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71 3 hours which halts daily activities should be reported to a healthcare provider. 3. Eat regular foods as tolerated. Do not eat food or drink liquids until a healthcare provider is consulted if pain occurs with nausea and vomiting, fever is present, or pain lasts longer than 3 hours. C. Pharmacotherapy. 1. Regardless of the cause, early use of analgesia before diagnosis is associated with improved diagnosis and treat-ment. a. Acetaminophen 1,000 g IV recommended regard-less of pain severity. b. IV narcotic analgesics can be added depending on the severity of pain. Morphine and opioids such as fentanyl can be considered in cases of acute abdomen. c. NSAIDs are effective for colic of biliary tract and ureteral stones. 2. If abdominal infections are suspected, blood cultures should be obtained and antimicrobial agents adminis-tered (within 1 hour in cases of suspected septic shock). Coverage of gram negative organisms is prudent. Broad antibiotic coverage is used if concern for sepsis. 3. When surgery is necessary, antimicrobial agents should be given just prior to the start of surgery (ideally within 30 minutes), which significantly reduces the risk of surgical site infection. D. Discharge instructions. 1. Surgery instructions depend on the procedure and surgeon preference, if applicable. 2. Stress the importance of follow-up, adherence to pre-scription instructions, and to call the healthcare provider with questions. Follow-Up A. If surgical intervention, perform as per surgeon instruc-tions. Consultation/Referral A. Consultation/referral depends on the underlying cause of acute abdomen. 1. Surgery. 2. Medicine (anticoagulation, antibiotic therapy man-agement). 3. Nutrition. 4. Oncology. 5. Gynecology. 6. Counseling. 7. Geriatric medicine. Special/Geriatric Considerations A. Consider that obesity distorts the abdominal examina-tion, making organ palpation or pelvic examination difficult. B. Men over 40 and women over 50 should warrant a high suspicion of cardiac origin of pain when epigastric. C. Geriatric patients have a higher incidence of: 1. Biliary disease. 2. Ischemic disease. 3. Mortality. 4. Hospital admission and complication rates. 5. Reliable history and physical can be difficult as find-ings in other age groups are often absent in the elderly. 6. Elderly individuals may have a vague or atypical pre-sentation of pain, varying in location, severity, and presentation of fever or nonspecific findings. Classical presentation of peritonitis rebound tenderness and local rigidity occurless often. Urinary tract infection (UTI) symptoms are more likely to be frequency, dysuria, or urgency. Abdom-inal pathology may advance to a dangerous point prior to symptom development, and altered mental status may play a role in assessment. 7. Aortic abdominal aneurysm (AAA) occurs most often in the elderly. Maintain a high level of suspicion in patients presenting with symptoms suggestive of renal colic or musculoskeletal back pain (approximately 65% of men older than 65 years have AAA). 8. Patients older than 65 have a 30% to 50% risk of gallstones and may not present with significant pain. 9. Fever and elevated white blood cell (WBC) count occur in less than half of elderly patients with diverticuli-tis. 10. Presence of peptic ulcer disease (PUD) is more com-mon in the elderly due to NSAIDs. The most common presenting symptom of PUD in the elderly is melena. Bibliography Banks, P. A., & Freeman, M. L. (2006). Practice guidelines in acute pancreatitis. The American Journal of Gastroenterology, 101, 2379-2400. Retrieved from https://journals. lww. com/ajg/Citation/ 2006/10000/Practice_Guidelines_in_Acute_Pancreatitis. 31. aspx Barkley, T. W., & Meyers, C. M. (2015). Practice considerations for adult-gerontology acute care nurse practitioners (Vol. 1, 2nd ed. ). West Holly-wood, CA: Barkley & Associates. Cartwright, S. L., & Knudson, M. P. (2008). Evaluation of acute abdominal pain in adults. American Family Physician, 77 (7), 971-978. Cash, J. C., Glass, C. A. (2017). Family practice guidelines (4th ed. ). New York, NY: Springer Publishing Company. Cervellin, G., Mora, R., Ticinesi, A., Meschi, T., Comelli, I., Catena, F., & Lippi, G. (2016). Epidemiology and outcomes of acute abdominal pain in a large urban emergency department: Retrospective analysis of 5,340 cases. Annals of Translational Medicine, 4 (19), 362. doi:10. 21037/atm. 2016. 09. 10 Chey, W. D., Leontiadis, G. I., Howden, C. W., & Moss, S. F. (2017). ACG clinical guideline: T reatment of Helicobacter pylori infection. American Journal of Gastroenterology, 112, 212-239. Retrieved from De Stigter, K. K., & Keating, D. P. (2009). Imaging update: Acute colonic diverticulitis. Clinics in Colon and Rectal Surgery, 22 (3), 147-155. doi:10. 1055/s-0029-1236158 El-Garem, H., Hamdy, E., Hamdy, S., El-Sayed, M., Elsharkawy, A., & Saleh, A. (2013). Use of the urinary trypsinogen-2 dipstick test in early diagnosis of pancreatitis after endoscopic retrograde cholangiopan-creatography (ERCP). Open Journal of Gastroenterology, 3, 289-294. doi:10. 4236/ojgas. 2013. 36049 Hardy, A., Butler, B., & Crandall, M. (2013). The evaluation of the acute abdomen. In L. Moore, K. T urner, & S. Todd (Eds. ), Common problems in acute care surgery (pp. 17-30). New York, NY: Springer Publishing Company. Kendal, J. L., & Moreira, M. (2018). Evaluation of the adult with abdom-inal pain in the emergency department. In J. Grayzel (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/evaluation-of-the-adult-with-abdominal-pain-in-the-emergency-department Macaluso, C. R., & Mc Namara, R. M. (2012). Evaluation and management of acute abdominal pain in the emergency department. International Journal of General Medicine, 5, 789-797. doi:10. 2147/IJGM. S25936 Malbrain, M. L., Chiumello, D., Pelosi, P., Bihari, D., Innes, R., Ranieri, V. M.,..., Gattinoni, L. (2005). Incidence and prognosis of intraab-dominal hypertension in a mixed population of critically ill patients: A multiple-center epidemiological study. Critical Care Medicine, 33 (2), 315-322. doi:10. 1097/01. CCM. 0000153408. 09806. 1B Mayumi, T., Yoshida, M., Tazuma, S., Furukawa, A., Nishii, O., Shigematsu, K., & Hirata, K. (2016). The practice guidelines for primary care of acute abdomen 2015. Japanese Journal of Radiology, 34, 80-115. doi:10. 1007/ s11604-015-0489-z Murray, H., Baakdah, H., Bardell, T., & T ulandi, T. (2005, October 11). Diagnosis and treatment of ectopic pregnancy. Canadian Medical Asso-ciation Journal, 173 (8), 905-912. doi:10. 1503/cmaj. 050222 Musson, R. E., Bickle, I., & Vijay, R. (2011). Gas patterns on plain abdomi-nal radiographs: A pictorial review. Journal of Postgraduate Medicine, 87, 274-287. doi:10. 1136/pgmj. 2009. 082396 Saccomano, S. J., & Ferrara, L. R. (2011). Evaluation acute abdomi-nal pain. The Nurse Practitioner, 38 (11), 46-53. doi:10. 1097/01. NPR. 0000433077. 14775. f1 Acute Abdomen https://journals. lww. com/ajg/Abstract/2017/02000/ACT_Clinical_ Guideline__T reatment_of_Helicobacter. 12. aspx

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72 Stollman, N., Smalley, W., & Hirano, I. (2015, December). Ameri-can Gastroenterological Association Institute guideline on the man-agement of acute diverticulitis. Gastroenterology, 149 (7), 1944-1949. doi:10. 1053/j. gastro. 2015. 10. 003 Vaidyanathan, S., Wadhawan, H., Welch, P., & El-Salamani, M. (2008). Ruptured abdominal aortic aneurysm masquerad-ing as isolated hip pain: An unusual presentation. Canadian Journal of Emergency Medicine, 10 (3), 251-254. doi:10. 1017/ S1481803500010186 Cirrhosis Robin Miller and Ann E. Burke Definition A. Cirrhosis: Chronic inflammation leading to fibrosis/ scarring of the liver. Causes of injury may be viral, autoim-mune, metabolic, drug induced, or due to alcohol and/ or fat. 1. Compensated: Mild portal hypertension but normal synthetic function (bilirubin, prothrombin time [PT], albumin, creatinine). 2. Decompensated: Progression of disease due to com-plications of portal hypertension which include variceal hemorrhage, hepatic encephalopathy, ascites, sponta-neous bacterial peritonitis (SBP). a. Median survival in decompensated cirrhosis is 6 months or less. b. MELD score—model to predict prognosis in patients with cirrhosis using the bilirubin, creatinine, and international normalized ratio (INR). Incidence A. Centers for Disease Control and Prevention (CDC) data from 2015 reports 3. 9 million people in the United States with cirrhosis (see Figure 4. 1). B. National Institutes of Health (NIH)—cirrhosis is the 12th leading cause of death in the United States. Pathogenesis A. Most common causes of cirrhosis in the United States include: Hepatitis C, alcoholic liver disease, and nonalcoholic fatty liver disease (NAFLD). These three causes account for 80% of patients on the liver transplant list during the years 2004 to 2013. B. Other less common causes include: Viral hepatitis B, hemochromatosis, autoimmune disease, primary biliary cholangitis, primary sclerosing cholangitis, drug-inducedliver injury (DILI), Wilson's disease, Alpha 1 antitrypsin defi-ciency, celiac disease, polycystic liver disease, sarcoidosis, and right-sided heart failure. Predisposing Factors A. Combination of more than one factor may lead to an accelerated progression to fibrosis. 1. Heavy alcohol use. 2. Viral hepatitis. 3. Fatty liver disease. 4. Genetic or metabolic disorder—that is, Wilson's, Alpha 1 antitrypsin, hemochromatosis. 5. Autoimmune disease. 6. Hepatic congestion, that is, heart failure. Subjective Data A. Common complaints/symptoms. 1. Nonspecific—anorexia, weight loss, fatigue. 2. Decompensated—jaundice, abdominal distension, confusion, g astrointestinal (GI) bleeding. B. Common/typical scenario. 1. May be incidental finding on lab tests or imaging without any symptoms. 2. There may be an acute presentation with hepatic decompensation. C. Family and social history. 1. Detailed history of alcohol use, drug use, sex partners, body piercings, tattoos. 2. Inquire about family history of autoimmune disease, liver disease, and liver cancer. 3. Living situation—household contacts with infected individuals with viral hepatitis. 4. Occupation—potential exposure to viral hepatitis. 5. T ravel—recent travel or country of origin. D. Review of systems. 1. May present with jaundice, pruritus, easy bruis-ing, hematemesis, melena, hematochezia, ascites, lower extremity edema, confusion, or sleep disturbances. Physical Examination A. May have no physical findings. B. In cirrhosis, one may see: 1. Jaundice. 2. Spider angiomata on the neck or chest. 3. Gynecomastia. 4. Ascites—associated with edema in the scrotum and/or lower extremities. 5. Firm nodular liver. 4. Gastrointestinal Guidelines Genetic/inherited Unknown Hepatitis B Hepatitis C Alcohol Nonalcoholic steatohepatitis FIGURE 4. 1 Common causes of cirrhosis. Source:Chaney,A. (2017). Fast Facts about GI and Liver Diseases for Nurses: What APRNs need to know in a nutshell. New York,NY:Springer Publishing Company.

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

73 6. Splenomegaly. 7. Palmar erythema. 8. Digital clubbing. 9. Asterixis: Bilateral flapping of dorsiflexed hands. 10. Low blood pressure. Diagnostic Tests A. Labs: Complete blood count (CBC), comprehensive metabolic panel (CMP), PT, INR. 1. All liver tests may be abnormal. In decompensated dis-ease, rising bilirubin, low albumin, elevated INR, and cre-atinine indicate synthetic dysfunction and progression of cirrhosis. 2. Thrombocytopenia: Related to portal hypertension and splenomegaly; platelets less than 150/L. 3. Anemia: Due to GI blood loss, chronic disease, renal disease, bone marrow suppression, or hemolysis. 4. Leukopenia: Secondary to hypersplenism. 5. Hyponatremia: Inability to excrete free water. B. Imaging. 1. Ultrasound (US): Shrunken nodular liver with or without splenomegaly/ascites. 2. US with Doppler: Portal hypertension, portal vein thrombosis, or collateral flow may be present. 3. MRI: Can identify cirrhosis, hepatocellular carci-noma, or other liver masses. It is the preferred study for cancer surveillance and staging. C. Liver biopsy. 1. It is the gold standard to diagnose or identify the cause of cirrhosis. 2. Fibroscan is a noninvasive tool to stage fibrosis. Differential Diagnosis A. Cirrhosis related to chronic hepatic inflammation due to: 1. Viral: Hepatitis A, B, C. 2. Alcohol. 3. Fatty liver. 4. Autoimmune: Autoimmune hepatitis, celiac, p rimary biliary cholangitis (PBC), p rimary sclerosing cholangitis (PSC). 5. Genetic/metabolic: Wilson's, hemochromatosis, Alpha 1 antitrypsin, polycystic liver disease. B. Extrahepatic causes of cirrhosis. 1. Congestive heart failure. 2. Sarcoidosis. 3. Budd Chiari. 4. Portal and splenic vein thrombosis. Evaluation and Management Plan A. General plan. 1. See Figure 4. 2. 2. Ascites and SBP. a. Ascites: Abdominal accumulation of fluid due to high portal pressures. It is typically treated with sodium restriction and diuretics. Refractory cases require paracentesis or transjugular intrahepatic por-tosystemic shunt (TIPS). b. SBP is an infection of the ascitic fluid unrelated to perforated viscus. Patients with high MELD scores are at most risk, and failure to identify the diagnosis can lead to refractory sepsis. Cultures will show high absolute polymorphonuclear leukocyte counts greater than 250 cells/mm. 3. Encephalopathy. a. Impairment in cognitive and neuromuscular func-tion associated with decompensated cirrhosis. b. Disturbance in sleep pattern, insomnia, and hypersomnia are common early features before more typical levels of consciousness alterations. c. Manifestations range from mild confusion to severe somnolence and coma. d. T reatment is based on underlying cause/trigger (e. g., GI bleeding, infection, dehydration, medication noncompliance). 4. GI bleeding. a. Acute variceal hemorrhage is the result of por-tal hypertension and usually occurs in the upper GI tracts. Other causes of GI bleeding in patients with liver disease include peptic ulcers, portal hyperten-sive gastropathy, and gastric antral vascular ectasias (GAVE). b. Bleeding presents as hematemesis and/or melena. c. Plan: Stabilization of patient. i. Blood and blood products: Goal hemoglobin of 7 to 9 g/d L. ii. Restoration of intravascular volume: I ntravenous (IV) fluids. iii. T reatment with endoscopic evaluation and interventions to stop the bleeding. Epinephrine, banding, Argon plasma coagulation, and clipping may be used alone or in combination. iv. Patients at high risk of rebleeding may be con-sidered a candidate for TIPS. v. Bleeding that is refractory to traditional mea-sures may require esophageal tamponade. Short-term only. vi. Prevention and management of complications (e. g., sepsis, renal failure, aspiration pneumonia) desired. 5. Hepatorenal syndrome (HRS). a. Chronic or acute kidney injury related to advanced hepatic failure and portal hypertension. Must exclude other causes (e. g., shock, nephrotoxic drugs, dehydra-tion). Can be precipitated by an acute insult such as SBP or GI bleeding. Without therapy, most patients with HRS die within weeks of the onset of renal impairment. i. Type I HRS: More severe with rapid onset and poor prognosis. May reverse if cause of hep-atic disease is treatable, that is, alcohol cessation, antiviral therapy. ii. Type II HRS: Less rapid progression. b. Plan. i. Correction of underlying hepatic cause, if able. ii. Medications to raise the mean arterial pressure and improve renal perfusion. iii. Monitor fluid status closely. iv. Dialysis as a bridge to transplant or renal recovery. v. May need dual renal/liver transplant. B. Patient/family teaching points. 1. Ascites and SBP. a. Ascitic fluid may reaccumulate despite diuretic therapy and will likely require multiple paracente-ses to manage fluids and mitigate side effects such as shortness of breath and edema. b. Daily weights. c. 2,000 mg sodium restricted diet. d. Laboratory monitoring of electrolytes and renal function for safe dosing of diuretics. e. Report any fever, abdominal pain, or altered men-tal status that may indicate SBP. Cirrhosis

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

74 Compensated Viral/Autoimmune Yes No Treat symptoms Refer to GI/hepatologist for liver biopsy/consider antiviral or immunosuppressive treatment Abnormal liver chemistries History, physical exam, routine blood tests, ultrasound Evidence of cirrhosis Decompensated (ascites, variceal bleeding, encephalopathy) Refer to hepatologist/transplant center for evaluation FIGURE 4. 2 Comprehensivemanagement of patients with cirrhosis. f. Prophylactic antibiotics for SBP is lifelong therapy or until transplant. 2. Encephalopathy. a. Review with family/caregiver to be alert for con-fusion, memory lapses, mood changes, speech abnor-malities, slowed movements, gait disturbance, or day/night reversal. b. Clearance of neurotoxins such as ammonia is important. This is primarily achieved through the stool. Medications for treatment target that means of clearance through promotion of several bowel move-ments daily. 3. GI bleeding. a. High risk of recurrent bleeding within 6 weeks of initial episode. b. If banding was performed, expect a sore throat for a few days. Soft diet recommended. c. Review signs of bleeding: Vomiting blood or coffee ground emesis, black tarry or maroon-colored stools, weakness, lightheadedness. d. If TIPS was placed, may see worsening encephalopathy. e. Avoid NSAIDs. 4. HRS. a. Avoid nephrotoxic drugs. b. Stop diuretic therapy. c. May require dialysis while awaiting transplant. d. Teach SQ injections for home therapy (e. g., octreotide). C. Pharmacotherapy. 1. Ascites and SBP. a. Combination diuretics, usually Lasix and Aldac-tone, to balance potassium. Diuretic starting dose is 20 mg Lasix with 50 mg Aldactone, which then increases using the same ratio. b. SBP is typically treated with third generation cephalosporin such as ceftriaxone or cefotaxime, typi-cally for 5 days. At discharge, switch to long-term pro-phylaxis using Cipro 500 mg po daily or Bactrim DS one tablet daily. 2. Encephalopathy. a. Lactulose: Synthetic disaccharide that is a mainstay of therapy and causes a purging of ammonia throughthe bowels. This has been shown to improve symp-toms in 70% to 80% of patients. Typical dose is 30 to 45 m L orally, two to four times per day. Dose is titrated to achieve two to three bowel movements per day. If comatose, it may be given as an enema. b. Xifaxan: Also known as rifaximin. A non-absorbable antibiotic that reduces the risk of hepatic encephalopathy recurrence. This is usually added to lactulose therapy or for patients who are intolerant of lactulose side effects. Dose is usually 550 mg orally twice daily. c. Benzodiazepines are contraindicated with cirrhotic patients who have encephalopathy. 3. GI bleeding. a. Vasoactive medication: Initiated at the time of presentation to decrease portal blood flow, that is, octreotide. Usually given 2 to 5 days. b. Proton pump inhibitor. c. Prophylactic antibiotics: Broad spectrum antibi-otics such as ceftriaxone 1 g IV daily for 7 days to prevent bacterial infections, which can occur in 20% of hospitalized cirrhotic patients (e. g., u rinary tract infection [UTI], bacteremia, respiratory infections). d. A nonselective beta blocker is often prescribed to reduce portal pressures for prevention of rebleeding after vasoactive medication has been discontinued. Titrate dose to a heart rate of 60 bpm. Propranolol or nadolol are commonly used. 4. HRS. a. Combined therapy with the goal to improve renal and systemic hemodynamics. b. Midodrine: Selective Alpha 1 adrenergic agonist; 7. 5 to 15 mg orally three times a day. c. Octreotide: Somatostatin analog; IV infusion: 50 mcg/hr or SQ 100 mcg three times a day. d. Albumin: Volume expander; IV bolus: 1 g per kg of body weight per day. D. Discharge instructions. 1. Ascites and SBP. a. Low sodium diet. b. Take diuretics as prescribed. c. Lab testing as recommended. d. Follow-up with hepatologist. 4. Gastrointestinal Guidelines

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

75 e. Call office or report to emergency department (ED) with abdominal pain, distension, shortness of breath, fever, or altered mental status. 2. Encephalopathy. a. Medication compliance is reinforced. b. Encourage two to three bowel movements daily for control of encephalopathy. c. Call the office or report to the ER with worsening confusion, fever, slurred speech, or lethargy. d. Follow-up with hepatologist. 3. GI bleeding. a. If esophageal band ligation was performed, will need a repeat e sophagogastroduodenoscopy (EGD) every 4 weeks until eradicated. b. Medication compliance with beta blockers. c. Monitor CBC. d. Follow-up visit with hepatology. 4. HRS. a. Compliance with medical regimen of dialysis and medications. b. Close monitoring of electrolytes and renal func-tion. c. Follow-up with hepatology. Follow-Up A. Follow-up with hepatology. B. Patients will need hepatocellular carcinoma and esophageal varices screening. 1. Imaging every 6 months: Alternating US and MRI of the abdomen. 2. Variceal surveillance: EGD every 2 to 3 years. C. Labs every 3 months: CBC, CMP, INR, alpha fetoprotein (AFP). D. Will need vaccination for hepatitis A and B if not immune. Consultation/Referral A. MELD score of 10 or higher will be referred to a trans-plant center. B. If alcohol-related cirrhosis, must complete a substance abuse program. C. Social services may need to help with insurance coverage if transplant is indicated. Special/Geriatric Considerations A. T ransplant eligibility varies between centers, but usually age greater than 70 is contraindicated. B. Cirrhosis is considered a high risk for abdominal, cardiac, or orthopedic surgeries due to high portal pressures and coag-ulopathies. It is usually determined by the surgeon on a case-by-case basis. Bibliography Bajaj, J. S., & Sanyal, A. J. (2017, May 5). Methods to achieve hemostasis in patients with acute variceal hemorrhage. In A. C. T ravis (Ed. ), Up To-Date. Retrieved from https://www. uptodate. com/contents/methods-to-achieve-hemostasis-in-patients-with-acute-variceal-hemorrhage Centers for Disease Control and Prevention. (2016, October 6). Chronic liver disease and cirrhosis. Retrieved from https://www. cdc. gov/nchs/ fastats/liver-disease. htm Chaney, A. (2016). Fast facts about GI and liver diseases for nurses: What APRNs need to know in a nutshell, New York, NY: Springer Publishing Company. Ferenci, P. (2019, February 5 ). Hepatic encephalopathy in adults: T reat-ment. In K. M. Robson (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/hepatic-encephalopathy-in-adults-treatment. Garcia-Tsao, G., Abraldes, J. G., Berzigotti, A., & Bosch, J. (2017). Por-tal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, andmanagement: 2016 practice guidance by the American Association for the study of liver diseases. Hepatology, 65 (1), 310-335. doi:10. 1002/ hep. 28906 Goldberg, E., & Chopra, S. (2018, September 5). Cirrhosis in adults: Etiologies, clinical manifestations, and diagnosis. In K. M. Robson (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/ cirrhosis-in-adults-etiologies-clinical-manifestations-and-diagnosis Goldberg, E., & Chopra, S. (2018, June 14). Cirrhosis in adults: Overview of complications, general management, and complications. In K. M. Robson (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/cirrhosis-in-adults-overview-of-complications-general-management-and-prognosis Runyon, B. A. (2018, September 21). Spontaneous bacterial peri-tonitis in adults: T reatment and prophylaxis. In K. M. Robson (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/ spontaneous-bacterial-peritonitis-in-adults-treatment-and-prophylaxis Runyon, B. A. (2018, February 13). Hepatorenal syndrome. In J. P. Forman (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/ hepatorenal-syndrome Sanyal, A. J. (2019, February 4). General principles of the man-agement of variceal hemorrhage. In K. M. Robson (Ed. ), Up To-Date. Retrieved from https://www. uptodate. com/contents/general-principles-of-the-management-of-variceal-hemorrhage Singleton, J. K., Di Gregorio, R. D., Green-Hernandez, C., Holzemer, S. P., Faber, E. S., Ferrara, L. R., & Slyer, J. T. (2015). Primary care: An inter-professional perspective (2nd ed. ). New York, NY: Springer Publishing Company. Such, J., & Runyon, B. A. (2018, August 13). Ascites in adults with cirrhosis: Initial therapy. In K. M. Robson (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/ascites-in-adults-with-cirrhosis-initial-therapy Drug-Induced Liver Injury Catherine Harris Definition A. Liver injury due to prescription medications, over-the-counter (OTC) medications, and herbal supplements. Incidence A. Estimated annual incidence is 10% of all cases of acute hepatitis; the most common cause of acute liver failure in the United States. Pathogenesis A. Over 1,000 medications and herbal products have been implicated in the development of drug-induced liver injury (DILI). B. Most common drug in acute DILI in the United States is acetaminophen. Predisposing Factors A. Women—more susceptible due to smaller size. B. Alcohol abuse. C. Malnutrition. Subjective Data A. Common complaints/symptoms. 1. Itching. 2. Jaundice. 3. Malaise. 4. Low grade fever. 5. Nausea and vomiting. 6. Right upper quadrant (RUQ) pain. 7. Dark urine. 8. Clay-colored stools. B. Common/typical scenario. 1. Patients may be asymptomatic with incidental finding of elevated liver tests. Drug-Induced Liver Injury

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

76 2. Ask patients about recent antibiotic use, herbal sup-plements, weight loss products, or OTC medications. 3. Thorough medication reconciliation. C. Family and social history. 1. Be culturally sensitive to nontraditional medicine and the patient's use of herbal products. 2. Alcohol use. D. Review of systems. 1. Same as common complaints. 2. Rash. 3. Pruritus. 4. Weight loss. Physical Examination A. Depending on the severity, no physical findings or the following: B. Scleral icterus. C. Generalized jaundice. D. Skin excoriations from scratching. E. RUQ tenderness. F. Hepatomegaly. Diagnostic Tests A. Lab workup includes: Complete blood count (CBC), comprehensive metabolic panel (CMP), international nor-malized ratio (INR), hepatitis A, B, and C serologies, antin-uclear antibody (ANA), antimitochondrial antibody (AMA), anti smooth muscle antibody (ASMA), liver kidney microso-mal type 1 (LKM1), ceruloplasmin (Wilson's disease), iron, ferritin (hemochromatosis), Alpha 1 antitrypsin. B. Hepatic function panel will show cholestatic, hepatocel-lular, or mixed pattern of injury. C. Imaging: Ultrasound (US), MRI. D. Liver biopsy: If labs and imaging are nondiagnostic, biopsy may be considered. Differential Diagnosis A. Acute viral hepatitis. B. Alcoholic liver disease. C. Nonalcoholic fatty liver disease. D. Autoimmune hepatitis. E. Wilson's disease. F. Biliary obstruction: P rimary biliary cholangitis (PBC) or p rimary sclerosing cholangitis (PSC). Evaluation and Management Plan A. General plan. 1. Obtaining a careful drug history and ruling out other causes. 2. Monitoring for improvement of symptoms and sero-logic markers after stopping the offending drug. B. Patient/family teaching points. 1. Regular liver tests at recommended interval to moni-tor for improvement. 2. Avoid alcohol. 3. Normalization of liver tests may take several months. 4. Do not start any new medications or OTC supple-ments. 5. Teach signs and symptoms associated with hepatic injury. 6. Follow-up with g astrointestinal (GI)/hepatology. C. Pharmacotherapy. 1. Primary treatment is withdrawal of the offending drug. 2. Recovery will occur in the majority of patients once the medication is stopped. 3. In acetaminophen toxicity, treatment is N-acetylcysteine. D. Discharge instructions. 1. Monitor labs. 2. Follow-up with gastroenterologist or hepatologist. Follow-Up A. Gastroenterologist/hepatologist should be monitoring labs and seeing the patient on a regular basis. Consultation/Referral A. May refer for liver transplant if there is no recovery of liver function. Special/Geriatric Considerations A. T reatment of older patients with liver disease may require different or longer interventions. B. Maintain pharmacokinetic precautions in geriatric patients. Bibliography Goldberg, E., & Chopra, S. (2018, June 14). Cirrhosis in adults: Overview of complications, general management, and com-plications. In K. M. Robson (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/cirrhosis-in-adults-overview-of-complicationsgeneral-management-and-prognosis Larson, A. M. (2017, July 10). Drug-induced liver injury. Retrieved from https://www. uptodate. com/contents/drug-induced-liver-injury Gastroesophageal Reflux Disease Catherine Harris Definition A. Gastric reflux that irritates and erodes the lining of the esophagus. Incidence A. 60% of adult population experience gastroesophageal reflux d isease (GERD) of some type. B. Affects up to 10 million adults in the United States on a daily basis. C. Many people experience heartburn two to three times per week. Pathogenesis A. The esophagus contracts to propel food into the stomach via peristalsis. B. A circular ring of muscle called the lower esophageal sphincter (LES) relaxes to allow food to enter the stomach, then contracts to avoid regurgitation of food or acid into the esophagus. C. When the LES is weak due to stomach distention, acid can wash up into the esophagus. D. Most episodes of heartburn occur shortly after meals. E. Functional or mechanical problem of LES is the most common cause of GERD. F. T ransient relaxation of LES can be caused by food (coffee, alcohol, chocolate, meals heavy in fat), medications (beta ago-nists, nitrates, calcium channel blockers, anticholinergics), hormones, and nicotine. Predisposing Factors A. Obesity. B. Smoking. C. Pregnancy. 4. Gastrointestinal Guidelines

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77 D. Certain medications. E. Peptic ulcers. F. Hiatal hernia. G. Diabetes (due to associated gastroparesis). H. Asthma (chronic, continuous coughing may contribute). I. Connective tissue disorders. J. Zollinger-Ellison syndrome. Subjective Data A. Common complaints/symptoms. 1. Heartburn or burning sensation after eating. 2. Nausea or vomiting. 3. Difficulty or pain when swallowing. 4. Regurgitation. 5. Hoarseness from irritation of the vocal cords. 6. Difficulty breathing. B. Common/typical scenario. 1. Most patients will complain of burning sensation or discomfort that occurs after eating or when lying supine or bending over. C. Family and social history. 1. Smoking. 2. Lifestyle. 3. Diet. D. Review of systems. 1. Head, ear, eyes, nose, and throat (HEENT): Laryngi-tis, dysphagia, hoarseness, teeth decay, ear infections. 2. Respiratory: Chronic cough, new or worsening asthma. 3. Cardiac: Burning sensations behind breastbone. Physical Examination A. HEENT: Evaluate throat for redness or irritation, look for enamel decay of the teeth, evaluate ears for possible infections if warranted. B. Respiratory: Listen for wheezing or decreased lung sounds. C. Cardiac: Evaluate for palpitations, murmurs, or a rapidor slow heart rate. Diagnostic Tests A. Diagnosis of GERD can be made upon symptoms and response to treatment alone. B. If a patient presents with chest pain or the diagnosis of GERD is not clear, then one or more of the following tests may be ordered. 1. Endoscopy: Evaluate for damage to the lining of the esophagus, stomach, and small intestine. 2. 24-hour esophageal p H study: Measure frequency of acid reflux. 3. Esophageal manometry: Evaluate functioning of LES. Differential Diagnosis A. Gastritis. B. Esophagitis. C. Irritable bowel syndrome. D. Peptic ulcer disease. E. Hiatal hernia. F. Gallstones. G. Coronary atherosclerosis. Evaluation and Management Plan A. General plan. 1. Stepwise approach. a. Control symptoms. b. Heal esophagitis. c. Prevent recurrence and complications of GERD. 2. Start with lifestyle modification and control of gastric acid secretion with medical therapy. a. Weight loss. b. Eat small, frequent meals. c. Avoid foods that trigger reflux such as alcohol, chocolate, tomato-based products, caffeine. d. Avoid lying down for 3 hours after a meal. e. Avoid bending or stooping for 3 hours after a meal. 3. Surgery may be indicated in the following cases. a. Symptoms not controlled with proton pump inhibitor (PPI) therapy. b. Presence of Barrett esophagus. c. Extraesophageal symptoms. d. Young patients. e. Poor compliance. f. Patients with cardiac conduction defects. B. Patient/family teaching points. 1. Stop smoking. 2. Reduce or eliminate alcohol intake. 3. Weight loss will improve symptoms. 4. Avoid tight fitting clothing. 5. Chew gum or use oral lozenges to increase saliva pro-duction. 6. If your symptoms are not controlled or last a long time, report this to your provider. 7. Chest pain can also be cardiac in nature; if the pain radiates to the jaw, left shoulder, or arm, be sure to seek medical attention immediately. C. Pharmacotherapy. 1. Antacids can be taken after each meal and before bed-time. 2. H2 Receptor antagonists: First-line agent for mild to moderate symptoms. 3. Proton pump inhibitors. a. Most powerful medications. b. Most commonly reported adverse reactions. i. Sore throat. ii. Flatulence. iii. Constipation. c. Superior to H2 receptor antagonists. 4. Prokinetics. a. Improve motility of esophagus. b. Somewhat effective in patients only with mild symptoms. c. May have long-term serious or potentially fatal complications. D. Discharge instructions. 1. Follow patient teaching points upon discharge for best results. 2. Lifestyle changes and medical therapy should resolve GERD symptoms within 4 weeks and esophagitis in 8 weeks. 3. Complications of untreated GERD include: a. Ulcers that can cause bleeding. b. Strictures of esophagus. c. Lung and throat problems. d. Barrett's esophagus. e. Esophageal cancer. Follow-Up A. As per your provider or if symptoms are not controlled. Consultation/Referral A. If symptoms are not controlled with one PPI. B. If symptoms do not confirm diagnosis or another prob-lem is potentially causing symptoms. Gastroesophageal Reflux Disease

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78 Special/Geriatric Considerations A. GERD can occur in pregnancy because of normal weight gain and hormone changes that allow muscles in the esopha-gus to relax more easily and frequently. B. As the uterus expands, particularly in the third trimester, pressure builds up in the stomach, which may cause food and acid to regurgitate into the esophagus. 1. Antacids are first-line agents in pregnancy but may not be sufficient. 2. Histamine blockers and proton pump inhibitors are also approved for treatment of GERD during pregnancy. Bibliography El-Serag, H. B. (2007). Time trends of gastroesophageal reflux disease: A systematic review. Clinical Gastroenterology and Hepatology, 5 (1), 17-26. doi:10. 1016/j. cgh. 2006. 09. 016 Giannini, E. G., Zentilin, P., Dulbecco, P., Vigneri, S., Scarlata, P., & Savarino, V. (2008). Management strategy for patients with gastroe-sophageal reflux disease: A comparison between empirical treatment with esomeprazole and endoscopy-oriented treatment. American Journal of Gastroenterology, 103 (2), 267-275. Retrieved from https://journals. lww. com/ajg/Abstract/2008/02000/Management_Strategy_for_Patients _With. 4. aspx Grant, A. M., Cotton, S. C., Boachie, C., Ramsay, C. R., Krukowski, Z. H., Heading, R. C., & Campbell, M. K. (2013). Minimal access surgery compared with medical management for gastro-oesophageal reflux dis-ease: Five year follow-up of a randomised controlled trial (REFLUX). BMJ, 346, f1908. doi:10. 1136/bmj. f1908 Hampel, H., Abraham, N. S., & El-Serag, H. B. (2005). Meta-analysis: Obe-sity and the risk for gastroesophageal reflux disease and its complications. Annals of Internal Medicine, 143 (3), 199-211. doi:10. 7326/0003-4819-143-3-200508020-00006 Oor, J. E., Roks, D. J., Ünlü, C., & Hazebroek, E. J. (2016). Laparoscopic sleeve gastrectomy and gastroesophageal reflux disease: A systematic review and meta-analysis. American Journal of Surgery, 211(1), 250-267. doi:10. 1016/j. amjsurg. 2015. 05. 031 Gastrointestinal Bleeding Catherine Harris Definition A. Gastrointestinal bleeding (GIB) is a symptom of a disease process or condition in the gastrointestinal (GI) tract. B. Bleeding that occurs in any part of the GI tract. C. Upper GI tract includes esophagus and stomach. D. Lower GI tract includes structures distal to the ligament of T reitz including small and large intestines, rectum, and anus. Incidence A. Upper gastrointestinal bleeding (UGIB). 1. Most common with approximately 100 cases per 100,000 population. 2. Mortality rates 6% to 10%. 3. Associated with comorbid illness. a. Peptic ulcer disease is most common cause of UGIB in up to 40% of cases. b. Mallory-Weiss tears account for 15% of UGIB cases. c. Caused by forceful vomiting, retching, coughing, or straining. d. Gastritis. e. Caused by acute stress, acute renal failure, and sepsis. B. Lower gastrointestinal bleeding (LGIB). 1. Annual incidence 20 to 27 cases per 100,000 popula-tion. 2. May be significantly underreported. 3. Four main types of LGIB. a. Anatomic (diverticulosis, hemorrhoids)—most common type, accounting for approximately 60% of cases. b. Vascular (ischemia, radiation-induced). c. Neoplasms account for approximately 12. 7% of cases. d. Inflammatory (infectious versus noninfectious such as Crohn's disease). 4. Segmented into significance of bleeding. a. Occult bleeding. b. Moderate bleeding. c. Massive bleeding. Pathogenesis A. UGIB. 1. Variceal hemorrhage—increases in blood pressure in portal vein system, usually from cirrhosis, can create enlarged veins (varices) which are prone to bleeding. 2. Nonvariceal hemorrhage—process occurs from either arterial hemorrhage, typically from ulcers, deep mucosal tears, or from low pressure venous hemorrhage from telangiectasias or arteriovenous malformations. B. LGIB. 1. The most common cause of LGIB is diverticulosis. Bleeding can occur in the absence of diverticulitis. Bleed-ing occurs when segmental weakness of the lumen of the bowel predisposes the artery to rupture. Bleeding can be massive and life-threatening. 2. Other forms of LGIB occur from ulceration or ero-sion of the mucosa, inflammatory changes that predis-pose the GI tract to mucosal friability, fissures, and fistulas that develop from infectious processes, radiation exposure, and vascular malformations. Predisposing Factors A. Occurs more frequently in men. B. Older age. C. Nonsteroidal anti-inflammatory drug (NSAID) use. D. Admission to ICU for sepsis, trauma, or ventilatory support. Subjective Data A. Common complaints/symptoms. 1. UGIB: Presence of bleeding from vomiting, black tarry stools, dyspepsia. 2. LGIB: Presence of bright red blood in stool, may present with or without abdominal pain. B. Common/typical scenario. 1. UGIB: Patients typically complain of presence of vomiting blood or passing black malodorous stool. They may present with weakness, dizziness, and possibly syncope. 2. LGIB: Depends on the amount of bleeding. a. Minor bleeding—may complain of some rectal bleeding, diarrhea, and abdominal pain. b. Moderate and massive bleeding—may present with signs and symptoms of shock including dehy-dration, hypotension, tachycardia, and fever. C. Family and social history. 1. Ask about family history of colon cancer. 2. Smoking or alcohol use. 3. NSAID use. 4. Gastrointestinal Guidelines

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79 D. Review of systems. 1. Constitutional: Dizziness or episodes of lightheaded-ness, may appear exhausted. 2. GI: Ask about color and consistency of stools, any pain during defecation, any associated nausea or vomit-ing, red streaking on toilet paper, abdominal pain sever-ity and location, presence of heartburn, or unintentional weight loss. Physical Examination A. Head, ear, eyes, nose, and throat (HEENT): Assess oropharynx and nasopharynx for sources of bleeding. B. GI: May have benign abdominal examination; check for hematemesis and melena, or rectal exam for bleeding. C. Cardiovascular: Hemodynamic instability in massive hemorrhage; assess for signs and symptoms of shock, or orthostatic hypotension. Diagnostic Tests A. Lab studies. 1. Complete blood count (CBC), basic metabolic panel (BMP), coagulation studies. 2. In suspected UGIB, check calcium level for increased levels, which can be associated with excessive acid secre-tion. 3. Test for Helicobacter pylori in UGIB. B. Imaging studies. 1. UGIB. a. Endoscopy to find source of bleeding. b. Chest radiography to exclude other causes of symptoms. c. CT may be used to find unusual causes of bleeding. d. Ultrasound can be useful to evaluate liver disease that may be associated with bleeding. e. Angiography offered when bleeding persists and a clear source has not been found or if an arterial UGIB does not respond to endoscopic management. 2. LGIB. a. Colonoscopy: Initial approach starts with colonoscopy unless the patient is unstable and offers ability to treat during diagnostic stage. b. Esophagogastroduodenoscopy (EGD): Can rule out UGIB. c. CT: Useful when endoscopy is limited. d. Computed tomography angiography (CTA): Has high positive predictive value for LGIB and often used as a first-line diagnostic study. e. Angiography: Useful in active bleeding where colonoscopy cannot be done or fails to identify a source. Also can be used emergently in massive ongo-ing LGIB. Differential Diagnosis A. Determine location in UGIB. 1. Esophagus. a. Barrett esophagus. b. Esophageal cancer. c. Esophageal varices. d. Esophagitis. 2. Stomach. a. Gastric cancer. b. Gastric outlet obstruction. c. Gastric ulcers. d. Peptic ulcer disease. B. Consider process in LGIB. 1. Anatomic: Diverticulosis. 2. Vascular. a. Arteriovenous malformations. b. Angiodysplasia. c. Vasculitides. 3. Neoplasm. a. Colon cancer. b. Polyps. 4. Inflammation. a. Inflammatory bowel disease. b. Colitis. c. Radiation induced. d. Ulceration. e. Abscess. f. Fistulas. g. Fissures. Evaluation and Management Plan A. General plan. 1. UGIB. a. Stabilize and fluid resuscitate patient by correcting states of shock and bleeding abnormalities. b. Insert nasogastric tube for lavage to determine if GIB is upper or lower. LGIB will result in bile aspirate but no bleeding. c. Risk assessment using predictive models. i. Rockall score. ii. Blatchford score. iii. AIMS65. d. Perform EGD to identify and treat source of bleeding. i. Contraindicated in uncooperative or unstable patients. ii. Consider surgical intervention if: 1)T wo attempts at endoscopic control are unsuccessful. 2)Failure of medical therapy or persistent bleeding. 3)Bleeding from perforation, obstruction, or malignancy. 4)Prolonged bleeding. e. Start proton pump inhibitors. f. Assess for complications of treatment with EGD. i. EGD can cause: 1)Aspiration pneumonia. 2)Perforation. 3)Arrhythmias. ii. Surgery. 1)Poor wound healing. 2)Rebleeding. 3)Ileus. 4)Sepsis. 2. LGIB. a. Stabilize and resuscitate patients with active bleed-ing and signs of hemodynamic instability. b. Insert nasogastric tube to rule out UGIB source. c. Risk assessment. d. Localize bleeding site. i. If stable colonoscopy should be performed for diagnosis and treatment. ii. Endoscopic hemostasis therapy can control active bleeding. iii. Angiography for embolization of source and to temporize bleeding with vasopressin infusion if needed. iv. Emergent surgery may be required if: 1)Medical and endoscopic therapy is unsuc-cessful. Gastrointestinal Bleeding

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80 2)Persistent hemodynamic instability with active bleeding. 3)Persistent, recurrent bleeding. 4)T ransfusion of more than four units of packed red blood cells in a 24-hour period with active or recurrent bleeding. e. Supportive measures. i. Fluid resuscitation. ii. Blood transfusions for hemoglobin less than 7 g/d L. iii. Management of coagulopathies or antiplatelet agents: Consider transfusing with fresh frozen plasma and platelets if prolonged prothrombin time with international normalized ratio greater than 1. 5 or low platelet count less than 50,000/L. f. Assess for complications of treatment of LGIB. i. Reactions to multiple blood transfusion. ii. Bleeding from surgery. iii. Sepsis. iv. Poor wound healing from surgery. v. Anastomotic strictures, incisional hernias after surgery. B. Patient/family teaching points. 1. UGIB. a. Lower the risk of UGIB by avoiding NSAIDs as much as possible. b. Anticoagulants and antiplatelet agents must be ordered in consultation with GI provider. The risk and benefits must be weighed in deciding which med-ications are necessary. c. Advise patient to take medications as prescribed for the entire duration. d. Follow-up with the necessary tests as determined by provider. e. If H. pylori positive, will need eradication therapy and confirmation of eradication in 4 to 6 weeks with a stool sample. f. Long-term acid suppression therapy is needed. 2. LGIB. a. If symptoms recur may need further workup. LGIB can be difficult to isolate in some cases. b. Avoid NSAIDs and aspirin use. c. Diet and lifestyle may prevent progression of cer-tain causes of LGIB. C. Pharmacotherapy. 1. UGIB. a. Proton pump inhibitors (PPIs): Reduce acid secre-tion. i. Inpatient start intravenous (IV) high dose therapy. 1)Bolus followed by twice daily injections. 2)Continuous infusions of PPIs have failed to show a difference in clinically relevant end-points. b. Prokinetics to promote gastric emptying; espe-cially useful to improve gastric visualization prior to endoscopy. i. Erythromycin. ii. Metoclopramide. c. Vasoactive medications treat variceal bleeding, may be used as adjunctive therapy in select cases of nonvariceal UGIB. i. Octreotide: IV bolus followed by a continuous infusion. d. Prophylactic antibiotics are used in patients with cirrhosis due to the high rate of bacterial infections associated with hospitalized events of UGIB. 2. LGIB. a. There are no medications specifically to treat LGIB. Medications used are supportive and depend heavily on identifying and treating the source of bleeding. D. Discharge instructions. 1. UGIB. a. Depending on the cause of UGIB, certain medica-tions will be prescribed. b. Follow-up with gastroenterologist within 2 weeks. c. Endoscopy typically repeated with ulcers to docu-ment healing. d. If symptoms recur, patient should call the office immediately. e. Diet and lifestyle changes. 2. LGIB. a. Will need to follow-up within 2 weeks. b. Start psyllium seed. c. Encourage fluids. d. Diet and lifestyle changes. e. May need repeat colonoscopy if recurrence of symptoms. Follow-Up A. Follow-up with gastroenterologist within 2 weeks of leav-ing the hospital. Consultation/Referral A. GIB is a sign of an underlying condition. Refer to gas-troenterologist for full workup. B. General surgery should be consulted as needed and emer-gently if there is massive bleeding. C. Patients who are hemodynamically unstable will require monitoring in the ICU. Special/Geriatric Considerations A. Older patients may present with minimal symptoms typ-ically in LGIB. Bibliography Cirocchi, R., Grassi, V., Cavaliere, D., Renzi, C., Tabola, R., Poli, G.,... Fingerhut, A. (2015, November). New trends in acute management of colonic diverticular bleeding: A systematic review. Medicine, 94 (44), e1710. doi:10. 1097/MD. 0000000000001710 Fujishiro, M., Iguchi, M., Kakushima, N., Kato, M., Sakata, Y., Hoteya, S.,... Fujimoto, K. (2016, February 22). Guidelines for endoscopic management of non-variceal upper gastrointestinal bleeding. Digestive Endoscopy, 28 (4), 363-378. doi:10. 1111/den. 12639 Jairath, V., & Desborough, M. J. (2015, December 28). Modern-day man-agement of upper gastrointestinal haemorrhage. Transfusion Medicine, 25(6), 351-357. doi:10. 1111/tme. 12266 Monteiro, S., Gonçalves, T. C., Magalhães, J., & Cotter, J. (2016, February 15). Upper gastrointestinal bleeding risk scores: Who, when and why? World Journal of Gastrointestinal Pathophysiology, 7 (1), 86-96. doi:10. 4291/wjgp. v7. i1. 86 Qayed, E., Dagar, G., & Nanchal, R. S. (2016, April). Lower gastrointestinal hemorrhage. Critical Care Clinics, 32 (2), 241-254. doi:10. 1016/j. ccc. 2015. 12. 004 Strate, L. L., & Gralnek, I. M. (2016, April). ACG clinical guideline: Management of patients with acute lower gastrointestinal bleeding. American Journal of Gastroenterology, 111 (4), 459-474. Retrieved from https://journals. lww. com/ajg/Abstract/2016/04000/ACG_Clinical_ Guideline__Management_of_Patients. 14. aspx Villanueva, C., Colomo, A., Bosch, A., Concepción, M., Hernandez-Gea, V., Aracil, C.,... Guarner, C. (2013, January 3). T ransfusion strategies for acute upper gastrointestinal bleeding. The New England Journal of Medicine, 368 (1), 11-21. doi:10. 1056/NEJMoa1211801 Wilkins, T., Embry, K., & George, R. (2013, May 1). Diagnosis and man-agement of acute diverticulitis. American Family Physician, 87 (9), 612-620. Retrieved from https://www. aafp. org/afp/2013/0501/p612. html4. Gastrointestinal Guidelines

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81Hepatitis-Alcoholic Robin Miller and Ann E. Burke Definition A. Syndrome of progressive inflammatory liver injury asso-ciated with long-term heavy intake of alcohol. B. Alcohol abuse is the most common cause of serious liver disease in Western society. Incidence A. In the United States, alcoholic liver disease affects more than 2 million people. B. The true prevalence of alcoholic hepatitis is unknown as the patient may be asymptomatic or never seek medical atten-tion. Pathogenesis A. Although the pathogenesis is not known, genetic, envi-ronmental, nutritional, metabolic, and immunologic factors may play a role. Predisposing Factors A. Majority of patients have a history of heavy alcohol use for two or more decades. Heavy is defined as greater than 100 g per day. B. Women are more susceptible than men. C. Peak age is 40 to 50 years old. D. Alcoholic liver disease is more common in minority groups, particularly among Native Americans. Subjective Data A. Common complaints/symptoms. 1. Anorexia. 2. Fever. 3. Right upper quadrant (RUQ) pain. 4. Abdominal distension. 5. Dark urine. 6. Clay-colored stools. B. Common/typical scenario. 1. History of daily alcohol use. 2. Stressful life events may trigger an increase in intake. 3. It is common for patients to cease alcohol intake several weeks prior to presentation due to feeling more ill. C. Family and social history. 1. It is essential that the healthcare provider take a careful alcohol history. 2. May need to elicit a more accurate history by includ-ing family members. 3. Drinking patterns may vary. Heavy drinking can be intermittent (e. g., weekends only) or hidden from family members. 4. A standard drink is defined as 14 g of alcohol. Exam-ples include: a. 12 ounces of beer. b. 5 ounces of wine. c. 1. 5 ounces of distilled spirits. d. 8 to 9 ounces of malt liquor. D. Review of systems. 1. Cognitive changes (encephalopathy). 2. Jaundice. 3. Anorexia. 4. Fever. 5. RUQ/epigastric pain. 6. Abdominal distension. Physical Examination A. Temporal wasting. B. Scleral icterus. C. Generalized jaundice. D. Hepatomegaly. E. Ascites. F. Spider angiomata, palmar erythema, and gynecomastia suggest advanced disease. G. Lower extremity edema. Diagnostic Tests A. Lab tests. 1. Hepatic function panel: Aspartate aminotransferase (AST)/a lanine aminotransferase (ALT) ratio is 2:1. 2. Complete blood count (CBC): Elevated white blood cell (WBC). 3. International normalized ratio (INR): Elevated. 4. Testing for hepatitis A, B, and C; autoimmune mark-ers (antinuclear antibody [ANA], AMA, ASMA, LKM1). B. Imaging. 1. Abdominal ultrasound with Dopplers to rule out biliary obstruction, Budd-Chiari malformation, or cirrhosis. C. Liver biopsy. D. If labs and imaging are nondiagnostic, biopsy may be considered. Differential Diagnosis A. Acute viral hepatitis. B. Autoimmune hepatitis. C. Drug-induced liver injury (DILI). D. Shock liver. E. Ischemic hepatitis. F. Budd-Chiari. G. Wilson's disease. H. Alpha 1 antitrypsin deficiency. I. Toxin-induced hepatitis (e. g., mushroom poisoning). Evaluation and Management Plan A. General plan. 1. Admission to ICU in patients that are unstable, that is, encephalopathic. 2. Fluid management and nutritional support. 3. Acuity of illness based on Maddrey Discriminant Function (DF) score and need for glucocorticoid ther-apy. DF is a calculation using bilirubin and prothrombin time (PT). 4. Alcohol withdrawal protocol per institutional guide-lines. 5. Infectious workup to rule out other causes of mental status change. 6. Prophylaxis against gastrointestinal (GI) bleeding. B. Patient/family teaching points. 1. Referral for substance abuse counseling. 2. Length of sobriety to meet transplant candidacy requirement per institution policy. 3. Steroid tapering schedule. C. Pharmacotherapy. 1. GI prophylaxis: Proton pump inhibitors (PPI) or H2 blocker. 2. Stop nonselective beta blocker during acute crisis due to risk of acute kidney injury (AKI). May resume later. Hepatitis-Alcoholic

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82 3. Nutritional support: Adequate calories and protein; vitamins thiamine, folate. 4. Glucocorticoids. a. Severe cases with DF greater than 32 receive pred-nisone/prednisolone for 28 days. b. Discontinue if no improvement after 7 days. This is based on the Lille score, a predictor of response to steroid treatment. 5. Lactulose or trial of xifaxan therapy for encephalopa-thy. D. Discharge instructions. 1. Review tapering schedule of steroids if applicable. 2. Set up outpatient substance abuse counseling or inpa-tient rehab. 3. Repeat lab tests in 1 week. 4. Close follow-up with hepatologist. Follow-Up A. As per discharge instructions, close follow-up with hepa-tologist and transplant center, if appropriate. Consultation/Referral A. Psychiatry: Addiction specialist. B. T ransplant center. Special/Geriatric Considerations A. Hemolysis, elevated liver enzymes, low platelet count in the setting of pregnancy (HELLP). Bibliography Friedman, S. L. (2018, August 13). Alcoholic hepatitis: Clinical manifes-tations and diagnosis. In K. M. Robson (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/alcoholic-hepatitis-clinical-manifestations-and-diagnosis Friedman, S. L. (2018, August 28). Management and prognosis of alco-holic hepatitis. In K. M. Robson (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/management-and-prognosis-of-alcoholic-hepatitis Heuman, D. M. (2016). Alcoholic hepatitis: Overview. In B. S. Anand (Ed. ), Medscape. Retrieved from https://emedicine. medscape. com/ article/170539-overview National Institute on Alcohol Abuse and Alcoholism. (n. d. ). What is a stan-dard drink? Retrieved from https://www. niaaa. nih. gov/alcohol-health/ overview-alcohol-consumption/what-standard-drink Hepatitis-Autoimmune Robin Miller and Ann E. Burke Definition A. Chronic: Clinical or biochemical evidence of liver disease greater than 6 months duration. B. Chronic inflammatory condition of the liver character-ized by transaminase elevation in the presence of autoanti-bodies. Incidence A. The exact prevalence in the United States is unknown but is estimated to be 1. 1 per 100,000 persons per year. B. Female predominance but occurs in both genders and all age groups. Pathogenesis A. Thought to result from an environmental trigger in a genetically predisposed individual. Predisposing Factors A. Strong genetic association with other autoimmune dis-eases from 26% to 49%. Subjective Data A. Common complaints/symptoms. 1. Presentation can vary from asymptomatic (up to 25%) to fulminant hepatic failure (rare). 2. May see anorexia, arthralgia, rash, or fatigue. B. Common/typical scenario. 1. Insidious onset with constitutional symptoms as listed earlier. 2. Asymptomatic patients will be diagnosed incidentally with laboratory testing. C. Family and social history. 1. Not applicable. D. Review of systems. 1. Flu-like symptoms. a. Nausea. b. Anorexia. c. Fatigue. d. Lethargy. e. Malaise. f. Abdominal pain. g. Itching. h. Arthralgia. Physical Examination A. Ranges from a normal physical examination to evidence of advanced disease, including: 1. Hepatomegaly. 2. Splenomegaly. 3. Jaundice. 4. Temporal wasting. 5. Spider angiomata. Diagnostic Tests A. Lab workup includes: Complete blood count (CBC), comprehensive metabolic panel (CMP), international nor-malized ratio (INR), hepatitis B and C serologies, antinu-clear antibody (ANA), AMA, ASMA, LKM1, quantitative immunoglobulins, ceruloplasmin (Wilson's disease), iron, ferritin (hemochromatosis), Alpha 1 antitrypsin. B. Lab abnormalities include: Elevated aspartate amino-transferase (AST)/alanine aminotransferase (ALT) 5 to 10X upper limit, elevated immunoglobin G (IMG), positive ANA, ASMA, or LKM1. C. Imaging: Abdominal ultrasound (US), MRI/magnetic resonance cholangiopancreatography (MRCP) to rule out other biliary disorders. D. Liver biopsy: Gold standard to confirm diagnosis and severity of disease. Differential Diagnosis A. Hepatitis A, B, and C. B. Primary biliary cholangitis (PBC). C. Primary sclerosing cholangitis (PSC). D. Wilson's disease. E. Hemochromatosis. F. Alpha 1 antitrypsin deficiency. G. Fatty liver disease. H. Drug-induced liver injury. I. Alcohol use. 4. Gastrointestinal Guidelines

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83 Evaluation and Management Plan A. General plan. 1. Decision to treat a patient is based on the severity of symptoms, magnitude of AST/ALT elevations, histologic findings, and the potential for side effects. 2. Supportive care. 3. Monitor liver function tests. 4. Glucocorticoid mono therapy or in combination with azathioprine. B. Patient/family teaching points. 1. Avoid alcohol or over-the-counter (OTC) supple-ments. 2. Discuss side effect management of steroid therapy. 3. Discuss importance of steroid tapering schedule; do not stop abruptly. C. Pharmacotherapy. 1. Glucocorticoids: Goal of therapy is to achieve quick remission and taper off steroids to minimize potential side effects. a. Moderate-severe activity: Prednisolone IV or oral prednisone starting at 60 mg daily. b. Mild activity: Lower dose of prednisone starting at 20 mg daily. 2. Nonsteroidal immunosuppressant: Imuran or 6 Mer-captopurine (6MP) in combination with steroids that are continued long term after steroid taper. This may also be appropriate for populations that are steroid sen-sitive. Thiopurine methyltransferase (TPMT) should be obtained prior to starting Imuran or 6MP. It measures the enzyme that breaks down azathioprine and helps guide dosing and risk for potential side effects. D. Discharge instructions. 1. Teaching points as listed earlier. 2. Avoid alcohol or OTC supplements. 3. Discuss side effect management of steroid therapy. 4. Discuss importance of steroid tapering schedule; do not stop abruptly. 5. Weekly CBC, glucose, and liver tests. 6. Follow-up with gastroenterology or hepatologist. Follow-Up A. Get baseline bone density scan. B. Follow-up with p neumocystis pneumonia (PCP) for lab monitoring. C. Follow-up with gastroenterologist or hepatologist within 1 month. Consultation/Referral A. Refer to transplant center; 10%-to 20% of patients with autoimmune hepatitis will require a liver transplant for acute liver failure, decompensated cirrhosis, and hepatocellular car-cinoma. Special/Geriatric Considerations A. Patients at increased risk for glucocorticoid side effects. 1. Prediabetes, diabetes. 2. Osteoporosis. 3. Emotional liability. 4. Sleep disturbance. Bibliography Fialho, A., Fialho, A., & Carey, W. (2015, July). Autoimmune hepatitis. Retrieved from http://www. clevelandclinicmeded. com/medicalpubs/ diseasemanagement/hepatology/chronic-autoimmune-hepatitis Heneghan, M. A. (2018, November 14). Autoimmune hepatitis: T reat-ment. In K. M. Robson (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/autoimmune-hepatitis-treatment Hepatitis A Robin Miller and Ann E. Burke Definition A. General: Inflammation of the liver. B. Acute: Clinical or biochemical evidence of liver disease less than 6 months. C. Vaccine preventable, communicable disease of the liver caused by the hepatitis A virus. D. Self-limited disease that does not result in chronic infection. Incidence A. Most common form of acute viral hepatitis in the world. B. In the United States, the estimated number of new infec-tions in 2015 was 2,800 people. Pathogenesis A. T ransmitted person-to-person by the fecal-oral route or consumption of contaminated food or water. Predisposing Factors A. International travel to developing countries. B. Day-care employees and children. C. Poor hygiene practices at restaurants/cafeterias. D. Living with an infected person. E. Men who have sex with men. Subjective Data A. Common complaints/symptoms. 1. Fatigue. 2. Fever. 3. Malaise. 4. Headache. 5. Nausea. 6. Right upper quadrant pain. 7. Loss of appetite. 8. Itching. 9. Myalgia. B. Common/typical scenario. 1. Onset of symptoms. 2. Vaccination history. 3. Recent travel. 4. Food history. C. Family and social history. 1. Living situation. 2. Sexual practices/preferences. D. Review of systems. 1. Dark urine. 2. Light-colored stool. 3. Jaundice. Physical Examination A. Jaundice. B. Scleral icterus. C. Fever up to 104∘F. D. Right upper quadrant (RUQ) tenderness. E. Hepatomegaly. Diagnostic Tests A. Workup includes: Complete blood count (CBC), com-prehensive metabolic panel (CMP), international normalized Hepatitis A

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84 ratio (INR), hepatitis A Ig M and Ig G antibodies, hepatitis B serologies (Hep B surface antibody, Hep B surface antigen, Hep B core antibody), hepatitis C antibody screen, hepatitis E antibody. B. Lab abnormalities include: Elevations of a spartate amino-transferase (AST)/alanine aminotransferase (ALT) often greater than 1,000 IU-L, followed by elevations of bilirubin up to 10 mg/d L. C. Ultrasound of the abdomen. Differential Diagnosis A. Hepatitis E. B. Alcoholic hepatitis. C. Autoimmune hepatitis. D. Acute drug-induced liver injury (DILI) E. Acute HIV infection. F. Cytomegalovirus (CMV) infection. G. Epstein-Barr virus (EBV). H. Herpes simplex virus (HSV). Evaluation and Management Plan A. General plan. 1. Supportive care. a. Intravenous (IV) fluids. b. Antiemetic medications. B. Patient/family teaching points. 1. Vaccination of close contacts. 2. Safe sex practices. 3. Good hand hygiene. C. Pharmacotherapy. 1. Acetaminophen may be cautiously administered but limited to 2 g per day. 2. Administration of immunoglobulin within 14 days of exposure to achieve passive immunization and reduce severity of illness. D. Discharge instructions. 1. Rest. 2. Return to work should be delayed for 10 days after the onset of jaundice. 3. Follow-up with primary care physician. Follow-Up A. Primary care doctor visit: Repeat liver tests. B. Vaccination for hepatitis B, if not immune. C. Most people have a full recovery; infection confers life-long immunity (positive hepatitis A antibody). D. Up to 10% of patients experience a relapse of symptoms during the 6 months following acute illness. Consultation/Referral A. Hepatologist for chronic elevated liver tests post infection. Special/Geriatric Considerations A. Liver transplant should be considered in fulminant disease. B. This occurs in less than 1% of patients and is most com-mon in individuals over 50, or with any other chronic liver disease. Bibliography Centers for Disease Control and Prevention. (n. d. ). Hepatitis A questions and answers for health professionals. Retrieved from https://www. cdc. gov/hepatitis/hav/havfaq. htm Gilroy, R. K. (2017, October 16). Hepatitis A. In B. S. Anand (Ed. ), Med-scape. Retrieved from https://emedicine. medscape. com/article/177484-overview Lai, M., & Chopra, S. (2018, December 17). Hepatitis A virus infection in adults: Epidemiology, clinical manifestations, and diagnosis. In E. L. Baron (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/ contents/hepatitis-a-virus-infection-in-adults-an-overview Mayo Clinic. (n. d. ). Hepatitis A. Retrieved from https://www. mayoclinic. org/diseases-conditions/hepatitis-a/symptoms-causes/syc-20367007. Hepatitis B Robin Miller and Ann E. Burke Definition A. Vaccine preventable, communicable disease of the liver caused by the hepatitis B virus. B. Global health problem. C. Acute or chronic forms. Incidence A. More than 250 million carriers worldwide. B. 600,000 deaths annually in the world. C. In the United States, the rate of hepatitis B-related hospitalizations, cancer, and death has doubled in the last decade. Pathogenesis A. T ransmission through activities that involve percutaneous or mucosal contact with infectious blood or body fluids. Predisposing Factors A. Intravenous (IV) drug use that involves sharing needles. B. Birth from an infected mother (vertical transmission). C. Needle sticks: Healthcare worker. D. Sex with an infected partner. E. T ravel to region that has high infection rates (e. g., Asia, Pacific Islands, Africa, Eastern Europe). Subjective Data A. Common complaints/symptoms. 1. Fever. 2. Fatigue/malaise. 3. Headache. 4. Nausea. 5. Vomiting. 6. Right upper quadrant (RUQ) pain. 7. Loss of appetite. 8. Itching. 9. Myalgias. B. Common/typical scenario. 1. Onset of symptoms. 2. Vaccination history. 3. Recent travel. 4. Food history. C. Family and social history. 1. Sexual activity (unprotected intercourse, gender, multiple partners). a. IV drug use. b. Alcohol use. c. Living situation (infected roommate or partner). d. Family history of hepatitis B. 2. Dialysis. D. Review of systems. 1. See common complaints in previous section (jaun-dice, dark urine, clay-colored stool). 4. Gastrointestinal Guidelines

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85 Physical Examination A. Acute illness. 1. Jaundice. 2. Scleral icterus. 3. Fever—low grade. 4. RUQ tenderness. B. Chronic illness. 1. Fatigue. 2. Anorexia. 3. Nausea. 4. Mild RUQ tenderness. C. Fulminant illness: Onset of liver failure as manifested by encephalopathy and systemic dysfunction within 8 weeks of the recognition of liver disease. 1. Ascites. 2. Hepatic encephalopathy. 3. Gastrointestinal (GI) bleeding. Diagnostic Tests A. Lab tests. 1. Hepatitis B surface antigen, surface antibody, core antibody, Ig M antibody. 2. Antibodies for hepatitis A, C, D, and E. 3. HIV. 4. Complete blood count (CBC). 5. International normalized ratio (INR). 6. Liver function tests. 7. Iron studies. 8. Alpha fetoprotein (AFP). B. Imaging. 1. Abdominal u ltrasound (US). 2. Abdominal MRI. C. Liver biopsy if indicated. Differential Diagnosis A. Hepatitis A, C, D, or E. B. Alcoholic hepatitis. C. Autoimmune hepatitis. D. Acute drug-induced liver injury (DILI). E. Hemochromatosis. F. Wilson's disease. Evaluation and Management Plan A. General plan. 1. Supportive care. a. The likelihood of liver failure from acute hepatitis B is less than 1%. b. Likelihood of progression to chronic hepatitis B is less than 5% in an immune competent adult. B. Patient/family teaching points. 1. Vaccination of close contacts. 2. Safe sex practices. C. Pharmacotherapy. 1. Antiviral medication—Tenofovir or entecavir for patients with acute liver failure or severe disease (elevated bilirubin, coagulopathic). 2. Fulminant hepatitis—refer for liver transplant. D. Discharge instructions. 1. Follow-up with p neumocystis pneumonia (PCP) or hepatologist. 2. Avoidance of alcohol or drugs that could harm the liver. 3. Do not share: Toothbrush, razor, needle. 4. Limit sexual partners, perform safe sex practices. 5. Call for fever, vomiting, bloody or black stool, dark urine, jaundice, ascites. Follow-Up A. See PCP if mild course. B. Antiviral medication as prescribed. C. Repeat lab tests to monitor recovery. D. Vaccination for hepatitis A if indicated. Consultation/Referral A. Hepatologist to manage if condition becomes chronic hepatitis B. B. T ransplant center per hepatologist. Special/Geriatric Considerations A. Hepatitis D coinfection: Requires the presence of hepati-tis B virus for infection. Should be treated by a hepatologist with peg interferon. B. Pregnancy: Child born to a hepatitis B mother receives immunoglobulin as well as vaccination after delivery. C. Fulminant failure: Consider for transplant. Bibliography Centers for Disease Control and Prevention. (n. d. ). Hepatitis B questions and answers for health professionals. Retrieved from https://www. cdc. gov/hepatitis/hbv/hbvfaq. htm Lok, A. (2017, September 29). Hepatitis B virus: Overview of management. In J. Mitty (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/hepatitis-b-virus-overview-of-management Mayo Clinic. (n. d. ). Hepatitis B. Retrieved from https://www. mayoclinic. org/diseases-conditions/hepatitis-b/symptoms-causes/syc-20366802. Pyrsopoulos, N. T. (2018, August 1). Hepatitis B workup. In B. S. Anand (Ed. ), Medscape. Retrieved from https://emedicine. medscape. com/article/177632-workup Hepatitis C Robin Miller and Ann E. Burke Definition A. Chronic: Clinical or biochemical evidence of liver disease greater than 6 months duration. B. One of the most common liver diseases. C. Blood-borne disease of the liver caused by the hepatitis C virus. D. 70% to 85% of those infected develop chronic illness. Incidence A. According to the Centers for Disease Control and Pre-vention (CDC), estimates of new hepatitis C infections from 2015 were 33,900 in the United States. B. Estimated prevalence is approximately 3. 6 million people. C. Accounts for 8,000 to 13,000 deaths each year in the United States. D. Infection rates have dramatically increased among young adults in the past decade due to the opioid epidemic. Pathogenesis A. T ransmission through blood from a contaminated indi-vidual or blood products. B. After 1990, blood and blood products underwent screening. Predisposing Factors A. Intravenous (IV) drug use and needle sharing. B. Healthcare worker. C. T ransfusion before 1990. D. Body piercing and tattoos. Hepatitis C

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86 E. Shared razors. F. Baby boomer—CDC recommendations to test those born between 1945 and 1965. G. Dialysis patient. H. Maternal history of hepatitis C virus (HCV)—vertical transmission rate is 5%. Subjective Data A. Common complaints/symptoms. 1. Most people have no symptoms. 2. Among those who do have symptoms, they complain of fatigue, muscle and joint pain, pruritus, nausea, loss of appetite, weakness, and weight loss. B. Common/typical scenario. 1. Incidental diagnosis for elevated liver tests, insurance screening, or p neumocystis pneumonia (PCP) following CDC recommendations. C. Family and social history. 1. Injection drug use. 2. Sexual or household contact. 3. Incarceration. D. Review of systems. 1. In chronic illness, there are very few symptoms unless advanced to cirrhosis. Physical Examination A. Generally there are no obvious features of chronic hepati-tis C unless cirrhosis is present. Diagnostic Tests A. Hepatitis C antibody. B. Hepatitis C viral RNA quantitative level and genotype. C. Screening tests to rule out coinfection for HIV or hepatitis B. D. Complete blood count (CBC), comprehensive metabolic panel (CMP), t hyroid-stimulating hormone (TSH), drug, and alcohol screen. E. Imaging—Ultrasound or MRI if advanced disease present. F. Procedure to assess the degree of fibrosis: Elastography (Fibro Scan), liver biopsy. Differential Diagnosis A. Autoimmune hepatitis. B. Cholangitis. C. Hepatitis A, B, D, and E. Evaluation and Management A. General plan. 1. T reatment with antiviral therapy is well tolerated and effective in curing the disease. 2. The decision to treat is based on genotype, the person's overall health and comorbidities, and stage of fibrosis. B. Patient/family teaching points. 1. If the decision is made to pursue antiviral treatment, medication adherence is essential to achieve optimal out-comes. 2. Skipping doses may lead to resistant strains and impact success of therapy. 3. Alcohol is prohibited as well as herbal supplements. 4. Successful treatment can mitigate progression to cir-rhosis. C. Pharmacotherapy. 1. Antiviral therapy—must be ordered by special-ist. Drug options include: Harvoni, Epclusa, Vosevi, Mavyret, Zepatier, Ribavirin. 2. Common side effects: Usually mild and may include fatigue, headaches, or nausea. D. Discharge instructions. 1. Follow-up with g astrointestinal (GI)/hepatologist. 2. Will need vaccinations for hepatitis A or B if indi-cated. 3. Avoid alcohol or any over-the-counter (OTC) supple-ments. Follow-Up A. GI/Hepatologist to initiate treatment and monitor ther-apy and side effects. B. For the cirrhotic patient, biannual imaging of the liver to screen for hepatocellular cancer. Consultation/Referral A. GI/Hepatologist. B. If they have hepatocellular carcinoma (HCC), will be referred to interventional radiology or oncology. C. Consider transplant for any patient with decompensated cirrhosis or HCC. Special/Geriatric Considerations A. Decision to treat any dialysis patient is undertaken on a case-by-case basis. B. A patient with HIV/hepatitis C coinfection may require changes in his or her highly active antiretroviral therapy (HAART) due to drug interactions with hepatitis C treat-ment. C. Pregnancy is contraindicated for treatment. Bibliography Centers for Disease Control and Prevention. (n. d. ). Hepatitis C information. Retrieved from https://www. cdc. gov/hepatitis/hcv/index. htm Chopra, S., & Pockros, P. J. (2018, June 5). Overview of the manage-ment of chronic hepatitis C virus infection. In A. Bloom (Ed. ), Up To-Date. Retrieved from https://www. uptodate. com/contents/overview-of-the-management-of-chronic-hepatitis-c-virus-infection Dhawan, V. K. (2019, January 17). Hepatitis C clinical presentation. In B. S. Anand (Ed. ), Medscape. Retrieved from https://emedicine. medscape. com/article/177792-clinical Inflammatory Bowel Disease Catherine Harris Definition A. Inflammatory bowel disease (IBD) is an umbrella term for a group of disorders that causes inflammation of the bowel such as ulcerative colitis (UC) and Crohn's disease (CD). Incidence A. Approximately 1 to 2 million people in the United States have UC or CD. B. IBD: 396 cases per 100,000/year. C. UC: 0. 5 to 24. 5 cases per 100,000. D. CD: 0. 1 to 16 cases per 100,000. 4. Gastrointestinal Guidelines

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87 Pathogenesis A. IBD causes inflammation of the mucosa of the intestinal tract. 1. Ulceration. 2. Edema. 3. Bleeding. 4. Fluid and electrolyte loss. B. Inflammatory mediators and cytokines disrupt intestinal mucosa, allowing chronic inflammatory processes to occur. C. UC: Inflammation begins in the rectum (always involved) with 25% of cases confined to the rectum. 1. Disease progresses in a contiguous manner and does not “skip” sections of bowel as common in CD. 2. Pancolitis occurs in 10%. D. CD: Can affect any part of the gastrointestinal tract from the mouth to the anus. 1. Three patterns of involvement. a. Inflammatory disease. b. Strictures. c. Fistulas. 2. Involves all layers of bowel, not just mucosa and submucosa. 3. Pattern is discontinuous (unlike UC) and typically has “skip” areas of interspersed disease in two or more areas. 4. May have rectal sparing. 5. Anorectal complications common. Predisposing Factors A. Higher prevalence rate in Jewish populations. B. Females have a slightly greater incidence. C. Young adults 15 to 40 years old. D. Living in a developed country, colder climates, and in urban areas. E. Genetic disposition. Subjective Data A. Common complaints/symptoms. 1. Diarrhea. 2. Constipation. 3. Bowel movement issues such as pain or bleeding. 4. Abdominal cramping and pain. a. Right lower quadrant pain in CD. b. Left lower quadrant or periumbilical in UC. 5. Nausea and vomiting. B. Common/typical scenario. 1. Patients typically complain of low grade fevers, sweats, malaise, or general fatigue with associated bowel move-ment changes that include pain or bleeding. 2. Patients may report irregular bowel patterns with either diarrhea or constipation or a combination of both. 3. Most patients report recurrent abdominal pain and diarrhea over several months to years. 4. May occur with or without blood or pus in the stool. C. Family and social history. 1. Family history of IBD, celiac disease, or colorectal cancer. 2. Use of nonsteroidal anti-inflammatory drugs (NSAIDs). 3. History of smoking. 4. Recent travel. 5. Stress. 6. Dietary problems. D. Review of systems. 1. Head, ear, eyes, nose, and throat (HEENT): Evidence or history of scleritis, anterior uveitis (redness, pain, itch-iness), aphthous stomatitis (mouth sores). 2. Dermatology: Psoriasis, erythema nodosum. 3. Rheumatology: Inflammatory arthritis, ankylosing spondylitis. 4. Arthritis. 5. Gastrointestinal (GI): Liver disease, gallstones, blood or pus in stool, diarrhea, constipation. 6. Genitourinary (GU): History of kidney stones. 7. Fatigue, night sweats, loss of appetite, fever, or recent infection. Physical Examination A. Constitutional: Patients who become dehydrated may have fever or appear lethargic. B. Gastrointestinal: Abdominal examination is often benign; a rectal examination can be done if there is con-cern for perianal fissures, fistulas, or evidence of rectal pro-lapse; occult stool may be present. C. Cardiovascular: Tachycardia from dehydration may be present. D. Skin: Pallor may be noted if there is anemia Diagnostic Tests A. Lab studies. 1. No laboratory test is specific for irritable bowel syn-drome (IBS). 2. Complete blood cell (CBC) count to assess for anemia or infection. 3. Markers of nutritional status may have value if con-cern for significant deficiencies. a. Albumin. b. Prealbumin. c. Vitamin B12. d. Folate. e. T ransferrin. 4. Erythrocyte sedimentation rate (ESR) and C-reactive protein are useful markers for inflammation. 5. Perinuclear antineutrophil cytoplasmic antibodies (p ANCA) and anti-Saccharomyces cerevisiae antibodies (ASCA). a. Positive p ANCA and negative ASCA is more spe-cific for UC. b. Negative p ANCA and positive ASCA is more spe-cific for CD. 6. Stool studies. a. Check stool culture, ova, and parasites. b. Check Clostridium difficile infection with toxin assay. B. Imaging studies. 1. Abdominal x-ray can be used to rule out other condi-tions. a. Free air is consistent with toxic megacolon. b. Dilated colon is consistent with colitis. c. Osteoporosis may explain some pain symptoms. 2. Barium enema studies: Can be useful in diagnosing UC versus CD. 3. Ultrasound, MRI, and CT may be useful in identify-ing fistulas, abscesses, and stenosis. C. Colonoscopy. 1. Most valuable tool to diagnose type of IBS. 2. Can be used to determine extent and severity. 3. Obtain tissue. 4. Document ulceration and assess inflammation. D. Flexible sigmoidoscopy. 1. Limited length of scope can help diagnosis rectal bleeding and diagnose distal UC. Inflammatory Bowel Disease

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88 E. Esophagogastroduodenoscopy (EGD). 1. Used to evaluate upper GI tract symptoms. 2. Can evaluate ulceration. Differential Diagnosis A. Gastritis. B. Colitis. C. Abdominal infections. D. Diverticulitis. E. Appendicitis. F. The differential diagnosis often depends on presentation. 1. If patients present with diarrhea consider: a. Celiac disease. b. Lactose intolerance. c. Gastrointestinal infections. d. Cancer of the GI tract. 2. If patients present with abdominal pain or gastroin-testinal bleeding. a. Arteriovenous malformations. b. Cancer of the GI tract. c. Colitis. Evaluation and Management Plan A. General plan. 1. Symptomatic therapy. a. T reat underlying inflammation in outpatient setting. b. Admit to hospital if surgical intervention required, uncontrolled pain, significant dehydration from vom-iting, evidence of emergent complications such as toxic megacolon, severe colitis, or bowel obstruction. c. Avoid antidiarrheals in acute phase because of risk of toxic megacolon. d. Supportive care. 2. Start stepwise medical therapy. a. Step 1: T reat with aminosalicylates +/-antibi-otics (controversial for prophylactic use). b. Step 2: T reat with corticosteroids. which provide rapid relief of symptoms. c. Step 3: T reat with immune modifying agents if steroids fail or are required for prolonged periods. d. Step 4: Experimental agents. i. Thalidomide. ii. Nicotine patch. iii. Butyrate enema. iv. Heparin subcutaneous injections. 3. Surgery. a. Not curative in CD because of the skip lesions and more diffuse nature of the disease. i. Performed in patients with complications such as strictures or fistulas. ii. Recurrent inflammation in 93% of cases at 1 year post surgery. b. Colectomy required in 2% to 30% of patients with UC. i. Intractable inflammation. ii. Medical therapy fails. iii. Precancerous changes. iv. Toxic megacolon. v. Perforation. 4. Remission therapy. a. Continue medications used to achieve remission. b. Taper off steroids: No role in maintaining remis-sion. B. Patient/family teaching points. 1. Dietary changes: Certain foods and drinks can make symptoms worse; avoid foods that cause flare ups, partic-ularly too much fiber, spicy food, alcohol, and caffeine. a. Eat smaller meals more often. b. Drink plenty of fluids. 2. Stress may exacerbate the condition. 3. Quit smoking to improve remission rates. 4. IBD may increase the risk of colon cancer. Colono-scopies should be done early and often. 5. If taking immunosuppressant therapy, the immune system's ability to fight infection is reduced. C. Pharmacotherapy. 1. Corticosteroids. a. T reatment of choice in acute attack in intra-venous form. b. Inhibitors of inflammation. c. Do not use for maintaining state of remission. 2. Immunosuppressants. a. Steroid sparing agents. b. Great in patients refractory to steroids. 3. 5-Aminosalicyclic acid derivatives. a. Reduce inflammatory reactions. b. Useful in mild to moderate UC. c. May be used to maintain remission in CD. 4. T umor necrosis factor alpha. a. Induces proinflammatory cytokines. b. Promotes mucosal healing. 5. Antibiotics: Broad spectrum antibiotics to treat intestinal bacteria are controversial. Antibiotics are thought to reduce recurrence rate, particularly in CD, though therapy is not well established in UC. Ameri-can College of Gastroenterology guidelines state that con-trolled trials have not consistently demonstrated efficacy. a. May be used for complications associated with IBS. b. Metronidazole. c. Ciprofloxacin. 6. Histamine H2 antagonists: Reduce gastric acid secre-tion. 7. Proton pump inhibitors. a. Reduce gastric acid secretion. b. Used in patients who fail H2 antagonist therapy. 8. Antidiarrheals for symptomatic relief. 9. Anticholinergic/antispasmodic agents. a. T reats spastic disorders or motility disturbances. 10. Probiotics: Certain strains ( Escherichia-coli Nissle 1917 & VSL # 3 [Mutaflor, Ardeypharm]) have shown to be effective in mild-moderate IBD (esp. UC) compa-rable to Metronidazole. 11. Supplements. a. Iron supplements. b. Nutritional supplements. c. Calcium and vitamin D supplements. D. Discharge instructions. 1. Avoid foods with caffeine, spicy foods, or milk products. 2. Eat small meals several times a day instead of fewer big meals. 3. Follow-up with gastroenterologist. Follow-Up A. Follow-up with gastroenterologist. 4. Gastrointestinal Guidelines i. Abscesses. ii. Fistulas. iii. Pouchitis.

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89 Consultation/Referral A. Refer to gastroenterology for medical management. B. Consult surgery in UC if medical therapy fails. C. Consult surgeon if severe disease or extraluminal compli-cations. D. Specialty consults to manage extracolonic manifestations. 1. Ophthalmology for uveitis. 2. Arthritis. 3. Dermatitis. 4. Dietician. Special/Geriatric Considerations A. The elderly may experience a delay in diagnosis because of the wide possibilities in the differential diagnosis. Bibliography Amezaga, A. J., & Van Assche, G. (2016). Practical approaches to “top-down” therapies for Crohn's disease. Current Gastroenterology Reports, 18(7), 35. doi:10. 1007/s11894-016-0507-z Ha, C., & Kornbluth, A. (2010). Mucosal healing in inflammatory bowel disease: Where do we stand? Current Gastroenterology Reports, 12 (6), 471-478. doi:10. 1007/s11894-010-0146-8 Henriksen, M., Jahnsen, J., Lygren, I., Sauar, J., Kjellevold, Ø, Schulz, T.,... Moum, B. (2006). Ulcerative colitis and clinical course: Results of a 5-year population-based follow-up study (the IBSEN study). Inflammatory Bowel Diseases, 12 (7), 543-550. doi:10. 1097/01. MIB. 0000225339. 91484. fc Khan, K. J., Ullman, T. A., Ford, A. C., Abreu, M. T., Abadir, A., Marshall, J. K.,... Moayyedi, P. (2011). Antibiotic therapy in inflammatory bowel disease: A systematic review and meta-analysis. The American Journal of Gastroenterology, 106 (4), 661-673. Retrieved from https://journals. lww. com/ajg/Abstract/2011/04000/Antibiotic_Therapy _in_Inflammatory_Bowel_Disease_. 14. aspx Kornbluth, A., & Sachar, D. B. (2010). Ulcerative colitis practice guide-lines in adults: American College of Gastroenterology, Practice Param-eters Committee. The American Journal of Gastroenterology, 105 (3), 501-523. Retrieved from https://journals. lww. com/ajg/Abstract/2010/ 03000/Ulcerative_Colitis_Practice_Guidelines_in_Adults_. 6. aspx Leighton, J. A., Shen, B., Baron, T. H., Adler, D. G., Davila, R., Egan, J. V.,... Fanelli, R. D. (2006). ASGE guideline: Endoscopy in the diagnosis and treatment of inflammatory bowel disease. Gastrointestinal Endoscopy, 63(4), 558-565. doi:10. 1016/j. gie. 2006. 02. 005 Lichtenstein, G. R., Abreu, M. T., Cohen, R., & T remaine, W. (2006). American Gastroenterological Association Institute medical position statement on corticosteroids, immunomodulators, and infliximab in inflammatory bowel disease. Gastroenterology, 130 (3), 935-939. doi:10. 1053/j. gastro. 2006. 01. 047 Molodecky, N. A., Soon, I. S., Rabi, D. M., Ghali, W. A., Ferris, M., Chernoff, G., & Kaplan, G. G. (2012). Increasing incidence and preva-lence of the inflammatory bowel diseases with time, based on systematic review. Gastroenterology, 142 (1), 46-54. e42. doi:10. 1053/j. gastro. 2011. 10. 001 Saez-Lara, M. J., Gomez-Llorente, C., Plaza-Diaz, J., & Gil, A. (2015). The role of probiotic lactic acid bacteria and bifidobacteria in the preven-tion and treatment of inflammatory bowel disease and other related dis-eases: A systematic review of randomized human clinical trials. Bio Med Research International. doi:10. 1155/2015/505878 Wilkins, T., Jarvis, K., & Patel, J. (2011). Diagnosis and management of Crohn's disease. American Family Physician, 84 (12), 1365-1375. Retrieved from https://www. aafp. org/afp/2011/1215/p1365. html Nonalcoholic Fatty Liver Disease Robin Miller and Ann E. Burke Definition A. Medical condition characterized by fatty infiltration in the liver without a history of alcohol use. B. T wo types exist based on presence of inflammation. 1. Nonalcoholic fatty liver disease (NAFLD)—benign condition without inflammation. 2. Nonalcoholic steatohepatitis (NASH)— Inflammation is present which leads to scarring. May progress to cirrhosis in 20% of the population. Incidence A. Most common liver disease in Western industrialized countries. B. In the United States, the prevalence of NAFLD is esti-mated at 10% to 46%. C. Incidence as high as 50% to 75% in obese patients. Pathogenesis A. Cause is not fully understood but thought to be linked to insulin resistance and oxidative stress in an individual with risk factors. Predisposing Factors A. Male sex. B. Higher prevalence in Hispanics. C. Commonly diagnosed at age 40 to 50. D. Metabolic syndrome is present with one or more of the following. 1. Obesity. 2. Diabetes. 3. Hypertension (HTN). 4. Dyslipidemia. E. Other disorders that may be associated: Polycystic ovarian syndrome (PCOS), sleep apnea, hypothyroidism. Subjective Data A. Common complaints/symptoms. 1. Most patients are usually asymptomatic. 2. May have fatigue, malaise, or r ight upper quadrant (RUQ) discomfort. B. Common/typical scenario. 1. Incidental findings of elevated alanine aminotrans-ferase (ALT) on lab testing or imaging suggestive of fatty infiltration. C. Family and social history. 1. Take a detailed history of alcohol intake to rule out alcohol-related liver disease. 2. Diet and weight history. D. Review of systems. 1. There are very few symptoms. 2. In advanced liver disease, they may have evidence of synthetic dysfunction. Physical Examination A. Most patients are obese. B. Hepatomegaly. C. In cirrhosis, may have stigmata of chronic liver disease. Diagnostic Tests A. Diagnosis made after exclusion of other causes and posi-tive findings of fatty infiltration on imaging or biopsy. B. Labs: Complete blood count (CBC), comprehensive metabolic panel (CMP), cholesterol, iron studies, ferritin, t hyroid-stimulating hormone (TSH), celiac antibody. C. Hepatitis A, B,and C serologies. D. Autoimmune markers antinuclear antibody (ANA), AMA, ASMA. E. Ceruloplasmin, Alpha 1 antitrypsin, HFE gene for hemochromatosis. F. Imaging: Ultrasound or MRI. G. Liver biopsy. Differential Diagnosis A. Viral hepatitis. B. Autoimmune disease. Nonalcoholic Fatty Liver Disease

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90 4. Gastrointestinal Guidelines C. Wilson's disease. D. Alpha 1 antitrypsin deficiency. E. Hemochromatosis. F. Alcohol-related hepatitis. G. Celiac disease. H. Thyroid disease. I. Medication induced: Amiodarone, methotrexate, tamox-ifen, steroids, antiretrovirals. Evaluation and Management A. General plan. 1. If no biopsy performed, consider noninvasive testing to assess degree of fibrosis, that is, Fibroscan. 2. Lifestyle modifications—weight loss, diet, and exercise. 3. Control of sugars. 4. T reatment of hyperlipidemia and HTN. 5. Monitor liver tests every 3 months. 6. Bariatric surgery may be considered if appropriate. B. Patient/family teaching points. 1. In general, control of risk factors contributing to metabolic syndrome. 2. Weight loss of 7% to 10% of current weight to improve fibrosis. 3. Avoid alcohol. 4. Good glucose control. 5. Vitamin E is not recommended if patient has heart disease or diabetes. 6. Reassure the patient that NAFLD is a chronic condi-tion. Most people will not develop advanced liver disease. C. Pharmacotherapy. 1. Vitamin E: Improves liver histology. 800 IU per day is recommended. 2. Statin therapy. 3. Clinical trials: Obeticholic acid (OCA) shows promise for future therapy. D. Discharge instructions. 1. Follow-up with g astrointestinal (GI)/hepatologist, p neumocystis pneumonia (PCP), and/or endocrinolo-gist. 2. Lifestyle modifications of diet and exercise. 3. Avoid alcohol. 4. Do not take any new medications/supplements with-out consulting your doctor. Follow-Up A. As noted in the discharge instructions, follow-up with PCP, GI/hepatology, and/or endocrinology. B. Patients with NASH cirrhosis will need hepatocellular carcinoma (HCC) screening and esophageal varices screen-ing under the supervision of a hepatologist. Consultation/Referral A. Dietician. B. Endocrinologist. C. Bariatric surgeon. D. Cardiologist. Special/Geriatric Considerations A. Another cause of hepatic steatosis is acute fatty liver of pregnancy. B. This is a rare condition and typically occurs in the third trimester to mothers with multiple gestation pregnancies. C. Early diagnosis and prompt delivery is primary treatment. Bibliography Chalasani, N., Younossi, Z., Lavine, J. E., Charlton, M., Cusi, K., Rinella, M.,... Sanyal, A. J. (2018). The diagnosis and management of nonal-coholic fatty liver disease: Practice guidance from the American Asso-ciation for the Study of Liver Diseases. Hepatology, 67 (2), 328-357. doi:10. 1002/hep. 29367 Chopra, S., & Lai, M. (2018, December 10). Management of nonalco-holic fatty liver disease in adults. In K. M. Robson (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/management-of-nonalcoholic-fatty-liver-disease-in-adults Sheth, S. G., & Chopra, S. (2018, April 3). Epidemiology, clini-cal features, and diagnosis of nonalcoholic fatty liver disease in adults. In K. M. Robson (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/epidemiology-clinical-features-and-diagnosis-of-nonalcoholic-fatty-liver-disease-in-adults Tendler, D. A. (2018, September 14). Pathogenesis of nonalcoholic fatty liver disease. In K. M. Robson (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/pathogenesis-of-nonalcoholic-fatty-liver-disease Pancreatitis Catherine Harris Definition A. Acute pancreatitis is a sudden inflammation of the pancreas. Incidence A. The incidence of acute pancreatitis ranges from 4. 9 to 13/100,000 persons. B. Leading gastrointestinal cause of hospitalization, with more than 300,000 admissions per year. C. 16. 5% to 25% of patients experience recurrent episodes in the first several years post diagnosis. D. Acute pancreatitis is frequently an isolated event, but may develop into chronic pancreatitis, particularly in the setting of chronic alcoholism. E. 60% to 90% of patients with pancreatitis have a history of chronic alcohol consumption; however, only a minority of alcoholics develop the disease. F. Mortality rate for acute pancreatitis has remained the same over the past decade at 10%. G. Optimal outcomes depend on recognition of acute pan-creatitis as quickly as possible. Pathogenesis A. Gallstones and alcohol account for about 80% of all cases of acute pancreatitis. B. Other causes of acute pancreatitis can be related to med-ications and very rarely to infections, trauma, or surgery of the abdomen. About 10% of cases are idiopathic. 1. Gallstones. a. Gallstones can lodge in the common bile duct and cause obstruction of the pancreatic fluid by impinging on the main pancreatic duct. b. Mechanism is not completely understood. 2. Alcohol. a. Alcohol is metabolized by the pancreas and is thought to have a toxic effect on key cells. b. Alcohol may also cause the production of excess collagen that contributes to fibrosis. c. Large amounts of alcohol (80 g/day; approxi-mately 10 to 11 drinks) for 6 to 12 years is required to produce symptomatic pancreatitis.

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91 3. Medications. a. Very rare and not well understood mechanism of how medications induce acute pancreatitis. b. Possible theories include pancreatic duct constric-tion, cytotoxic, and metabolic effects. c. Medications associated with acute pancreatitis. i. Angiotensin-converting enzyme inhibitors. ii. Statins. iii. Oral contraceptives. iv. Diuretics. v. Valproic acid. vi. Glucagon-like peptide 1 (GLP-1) hypo-glycemic agents. 4. T rauma or surgery. a. Injury to pancreas from trauma or surgery typi-cally occurs from hemorrhage and sepsis related to pri-mary injury. b. Least commonly injured organ in abdominal trauma due in part to its location. Predisposing Factors A. Choledocholithiasis. B. Chronic alcoholism. C. Hypertriglyceridemia (greater than 1,000 mg/d L). Subjective Data A. Common complaints/symptoms. 1. Severe abdominal pain. 2. Nausea and vomiting. 3. Diarrhea. B. Common/typical scenario. 1. Patients may start with sudden onset dull pain in the abdomen that becomes increasingly more severe. 2. Pain localizes to the upper abdomen and may radiate to back. 3. Usually associated with nausea and vomiting. 4. Patients usually restless and bending forward to try to alleviate the constant pain. C. Family and social history. 1. Alcoholism. 2. Familial history of hypertriglyceridemia. 3. Recent abdominal surgery or trauma. D. Review of systems. 1. Constitutional: Ask about any fever. 2. Cardiovascular: May have rapid heartbeat or feel light-headed. 3. Respiratory: Ask about any difficulty breathing or trouble getting air in. 4. Gastrointestinal: Ask about nausea, vomiting, diar-rhea, pain location and intensity, and if any radiation. 5. Weight loss. Physical Examination A. Gastrointestinal—abdominal tenderness, distention, guarding, bowel sounds may be diminished or absent, may have jaundice. B. Respiratory—dyspnea from diaphragmatic inflamma-tion. C. Cardiovascular—hemodynamic instability in severe acute pancreatitis; assess for signsand symptoms of shock. D. Skin—physical findings consistent with severe necrotiz-ing pancreatitis. 1. Cullen sign: Periumbilical bluish discoloration. 2. Grey T urner sign: Reddish brown discoloration along flanks consistent with extravasated pancreatic exudate. Diagnostic Tests A. Lab studies. 1. Amylase and lipase are routinely ordered and will be elevated at least 3 ×above normal reference range in acute pancreatitis. The serum level of amylase or lipase does not correlate with severity. a. Amylase: Half-life is short (less than 12 hours) and will return to normal; not specific to acute pancreatitis. b. Lipase elevations support diagnosis of acute pan-creatitis and is more specific than amylase to the pan-creas. 2. Liver function tests (LFTs). a. Alkaline phosphatase. b. Total bilirubin. c. Aspartate aminotransferase (AST). d. Alanine aminotransferase (ALT) greater than 150 U/L suggests gallstone pancreatitis. 3. Basic metabolic panel, electrolytes, cholesterol, and triglycerides. a. Hypertriglyceridemia (greater than 1,000 mg/d L). 4. C-reactive protein. a. Higher levels (greater than 10 mg/d L) associated with severe pancreatitis, but is not specific for pancre-atitis. 5. Lactic dehydrogenase (LDH) should be checked to provide prognosis based on the Ranson criteria (see sec-tion “Evaluation and Management Plan”). 6. Immunoglobulin G4 (Ig G4) if concern for autoim-mune pancreatitis. B. Imaging studies. 1. Ultrasound. a. Good screening test for determining the etiology of pancreatitis and standard of care for detecting gall-stones. b. Cannot measure severity of disease. 2. Endoscopic ultrasonography. a. High frequency ultrasound can provide more detailed imagery. 3. Contrast-enhanced CT or MRI only necessary if a diagnosis is uncertain with clinical presentation and lab-oratory data. C. Endoscopic retrograde cholangiopancreatography (ERCP). 1. Endoscopic procedure used in patients with severe acute pancreatitis with suspected gallstones or biliary pan-creatitis with worsening clinical examination. 2. Not used routinely in patients with acute pancreatitis and should be used with caution and only in cases where gallstones are suspected to be the underlying etiology. Differential Diagnosis A. Cholecystitis. B. Acute abdomen. C. Pneumonia. D. Peptic ulcer disease. E. Hepatitis. F. Irritable bowel syndrome. G. Myocardial infarction. H. Chronic pancreatitis. I. Gastroenteritis. J. Peritonitis. Evaluation and Management Plan A. General plan. Pancreatitis

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92 1. Stage acute pancreatitis to determine prognosis using the 11-point Ranson criteria within 48 hours. Each cri-teria is 1 point. Ranson score 0 to 2: Minimal mortality; Ranson score 3 to 5: 10% to 20% mortality; Ranson score greater than 5 after 48 hours has a mortality rate greater than 50%. a. Present on admission. i. Patient older than 55 years. ii. White blood cell (WBC) count higher than 16,000 u L. iii. Blood glucose higher than 200 mg/d L. iv. Serum LDH level higher than 350 IU/L. v. AST level higher than 250 IU/L. b. Develops within 48 hours. i. Drop of hematocrit more than 10%. ii. Blood urea nitrogen (BUN) increases more than 8 mg/d L. iii. Fluid retention greater than 6 L. iv. Base deficit greater than 4 m Eq/L. v. Pa O2 less than 60 mm Hg. vi. Serum calcium less than 8 mg/d L. 2. Supportive medical care. a. Bowel rest for several days except in mild cases where there is no nausea or vomiting. b. Nutritional support with dextrose 5% in water for mild pancreatitis. c. In moderate to severe pancreatitis, start nasojejunal feeds with low fat formulation. d. Parenteral nutrition should be avoided except in very severe cases in order to minimize the risk of infections. e. Pain management. f. Aggressive rehydration with intravenous fluids within the first 12 to 24 hours of symptom onset— monitor patients with cardiovascular and renal comorbidities very closely. 3. Surgical therapy. a. ERCP within 24 hours of admission if patient has concurrent acute cholangitis. b. Gallstones may require surgical intervention. c. Resection of necrotic tissue if necrotizing pancre-atitis or abscess. d. Sphincteroplasty may be performed if sphincter dysfunction is found. 4. Monitor for complications associated with severe acute pancreatitis. a. Shock. b. Pulmonary complications. c. Inflammatory changes. i. Kidney dysfunction. ii. Gastrointestinal bleeding. iii. Colitis. iv. Splenic vein thrombosis. d. Localized complications are more likely to occur in patients with alcoholic and biliary pancreatitis. i. Fluid collection. ii. Ascites. iii. Pseudocysts. B. Patient/family teaching points. 1. Acute pancreatitis is typically relieved after a couple days but can become severe. 2. Avoid binge drinking. 3. Smoking cessation is thought to exacerbate episodes of acute pancreatitis but the studies are not conclusive. 4. Recurrence of acute pancreatitis may occur and pre-vention depends on the cause. a. If gallstones caused acute pancreatitis, you may need to have your gallbladder removed. b. If alcohol is the cause, you should stop drinking. 5. Diet changes may be required in people with high fat intake. 6. Medication changes may be necessary if acute pancre-atitis is associated with a particular drug. 7. Some patients may develop chronic pancreatitis but acute pancreatitis is more frequently a one off event, espe-cially if the underlying cause is treated. C. Pharmacotherapy. 1. No specific pharmacological therapy for acute pancre-atitis. 2. Supportive fluid resuscitation and management of pain. 3. Antibiotic therapy only in cases of suspected infection. D. Discharge instructions. 1. Eliminate alcohol from diet. 2. Eat small frequent meals. 3. Reduce fat in diet. 4. Don't smoke. 5. Follow-up with the gastroenterologist. Follow-Up A. No guidelines established for long-term follow-up. B. Depending on etiology, may need follow-up imaging or lab monitoring. Consultation/Referral A. Gastroenterology should evaluate all cases of pancreatitis. B. Surgical consult for acute pancreatitis related to gall-stones. C. Endocrinology consult if patient has hyperparathy-roidism, hypertriglyceridemia, or hypercalcemia-induced pancreatitis. D. Refer patients to social work if alcohol abuse suspected. Special/Geriatric Considerations A. Gallstone pancreatitis is much more likely in elderly and pregnant persons. B. Presenting abdominal pain may be more vague in elderly patients. C. Acute pancreatitis is rare during pregnancy but typically occurs in the third trimester and is mostly due to gallstones, which can cause preterm labor or in utero fetal demise. Bibliography Balthazar, E. J. (2002). Staging of acute pancreatitis. Radiologic Clinics, 40(6), 1199-1209. doi:10. 1016/S0033-8389(02)00047-7 Banks, P. A., Bollen, T. L., Dervenis, C., Gooszen, H. G., Johnson, C. D., Sarr, M. G.,... Vege, S. S. (2013). Classification of acute pancreatitis— 2012: Revision of the Atlanta classification and definitions by inter-national consensus. Gut, 62 (1), 102-111. doi:10. 1136/gutjnl-2012-302779 Ducarme, G., Maire, F., Chate, P., Luton, D., & Hammel, P. (2014). Acute pancreatitis during pregnancy: A review. Journal of Perinatology, 34, 87-94. doi:10. 1038/jp. 2013. 161 Imrie, C. W. (2003). Prognostic indicators in acute pancreatitis. Canadian Journal of Gastroenterology, 17 (5), 325-358. doi:10. 1155/2003/250815 Jones, M., Hall, O., Kaye, A. M., & Kaye, A. D. (2015). Drug-induced acute pancreatitis: A review. Ochsner Journal, 15 (1), 45-51. Retrieved from http://www. ochsnerjournal. org/content/15/1/45 Strate, T., Yekebas, E., Knoefel, W., Bloechle, C., & Izbicki, J. (2002). Pathogenesis and the natural course of chronic pancre-atitis. European Journal of Gastroenterology & Hepatology, 14 (9), 929-934. Retrieved from https://journals. lww. com/eurojgh/Fulltext/ 2002/09000/Pathogenesis_and_the_natural_course_of_chronic. 2. aspx4. Gastrointestinal Guidelines

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93 Tenner, S., Baillie, J., De Witt, J., & Vege, S. S. (2013). American College of Gastroenterology guideline: Management of acute pan-creatitis. The American Journal of Gastroenterology, 108 (9), 1400-1416. Retrieved from https://journals. lww. com/ajg/Abstract/2013/ 09000/American_College_of_Gastroenterology_Guideline_. 6. aspx Vege, S. S., Ziring, B., Jain, R., & Moayyedi, P. (2015). American Gastroen-terological Association institute guideline on the diagnosis and man-agement of asymptomatic neoplastic pancreatic cysts. Gastroenterology, 148(4), 819-822. doi:10. 1053/j. gastro. 2015. 01. 015 Whitcomb, D. C. (2006). Clinical practice. Acute pancreatitis. New England Journal of Medicine, 354 (20), 2142-2150. doi:10. 1056/ NEJMcp054958 Whitcomb, D. C., Yadav, D., Adam, S., Hawes, R. H., Brand, R. E., Ander-son, M. A.,... Barmada, M. M. (2008). Multicenter approach to recur-rent acute and chronic pancreatitis in the United States: The North American Pancreatitis Study 2 (NAPS2). Pancreatology, 8 (4-5), 520-531. doi:10. 1159/000152001 Peptic Ulcer Disease Catherine Harris Definition A. An ulcer that forms in the lining of the esophagus, stom-ach, or small intestine. Incidence A. 10% of the population is thought to have evidence of peptic ulcer disease (PUD). B. Similar occurrence in males and females. C. Mortality rate due to hemorrhagic ulcer is approximately 5%. Pathogenesis A. Defect of mucosal lining of digestive tract; frequently occurs when there is an imbalance between gastric acid secre-tion and degradation of the mucosal defense mechanism caused by use of anti-inflammatory drugs, Helicobacter pylori infection, alcohol, acid, and pepsin. B. H. pylori infection can colonize the gastric mucosa and cause inflammation. C. Nonsteroidal anti-inflammatory drug (NSAID) use can disrupt the mucosal barrier. D. Alcohol is a gastric mucosal irritant. E. Stress ulceration can occur and is associated with serious systemic illnesses. F. Brain injury or tumors are associated with high gastric acid output. G. Hypersecretory states can also cause PUD, most notably Zollinger-Ellison syndrome. H. Three types of ulcers (location based). 1. Gastric ulcers. 2. Esophageal ulcers. 3. Duodenal ulcers. I. Major risk of perforation, which carries a mortality rate of up to 30%. Predisposing Factors A. Taking NSAIDs including ibuprofen, aspirin. B. Smoking. C. Excessive alcohol. D. Excess stress. E. Obesity. F. Zollinger-Ellison disease. Subjective Data A. Common complaints/symptoms. 1. Gnawing or burning sensation that occurs shortly after meals (gastric ulcers) or at 2 to 3 hours (duodenal ulcers). 2. Heartburn. 3. Belching. 4. Bloating. 5. Distention. B. Common/typical scenario. 1. Gastric and duodenal ulcers typically cannot be dif-ferentiated with history alone, but there are some differ-ences. a. Most patients regardless of type of PUD complain of epigastric pain. b. Patients with gastric ulcers typically complain of pain shortly after meals. c. In patients with duodenal ulcers: i. Antacid use commonly ineffective. ii. Complaints of pain 2 to 3 hours after a meal. iii. Frequent night waking. C. Family and social history. 1. Ask about smoking and alcohol use. 2. Ask about family history of any type of gastric cancer. D. Review of systems. 1. Evaluate for dysphagia, nausea, vomiting, or blood in stool. 2. Evaluate pain intensity, timing, and duration. 3. Inquire about back pain (which may indicate gall-stones or pancreatitis). Physical Examination A. Gastrointestinal focus. 1. Epigastric tenderness. 2. Typically pain will be vague and nonlocalizing. 3. Melena may be present. B. If the ulcer perforates. 1. Sudden onset of severe abdominal pain that is gener-alized and worsens with movement. 2. Rebound abdominal tenderness. 3. Guarding. 4. Rigidity. 5. May have signs of shock including: a. Tachycardia. b. Hypotension. c. Anuria. Diagnostic Tests A. Obtain complete blood count (CBC) and l iver function tests (LFTs) in all suspected cases of PUD. B. Use amylase or lipase to rule out other causes of epigastric pain. C. Test for H. pylori. D. Upper g astrointestinal (GI) endoscopy is the preferred diagnostic test in PUD. 1. Differentiates gastric and duodenal ulcers. 2. Allows for biopsy if indicated. E. Angiography may be needed in cases with massive GI bleeding. F. If Zollinger-Ellison syndrome is suspected, obtain serum gastrin level: If inconclusive, order secretin stimulation test. G. Biopsy if concern for cancer. Differential Diagnosis A. Gastritis. B. Gastroesophageal reflux disease (GERD). C. Inflammatory bowel disease. D. Cholecystitis. Peptic Ulcer Disease

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94 E. Coronary artery disease. F. Esophageal rupture. G. Diverticulitis. H. Pancreatitis. I. Viral hepatitis. Evaluation and Management Plan A. General plan. 1. Gastric ulcers can be staged according to Johnson clas-sification. a. Type I—normal or decreased gastric acid secre-tion. b. Type II—combination of stomach and duodenal ulcers with normal or increased gastric acid secretion. c. Type III—prepyloric associated with normal or increased gastric acid secretion. d. Type IV—near gastroesophageal junction with normal or decreased gastric acid secretion. 2. T reatment plans vary on the location of the peptic ulcer and clinical presentation. 3. Typical treatment options include: a. Empiric antisecretory therapy. b. T riple therapy for H. pylori infection. c. Endoscopy 6 to 8 weeks after diagnosis to docu-ment healing of ulcers. d. Document H. pylori cure with noninvasive test. i. Urea breath test. ii. Fecal antigen test (complicated ulcers). B. Patient/family teaching points. 1. Avoid NSAIDs and aspirin. 2. Reduce or eliminate alcohol. 3. Smoking cessation. 4. Reduce or eliminate caffeine from diet. 5. Weight loss. 6. Stress reduction. C. Pharmacotherapy. 1. H. pylori infection. a. Option 1—10 to 14 days of quadruple therapy. i. Bismuth. ii. Proton pump inhibitor. iii. Tetracycline. iv. Nitroimidazole. b. Option 2—10 to 14 days. i. Proton pump inhibitor. ii. Clarithromycin. iii. Amoxicillin. iv. Nitroimidazole. c. Option 3—10 to 14 days of triple therapy (no previous macrolide exposure and clarithromycin resis-tance low). i. Clarithromycin. ii. Proton pump inhibitor. iii. Amoxicillin or metronidazole. d. Other suggested options per guidelines. 2. H. pylori infection persists. a. Avoid previously used antibiotics. b. Choose a new option from the aforementioned list. D. Discharge instructions. 1. Follow-up with primary care provider for long-term monitoring and further evaluation. Follow-Up A. Follow-up routinely with primary care provider to assure proper maintenance therapy is initiated and symptoms are controlled. B. If H. pylori eradication is not achieved, antisecretory ther-apy should be recommended. Consultation/Referral A. Consult to gastroenterology for bleeding (hematemesis or melena), anemia, unexplained weight loss, associated vomit-ing, or family history of gastrointestinal cancer. B. Surgical consultation for all bleeding ulcers or suspected perforations. C. Urgent referral for sudden and severe onset of symptoms, which may indicate perforation. D. Failure of medical management. Special/Geriatric Considerations A. NSAID-induced PUD may not be overtly symptomatic in elderly patients. B. Elderly patients may also present with significantly less profound signs and symptoms of shock in the case of perfo-rated ulcers. 4. Gastrointestinal Guidelines Bibliography Boparai, V., Rajagopalan, J., & T riadafilopoulos, G. (2008). Guide to the use of proton pump inhibitors in adult patients. Drugs, 68 (7), 925-947. doi:10. 2165/00003495-200868070-00004 Chey, W. D., Leontiadis, G. I., Howden, C. W., & Moss, S. F. (2017). ACG clinical guideline: T reatment of Helicobacter pylori infection. The American Journal of Gastroenterology, 112, 212-238. Retrieved from https://journals. lww. com/ajg/Abstract/2017/02000/ACG_Clinical_ Guideline__T reatment_of_Helicobacter. 12. aspx Chey, W. D., & Wong, B. C. (2007). American College of Gastroenterology guideline on the management of Helicobacter pylori infection. The Amer-ican Journal of Gastroenterology, 102 (8), 1808-1825. Retrieved from https://journals. lww. com/ajg/Abstract/2007/08000/American_College _of_Gastroenterology_Guideline_on. 36. aspx Ford, A. C., Marwaha, A., Lim, A., & Moayyedi, P. (2010). What is the prevalence of clinically significant endoscopic findings in subjects with dyspepsia? Systematic review and meta-analysis. Clinical Gastroenterol-ogy and Hepatology, 8 (10), 830-837. e2. doi:10. 1016/j. cgh. 2010. 05. 031 Leontiadis, G. I., Sreedharan, A., Dorward, S., Barton, P., Delaney, B., Howden, C. W.,... Forman, D. (2007). Systematic reviews of the clinical effectiveness and cost-effectiveness of proton pump inhibitors in acute upper gastrointestinal bleeding. Health T echnology Assessment, 11(51), 1-164. doi:10. 3310/hta11510 Ramakrishnan, K., & Salinas, R. C. (2007). Peptic ulcer disease. American Family Physician, 76 (7), 1005-1012. Retrieved from https://www. aafp. org/afp/2007/1001/p1005. html Schubert, M. L., & Peura, D. A. (2008). Control of gastric acid secretion in health and disease. Gastroenterology, 134 (7), 1842-1860. doi:10. 1053/ j. gastro. 2008. 05. 021 Sung, J. J., Tsoi, K. K., Ma, T. K., Yung, M.-Y., Lau, J. Y., & Chiu, P. W. (2010). Causes of mortality in patients with peptic ulcer bleeding: A prospective cohort study of 10,428 cases. The American Journal of Gas-troenterology, 105 (1), 84-89. Retrieved from https://journals. lww. com/ ajg/Abstract/2010/01000/Causes_of_Mortality_in_Patients_With_ Peptic_Ulcer. 15. aspx

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5 Nephrology Guidelines Acute Kidney Injury Alexis Chettiar Definition A. Abrupt decline in renal function associated with an increase in nitrogen waste products over the course of a short time frame (hours to days). B. Can be defined by the RIFLE criteria (also has implied staging built into the definition). 1. Risk: Increase in serum creatinine 50% to 99% (increased SCreat ×1. 5 or glomerular filtration rate [GFR] decrease >25%) OR Urine output less than 0. 5 m L/kg/hr for 6 to 12 hours. 2. Injury: Increase in serum creatinine 100% to 199% (increased SCreat ×2 or GFR decrease >50%) OR Urine output less than 0. 5 m L/kg/hr for 12 to 24 hours. 3. Failure—Increase in serum creatinine greater than 200% (increase SCreat ×3 GFR decrease >75% OR SCreat >4. 0 mg/d L) OR increase in serum creatinine by 0. 5 mg/d L to greater than 4. 0 mg/d L OR urine output less than 0. 3 m L/kg/hr for greater than 24 hours or anuria for greater than 12 hours OR Initiation of renal replace-ment therapy. 4. Loss—Persistent acute renal failure (ARF) and com-plete loss of kidney function; need for renal replacement therapy for greater than 4 weeks. 5. End-stage renal disease (ESRD)—End-stage kidney disease greater than 3 months; need for renal replacement therapy for greater than 3 months. Incidence A. The true incidence of acute kidney injury (AKI) is diffi-cult to determine due to variation in diagnostic criteria. B. The incidence is estimated at 1% to 25% of ICU patients. 1. This increases the odds ratio of mortality from 2. 2 to 8. 8, depending on the AKI stage. 2. Even small increases in serum creatinine are associated with a significant increase in mortality. Pathogenesis A. AKI is the reduction of renal blood flow and decrease of GFR typically from one of three main mechanisms. 1. Prerenal: Decreased renal perfusion from hypotension or hypovolemia. 2. Intrinsic: Renal failure from diseases of the kidney, with ischemic causes being the most common. May also result from medications and poorly controlled chronic kidney disease. 3. Obstructive—build up of tubular pressure caused by an obstruction of the urinary tract. Predisposing Factors A. Prerenal. 1. Hemorrhage. 2. Diarrhea. 3. Diuretics. 4. Heart failure. 5. Acute myocardial infarction (MI). 6. Pulmonary embolus. 7. Sepsis. 8. Anaphylaxis. 9. Medications, including nonsteroidal anti-inflammatory drugs (NSAIDs). 10. Hepatorenal syndrome. 11. Any condition that causes hypovolemia. B. Intrinsic. 1. Renal artery or vein obstruction. 2. Severe hypertension. 3. Atherosclerosis. 4. Nephrotoxic medications (amphotericin B, NSAIDs, radiocontrast agents). 5. Goodpasture's syndrome. 6. Glomerulonephritis from lupus. 7. Systemic diseases such as lymphoma, Sjögren's syn-drome, leukemia. C. Postrenal. 1. Urinary stones. 2. Strictures. 3. T umors of urinary tract. 4. Thrombosis. Subjective Data A. Common complaints/symptoms. 1. Usually asymptomatic. a. However, patients may experience symptoms related to the underlying cause of AKI (see s ection “Differential Diagnosis”). 2. If symptomatic, patients may complain of: a. Edema. b. Decreased urine output. c. Nausea. d. Anorexia. B. Family and social history. 1. May not be relevant; history of chronic kidney disease. C. Review of systems. 1. Ask patient about the presence of: Acute Kidney Injury95

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a. Any new medications, especially: i. Statins (rhabdomyolysis). ii. Antibiotics (nephrotoxicity, intrarenal AKI). iii. Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). iv. NSAIDs. b. Chemotherapy treatment. c. Exposure to toxic substances such as ethyl alcohol or ethylene glycol. d. Changes in blood pressure or blood pressure man-agement (prerenal AKI, vasculitis intrarenal AKI). e. Blood loss or transfusion. f. History of liver disease (cirrhotic prerenal AKI). g. Recent or past history of thrombus or embolisms (prerenal AKI due to renal artery thrombosis). h. History of renal artery stenosis. i. Recent history of infectious disease (post infec-tious glomerulonephritis). j. Recent procedures or diagnostic examinations involving the use of IV radiocontrast. i. Examples: Angiography or CT. k. Extreme exercise or trauma (rhabdomyolysis). l. History of myeloma. i. Bone pain. ii. Fractures. iii. Weight loss. m. History of kidney stones or gout (acute tubular necrosis [ATN]) due to intratubular crystal deposi-tion. n. Rash (vasculitis). Physical Examination A. Skin. 1. Livedo reticularis (systemic vasculitis). a. Digital ischemia. b. Butterfly rash. c. Palpable purpura. 2. Maculopapular rash (allergic interstitial nephritis). 3. T rack marks (endocarditis). 4. Mucosal or cartilaginous lesions (Wegener's granulo-matosis). 5. Skin turgor (hypovolemic AKI). B. Ophthalmic examination. 1. Conjunctival jaundice. 2. Band keratopathy (hypercalcemia due to multiple myeloma). 3. Symptoms of malignant hypertension. a. Papilledema. b. Flame-shaped hemorrhages. 4. Atheroemboli (renal ischemia due to atheroemboli or renal artery thrombosis). 5. Uveitis (interstitial nephritis/necrotizing vasculitis). 6. Ocular palsy (ethylene glycol poisoning). C. Ears. a. Hearing acuity (hearing loss related to aminogly-coside). D. Cardiovascular system. 1. Assessment of volume status (intra-and extra-vascular volume). a. Blood pressure and pulse: Sitting and standing. b. Jugular vein distention. c. S3heart sounds (heart failure). d. Peripheral/dependent edema. e. Hourly intake and output records. f. Daily weight. 2. Heart rate/rhythm. a. Atrial fibrillation (thromboembolism, decreased cardiac output). b. Murmurs (endocarditis). c. Pericardial friction rub (endocarditis). E. Pulmonary system. 1. Auscultation of lung sounds. a. Pulmonary vascular congestion (congestive heart failure). b. Rales (pulmonary-renal syndromes). 2. Hemoptysis. 3. Respiratory rate and effort (congestive heart failure). F. Abdomen. 1. Pulsatile mass or bruit (atheroemboli). 2. Abdominal or costovertebral angle tenderness (nephrolithiasis, renal artery thrombosis, renal vein thrombosis). 3. Abdominal fluid wave (ascites, cirrhosis, or elevated intra-abdominal pressure). 4. Symptoms of urinary obstruction. a. Pelvic/rectal masses. b. Prostatic hypertrophy. c. Distended bladder. Diagnostic Tests A. Comprehensive blood chemistry panel, with serum osmolality. B. Complete blood count (CBC). 1. Prolonged AKI causes nephrogenic anemia (due to reduced renal erythropoietin synthesis). C. Renal ultrasound. 1. Rule out hydronephrosis due to obstructive process. 2. Assess underlying state of kidney mass and sclerosis. D. 24-hour creatinine clearance. 1. Gives an accurate assessment of current renal clear-ance. Serum creatinine is a late indicator of renal dysfunc-tion. E. Hourly urine output. F. Urinalysis with microscopy. 1. Granular, muddy casts in urine sediment suggest tubular necrosis. 2. Oxalate crystals also observed in ATN. 3. Eosinophils common in interstitial nephritis. G. Urine sodium and osmolality. H. Fractional Excretion of Sodium and Urea (FENa) helps differentiate cause of AKI in the presence of oliguria. 1. FENa =(UNa/PNa)/(U Cr/PCr) x 100. a. FENa lessthan 1% is usually prerenal azotemia. b. FENa greater than 1% is usually ATN caused by contrast, burns, rhabdomyolysis, or acute glomeru-lonephritis. I. Further testing depends on the suspected cause of AKI. J. Renal biopsy: May be indicated if the cause cannot be determined and renal function does not return for a pro-longed period of time. Differential Diagnosis A. Prerenal. 1. Hemorrhage. 2. Volume depletion. 3. Congestive heart failure. 4. Cirrhosis. 5. Renal artery. 6. Stenosis. 7. Thrombosis/embolism. 8. NSAIDs. 9. ACE inhibitor and ARB. 5. Nephrology Guidelines96 96

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B. Intrarenal. 1. ATN. a. Ischemic. b. Toxic. i. Exogenous. 1)Antibiotics. 2)Contrast. 3)Chemotherapy. ii. Endogenous. 1)Pigment (hemoglobinuria, myoglobin-uria). 2)Intratubular proteins (myeloma). 3)Intratubular crystals (uric acid, oxalate). 2. Acute interstitial nephritis. a. Drug associated. b. Acute glomerulonephritis. c. Post infectious. d. Vascular. i. Vasculitis. ii. Malignant hypertension. C. Postrenal. 1. Obstructive. 2. Bladder outlet obstruction. 3. Bilateral ureteral obstruction. Evaluation and Management Plan A. General plan. 1. Use the ABCDE-IT mnemonic to quickly deter-mine a treatment plan (see Box 5. 1, AKI ABCDE-IT Mnemonic). 2. Determine the stage of AKI using the RIFLE criteria and manage accordingly (see Figure 5. 1, AKI T reatment Algorithm). 3. Monitor serum creatinine. 4. Avoid further renal insult. 5. Ensure that blood pressure is in the target range (varies depending on the patient's age and comorbid disease sta-tus). 6. Correct fluid overload to achieve volume homeostasis. 7. Correct any acidosis or electrolyte abnormalities. BOX 5. 1 Acute Kidney Injury ABCDE-IT Mnemonic Assess for acute complications (high potassium, acidosis, fluid overload). BP check (if systolic BP <110, consider fluid challenge). Catheterize (to eliminate postbladder obstructive process and monitor I/O). Drugs; stop/avoid nephrotoxins, hold ACE inhibitors. Exclude obstruction (Renal US). Investigations; urinalysis with micro, for stage 2/3 AKI add ANCA, Anti GBM Ab, DSDNA, ANA, immunoglobulin, electrophoresis. Treat the cause. ACE, angiotensin-converting enzyme; AKI, acute kidney injury; ANA, antinuclear antibody; ANCA; antineutrophil cytoplasmic antibodies; BP, blood pressure; DSDNA, double stranded deoxyribonucleic acid; US, ultrasound B. Patient/family teaching points. 1. Signs/symptoms to monitor: Edema, headache, dizzi-ness, or syncope. 2. Common occurrences: Hypotension or hypertension. 3. Readmission concerns. a. Recurrent AKI due to secondary renal insult that is often due to inappropriate resumption of medications (ACE inhibitors/ARBs, NSAIDs) or hypotension/ hypertension. b. Patients should be clear about which medications to hold/restart after discharge and check home blood pressure. If the patient is able to check home blood pressure, provide high and low parameters for report-ing readings. c. These parameters will vary according to the clin-ical context, but generally patients should call the provider to report a systolic blood pressure less than 130 mm Hg, systolic blood pressure greater than 180 mm Hg, and diastolic blood pressure greater than 100 mm Hg. d. Renal vasculature is sensitive to blood pressure fluctuations in the recovery phase of AKI, and hypotension or hypertension can precipitate further renal injury. C. Pharmacotherapy. 1. No pharmacotherapy treatment in AKI. The primary cause must be reversed. 2. Intravenous isotonic sodium chloride solution should be used to maintain euvolemia as clinically indicated. 3. Medications. a. Hold ACE inhibitors, ARBs, NSAIDs, and any other medications associated with renal insult (e. g., nephrotoxic chemotherapy, aminoglycoside, and beta lactam antibiotics) until patient's serum creatinine has stabilized at baseline. b. Note that renal dose dopamine may cause some dilatation to enhance renal perfusion. However, no study has been able to demonstrate a beneficial role of vasodilator use. D. Discharge instructions. 1. Serum creatinine has either returned to baseline OR, 2. It has significantly improved with a downward trend and resolution of AKI etiology. Follow-Up A. Monitor. 1. Serum creatinine and electrolytes. 2. Urine output. 3. Volume status. B. Pursue other follow-up as indicated specific to the under-lying cause of the AKI. C. Check creatinine within 1 to 2 weeks after discharge to confirm improvement. D. If medications are on hold due to AKI, follow to deter-mine when medications should be restarted. Consultation/Referral A. Early nephrology consultation should occur after hospi-talization. Acute Kidney Injury97

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Special/Geriatric Considerations A. Geriatric considerations. 1. Elderly patients are at high risk for AKI, particularly those treated with diuretics, ACE inhibitors, ARBs, and NSAIDs. 2. Serum creatinine in elderly patients with diminished muscle mass underestimates the extent of renal impair-ment. Bibliography Brivet, F. G., Kleinknecht, D. J., Loirat, P., & Landais, P. J. (1996). Acute renal failure in intensive care units-causes, outcome, and prognostic factors of hospital mortality: A prospective, multicenter study. French Study Group on Acute Renal Failure. Critical Care Medicine, 24 (2), 192-198. doi:10. 1097/00003246-199602000-00003 Hoste, E. A. J., Clermont, G., Kersten, A., Venkataraman, R., Angus, D. C., De Bacquer, D., & Kellum, J. A. (2006). RIFLE criteria for acute kidney5. Nephrology Guidelines98 98 AKI T reat ment Stage 1 AK I Remo ve ris k fact ors o Neph rotoxic agen ts o Vasodilat ors o ACE/ARB o NSAIDs o Stop/reduce diuretics Treat i denti/f_ied c ause(s) o Infections o Hyp ovolemia Resolution Stable Progression Follo w-up Further treatment dic tate d by underlying cau se and clinical c ontext Stag e 2 and 3 AKI Stop diuretics Volu me expansion with albumin, if indicated (1 g/kg) Response Yes No Meets c riteria for h epato-renal syndrome Yes No Vasocon stric tors and albumin Treat ment speci/f_ic to AK I etio logy FIGURE 5. 1 Acute kidney injury treatment algorithm. ACE, angiotensin-converting enzyme; AKI, acute kidney injury; ARB, angiotensin II receptor blockers; NSAIDs, nonsteroidal anti-inflammatory drugs.

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injury are associated with hospital mortality in critically ill patients: A cohort analysis. Critical Care, 10 (3), R73. doi:10. 1186/cc4915 Kidney Disease, Improving Global Outcomes. (2012). KDIGO clinical prac-tice guideline for acute kidney injury. Cranford, NJ: International Society of Nephrology. Retrieved from https://kdigo. org/wp-content/uploads/ 2016/10/KDIGO-2012-AKI-Guideline-English. pdf Leblanc, M., Kellum, J. A., Gibney, R. T. N., Lieberthal, W., T umlin, J., & Mehta, R. (2005). Risk factors for acute renal failure: Inherent and modifiable risks. Current Opinion in Critical Care, 11 (6), 533-536. doi:10. 1097/01. ccx. 0000183666. 54717. 3d Liaño, F., & Pascual, J. (1996). Epidemiology of acute renal failure: A prospective, multicenter, community-based study. Madrid Acute Renal Thakar, C. V., Christianson, A., Freyberg, R., Almenoff, P., & Render, M. L. (2009). Incidence and outcomes of acute kidney injury in intensive care units: A Veterans Administration study*. Critical Care Medicine, 37 (9), 2552-2558. doi:10. 1097/CCM. 0b013e3181a5906f Uchino, S. (2005). Acute renal failure in critically ill patients: A multina-tional, multicenter study. Journal of the American Medical Association, 294(7), 813. doi:10. 1001/jama. 294. 7. 813 Benign Prostatic Hypertrophy Suzanne Barron Definition A. A histological change that develops within the prostate gland, which may lead to the presence of an enlarged prostate gland and associated lower urinary tract symptoms. Incidence A. 50% of men over the age of 40 develop histologic evi-dence of benign prostatic hypertrophy (BPH). 1. 30%-50% of these men develop bothersome lower urinary tract symptoms (LUTS). B. Prevalence of BPH increases with age. 1. 60% for men in their 60s. 2. Up to 90% for men in their 70s and 80s. Pathogenesis A. There is abnormal microscopic hyperplasia and macro-scopic growth. B. The detrusor muscle generates higher pressures, leading to frequency, urgency, and nocturia. C. BPH may lead to bladder decompensation, with the blad-der muscle no longer able to provide enough pressure to uri-nate. D. The role of hormonal involvement in the development of BPH is still poorly understood, but there is evidence that the hormone androgen, which becomes dihydrotestosterone (DHT), plays a critical role in the growth of prostatic tissue. Predisposing Factors A. Advancing age. B. Family history of BPH. C. Ethnic background. 1. The risk of BPH is higher in black and Hispanic men than in white men and Asian men. D. Diabetes and heart disease: Possible increased incidence in BPH. E. Obesity: Possible association with increased prostate vol-ume and LUTS. Subjective Data A. Common complaints/symptoms: LUTS. 1. Storage symptoms or irritative voiding symptoms: Frequency, nocturia, dysuria, decreased volume, urgency, or urge incontinence. 2. Voiding symptoms or obstructive voiding symptoms: Weak stream, intermittent stream, hesitancy, retention, abdominal straining, incomplete emptying, or post void dribbling. B. Common/typical scenario. 1. Onset is gradual, with symptoms increasing over time. 2. Symptoms are often aggravated at night with sig-nificant nocturia, which may often cause difficulty sleeping. 3. Symptoms may be aggravated by cough/cold medica-tions (antihistamines, pseudoephedrine). C. Family and social history. 1. Increased likelihood if father or brother have history of BPH. 2. Increased physical activity: Possible protection against BPH. D. Review of systems. 1. Constitutional: Weight loss or insomnia. 2. Neurological: Dizziness, weakness, tremors, or other signs that may indicate a neurological condition such as multiple sclerosis or Parkinson's disease. 3. Genitourinary: LUTS; usually no flank pain. a. Possible report of suprapubic fullness/tenderness. b. Hematuria: Possible indication of genitourinary malignancy (bladder cancer). 4. Cardiovascular: Lower extremity edema that may indicate heart failure or diuretic use. 5. Endocrine: Polyuria, polyphagia, or polydipsia that may indicate diabetes mellitus or diabetes insipidus. Physical Examination A. Neurological. 1. Evaluate for musculoskeletal weakness, especially lower extremity motor and sensory function. 2. Evaluate gait. B. Digital rectal examination (DRE). 1. To estimate prostate size, assess for prostatitis, or eval-uate prostate nodules that may indicate prostate cancer. 2. Assess for anal sphincter tone; if absent or decreased, possible neurological disorder. C. Abdominal. 1. Palpate for masses that may be pressing on the bladder. D. Genitourinary. 1. Assess for costovertebral angle tenderness. 2. Assess for obvious urethral strictures and phimosis. Diagnostic Tests A. Urinalysis to exclude hematuria or possible infection. B. Blood work. 1. Prostate specific antigen (PSA), especially if prostatic nodules are palpated on DRE or high concern for prostate cancer. 2. Basic metabolic panel to assess for renal function, elec-trolyte abnormalities, and hyperglycemia. C. Imaging: CT or MRI generally not indicated. D. Uroflowmetry: Measures the volume/time of urine accu-mulation. E. Post void residual: Volume of urine remaining in bladder after voiding. 1. Obtain from bladder ultrasound/bladder scan if pos-sible. 2. Straight catheterization if bladder ultrasound not available. F. Urodynamic study to differentiate between bladder outlet obstruction and hypocontractile bladder. This may be neces-sary prior to surgical intervention for BPH. Benign Prostatic Hypertrophy Failure Study Group. Kidney International, 50 (3),811-818. doi:10. 1038/ki. 1996. 38099

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Differential Diagnosis A. Foreign body in urethra/bladder (stone or retained ureteral stents) B. Meatal stenosis. C. Urethral stricture. D. Detrusor sphincter dyssynergia. E. Neurogenic bladder (e. g., multiple sclerosis, Parkinson's disease). F. Bladder cancer. G. Prostate cancer. H. Overactive bladder. I. Interstitial cystitis. J. Infectious source: Acute cystitis, acute prostatitis/chronic prostatitis, or prostatic abscess. K. Pelvic floor dysfunction. L. Radiation cystitis. M. Diabetes insipidus causing polyuria. N. Diabetes mellitus causing polyuria. Evaluation and Management Plan A. General plan. 1. Obtain urinalysis/urine culture. 2. Obtain PSA if concern for prostate cancer. 3. Place Foley catheter for urinary retention or teach patient how to perform clean intermittent catheteriza-tion. 4. Observe for post obstructive diuresis with urinary retention. 5. Advise watchful waiting, with no treatment for men with mild symptoms and good quality of life. 6. Use pharmacotherapy: Alpha blockers or 5-alpha-reductase inhibitors (5-ARIs). 7. Obtain prostate biopsy if elevated PSA or prostatic nodule. 8. Order uroflowmetry/post void residual. 9. Order urodynamic study if indicated. 10. Advise surgery if indicated. B. Patient/family teaching points. 1. Have a thorough discussion with patient and family about the usefulness of PSA screening test in detecting prostate cancer. a. If the PSA is elevated, this will prompt prostate biopsy and possible treatment for prostate cancer, which may be a slow-growing disease. b. In 2010, the U. S. Preventive Task Force recom-mended against PSA screening, stating that the test has no net benefit and that the harms outweigh ben-efits. The American Urologic Association in 2013 also started to recommend against routine cancer screening. 2. Discuss keeping a voiding diary. 3. Discuss possible side effects of medical therapy, including orthostatic hypotension, dizziness, and retro-grade ejaculation. 4. Educate the patient with retention regarding how to perform clean intermittent catheterization because this is a better alternative to an indwelling Foley catheter. 5. Avoid becoming constipated because this aggravates symptoms. C. Pharmacotherapy. 1. Alpha blockers, which rapidly relax the smooth mus-cles of the bladder neck and prostate without impairing bladder body contractility. a. Most commonly used: Tamsulosin 0. 4 mg daily (max 0. 8 mg daily). 2. 5-ARIs, which block intracellular DHT conversion. a. Best for larger prostate glands ( >40 m L). b. Most commonly used: Finasteride 5 mg. 3. Antimuscarinic agents, which help with bladder over-activity. a. Most commonly used: Oxybutynin 5 mg TID. 4. Phosphodiesterase-5 inhibitor, which is Food and Drug Administration (FDA) approved for LUTS sec-ondary to BPH. a. Tadalafil (Cialis): 2. 5 to 5 mg; contraindicated in men taking nitrates, nonselective alpha blockers, and cytochrome P 450 inhibitors. D. Discharge instructions. 1. Advise patients to limit caffeine, fluids, and alcohol. These may increase LUTS. 2. Advise them to avoid cold medications, antihis-tamines, and pseudoephedrine. 3. Advise them to seek medical attention if they are unable to void or have flank pain, gross hematuria, or pas-sage of clots. 4. Advise them to discontinue alpha blockers with dizzi-ness, lightheadedness, or falls. Follow-Up A. Monitor response to treatment with uroflowmetry, post void residual, and presence of symptoms. B. Advise that urodynamic studies may be indicated if there is no improvement of symptoms with medical therapy. C. Advise that surgery may provide relief in the case of exces-sive symptoms refractory to medical management. Some of the more common options include: 1. T ransurethral resection of the prostate (TURP). 2. Holmium laser enucleation of the prostate (Ho LEP). 3. Simple prostatectomy for large prostates greater than 100 m L. Consultation/Referral A. Urology. 1. Urinary retention. 2. Hematuria/clot retention. 3. PSA elevation, will need prostate biopsy. 4. Suspected genitourinary malignancy. 5. Failed medical treatment with moderate to severe symptoms. B. Neurology: With any concern for neurological condition that may be causing LUTS. C. Endocrinology. 1. For hyperglycemia. 2. Concern for diabetes insipidus. Special/Geriatric Considerations A. Many patients limit fluids due to symptoms; this may lead to dehydration, especially in geriatric individuals. Assess for dehydration and provide education to maintain a normal fluid intake. B. Monitor the geriatric population for medication side effects. 1. Alpha-blockers: Hypotension and dizziness. 2. Anti-muscarinic agents: Dry mouth, constipation, and mental status changes. a. Monitor for polypharmacy with other possible anticholinergic medications that patients may be pre-scribed or taking over the counter. 5. Nephrology Guidelines100

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b. Studies have shown that transdermal oxybu-tynin and the newer anticholinergics may be better tolerated. Bibliography Deters, L. A. (2019, January 15 ). Benign prostatic hypertrophy (BPH) dif-ferential diagnoses.,In E. D. Kim (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/article/437359-differential Kim, E. H., Larson, J. A., & Andriole, G. L. (2016). Management of benign prostatic hyperplasia. Annual Review of Medicine, 67, 137-151. doi:10. 1146/annurev-med-063014-123902. Nicholson, T., & Ricke, W. (2011, November-December). Androgens and estrogens in benign prostatic hyperplasia, past, present and future. National Institutes of Health, 82 (4-5), 184-189. Retrieved from https://www. ncbi. nlm. nih. gov/pmc/articles/PMC3179830 Chronic Kidney Disease Jane S. Davis, Kim Zuber, and Christine M. Chmielewski Definition A. Reduction of kidney function: An estimated glomerular filtration rate (GFR) less than 60 m L/min/1. 73 m2for greater than 3 months. OR B. Evidence of kidney damage, including persistent albuminuria—defined as greater than 30 mg of urine albu-min per gram of urine creatinine for greater than 3 months. 1. Anatomical abnormalities including, but not limited to, polycystic kidneys, kidney transplant, and genetic abnormalities. 2. Chronic kidney disease (CKD) versus acute kidney injury (AKI). A 3-month time frame is used to distin-guish CKD from AKI. C. Classification. 1. CKD stages are defined by a presence of albuminuria and the GFR (see Table 5. 1). 2. The GFR requires age, race, gender, and serum crea-tinine for calculation. TABLE 5. 1 Stages of CKD Stage of CKDGFR (m L/min/1. 73 m2)Albuminuria 1 ≥90 Normal or high 2 60-89 Mildly decreased 3a 45-59 Mildly to moderately decreased 3b 30-44 Moderately to severely decreased 4 15-29 Severely decreased 5 <15 Kidney failure/ESRD Albuminuria categories in CKD (ACR in mg/g) A1 <30 Normal to mildly increased A2 30-300 Moderately increased A3 >300 Severely increased Notes: ACR, albumin-to-creatinine ratio; CKD, chronic kidney disease; ESRD, end-stage renal disease; GFR, glomerular filtration rate. Incidence A. It is estimated that approximately 14. 8% of the adults in the United States have CKD. B. Approximately 96% of those with mild to moderate reduced kidney function are unaware that they have CKD. C. Approximately 48% of those with severely reduced kid-ney function are unaware that they have CKD. D. Approximately 661,000 individuals in the United States have end-stage renal disease (ESRD); of these, 468,000 are on dialysis and 193,000 have a functioning kidney transplant. Pathogenesis A. Initial kidney injury or insult leads to the loss of func-tioning nephrons (nephron loss). B. Hyperfiltration of the remaining intact nephrons occurs (glomerular hypertrophy). C. Initial beneficial, adaptive response leads to ongoing damage (interstitial inflammation, fibrosis, and endothelial/ vascular injury). D. This injury eventually leads to further nephron loss (dis-ease progression). Predisposing Factors A. General risk factors. 1. Diabetes mellitus. 2. Hypertension. 3. Cardiovascular disease (CVD). 4. History of kidney disease. 5. Family history of CKD. 6. Race/ethnicity. a. African Americans. b. Hispanics. c. Native Americans. d. Asians. 7. AKI. 8. Older age. 9. Smoking. 10. Exposure to nephrotoxins. 11. Obesity. B. Risk factors for progression of CKD to next stage. 1. Male gender. 2. African American race. 3. Diabetes mellitus. 4. Hypertension. 5. Proteinuria. 6. Prior trajectory of kidney function. Subjective Data A. Common complaints/symptoms. 1. Often silent. 2. Lethargy due to low hemoglobin. 3. Metallic taste due to uremia. 4. Increased incidence of confusion with uremia. 5. Edema. B. Medication history. 1. Medication review. a. Prescription drugs. b. Over-the-counter drugs. c. Herbal supplements. 2. Medication-associated risk. a. Clearance by kidney. b. Narrow therapeutic window. Chronic Kidney Disease101

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c. High risk in older population. d. Potential central nervous system (CNS) effects. e. Drug dosing data availability. C. Review of systems. 1. Constitutional: Change in activity, appetite changes. 2. Head, ear, eyes, nose, and throat (HEENT): Changes in vision, facial swelling, nosebleeds. 3. Cardiovascular: Any pain in chest. 4. Respiratory: Difficulty breathing. 5. Gastrointestinal: Nausea or vomiting, hiccups, blood in stool. 6. Genitourinary: Difficulty urinating or pain on uri-nation. 7. Musculoskeletal: Back pain, muscle cramps. 8. Neurological: Dizziness or balance problems. 9. Integumentary: Dry skin, itching, or rash. 10. Psychiatric: Confusion or difficulty concentrating, sleep disturbance. 11. Endocrine: Cold intolerance. 12. Hematologic: Bruising easily. Physical Examination A. Vital signs, including orthostatic signs. B. Constitutional. C. Eyes: Funduscopic examination. 1. Look for retinopathy secondary to diabetes mellitus. D. Cardiovascular: Palpitations, dysrhythmia, tachycardia, heart sounds (S3 and S4, murmurs, rubs), distal pulses, lower extremity edema, carotid bruit, jugular venous distension (JVD). E. Pulmonary: Breath sounds, effort (use of accessory mus-cles), wheezing. F. Abdominal: Abdominal palpation, bowel sounds, dys-geusia, melena. G. Genitourinary: Dysuria, flank pain, proteinuria, hema-turia, oliguria, anuria. H. Musculoskeletal: Arthralgias, gait disturbances, myalgias. I. Integumentary/nails: Rash, pruritus, uremia. J. Confusion, asterixis. K. Endocrine: Polydipsia, polyphagia, polyuria. L. Hematologic/lymphatic: Bruising, petechiae, ecchymosis. Diagnostic Tests A. Renal function panel. B. Complete blood count (CBC) with differential. C. Serum albumin. D. Fasting lipid panel. E. Urinalysis. F. Urine albumin to creatinine ratio (UACR). G. Urine culture and sensitivity (C & S; if indicated). H. Renal ultrasound with post void residual. I. Specialty serologic studies if indicated: Antinuclear anti-body (ANA), C3, C4, hepatitis B and C serologies. J. CKD mineral bone disorder: Calcium, phosphorus, intact parathyroid hormone (PTH), 25(OH) vitamin D. K. Anemia. 1. Microcytic: Iron studies (iron, total iron-binding capacity [TIBC], ferritin). 2. Macrocytic: Folate and B12levels. L. Multiple myeloma/paraprotein. 1. Serum protein electrophoresis (SPEP), urine protein electrophoresis (UPEP). 2. Serum and urine for immunoelectrophoresis. 3. Serum for free light chains. M. Renal biopsy: Reserved to guide management or when the cause of CKD is unclear. Differential Diagnosis A. AKI. 1. Prerenal. 2. Intrinsic. 3. Postrenal. B. Multiple myeloma. C. Nephrolithiasis. D. Diabetic nephropathy. E. Glomerulonephritis. Evaluation and Management Plan A. General plan. 1. Determine CKD stage (see Table 5. 2). a. CKD Stage 1: Manage comorbid conditions and identify CVD risk factors. b. CKD Stage 2: Monitor CKD progression. c. CKD Stages 3a and 3b: T reat CKD complications. d. CKD Stage 4: Refer to nephrology. e. CKD Stage 5: Start kidney replacement therapy (KRT). 2. Manage complications. a. Acidosis. b. Anemia. c. Hypertension. d. CKD mineral bone disorder. e. Dyslipidemia. f. Diabetic complications: Indications for initiation of dialysis. i. Hyperkalemia. ii. Uremic pericarditis. iii. Refractory metabolic acidosis. iv. Volume overload. v. Pulmonary edema. vi. Uremic encephalopathy. vii. Refractory hypertension. viii. Persistent nausea and vomiting. ix. Blood urea nitrogen (BUN) greater than 100 mg/d L. B. Patient/family teaching points. 1. Patient-centered educational efforts: A conceptual model. a. Prevent kidney disease. i. Awareness of risk. ii. Knowledge of prevention. b. Identify kidney disease. i. Awareness of diagnosis. ii. Knowledge of health implications. c. Manage kidney disease. i. Knowledge of management goals and how to achieve them. d. Comprehensive conservative care for ESRD. i. Knowledge of treatments, risks, benefits, and management goals. 2. Dietary modifications. a. Sodium intake: L ess than 2 g/day. b. Potassium intake: 2 g/day. c. Protein intake. i. Avoid high protein intake. ii. Lower protein intake to 0. 8 g/kg/day in adults with diabetes or without diabetes and a GFR less than 30 m L/min/ 1. 73 m2. d. Phosphorus intake: 800 to 1,000 mg/day. 5. Nephrology Guidelines102

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TABLE 5. 2 Stages of CKD With Monitoring Recommendations e. Diabetes dietary guidelines: Target hemoglobin A1c (Hb A1c) of ∼7. 0%. f. Target Hb A1c can be extended above 7. 0% (53 mmol/mol) in individuals with comorbidities or lim-ited life expectancy and risk of hypoglycemia. g. Hyperlipidemia dietary modifications. i. Decrease intake of saturated and trans fat foods. ii. Substitute with monounsaturated fats and moderate intake of polyunsaturated fats. C. Pharmacotherapy: Targeted at preventing complications. 1. Acidosis: Maintenance of carbon dioxide/bicarbonate level with sodium citrate tablets. 2. Anemia: Performance of iron studies to determine iron supplementation plan. a. Ferrous sulfate tablets. b. Folic acid replacement tablets. c. Cobalamin for vitamin B 12replacement/supple-mentation. d. Erythropoiesis stimulating agents (not recom-mended in patients with active malignancy or recent history of malignancy). 3. Hypertension: CKD with or without diabetes: Use an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB). a. Obtain a baseline serum creatinine and serum potassium and follow. b. Recheck those levels 1 week after starting or increasing dose to avoid further decreases in GFR and/or hyperkalemia. 4. CKD mineral bone disorder: Follow common miner-als and replace as needed. a. Phosphate binders: Example of calcium-based binders is calcium acetate. b. Vitamin D replacement. c. Bisphosphonates (avoid in CKD with GFR less than 30 m L/min/1. 73 m2). 5. Dyslipidemia: Lipid lowering agent. 6. Diabetic complications: Keep Hb A1c ∼7%. 7. Malnutrition: High biologic value protein intake. 8. Proteinuria: ACE inhibitor/ARB or non dihydropyri-dine calcium channel blocker. Follow-Up A. Follow-up in CKD is important to mitigate progression of disease and to manage risk factors that may contribute to worsening of the patient's clinical health. B. A nephrologist should be consulted if there is an increase in urine protein or abrupt decline in GFR. Chronic Kidney Disease CKD classified based on: GFR (G) Albuminuria (A) KDIGO 2012Albuminuria categories Description and range A1 A2 A3 Normal to mildly increased Moderately increased Severely increased <30 mg/g <3 mg/mmol30-299 mg/g 3-29 mg/mmol≥300 mg/g ≥30 mg/mmol GFR categories (/min/1. 73 m2 Description and range G1 Normal or high ≥90 Monitor 1 Monitor 1 Refer* 2 G2Mildly decreased60-90 Monitor 1 Monitor 1 Refer* 2 G3a Mildly to moderately decreased45-59 Monitor 1 Monitor 2 Refer 3 G3b Moderately to severely decreased30-44 Monitor 2 Monitor 3 Refer 3 G4 Severely decreased 15-29 Refer* 3 Refer* 3 Refer* 4 + G5 Kidney failure <15 Refer* 4 + Refer* 4 + Refer* 4 +m L103 Shades: Represents the risk for progression, morbidity, and mortality by shades, from best to worst. White:Lowrisk(ifnoothermarkersofkidneydisease,no CKD)Lightgray:Moderatelyincreasedrisk. Mediumgray:Highrisk. Darkgray:Very high risk. Black: High risk +4 times per year. Numbers: Represent a recommendation for the number of times per year the patient should be monitored. Refer: Indicates that nephrology referral and services are recommended. CKD, chronic kidney disease; GFR, glomerular filtration rate; KDIGO, Kidney Disease: Improving Global Outcomes. *Referring clinicians may wish to discuss with their nephrology service depending on local arrangements regarding monitoring or referral. Source : Modified with permission from KDIGO. (2012). Clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int, 2013 (Suppl. 3), 1-150..

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C. Regular visits with a primary provider are essential for long-term health maintenance. Consultation/Referral A. Consult nephrology in the acute care setting for patients with the following. 1. An estimated GFR less than 30 m L/min/1. 73 m2. 2. Significant albuminuria or overt proteinuria. 3. An abrupt decrease in estimated GFR/acute rise in serum creatinine. 4. Evidence of worsening kidney function/CKD pro-gression. 5. Persistent hematuria. 6. Resistant hypertension. Special/Geriatric Considerations A. The incidence of cardiovascular death increases with each stage of CKD. Individuals are more likely to die than to reach the next stage of CKD. In addition, the incidence of death related to cardiovascular procedures increases with CKD stage. B. The incidence of hospitalization increases with CKD stage, although in the past 10 years, the number of hospi-talizations has decreased. C. It is important to identify CKD in hospitalized patients because it is an important prognostic factor for increased risk of in-hospital AKI. D. The incidence of CKD and AKI increase with age. 1. Polypharmacy is more common in the elderly. It is important to review medications regularly to identify medications that are actual or potential nephrotoxins that require dose or schedule changes, as these should be avoided. E. Older individuals have an increased prevalence of decreased estimated GFR and increased ACR. 1. There is a debate concerning whether decreased GFR or increased urine albumin-to-creatinine ratio in older individuals represents disease or normal aging. Bibliography Alleman, K., & Houle, K. (2015). Module 6. The APRN's approaches to care in nephrology. In C. S. Counts (Ed. ), Core curriculum for nephrology nursing (6th ed., pp. 1-206). Pitman, NJ: AJ Jannetti, Inc. Fliss, E. M., Burns, A., Moranne, O., Morton, R. L., & Naicker, S. (2016). Supportive care: Comprehensive care in end-stage kidney disease. Clin-ical Journal of the American Society of Nephrology, 11 (10), 1909-1914. doi:10. 2215/CJN. 04840516 Jayadevappa, R., & Chhatre, S. (2011). Patient centered care—A conceptual model and review of the state of the art. Open Health Services and Policy Journal, 4, 15-25. doi:10. 2174/1874924001104010015 Kidney Disease: Improving Global Outcomes (KDIGO) Anemia Work Group. (2012). KDIGO clinical practice guideline for anemia in chronic kidney disease. Kidney International, 2 (Suppl. ), 279-335. doi:10. 1038/ki. 2012. 270 Kidney Disease: Improving Global Outcomes CKD-MBD Work Group. (2009). KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease—mineral and bone disorder (CKD-MBD). Kidney International, 76 (113 Suppl), S1-S130. Kidney Disease: Improving Global Outcomes CKD Work Group. (2013). KDIGO 2012 clinical practice guideline for the evaluation and man-agement of chronic kidney disease. Kidney International, 3 (1 Suppl. 3), 1-150. Kidney Disease: Improving Global Outcomes Lipid Work Group. (2013). KDIGO clinical practice guideline for lipid management in chronic kid-ney disease. Kidney International, 3 (Suppl. 3), 1-305. National Kidney Disease Education Program. (2014, July). Making sense of CKD a concise guide for managing chronic kidney disease in the primary care setting. Bethesda, MD: National Institutes of Health. Nissenson, A. R., & Fine, R. N. (2017). Handbook of dialysis therapy (5th ed. ). Philadelphia, PA: Elsevier. Ponnaluri, S.,&King, M. J. (2016). A retrospective study of research data on end stage renal disease. Journal of Emerging Investigators, 5. doi:10. 1177/2054358118799689 Rosenberg, M. ( 2018, June 29). Overview of the management of chronic kidney disease in adults. In S. Motwani (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/overview-of-the-management-of-chronic-kidney-disease-in-adults Shingarev, R., Wille, K., & Tolwani, A. (2011). Management of complica-tions in renal replacement therapy. Seminars in Dialysis, 24 (2), 164-168. doi:10. 1111/j. 1525-139X. 2011. 00828. x U. S. Renal Data System. (2014). USRDS 2014 annual data report: Atlas of chronic kidney disease and end-stage renal disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Dia-betes and Digestive and Kidney Diseases. Weir, M. R., & Fink, J. C. (2014). Safety of medical therapy in patients with chronic kidney disease and end-stage renal disease. Current Opin-ion in Nephrology Hypertension, 23 (3), 306-313. doi:10. 1097/01. mnh. 0000444912. 40418. 45 Hematuria Suzanne Barron Definition A. Gross hematuria: Visible blood in the urine. 1. Visible blood in the urine may be seen with as little as 1 m L of blood in 1 L of urine. B. Microscopic hematuria: Greater than three red blood cells (RBCs) per high power field in a single urinalysis. Incidence A. Population-based studies have shown prevalence rates of less than 1% to as high as 16%. B. Older men have a higher prevalence of hematuria. C. Associated conditions. 1. No diagnosis after workup: 60. 5%. 2. Urinary tract infection (UTI): 13%. 3. Stone disease: 3. 6%. 4. Cancer: 13%. 5. Glomerular disease: 9. 8%. Pathogenesis A. Glomerular or nephronal hematuria (originates from nephron). 1. On microscopic evaluation, RBCs that are dysmor-phic (irregular shapes and uneven hemoglobin distribu-tion) often represent glomerular disease. There may be casts. 2. On urinalysis, the combination of RBCs and protein-uria most often indicates a glomerular source of hema-turia. B. Extraglomerular hematuria (originates from urologic source): Anything that disrupts the genitourinary (GU) epithelium, which may include irritation, trauma, inflamma-tion, or invasion. 1. On microscopic evaluation, the RBCs in the urine are isomorphic; have smooth, round membranes; and display even hemoglobin distribution. 2. Associated conditions include tumors, kidney stones, trauma, infection, anatomic abnormalities of the uri-nary tract such as ureteropelvic junction obstruction, and benign prostatic hypertrophy (BPH). Predisposing Factors A. Age greater than 35. B. Smoking history. 5. Nephrology Guidelines104

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C. Recent trauma. D. Recent urinary tract surgery or instrumentation. E. BPH. F. Family history of renal disease. G. Personal history of nephrolithiasis. H. Pelvic radiation. I. Recent febrile illness. J. Frequent UTIs. K. Occupational exposure to chemicals and dyes (benzenes or aromatic amines). L. Medications (abuse of analgesics such as nonsteroidal anti-inflammatory drugs [NSAIDs]). M. Chronic indwelling catheters (Foley, suprapubic tube). Subjective Data A. Common complaints/symptoms. 1. Flank pain: Possible recent trauma, stones, renal can-cer, ureteral tumor, or pyelonephritis. 2. Dysuria/lower urinary tract symptoms (LUTS) such as urgency/frequency and urinary retention: Possible UTI/prostatitis, BPH, or bladder stones. 3. Fever: Possible UTI, prostatitis, or pyelonephritis. 4. Worm-like (vermiform) clots: Possible origin from upper urinary tract. B. Common/typical scenario. 1. Visual appearance of blood in the urine or presence with microscopic hematuria. 2. Timing of hematuria during urinary stream: May indicate the site of pathology (i. e., initiation of stream— anterior urethral pathology; termination of stream— bladder neck, prostate, or urethra inflammation/pathol-ogy; throughout stream—bladder or upper urinary tract origin). 3. Aggravating factors. a. Pain, recent trauma, or recent vigorous activity/ exercise. b. Recent upper respiratory infection (associated with glomerulonephritis). c. Ingestion of certain foods and drugs (pseudohe-maturia). d. Excessive use of analgesics such as NSAIDs. C. Family and social history. 1. Smoking (past or present). 2. Excessive ingestion of barbecued/smoked foods (asso-ciated with link to bladder cancer). 3. Sexual history (recent sexually transmitted infections [STIs]). 4. Work history: Exposure to chemicals and dyes in rub-ber and/or petroleum industries (associated with bladder cancer). 5. Family history. a. GU malignancies. b. Primary renal disease. c. Polycystic kidney disease. d. Nephrolithiasis. e. Hypertension. D. Review of systems. 1. Constitutional symptoms: Recent weight loss, fevers, or night sweats that may indicate malignancy. 2. Respiratory: Cough or shortness of breath that may indicate recent upper respiratory infection or tumor inva-sion. 3. Musculoskeletal: Generalized pain may indicate excessive NSAID use. 4. GU: LUTS, flank pain, dysuria, cloudy urine, or foul smelling urine. 5. Gynecologic: Menorrhagia. 6. Gastrointestinal: Nausea, vomiting, or abdominal pain may indicate renal mass, or nephrolithiasis. 7. Neurological: Confusion, dizziness, or mental status changes may indicate metastatic malignant disease (renal cancer). 8. Skin: Rashes or pallor that may be associated with systemic lupus erythematosus. 9. Hematologic: Excessive bruising or petechiae may indicate blood clotting disorder. 10. Ear, nose, and throat (ENT): Frequent nosebleeds, rhinorrhea, or sinus congestion. Physical Examination A. Vital signs. 1. Temperature: Measurement greater than 101. 5∘F may indicate UTI, pyelonephritis, or prostatitis. 2. Blood pressure. a. Hypertension: Glomerular source or renal failure. b. Hypotension: Possible acute blood loss anemia from gross hematuria. 3. Pulse: Tachycardia, sepsis, or hypovolemia from acute blood loss anemia. B. Skin: Rashes, pallor, or bruising/lacerations from recent trauma. C. Edema: Possible nephrotic syndrome; rule out deep vein thrombosis (DVT) from GU malignancy. D. GU examination. 1. Costovertebral angle tenderness: Nephrolithiasis; pyelonephritis. 2. Urethral trauma: Urethral caruncle, vaginal prolapse, phimosis, obvious urethral stricture. E. Digital r ectal exam (DRE). 1. Boggy, tender warm prostate: Acute prostatitis. 2. Nodularity: Prostate cancer. Diagnostic Tests A. Urinalysis. 1. Color: Red (recent bleeding, most likely urologic source) versus brown or tea color (old blood clots or renal disease). 2. Proteinuria: Heavy 3 to 4 +(renal disease). 3. Leukocyte positive and/or nitrite positive: Infection. 4. Pyuria: Infection. 5. Red cell casts: Glomerular bleeding. 6. Crystalluria: Possible nephrolithiasis. B. Phase contrast microscopy: Helps differentiate renal (presence of distorted RBCs) versus nonglomerular bleeding. C. Urine culture: Evaluate for infectious sources. D. Laboratory/blood work. 1. Complete blood count (CBC): Anemia. 2. Basic metabolic panel: Renal function. 3. Prothrombin time (PT)/partial thromboplastin time (PTT) and international normalized ratio (INR): Bleed-ing disorders. E. Urine cytology. 1. Recommended for all patients with risk factors for GU malignancy and with LUTS and voiding symptoms. 2. Not recommended by the American Urologic Associ-ation as part of the routine evaluation of asymptomatic microhematuria. 3. Negative result does not rule out malignancy. 4. False positive results can be seen with calculi or inflam-mation. Hematuria105

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F. Imaging. 1. Computed tomographic urogram (CTU) with and without contrast: Gold standard. a. Three phase test. b. Used to assess for stones (non contrast image); tumors of bladder or kidneys; hydronephrosis; other anatomic abnormalities (contrast image); tumors of upper tract; and collecting system filling defects (excretory phase). c. Contraindicated with a serum creatinine greater than 2 mg/d L. d. Highest sensitivity and specificity. 2. MRI/m agnetic resonance urography (MRU; MRI urogram): Alternative imaging modality when not able to perform CTU due to renal insufficiency, contrast allergy, or pregnancy. a. Less sensitivity at recognizing calculus of the GU tract. 3. Renal ultrasound: Not as specific or sensitive. a. Can be used to grossly rule out clots in bladder or to detect hydronephrosis. G. Diagnostic procedures/surgery. 1. Cystoscopy. a. Indicated for all patients older than 35 years of age with microscopic hematuria or gross hematuria. b. Also indicated for patients younger than 35 years of age with risk factors for GU malignancies and smoking history. 2. Retrograde pyelogram with or without ureteroscopy: May be performed to evaluate the upper tract in patients who are unable to have intravenous contrast for the CTU/MRU imaging. 3. Renal biopsy: Nephrology referral if glomeru-lonephritis is suspected. Differential Diagnosis A. Pseudohematuria: Certain foods, beets/certain drugs, or phenazopyridine (Pyridium). B. Hereditary disorders: Polycystic kidney disease, nephropathy, renal tubular acidosis, or cystinuria. C. Hematologic abnormalities: Bleeding disorders or sickle cell disease. D. Anatomic abnormalities: Urethral strictures, ureteral strictures, ureteropelvic junction obstruction, urethral carun-cle, or phimosis. E. Vascular malformations (hemangioma). F. T rauma: Abdominal and pelvic injury (degree of hema-turia is a poor indicator of the severity of the injury). G. Exercise-induced hematuria. H. Foreign bodies (catheters, ureteral stents, self-introduced foreign body into urethra). I. Infectious (UTI, pyelonephritis, prostatitis, schistosomi-asis, tuberculosis). J. Radiation (radiation cystitis and nephritis). K. Stones of the GU tract. L. Malignancy (renal, bladder, ureteral, prostate, penile, urethral, vulvar). M. Benign tumor. N. BPH. O. Endometriosis of urinary tract (cyclic hematuria). P. Benign essential hematuria. Q. Glomerulonephritis or renal disorders (Ig A nephropathy, drug-induced nephropathy). R. Overanticoagulation with medications such as warfarin. 1. Clinical caveat—patients should still be thoroughly evaluated for other possible causes. Evaluation and Management Plan A. General plan. 1. Urinalysis, urine culture, and laboratory tests (see s ection “Diagnostic Tests”). 2. Urine cytology if indicated. 3. Imaging (CTU). 4. Patients with gross hematuria and/or urinary reten-tion. a. Place three-way Foley catheter (22-24 French most commonly used) and irrigate clots (continuous bladder irrigation with sterile saline solution). b. If bleeding is not controlled, propose evaluation with urologic surgery for cystoscopy under anesthesia for clot evacuation/fulguration. 5. Patients who are voiding without clots or urine reten-tion: Observation, with increase in oral fluid intake. 6. Patients with gross hematuria or history of trauma for acute blood loss anemia: Monitor with serial hemoglobin and hematocrit and transfuse as indicated. B. Patient/family teaching points. 1. Provide patient education and prognosis depending on the cause of the hematuria. 2. Explain the various tests that are necessary to deter-mine the cause of bleeding and the treatments that may be necessary for control of gross hematuria (e. g., cystoscopy, clot evacuation, Foley catheter placement for bladder irri-gation). 3. Help to ease anxiety by providing appropriate anal-gesics (e. g., lidocaine jelly before placing a three-way catheter or narcotics/anticholinergics for painful bladder spasms due to clot retention/catheter placement). C. Pharmacotherapy. 1. No specific medications are primarily indicated to treat hematuria. 2. Appropriate antimicrobials may be used to treat underlying infections. 3. Finasteride may be helpful in controlling bleeding from the prostate. D. Discharge instructions. 1. Advise patients to refrain from vigorous activity for one week after gross hematuria has resolved. 2. Avoid NSAIDs and aspirin (if possible, some patients may need to continue based on history of coronary artery disease) for 3 days. 3. Advise patients that it is normal to have tea-colored urine for a few days as the hematuria is resolving. 4. Recommend that patients drink plenty of fluids. 5. Suggest that patients prevent constipation and strain-ing by taking stool softeners such as docusate sodium. 6. Advise that patients should seek medical attention promptly if they develop bright red urine, pass clots, are unable to urinate, or have fevers or chills. Follow-Up A. Follow-up as indicated for the condition that is causing the hematuria. B. Once the condition has resolved, reevaluate for microhe-maturia. 5. Nephrology Guidelines106

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C. In asymptomatic microhematuria with a negative work-up, follow-up annually for repeat urinalysis/microscopy. If negative for 2 years, release from care. If positive, repeat imag-ing every 3 years and refer for renal evaluation. Consultation/Referral A. Nephrology consult for nephrogenic source of hematuria. B. Urology consult for stones, tumors of the GU tract, BPH, anatomic evaluation, and control of bleeding. C. Infectious disease consult for treatment of infectious sources (pyelonephritis, prostatitis, UTIs, possible tubercu-losis work-up, or possible schistosomiasis). D. Rheumatology consult for autoimmune disorders such as systemic lupus erythematosus. E. Hematology consult for bleeding disorders. Special/Geriatric Considerations A. Screen elderly individuals appropriately for renal function prior to obtaining imaging studies with contrast. B. The reduced capacity to retain salt and water increases as the kidney ages, predisposing to dehydration. C. Older individuals are more susceptible to acute kidney injury from acute blood loss anemia and certain medications such as NSAIDs. D. Elderly patients should be monitored closely for hypov-olemia that present with gross hematuria. Bibliography Diagnosis, Evaluation and Follow-Up of Asymptomatic Microhematuria (AMH) in Adults. American Urologic Association. Published 2012. Reviewed and Validity Confirmed 2016. Fatica, R., & Fowler, A. (2009, January). Hematuria. Cleveland Clinic for Continuing Education. Retrieved from https://www. auanet. org/ guidelines/asymptomatic-microhematuria-(amh)-guideline#x2396 Lambert, M. (2013, May). AUA guideline addresses diagnosis, evaluation and follow-up of asymptomatic microhematuria. American Family Physi-cian, 87 (9), 649-653. Hypercalcemia Jessica S. Everitt, Divya Monga, and Catherine Wells Definition A. Serum total calcium greater than 10. 2 mg/d L (corrected for low albumin; see Box 5. 2). Incidence A. Hypercalcemia is a relatively common abnormality that is usually mild in presentation. B. Approximately 90% of cases of hypercalcemia may be caused by some type of malignancy or hyperparathyroidism. C. Other causes may be from vitamin D deficiencies or kid-ney transplantation. Pathogenesis A. Calcium is controlled by three major hormones: Parathy-roid, calcitonin, and vitamin D. B. Dysregulation in these hormones can lead to hypercal-cemia. C. Calcium is tightly regulated in the bloodstream; there-fore, even mild cases of hypercalcemia are concerning and should be investigated for possible malignancy. Predisposing Factors A. Women over the age of 50. B. Patients taking excessive calcium or vitamin D supple-ments. C. Cancer. D. Genetics. E. Immobility may contribute to release of calcium. F. Lithium. Subjective Data A. Common complaints/symptoms. 1. Gastrointestinal, including nausea, vomiting, and constipation. 2. Anorexia. 3. Fatigue and lethargy. 4. Confusion. 5. Severe hypercalcemia. a. Cardiac effects, including bradycardia or arrhyth-mias with EKG changes. b. Volume depletion secondary to polyuria and hypercalcemia-induced natriuresis. c. Possible acute renal failure if severe and prolonged. 6. Chronic hypercalcemia: Possible nephrolithiasis, sys-temic calcifications (e. g., vascular), and renal failure. Physical Examination A. Volume status. B. Cardiac examination. C. Neurological examination. D. Reflexes. E. Musculoskeletal examination. Diagnostic Tests A. Serum calcium and phosphorus. B. 25-hydroxyvitamin D. C. Intact parathyroid hormone (PTH). D. Creatinine, b lood urea nitrogen (BUN). E. Protein electrophoresis and immunofixation (serum and urine). F. Thyroid-stimulating hormone (TSH). G. EKG. Differential Diagnosis A. Malignancy: Local osteolytic hypercalcemia, or hemato-logical malignancies. B. Hyperparathyroidism: Primary, secondary, and tertiary. C. Paget's disease. D. Milk-alkali syndrome. E. Thyrotoxicosis. F. Granulomatous diseases (such as sarcoidosis and tubercu-losis). G. Immobilization. H. Medication-induced. 1. Vitamin A and D overdose/toxicity. 2. Parenteral nutrition. 3. Thiazide diuretics. 4. Lithium. 5. Estrogens, antiestrogens, and androgens. 6. Calcium supplements and calcium-containing phos-phorus binders. I. Impaired renal function (c hronic kidney disease [CKD] or a cute kidney injury [AKI])—usually due to clearance of drugs. Hypercalcemia107

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BOX 5. 2 Calcium in Humans Normal total serum calcium is 8. 6 to 10. 2 mg/d L. Normal ionized serum calcium is 1. 12 to 1. 3 mmol/L. Extracellular calcium is found in three forms. b40% of calcium in serum is protein-bound, primarily to albumin. b50% is free (ionized or unbound) calcium. b10% is complexed (i. e., calcium citrate). Total serum calcium underestimates active calcium. b Ionized or unbound calcium is the biologically active form. b Correct serum calcium in hypoalbuminemic patients for actual total calcium. ■Corrected calcium =serum total calcium +(0. 8×[4-serum albumin concentration]). 99% of total body calcium is found in bones. PTH and vitamin D regulate serum calcium. Physiologic functions. b Bone metabolism. b Electrophysiology of cardiac and smooth muscle. b Coagulation. b Endocrine and exocrine secretory functions. Phosphorus and calcium directly affect each other. b Elevated phosphorus binds to ionized calcium, decreasing unbound, active calcium. b Maintain the optimal relationship between calcium and phosphorous. ■For bone health. ■To prevent vascular and soft tissue calcifications. Calcium is an inotrope if given at accelerated doses (due to its effects on cardiac and smooth muscle). Calcium is critical to the coagulation cascade; thus, low calcium or blocking calcium can lead to bleeding. PTH, parathyroid hormone. Evaluation and Management Plan A. Goal: To correct the underlying cause of hypercalcemia and prevent complications of hypercalcemia. B. Step 1 —T reat symptoms. 1. Use aggressive volume resuscitation with intravenous (IV) normal saline 0. 9% (200-500 m L/hr) in patients with volume depletion and normal heart and kidney function. 2. Manage cardiac effects: EKG changes and hypoten-sion or hypertension. 3. Replace phosphorus if hypophosphatemia is present. C. Step 2 —T reat hypercalcemia and identify the underlying cause. 1. Discontinue all vitamin D and calcium (oral and intravenous). 2. Acute, severe hypercalcemia. a. Give loop diuretics (such as furosemide 40-100 mg IV), once volume resuscitation has taken place, to increase renal calcium excretion and avoid volume overload. b. Possibly arrange for hemodialysis in patients with renal dysfunction. 3. Mild or asymptomatic hypercalcemia. Some therapies may also be beneficial in combination with severe hyper-calcemia management. a. Calcitonin. i. Rapid onset of action but with short-term effectiveness ( <48 hours) due to tachyphylaxis. ii. Can be used in initial treatment of severe hypercalcemia along with intravenous hydration. iii. Increases renal excretion and decreases osteoclast-mediated bone resorption of calcium. iv. Dose: 4 to 8 units/kg IV or intramuscularly (IM) every 12 hours. b. Glucocorticoids. i. Useful in patients with granulomatous disor-ders or lymphoma. ii. Decreases calcitriol production, which subse-quently lowers intestinal calcium absorption. iii. Sample regimens: Prednisone 20-60 mg/day PO or hydrocortisone 200 mg/day IV. c. Bisphosphonates. i. Examples: Pamidronate and zoledronate. ii. Potent inhibitors of osteoclast-mediated bone resorption frequently used in hypercalcemia of malignancy. iii. Due to delayed onset of action, limited role in severe, acute hypercalcemia. d. Cinacalcet or etelcalcetide. i. Indication: For outpatient management of pri-mary hyperparathyroidism and secondary hyper-parathyroidism of renal origin. ii. Mimics the effects of calcium (calcimimetic) by binding to the calcium-sensing receptor on the parathyroid gland, thus reducing PTH and serum calcium. iii. Dosing. 1)Cinacalcet: Initially at 30 mg one to two times daily to max of 180 mg/day. 2)Etelcalcetide: Initial dosing 5 mg three times weekly IV (after dialysis) to a maximum of 15 mg three times weekly IV (after dialysis). e. Denosumab. i. Indicated for hypercalcemia of malignancy. 5. Nephrology Guidelines108

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ii. Delayed onset of action. iii. Binds to receptor activator of nuclear factor-kappa ligand (RANKL), leading to decreased bone resorption. iv. Given subcutaneously every 4 weeks with additional doses during the first month of treat-ment. D. Step 3 —T reat other electrolyte and acid-base disorders. Follow-Up A. Hypercalcemia can lead to osteoporosis, kidney stones or failure, nervous system disorders, and arrhythmias. B. Follow-up of calcium levels is essential to prevent adverse outcomes. Consultation/Referral A. Patients should be referred to the appropriate service to treat the underlying disorder. B. Oncology may be needed for patients with cancer. C. Endocrine can be consulted for hormonal disorders con-tributing to hypercalcemia. D. Nephrology should be consulted if there is renal involve-ment. Special/Geriatric Considerations A. Geriatric patients may be at increased risk due to immo-bility and dehydration. B. Sitting or lying for long periods of time can cause calcium to leak into the bloodstream. C. Severe dehydration can also transiently increase calcium concentration secondary to hypovolemia. D. Hypercalcemia can contribute to arrhythmias that further put geriatric patients at risk for adverse events. Bibliography Kraft, M. D., Btaiche, I. F., Sacks, G. S., & Kudsk, K. A. (2005, August). T reatment of electrolyte disorders in adult patients in the intensive care unit. American Journal of Health System Pharmacy, 62 (16), 1663-1682. doi:10. 2146/ajhp040300 Moe, S. M., & Daoud, J. R. (2004). Disorders of mineral metabolism: Cal-cium, phosphorous, and magnesium. In D. S. Gipson, M. A. Perazella, & M. Tonelli (Eds. ), National kidney foundation's primer on kidney dis-eases (6th ed., pp. 100-112). Philadelphia, PA: Elsevier Saunders. Shane, E. (2018, August 13). Diagnostic approach to hypercalcemia. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/diagnostic-approach-to-hypercalcemia Shane, E., & Berenson, J. R. (2017). T reatment of hypercal-cemia. In J. E. Mulder (Ed. ), Up To Date. Retreived from https://www. uptodate. com/contents/treatment-of-hypercalcemia Hyperkalemia Jessica S. Everitt, Divya Monga, and Catherine Wells Definition A. Serum potassium concentration of greater than 5. 5 m Eq/L (see Box 5. 3). Incidence A. Most common in patients with renal disease (impaired potassium elimination). Pathogenesis A. Causes. 1. Redistribution (a net shift of potassium from intracel-lular to extracellular space). 2. Total body excess (due to increased potassium inges-tion or impaired potassium elimination). BOX 5. 3 Potassium in Humans Normal serum potassium concentration is 3. 5 to 5. 5 m Eq/L. b Serum potassium levels represent extracellular potassium. b The vast majority ( 98%) of total body potassium is intracellular. Kidneys excrete 90% to 95% of dietary potassium, with the remaining excreted by the gut. Physiologic functions. b Cellular metabolism. b Glycogen and protein synthesis. b Regulation of the electrical action potential across cell membranes. Predisposing Factors A. High potassium, low sodium diets. B. Potassium supplements. C. Renal insufficiency. Subjective Data A. Common complaints/symptoms. 1. General malaise. 2. Weakness. 3. Gastrointestinal complaints. a. Nausea and vomiting. b. Diarrhea. 4. Neuromuscular. a. Muscle twitching. b. Cramping. c. Weakness. d. Ascending paralysis. e. Paresthesia. f. Hyperreflexia. Physical Examination A. Inspect and assess for volume/hydration status: Skin, mucous membranes, and jugular venous distension. B. Assess for cardiac and renal comorbidities. 1. Auscultate and evaluate heart and lung. 2. Perform neurological examination. Diagnostic Tests A. Initial laboratory tests. 1. Serum potassium (preferably plasma). 2. Venous or arterial CO2or HCO3and/or p H. Hyperkalemia109

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B. Other laboratory tests. 1. Complete chemistry panel. 2. Complete blood count. 3. Drug levels (i. e., digoxin). 4. T rans-tubular potassium gradient (TTKG). a. [Urine potassium/plasma potassium]/[urine osmolarity/plasma osmolarity]. b. Assessment of the kidney's capability to appropri-ately conserve potassium. c. Valid only if the patient is not taking any diuretics or drugs to block the renin-angiotensin-aldosterone system (RAAS), the urine osmolarity is greater than 300 m Osm/kg, and the urine sodium is greater than 25 m Eq/L. d. Should be greater than 10 during hyperkalemia, indicating that the kidneys are trying to remove potas-sium. C. Cardiac function tests. 1. EKG changes including: a. Peaked T-waves, prolonged PR-interval, widened QRS complex, and shortened QT-interval. b. Progressive worsening as potassium rises. c. Brady arrhythmias. d. Ventricular fibrillation. e. Asystole. Differential Diagnosis A. Pseudohyperkalemia. 1. Hemolysis during blood draw. 2. Preexisting hemolysis (e. g., sickle cell disease, transfu-sion reaction, drug induced). 3. Sampling error (i. e., collected above the level of an infusion). 4. Polycythemia. 5. Thrombocytosis ( >500,000 to 1 million/mm3): Potassium release when clots are formed. 6. Leukocytosis ( >100-200,000/mm3): Elevated potas-sium in serum but not in plasma. 7. Familial pseudohyperkalemia. B. Redistribution of intracellular potassium (shifts from intracellular to extracellular fluid). 1. Metabolic acidosis or diabetic ketoacidosis: Insulin deficiency. 2. Muscular injury (e. g., trauma and rhabdomyolysis). 3. Succinylcholine. 4. Digoxin overdose. 5. Reduced effective plasma volume/hypertonic state. a. Severe dehydration. b. Heart failure. c. Liver failure. 6. Hyperkalemic periodic paralysis. 7. Medications (toxicity): Beta-blockers, succinyl-choline;,and digitalis. C. Impaired elimination. 1. Kidney failure: Acute versus chronic. 2. Medication-induced. a. Potassium-sparing diuretics. b. Angiotensin-converting enzyme (ACE) inhibitors. c. Angiotensin receptor blockers (ARBs). d. Aldosterone antagonists. e. Nonsteroidal anti-inflammatory drugs (NSAIDs). f. T rimethoprim. g. Heparin. 3. Decreased action of aldosterone/aldosterone defi-ciency. a. Medications: ACE inhibitors; ARBs; NSAIDs; potassium-sparing diuretics; antibiotics(trimethoprim, penicillin G potassium); clonidine; cyclosporine; heparin; and others. b. Type IV renal tubular acidosis. c. Hyporeninemic hypoaldosteronism. d. Addison's disease (primary adrenal insufficiency). e. Gordon's syndrome (Type II pseudohypoaldos-teronism). 4. Hypocalcemia. D. Increased ingestion (requires impaired elimination). Evaluation and Management Plan A. Step 1 —Cardiac stabilization (stabilize the action poten-tial in the myocardium). 1. Intravenous calcium administered as calcium glu-conate or calcium chloride transiently stabilizes cardiac muscle but does not decrease serum potassium. a. Calcium gluconate contains 4. 65 m Eq Ca++/g and calcium chloride contains 13. 6 m Eq Ca++/g. Adjust doses accordingly. 2. T ransient but immediate effect. 3. 1 to 2 g given immediately and prior to other therapies (i. e., intravenous bicarbonate), and may be repeated as needed. 4. Central line preferred (especially for calcium or high doses of calcium gluconate). B. Step 2 —Shift potassium to intracellular space. 1. 10 units intravenous insulin with 50 m L dextrose 50% to prevent hypoglycemia. Repeat as needed. Moni-tor glucose and potassium. 2. High dose 𝛽-agonists such as nebulized albuterol. 3. Sodium bicarbonate in acidotic patients. a. Note: Correcting acidosis can also lower calcium levels. Give intravenous calcium before intravenous bicarbonate. C. Step 3 —Remove excess potassium. 1. Potassium-wasting diuretics; adequate dosing for renal function. 2. Potassium binders. a. Sodium polystyrene sulfonate (Kayexalate) given as 15 to 30 g PO every 4 to 6 hours or 30 to 60 g per retention enema. b. Patiromer (Veltassa) as 8. 4 g PO once daily. D. Step 4 —Dialysis. Consult a nephrology expert. 1. Assess all electrolytes and acid-base balance and treat as indicated with nephrology. Follow-Up A. Continue to monitor potassium levels for 24 to 48 hours after the last dose of medication to account for the half-life of all medications. B. Consider chronic treatment, which also includes potas-sium restriction and increased potassium elimination. 1. Dietary potassium restriction. 2. Discontinuation of medications associated with hyperkalemia. 3. Potassium-wasting medications (diuretics or potas-sium binders). C. Follow-up with nephrology and cardiology as needed until potassium is normalized. Consultation/Referral A. Consult nephrology for any refractory electrolyte disorder with or without a cute kidney i njury (AKI) or c hronic kidney disease (CKD). B. Consult endocrinology for any uncontrolled diabetes. 5. Nephrology Guidelines110

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Special/Geriatric Considerations A. Sodium polystyrene sulfonate (Kayexalate) is associated with bowel obstruction. Use with caution in all popula-tions but especially patients at risk for slow gastrointestinal motility. B. The high doses of 𝛽-agonists required to shift potas-sium intracellularly can cause tachycardia. Use with caution in patients with preexisting arrhythmias, and other at-risk populations. C. Patients with CKD and e nd-stage renal disease (ESRD) as well as high risk of history of cardiac arrhythmias have a higher risk of mortality with hypokalemia than hyper-kalemia. Monitor carefully. D. Patients with chronic hyperkalemia may not require acute lowering of potassium levels for baseline potassium in the absence of EKG changes or other signs/symptoms. Bibliography Allon, M. (2014). Disorders of potassium metabolism. In D. S. Gipson, M. A. Perazella, & M. Tonelli (Eds. ), National Kidney Foundation's primer on kidney diseases (6th ed., pp. 90-99). Philadelphia, PA : Elsevier Saunders. Choi, M. J., & Ziyadeh, F. N. (2008, March). The utility of the transtubu-lar potassium gradient in the evaluation of hyperkalemia. Journal of the American Society of Nephrology, 19 (3), 424-426. doi:10. 1681/ASN. 2007091017 Cohnm, J. N., Kowey, P. R., Whelton, P. K., & Prisant, L. M. (2000). New guidelines for potassium replacement in clinical practice. Archivesof Internal Medicine, 160, 2429-2436. doi:10. 1001/ archinte. 160. 16. 2429 Ethier, J. H., Kamel, K. S., Magner, P. O., Lemann, J., & Halperin, M. L. (1990, April). The transtubular potassium concentration in patients with hypokalemia and hyperkalemia. American Journal of Kidney Dis-eases, 15 (4), 309-315. doi:10. 1016/s0272-6386(12)80076-x Kraft, M. D., Btaiche, I. F., Sacks, G. S., & Kudsk, K. A. (2005). T reat-ment of electrolyte disorders in adult patients in the intensive care unit. American Journal Health System Pharmacy, 62 (16), 1663-1682. doi:10. 2146/ajhp040300 Pepin, J., & Sheilds, C. (2012). Advances in diagnosis and management of hypokalemic and hyperkalemic emergencies. Emergency Medical Practice, 14(2), 1-20. Sood, M. M., Sood, A. R., & Richardson, R. (2007). Emergency man-agement and commonly encountered outpatient scenarios in patients with hyperkalemia. Mayo Clinic Proceedings, 82 (12), 1553-1561. doi:10. 1016/S0025-6196(11)61102-6 Hypermagnesemia Jessica S. Everitt, Divya Monga, and Catherine Wells Definition A. See Box 5. 4. B. Mild hypermagnesemia 2. 5 to 4 mg/d L. C. Moderate hypermagnesemia 4 to 12. 5 mg/d L. D. Severe hypermagnesemia greater than 12. 5 mg/d L. BOX 5. 4 Magnesium in Humans Normal serum range is 1. 5 to 2. 4 mg/d L. Found primarily in soft tissue, bone, and muscle. Approximately 1% of total body magnesium is found in the extracellular fluid. Homeostasis managed primarily by the kidneys, but gastrointestinal tract, parathyroid hormone, and serum magnesium con-centrations also involved. Serves as a cofactor in many enzymatic and biochemical reactions, including reactions involving adenosine triphosphate. Incidence A. Hypermagnesemia is rare in patients with normal renal function. Pathogenesis A. Magnesium is the second most abundant intracellular cation in the body after potassium. B. It is critical in the functioning of neuromuscular, cardiac, and nervous system functions. C. Magnesium is vital to vascular tone, heart rhythm, bone formation, and muscle contraction among many other criti-cal functions. Predisposing Factors A. Excessive intake of magnesium. B. Lithium. C. Hypothyroidism. D. End-stage renal disease. Subjective Data A. Common complaints/symptoms. 1. Typically asymptomatic until serum concentrations exceed 4 mg/d L. 2. Mild hypermagnesemia. a. Nausea and vomiting. b. Loss of deep tendon reflexes. c. Hypotension. d. Bradycardia. e. EKG changes such as increased PR interval, and increased QRS interval. 3. Severe hypermagnesemia. a. Respiratory paralysis. b. Refractory hypotension. c. Atrioventricular block. d. Cardiac arrest. Physical Examination A. Check reflexes. B. Check blood pressure. C. Perform cardiac examination. Diagnostic Tests A. Serum magnesium. B. Serum creatinine/b lood urea nitrogen (BUN). C. EKG. D. Evaluation for pregnancy. Differential Diagnosis A. Ingestion. 1. Magnesium-containing laxatives or antacids. Hypermagnesemia111

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2. Accidental ingestion of Epsom salts (magnesium sul-fate). B. Intravenous magnesium infusion (intentional overdose). 1. Therapy for preeclampsia and eclampsia. 2. Parenteral nutrition or magnesium supplementation. C. Reduced excretion. 1. Reduced renal function due to chronic kidney disease or acute kidney injury. D. Theophylline intoxication. E. Acromegaly. F. T umor lysis syndrome. G. Familial hypocalciuric hypercalcemia. H. Adrenal insufficiency. Evaluation and Management Plan A. Step 1 —If severe cardiac symptoms exist, give intra-venous calcium immediately. It can transiently stabilize the cardiac effects of severe, symptomatic hypermagnesemia. 1. Calcium chloride 1 gm or calcium gluconate 3 gm (see s ection “Hypocalcemia” for safety details regarding intravenous calcium). B. Step 2 —Determine the cause. 1. Intentional overdose for medical reasons should not be corrected. 2. If indicated, restrict or discontinue all magnesium-containing agents. C. Step 3 —T reat other electrolyte and acid-base disorders. D. Step 4 —Accelerate renal magnesium clearance. 1. Loop diuretics, which can increase urinary excretion of magnesium. 2. Hemodialysis, which can remove excess magnesium. Follow-Up A. Hypermagnesemia is a rare occurrence. Follow-up with nephrology if persistent. Consultation/Referral A. Nephrology should be consulted if hypermagnesemia cannot be explained or requires intervention such as dialysis. Special/Geriatric Considerations A. This is a rare condition that is typically caused by inges-tion of excessive magnesium. Bibliography Kraft, M. D., Btaiche, I. F., Sacks, G. S., & Kudsk, K. A. (2005, August). T reatment of electrolyte disorders in adult patients in the intensive care unit. American Journal of Health System Pharmacy, 62 (16), 1663-1682. doi:10. 2146/ajhp040300 Moe, S. M., & Daoud, J. R. (2014). Disorders of mineral metabolism: Cal-cium, phosphorous, and magnesium. In D. S. Gipson, M. A. Perazella, & M. Tonelli (Eds. ), National Kidney Foundation's primer on kidney dis-eases (6th ed., pp. 100-112). Philadelphia, PA: Elsevier Saunders. Hypernatremia Jessica S. Everitt, Divya Monga, and Catherine Wells Definition A. Serum sodium greater than 145 m Eq/L (see Box 5. 5). Incidence A. Up to 80% of hypernatremia is hospital acquired. Only 0. 1% to 1. 4% of hypernatremia is present on admission. B. Overall inpatient incidence is 1% to 5%, and incidence in critically ill patients is 9% to 26%. C. Hypernatremia is associated with increased length of stay and is an independent predictor of mortality (increased >40%). D. Populations at increased risk. 1. Extremes of age (infants and elderly), especially patients with pulmonary or urinary tract infections. 2. Restricted access to water. 3. Altered mental status/neurological illness. 4. Chronic debilitating illnesses associated with impaired thirst/dehydration. Pathogenesis A. Reflects a water deficit relative to total body sodium. B. Can occur in hypovolemic, euvolemic, and hypervolemic patients. C. Causes plasma hypertonicity (effect of plasma on cells that causes cells to shrink). D. Almost always requires reduced intake of water with or without loss of the normal thirst response. Otherwise, indi-viduals' normal thirst would encourage them to drink a suf-ficient amount to correct plasma hypertonicity. BOX 5. 5 Sodium in Humans Normal serum concentration 135 to 145 m Eq/L. Most abundant extracellular cation. The majority of total body sodium is found in cells and plasma water. Additional bound sodium is found (and can accumulate) in bone, cartilage, and connective tissue. Plasma sodium is approximately the same as interstitial sodium. Sodium does not cross the blood-brain barrier, but plasma sodium levels and tonicity of plasma affect brain cells. Changes in serum sodium concentration typically reflect changes in water balance rather than actual changes in total body sodium. E. Hypovolemic hypernatremia: Represents a pronounced water deficit with a mild sodium deficit and requires impaired thirst or decreased intake of water in addition to losses. F. Euvolemic hypernatremia: Represents a pure body water deficit. G. Hypervolemic hypernatremia: Represents minimal decrease or no change in total body water (TBW) with an increase in total body sodium. H. Acute salt poisoning: Large intake of sodium (whether accidental or intentional), resulting in a rapid rise in sodium and subsequent severe hypertonicity. 5. Nephrology Guidelines112

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Predisposing Factors A. Alterations in thirst. B. Volume depletion. C. Hyperglycemia. D. Certain brain tumors such as pituitary tumors. Subjective Data A. Common complaints/symptoms. 1. Vary depending on cause, severity, and rate of devel-opment of hypernatremia. a. Altered skin turgor commonly found in hypov-olemic or euvolemic hypernatremia. b. Signs of volume overload: Hypervolemic hyperna-tremia. 2. Spectrum of neurological symptoms: Beginning with irritability, dizziness, fatigue, lethargy, and confusion; can progress to seizures and coma. 3. Other symptoms: Nausea, vomiting, and generalized muscle weakness. 4. Polyuria. a. Definition: 3 L or more per day. b. Urine output exceeding 5 to 10 L per day indi-cates antidiuretic hormone (ADH) deficiency (as in diabetes insipidus [DI]); these affected patients often crave ice. 5. Acute salt poisoning: High fever, intracranial hemor-rhage, seizures, and coma. Physical Examination A. Physical examination to assess volume status. 1. Check skin, mucous membranes, heart, lungs, jugular venous distension (JVD), edema. 2. Assess blood pressure and orthostatic changes. 3. Determine weight changes. B. Neurological assessment (initial and ongoing). Diagnostic Tests A. Serum sodium. B. Complete chemistry panel to assess causes. C. Serum osmolality. D. Spot urine osmolality (measured). 1. G reater than 300 m Osm/kg: Urine is concentrated and hypertonic but not necessarily because of sodium. This indicates a relative increase in solute compared to water. 2. Less than 100 m Osm/kg: Urine is dilute and hypo-tonic. This indicates a relative increase in water and/or decrease in solute. E. Spot urine sodium. 1. Less than 20 m Eq/L: Renal sodium retention as in low effective arterial blood volume. a. Common with extra-renal volume losses. 2. G reater than 20 to 30 m Eq/L: Renal-related losses of electrolytes (sodium). a. Common with loop diuretics, osmotic diuresis, or hyperglycemia. b. Post-AKI diuresis and post obstructive diuresis. F. Determination of patient volume status. 1. Consider volume assessment to be unreliable initial diagnostic criteria but is necessary when interpreting hypernatremia-related lab tests. 2. Review and calculate history of fluid intake and out-put. Differential Diagnosis A. Hypovolemic hypernatremia. 1. Water and salt deficit. 2. Renal losses (Urine sodium >20 m Eq/L). a. Loop diuretics (spot urine osmolality <100 m Osm/kg [hypotonic]). b. Post-obstructive or post-a cute kidney i njury (AKI) diuresis. c. Osmotic diuresis: Hyperglycemia, mannitol, urea (enteral tube feedings; spot urine osmolality >300 m Osm/kg or 24-hour urine osmolality >1,200 m Osm/kg). 3. Extrarenal losses: Urine sodium less than 20 m Eq/L; urine osmolality greater than 300 m Osm/kg (hyper-tonic). a. Gastrointestinal losses such as vomiting, diarrhea (i. e., acute infectious, osmotic [enteral tube feed-ings]), nasogastric suctioning, or enterocutaneous fis-tula. b. Skin losses: Perspiration, burns, or severe wounds. B. Euvolemic hypernatremia. 1. Pure water deficit; body sodium preserved. 2. Renal losses: Hypotonic urine (urine osmolality/ plasma osmolality <1). a. DI: Inadequate ADH release (spot urine osmolal-ity<100 m Osm/kg). i. Central DI: Congenital, head trauma, post neurosurgical surgery, neoplasms, infiltrative disorders (i. e., sarcoidosis), hypoxic encephalopa-thy, bleeding, infection, aneurysm, meningitis/ encephalitis. b. Gestational DI: Peripheral degradation of ADH. c. Nephrogenic DI (hereditary): Inadequate renal response to ADH. i. X-linked nephrogenic DI. ii. Autosomal recessive nephrogenic DI. d. Acquired nephrogenic DI: ADH independent urine concentrating defect. i. Hypercalcemia or hypokalemia. ii. Medication-induced: Lithium, vasopressin V2 receptor antagonists, demeclocycline, ampho-tericin B, methoxyflurane, or foscarnet. iii. Chronic kidney diseases (i. e., medullary cyst disease, sickle cell disease, amyloidosis, Sjögren's syndrome). iv. Bartter's syndrome. v. Malnutrition. 3. Extrarenal losses: Hypertonic urine (urine osmolality/ plasma osmolality >1). a. Insensible losses. i. Cutaneous: Fever, sweating, burns, or increased ambient temperature. ii. Respiratory: Tachypnea or mechanical venti-lation. b. Decreased water intake. i. Primary hypodipsia. ii. Reset osmostat. iii. Decreased access to water (i. e., altered mental status, iatrogenic). iv. Water loss intracellular (i. e., seizures, extreme exercise). C. Hypervolemic hypernatremia. 1. Increased sodium intake (TBW and sodium can be variable). Hypernatremia113

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2. Iatrogenic causes. a. Sodium administration (e. g., normal saline, 3% saline, or sodium bicarbonate) via intravenous or oral routes. b. Hyperalimentation. 3. Mineralocorticoid excess. 4. Medications: Lithium, demeclocycline, glyburide, amphotericin, colchicine, vinblastine, and others. 5. Hypertonic dialysis. 6. Salt ingestion. Evaluation and Management Plan A. Initial goal: To replace free water deficit and prevent ongoing water loss. 1. Assess volume status. 2. Calculate water losses and exact replacement necessary to avoid overcorrection. a. TBW for lean men is usually 60% of weight in kilogram, and for lean women is usually 50% of weight in kilogram. TBW is lower (approximated to 45%) in obese patients because of adipose tissue. Elderly patients also have a lower TBW (commonly estimated around 50%). b. Free water deficit (L) =Normal TBW ×[140 m Eq/l / (Current NA Plasma )-1]. 3. Choose appropriate replacement fluid and initial rate of repletion based on acuity and degree of hypovolemia. 4. Estimate ongoing water losses: Renal and extrarenal. 5. Choose an appropriate replacement fluid based on sodium level and underlying cause/diagnosis. 6. Choose replacement rate based on water losses. B. Hypovolemic hypernatremia. 1. Step 1 —Replace intravascular volume deficit (plasma volume deficit) with isotonic crystalloids within the first several hours. The goal is stable hemodynamics. 2. Step 2 —Replace total free water deficit/loss over 3 to 4 days (include ongoing losses). a. Calculate free water deficit (as previously noted). b. Choose hypotonic replacement fluid. i. 0. 45% Na Cl IV (1/2 of the volume given is water). ii. Water (D 5NS, D 5W, oral/gastric tube water). c. Replacement rate. i. Acute rise in sodium (hypernatremia devel-oped over <48 hours). 1)Rapid water replacement/correction over 24 hours. ii. Chronic rise in sodium (hypernatremia devel-oped over >48 hours; NOTE: If unknown whether hypernatremia is acute or chronic—treat as chronic). 1)Maximum rate for sodium correction = 10 m Eq/l per day over 2 to 3 days. 2)Less than 6 m Eq/L per day in elderly patients. d. Monitor fluid intake and output closely. e. With low sodium intake, do not allow sodium intake to exceed output as this will exacerbate hyper-natremia. f. Determine and treat the underlying cause. g. Perform neurological checks frequently. h. Monitor sodium levels every 4 hours, then daily. i. Monitor all electrolytes and replace as indicated. j. Initially monitor closely in an intensive care setting. 3. Step 3 —Replace ongoing water losses. a. Choose fluid with less sodium than current urine concentration. b. Monitor sodium at least daily. c. Monitor fluid intake and output closely. d. Give a low salt diet. 4. Step 4 —Monitor/replace other electrolyte losses due to polyuria (e. g., hypokalemia, bicarbonate). C. Euvolemic and hypervolemic hypernatremia. 1. Step 1 —If necessary, correct water deficit (as previ-ously noted). 2. Step 2 —Monitor fluid intake and output closely. Low salt diet. Do not allow sodium intake to exceed output as this will exacerbate hypernatremia. 3. Step 3 —Define/treat underlying cause. a. Review medications. b. Consider desmopressin (d DAVP) for central DI (synthetic ADH analog; also increases factor VIII and von Willebrand factor levels—monitor for clotting) at ONE of the following doses. i. 0. 05-0. 6 mg BID PO. ii. 1-2 mcg BID IV. iii. 10-20 mcg BID intranasal. c. Perform neurological checks frequently. d. Monitor sodium levels every 4 hours then daily. e. Monitor all electrolytes and replace as indicated. f. Initially monitor closely in an intensive care set-ting. 4. Step 4 —T reat other electrolyte and acid-base disor-ders. D. Acute salt poisoning—rapid rise in sodium. 1. Give a rapid infusion of water to correct at a rate of 1 m Eq/L per hour. 2. Consider hemodialysis for sodium correction. 3. Closely monitor and avoid overcorrection. Follow-Up A. Follow-up depends on the nature of the underlying con-dition. B. Hypernatremia needs to be corrected and maintained. Consultation/Referral A. Consult nephrology to help regulate hypernatremia. B. Consult neurosurgery if central DI is responsible for hypernatremia. Special/Geriatric Considerations A. Increased age: Decline in TBW, decreased urinary con-centrating ability, and impaired thirst; thus, elderly patients lack the same defenses against hypernatremia as younger patients. Bibliography Kraft, M. D., Btaiche, I. F., Sacks, G. S., & Kudsk, K. A. (2005, August). T reatment of electrolyte disorders in adult patients in the intensive care unit. American Journal of Health System Pharmacy, 62 (16), 1663-1682. doi:10. 2146/ajhp040300 Lindner, G.,Funk, G. C., & Schwarz, C. (2007). Hypernatremia in the crit-ically ill is an independent risk factor for mortality. American Journal of Kidney Diseases, 50, 952. doi:10. 1053/j. ajkd. 2007. 08. 016 Sterns, R. H. (2015). Disorders of plasma sodium. The New England Journal of Medicine, 372 (1), 55-65. doi:10. 1056/NEJMc15013425. Nephrology Guidelines114

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Hyperphosphatemia Jessica S. Everitt, Divya Monga, and Catherine Wells Definition A. Serum phosphorus greater than 4. 5 mg/d L (see Box 5. 6). Incidence A. Hyperphosphatemia is most common in renal impair-ment (acute or chronic). B. Sustained hyperphosphatemia is rare in the absence of renal disease. Pathogenesis A. Homeostasis of phosphate is maintained through g astrointestinal (GI) absorption and renal excretion. Imbal-ances in either of these mechanisms can result in hyperphos-phatemia. Predisposing Factors A. Excessive intake is rare, but potential cause. B. Patients with renal failure. BOX 5. 6 Phosphorus in Humans 85% of total body phosphorus is located in bones. b Approximately 14% is intracellular. b Remaining 1% is extracellular. Two-thirds of ingested phosphorus is excreted in the urine with the remainder excreted in stool. Normal serum phosphorus is 2. 5 to 4. 5 mg/d L. Many physiological functions. b Bone and cell membrane composition. b Nerve conduction. b Muscle function. b Energy-rich bonds of adenosine triphosphate. Subjective Data A. Common complaints/symptoms. 1. Most common and significant manifestations are signs/symptoms of hypocalcemia due to calcium-phosphate precipitation with decrease in ionized calcium. 2. Can lead to soft-tissue calcification due to precipita-tion of calcium-phosphate crystals in soft tissues produc-ing symptoms of pruritus, dermatologic changes, and (in severe cases) calciphylaxis. Physical Examination A. Respiratory examination. B. Musculoskeletal examination. C. Dermatological examination. Diagnostic Tests A. Serum phosphorus. B. Serum total calcium, ionized calcium. C. Venous CO2. D. Renal function evaluation (b lood urea nitrogen [BUN] and serum creatinine). Differential Diagnosis A. Renal failure or decreased renal excretion. 1. In chronic dialysis patients, poor compliance with phosphorus binding medications. B. Increased intestinal absorption: Rapid shifts from intra-cellular to extracellular. 1. Acidosis (respiratory or metabolic). 2. Hemolysis. 3. Rhabdomyolysis. 4. T umor lysis syndrome. C. Hypoparathyroidism. D. Vitamin D toxicity. E. Phosphorus containing laxatives or enemas. F. Hypocalcemia (reciprocal rise). G. Thyrotoxicosis, acromegaly (rare). Evaluation and Management Plan A. Step 1 —Volume expansion despite fluid volume status. 1. Initial bolus resuscitation. 2. Continue isotonic intravenous hydration. B. Step 2 —Emergency treatment for acute and severe hyperphosphatemia due to risk of renal failure. 1. Calcium replacement (see s ection “Hypocalcemia”). Acute, severe hyperphosphatemia can cause reciprocal hypocalcemia. 2. Emergency treatment: Continuous renal replacement therapy. Consult nephrology. 3. Additional management. a. Phosphorus binders (as noted in the text that follows) at large doses with three meals, snacks, plus a dose at bedtime. b. Consultation with a renal dietician for dietary counseling. i. Tightly restrict unnecessary sources of phos-phorus in the diet such as food preservatives and higher phosphorus grains and vegetables. ii. Choose an individualized target for protein intake that will not place the patient at risk for nutrition deficiencies or allow excessive phospho-rus intake from protein sources. c. Continuation of isotonic intravenous hydration. Consider loop diuretics if needed to increase urine output. C. Step 3 —If nonemergent, assess for cause of hyperphos-phatemia. 1. Hyperphosphatemia management is oral phosphate binders and dietary restriction in patients with chronic renal disease. Hyperphosphatemia115

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a. Give phosphate binders with food in order to bind dietary phosphorus in the intestinal tract and prevent absorption. b. Avoid magnesium-and aluminum-based binders because of risk of accumulation in renal disease. 2. Phosphorus binders should not be given to patients with acute kidney injury (AKI) due to risk for overcor-rection (hypophosphatemia) during recovery. 3. Current available formulations. a. Calcium-based (calcium acetate or calcium car-bonate). b. Sevelamer. c. Lanthanum. d. Iron-based (ferric citrate or sucroferric oxyhydrox-ide). e. Dose is specific to formulation used. D. Step 4 —T reat underlying cause if possible. E. Step 5 —T reat other electrolyte and acid-base disorders. Follow-Up A. Calcium levels, phosphate levels, and renal function should be monitored at intervals consonant with the sever-ity of the underlying disorder. Consultation/Referral A. Nephrology may be consulted if the hyperphosphatemia is associated with renal failure. Endocrinology may be consulted if the patient has hypoparathyroidism. Special/Geriatric Considerations A. Elderly patients with c hronic kidney disease ( CKD) are at risk for hyperphosphatemia. Bibliography Hypocalcemia Jessica S. Everitt, Divya Monga, and Catherine Wells Definition A. Total serum calcium less than 8. 6 mg/d L or ionized cal-cium less than 1. 1 mmol/L (see Box 5. 2). Incidence A. The incidence of hypocalcemia is difficult to quantify. B. In intensive care patients, hypocalcemia is estimated between 15% and 88% of all patients. Pathogenesis A. Calcium is necessary for bone mineralization, nerve con-duction, muscle relaxation, and cardiac conduction. Predisposing Factors A. Renal failure. B. Advancing age. C. Volume depletion. D. Hepatic insufficiency. E. Chronic heart failure. Subjective Data A. Common complaints/symptoms. 1. Most specific symptoms are perioral numbness and spasms of upper and lower extremities. 2. Severe hypocalcemia can lead to tetany and seizures. 3. Other neuromuscular, central nervous system (CNS), and cardiovascular symptoms may be present, even with mild to moderate hypocalcemia. a. Prolonged QT interval. b. Paresthesia. 4. Chronic hypocalcemia may present with skin mani-festations such as brittle and grooved nails, hair loss, der-matitis, and eczema. Physical Examination A. Cardiac examination. B. Neurological examination (reflexes). C. Possible bleeding. D. Chvostek's sign or T rousseau's sign: Increased neuromus-cular activity can be demonstrated by tapping over the facial nerve. Diagnostic Tests A. Total and ionized serum calcium. B. Serum phosphorus. C. Serum magnesium. D. 25-hydroxyvitamin D. E. Intact p arathyroid hormone (PTH). Differential Diagnosis A. Hypoparathyroidism. B. Pseudohypoparathyroidism (low calcium with low phos-phorus also known as i PTH resistance). C. Hypomagnesemia. D. Vitamin D deficiency. 1. Poor intestinal absorption (e. g., short bowel, poor nutritional intake). 2. Lack of sun exposure. 3. Decreased activation of vitamin D (e. g., cirrhosis). E. Tissue consumption of calcium. 1. Acute severe pancreatitis. 2. Sepsis. 3. Acute malignancies/blastic bone metastases (excess bone formation). 4. “Hungry bone syndrome” post parathyroidectomy in c hronic kidney disease (CKD) or e nd-stage renal disease (ESRD) patients with history of hyperparathyroidism. 5. Acute hyperphosphatemia (i. e., rhabdomyolysis, tumor lysis syndrome). 6. Citrate infusion (citrate binds to ionized calcium decreasing unbound, active calcium). a. T ransfusion of blood products preserved with citrate. b. Circuit anticoagulation for dialysis/apheresis. Evaluation and Management Plan A. Step 1 —Replace acute calcium needs. 1. Intravenous administration used when rapid correc-tion is required. 5. Nephrology Guidelines Kraft, M. D., Btaiche, I. F., Sacks, G. S., & Kudsk, K. A. (2005, August). T reatment of electrolyte disorders in adult patients in the intensive care unit. American Journal of Health System Pharmacy, 62 (16), 1663-1682. doi:10. 2146/ajhp040300 Moe, S. M., & Daoud, J. R. (2014). Disorders of mineral metabolism: Cal-cium, phosphorous, and magnesium. In D. D. Gipson, M. A. Perazella, & M. Tonelli (Eds. ), National Kidney Foundation's primer on kidney dis-eases (6th ed., pp. 100-112). Philadelphia, PA: Elsevier Saunders. Stubbs, J. R., & Yu, A. S. L. (2017). Overview of the causes and treatment of hyperphosphatemia. In S. Goldfarb & A. Q. Lam (Eds. ), Up To Date, Waltham, MA: Retrieved from https://www. uptodate. com/contents/overview-of-the-causes-and-treatment-of-hyperphosphatemia116

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2. Initial dose: 1 g calcium chloride or 3 g calcium gluconate. a. Repeat dose as needed. b. Calcium chloride contains three times more elemental calcium than calcium gluconate. 3. Caution: Intravenous calcium can cause vascular and tissue necrosis if extravasation occurs as both calcium chloride and calcium gluconate. A central intravenous line is recommended for all calcium infusions. B. Step 2 —Assess for ongoing calcium replacement needs and replace as indicated. 1. Use intravenous or oral calcium replacement. 2. Oral calcium supplements used in asymptomatic patients and patients with chronic hypocalcemia. a. Calcium carbonate contains maximum elemental calcium compared to other formulations. b. Typical dose is calcium carbonate 1,250 mg (equivalent to 500 mg elemental calcium) twice daily. c. Take on empty stomach to maximize absorption of calcium. 3. Administer vitamin D to increase intestinal absorp-tion of calcium if vitamin is deficient. a. NOTE: Patients with renal failure need activated formulas of vitamin D replacement. Consult nephrol-ogy for assistance. C. Step 3 —T reat other electrolyte and acid-base disorders (i. e., hypomagnesemia). Follow-Up A. Follow-up with an outpatient provider to monitor labs would be advised. Consultation/Referral A. Consider consults based on the underlying cause of hypocalcemia and the severity of the condition. Special/Geriatric Considerations A. Severe hypocalcemia may result in seizures, tetany, refrac-tory hypotension, or arrhythmias that require a more aggres-sive approach. Bibliography Goltzman, D. (2000, updated 2016). Approach to hypercalcemia. In K. R.,Feingold,B. Anawalt,&B,A. Boyceetal(Eds. ), Endotext, South Dartmouth, MA: MDText. com. Retrieved from https://www. ncbi. nlm. nih. gov/books/NBK279129/ Kraft, M. D., Btaiche, I. F., Sacks, G. S., & Kudsk, K. A. (2005, August). T reatment of electrolyte disorders in adult patients in the intensive care unit. American Journal of Health System Pharmacy, 62 (16), 1663-1682. doi:10. 2146/ajhp040300 Moe, S. M., & Daoud, J. R. (2014). Disorders of mineral metabolism: Cal-cium, phosphorous, and magnesium. In D. S. Gipson, M. A. Perazella, & M. Tonelli (Eds. ), National Kidney Foundation's primer on kidney dis-eases (6th ed., pp. 100-112). Philadelphia, PA: Elsevier Saunders. Hypokalemia Jessica S. Everitt, Divya Monga, and Catherine Wells Definition A. Serum potassium concentration of less than 3. 5 m Eq/L (see Box 5. 3). Incidence A. Hypokalemia occurs in 20% of hospitalized patients. Pathogenesis A. Causes. 1. Total body deficiency (increased losses or decreased intake). This condition may develop as a result of: a. Gastrointestinal losses. b. Renal losses with or without metabolic abnormal-ities. c. Decreases in intake that surpass the kidneys' ability to compensate. 2. Redistribution (a net shift of potassium from extracel-lular to intracellular space). 3. Hypomagnesemia. This causes the kidneys to secrete potassium into the urine at a higher rate than they would with the same potassium levels and higher magnesium levels, leading to hypokalemia or accelerating it. 4. Elevated plasma sodium levels (due to a high salt diet). These cause the kidneys to lose potassium while mak-ing an effort to balance ion neutrality via available ion exchange transporter. Predisposing Factors A. Nonpotassium sparing diuretics. B. Eating disorders. C. Alcoholism. Subjective Data A. Common complaints/symptoms. 1. Palpitations or arrhythmias. 2. Gastrointestinal. a. Nausea and vomiting. b. Constipation, ileus. 3. Muscle weakness (severe hypokalemia). a. Skeletal muscle weakness and paralysis. b. Respiratory compromise due to diaphragmatic paralysis. c. Rarely, rhabdomyolysis. 4. Cramping (lower legs). B. Postural hypotension. Physical Examination A. EKG changes include ST-segment depression, T-wave flattening, T-wave inversion, and the presence of U-waves. B. Can progress to life-threatening and/or fatal arrhythmias and sudden cardiac death. 1. Check gastrointestinal system: Abdominal pain and bowel sounds. 2. Inspect musculoskeletal system: Strength. 3. Perform neurological examination. Diagnostic Tests A. Initial lab tests. 1. Serum potassium (preferably plasma). 2. Venous or arterial CO2or HCO3and/or p H. B. Other lab tests. 1. Complete chemistry panel. 2. Blood urea nitrogen (BUN) and creatinine to assess kidney function. C. Estimate of total body extracellular potassium and potas-sium deficit. 1. Total body potassium (m Eq/L) =Extracellular fluid volume (ECFV) ×Serum potassium (m Eq/L). a. ECFV =Total body water [0. 6 ×weight (kg)] × 1/3. Hypokalemia117

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2. Potassium deficit (m Eq/L) = a. ECFV ×Desired serum potassium (4. 0 or 4. 5 m Eq/L)-ECFV ×Serum potassium (m Eq/L). b. NOTE: This calculation does not account for ongoing losses or intracellular deficits. D. Assessment for cause of potassium losses. 1. T rans-tubular p otassium g radient (TTKG): Assess-ment of the kidney's capability to appropriately conserve potassium. a. Valid only if the patient is not taking any diuretics or drugs to block the renin-angiotensin-aldosterone system (RAAS). b. During hypokalemia, TTKG should be less than 3, indicating the kidneys are conserving potassium. 2. Urine potassium concentration—24-hour collection. E. Cardiac function. 1. EKG changes including peaked T-waves, prolonged PR-interval, widened QRS complex, shortened QT-interval. 2. Bradyarrhythmias. 3. Ventricular fibrillation. 4. Asystole. Differential Diagnosis A. Spurious hypokalemia or pseudohypokalemia. 1. Leukocytosis greater than 100,000/mm3. 2. Insulin dosing/timing of lab draw. B. Redistribution. 1. Metabolic alkalosis. 2. Catecholamine excess. a. Alkalemia. b. Familial hypokalemic periodic paralysis. c. Thyrotoxicosis. d. Factor replacement in megaloblastic anemia. e. Medications: Insulin, theophylline toxicity, 𝛽-adrenergic activity/agents (epinephrine), bron-chodilators, caffeine-containing drugs. C. Increased potassium losses. 1. Gastrointestinal losses: Prolonged vomiting or diar-rhea. 2. Extra-renal potassium loss (urine potassium <20 m Eq/24 hours). a. Prolonged diarrhea. b. Nasogastric suctioning. c. Intestinal potassium binders (e. g., sodium polystyrene sulfonate or patiromer). d. Poor intake/malnutrition. e. Laxative abuse. f. Excessive sweating. g. Villous adenoma recto-sigmoid colon. 3. Renal potassium loss (urine potassium >20 m Eq/24 hours): Non anion gap metabolic acidosis. a. Renal tubular acidosis Type I (distal) and Type II (proximal). b. Liddle's syndrome (decreased aldosterone secre-tion; normal renin level). c. Diabetic ketoacidosis, lactic acidosis. d. Ureterosigmoidostomy. e. Medications: Carbonic anhydrase inhibitors, laxa-tive overuse, topiramate. 4. Renal potassium loss (urine potassium >20 m Eq/24 hours): Metabolic alkalosis. a. Vomiting or nasogastric suction. b. Mineralocorticoid excess syndromes (normoten-sive primary hyperaldosteronism). c. Bartter's syndrome. d. Gitelman's syndrome. e. Medications: Diuretics (loop, thiazide), especially in the setting of high salt intake. 5. Renal potassium loss (urine potassium >20 m Eq/24 hours): No acid-base disorder. a. Elevated renin levels: Malignant hypertension, ren-ovascular disease, renin-secreting tumor. b. Low renin levels: Elevated aldosterone levels (pri-mary hyperaldosteronism, bilateral adrenal hyperpla-sia, dexamethasone suppression). c. Low aldosterone levels. i. Mineralocorticoid ingestion. ii. Congenital adrenal hyperplasia. iii. Cushing's syndrome. iv. Ectopic ACTH. v. Tobacco. vi. Black licorice. d. Hypomagnesemia. e. Enuresis/polyuria: Hypercalcemia, acute kidney injury recovery, postobstructive diuresis, osmotic diuresis (e. g., hyperglycemia). f. Medications: Aminoglycosides, amphotericin B, high dose corticosteroids, mineralocorticoids. 6. Other. a. Leukemia. b. Any disorder causing severe or progressive weak-ness: Myasthenia gravis, polyneuropathy. Evaluation and Management Plan A. Goal: To avoid or resolve the cause of the hypokalemia and treat the condition and its related symptoms. B. Step 1 —Immediate treatment: Potassium supplementa-tion. The total dose is at least equal to the calculated potas-sium deficit. The calculated dose to replace potassium in extracellular fluid is: 1. [Ideal plasma potassium mmol/L-Actual plasma potassium] ×[TBW (L) ×Extracellular fluid (%)]. a. TBW =Weight (kg) ×0. 5 (women), 0. 6 (men), 0. 45 (elderly). b. ECFV is 26% to 30% of TBW. 2. [4. 0 mmol/L-2. 5] ×[(80 kg ×0. 5)×0. 26] =1. 5× [40 x 0. 26] =1. 5×10. 4=15. 6 mmol/L or 16. a. 16 mmol/L-16 m Eq/L b. Deliver intravenously. Oral doses will be higher due to poor absorption. C. Step 2 —Repeated calculations and doses for ongoing potassium losses. 1. Intravenous supplementation. a. Initial dose of 20 to-40 m Eq: Common, but in severe hypokalemia will likely need to be repeated. b. Dose: 10 to 20 m Eq/hr. c. Reserved for severe and/or symptomatic hypokalemia or for patients unable to tolerate oral supplementation. 2. Oral supplementation. a. Available in tablet, capsule, or liquid formulations. b. Total daily doses: 40 to 100 m Eq; sufficient replacement in most cases. c. Divided into two to four doses to reduce gastroin-testinal side effects. d. Patients with renal dysfunction: Decrease dose by 50% and avoid repeating doses. D. Step 3 —T reatment of underlying disorder. 1. Correct hypomagnesemia as it can result in refractory hypokalemia. 5. Nephrology Guidelines118

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2. Decrease or discontinue medications associated with hypokalemia if possible. 3. Decrease sodium intake (especially with diuretic use). E. Step 4 —T reatment of other electrolyte and acid-base disorders. F. Step 5 —Assessment of need for chronic management. 1. Some patients will require chronic oral potassium sup-plements or high potassium diets. 2. Consider potassium-sparing diuretics (e. g., spirono-lactone, amiloride, triamterene) in patients on potassium-depleting medications. 3. All patients on potassium-depleting medications need a low-salt diet. Follow-Up A. For hypokalemia related to acute episodes, such as severe diarrhea, no follow-up is necessary. B. However, patients on long-term diuretic therapy should have periodic monitoring of serum potassium levels. Consultation/Referral A. Consult nephrology for any refractory electrolyte disorder with or without acute kidney injury or chronic kidney disease (CKD). B. Consult endocrinology for any uncontrolled diabetes or other hormone disorders. C. Consult gastroenterology for refractory symptoms and suspected villous adenoma. Special/Geriatric Considerations A. Monitor patients with CKD, congestive heart failure, or medications associated with hypokalemia carefully to avoid overcorrecting. Bibliography Allon, M. (2014). Disorders of potassium metabolism. In D. S. Gipson, M. A. Perazella, & M. Tonelli (Eds. ), National Kidney Foundation's primer on kidney diseases (6th ed., pp. 90-99). Philadelphia, PA: Elsevier Saunders. Cohnm, J. N., Kowey, P. R., Whelton, P. K., & Prisant, L. M. (2000). New guidelines for potassium replacement in clinical practice. Archives of Internal Medicine, 160, 2429-2436. doi:10. 1001/archinte. 160. 16. 2429 Kraft, M. D., Btaiche, I. F., Sacks, G. S., & Kudsk, K. A. (2005, August). T reatment of electrolyte disorders in adult patients in the intensive care unit. American Journal of Health System Pharmacy, 62 (16), 1663-1682. doi:10. 2146/ajhp040300 Pepin, J., & Shields, C. (2012). Advances in diagnosis and management of hypokalemic and hyperkalemic emergencies. Emergency Medical Practice, 14(2), 1-20. Hypomagnesemia Jessica S. Everitt, Divya Monga, and Catherine Wells Definition A. Serum magnesium less than 1. 5 mg/d L (see Box 5. 4). Incidence A. 2% of general population. B. 10% to 20% hospitalized patients. Pathogenesis A. Magnesium is the second most abundant intracellular cation in the body after potassium. B. It is critical in the functioning of neuromuscular, cardiac, and nervous system functions. Magnesium is vital to vasculartone, heart rhythm, bone formation, and muscle contraction, among many other critical functions. Predisposing Factors A. Starvation. B. Alcohol use. C. Diarrhea. D. Vomiting. E. Gastrointestinal fistulas. Subjective Data A. Common complaints/symptoms. 1. Neuromuscular symptoms similar to hypocalcemia. a. Hyperreflexia. b. Carpopedal spasm. c. Tetany. d. Seizures. e. Positive Chvostek's and T rousseau's signs. 2. Severe hypomagnesemia: Possible EKG changes and life-threatening arrhythmias (including torsades de pointes). Physical Examination A. Reflexes. B. EKG. C. Blood pressure. D. Cardiac examination. Diagnostic Tests A. Serum magnesium. B. Total calcium and ionized calcium (hypomagnesemia is often accompanied by hypokalemia and/or hypocalcemia). C. Potassium. D. Serum creatinine and b lood urea nitrogen (BUN). Differential Diagnosis A. Decreased intake. 1. Chronic alcoholism. 2. Prolonged fasting. 3. Protein-calorie malnutrition. 4. Inadequate supplementation in parenteral nutrition-dependent patients. B. Gastrointestinal losses. 1. Inflammatory bowel disease. 2. Chronic diarrhea. 3. Laxative abuse. 4. Malabsorption syndromes. 5. Surgical bowel resection or small intestinal bypass surgery. C. Renal losses. 1. Drugs. a. Diuretics. b. Amphotericin B. c. Aminoglycosides. d. Cyclosporine. e. Tacrolimus. f. Pentamidine. g. Proton pump inhibitors. h. Foscarnet. i. Cetuximab. j. Cisplatin. 2. High urinary output. a. Post-obstructive or resolving acute tubular necrosis (ATN) diuresis. Hypomagnesemia119

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b. Post-transplant polyuria. c. Hypercalcemia. 3. Inherited hypomagnesemia. a. Gitelman's syndrome. b. Bartter's syndrome. c. Phosphate depletion. 4. Primary hyperaldosteronism. 5. Chronic metabolic acidosis. 6. Idiopathic renal wasting. Evaluation and Management Plan A. Step 1 —Initiate intravenous (IV) magnesium replace-ment 4 g for all patients with severe symptoms or eclamp-sia/preeclampsia. 1. Deliver first dose quickly (over 4-5 minutes) if fol-lowed by an infusion or repeat slow IV bolus (over 6-12 hours). 2. Infuse 4 to 6 g over 8 to 12 hours. a. Magnesium distributes into tissues slowly, but is rapidly eliminated by the kidney. B. Step 2 —Replace magnesium. 1. Available in IV and oral forms. a. Use IV replacement for patients with severe deple-tion, those who cannot tolerate oral replacement, those who have eclampsia/preeclampsia, and those who are symptomatic. b. Use oral supplements for chronic hypomagne-semia and asymptomatic states. i. Absorption is unpredictable with oral supple-ments, and diarrhea is common. ii. Repletion of total body stores takes several days. 2. Recommended IV doses of magnesium sulfate (dose should be decreased by 50% in patients with renal impair-ment). a. 1 to 4 g if serum magnesium 1 to 1. 5 mg/d L. b. 4 to 8 g if serum magnesium less than 1 mg/d L. 3. Oral supplements. a. Magnesium oxide 400 mg BID. C. Step 3 —T reat other electrolyte and acid-base disorders. D. Step 4 —Assess cause and initiate a plan for prevention. 1. Potassium-sparing diuretics can reduce renal magne-sium wasting. Follow-Up A. Follow-up depends on underlying cause. B. Patients who have cardiac arrhythmias should be closely followed until magnesium levels are restored. Consultation/Referral A. Consult cardiology as needed for cardiac arrhythmias. B. Consult nephrology for management of renal impair-ment. Special/Geriatric Considerations A. Geriatric patients are at high risk for cardiac arrhythmias and renal impairment. B. Caution should be used to assure magnesium levels are optimized in this patient population. Bibliography Kraft, M. D., Btaiche, I. F., Sacks, G. S., & Kudsk, K. A. (2005, August). T reatment of electrolyte disorders in adult patients in the intensive care unit. American Journal of Health System Pharmacy, 62 (16), 1663-1682. doi:10. 2146/ajhp040300Moe, S. M., & Daoud, J. R. (2014). Disorders of mineral metabolism: Cal-cium, phosphorous, and magnesium. In D. S. Gipson, M. A. Perazella, & M. Tonelli (Eds. ), National Kidney Foundation's primer on kidney dis-eases (6th ed., pp. 100-112). Philadelphia, PA: Elsevier Saunders. Hyponatremia Jessica S. Everitt, Divya Monga, and Catherine Wells Definition A. See Box 5. 5 for further details. B. Serum sodium less than 135 m Eq/L (measured by ion-specific electrode; see Box 5. 5). a. Mild: 130 to 135 m Eq/L. b. Moderate: 125 to 129 m Eq/L. c. Severe or profound: L ess than 125 m Eq/L. C. Acute hyponatremia: Low serum sodium documented for 48 or fewer hours. D. Chronic hyponatremia: Low serum sodium that is either documented for greater than 48 hours or onset is unknown. Incidence A. The incidence is 15% to 38% in hospitalized patients, with only ∼7% incidence in ambulatory settings. B. In institutionalized geriatric patients, an incidence as high as 53% has been reported. C. The incidence of moderate and severe hyponatremia (serum sodium <130 m Eq/L) is 1%, with a prevalence of 2. 5%. 1. 67% of cases are hospital acquired, and 30% occur in the ICU. D. Admission of patients with hyponatremia is directly asso-ciated with inpatient mortality. Pathogenesis A. Pseudohyponatremia. 1. Apparent low sodium with plasma and urine osmo-lality and tonicity, as well as hyperlipidemia or hyperpro-teinemia. 2. Normal serum sodium that appears falsely low when using indirect ion-selective electrode (ISE) method to assess plasma for sodium. a. The original sample is diluted to 1:10 ratio, mea-suring whole plasma sodium, assuming the sample contains 93% water and 7% proteins/lipids. b. But increased proteins or lipids decrease the ratio of total water, causing a perceived lower than actual sodium level. 3. Solution: Measurement of sodium via direct ion-sensitive electrode and serum sample (undiluted blood). a. This is usually a point of care test. B. Dilutional hyponatremia ( ↑total body water [TBW] +/-↓Solutes). 1. Due to transcellular water shifts—hypertonicity. a. Hyperglycemia ( >250 mg/d L). b. Hypertonic solutions (e. g., mannitol, intravenous immunoglobulin [IVIG]). C. Solute depletion hyponatremia ( ↓Solutes + ↑ TBW; requires water intake). 1. Loss of solute while maintaining water intake. D. Potassium and sodium. 1. Potassium is an active cation; Sodium is an anion. To maintain electroneutrality, potassium +chloride exchange across cell membranes for sodium. 5. Nephrology Guidelines120

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2. As a result, when infusing potassium, some potassium ions become intracellular, and some sodium ions become extracellular, thus raising sodium levels. Predisposing Factors A. Elderly patients. B. Taking psychiatric medications. C. Cardiac disease. D. Chronic kidney disease. E. Malignancy. F. Alcoholism. Subjective Data A. Common complaints/symptoms. 1. Neurological symptoms: Range from mild and non-specific to severe and potentially fatal. a. Severity of symptoms increases with acuity of onset. i. Chronic hyponatremia often presents with rel-atively mild symptoms. ii. Acute, severe hyponatremia is associated with marked neurological deficits. 2. Neurological and other symptoms grouped by sever-ity. a. Mild symptoms (nonspecific and rarely progress to herniation). i. Headache. ii. Nausea and vomiting. iii. Mild confusion. b. Moderate (sometimes known as moderately severe): Most often seen in chronic hyponatremia, and thus not associated with impending herniation. i. Anorexia. ii. Fatigue/malaise. iii. Confusion, agitation, disorientation, or for-getfulness. iv. Gait disturbance. v. Abnormal sensorium (i. e., dizziness). c. Severe. i. Vomiting. ii. Cardiopulmonary distress. 1)Pulmonary edema. 2)Acute respiratory failure secondary to tentorial herniation with subsequent brain-stem compression. 3)Cheyne-Stokes respiration. iii. Delirium. iv. Somnolence/obtundation. v. Seizures (10% incidence with severe hypona-tremia). vi. Pathologic or depressed reflexes. vii. Pseudobulbar palsy. viii. Coma (Glasgow Scale ≤8). d. Other signs (e. g., falls). 3. Possible hypovolemia or hypervolemia depending on the etiology of the hyponatremia. Physical Examination A. Physical examination to assess volume status. 1. Check skin, mucous membranes, heart, lungs, jugular venous distension (JVD), edema. 2. Assess blood pressure and orthostatic changes. 3. Determine weight changes. B. Neurological assessment (initial and ongoing). Diagnostic Tests A. Serum sodium. B. Serum osmolality. C. Complete chemistry panel including potassium. D. Spot urine osmolality. 1. G reater than 300 m Osm/kg: Urine is concentrat-ed/hypertonic but not necessarily because of sodium. This indicates a relative increase in solute compared to water. 2. L ess than 150 m Osm/kg: Urine is dilute/hypotonic. This indicates a relative increase in water and/or decrease in solute. E. Spot urine sodium. 1. L ess than 20 m Eq/L: Renal sodium retention as in low effective arterial blood volume. 2. 20 m Eq/L or more: Diuretics will induce increased urine sodium. F. Determination of patient volume status. 1. Volume assessment is known to be unreliable as initial diagnostic criteria in hyponatremia but is necessary when interpreting hyponatremia-related lab tests. 2. Physical examination to include assessments. a. Skin, mucous membranes, heart, lungs, JVD, edema, and weight changes. b. Blood pressure and orthostatic changes (especially in patients using diuretics). G. Other lab tests to consider. 1. Fractional excretion of uric acid (FE UA%) or chloride (FE CL%). a. These have better specificity and sensitivity than fractional excretion of sodium (FE NA%) to help determine volume status and renal clearance of solutes. 2. Vasopressin levels. 3. Thyroid-stimulating hormone (TSH). 4. Glucose and glycosylated hemoglobin. 5. Cortisol. Differential Diagnosis A. Pseudohyponatremia. 1. Hypertriglyceridemia greater than 1,000 mg/d L. 2. Familial hypercholesterolemia. 3. Proteinemia greater than 10 gm/d L (i. e., multiple myeloma). B. Dilutional hyponatremia ( ↑TBW +/-↓Solutes). 1. Impaired free water excretion: Renal tubular water losses. a. Endocrine: Hypothyroidism or adrenal/ glucocor-ticoid insufficiency. b. Physical/emotional stress. c. Syndrome of inappropriate antidiuretic hormone (SIADH). i. C entral nervous system (CNS) etiologies: T umor, meningitis, intracranial hemorrhage/ hematoma, stroke, or trauma. ii. Pulmonary disease: Pneumonia, acute respira-tory failure, tuberculosis, or aspergillosis. iii. Neoplasm: Small cell carcinoma lung, pancre-atic cancer, or duodenal cancer. iv. HIV/AIDS. v. Postoperative. d. Edema syndromes: Nephrotic syndrome, cirrho-sis, or heart failure. e. Drugs: Amitriptyline, carbamazepine, chlor-propamide, clofibrate, cyclophosphamide, haloperidol, narcotics, nicotine, nonsteroidal Hyponatremia121

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anti-inflammatory drugs (NSAIDs), serotonin reup-take inhibitors, thiothixene, thioridazine, vincristine, ecstasy, or oxytocin. f. Thiazide diuretics. g. Diminished solute intake with ongoing water intake: “Tea and toast” diet or beer potomania. 2. Excess water intake. a. Primary polydipsia. b. Dilute infant formula. c. Hypotonic intravenous (IV) fluids. C. Solute depletion hyponatremia ( ↓Solutes + ↑ TBW; requires water intake). 1. Renal solute loss. a. Diuretic. b. Solute diuresis: Bicarbonaturia, ketonuria, glu-cose, mannitol, or urea diuresis. c. Salt wasting nephropathy (i. e., cystic renal dis-eases, interstitial disease, chronic glomerular disease, partial obstruction). d. Mineralocorticoid deficiency. 2. Nonrenal solute loss. a. Gastrointestinal loss (diarrhea, vomiting, pancre-atitis, bowel obstruction). b. Cutaneous (sweating, burns). c. Blood loss. d. Excessive intake of water and sports drinks in ath-letes, combined with excessive body fluid losses. Evaluation and Management Plan A. Step 1 —Choose therapy goal and timing of sodium cor-rection based on the following (obtained from history). 1. Acute hyponatremia with severe symptoms: Emer-gency treatment (more aggressive treatment). a. Sodium 129 m Eq/L or less that fell within the past 48 hours, causing severe patient symptoms. 2. Acute hyponatremia with moderately severe symp-toms: Emergency treatment. a. Sodium 129 m Eq/L or less that fell within the past 48 hours. causing moderate patient symptoms. 3. Acute hyponatremia with mild symptoms: Nonemer-gency treatment (most cases). a. Sodium 129 m Eq/L or less that fell within the past 48 hours, causing mild patient symptoms. 4. Acute hyponatremia asymptomatic: Nonemergency treatment (most cases). a. Sodium 129 m Eq/L or less that fell within the past 48 hours, without causing symptoms. 5. Chronic hyponatremia with any symptoms: None-mergency treatment. a. Sodium 129 m Eq/L or less for greater than 48 hours or an unknown period of time, causing any related patient symptoms. 6. Chronic hyponatremia asymptomatic: Outpatient treatment. a. Sodium 129 m Eq/L or less for greater than 48 hours, without causing symptoms. B. Step 2 —Set up appropriate monitoring to provide safe care and prevent overcompensation of sodium levels. 1. Emergency treatment. a. Monitor closely in an intensive care setting. b. Monitor complete fluid intake and output hourly. i. Do not allow water intake to exceed output as this will exacerbate hyponatremia. c. Perform neurological and symptom assessment frequently. d. Measure sodium levels every 2 to 4 hours; then take them once daily until stable and sodium greater than 130 m Eq/L. 2. Nonemergency treatment. a. Monitor in an ED, ICU, or other nursing floor with trained staff. b. Monitor complete fluid intake and output hourly. i. Do not allow water intake to exceed output as this will exacerbate hyponatremia. c. Perform neurological and symptom assessment frequently. d. Measure sodium levels every 4 to 6 hours; then take them once daily until stable and sodium greater than 130 m Eq/L. 3. Outpatient treatment. a. Only for chronic patients with stable but low sodium. b. Monitoring and follow-up vary according to cause of hyponatremia. C. Step 3 —Initiate volume correction if hypovolemic. D. Step 4 —Initiate sodium correction therapy according to severity of symptoms. 1. Acute or severe symptomatic hyponatremia. a. Initial treatment: 3% sodium chloride 100 m L bolus over 10 to 20 minutes. i. Repeat as needed: Up to 3 times. ii. Goal: To raise sodium 5% or 4 to 6 m Eq/L and resolve symptoms. iii. Once goal is met, change to 3% sodium chloride infusion initiated at 0. 5 to 2 m L/kg/hr and titrated based on sodium levels until sodium reaches 130 m Eq/L. 1)Raise the sodium: 1 m Eq/hour. 2)Maximum rise in sodium: 10 m Eq/L above baseline per 24 hours. b. Day 1 (first 24 hours): Maximum rise in sodium: 10 m Eq/L or 10%. c. Following days: Raise the sodium 8 m Eq/L or 10%. 2. Acute or moderate symptomatic hyponatremia. a. Initial treatment: 3% sodium chloride infusion given at 0. 5 to 2 m L/kg/hour and titrated based on sodium levels until sodium reaches 130 m Eq/L. b. Day 1 (first 24 hours). i. Goal for day 1: To raise sodium 5% or 4 to 6 m Eq/L and resolve symptoms. ii. Maximum rise in sodium: 10 m Eq/L or 10%. c. Following days. i. Raise the sodium 8 m Eq/L or 10%. 3. Asymptomatic hyponatremia. a. Water diuresis (unless hypovolemic): Loop diuret-ics. b. If not resolved: 3% sodium chloride infusion ini-tiated at 0. 5 to 2 m L/kg/hour and titrated based on sodium levels until sodium reaches 130 m Eq/L. c. Day 1 (first 24 hours). i. Maximum rise in sodium: 10 m Eq/L or 10%. d. Following days. i. Raise the sodium 8 m Eq/L or 10%. E. Step 5 —Other related interventions. 1. T reatment of other electrolyte and acid-base disor-ders; correct hypokalemia to a potassium of 3. 5 to 4. 5 m Eq/L. 2. Strict fluid intake and output; restrict or supplement intake as needed. 5. Nephrology Guidelines122

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3. Head trauma or hemodynamic instability: Consider consulting nephrology for continuous renal replacement therapy (CRRT) hyponatremia protocols. a. Slower sodium titration. b. Controlled management of sodium levels using CRRT. 4. Chronic hyponatremia. a. Initial therapy. i. Restrict all water intake (enteral and par-enteral) to 1,000 to 2,000 m L/day. ii. Correct hypokalemia to a potassium of 3. 5 to 4. 5 m Eq/L. iii. Euvolemic and hypovolemic patients. 1)Administer isotonic saline or balanced crystalloid solution. 2)Discontinue existing/chronic diuretics (assess as possible cause). iv. Hypervolemic patients. 1)Further restrict all water intake (enteral and parenteral) to 800 to 1,500 m L/day. 2)Give loop diuretics. v. Replace sodium deficit only if necessary. 1)3% sodium chloride infusion initiated at 0. 5 to 2 m L/kg/hour and titrated based on sodium levels until sodium reaches 130 m Eq/L. 2)+/-desmopressin (d DAVP) 1 to 2 mcg IV or SC every 8 hours for 24 to 48 hours. Only use d DAVP to support a therapy plan that includes sodium replacement and water restriction; d DAVP alone will not correct hyponatremia. Do not use d DAVP in psy-chogenic polydipsia, or edematous hypona-tremia (i. e., congestive heart failure [CHF], cirrhosis). 3)Day 1 (first 24 hours): Maximum rise in sodium: 10 m Eq/L or 10%. 4)Following days: Raise the sodium 8 m Eq/L or 10%. b. Patients with high urine cation concentrations. i. Give loop diuretics. ii. Give vasopressin type 2 (V 2) receptor antago-nists, also called vaptans. iii. Give salt tablets. iv. If resistant to the previously noted therapies, consider demeclocycline, or urea in conjunction with nephrology (demeclocycline likely to dam-age kidney function). 5. Overcorrecting hyponatremia. a. Risks: Seizures, cerebral edema, osmotic demyeli-nating syndrome (ODS), and death. b. If baseline serum sodium is 120 m Eq/L or more, no intervention necessary. c. If baseline serum sodium is less than 120 m Eq/L or if correction exceeds 6 to 8 m Eq/L or 10% per day. i. Give electrolyte free water (D 5W) 10 m L/kg and repeat as needed. ii. Consider also d DAVP 2 mcg IV. iii. Correct sodium level back to the most recent sodium that was within guidelines for correcting at 6 to 8 m Eq/L or 10% per day. iv. Correct sodium quickly, within a few hours of overcorrecting. Follow-Up A. Follow-up depends on underlying cause of hyponatremia. B. Follow-up should be managed by the primary service who is managing the underlying cause. Consultation/Referral A. Consult nephrology if hyponatremia is due to renal dis-orders. B. Consult neurology for CNS disorders causing hypona-tremia. Special/Geriatric Considerations A. A spectrum of diseases and disorders is associated with the geriatric population that predisposes them to hyponatremia, including pulmonary, endocrine, and CNS diseases, as well as cancers. B. A careful assessment of overall fluid status in elderly patients should be ascertained. C. Bone stress and fractures. 1. Sodium is stored in bone. Hyponatremia induces osteoclasts and thus bone loss. 2. Chronic hyponatremia is associated with a fourfold increase in osteoporosis (dose and time dependent), gait instability, falls in the elderly, and increased risk of frac-tures. D. Cerebral edema. 1. Sodium enters the brain only in plasma. Acute changes to plasma tonicity/osmolality cause water to shift in and out of astrocytes. Acute rises in osmolality cause astrocytes to shrink. 2. Within 48 hours, astrocytes adapt to hyponatremia and intracellular osmolality becomes equal to plasma osmolality without changing cell volume due to adaptive solutes and osmolytes. 3. However, this adaptation has consequences such as increased astrocyte susceptibility to injury and poor long-term outcomes. E. ODS. 1. Sudden rises in extracellular tonicity/osmolality caused by the treatment/overcorrection of hypona-tremia can cause osmotic stress on astrocytes, resulting in demyelination. 2. ODS initially seems to improve with improvement of hyponatremia. 3. There is a delayed onset of additional symptoms: Seizures, behavior changes, delusions, swallowing and speech dysfunction, movement disorders, paralysis, and potentially death. Symptoms can be temporary or permanent. F. Mortality: Mild hyponatremia is associated with increased mortality, but deaths from cerebral edema and ODS are rare. G. Monitor sodium closely in high risk populations. 1. Geriatrics. 2. Liver disease. 3. CHF. 4. CKD. H. Before treating hyponatremia, rule out and/or treat hypothyroidism, adrenal insufficiency, hyperglycemia, hypertriglyceridemia, and hyperproteinemia. I. For refractory hyponatremia in patients with CHF, con-sider adding a low dose a ngiotensin-converting enzyme (ACE) inhibitor to the diuretic regimen. Consult nephrology and cardiology experts. J. For patients with cirrhosis, primary therapy for hypona-tremia is water restriction and a low salt diet. If diuretics are required, use loop diuretics in combination with potassium-sparing diuretics and monitor potassium carefully. Hyponatremia123

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K. Thiazide diuretics impair urine-diluting capacity, thus exacerbating hyponatremia. Bibliography Hoorn, E. J., & Zietse, R. (2017). Diagnosis and treatment of hyponatremia: Compilation of the guidelines. Journal of American Society Nephrology, 28, 1-10. doi:10. 1681/ASN. 2016101139 Kraft, M. D., Btaiche, I. F., Sacks, G. S., & Kudsk, K. A. (2005, August). T reatment of electrolyte disorders in adult patients in the intensive care unit. American Journal of Health System Pharmacy, 62 (16), 1663-1682. doi: 10. 2146/ajhp040300 Spasovski, G., Vanholder, R., Allolio, B., Annane, D., Ball, S., Bichet, D.,... Nagler, E. (2014, April). Clinical practice guideline on diagnosis and treatment of hyponatremia. Nephrology, Dialysis, Transplantation, 29(Suppl. 2), i1-i39. doi:10. 1093/ndt/gfu040 Sterns, R. H. (2015). Disorders of plasma sodium. The New England Journal of Medicine, 372 (1), 55-65. doi:10. 1056/NEJMra1404489 Sterns, R. H., & Silver, M. S. (2016). Complications and management of hyponatremia. Current Opinion Nephrology Hypertension, 25 (2), 114-119. doi:10. 1097/MNH. 0000000000000200 Sterns, R. H. (2018, September 18). Causes of hypotonic hypona-tremia in adults. In J. P. Forman (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/causes-of-hypotonic-hyponatremia-in-adults Sterns, R. H. (2018, December 6). Overview of the treatment of hyponatremia in adults. In J. P. Forman (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/overview-of-the-treatment-ofhyponatremia-in-adults;Sterns Verbalis, J. G. (2014). Hyponatremia and hypoosmolor disorders. In D. S., Gipson, M. A. Perazella, & M. Tonelli (Eds. ), National Kidney Founda-tion's primer on kidney diseases (6th ed., pp. 62-69). Philadelphia, PA: Elsevier Saunders. Hypophosphatemia Jessica S. Everitt, Divya Monga, and Catherine Wells Definition A. See Box 5. 6. B. Serum phosphorus less than 3. 5 mg/d L. C. Moderate hypophosphatemia less than 2. 5 mg/d L. D. Severe hypophosphatemia less than 1 mg/d L. Incidence A. Incidence in general population is typically asymptomatic and estimated to be around 1% to 5%. The incidence rises sharply in patients with diabetic ketoacidosis, sepsis, or history of alcoholism. Pathogenesis A. Homeostasis of phosphate is maintained through g astrointestinal (GI) absorption and renal excretion. B. Imbalances in either of these mechanisms can result in hypophosphatemia. Predisposing Factors A. Eating disorders. B. Alcoholism. C. T umors. D. Vitamin D deficiency. E. Refeeding syndrome. F. Malabsorption. Subjective Data A. Common complaints/symptoms. 1. Depend on magnitude of hypophosphatemia: Mod-erate and severe before symptomatic. 2. Muscle weakness. a. Diaphragmatic weakness and difficulty with ven-tilation or weaning mechanical ventilation. b. Impaired myocardial contractility. 3. Neurological dysfunction. a. Irritability ranging to seizures or coma. b. Paresthesias. 4. Hematologic dysfunction, including hemolysis and platelet dysfunction. Physical Examination A. Respiratory examination. B. Musculoskeletal examination. C. Neurological examination. D. Gastrointestinal examination. Diagnostic Tests A. Serum phosphorus. B. Total calcium and ionized calcium. Differential Diagnosis A. Decreased intestinal absorption. 1. Malabsorption and chronic diarrhea. 2. Antacid abuse, excessive calcium supplement use, or overdose of phosphate binders. 3. Vitamin D deficiency. 4. Alcoholism. 5. Malnutrition, starvation, or anorexia. B. Increased urinary losses. 1. Primary hyperparathyroidism. 2. Fanconi syndrome. 3. Osmotic diuresis. a. Post-obstructive or resolving acute tubular necro-sis (ATN) diuresis. b. Glucosuria. 4. Acetazolamide. 5. Rickets (X-linked or vitamin D dependent). 6. Oncogenic osteomalacia. 7. Enuresis/polyuria. a. Postoperative, especially immediately after kidney transplant. b. Extracellular volume expansion. C. Redistribution (shift to intracellular space). 1. Respiratory alkalosis. 2. Diabetic ketoacidosis/treatment of hyperglycemia. 3. Refeeding syndrome (shift of phosphorus intracellu-larly in response to carbohydrate load). a. Malnourished patients are at high risk with total parenteral nutrition. 4. Alcohol withdrawal. 5. Severe burns. 6. Leukemic blast crisis. Evaluation and Management Plan A. Step 1 —If acute, severe, or symptomatic, replace phos-phate intravenously. 1. Give intravenous repletion for symptomatic patients with moderate or severe hypophosphatemia or those who cannot tolerate or receive oral supplementation. a. Potassium phosphate or sodium phosphate may be given. Sodium phosphate is recommended unless the patient also has hypokalemia. b. The initial dose is 0. 16 to 0. 25 mmol/kg, not to exceed 0. 5 mmol/kg. i. Give dose over a minimum of 4 to 6 hours. 5. Nephrology Guidelines124

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ii. Reduce dose by 50% in patients with renal dysfunction. B. Step 2 —Assess for ongoing losses or further phosphorus replacement needs. 1. Give intravenous replacement to patients who cannot take or absorb oral phosphorus or patients with ongoing symptoms. 2. Use oral supplements in patients with asymptomatic mild hypophosphatemia. a. May cause or worsen diarrhea. b. Gastrointestinal absorption is variable. c. Oral formulations contain various amounts of phosphorus, sodium, and potassium. d. Common regimen is 250 mg of elemental phos-phorus four times daily. 3. If oral supplements fail to maintain phosphorous lev-els, supplement with intravenous phosphorus. C. Step 3 —Identify and treat cause. D. Step 4 —T reat other electrolyte and acid-base disorders. Follow-Up A. Follow-up should occur with the provider who treats the underlying condition causing the electrolyte imbalance. Consultation/Referral A. Depends on underlying condition causing hypophos-phatemia. B. Endocrinology should be consulted if the diagnosis is related to hyperparathyroidism. C. Gastroenterology should be consulted if there is a malab-sorption condition. D. Nephrology should be consulted in renal phosphate wasting. E. Psychiatry should be consulted for eating disorders. Special/Geriatric Considerations A. Elderly patients can develop osteomalacia and be prone to bone pain and fractures. Bibliography Kraft, M. D., Btaiche, I. F., Sacks, G. S., & Kudsk, K. A. (2005, August). T reatment of electrolyte disorders in adult patients in the intensive care unit. American Journal of Health System Pharmacy, 62 (16), 1663-1682. doi:10. 2146/ajhp040300 Moe, S. M., & Daoud, J. R. (2014). Disorders of mineral metabolism: cal-cium, phosphorous, and magnesium. In D. S. Gipson, M. A. Perazella, & M. Tonelli (Eds. ), National Kidney Foundation's primer on kidney dis-eases (6th ed., pp. 100-112). Philadelphia, PA: Elsevier Saunders. Yu, A. S. L., & Stubbs, J. R. (2019, February 12). Evaluation and treatment of hypophosphatemia. In A. Q. Lam (Ed. ), Up To-Date. Retrieved from https://www. uptodate. com/contents/evaluation-and-treatment-of-hypophosphatemia Metabolic Acidosis Mary Rogers Sorey Definition A. Low arterial p H and low HCO3. B. Low p CO2after respiratory compensation. Incidence A. Metabolic acidosis occurs frequently in acute and chronic renal disease and in patients with any type of poisoning from drugs or chemicals. It is a common finding in the hospital setting for a variety of reasons. B. It is typically classified as having a normal anion gap (non-AG) or a high anion gap (AG). Pathogenesis A. Metabolic acidosis can be determined by calculating the AG, the first step in distinguishing the type of metabolic aci-dosis. 1. The equation to calculate the AG: AG =Na+-(Cl-+HCO 3). 2. The normal AG is 12 m Eq/L. B. The causes of metabolic acidosis can be a loss of bicarbon-ate or the addition of acid. C. In metabolic acidosis caused by loss of bicarbonate, there is a non-AG. 1. Gastrointestinal (GI) losses. a. Diarrhea. b. Ileostomy. c. Surgical drains. 2. Renal losses. a. Proximal and distal renal tubular acidosis. b. Hypoaldosteronism. D. In metabolic acidosis caused by addition of acid, the AG is elevated above 12. 1. Renal failure or uremia. 2. Lactic acidosis. 3. Ketoacidosis. a. Diabetes. b. Ethanol. c. Starvation. 4. Ingestion. a. Ethylene glycol. b. Methanol. c. Paraldehyde. d. Salicylate intoxication. E. In metabolic acidosis, the PCO 2falls predictably depend-ing on HCO 3concentration. 1. To calculate expected change, PCO 2=(1. 5 HCO 3-) +8+2. 2. If the PCO 2is not as expected, there is a respiratory acid-base disturbance, too. F. In AG metabolic acidosis,-can be used to discover a sec-ond metabolic acid-base disorder. 1. Gap/HCO 3-=(measured AG-ideal AG)/(ideal HCO 3-measured HCO 3-). a. If less than 1 then there is a non-AG metabolic acidosis present. b. If greater than 2 then there is a metabolic alkalosis present. Predisposing Factors A. There are none. Metabolic acidosis is dependent on cause, which determines the predisposing factors. Subjective Data A. Common complaints/symptoms. 1. Increased respiratory rate. 2. Drowsiness. 3. Nonspecific. B. Family and social history. 1. Alcohol use or drug abuse. 2. Occupational history and potential exposure to metals or chemicals. 3. Genetic disorder associated with a family history of acidosis, typically discovered in childhood. Metabolic Acidosis125

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C. Review of systems. 1. Neurological: Blurred vision, vertigo, headache, con-fusion, generalized weakness. 2. Head, ear, eyes, nose, throat: Ringing in the ears, light bothering eyes, seeing floaters. 3. Respiratory—increased breathing. 4. Cardiovascular—chest pain, palpitations. 5. GI—diarrhea, vomiting, pain in the chest that feels like heartburn. 6. Renal—increased urination, increased thirst, urina-tion at night. 7. Psychiatric: Any history of drug use or depression. Physical Examination A. Nonspecific physical examination that depends on the underlying cause. 1. Renal failure: Pallor, drowsiness, asterixis, pericardial rub. 2. Diabetic ketoacidosis: Reduced skin turgor, dry mucous membranes, fruity breath. 3. Sepsis—fever, confusion or coma, hypotension, Kuss-maul respirations. Diagnostic Tests A. Serum electrolytes: Check serum bicarbonate. B. Arterial blood gas (ABG): p H less than 7. 40. C. AG determination. D. Base excess/deficit determination to determine the degree of acidosis. E. CBC: Look for severe anemia which can affect oxygen delivery. F. Urinalysis: Urine p H greater than 5. 5 may be associated with certain renal diseases. 1. Calcium oxalate crystals seen in ethylene glycol toxicity. G. Beta-hydroxybutyrate. H. Lactate level. I. Necessary in certain situations. 1. Salicylate levels. 2. Iron levels. 3. Aldosterone levels. 4. Ammonium levels. Differential Diagnosis A. For normal AG metabolic acidosis. 1. Abdomen. a. Diarrhea. b. Fistulas. 2. Renal. a. Renal tubular acidosis: Addison's disease. b. Carbonic anhydrase inhibitors. c. Post hypocapnia. d. Excessive chloride (large volumes of saline). B. For a high AG metabolic acidosis, use the mnemonic MUDPILES to remember the differential diagnosis. 1. Methanol. 2. Uremia. 3. Diabetic ketoacidosis. 4. Paraldehyde. 5. Infection, iron, isoniazid, ibuprofen. 6. Lactic acidosis. 7. Ethylene glycol. 8. Salicylates. Evaluation and Management Plan A. General plan. 1. T reat with an alkali therapy to raise plasma p H greater than 7. 20. 2. Calculate the sodium bicarbonate deficit to determine how much must be administered intra-venously to raise the serum bicarbonate level to increase the p H greater than 7. 20. 3. Determine the underlying cause of the metabolic acidosis and treat appropriately. B. Pharmacotherapy. 1. Metabolic acidosis of any type. Sodium bicarbonate can be used, but treating the underlying issue is critical. a. Be cautious of volume overload; loop diuretics can be used to reduce volume as needed. 2. Methanol or ethylene glycol poisoning. Fomepizole can be used to treat ethylene glycol poisoning. 3. Uremia. Sodium bicarbonate can be used to keep serum bicarbonate levels above 20 m Eq/L. 4. Diabetic ketoacidosis. Insulin can be used to treat ketoacidosis. 5. Paraldehyde poisoning. Alkali therapy can be used to correct metabolic acidosis during supportive care; no spe-cific antidote exists. 6. Infection, iron, isoniazid, or ibuprofen. Antibiotics can be used to treat sepsis and activated charcoal can be used for the treatment of poisoning caused by drugs and chemicals. 7. Lactic acidosis. Alkali therapy such as sodium bicar-bonate or tromethamine can be used. a. The role of alkali therapy can be controversial. 8. Ethylene glycol—Fomepizole or ethanol can be used to treat cases of poisoning. 9. Salicylates—Acetazolamide can treat salicylate poi-soning by inducing alkaline diuresis. Follow-Up A. The patient needs to follow-up with the primary care provider and any appropriate service providers involved in regulating the underlying disease process that causes the metabolic acidosis. Consultation/Referral A. Refer to the appropriate service provider related to the cause of the metabolic acidosis. B. Consult nephrology as quickly as possible in cases that may require hemodialysis. C. Consult endocrine for patients who present with diabetic ketoacidosis. Special/Geriatric Considerations A. Metabolic complications are common in the elderly and can be exacerbated in chronic kidney disease. B. Special care to monitor and detect metabolic disturbances should be instituted. Bibliography Kraut, J. A., & Madias, N. E. (2015, October 15). Metabolic acidosis of CKD: An update. American Journal of Kidney Diseases, 67 (2), 307-317. doi:10. 1053/j. ajkd. 2015. 08. 028 Kraut, J. A., & Madias, N. E. (2016, September). Lactic acidosis: Current treatments and future directions. American Journal of Kidney Diseases, 68(3), 473-482. doi:10. 1053/j. ajkd. 2016. 04. 0205. Nephrology Guidelines126

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Rastegar, M., & G. T. Nagami (2017, February). Non-anion gap metabolic acidosis: A clinical approach to evaluation. American Journal of Kidney Diseases, 69 (2), 296-301. doi:10. 1053/j. ajkd. 2016. 09. 013 Reddy, P., & Mooradian, A. D. (2009, October). Clinical utility of anion gap in deciphering acid-base disorders. International Journal of Clinical Practice, 63 (10), 1516-1525. doi:10. 1111/j. 1742-1241. 2009. 02000. x Thomas, C. P. (2018, October 10). Metabolic acidosis. In V. Batu-man (Ed. ), Medscape. Retrieved from https://emedicine. medscape. com/ article/242975-overview Nephrolithiasis Juan A. Medaura Definition A. Formation of a kidney stone, an organized mass of crystals that grows on the surface of a renal papilla. Incidence A. Renal and ureteral stones are a common problem. In the United States, almost 2 million outpatient visits with urolithiasis as primary diagnosis were recorded in the year 2000. B. The prevalence is increasing from 3. 8% (1976-1980) to 8. 4% (2007-2010). It coincidentally has increased in concor-dance with the rising incidence in obesity, insulin resistance, and metabolic syndrome. C. The condition is more common in males than females. However, the ratio has gone from 1:4 to 1:1. 4, as a result of a significant spike in the incidence of the condition in women in the past decades. D. The average age of onset is 20s to 30s with a second peak in the mid-50s. Up to 16% of men and 8% of women will have at least one symptomatic stone by the age of 70 years. E. It is more common in whites compared with blacks, Asians, and Hispanics. F. It is more common in the south-eastern United States and more common in summer because of heat, sunlight exposure, and dehydration, leading to low urine volumes. G. In stone formers, the rate of recurrence is 30% at 5 years, 50% at 10 years, and 80% at 20 years. H. In the United States ∼80% of kidney stones are calcium-containing stones, of which 80% are mainly calcium oxalate stones. Less often they are calcium phosphate stones. Pathogenesis A. Kidney stones occur as the result of an increased burden of a poorly soluble salt excreted into a volume of urine that is insufficient to dissolve it (supersaturation). 1. In addition to an individual predisposition and/or other factors, there is, especially, lack of inhibitors of crys-tallization. 2. Supersaturation of poorly soluble salts (i. e., calcium oxalate) in urine is one factor. B. However, the main factor, especially in calcium-containing stones, is the accumulation of apatite (calcium phosphate) in the medullary interstitium; this may develop in idiopathic hypercalciuria. 1. A stone starts to accumulate in the basement mem-brane of the thin loop of Henle and grows into the medullary interstitium, to finally form the “Randall's plaque” that will erupt breaking the urothelium of the papilla. 2. This favors the deposition and aggregation of crystals, resulting in the organized stone. Predisposing Factors A. Idiopathic hypercalciuria. B. Obesity, diabetes, and metabolic syndrome: Uric acid stones and calcium oxalate stones. C. Dehydration, low fluid intake, and low urine volume (summer months, hot and/or dry weather, athletic, or occu-pational activities). D. High dietary salt. E. High oxalate food intake (e. g., spinach, nuts, chocolate, berries, tea, rhubarb, star fruit). F. High animal protein diet. G. Protein supplements. H. Excessive vitamin C supplementation (metabolized to oxalate). I. Low calcium diet with main meals of the day. J. Bariatric surgery (gastric bypass). K. Rapid weight loss/starvation. L. Hypocitraturia, metabolic acidosis, hypokalemia, or hypomagnesemia. M. Intestinal malabsorption. N. Antibiotics (leading to loss of Oxalobacter formigenes, a protecting bacteria of the gut microbiota against excess oxalate absorption). O. Chronic or recurrent u rinary tract infection (UTIs) with urea-splitting organisms such as Proteus, Providencia, or Ure-aplasma (struvite stones). P. Medications: Topiramate, acetazolamide, atazanavir, indinavir, triamterene, sulfadiazine, sulfasalazine, or felba-mate. Q. Systemic diseases: Primary hyperparathyroidism, dis-tal renal tubular acidosis (type 1), sarcoidosis/tuberculo-sis, medullary sponge kidney, malignancy, intestinal mal-absorption (i. e., Crohn's disease), hyperthyroidism, and so forth. Subjective Data A. Common complaints/symptoms. 1. Flank pain (radiates downward and anteriorly to the abdomen, pelvis, and groin/genitals). 2. Nausea and vomiting. 3. Hematuria (gross or microscopic). 4. Stone passage. B. Common/typical scenario. 1. Fever. 2. Dysuria. 3. Calculous anuria. 4. Interruption of urinary stream. C. Review of systems. 1. Establish onset and characteristics of the pain. 2. Ask about witnessed stone passage. 3. Ask about stone history. a. Age when first stone developed. b. Number of stones. c. Frequency of stone episodes. d. Size of stone (passed or still retained). e. Type of stone (if known). f. Kidney involved (left, right, or both). g. Need of urologic intervention (if yes, response to the intervention). h. UTI associated (yes or no). 4. Inquire about diet, at-risk occupations (e. g., pilots, taxi drivers, teachers, athletes), family history, medica-tions, dietary supplements, medical conditions, previous episodes of urolithiasis, and frequency of UTIs. Nephrolithiasis127

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Physical Examination A. The physical examination is most important for ruling out other conditions. Kidney and ureteral stones have no spe-cific manifestations on physical examination. B. C erebrovascular accident (CVA) tenderness can be posi-tive in some cases. Diagnostic Tests A. Noncontrast CT scan (stone protocol) is the gold standard. B. Renal ultrasound (inexpensive, safe) is a good diagnos-tic tool to diagnose urolithiasis and rule out hydronephro-sis, especially for frequent stone formers or patient with contraindication for radiation (i. e., pregnancy). C. Plain radiography of the abdomen shot at 60 k V (kidney-ureter-bladder [KUB]) is useful for the frequent calcium stone former to reduce the amount of radiation and is more economic. 1. Does not detect non-calcium stones (i. e., uric acid stones). D. Laboratory analysis should be performed after the first kidney stone episode. 1. Serum electrolytes, including calcium and phospho-rus. 2. Blood urea nitrogen (BUN) and creatinine. 3. Uric acid level. 4. In patients with hypercalcemia. a. Parathyroid hormone (PTH) level. b. 25-OH vitamin D. c. 1,25 dihydroxyvitamin D. 5. A low-serum bicarbonate concentration. a. Urine p H. i. 6. 0 or more: Suggests renal tubular acidosis. ii. G reater than 8 urine p H or pyuria: Should lead to urine cultures and consideration of stru-vite stones. 6. Ancillary 24-hour urine collection for stone-risk pro-file is recommended in these situations. a. All children with kidney stones. b. Metabolically active stones (growing in size or in number within 1 year). c. Frequent stone formers (more than two to three episodes). d. Non-calcium (e. g., cystine, uric acid) stone form-ers. e. Patient in demographic group not typically prone to stone formation (e. g., African Americans). Differential Diagnosis A. Pyelonephritis (although in many situations coexist with nephrolithiasis). B. Peritonitis. C. In women: Ovarian torsion, ovarian cyst, or ectopic preg-nancy. Evaluation and Management Plan A. General plan. 1. Pain relief. a. Patients can be managed at home if they are able to take oral medications and fluids. b. Combination of nonsteroidal anti-inflammatory drugs (NSAIDs) and opioids is superior than each agent alone (i. e., morphine 5 mg +ketorolac 15 mg). 2. Fluid intake. a. The mainstay of therapy is to increase the urine volume to more than 2 L per day. b. Therefore, the patient has to be encouraged to drink around 3 L of fluid per day. Because the risk of stone formation is highest during the night time, patients should be encouraged to drink plenty of flu-ids in the evening. 3. Sodium intake. a. Urine sodium excretion augments urine calcium excretion. b. Hence, the patient should be instructed to limit dietary sodium to 2 g per day. 4. Dietary calcium. a. It has been demonstrated that an adequate calcium intake in the diet decreases kidney stone incidence. This is likely due to intestinal binding of calcium to oxalate, preventing its absorption. b. An age-and gender-appropriate calcium diet is therefore recommended. Calcium supplementation outside of meals should be avoided. B. Specific treatment (for each stone type). 1. Calcium stones. a. Potassium citrate 30 to 60 m Eq/day PO. i. Would start with 60 m Eq/day if 24-hour uri-nary citrate is less than 150 mg/day. ii. Titrate dose to a 24-hour urinary citrate 320 to 640 mg/day and a urinary p H 6. 0 to 7. 0, to inhibit stone formation. b. Thiazide diuretic: Patients with hypercalciuria (24-hour urinary calcium >250 mg/day). i. Chlorthalidone 12. 5 mg PO daily, or hydrochlorothiazide 12. 5 mg PO daily, or inda-pamide 1. 25 mg PO daily. ii. If the calcium excretion remains elevated in follow-up 24-hour urinary calcium several months after, the thiazide dose should be increased. c. Dietary oxalate restriction: Patients with hyper-oxaluria (24-hour urinary oxalate >25-30 mg/day). Supplement each meal with calcium carbonate 1 to 1. 5 g and snack to bind dietary oxalate in the intes-tine and prevent absorption. d. Specific therapy for malabsorptive disorder: First-line treatment for enteric hyperoxaluria. 2. Uric acid stones. a. Potassium citrate: 30 to 60 m Eq/day or twice daily orally to dissolve retained uric acid stones. i. For prevention of new stones: 30 to 60 m Eq/ day or three times a week titrating urinary p H to greater than 7. 0. ii. Patient use of colorimetric p H-sensitive urine strips: Check the urinary p H 3 to 4 hours after taking potassium citrate. b. Low purine and low animal protein diet, if in follow-up the 24-hour urine uric acid is still high (>700 mg/day). i. May need to add allopurinol 100 mg/day PO, increasing weekly to 200 to 300 mg/day. 3. Struvite stones (staghorn calculi). a. Aggressive medical and surgical treatment, since this can lead to renal failure. i. Early urologic intervention is advised. b. Antibiotic therapy, to prevent further stone forma-tion due to urease splitting organisms. 4. Cystine stones. a. T reatment to decrease cysteine concentration: Water intake as mainstay of therapy. i. T rying to achieve 3 to 4 L of urine a day. 5. Nephrology Guidelines128

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ii. Goal urine cystine concentration less than 243 mg/L. b. Low sodium diet 2 g/day. c. Low animal protein diet. d. Potassium citrate: Goal urine p H greater than 7. 0 (maintained), which is a difficult task. i. Start 20 m Eq TID and titrate up to a p H greater than 7. 0. e. Tiopronin 400 to 1,200 mg/day in three divided doses (comes in 100 mg tablets). i. Fewer side effects than D-penicillamine, but still can cause the same side effects (i. e., protein-uria, fever, rash, abnormal taste, arthritis, leukope-nia, aplastic anemia, and hepatotoxicity). C. Hospitalization. 1. Stone greater than 5 mm (98% of stones <5 mm will pass spontaneously). 2. Nausea and vomiting; unable to take oral medicine or fluids. 3. Requiring parenteral therapy for pain. 4. Pyelonephritis/UTI. Follow-Up A. For adult patients with history of only one calcium-containing kidney stone that passed spontaneously, no spe-cial follow-up is required. B. For frequent stone formers (two to three or more episodes), children, or individuals who form non-calcium stones or rare stone types, they need a follow-up in 4 to 6 months with a 24-hour stone risk analysis to monitor the effect of therapy. Consultation/Referral A. Urology consultation is recommended for stones greater than 5 mm as the likelihood of spontaneous passage of stones of this magnitude is low, or consult when complications occur. UTI with obstruction is the most urgent indication for urologic consultation. B. Nephrology consultation is recommended for frequent stone formers, patients who form non-calcium stones, those who form rare stone types, and those with nephrolithiasis and chronic kidney disease (CKD). Children should be referred to pediatric nephrology. Special/Geriatric Considerations A. Common in the elderly and is associated with multiple comorbidities, including hypertension, coronary artery dis-ease, diabetes mellitus, and CKD. Bibliography Assimos, D. G., Krambeck, A., Miller, N. L., Monga, M., Murad, M. H., Nelson, C. P., & Matlaga, B. R. (2016). Surgical man-agement of stones: American Urological Association/Endourological Soci-ety Guideline. Linthicum, MD: American Urological Association. Retrieved from https://www. auanet. org/education/guidelines/surgical-management-of-stones. cfm Jindal, G., & Ramchandani, P. (2007, May). Acute flank pain sec-ondary to urolithiasis: Radiologic evaluation and alternate diag-noses. Radiologic Clinics of North America, 45 (3), 395-410, vii. doi:10. 1016/j. rcl. 2007. 04. 001 Singh, A., Alter, H. J., & Littlepage, A. (2007, November). A systematic review of medical therapy to facilitate passage of ureteral calculi. Annals of Emergency Medicine, 50 (5), 552-563. doi:10. 1016/j. annemergmed. 2007. 05. 015 Wen, C. C., & Nakada, S. Y. (2007, August). T reatment selection and out-comes: Renal calculi. The Urologic Clinics of North America, 34 (3), 409-419. doi:10. 1016/j. ucl. 2007. 04. 005 Worcester, E. M., & Coe, F. L. (2008, June). Nephrolithiasis. Primary Care, 35(2), 369-391. doi:10. 1016/j. pop. 2008. 01. 005Ziemba, J. B., & Matlaga, B. R. (2017, September). Epidemiology and eco-nomics of nephrolithiasis. Investigative and Clinical Urology, 58 (5), 299-306. doi:10. 4111/icu. 2017. 58. 5. 299 Nephrotic Syndrome Debra Hain Definition A. Nephrotic syndrome (NS) is a clinical syndrome with specific features of proteinuria and hypoalbuminemia or hypoproteinemia. B. The National Kidney Foundation defines NS as total urine protein excretion in excess of 3,500 mg/d (equivalent to a total protein-creatinine ratio of >3,000 mg/g), with a decreased serum albumin concentration and edema with or without a decrease in glomerular filtration rate (GFR). C. The term nephritic syndrome is an outdated term charac-terized by hematuria with red blood cell casts, hypertension, and edema with or without decreased GFR. Incidence A. Annual incidence in adults is three per 100,000 individ-uals. B. About 80% to 90% of the NS cases are primary (idio-pathic). 1. Membranous nephropathy (MN) is the leading cause of idiopathic NS. a. MN NS is common in white individuals and focal segmental glomerulosclerosis (FSGS) is more common in black individuals. b. FSGS NS accounts for about 30% to 35% of NS cases. 2. Minimal change disease (MCD) and immunoglobu-lin A nephropathy (about 15% of cases) are less frequent. C. About 10% of NS cases are secondary (due to underlying medical conditions). 1. Systemic lupus erythematosus (SLE). 2. Malignancy. 3. Infections (hepatitis B and C, HIV, and malaria). 4. Diabetic nephropathy. Pathogenesis A. Pathogenesis of NS is related to increased glomerular per-meability to albumin and other plasma protein as a conse-quence of a damaged basement membrane. B. MN is characterized by immune deposits that form at the base of the foot processes of the glomerular visceral epithelial cell or podocyte. C. FSGS is multifactorial, but the injury to the foot pro-cess on the podocytes seem to be the main cause. Mech-anisms include a T-cell mediated circulating permeability factor, transforming growth factor (TGF), B-cell mediated matrix synthesis, and genetic podocyte abnormalities. Predisposing Factors A. Amyloidosis. B. Diabetes mellitus. C. Cryoglobulinemia. D. Sjögren syndrome. E. SLE. F. Carcinoma. G. Leukemia, lymphoma. H. Melanoma. Nephrotic Syndrome129

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I. Multiple myeloma. J. Infection (bacterial, protozoan, viral). K. Allergic reaction to insect stings or bites, antitoxins, posi-tion ivy, or oak. L. Malignant hypertension. M. Sarcoidosis. N. Genetic syndromes (e. g., familial FSGS, hereditary nephritis [Alport syndrome]). Subjective Data A. Common complaints/symptoms. 1. Progressive lower extremity edema. 2. Significant fluid weight gain. 3. Fatigue. 4. Exertional dyspnea. B. Common/typical scenario. 1. Periorbital, genital edema. 2. Ascites. 3. Pleural or pericardial effusion. 4. Adults who present with new onset of edema or ascites and do not have the typical dyspnea seen with heart fail-ure or present with cirrhosis. C. Review of systems. 1. Determine onset and duration of symptoms. 2. Determine if weight change has occurred (normal weight). a. If weight gain: How much and over what period of time? 3. Ask if any changes in urine output; foamy urine? 4. Identify medication or toxin exposure: Risk factors for HIV or hepatitis and symptoms that could be indicative of other causes for edema (e. g., heart failure). 5. Underlying health conditions such as diabetes, SLE, or other systemic disease. 6. Previous history of NS; if yes, when and, if known, what was the cause and treatment? Physical Examination A. Check vital signs, blood pressure, temperature, heart rate, and respirations; obtain body weight. 1. Possible hypertension. B. Inspect periorbital area, abdomen, and lower extremities assessing for edema or ascites. C. Auscultate heart, lungs, and abdomen. D. Palpate abdomen assessing for ascites and lower extremi-ties for edema. Diagnostic Tests A. The goal of diagnostic testing is to (a) assess for complica-tions; (b) identify underlying disease; and (c) possibly deter-mine the histological type of idiopathic NS. B. Serum and urine tests. 1. Serum chemistry panel to evaluate kidney function (b lood urea nitrogen [BUN], creatinine, estimated GFR), electrolytes. 2. Assess for acute kidney injury (AKI; see s ection “Acute Kidney Injury” for specific information). 3. Glucose for diabetes mellitus. 4. Blood count and coagulation panel (abnormal sugges-tive of bleeding disorder). 5. Serum albumin. 6. Lipid panel to assess for hyperlipidemia. 7. Urine dipstick to confirm proteinuria; protein-to-creatinine ratio from a random (spot) urine sample to evaluate for nephrotic-range proteinuria (24-hour urinecollection is cumbersome for patients and the collection is done incorrectly). a. Early morning specimen is best. b. Protein-to-creatinine ratio greater than 3. 0 to 3. 5 mg protein/mg creatinine (300-350 mg/mmol). c. Spot urine may be inaccurate in person who exer-cises heavily or someone who is gaining or losing mus-cle mass. d. Hematuria or casts are suggestive of nephritis. C. Additional tests depending on patient presentation. 1. HIV screening. 2. Liver panel; elevated transaminase may indicate viral hepatitis (if abnormal, obtain viral hepatitis panel). 3. Serum or urine protein electrophoresis (amyloidosis or multiple myeloma). 4. Rapid plasma regain to determine if syphilis present. 5. Antinuclear antibodies, anti-double-stranded DNA antibody, and complement values (C3 and C4) if suspect connective tissue disorder. D. Imaging studies. 1. Chest x-ray: To evaluate for pleural effusion. 2. CT or MRI: Possible to evaluate for neoplastic diseases as secondary cause. 3. Ultrasound. a. Renal: For reduced GFR. b. Abdominal to evaluate for ascites. c. Lower extremity Doppler ultrasound, CT, MRI, or lung ventilation/perfusion scan if suspect thrombosis or pleural effusion. 4. Echocardiography: For suspected heart failure. E. Renal biopsy. 1. The role of renal biopsy is controversial and there is a lack of evidence-based guidelines. In those with NS from a known secondary cause who are responding to treat-ment, the renal biopsy will not likely add to the treat-ment. 2. It may prove beneficial when trying to determine best treatment and prognosis in adults with idiopathic NS of unknown histologic disease type and in those in which the provider is considering underlying SLE as the cause. Differential Diagnosis A. Liver disease (e. g., cirrhosis). B. Heart failure. C. Differential for AKI in NS. 1. Allergic interstitial nephritis. 2. AKI. a. Acute tubular necrosis. b. Prerenal azotemia. 3. Adverse effects from drug therapy. 4. N onsteroidal anti-inflammatory drug (NSAID) nephropathy. 5. Renal venous thrombosis. Evaluation and Management Plan A. General plan. 1. Confirm NS (evidence of proteinuria and hypoalbu-minemia); once confirmed, consult nephrology expert (e. g., physician, nurse practitioner). 2. Assess for common causes (see section “Incidence”). 3. Assess for complications. a. Venous thrombosis. i. Renal veins affected; possible cause of pul-monary embolism. 5. Nephrology Guidelines130

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ii. No evidence for prophylactic anticoagulation: Decision to treat should be considered individu-ally. b. Infection, especially cellulitis. i. Maintenance of standard infection control practices. ii. No strong evidence supporting any specific intervention to prevent infection in adults with NS. c. AKI. d. Markedly elevated lipid levels. B. Patient/family teaching points. 1. Restrict sodium intake to less than 3 g per day. 2. Restrict fluid to less than 1,500 m L per day. C. Pharmacotherapy. 1. Diuretic therapy to treat edema. a. Loop diuretics (act in renal tubule and must be protein-bound to be effective). i. Oral loop diuretics twice a day are more effec-tive than once daily. 1)Furosemide 40 mg PO twice daily or bumetanide 1 mg PO twice daily is used to start. 2)The dose may be doubled every 1 to 3 days if edema not improved or patient experienc-ing hypervolemia. 3)Maximum dose of furosemide is 240 mg per dose or 600 mg total per day. If no response to oral drug, consider intravenous form. 4)Serum protein is decreased so higher dose may be necessary. 5)Intravenous bolus of 20% human albu-min prior to intravenous diuretic may be con-sidered. ii. When edema is severe, it may be necessary to start with intravenous diuretics. b. Diuresis should be gradual and guided by daily weights (1-2 kg per day). 2. Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers ( ARBs) are used to reduce proteinuria. 3. Immunosuppressive therapy: Should be prescribed in collaboration with nephrology expert. a. Corticosteroids: Used frequently (despite lack of supportive data). b. Azathioprine (Imuran). c. Biologics (rituximab, eculizumab). d. Cyclophosphamide. e. High dose immune globulin. f. Mycophenolate mofetil (Cell Cept). Follow-Up A. The prognosis is variable depending on the underlying cause, disease histology, and patient clinical factors. 1. Many patients will improve and some will require dialysis. 2. Patients with volume overload and cardiopulmonary decompensation for intravenous diuresis versus ultrafil-tration for fluid removal require admission. 3. Follow-up is on an individual basis, but patients should continue with nephrology expert and primary care provider. Consultation/Referral A. Nephrology expert. B. Other specialist depending on underlying cause (e. g., infectious disease, endocrinology, liver specialist). Special/Geriatric Considerations A. Consider underlying kidney function when treating with medications. B. In NS due to AKI requiring dialysis, avoid hypovolemia and hypotension to preserve residual kidney function. Reso-lution of AKI to baseline kidney function (without requiring dialysis) is possible. C. Older adults may seem to have a creatinine within nor-mal range due to loss of muscle mass. Use estimated GFR to determine kidney function. Bibliography Beck, L. H., & Salant, D. J. (2010). Membranous nephropathy: Recent travels and new roads ahead. Kidney International, 77 (9), 765-770. doi:10. 1038/ki. 2010. 34 Cattran, D. C., & Brenchley, P. E. (2017). Membranous nephropathy: Inte-grating basic science into improved clinical management. Kidney Inter-national, 91 (3), 566-574. doi:10. 1016/j. kint. 2016. 09. 048 Floege, I. (2015). Introduction to glomerular disease: Clinical presentations. In R. J. Johnson, J. Feehally, & J. Floege(Eds. ), Comprehensive clinical nephrology (5th ed., pp. 184-197). Philadelphia, PA: Elsevier Saunders. Kerlin, B. A., Ayoob, R., & Smoyer, W. E. (2012). Epidemiology and patho-physiology of nephrotic syndrome—Associated thromboembolic dis-ease. Clinical Journal of the American Society of Nephrology, 7 (3), 513-520. doi: 10. 2215/CJN. 10131011 Kodner, C. (2009). Nephrotic syndrome in adults: Diagnosis and manage-ment. American Family Physicians, 80 (10), 1129-1134. Kodner, C. (2016). Diagnosis and management of nephrotic syndrome in adults. American Family Physician, 93 (6), 479-485. Korbet, S. M. (2012). T reatment of primary FSGS in adults. Journal of the American Society of Nephrology, 23 (11), 1769-1776. doi:10. 1681/ASN. 2012040389 National Kidney Foundation. (2019). Retrieved from https://www. kidney. org/atoz/content/nephrotic Nishi, S., Ubara, Y., Utsunomiya, Y., Okada, K., Obata, Y., Kai, H., & Sato, Y. (2016). Evidence-based clinical practice guidelines for nephrotic syndrome 2014. Clinical and Experimental Nephrology, 20 (3), 342-370. doi:10. 1007/s10157-015-1216-x Radhakrishnan, J., & Cattran, D. C. (2012). The KDIGO practice guideline on glomerulonephritis: Reading between the (guide) lines—application to the individual patient. Kidney International, 82 (8), 840-856. doi:10. 1038/ki. 2012. 280 Segal, P. E., & Choi, M. J. (2012). Recent advances and prognosis in idio-pathic membranous nephropathy. Advances in Chronic Kidney Disease, 19(2), 114-119. doi:10. 1053/j. ackd. 2012. 01. 007 Prostatitis Catherine Harris Definition A. Inflammation of the prostate gland, which can be caused by infection or persistent irritation of the gland. B. Can be acute or chronic, lasting for more than 3 months. Incidence A. Almost 10% of males will have prostatitis over their life-time. B. About 90% of these conditions will be related to chronic nonbacterial prostatitis. Pathogenesis A. Any bacteria can cause prostatitis, although 80% of pathogens are gram negative. Sexual transmission is very common. B. Chronic nonbacterial prostatitis is inflammation of the prostate gland from persistent irritation that is nonbacterial. Prostatitis131

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Predisposing Factors A. Blockage of urine out of the bladder. B. Phimosis. C. Injury to the perineum. D. Foley catheters. E. Procedures such as cystoscopy or biopsy of the prostate. F. B enign prostatic hypertrophy (BPH). Subjective Data A. Common complaints/symptoms. 1. Acute bacterial prostatitis: Fever, chills, malaise, dysuria, low abdominal pain, or urethral discharge. 2. Chronic bacterial prostatitis: Intermittent dysuria or recurrent urinary tract infections (UTIs). B. Common/typical scenario. 1. Possible fever, chills, and malaise. 2. Possible pain with intercourse or defecation. 3. Arthralgias. 4. Nocturia. C. Family and social history. 1. Ask about number of sexual partners or history of sex-ually transmitted infections (STIs). D. Review of systems. 1. Assess patient for discharge, pain, hematuria, back pain, and weight loss. Physical Examination A. Check for urethral discharge and inspect the foreskin and penis for any lesions or fluid. B. Palpate testes and epididymides for inflammation and tenderness. C. Check for costovertebral angle (CVA) tenderness. D. Perform rectal examination to evaluate prostate for sym-metry, swelling, and tenderness and to determine if the prostate gland is boggy. E. Avoid massage if acute prostatitis is suspected. Diagnostic Tests A. Check for infection. 1. Complete blood count (CBC) with differential. 2. Urinalysis with urine culture. 3. Gram stain and culture-expressed prostatic secretions (EPS). 4. Presence of STI. B. For chronic prostatitis, check: 1. CBC, serum creatinine, and b lood urea nitrogen (BUN). 2. Ultrasound, MRI, or biopsy if necessary to rule out other possibilities. Differential Diagnosis A. Anal fistulas. B. UTI. C. Epididymitis. D. Urethritis. E. Urinary obstruction. F. Pyelonephritis. Evaluation and Management Plan A. General plan. 1. Acute prostatitis may need intravenous (IV) therapy for severe infection or if patient looks toxic. 2. Increase fluid intake. 3. Decrease caffeine and alcohol intake. B. Patient/family teaching points. 1. Teach patients how the infection is transmitted. 2. Suggest that sexual partners may need treatment. 3. Tell patients to use condoms. 4. Tell patients to urinate when the urge comes. C. Pharmacotherapy. 1. Acute bacterial prostatitis. a. Broad-spectrum penicillin, third generation cephalosporins, or fluoroquinolones. b. N onsteroidal anti-inflammatory drugs (NSAIDs) for treating discomfort may be considered. 2. Chronic bacterial prostatitis. a. Fluoroquinolones for 4 to 6 weeks. b. NSAIDs. c. Alpha blockers, which reduce bladder outlet syn-drome, may be beneficial. D. Discharge instructions. 1. Prevent infection with good hygiene. 2. Complete the antibiotic treatment as prescribed, which may take up to 1 month. Follow-Up A. Evaluate the effectiveness of the treatment plan and reso-lution of symptoms. B. Admit patients who appear toxic to the hospital for IV antibiotics. Consultation/Referral A. Consult urology for acute recurrent bacterial infections or persistent infections. Cystoscopy may be required. Special/Geriatric Considerations A. Prostatitis may lead to sepsis, particularly in patients with diabetes or chronic renal failure, patients on dialy-sis, immunocompromised patients, and postsurgical patients with urethral instrumentation. There should be a low thresh-old to hospitalize these patients if there is a concern. B. Urinary retention association with acute prostatitis may also require hospitalization. Bibliography Center for Urology, Rochester, N. Y. (n. d. ). Discharge instructions for prostatitis. Retrieved from http://www. cfurochester. com/pdf/discharge-prostatitis. pdf 5 Foods that can cause prostatitis. (n. d. ). Retrieved from http://prostate. net/ articles/foods-that-cause-prostatitis Gupta, N., Mandal, A., & Singh, S. (2008). T uberculosis of the prostate and urethra. Indian Journal of Urology, 24 (3), 388-391. doi:10. 4103/0970-1591. 42623 Luzzi, G. (2007). Editorial letter. Chronic prostatitis. New England Journal of Medicine, 356, 423-424. doi:10. 1056/NEJMc063135 Stevermer, J., & Easley, S. (2000, May). T reatment of prostatitis. American Family Physician, 61 (10), 3015-3022. Strauss, A., & Dimitrakov, J. (2010, March). New treatments for chronic prostatitis/chronic pelvic pain syndrome. Nature Reviews Urology, 7 (3), 127-135. T urek, P. J. (2019, December 6). In J. P. Taylor 3rd (Ed. ), Med-scape. Retrieved from http://emedicine. medscape. com/article/785418-overview Prostatitis Yavasscaoglu, I., Oktay, B., Simpseck, U., & Ozyurt, M. (1999, March). Role of ejaculation in the treatment of chronic non-bacterial prostatitis. International Journal of Urology, 6 (3), 130-134. 5. Nephrology Guidelines132

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Pyelonephritis Suzanne Barron Definition A. An infection (usually from bacteria but also from viruses, fungi, or parasites) that results in swelling of the kidney. It may affect one or both kidneys. 1. Uncomplicated. 2. Complicated—associated with obstruction, anatomic anomaly, or kidney stones. Incidence A. Population-based study of acute pyelonephritis in the United States found overall annual rates of 15 to 17 cases per 10,000 females and 3 to 4 cases per 10,000 males. B. At least 250,000 cases of pyelonephritis are diagnosed annually in the United States. Pathogenesis A. Usually results from bacterial invasion by ascending from the lower urinary tract (urethra and bladder). B. Can result from colonization of the vagina with fecal flora. C. Hematogenous source—from bloodstream infection that reaches renal parenchyma (uncommon). Most likely gram-positive organisms from endocarditis. D. Evidence suggests that bacteria attaches to the urothe-lium and causes an inflammatory response. Hemolysins allow for bacterial invasion by damaging cells. Infection is most commonly associated with gram-negative bacteria such as Escherichia coli and Klebsiella pneumoniae. Predisposing Factors A. Female sex: Shorter urethra, allowing organisms to ascend to bladder and kidneys. B. Functional abnormalities: High post void residuals or incomplete bladder emptying, neurogenic bladder. C. Anatomic conditions: Bladder outlet obstruction/BPH or vesicoureteral reflux. D. Chronic indwelling catheters. E. Nephrolithiasis. F. Diabetes mellitus. G. Immunosuppression. H. Alcohol or drug abuse. I. Previous history of pyelonephritis. J. Pregnancy. K. New or multiple sexual partners. L. History of recent cystitis. Subjective Data A. Common complaints/symptoms. 1. Flank pain. 2. Fever. 3. Nausea and vomiting. 4. Weakness. 5. Dysuria. 6. Foul-smelling urine. 7. Hematuria. B. Common/typical scenario. 1. Onset: Abrupt, usually 1 to 2 days of symptoms. 2. Location/character. a. Sharp and persistent flank pain in one or both kid-neys. b. Abdominal pain, suprapubic tenderness. c. Possible groin pain. d. Strong urge to urinate. e. Burning on urination. 3. Fevers/chills: Generally feeling unwell. 4. Possible past medical history of kidney stones, pyelonephritis, or neurogenic bladder with chronic indwelling catheter. C. Family and social history. 1. Family history. a. Congenital anomalies of genitourinary (GU) tract. b. Nephrolithiasis. c. Diabetes mellitus. d. History of frequent u rinary tract infections (UTIs). 2. Social history. a. Alcohol use. b. Drug use (intravenous [IV] drug abuse may be associated with hematogenous spread of staphylococ-cal infection to kidney). c. Multiple sexual partners. d. New sexual partners. e. Use of spermicide. f. Poor perineal hygiene (fecal incontinence, soiling). D. Review of systems. 1. Constitutional: Fevers, chills, or malaise. 2. Cardiovascular: Palpitations or fast heart rate. 3. Gastrointestinal—nausea and vomiting, abdominal pain, fecal incontinence. 4. Genitourinary—flank pain, dysuria, foul-smelling urine, hematuria, urgency/frequency, incontinence. 5. Neurological—confusion and dizziness, especially in elderly. 6. Gynecologic—vaginal discharge. 7. Endocrine—polyuria, polydipsia, polyphagia (symp-toms of diabetes), night sweats. Physical Examination A. Vital signs: Evaluate for systemic inflammatory response/ sepsis. 1. Fever. 2. Tachycardia. 3. Hypotension. B. Generalized: Check to see if the patient appears ill; he or she may have rigors. C. Genitourinary—evaluate for cerebrovascular accident (CVA) tenderness (positive in most cases on side of infected kidney). D. Abdominal—evaluate for suprapubic tenderness (with-out guarding) and rigidity to rule out other causes of abdom-inal pain (e. g., acute abdomen, appendicitis). E. Respiratory—assess for crackles, decreased breath sounds (signs of pneumonia). F. Gynecological examination—perform if necessary in females to rule out gynecological disorder or pelvic inflamma-tory disease. Diagnostic Tests A. Blood work. 1. Complete blood count (CBC) with differential: Leukocytosis with neutrophil predominance. 2. Basic metabolic panel: Renal failure. Uncommon unless obstruction or sepsis is present. 3. Blood culture: Possible bacteremia. Pyelonephritis133

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B. Urinalysis. 1. Pyuria greater than 5 to 10 white blood cells (WBCs)/high power field (HPF). 2. Leukocytes positive. 3. WBC casts: Often indicative of pyelonephritis. 4. Nitrites: Positive in most cases if infection caused by gram-negative bacteria. 5. R ed blood cells (RBCs): May be positive. C. Urine culture. 1. Positive with greater than 100,000 bacteria/m L; 10,000 bacteria/m L in patients with catheterized urine samples. 2. Possibly negative if the patient was on antimicrobials prior to presentation. D. Imaging: Not necessary in uncomplicated pyelonephritis but failure to respond to appropriate therapy requires imag-ing to rule out ureteral obstruction or abscess. 1. Abdominal x-ray (kidney-ureter-bladder [KUB]): Stones, intraparenchymal gas; may be emphysematous pyelonephritis. 2. CT scan (non contrast): Enlarged kidney with per-inephric fat stranding. 3. Renal ultrasound: Imaging modality of choice for pregnant females (no radiation). a. Shows renal enlargement with hypoechoic parenchyma and loss. Differential Diagnosis A. Abdominal disorders. 1. Appendicitis. 2. Cholecystitis. 3. Pancreatitis. 4. Diverticulitis. 5. Peptic ulcer disease. B. Gynecologic disorders. 1. Ectopic pregnancy. 2. Pelvic inflammatory disease. 3. Ruptured ovarian cyst. C. Urologic disorders. 1. Nephrolithiasis. 2. Epididymitis. 3. Renal or perinephric abscess. 4. Urethritis. 5. Cystitis. Evaluation and Management Plan A. General plan. 1. See Figure 5. 2. 2. Obtain urinalysis and urine culture. 3. Obtain blood work: CBC, blood cultures, and basic metabolic panel. 4. Start broad-spectrum antibiotics. a. Can tolerate oral agents (e. g., ciprofloxacin, trimethoprim, and sulfamethoxazole). Nitrofurantoin should be avoided (does not penetrate kidney well). b. Unable to tolerate oral agents (e. g., ampicillin 2 g IV every 6 hours and gentamicin 1. 5 mg/kg every 8 hours). 5. Use imaging studies for high suspicion of ureteral obstruction and abscess. 6. Hospitalize patients who have systemic inflamma-tory response syndrome (SIRS), sepsis, dehydration, or uncontrollable pain. 7. Consult urology if ureteral obstruction is found for stent placement or possible percutaneous nephrostomy drain. B. Patient/family teaching points. 1. Increase fluids to promote hydration and flushing of the bacteria. 2. Encourage good hygiene and wiping from front to back after urinating to prevent bacteria from colonizing the urethra. 3. Urinate after sexual intercourse to help wash away bacteria. 4. Counsel patient and family that the patient may con-tinue to have fever and flank pain for 2 to 3 days after appropriate treatment has been given. 5. Reinforce the importance of completing antibiotics for the recommended 14-to 21-day course. C. Pharmacotherapy. 1. Once urine culture has finalized, switch to an appro-priate antimicrobial for 14 to 21 days. Oral antibiotics can be used depending on susceptibilities. 2. Supportive care. a. Phenazopyridine as possible help for dysuria. b. Antipyretics such as acetaminophen to control fever. c. Analgesics for appropriate pain management. d. IV fluid hydration to prevent and treat dehydra-tion and sepsis. D. Discharge instructions. 1. Advise patients to seek medical care for any recurrent symptoms such as fevers, flank pain, nausea, and vomit-ing. 2. Advise patients to call if they are unable to tolerate oral antibiotic or develop adverse effects such as rash or diarrhea. 3. Advise patients to drink plenty of fluids. Follow-Up A. Instruct patients to follow-up within 4 to 6 weeks after completion of antibiotics with a repeat urine culture to verify that infection has cleared. B. Advise patients to follow-up with recurrent symptoms because relapse can occur requiring a second 14-day course of antibiotics. Consultation/Referral A. Urology consult. 1. Obstructive ureteral stones. 2. Nephrolithiasis as a chronic nidus of infection. 3. Recurrent episodes of pyelonephritis, which warrant evaluation for anatomic anomalies. B. Infectious disease consult: Complicated infections and recommendations of duration of treatment. C. Home infusion consult/home health nursing: If IV antibiotics recommended. D. Interventional radiology consult: If percutaneous nephrostomy tube is indicated due to ureteral obstruction or for percutaneous drain placement for an abscess. Special/Geriatric Considerations A. Diabetic patients; increased risk of developing emphyse-matous pyelonephritis. B. Long-term/recurrent pyelonephritis patients: Develop-ment of significant renal scarring. C. Geriatric individuals: Dosing of antibiotics based on renal function/creatinine clearance. D. Pregnant patients: Increased risk of preterm delivery, sep-sis, and adult respiratory distress syndrome. 5. Nephrology Guidelines134

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Bibliography Czaga, C., Scholes, D., Hooton, T., & Stamm, W. (2007, August). Population-based epidemiologic analysis of acute pyelonephritis. Clini-cal Infectious Diseases, 45 (3), 273-280. doi:10. 1086/519268 Fulop, T. (2018, December 12). Acute pyelonephritis. In V. Batu-man (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/ article/245559-overview Naderi, A., & Reilly, R. (2008, December). Primary care approach to pro-teinuria. The Journal of the American Board of Family Medicine, 21 (6), 569-574. doi:10. 3122/jabfm. 2008. 06. 070080Urinary Incontinence Suzanne Barron Definition A. Unintentional loss of urine. B. Types. Urinary Incontinence135 Acute Cyst itis Obtain u rinalysis Negative urology If positive for epith elial Midstrea m cath eterizati on Firs t Line Antib iotics dose Seco nd Line Antib iotics Third Line Antibiot ics Irrita tive voiding symp toms: Dysuria, frequenc y, urgen cy If negative n itrites an d neg ative leukocytes, th en obtain urine culture culture Consid er other causes of irritative voiding symptom s (interstitial cystitis) Consid er referral to Positive cultu re Treat with culture-sp eci/f_ic antibiotic s Resolution of symptom s? Yes Fem ale patient s: No furth er treat ment in female patien ts Male pa tients : Consid er referral to urology No Repeat urin e culture Refer to u rology with rec urrent infections cells >5 per HPF u sually represen ts conta mination Repeat specimen catc h Straight for spec imen If positive for leukocytes and/or positive n itrites and /or more than 10 WBCs per H PF Treat with antibiotic s Tailor treat men t after urine culture /f_inaliz ed Bactrim D S BID × 3 da ys Nitrofuranto in 100 mg BID × 5-7 da ys Fosf omycin 3 g × 1 Cipro 250 m g BID × 3 days Levaquin 25 0 mg da ily × 3 da ys Aug mentin 50 g /125 mg BID × 5 days Cefdinir 3 00 m g BID × 10 d ays Cefpodoxime 1 00 mg BID × 7 days FIGURE 5. 2 Acute cystitis algorithm. HPF, high power field; WBC, white blood cells.

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1. Stress urinary incontinence (SUI): Occurs during physical exertion (sneezing, coughing, exercise). 2. Urgency incontinence (UI): Involuntary loss of urine associated with urgency (bladder spasms). 3. Mixed urinary incontinence: Combination of SUI and UI. 4. Overflow incontinence (OI): Occurs with urinary retention or high post void residuals. The overdistended bladder leads to leakage. 5. Functional incontinence: Loss of urine due to deficits of cognition and mobility. Incidence A. Urinary incontinence has been reported to affect 12% to 43% of women and 3% to 11% of men. B. Prevalence rapidly increases in both genders after the age of 70, but severe incontinence in men is reported at about half that in women. Pathogenesis A. SUI: Hypermobility of the urethra and/or intrinsic sphincter deficiencies. 1. Women: Related to the number of vaginal deliveries. 2. Men: Rare, unless history of prostatectomy, trauma, or neurological disorder. B. UI: Detrusor muscle over-activity. 1. Detrusor myopathy. 2. Detrusor neuropathy. C. OI: Overdistention of the bladder with subsequent leak-age from either impaired detrusor contractility or bladder outlet obstruction. 1. Diabetes mellitus. 2. Lumbosacral nerve disease. 3. Multiple sclerosis. 4. Spinal cord injuries. 5. Prolapsed intervertebral discs. 6. Severe cases of bladder outflow obstruction. Predisposing Factors A. Sex (female >male). B. Advanced age. C. Vaginal childbirth. D. Cognitive impairment. E. Chronic obstructive pulmonary disease (COPD). F. Obesity. G. Pelvic organ prolapse. H. Smoking. I. Pregnancy. J. Previous history of pelvic surgery (hysterectomy, prosta-tectomy) or pelvic radiation. K. Poor mobility. L. Neurological disorders. M. Anatomical disorders (e. g., vesicovaginal fistula). N. Certain medications (diuretics, narcotic pain medication). O. History of pelvic trauma. Subjective Data A. Common complaints/symptoms. 1. SUI: Leakage of urine involuntarily when laughing, coughing, or sneezing. 2. UI: Uncontrollable urge to urinate with associated leakage; occurs frequently. 3. OI: Dribbling of urine, weak stream, and incomplete bladder emptying. B. Common/typical scenario. 1. Onset of symptoms: Gradual versus sudden. 2. Associated pain with incontinence. 3. Severity: Minimal amount of leakage versus large amount of leakage and soaking through clothes. 4. Timing and frequency of the incontinence (after sneezing, only occurs at night). 5. Aggravating factors (e. g., caffeine, citrus). 6. Alleviating factors (pessary). 7. Risk factors (vaginal prolapse, recent u rinary tract infection [UTI], benign prostatic hypertrophy [BPH], neurological disorders, trauma). C. Family and social history. 1. Smoking. a. Tobacco: Irritant to the bladder, causing UI. b. Tobacco addiction: Possibly leading to a chronic cough and increased intra-abdominal pressure, dam-aging the muscles of the pelvic floor and resulting in SUI. 2. Alcohol: Diuretic affect/central nervous system (CNS) depressant causing OI and UI. 3. Illicit drugs: Abuse of prescription drugs such as opioids/sedatives causing OI or functional incontinence. D. Review of systems. 1. Constitutional: Fevers, chills, and weight gain. 2. Neurological: Confusion, altered speech, altered men-tal status, lower extremity weakness, dizziness, tremors, decreased mobility, and paresthesia (saddle anesthesia). 3. Respiratory: Chronic cough and chronic bronchitis. 4. Cardiovascular: Shortness of breath or edema associ-ated with congestive heart failure (CHF). 5. Abdominal: Constipation, obstipation, or reflux that causes cough. 6. Genitourinary: Frequency, urgency, hematuria, reten-tion, incomplete bladder emptying, or suprapubic pain. 7. Gynecologic: Pelvic organ prolapse or leakage of urine from vagina. 8. Musculoskeletal: Lower back pain. Physical Examination A. Neurological. 1. Assess mental status, motor strength, and sensory status, as well as deep tendon reflexes. 2. Observe gait. B. Respiratory: Assess for rhonchi and barrel chest. C. Cardiovascular: Assess for JVD and edema. D. Abdomen: Assess for suprapubic tenderness, palpable bladder, and abdominal/pelvic masses. E. Genitourinary. 1. Perform digital r ectal e xamination (DRE) to evaluate for BPH, prostatitis, and prostate nodules. 2. Evaluate for rectal fissures and/or fecal impaction. F. Gynecologic. 1. Perform Q-tip test: Used to demonstrate urethral hypermobility, which may indicate SUI. a. A sterile, well-lubricated Q-tip is placed into the urethra, and the patient is then told to cough or strain. b. The degree of Q-tip movement is measured. The test is considered positive if the Q-tip moves more than 30∘. 2. Evaluate for vaginal atrophy. 3. Evaluate for pelvic organ prolapse. G. Dermatological: Assess for excoriated skin due to incon-tinence or presence of fungal infection. 5. Nephrology Guidelines136

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Diagnostic Tests A. Urinalysis and urine culture: Evaluate for infectious source. B. Blood work: Basic metabolic panel to evaluate renal func-tion, which may indicate obstructive source. C. Imaging: Generally not indicated. D. Urodynamic studies/video-urodynamic studies. 1. Filling study: Detrusor overactivity, leak point pressure. 2. Voiding study: Urinary flow rate, post void residual, detrusor sphincter synergy. E. Cystoscopy: If there is concern for fistula or malignancy. Differential Diagnosis A. UTI (Cystitis, prostatitis). B. Interstitial cystitis. C. Nocturnal enuresis. D. Urethral diverticulum. E. Vesicovaginal fistula. F. Cauda equina syndrome. G. Constipation/obstipation. H. Bladder cancer. I. Bladder outlet obstruction. Evaluation and Management Plan A. General plan. 1. Obtain thorough history to determine type of urinary incontinence to target treatment. 2. Obtain laboratory studies such as urinalysis, urine cul-ture, and basic metabolic panel. 3. If possible, obtain post void residual with bladder scan. B. Patient/family teaching points. 1. Encourage smoking cessation and avoidance of alcohol/caffeine. 2. Encourage keeping a 24-hour voiding diary to help patients understand voiding patterns. 3. Educate patient about timed voiding, which will help avoid significant bladder distention. 4. Educate patients with SUI about how to perform Kegel exercises to strengthen pelvic floor muscles. Discuss the role of biofeedback in helping control these muscles. 5. Educate patients with UI about bladder training (delay voiding for increasing periods of time by inhibiting the desire to void). 6. Encourage weight loss in obese patients. 7. Teach patients with overflow incontinence about how to perform clean intermittent catheterization if necessary. C. Pharmacotherapy. 1. SUI. a. Currently, no Food and Drug Administration (FDA) approved medication for SUI. b. Topical estrogen in post menopausal women: Mild benefit. 2. UI. a. Anticholinergic medications: Act to inhibit blad-der contractions and increase capacity. i. Most common: Oxybutynin and tolterodine. ii. Others: T rospium chloride, solifenacin, darife-nacin, and fesoterodine. b. T ricyclic antidepressants. i. Direct relaxant effect on bladder muscle. ii. Not commonly used due to side effects. c. Beta 3-adrenergic receptor agonist (mirabegron): Associated with much less dry mouth andconstipation (side effects of anticholinergic medi-cations) but may cause hypertension. D. Discharge instructions. 1. Discuss with the patient to call with side effects of medication such as dry mouth, constipation, confusion, or vision changes. 2. Instruct the patient to seek medical attention with any fevers, chills, flank pain, or hematuria, which may indi-cate UTI. 3. Advise the patient about appropriate care of the skin due to incontinence. Keep the skin clean and dry. Wear-ing pads may help to protect the skin. 4. Mention that stool softeners or mild laxatives may be needed to prevent constipation. Follow-Up A. Follow-up in 3 to 4 weeks for symptom assessment/ response to therapy. B. Biofeedback often requires multiple visits. C. Instruct the patient to bring his or her voiding diary to follow-up appointment. D. For patients on an anticholinergic, check post void resid-ual to monitor for urinary retention. Consultation/Referral A. Refer to urologist/urogynecologist for persistent symp-toms or concern for malignancy or anatomic abnormality. 1. SUI. a. Periurethral bulking agents such as calcium hydroxylapatite. b. Pubovaginal sling placement. c. Surgical repair of pelvic organ prolapse. d. Surgery for BPH (t ransurethral resection of the prostate [TURP]). e. Artificial urinary sphincter for men. f. Fit for pessary. 2. UI. a. Percutaneous tibial nerve stimulation. b. Intravesical botulinum toxin: High efficacy in patients who have failed other medical treatment. 3. Cystoscopy to rule out malignancy or anatomic abnormality. B. Refer to neurology/neurosurgery with any concern for spinal cord injury, compression (Cauda equine), or neuro-logical disorder. Special/Geriatric Considerations A. Avoid anticholinergic medication in patients who have a history of acute angle glaucoma. B. Anticholinergic medication may cause confusion in geri-atric individuals. C. Assess geriatric patients for polypharmacy. Various med-ications that are commonly given may cause overflow incon-tinence (antidepressants, calcium channel blockers, opioid pain medication, sedatives, antihistamines) or UI due to the high volume of urine (diuretics). D. Consider the cost of pads in geriatric individuals who are on a fixed income. It is estimated that women with severe incontinence pay up to $900 per year for incontinence pads. Bibliography Albala, D., Morey, A., Gomella, L., & Stein, J. (2011). Oxford American handbook of urology, New York, NY: Oxford University Press. Cameron, A., Jimbo, M., & Heidelbaugh, J. (2013). Diagnosis and office-based treatment of urinary incontinence in adults. Part two: Urinary Incontinence137

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T reatment. Therapeutic Advances in Urology, 5 (4), 189-200. doi:10. 1177/1756287213495100 Cohn, J. A., Brown, E. T., Reynolds, W. S., Kaufman, M. R., Milam, D. F., & Dmochowski, R. R. (2016). An update on the use of transdermal oxy-butynin in the management of overactive bladder disorder. Therapeutic Advances in Urology, 8 (2), 83-90. doi:10. 1177/1756287215626312 Gomella, L., Andriole, G., Burnett, A., Flanigan, R., Keane, T., Koo, H., & Thomas, R. (2015). The 5-minute urology consult 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins. Herbruck, L. (2008). Stress urinary incontinence: An overview of diagno-sis and treatment options. Urology Nursing, 28 (3), 186-198. Retrieved from www. Medscape. com/viewarticle/57833_4 Hesch, K. (2007, July). Agents for treatment of overactive bladder: A thera-peutic class review. Proceedings (Baylor University Medical Center), 20 (3), 307-314. Khandelwal, C., & Kistler, C. (2013, April). Diagnosis of urinary inconti-nence. American Family Physician, 87 (8), 543-550. Mac Diarmid, S. (2008, Winter). Maximizing the treatment of overactive bladder in the elderly. Reviews in Urology, 10 (1), 6-13. Salzman, B., & Hersch, L. (2013, May). Clinical management of urinary incontinence in women. American Family Physician, 87 (9), 634-640. Subak, L., Brown, J., Kraus, S., Brubaker, L., Lin, F., Richter, H.,... Grady, D. (2006). The “costs” of urinary incontinence for women. Obstet-ric Gynecology, 107 (4), 908-916. doi: 10. 1097/01. AOG. 0000206213. 48334. 09 Thomas, B. (2015). The pathophysiology of urinary incontinence: Part 2. Retrieved from https://www. gmjournal. co. uk/the_pathophysiology_ of_urinary_incontinence_part_2_25769830611. aspx Urinary Tract Infection Swetha Rani Kanduri & Karthik Kovvuru Definition A. Infection of the urinary tract in the absence of comorbidi-ties such as diabetes, pregnancy, or physiologic and structural anomalies. Incidence A. Urinary tract infections ( UTIs) account for about 7 mil-lion office visits annually, affecting men and women. B. These infections are more common in young, sexually active women than men. C. 30% to 40% of women will experience one episode/year. Pathogenesis A. UTIs are more common in women because the female urethra: 1. Is shorter and in closer proximity to the rectum. 2. Allows bacteria to colonize more easily. B. UTIs peak in two different age groups in women. 1. 20 to 40 age group: Predisposed by intercourse. 2. 55 to 60 age group: Related to declining estrogen levels. Predisposing Factors A. Conditions that reduce urine flow. 1. Outflow obstruction: Prostatic hyperplasia, prostatic carcinoma, urethral stricture, or foreign body (calculus). 2. Neurogenic bladder. 3. Inadequate fluid uptake. B. Conditions that promote colonization. 1. Sexual activity: Increased inoculation. 2. Spermicide: Increased binding. 3. Estrogen depletion: Increased binding. 4. Antimicrobial agents: Decreased indigenous flora. C. Conditions that facilitate ascent. 1. Catheterization. 2. Urinary incontinence. 3. Fecal incontinence. D. Conditions in older women, who may be at higher risk for UTIs due to a combination of factors. 1. Atrophic changes. 2. Impaired urethral function. 3. Insufficient fluid intake. 4. Constipation. 5. Increased residual urine volume. Subjective Data A. Common complaints/symptoms. 1. Foul-smelling urine. 2. Dysuria, increased frequency, or urgency. 3. Suprapubic pain and discomfort. 4. Occasional hematuria. B. Atypical symptoms in older patients. 1. Confusion. 2. Delirium. 3. Falls or adverse behaviors. Physical Examination A. Possible suprapubic tenderness on palpation. B. Increasing discharge from vagina. C. Urinary meatus that may be erythematous or edematous. D. Negative costovertebral angle (CVA) tenderness. E. Negative pelvic or prostate examination. F. Urological evaluation is required for men with UTI. Diagnostic Tests A. Urinalysis. 1. Urine dipstick with clean catch urine necessary. 2. Positive for blood, leukocyte esterase, or nitrate. 3. Sensitivity of 75% to 96% and a specificity of 94% to 98%. B. Urine gram stain. 1. 10 white blood cells (WBC)/high power field (HPF; may not be present). 2. Bacteria greater than 15 bacteria/HPF. C. Urine culture. 1. More than 10,000 bacteria/m L in fresh, midstream specimen. Differential Diagnosis A. Genital herpes (herpes simplex virus [HSV]). B. Urethritis. C. Chlamydia. D. Trichomonas. E. Vaginitis. F. Prostatitis. G. Nephrolithiasis. H. T rauma. I. Urinary tract tuberculosis. J. Urinary tract neoplasm. K. Intra-abdominal abscess. Evaluation and Management Plan A. General plan. 1. See Figure 5. 3. 2. Advise patients on condition, timeline of treatment, and expected course of disease process. 3. Collect urine culture before starting antibiotics. 4. Complete all antibiotic regimens. 5. Nephrology Guidelines138

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FIGURE 5. 3 Urinary tract infection flipped in chronic kidney disease. ESRD, end-stage renal disease; IV, intravenous; LE, leukocyte esterase; UTI, urinary tract infection. B. Patient/family teaching points. 1. Counsel patients about appropriate use of medica-tions (dose, frequency, side effects, need to complete entire course of medications). 2. Recommend increasing fluid intake to 8 to 10 glasses per day. 3. Suggest that sitting in a warm tub may relieve symp-toms of dysuria. 4. For women, advise that they wipe front to back after a bowel movement. 5. For women, advise against using douches. 6. Tell patients to avoid bubble baths. 7. Advise that voiding after intercourse may be beneficial. 8. Use appropriate cleaning for sex toys and advise against sharing sex toys. C. Pharmacotherapy. 1. First-line antibiotics. a. Bactrim, double strength orally twice a day for 3 days. b. Nitrofurantoin, 100 mg twice a day for 5 days. c. Fosfomycin 3 g single dose. Urinary Tract Infection139 Anti biotic Treat ment Op tions Urine Fever Dysuria Urgency Frequency Stable Not ill appearing Immunocom petent Stable vitals Hypotension ESRD with symptoms Severe /f_lank pain Immunosuppressed Instrumentation/Stents Hematuria Acute uncomplicated UTI Complicated UTI (+) LE (+) Nitrate Pyuria U rine culture IV antibiotics CT abdomen/pelvis R enal ultrasound (-) LE (-) Nitrate + Symptoms Urine culture + Oral antibiotics Urine culture + Oral antibiotics Stop if cultures are negative Oral antibiotics Fluoroquinolones Amoxicillin-clavulanate Nitrofurantoin (if Cr Cl >50) Cefaclor Cefpodoxime Cefdinir Tmp-Smx Intraven ous antibiotics Cefepime Piperacillin-tazobactam Levo/f_loxacin Carbapenem for resistant organisms

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2. Second-line antibiotics. a. Ciprofloxacin 250 mg orally twice a day for 3 days. b. Amoxicillin/clavulanate 500/125 mg orally twice a day for 5 days. 3. T reatment during pregnancy. a. Ampicillin 500 mg orally every 8 hours for 3 to 7 days. b. Amoxicillin/clavulanate 500 mg every 8 hours for 3 to 7 days. c. Cephalexin 500 mg every 6 hours for 3 to 7 days. d. Nitrofurantoin 100 mg twice a day for 5 to 7 days (avoid during first trimester and at term). e. Bactrim DS twice a day for 5 days (avoid during first trimester and at term). f. Fosfomycin 3 g orally as single dose. D. Discharge instructions. 1. Return to clinic for fever or if symptoms do not improve/progress in 48 to 72 hours. Follow-Up A. Follow-up with primary care provider. Consultation/Referral A. Consult or refer to urology only if complications occur. Special/Geriatric Considerations A. Geriatric patients may present with atypical symptoms and require close monitoring of intake versus output during UTI. B. Patients with chronic kidney disease or e nd-stage renal disease (ESRD) may require antibiotic dose adjustments. Bibliography Lane, D. R., & Takhar, S. S. (2011, August). Diagnosis and management of urinary tract infection and pyelonephritis. Emergency Medicine Clinics of North America, 29 (3), 539-552. doi:10. 1016/j. emc. 2011. 04. 001 Wagenlehner, F. M., Schmiemann, G., Hoyme, U., Fünfstück, R., Hummers-Pradier, E., Kaase, M., & Naber, K. G. (2011, Febru-ary). National S3 guideline on uncomplicated urinary tract infection: Recommendations for treatment and management of uncomplicated community-acquired bacterial urinary tract infections in adult patients. Urologe A, 50 (2), 153-169. doi:10. 1007/s00120-011-2512-z Workowski, K. A., & Bolan, G. A. ( 2015, June 5). Sexually transmitted diseases treatment guidelines, 2015. Morbidity and Mortality Weekly Report. Recommendations and Reports. 64 (RR-03), 1-137. Retrieved from https://www. cdc. gov/mmwr/preview/mmwrhtml/rr6403a1. htm5. Nephrology Guidelines140

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141 6 Neurology Guidelines Nicole Thomer Anoxic Brain Injury Nicole Thomer and Syed Omar Shah Definition A. Deprivation of oxygen to the brain often due to car-diac arrest, but can occur from any cause including car-bon monoxide poisoning, severe asthma attacks, suffocation, drowning, and strokes. B. Can be classified into four categories. 1. Diffuse cerebral hypoxia. 2. Focal cerebral ischemia. 3. Global cerebral ischemia. 4. Cerebral infarction. Incidence A. No specific numbers are available to document the inci-dence or prevalence of anoxic brain injury. B. Main cause of anoxic brain injury is cardiac arrest (82. 4%). C. Other main causes include: Poisoning, drug overdose, head trauma, stroke, seizures, and severe asthma attacks. Pathogenesis A. The delivery of oxygen to the brain is highly dependent on its metabolic demand. Overall, this drive is usually higher compared to the rest of the body. B. Thus, any interruption of blood supply to its rich vascu-lature, even in short amounts of time such as a cardiac arrest, can cause significant brain injury. 1. Primary brain injury. a. Decreased perfusion to the brain, leading to deprivation of oxygen, glucose, and other nutrients required for brain metabolism. b. Glutamate, an excitatory neurotransmitter, release. This, along with the release of other exci-tatory amino acid neurotransmitters, leads to the formation of free radicals and lipid peroxidation. c. Large amounts of sodium and calcium entering the cells. This leads to cytotoxic edema. d. Lost regulatory mechanisms of the cell. This results in cell death. 2. Secondary brain injury. a. Microvascular dysfunction: Occurs from poor per-fusion. Small capillaries and arterioles can continue to have low perfusion despite restoration of blood flow. This can result in cerebral edema. b. Cerebral edema: Can occur from microvascular dysfunction as well as cytotoxic edema from cell death. c. Impaired autoregulation: Pressure passive cerebral hemodynamics with a right shift in autoregulation. d. Hyperoxia: Occurs from increased free radicals. e. Hyperthermia: Occurs from increased metabolic demand and induction of apoptosis. Predisposing Factors A. In cardiac arrest, patients have risk factors associated with cardiac disease. B. In other causes, patients tend to be younger, especially in respiratory-related anoxic brain injury cases. Subjective Data A. Patients with anoxic brain injury will not be able to pro-vide any subjective information, so subjective data is not rel-evant in this situation. B. However, the interviewer should obtain as much history from others as possible. 1. Obtain a thorough patient social history through fam-ily, friends, or witnesses. 2. Obtain any information about time, place, and onset. a. How long was the person in cardiac arrest or deprived of oxygen? Studies have shown that pro-longed CPR (typically >15 minutes) has not led to a good prognosis. These people generally die from this injury within 6 weeks. 3. Obtain the patient's medical history, medication use, any history of drug or alcohol abuse, or any recent com-plaints. Physical Examination A. Thorough neurological exam: Required. B. Levels of consciousness. 1. Coma: State of unresponsiveness. Patients are unaware of their surroundings and are unarousable. 2. Vegetative state: State of wakefulness without aware-ness or return of sleep-wake cycles. This results from a severe anoxic injury. a. Persistent vegetative state: Vegetative state 1 month after injury. b. Permanent vegetative state (PVS): Irreversible. This may occur 3 months after a nontraumatic injury and 1 year following a traumatic brain injury. 3. Minimal consciousness: State that does not fit the definition for PVS. Patients show limited evidence of awareness of themselves or environment that is repro-ducible. They may have brief periods of meaningful inter-action (e. g., simple commands or tracking). Anoxic Brain Injury

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142 4. Locked-in syndrome: Sustained eye opening, aware-ness of environment with quadriplegia. Cognition is intact. Vertical eye movements and/or blinking of eyes to communicate. 5. Brain death: Death by irreversible cessation of cerebral blood flow. Absence of all brainstem functions is charac-teristic (see section “Brain Death” for additional informa-tion). Diagnostic Tests A. Diagnostic tests can be performed but these can be affected by timing and patient temperature. Overall, time is essential to the prognostication process. The longer a clinician waits to prognosticate, the better. In most cases, it is neces-sary to wait at least 72 hours after rewarming or postarrest without hypothermia to give a prognosis. B. However, timing should be on a case-to-case basis. Some patients with hypothermia that requires heavy sedation should be given longer than 72 hours because hypothermia can delay drug metabolism. C. Clinical examination: T raditionally the strongest predic-tor of outcome. Predictors of poor outcome include: 1. Absent pupillary reflexes. 2. Absent corneal reflexes. 3. Motor response of extensor posturing or no move-ment. D. Biochemical markers. E. Neuroimaging. 1. MRI of the brain: Loss of gray/white matter. This indicates significant brain injury and is a sign of poor prognosis. 2. CT of the head: Initially, this can be normal but after about 3 days it shows brain edema and loss of gray/white differential. F. Electrophysiology. 1. Somatosensory evoked potential (SSEP). 2. EEG: Used to determine the presence of underlying brain activity as well as seizures (commonly seen after an anoxic injury). Differential Diagnosis A. Seizure. B. Hypoglycemia. Evaluation and Management Plan A. Hypothermia (see Chapter 7). B. Supportive care. 1. Ventilatory support. 2. Seizure management: Continuous EEG monitoring during entire duration of hypothermia as well as post rewarming. a. This should be considered. It allows monitoring of not only seizures but the patient's background rhythms. 3. Monitoring of basic labs and evidence of nosocomial infection. 4. Monitoring for evidence of end organ damage. C. Family counseling. 1. Inform families of the studies that are performed, including the timeline of these studies; this helps set expectations. 2. Review the results and provide the likelihood of a meaningful recovery versus the possibility of long-term placement. Follow-Up A. Case management consultation: Necessary for placement options (long-term facility vs. hospice care). Consultation/Referral A. Prompt consultation with a neurologist. B. Potential consultation with palliative care. Special/Geriatric Considerations A. Poor neuroprognostication increases with age of patient and time sustained in a coma. Bibliography Heinz, U., & Rollnik, J. (2015). Outcome and prognosis of hypoxic brain damage patients undergoing neurological early rehabilitation. BMC Research Notes, 8, 243. doi:10. 1186/s13104-015-1175-z Romergyrko, G., Koenig, M., Jia, X., Stevens, R., & Peberdy, M. (2008). Management of brain injury after resuscitation from cardiac arrest. Neu-rologic Clinics, 26 (2), 487-506. doi:10. 1016/j. ncl. 2008. 03. 015 Weinhouse, G., & Young, B. (2015). Hypoxic-ischemic brain injury in adults: Evaluation and prognosis. In J. L. Wilterdink (Ed. ), Upto Date. Retrieved from https://www. uptodate. com/contents/hypoxic-ischemic-brain-injury-in-adults-evaluation-and-prognosis Brain Death Nicole Thomer and Syed Omar Shah Definition A. Often defined as the irreversible loss of all function of the brain, including the loss of brainstem functions. 1. U. S. law associates brain death with cardiopulmonary death, but specific criteria are not mandatory. 2. Some states, such as New Jersey, have very specific diagnostic mandates. 3. Most clinicians rely on guidelines to help guide their decision making. B. Three key findings suggest brain death and must be exam-ined. 1. Coma. 2. Absence of brainstem reflexes. 3. Apnea. C. Once brain death criteria have been established and irre-versible loss of brain function is proven, patients can be declared brain dead and therefore legally deceased. Incidence A. Brain death is declared in approximately 2. 3% to 7. 5% of all deaths annually. Pathogenesis A. Causes: Devastating, identifiable, and irreversible neuro-logical injuries, such as subarachnoid hemorrhages. B. Main processes resulting in brain death: Mass cerebral edema and downward herniation. Physical Examination (Neurological Assessment) A. Prerequisites for clinical examination. (Note that these could vary by institution; it is important to be familiar with institution guidelines. ) 1. Clear clinical or radiographic evidence of widespread brain injury that is compatible with a diagnosis of brain death. 6. Neurology Guidelines

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143 2. Core body temperature greater than or equal to 36∘C or 96. 8∘F. 3. Ruling out of the use of any drug or intoxication that could cause central nervous system (CNS) depression. This must be done through history taking through fam-ily and friends, clinical and laboratory testing, and drug screening. 4. Absence of severe metabolic disturbances as identi-fied by clinical and laboratory data (i. e., severe electrolyte, endocrine, or acid-base abnormalities). 5. Systolic blood pressure greater than 100 mm Hg. 6. Identification of an examiner. This can vary accord-ing to state and national laws. The examiner should be confident in his or her understanding of the criteria and comfortable performing all aspects of the examination. B. Clinical examination: All of the following factors must be checked and confirmed to be absent to determine brain death. 1. Level of consciousness/mental status. a. The patient must be in a nonmedically induced coma. 2. Motor examination. a. The patient must have an absence of brain-originating responses to noxious stimuli. b. It is not uncommon to witness spinal medi-ated reflexive movements, which are not to be confused with purposeful movements. Examples of spinal-mediated movements include rhythmic facial nerve-innervated muscles, finger flexor movements, “Lazarus sign,” triple flexion, positive Babinski sign, or fasciculations of trunk and extremities. 3. Cranial nerve assessment. a. Pupillary response: Absent. Pupils are dilated and fixed in a neutral position. b. Ocular movement: Absence of oculovestibular reflexes. i. Cold calorics: Testing that injects ice cold water into the ear canal. The provider then watches the eyes for 2 minutes to ensure there are no findings of eye movements. ii. This is done on both ears. c. Brainstem reflexes. i. Absence of corneal reflexes. ii. Absence of a gag/sucking/rooting reflex. iii. Absence of a cough with tracheal suctioning. d. Respiratory function: Confirmation of apnea. Diagnostic Tests A. Apnea test. 1. Prerequisites. a. Clinical examination has been performed as described earlier and the findings are consistent with brain death. b. Patient has been preoxygenated for 10 minutes and then an arterial blood gas is performed. i. A Pa O2greater than 200 mm Hg and a Pa CO2 greater than 35 to 45 mm Hg must be present. c. Any prior evidence of CO2retention must be ruled out (e. g., patient with chronic obstructive pulmonary disease [COPD] or severe obesity). i. If a patient does have retention, an apnea test cannot be safely and accurately performed and thus a confirmatory ancillary test must be consid-ered. 2. Actual testing. a. Ensure that a physician, respiratory therapist, and nurse are present for the entirety of this test. Testingcan range from 8 minutes up to 12 minutes, depend-ing on the stability of the patient during testing. Dis-connect the patient from the ventilator and provide oxygen via a nasal cannula at 6 L/min into the endo-tracheal tube at the level of the carina. i. Alternatively, use a T-piece system with oxy-gen flow at 12 L/min and use continuous positive airway pressure (CPAP) 10 to 20 cm H2O, with oxygen flow at 12 L/min. ii. Observe for respiratory movements. iii. Ensure that all clothing is removed and the patient's chest is completely exposed. iv. If any respiratory movements are present, then place the patient back on the ventilator and abort the test. b. After the 8 to 12 minute test is performed, draw another arterial blood gas sample and result immedi-ately, then place the patient back on the ventilator. Be sure not to place the patient on the ventilator before drawing the arterial blood gas. i. If the Pa CO2is greater than or equal to 60 mm Hg or greater than or equal to 20 mm Hg above the baseline, then the test is confirmatory. Therefore, apnea is present. 3. Complications during apnea testing. a. If respiratory instability defined as Sa O2<90% or hemodynamic instability defined as systolic blood pressure less than 90 mm Hg occurs, it is necessary to draw an arterial blood gas and place the patient back on the ventilator. If the earlier criteria are met prior to the 8-minute minimum, the test remains confir-matory. b. If the patient remains hemodynamically stable and maintains adequate saturations but the test is incon-clusive, the test may be repeated for a longer period (10-15 minutes). c. If the patient does not meet criteria for confirma-tory apnea, ancillary testing may be required. 4. Observation period. a. Observing for adults is considered optional. b. Six hours is often recommended with longer peri-ods, up to 24 hours, recommended in cases of hypoxic ischemic encephalopathy. c. The 2010 American Academy of Neurology guide-lines found insufficient evidence to determine a min-imally acceptable observation period. B. Ancillary testing. 1. Indications: Limitations to performing the clinical examination or apnea testing. Reasons for considering ancillary testing include: a. Presence of factors that may affect accurate test-ing of cranial nerve functions (e. g., preexisting pupil-lary abnormalities complicating assessment of func-tion and facial trauma). b. Inability to perform clinical examination or apnea testing. c. Inability to perform apnea testing because of pre-existing CO2retention diagnosis. d. Presence of heavy sedation or neuromuscular paralysis. 2. Specific tests. a. Angiography: “Gold Standard” for ancillary test-ing. A positive study reflects the absence of cere-bral perfusion at or beyond the carotid bifurcation or circle of Willis and demonstrates that the exter-nal carotid system has blood flow. However, this is invasive, high risk, and requires transportation to the Brain Death

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144 radiology department with an unstable patient. It also carries the risk of false positives when the cranial vault is breached by trauma, surgery, or ventricular drains. b. Cerebral scintigraphy or nuclear testing. This method closely resembles the cerebral angiography. A positive finding consistent with no cerebral perfusion is the “hollow skull” appearance. c. T ranscranial ultrasound or transcranial Doppler. This method is safe, noninvasive, and inexpensive. However, this method is reliable only if there is a good quality signal and requires expertise in testing both anterior and posterior circulations. Abnormal find-ings include reverberating flow or small early systolic peaks without diastolic flow. d. EEG. Testing should be performed for at least 30 minutes. This testing must demonstrate no electrical activity and no reactivity to visual, auditory, or sen-sory stimuli. Testing results can be skewed, especially in an ICU setting; outside activity can be mistaken for cortical activity. Also, the EEG may be flat or iso-electric but cannot evaluate a brainstem that may have viable neurons. e. Somatosensory evoked potentials (SSEPS). In SSEPS, when the median nerve is stimulated and the response is bilateral absence of the parietal sensory cortex, brain death is indicated. Differential Diagnosis A. Various scenarios have been studied and closely resem-ble brain death. Conditions that therefore must be ruled out include: 1. Metabolic encephalopathy. 2. Drug intoxications. 3. Neuromuscular paralysis. 4. Guillain-Barre syndrome. 5. Locked-in syndrome. 6. Hypothermia. Evaluation and Management Plan A. Prognosis and pronouncement of death. 1. There are no published reports of neurological recov-ery after a diagnosis of brain death. 2. Once brain death criteria are met and determination of brain death is made, that person is legally dead, and a time of death is given. An attending physician must pro-nounce a person deceased. 3. Often, there are family objections and delays in dis-continuation of life support. This can often be mitigated by good education as well as guidance for the family from the medical team. As the provider, it is important to include the family early in the process. a. Be concise and clear in your communication to them. Be sensitive and ensure that an understanding of the process is being met. By doing so, when it comes time to remove life sustaining measures, the family has a better understanding as to why. b. Once an understanding is reached, this would be an appropriate time to introduce the organ procure-ment team. B. Organ procurement. 1. Each state has an organization that offers its ser-vices to hospitals and patients' families to discuss the opportunity for organ donation. This is most often an outlet for families to help cope in a devastating situation. 2. If a family does decide to donate organs, it may be necessary to treat certain medical problems to preservethe patient's organs. Diabetes insipidus and pulmonary hypertension are two complications that develop early in patients who are diagnosed with brain death and are important to consider. 3. There are two types of organ donations after death. a. Donation after cardiac death. If the person does not satisfy brain death criteria but does not have a meaningful recovery of life and the family decides to withdraw care but wants to proceed with donation, it can do so. The patient is extubated in the operating room and prepped for surgery, with transplant teams standing by. If the patient dies by cardiac death, he or she is reintubated and surgery is performed immedi-ately for organ procurement. If the patient does not die within 60 minutes, surgery for donation legally cannot proceed and therefore the patient is made comfortable and allowed to die in a private room. b. Donation after brain death. The patient has already been determined to be brain dead and given a time of death. He or she can then be taken to the oper-ating room for organ procurement, once all arrange-ments have been made. Bibliography Baker, A., Beed, S., Fenwick, J., Kjerulf, M., Bell, H., Logier, S., & Shep-herd, J. (2006). Number of deaths by neurological criteria, and organ and tissue donation rates at three critical care centres in Canada. Cana-dian Journal of Anesthesia, 53 (7), 722-726. doi:10. 1007/BF03021632 Burkle, C. M., Schipper, A. M., & Wijdicks, E. F. (2011). Brain death and the courts. Neurology, 76, 837-841. doi:10. 1212/WNL. 0b013e31820e7bbe Gardiner, D., Shemie, S., Manara, A., & Opdam, H. (2012). International perspective on the diagnosis of death. British Journal of Anaesthesia, 108(Suppl. 1), i14-i28. doi:10. 1093/bja/aer397 Hocker, S., Whalen, F., & Wijdicks, E. F. (2014). Apnea testing for brain death in severe acute respiratory distress syndrome: A possible solution. Neurocritical Care, 20, 298-300. doi:10. 1007/s12028-013-9932-0 The Quality Standards Subcommittee of the American Academy of Neurol-ogy. (1995). Practice parameters for determining brain death in adults (summary statement). Neurology, 45, 1012-1014. Wijdicks, E. F., Varelas, P. N., Gronseth, G. S., & Greer, D. M. (2010). Evidence-based guideline update: Determining brain death in adults. Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology, 74, 1911-1918. doi:10. 1212/WNL. 0b013e3181e242a8 Headaches Asha Avirachen and Muhammed Athar Definition A. Diffuse pain in some part of the head or pain located above the orbitomeatal line of the head. B. The International Headache Society divides headaches into primary and secondary headaches. 1. Primary: Benign headaches without any abnormal pathology. More than 90% of headaches are primary. Three types are recognized. a. Migraine: Characterized by attacks of moderate to severe throbbing headaches that are often unilateral in location, worsened by physical activity, and associ-ated with nausea and/or vomiting, photophobia, and phonophobia. Migraine headaches may last from 4 to 72 hours. i. Classic migraine: Migraine with aura—the aura usually only lasts up to 60 minutes. ii. Common migraine: Migraine without aura. iii. Status migrainosus: Migraine lasting more than 3 days. 6. Neurology Guidelines

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145 b. Tension-type headache: Most common form of headache that can last from 30 minutes to 7 days. Characterized by bilateral mild to moderate non-throbbing pressure such as pain, without associated symptoms. Mostly described as tight band around the head. c. Cluster headache: Less common. Brief episodes of severe unilateral throbbing pain, mostly in the retro-orbital area that usually last from 15 minutes to 3 hours. Ipsilateral autonomic symptoms such as eye-lid edema, nasal congestion, and lacrimation may be present. 2. Secondary: Malignant headaches caused by structural lesion or organic pathology. Less than 10% of headaches are secondary. a. Examples include headaches due to brain tumor, meningitis, substance withdrawal, and intracerebral hemorrhage. Incidence A. Many headache sufferers do not seek medical attention. B. An estimated 23 million Americans and 240 million peo-ple worldwide have migraine headaches each year. C. Migraine headaches occur in a 3:1 female-to-male ratio. D. Episodic tension-type headaches are present in about 46% of the U. S. population. E. Chronic tension-type headaches are present in approxi-mately 2% of the U. S. population. Pathogenesis A. The exact mechanism involved in the development of pri-mary headaches is unknown. B. Headaches usually result from vasodilation/constriction of blood vessels. C. Migraine headaches are thought to result from activation of meningeal and blood vessel nociceptors, combined with a change in central pain modulation. D. Activation of trigeminal system results in release of neu-ropeptides, which, in turn, causes neurogenic inflammation and increase in vascular permeability and local dilation of blood vessels, causing pain and associated symptoms via the trigeminal pathway. E. Decrease in levels of serotonin (5-hydroxytryptamine [5-HT]) have shown to induce migraine. Predisposing Factors A. Foods containing tyramine (aged cheeses, pickled foods), nitrites (cured meats), monosodium glutamate, or sulfites. B. Alcoholic beverages, especially red wine and beer. C. Emotional factors such as stress, anxiety, and depression. D. Hormonal fluctuations. E. Decreased sleep or sleep deprivation. F. Medications: Estrogen, nitroglycerine, or ranitidine. G. Physical fatigue. H. Environmental: Weather, odors, sound, bright lights, and barometric changes. Subjective Data A. Common complaints/symptoms (red flag symptoms). 1. Every headache evaluation should begin with a search for certain signs and symptoms. The presence of any ofthese “red flag” symptoms warrants an urgent extensive workup. 2. Systemic symptoms (fever, weight loss) or secondary risk factors (HIV, systemic cancer). 3. Neurologic symptoms or abnormal signs (impaired alertness or consciousness, confusion, weakness, visual loss). 4. Onset: Sudden, abrupt, or split-second. 5. Increased age: New-onset and progressive headache, especially in middle age ( >50 years [giant cell arteritis]). 6. Previous headache history: First headache or different headache (marked change in attack, frequency, severity, or clinical features). B. Diagnostic criteria. 1. The gold standard for diagnosis of headache is a detailed interview and clinical examination. 2. Headache onset (age, sudden or gradual onset, fac-tors associated with onset such as exercise, sexual activity, Valsalva maneuver, febrile illness). 3. Location of pain: Unilateral, bilateral, global. 4. Duration (see section “Definition” for details). 5. Frequency. 6. Quality: Throbbing, squeezing, band like, stabbing. 7. Severity (at onset, at peak, and duration from onset to peak). 8. Associated symptoms such as nausea, vomiting, blurred vision, nasal congestion, mood swings, and so forth. 9. Presence or absence of an aura: Visual scotomas, flashing lights, or facial numbness. 10. Aggravating and relieving factors: Body position or darkness. C. History. 1. Medication history: Contraceptives, hormonal ther-apy, vitamins, herbals, and painkillers. 2. General medical history. 3. Family history of headaches. Physical Examination A. Perform a complete general examination with focus on the head and neck and a full neurological examination. Gen-erally, these are normal, with no neurological deficits in primary headaches. A focal neurological deficit with acute headache predicts central nervous system (CNS) pathology. B. Observe the body habitus. Patients with pseudo tumor cerebri tend to be obese. C. Perform a funduscopic examination to rule out papilledema as in pseudo tumor cerebri or diseases with increased intracranial pressure (ICP). D. Auscultate the skull and orbits for bruits as heard in arteriovenous malformation and fistulas. E. Palpate and tap the sinus for tenderness in sinus inflam-mation. F. Arteries may be tender and harder to palpate in temporal arteritis. G. Palpate both temporomandibular joints for tenderness and crepitus while the patient opens and closes the jaw. Diagnostic Tests A. The diagnosis of primary headache is usually made on the basis of headache history, physical examination, and neuro-logical examination. No specific diagnostic tests are available. B. The diagnosis of secondary headache involves the following. Headaches

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146 1. Complete blood count (CBC), chemistry panel, uri-nalysis, liver function test, and thyroid profile. 2. Sedimentation rate and C-reactive protein: Elevated in temporal arteritis. 3. Neurological imaging, which should be considered in patients with any of the following findings. a. Thunderclap headache/worst headache of life. b. Altered mental status. c. Meningismus. d. Papilledema. e. Acute neurological deficit. f. New onset headache after age 50. g. History of cancer or HIV or immunocompro-mised state. 4. CT of head: Best to rule out acute injury and bleed. 5. CT of paranasal sinuses: To rule out sinusitis. 6. MRI of brain (more sensitive than CT): Useful to rule out space occupying lesions, demyelinating lesions, ischemia, and abscess. 7. Magnetic resonance angiography (MRA): Helpful in identifying vascular abnormalities such as aneurysms and arteriovenous malformation. 8. Lumbar puncture: Useful in diagnosing infections, malignancy and subarachnoid hemorrhage, and idio-pathic intracranial hypertension. 9. Tonometry: If symptoms suggest acute narrow angle glaucoma (visual halos, corneal edema, shallow anterior chamber). Differential Diagnosis A. Differential diagnosis. B. Brain tumor. C. Brain hemorrhage. D. Seizure. E. Meningitis. F. Dissection. G. Cerebral aneurysm. Evaluation and Management Plan A. Migraine headache. 1. General interventions. a. Lifestyle modifications and trigger prevention should be emphasized. b. Analgesics such as aspirin, acetaminophen, ibuprofen, and naproxen can be used in mild headache. Opioids are generally avoided in primary headaches. 2. Acute migraine: Abortive treatment in inpatient or ED setting. a. Nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids: Caution necessary in patients with hepatic or renal impairment, diabetes, or gastri-tis. One of the following drugs can be used. i. Ketorolac 30 mg IV. ii. Methylprednisolone 100 to 200 mg. iii. Dexamethasone 10 to 40 mg. b. Neuroleptics: Can be used alone and as pretreat-ment to ergot derivatives to offset nausea. i. Diphenhydramine 25 to 50 mg, lorazepam 0. 5 to 1 mg, and/or benztropine 1 mg is often given before neuroleptic to prevent akathisia. ii. ECG: Check and avoid neuroleptics if QTc is prolonged. c. Anti-nausea medications can be used to alleviate the sense of nausea, but are also effective in controlling migraines in select patients. i. Metoclopramide 10 to 20 mg IV. ii. Prochlorperazine 10 to 20 mg IV, IM. iii. Droperidol 0. 625 to 2. 5 mg IV or IM. iv. Chlorpromazine 12. 5 to 100 mg PO, IV (up to 50 mg only). d. Dihydroergotamine 0. 5 to 1 mg IV push: Migraine-specific but also helpful in cluster headache. This drug must not be administered if a triptan has been taken in the preceding 24 hours, and it is contraindicated in patients with a history of, or at high risk for, myocardial infarction (MI), or stroke. e. Anticonvulsants: Can be useful; given as rapid infusions (over 10-20 minutes). i. Valproic acid: 500 to 1,000 mg; can also be useful for cluster headache. ii. Levetiracetam: 1,000 to 2,000 mg, maximum recommended dose is 3,000 mg/d. f. Magnesium sulfate: 1 to 2 g IV piggyback. g. Serotonin (5-HT) receptor agonists: Sumatriptan 6 mg SC or 10 mg intranasal. 3. Migraine prophylaxis: Used when attacks exceed two per month or when acute attacks are refractory. One of the following drugs can be used. a. Beta adrenergic blockers: Propranolol—drug of choice. b. T ricyclic antidepressants: Amitriptyline 25 to 125 mg PO hs. c. Serotonin antagonists: Methysergide 1 to 2 mg PO TID. d. Calcium channel antagonist: Verapamil 40 to 80 mg TID. e. Anticonvulsant: Valproic acid total 250 mg BID or TID. B. Tension-type headache. 1. Usual abortive treatment can be any simple analgesic. 2. Drug of choice for prophylaxis is amitriptyline 50 to 150 mg/d. 3. Concurrent depression or anxiety disorder needs to be addressed if present. C. Cluster headache. 1. Abortive treatment. a. Inhalation of 100% of oxygen for 10 to 15 min-utes. b. Sumatriptan 6 mg SC. c. Dihydroergotamine IV. 2. Preventive therapy with one of the following. a. Verapamil—drug of choice—80 mg TID; max dose is 360 mg/d. b. Lithium 600 to 1,200 mg/d; monitor lithium levels. c. Topiramate 100 to 400 mg/d. d. Gabapentin 1,200 to 3,600 mg/d. e. Melatonin 9 to 12 mg/d. D. Nonpharmacologic treatment for all types of headaches. 1. Interventions such as acupuncture, biofeedback, nerve block, neurotoxin injections, neurostimulators, and behavioral and psychological therapies are found to be effective in managing headaches. Follow-Up A. Patients can follow-up with primary providers if headaches are infrequent. B. Follow-up with a headache specialist for more com-plicated or refractory cases or treatment of persistent headaches. 6. Neurology Guidelines

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147 Consultation/Referral A. Refer to a headache specialist if there is concern for an underlying pathology for the headaches or if there are any unusual features or symptoms associated with the headaches. B. Also consider referring patients who are refractory to con-ventional treatment. Special/Geriatric Considerations A. New onset of severe headache in pregnancy or postpar-tum period should be investigated to rule out cortical sinus thrombosis. MRI is considered safe during pregnancy. B. T reatment of headache in pregnancy should be coordi-nated with obstetrician. C. Metoclopramide and prochlorperazine are generally con-sidered safe in pregnancy. D. Ergotamines are absolutely contraindicated in pregnancy. Bibliography American Association of Neuroscience Nurses. (2004). Headaches. In M. Bader, & L. Littlejohns (Eds. ), AANN core curriculum for neuroscience nursing (4th ed., Vol. 1, pp. 836-849). Maryland Heights, MO: Saun-ders. Hainer, B., & Matheson, E. (2013). Approach to acute headache in adults. American Family Physician, 87 (10), 682-687. Retrieved from https://www. aafp. org/afp/2013/0515/p682. html Hickey, J. (2003). Headaches. In J. HIckey (Ed. ), The clinical practice of neu-rological and neurosurgical nursing (5th ed., pp. 603-615). Philadelphia, PA: Lippincott Williams. International Headache Society. (n. d. ) Retrieved from http://www. ihs-headache. org Singh, G., Gupta, P., Gupta, A., & Khanal, M. (2011). Clinical approach to a patient with headache. In Neurology (Vol. 1, pp. 514-517). Elsevier. Young, W., Silberstein, S., Nahas, S., & Marmura, M. (2011). Jefferson headache manual. New York, NY: Demos Medical. Intracerebral Hemorrhage Bridget Gibson and Syed Omar Shah Definition A. A pathologic accumulation of blood within the parenchyma of the brain. B. Often confused with intracranial hemorrhage, an umbrella term that encompasses subdural hematoma, epidu-ral hematoma, and subarachnoid hemorrhage, as well as intracerebral hemorrhage (ICH). Incidence A. ICH affects 12 to 15 per 100,000 people. It increases with age, doubling every 10 years after age 35. B. The incidence is higher in populations with higher fre-quencies of hypertension such as African Americans. The prevalence is increased in Asian populations compared with Caucasian populations because of environmental and genetic factors. Pathogenesis A. Hypertensive damage to intracranial blood vessels caus-ing small vessel vasculopathy resulting from chronic or acute hypertension or drug abuse. B. Autoregulatory dysfunction with excessive cerebral blood flow resulting from reperfusion or the hemorrhagic transfor-mation of ischemic strokes. C. Vascular malformations resulting from aneurysm rupture or hemorrhage of an arteriovenous malformation. D. Coagulopathy resulting from anticoagulation, thrombol-ysis, or a bleeding disorder. E. Hemorrhagic necrosis resulting from tumor or infection. F. Venous outflow obstruction resulting from cerebral venous thrombosis. G. T rauma. Predisposing Factors A. Modifiable risk factors: Hypertension, cocaine/stimulant use, low cholesterol levels, oral anticoagulants, and excessive alcohol intake. B. Nonmodifiable risk factors: Age, male gender, African American/Japanese ethnicity, and cerebral amyloid angiopa-thy (CAA). Subjective Data A. Common complaints/symptoms. 1. Headache, seizures, vomiting, or worsening score on the Glasgow Coma Scale (GCS). 2. Focal neurological signs (such as unilateral limb weak-ness, facial weakness, or cranial nerve palsies) can present to varying degrees of severity depending on the location and size of hemorrhage. 3. Frequency of clinical seizures within 1 week of ICH is 16% with majority occurring at onset. B. Common/typical scenario. 1. Severe headache with or without vomiting prompts patient to go to the hospital or the patient has a change in mental status and emergency personnel are called to the scene. Typically bystanders will report nothing unusual occurred until the moment of the intracranial injury. C. Family and social history. 1. Ask about smoking and alcohol use. 2. Drug use is often associated with ICH in younger patients. 3. Family history of stroke. D. Review of systems. 1. Neurological—ask about headache, any weakness, or difficulty speaking. 2. Cardiac—ask about history of high blood pressure, if the patient is taking any blood thinning medications for irregular heart rate. Physical Examination A. Neurological—perform full neurological examination. 1. Motor assessment—note any weakness of limbs. 2. Sensory assessment—note any decrease in or lack of sensation on a limb. 3. Assess cranial nerves for deficits, in particular the extraocular movements and facial nerves. 4. Assess speech for difficulty speaking or finding words. 5. Assess language for difficulty understanding. 6. Determine level of consciousness. 7. Check for symptoms that may provide a clue to a loca-tion of the hemorrhage. a. Basal ganglia/thalamus location: Hemisensory loss, hemiplegia, aphasia, homonymous hemianopsia, eye deviation away from lesion, upgaze palsy. b. Lobar location: Seizures, homonymous hemi-anopsia, plegia, or paresis of leg greater than arm. c. Cerebellar location: Ataxia, nystagmus, intractable vomiting, and/or symptoms related to obstructive hydrocephalus (drowsiness, leg weakness, impaired upgaze, blurred, or double vision). Intracerebral Hemorrhage

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148 A B FIGURE 6. 1 Head CT scans showing (A) basal ganglia hemorrhage due to hypertension, (B) right frontal hemorrhage due to amyloid angiopathy. d. Pons location: Pinpoint pupils, quadriparesis, coma, locked-in syndrome. Diagnostic Tests A. Noncontrast head CT: Should be obtained as soon as possible and then 24 hours after admission (see Figure 6. 1). Repeat imaging may be warranted if the patient bleeds on anticoagulation while reversal of coagulopathy is in process. Also, obtain a STAT noncontrast head CT with any neuro-logical examination change. 1. Fluid levels seen within hemorrhage on CT scan indi-cate a coagulopathy (slow oozing of blood over time as seen by different intensities of blood on CT scan). 2. Hemorrhage volume calculation: ABC/2 (or ABC/3 for hemorrhages secondary to warfarin). 3. A (diameter in cm on CT slice where hemorrhage is largest) × 4. B (largest diameter in cm 90∘to A)× 5. C (number of 10 cm CT slices)/2 B. CT angiogram of head and neck: May be helpful to rule out subarachnoid hemorrhage, arteriovenous/cavernous mal-formation, and brain tumor. C. MRI brain with and without contrast: Should be obtained 4 to 6 weeks posthemorrhage to evaluate for under-lying mass if etiology remains unclear. Differential Diagnosis A. Clinical suspicion is warranted when there is a rapid alter-ation in neurological status often in conjunction with signs of an elevation in intracranial pressure. Increased intracranial pressure may be evidenced by change in level of conscious-ness, nausea, vomiting, or headache. B. The type of neurological dysfunction brought about by ICH may indicate the location, etiology, and severity of the hemorrhage. C. Conditions to rule out include arteriovenous mal-formations, severe hemiplegic migranes, seizures, cerebral aneurysms, and tumors. Evaluation and Management Plan A. General plan. 1. Determine the location of the hemorrhage, which will assist in secondary prevention. a. Hypertensive hemorrhages tend to occur in basal ganglia/thalamus greater than lobar more than cerebellum greater than pons. b. Amyloid hemorrhages are mostly in lobar locations. c. Hemorrhages secondary to vascular malforma-tions, tumors, and coagulopathies can occur any-where. 2. Medical management. a. Blood pressure. i. Hypertension is associated with hematoma expansion, neurological deterioration, depen-dency, and death. Early control is essential. 1)Antihypertensive treatment of acute cere-bral hemorrhage (ATACH) and intensive blood pressure reduction in acute cerebral hemorrhage (INTERACT) found reduction of systolic blood pressure less than 140 mm Hg to be safe and beneficial in improving func-tional outcomes. 2)Arterial line and peripheral intravenous lines should be placed for close monitoring and tight control of blood pressure. 3)Continuous infusions should be used to maintain blood pressure parameters. a)Clevidipine, start 1 to 2 mg/hr (max 21 mg/hr). b)Labetalol, 1 to 2 mg/min (max 2 mg/min). c)Nicardipine, start 5 mg/hr (max 15 mg/hr). b. Coagulopathies. i. Any coagulopathies should be addressed and reversed if possible. c. Seizures. i. Clinical seizures should be treated with intra-venous anti-epileptics. ii. Continuous EEG monitoring is necessary for patients with depressed mental status out of pro-portion to injury. 6. Neurology Guidelines

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149 iii. Prophylactic anti-epileptic medication is not recommended. d. Intracranial pressure. i. Monitor intracranial pressure with an external ventricular device if patient has a Glasgow Coma Score of 8 or less. e. Other medical issues. i. Hypoglycemia and hyperglycemia should be avoided. ii. Normothermia should be maintained. iii. Deep venous thrombosis (DVT) prophylaxis: After radiographic evidence of hematoma stabil-ity, subcutaneous heparin should be considered for patients with lack of mobility after 1 to 4 days from onset. 3. Surgical management: Surgical management is not warranted in all cases of ICH and is limited in hyperten-sive hemorrhages to the acutely deteriorating patient as a lifesaving measure. Surgical management is the standard of care in subdural or epidural hematomas or in patients who have an ICH secondary to a tumor. a. Craniotomy. i. This procedure should be considered in patients with a subdural hematoma that is causing midline shift and increased intracranial pressure, epidural hematomas, and for removal of tumors associated with ICH. ii. Patients with cerebellar ICH who deterio-rate neurologically or have brainstem compression and/or hydrocephalus should undergo emergent surgical hematoma evacuation. b. Decompressive hemicraniectomy. i. This procedure may reduce mortality for comatose patients, those who have large hematomas with significant midline shift, or those with elevated ICP refractory to medical management. ii. Decompressive hemicraniectomy is contro-versial because although it reduces mortality in comatose patients, morbidity is very profound and outcomes are generally poor, leading to sig-nificant impairments of motor, speech, language, and quality of life. 4. Determine prognosis. a. Prognosis can be determined by using the ICH score. i. This simple clinical grading scale (see Table 6. 1) aids in prognostication at presentation. ii. The total score (see Table 6. 2) represents 30-day mortality risk based on a combination of criteria. B. Patient/family teaching points. 1. Depends on the extent of the injury. a. If patients are able to participate in their own care, they should be instructed on diet and lifestyle changes, blood pressure control, avoidance of alcohol, and smoking cessation. b. If patients are unable to participate in their own care, families need to be given options to care for the patient at home or in a nursing home. C. Pharmacotherapy. 1. There are no specific medications for the treatment of spontaneous ICH. a. Antihypertensive medications to maintain nor-motension. TABLE 6. 1 ICH Score Points Score on GCS 3-4 2 5-12 1 13-15 0 Intracerebral Volume ≥30 cm31 <30 cm30 Intraventricular Hemorrhage Yes 1 No 0 Location Infratentorial 1 Supratentorial 0 Age Age≥80 y 1 Age<80 y 0 GCS, Glasgow Coma Scale; ICH, intracerebral hemorrhage. Source: Hemphill, J. C., 3rd, Bonovich, D. C., Besmertis, L., Manley, G. T., & Johnston, S. C. (2001). The ICH score: A simple, reliable grading scale for intracerebral hemorrhage. Stroke, A Journal of Cerebral Circulation, 32,891-897. doi: 10. 1161/STR. 0000000000000069 TABLE 6. 2 30-Day Mortality Risk for Spontaneous Intracranial Hemorrhage ICH Score Mortality (%) 0 0 1 13 2 26 3 72 4 97 5 100 6 100 ICH, intracerebral hemorrhage. b. Antilipid medications for the treatment of atherosclerotic disease. c. Patients who need to take antiplatelet medications or need anticoagulation should consult with the neu-rologist prior to starting. D. Discharge instructions. 1. If the ICH is small, patients may return home with instructions to slowly return to daily activities. 2. If the patient requires rehabilitation, families should be given instructions to follow-up with the neurologist afterward. 3. If the patient requires a nursing home, follow-up can be on an as needed basis. 4. All patients should receive clearance from the neu-rologist prior to starting antiplatelet or anticoagulation therapy. Intracerebral Hemorrhage

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150 Follow-Up A. Patients should follow-up with the neurologist in 6 to 8 weeks from discharge from the hospital or rehabilitation center. B. Patients who require a nursing home can follow-up with specific issues on an as needed basis. Consultation/Referral A. Consult neurology on every ICH patient who comes into the hospital. All patients will require secondary prevention. B. Consult neurosurgery if there is a concern for increased intracranial pressure or in patients with a GCS of less than 13. Patients who have large ICHs should be evaluated for possible surgery. Special/Geriatric Considerations A. Elderly patients who present with spontaneous ICH fre-quently have the condition amyloid angiopathy. There is no treatment for amyloid and recurrence is high, up to 30%. B. Elderly patients with significant volume loss associated with aging or certain disease states, such as dementia or alco-holism, may tolerate larger ICHs with fewer deficits. How-ever, recovery from any lost function in the elderly is generally poor. Bibliography Anderson, C. S., Heeley, E., Huang, Y., Wang, J., Stapf, C., Delcourt, C.,... Chalmers, J. (2013). Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. The New England Journal of Medicine, 368, 2355-2365. doi:10. 1056/NEJMoa1214609 Ariesen, M. J., Claus, S. P., Rinkel, G. J., & Algra, A. (2003). Risk factors for intracerebral hemorrhage in the general population: A systematic review. Stroke, 34, 2060-2065. doi:10. 1161/01. STR. 0000080678. 09344. 8D Arima, H., Huang, Y., Wang, J. G., Heeley, E., Delcourt, C., Parsons, M., & Anderson, C. (2012). Earlier blood pressure-lowering and greater atten-uation of hematoma growth in acute intracerebral hemorrhage: INTER ACT pilot phase. Stroke, 43, 2236-2238. doi:10. 1161/STROKEAHA. 112. 651422 De Herdt, V., Dumont, F., H ́enon, H., Derambure, P., Vonck, K., Leys, D., & Cordonnier, C. (2011). Early seizures in intracerebral hemorrhage: Incidence, associated factors, and outcome. Neurology, 77, 1794-1800. doi:10. 1212/WNL. 0b013e31823648a6 Hemphill, J. C., Bonovich, C. D., 3rd, Besmertis, L., Manley, G. T., & Johnston, S. C. (2001). The ICH score: A simple, reliable grading scale for intracerebral hemorrhage. Stroke, 32, 891-897. doi:10. 1161/ 01. STR. 32. 4. 891 Hemphill, J. C., Greenberg, M. S., 3rd, Anderson, C. S., Becker, K., Ben-dok, B. R., Cushman, M., & Woo, D. (2015). Guidelines for the management of spontaneous intracerebral hemorrhage: A guideline for healthcare professionals from the American Heart Association/Amer-ican Stroke Association. Stroke, 46, 2032-2060. doi:10. 1161/STR. 0000000000000069 Labovitz, D. L., Halim, A., Boden-Albala, B., Hauser, W. A., & Sacco, R. L. (2005). The incidence of deep and lobar intracerebral hemorrhage in Whites, Blacks, and Hispanics. Neurology, 65, 518-522. doi:10. 1212/ 01. wnl. 0000172915. 71933. 00 Mendelow, A. D., Gregson, B. A., Fernandes, H. M., Murray, G. D., Teas-dale, G. M., Hope, D. T., & Barer, D. H. (2005). Early surgery ver-sus initial conservative treatment in patients with spontaneous supra-tentorial intracerebral haematomas in the International Surgical T rial in Intracerebral Haemorrhage (STICH): A randomised trial. Lancet, 365, 387-397. doi:10. 1016/S0140-6736(05)17826-X Mendelow, A. D., Gregson, B. A., Rowan, E. N., Murray, G. D., Gholkar, A., & Mitchell, P. M. (2013). Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): A randomised trial. Lancet, 382, 397-408. doi:10. 1016/S0140-6736(13)60986-1 Mould, W. A., Carhuapoma, J. R., Muschelli, J., Lane, K., Morgan, T. C., Mc Bee, N. A., & Hanley, D. F. (2013). Minimally invasive surgery plus recombinant tissue-type plasminogen activator for intracerebral hemor-rhage evacuation decreases perihematomal edema. Stroke, 44, 627-634. doi:10. 1161/STROKEAHA. 111. 000411Naff, N., Williams, M. A., Keyl, P. M., T uhrim, S., Bullock, M. R., Mayer, S. A., & Hanley, F. D., Jr. (2011). Low-dose recombinant tissue-type plas-minogen activator enhances clot resolution in brain hemorrhage: The intraventricular hemorrhage thrombolysis trial. Stroke, 42, 3009-3016. doi:10. 1161/STROKEAHA. 110. 610949 Qureshi, A. I., Palesch, Y. Y., Martin, R., Novitzke, J., Cruz-Flores, S., Ehtisham, A.,... Tariq, N. (2010). Effect of systolic blood pres-sure reduction on hematoma expansion, perihematomal edema, and 3-month outcome among patients with intracerebral hemorrhage: Results from the antihypertensive treatment of acute cerebral hemorrhage study. Archives of Neurology, 67, 570-576. doi:10. 1001/archneurol. 2010. 61 Rincon, F., & Mayer, S. A. (2013). The epidemiology of intracerebral hem-orrhage in the United States from 1979 to 2008. Neurocritical Care, 19, 95-102. doi:10. 1007/s12028-012-9793-y Stein, M., Misselwitz, B., Hamann, G. F., Scharbrodt, W., Schummer, D. I., & Oertel, M. F. (2012). Intracerebral hemorrhage in the very old: Future demographic trends of an aging population. Stroke, 43, 1126-1128. doi:10. 1161/STROKEAHA. 111. 644716 van Asch, C. J., Luitse, M. J., Rinkel, G. J., van der T weel, I., Algra, A., & Klijn, C. J. (2010). Incidence, case fatality, and functional outcome of intracerebral haemorrhage over time, according to age, sex, and eth-nic origin: A systematic review and meta-analysis. The Lancet Neurology, 9(2), 167-176. doi:10. 1016/S1474-4422(09)70340-0 Ischemic Stroke/Cerebrovascular Accident Catherine Harris Definition A. A sudden interruption of blood flow to the brain. B. Classification. 1. Thrombotic strokes—55 +%. 2. Embolic strokes—10% to 30%. 3. Lacunar strokes—10%. 4. Cryptogenic strokes—10%. Incidence A. Approximately 800,000 strokes occur each year. 1. 610,000 are first-time strokes. 2. 185,000 are recurring strokes. B. Stroke is the fifth leading cause of death. C. Stroke is the leading cause of disability. There are approx-imately 7 million stroke survivors in the United States. Pathogenesis A. Stroke results from decreased cerebral blood flow that can be the result of an obstruction (e. g., thrombus or embolus), vasoconstriction, low blood flow states (shock), or anything that deprives oxygen or glucose to the brain. B. Anaerobic metabolism and lactic acid production com-promise surrounding brain tissue (penumbra), causing ischemia followed by infarction if blood flow is now restored. Predisposing Factors A. Nonmodifiable. 1. Age greater than 55 years. 2. Gender: Women greater than men. 3. Race: African Americans have a 2 to 3x increased risk compared to Caucasians. 4. Prior stroke or transient ischemic attack (TIA). 5. Family history. B. Modifiable. 1. Hypertension. 2. Hypercholesterolemia. 3. Diabetes. 4. Atrial fibrillation. 5. Hypercoagulable states. 6. Coronary artery disease. 6. Neurology Guidelines

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151 7. Sleep apnea. 8. Smoking. 9. Alcohol consumption. 10. Use of oral contraceptives. 11. Obesity. 12. Drug use. Subjective Data A. Common complaints/symp toms. 1. Depend on the location of the stroke (see section “TIA” discussion). B. Common/typical scenario. 1. Sudden, abrupt onset. 2. Typical report of family members: Patient is perfectly fine one moment and then instantly changes. 3. Relationship between typical symptoms and location of stroke (see section “TIA” discussion). C. Review of systems. 1. Ask patient about following (see Table 6. 3). a. Headaches. b. Speech difficulties. c. Falls. d. Dropping objects. e. Weakness of arms/legs/face. f. Numbness/tingling. g. Loss of urine/bowel control. h. Visual changes—blurriness, double vision, loss of vision. Physical Examination A. Objective data. 1. Level of consciousness. 2. Visual examination. 3. Motor and sensory examination. 4. Speech assessment. 5. Cognitive test. 6. Cranial nerve examination. B. Use the National Institute of Health Stroke Scale (NIHSS) to objectively score stroke severity. The tool uses a point range from 0 to 42, with severity increas-ing with score and can be accessed through the National Institutes of Health: www. ninds. nih. gov/sites/default/ files/NIH_Stroke_Scale. pdf. 1. Use dynamically to assess and then reassess the patient's condition. TABLE 6. 3 Typical Findings of Stroke Symptoms Based on Hemisphere Left hemisphere Right-sided weakness (face, arm, leg) Left gaze preference Speech slurred Aphasia Right hemisphere Left-sided weakness (face, arm, leg) Right gaze preference Speech slurred Flat affect May neglect the left side of the body Brainstem or cerebellum May have multiple cranial nerve palsies Ataxia Dysmetria Visual disturbances especially diplopia May have hemiparesis or quadriparesis Locked-in syndrome Vertigo2. Scores greater than 13 indicate very severe stroke that may warrant surgical intervention and carry a very high probability of severe disability or death. Diagnostic Tests A. Initial tests to be done immediately. 1. CT head. a. Should be done immediately if stroke is in the dif-ferential diagnosis. From the moment a stroke is sus-pected, a CT head should be completed within 25 minutes. b. Do NOT delay a CT head. 2. Lab tests: Should be done simultaneously as preparing to go to CT head. a. Minimum: Obtain a glucose done prior to CT, but if the patient is a difficult stick, obtain the rest of the lab tests after CT of the head. b. Complete blood count (CBC), basic metabolic panel, prothrombin time (PT)/partial thromboplastin time (PTT)/international normalized ratio (INR). 3. Electrocardiogram. B. Other tests to be considered in select patients. 1. CT angiogram (CTA)/CT perfusion (CTP): Shows blood vessels, area of occlusion, and if there is collateral circulation. It can quantify cerebral blood flow, blood vol-ume, and the presence or absence of penumbra. 2. MRI/magnetic resonance angiography: To evaluate extent of stroke. 3. Arterial blood gas (ABG). 4. Cerebral angiography: If a candidate for thrombec-tomy. 5. Ultrasound of carotids: To evaluate for carotid plaque as the source of stroke. 6. EEG: If seizure suspected. Differential Diagnosis A. Ischemic stroke. B. Hemorrhagic stroke. C. Migraine. D. Bell's palsy. E. Seizure. F. Hypoglycemic/hyperglycemia episode. G. Sepsis. H. Vertigo. I. Neuromuscular or neurodegenerative disease. J. Brain tumor. K. Meningitis. L. Syncope. M. Multiple sclerosis. Evaluation and Management Plan A. The treatment of stroke should be broken up into three main phases. In the first phase, after the stroke has been iden-tified, the goal of treatment is to minimize the damage as quickly as possible. In the second phase of the treatment of stroke, the goal is to prevent further strokes from occurring. In the third phase of treatment, the goal is to return the patient to his or her functional baseline prior to the stroke occurring. B. Phase I plan. 1. Medical management. a. Blood pressure (BP) control—the goal of BP man-agement is to avoid complications. BP that is lowered too rapidly can cause increased ischemia and BP that is too high may cause a hemorrhagic conversion. Ischemic Stroke/Cerebrovascular Accident

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152 i. If no thrombolytics are given, treat the follow-ing BP. 1)Diastolic BP >140 mm Hg: Intravenous infusion. 2)Systolic BP >220 mm Hg, diastolic BP 121 to 40 mm Hg: Intravenous push medica-tions. 3)Systolic BP <220 mm Hg or diastolic BP <120 mm Hg: Monitor in the absence of other compelling indications. ii. If thrombolytics are to be given or have been given, treat the following BP. 1)Systolic BP >180 mm Hg. 2)Diastolic BP >105 mm Hg. b. Glucose monitoring. i. The brain requires glucose for energy. Persis-tent hyperglycemia is associated with poor neuro-logical outcomes. Hypoglycemia can cause wors-ening of ischemia. ii. Goal of glucose monitoring: Maintain eug-lycemia less than 180 mg/d L. c. Intravenous tissue plasminogen activator (t PA) administration. i. Given to patients with the diagnosis of ischemic stroke where intracranial hemorrhage has been ruled out who present within a 3-hour time frame for treatment from symptom onset. ii. Some patients may qualify for treatment with intravenous t PA up to 4. 5 hours. However, this is not Food and Drug Administration (FDA) approved. 2. Surgical management. a. Endovascular intervention. b. Intra-arterial t PA administration. i. Intra-arterial delivery directly into the clot via endovascular intervention. ii. Given within 6 hours of symptom onset. iii. Delivered directly into the clot. iv. Often used with mechanical clot extraction in large vessel strokes. c. Carotid endarterectomy: Rarely done as an emer-gency. d. Hemicraniectomy used for large hemispheric strokes with significant edema. C. Phase II plan: Medical management begins 48 to 72 hours after stroke presentation. 1. Antiplatelet—low dose aspirin or clopidogrel should be initiated as soon as intracranial hemorrhage has been ruled out. a. Aspirin 81 to 325 mg. b. Clopidogrel. 2. Anticoagulants—prescribe only if there is an increased cardioembolic risk as determined by the CHA 2DS2-VAS c Score (see Table 6. 4 and section “TIA” discussion). 3. DVT prophylaxis. 4. BP management (see Chapter 3). D. Phase III plan: Rehabilitation. 1. Speech. 2. Physical therapy. 3. Occupational therapy. E. Patient/family teaching. 1. Note that depression is very common after stroke. 2. Provide education about the cognitive limitations of the patient. 3. Emphasize that rehabilitation may last as long as 1 year. 4. Encourage lifestyle changes, including smoking cessa-tion, physical activity, and changes in dietary intake. Follow-Up A. Patients need to follow-up with neurology. If there has been any intervention, the patient should follow-up with the neurosurgeon. Consultation/Referral A. Provide referrals to rehabilitation, physical and occupa-tional therapy, nutrition, and speech. Special/Geriatric Considerations A. Stroke in adults under 40 is rare. 1. If it does occur in younger adults, a hypercoagulable workup should be initiated in the hospital. 2. Also consider mechanical causes such as carotid dis-section, arteriovenous malformations, or fistulas. B. Older adults should not be denied treatment due to age alone. 1. Make sure the patient is assessed for the degree of frailty to help the family make decisions on treatment. 2. The goal of treatment is to return the patient to base-line. If the baseline for the patient is extremely poor at any age, this should play a stronger role in the decision-making process. Bibliography Adams, H. P., Jr., del Zoppo, G., Alberts, J. M., Bhatt, D. L., Brass, L., Furlan, A.,,... Wijdicks, E. F. (2007, May). Guidelines for the early management of adults with ischemic stroke: A guideline from the American Heart Association/American Stroke Association Stroke Coun-cil, Clinical Cardiology Council, Cardiovascular Radiology and Inter-vention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke, 38 (5), 1655-1711. doi:10. 1161/STROKEAHA. 107. 181486 Goldstein, L. B., Bushnell, C. D., Adams, R. J., Appel, L. J., Braun, L. T., Chaturvedi, S.,... Pearson, T. A. (2011, February). Guidelines for the primary prevention of stroke: A guideline for healthcare profession-als from the American Heart Association/American Stroke Association. Stroke, 42 (2), 517-584. doi:10. 1161/STR. 0b013e3181fcb238 Hughes, S. (2014, May 2). New AHA/ASA stroke secondary pre-vention guidelines. Medscape Medical News, (pp. 870-947). doi: 10. 1161/STR. 0b013e318284056a Jauch, E. C., Saver, J. L., Adams, Jr., H. P., Bruno, A., Connors, J. J., Demaerschalk, B. M., Khatri, P., Mc Mullan, P. W.,... Howard Yonas, H. (2015, June 29). AHA/ASA focused update of the 2013 guidelines for the early management of patients with acute ischemic stroke regarding endovascular treatment: A guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke, 38(5), 1655-1711. Mozaffarian, D., Benjamin, E. J., Go, A. S., Arnett, D. K., Blaha, M. J., Cushman, M.,... T urner, M. B. (2015, January 27). Heart dis-ease and stroke statistics—2015 update: A report from the Ameri-can Heart Association. Circulation, 131 (4), e29-e322. 10. 1161/CIR. 0000000000000152 National Institutes of Health. (2003). NIH stroke scale. Retrieved from https://www. ninds. nih. gov/sites/default/files/NIH_Stroke_Scale. pdf Status Epilepticus Asha Avirachen and M. Kamran Athar Definition A. Five minutes or more of continuous clinical and /or elec-trographic seizure activity or recurrent seizure activity with-out return to baseline between seizures. 6. Neurology Guidelines

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153 B. Classification of the type of status epilepticus ( SE) based on semiology, duration, and underlying etiology. 1. Convulsive SE: Associated with generalized tonic-clonic movements of extremities and mental status impairment; a life-threatening medical emergency. 2. Nonconvulsive status epilepticus (NCSE): Seizure activity only seen on EEG without any correlating clinical findings; requires emergent treatment to prevent cortical neuronal damage. 3. Refractory SE: Clinical or electrographic seizures that do not respond to adequate doses of initial benzodi-azepines, followed by a second antiepileptic drug (AED) agent. Incidence A. Annual incidence of SE is 100,000 to 200,000 cases in the United States. B. Refractory SE occurs in up to 43% of patients with SE. C. Up to a third of neuro ICU patients have NCSE. D. 10% of medical ICU patients develop NCSE. Pathogenesis A. SE results from a neuronal imbalance between excita-tory and inhibitory neurotransmitters (gamma-aminobutyric acid [GABA], N-methyl-D-aspartate [NMDA], glutamate) within the central nervous system (CNS). B. Prolonged epileptic seizures result in lack of oxygen and glucose in brain cells, stimulating the release of excessive amounts of glutamate. Glutamate alters membrane channels, leading to an influx of calcium, which in turn triggers oxy-gen free radicals. These make brain cells electrically stable and cause cell injury. Predisposing Factors A. Acute processes. 1. T raumatic brain injury. 2. Metabolic disturbances: Electrolyte abnormalities, hypoglycemia, and renal failure. 3. CNS infections. 4. Cerebrovascular pathology: Ischemic stroke, hem-orrhage, cerebral sinus thrombosis, and hypertensive encephalopathy. 5. Autoimmune encephalitis, paraneoplastic syndromes. 6. Sepsis. 7. Drugs: Toxicity; noncompliance with AEDs; and withdrawal from opioids, benzodiazepine, barbiturates, or alcohol. 8. Anoxic brain injury. B. Chronic processes. 1. Preexisting epilepsy. 2. CNS tumors. 3. History of CNS pathology (traumatic brain injury, abscess, stroke). 4. Chronic ethanol abuse. Subjective Data A. Common complaints/symptoms. 1. Generalized convulsive status epilepticus (GCSE): Tonic extension of trunk and extremities, followed by clonic extension. Consciousness is usually lost. 2. Myoclonic SE: Bursts of brief myoclonic jerks, which increase in intensity until a convulsion occurs. This condition is seen mostly in anoxic encephalopathy or metabolic disturbances, particularly renal failure. 3. NCSE: Absence of awakening or returning to baseline even after 20 minutes of successful termination of clin-ical seizures. Symptoms may include coma, confusion, aphasia, staring, automatisms, facial twitching, eye devi-ation, and agitation. B. Common/typical scenario. 1. GCSE usually presents with the classic full body con-vulsions and the patient is not aware of the occurrence. 2. Myoclonic SE typically is seen in what people describe as limb shaking or twitching. Patients are awake and are able to describe the sensation. 3. In NCSE, patients do not have any signs of twitching or abnormal movements. The only clue to lead to NCSE is the absence of the patient waking up or returning to baseline after an event such as cardiac arrest, intracranial hemorrhage, or any surgery. C. Family and social history. 1. Most common cause of SE is a prior history of epilepsy. 2. Ask about changes in antiepileptic medications. 3. Alcohol and drug use can lower the seizure threshold in patients with a history of epilepsy. D. Review of systems. 1. In patients with GCSE or NCSE, a review of systems is generally not possible to the altered level of conscious-ness. Physical Examination A. Neurological examination. 1. Assess for any sensory or motor deficits in all limbs. 2. Assess for any speech, memory, or language impair-ment. 3. Assess for cranial nerve palsies. 4. Assess level of consciousness and response to stimuli. Diagnostic Tests A. Workup should occur simultaneously and in parallel with treatment. 1. Finger stick glucose. 2. Complete blood count (CBC), comprehensive metabolic panel (CMP), drug screen, AED levels, alcohol levels, arterial blood gas (ABG), serum magnesium, and calcium (total and ionized). 3. CT of brain to rule out intracranial pathology. 4. Continuous EEG monitoring: 24-hour EEG is the gold standard. Most typical pattern in SE is rhyth-mic high frequency ( >12 hz) activity that increases in amplitude and decreases in frequency, finally ter-minating abruptly and leaving postictal low amplitude slowing. 5. Brain MRI: Seizure focus may show up as a bright signal on diffusion weighted imaging (DWI) and dark signal on apparent diffusion coefficient (ADC) imaging in a nonvascular territory possibly with leptomeningeal enhancement. 6. Lumbar puncture and cerebrospinal fluid (CSF) studies. 7. Toxicology panel: Check for toxins that frequently cause seizures (i. e., isoniazid, tricyclic antidepressants (TCAs), antidepressants, theophylline, cocaine, sympath-omimetic, organophosphates, and cyclosporine). Differential Diagnosis A. Movement disorders. B. Herniation syndromes (decerebrate /decorticate posturing). Status Epilepticus

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154 C. Psychiatric disorders: Psychogenic nonepileptic seizures, conversion disorder, acute psychosis, or catatonia. Evaluation and Management Plan A. General plan. 1. T reatment of SE should occur rapidly and continue sequentially until clinical and electrographic seizures are stopped. 2. Simultaneous assessment and management of airway, breathing, and circulation should be performed. 3. Do not withhold seizure medications because of fear of respiratory compromise. 4. Definitive control of SE should be established within 60 minutes of onset. 5. Emergent treatment. a. Stabilize patient (airway, breathing, circulation). b. Perform cardiac monitoring. c. Consider intubation as needed. d. Use nutritional resuscitation with 100 mg of thi-amine IV followed by 50 m L of 50% dextrose IV push. e. Lorazepam (drug of choice for intravenous admin-istration): 0. 1 mg/kg IV at the rate of 2 mg/min (max 4 mg per dose); max total dose 8 mg. f. Midazolam is preferred for IM. 0. 2 mg/kg IM; max dose 10 mg. g. Diazepam (preferred for rectal administration): One time dose of 10 mg per rectum. 6. Urgent treatment. a. Recommended AEDs include intravenous fos-phenytoin or phenytoin (PHT), valproic acid, leve-tiracetam, and lacosamide. Initial total levels should be drawn after 2 hours of intravenous loading dose to determine maintenance dose and need to reload. i. Load with fosphenytoin 20 mg pheny-toin sodium equivalent (PE)/kg at the rate of 150 mg/min. If using phenytoin, the rate should not be more than 50 mg/min. Cardiac monitor-ing should occur during infusion due to increased risk of QT prolongation and cardiac arrhythmia. An additional 10 mg/kg IV can be given if seizures persist. The maintenance dose is phenytoin 100 mg q8h. The target free phenytoin level is 2 to 3 mcg/m L. Check serum levels daily. ii. Valproic acid: Load with 20 mg/kg (max 2,000 mg) at a rate of 3 to 6 mg/kg/min. If seizure persists, additional 20 mg/kg can be given. Main-tenance dose is 30 to 60 mg/kg/d in divided doses. Serum valproic goal is 70 to 100 mcg/m L. Check levels daily. iii. Levetiracetam is usually loaded with 1,000 mg. Maintenance dosing is 1,000 to 1,500 mg q12. Blood levels are not monitored. iv. Lacosamide: Load with 400 mg. Maintenance dosing is 100 to 200 mg twice daily. Max dose is 400 mg daily. Blood levels are not monitored. 7. Refractory therapy. a. If seizures persist, consider continuous infusion of AEDs. The most recommended are midazolam, propofol, and pentobarbital. Dosing of continuous infusion of AEDs should be titrated to cessation of electrographic seizures or burst suppression. b. A period of 24 to 48 hours of electrographic seizure control is recommended prior to slow withdrawal of continuous infusion of AEDs. It is recommended that EEG findings, not serum drug levels, guide therapy. i. Midazolam infusion: Load with 0. 2 mg/kg, at an infusion rate of 2 mg/min. Begin continuous infusion: 0. 05 to 2 mg/kg/hr. For breakthrough seizures: Give 0. 1 to 0. 2 mg/kg bolus and increase infusion by 0. 05 to 0. 1 mg/kg/hr every 3 to 4 hours. ii. Propofol infusion: Load with 1 to 2 mg/kg, infused over 1 minute. Begin continuous infu-sion at 20 to 200 mcg/kg/min. Use caution when administering high doses ( >80 mcg/kg/min) for extended periods of time ( >48 hours) to avert risk of propofol infusion syndrome. For break-through seizures: Increase infusion rate by 5 to 10 mcg/kg/min every 5 minutes until seizure ces-sation. iii. Pentobarbital infusion: Load with 3 to 5 mg/kg IVPB over 10 to 30 minutes. Begin continuous infusion at 0. 5 to 5 mg/kg/hr. For breakthrough seizures: Titrate 1 mg/kg/hr every 10 minutes to continuous EEG of 4 to 6 bursts/minute. Follow-Up A. Patients will need to follow-up with an epileptologist to monitor and control the antiepileptic medications that will be required. Consultation/Referral A. A neurologist must be consulted on cases of SE. A neu-rologist with continuous EEG training and specialty training in epileptology is preferred. B. Centers without the ability to perform or interpret con-tinuous EEG in patients with SE or NCSE should consider rapid transfer to a higher level of care. Special/Geriatric Considerations A. Pregnancy: Lorazepam and fosphenytoin are recom-mended as initial and urgent therapy. Levetiracetam has shown to be safe in recent studies. 1. Eclampsia must be considered in patients with SE in pregnancy; delivering the fetus is the best therapy in this situation. 2. Also, magnesium sulfate is proved to be supe-rior to AEDs in pregnant women with seizures and eclampsia. B. Anoxic brain injury: Prognosis of SE after hypoxic or anoxic brain injury is really poor. C. Ketamine, an NMDA receptor antagonist, has emerged as a potential treatment for refractory SE associated with autoimmune encephalitis. 6. Neurology Guidelines Bibliography Bleck, T. (2008). Seizures in the critically ill. In J. E. Parrillo & R. P. Dellinger (Eds. ), Critical care medicine: Principles of diagnosis and management in the adult (3rd ed., pp. 1367-1383). Maryland Heights, MO: Mosby. doi:10. 1016/b978-032304841-5. 50068-6 Brophy, G. M., Bell, R., Classen, J., Alldredge, B., Bleck, T., Glauser, T., & Vespa, P. (2012). Guidelines for the evaluation and management of sta-tus epilepticus. Neurocritical Care, 17, 3-23. doi:10. 1007/s12028-012-9695-z Claassen, J., & Hirsch, L. J. (2009). Status epilepticus. In J. Frontera (Ed. ), Decision making in neurocritical care (1st ed., Vol. 1, pp. 63-75). New York, NY: Thieme Medical. Gilmore, R. L., Cibula, J. E., Eisenschenk, S., & Roper, S. N. (2013). Seizures. In J. Layon, A. Gabrielli, & W. Friedman (Eds. ), T extbook of neurointensive care (2nd ed., Vol. 1, pp. 799-811). New York, NY: Springer Publishing Company.

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155Transient Ischemia Attack Catherine Harris Definition A. Temporary blockage of blood flow to the brain ( <24 hours) that does not result in permanent damage; often referred to as a “mini-stroke. ” B. Majority of transient ischemia attacks (TIAs): Complete resolution in less than 10 minutes. Incidence A. It is estimated that up to 500,000 people a year have a TIA in the United States. B. Up to 30% of people who report a TIA have a stroke within 5 years. C. The incidence of a cerebrovascular accident (CVA) has been reported as high as 11% within 7 days. Pathogenesis A. A TIA occurs when there is blockage of blood to the brain from atherosclerosis, any type of emboli, decreased blood flow/volume to the brain, or constriction of the arteries in the brain. B. The exact symptoms of a TIA correlate with the particular artery that is affected. The hallmark of a TIA is resolution of symptoms within 24 hours from onset. Predisposing Factors A. Medical factors. 1. Hypertension. 2. Diabetes. 3. Hyperlipidemia. 4. Coronary artery disease: Arrhythmias, heart defects, heart infections, or valvular disease. 5. Peripheral artery disease. 6. Obesity. 7. Elevated homocysteine levels. 8. Sickle cell disease. B. Nonmodifiable risk factors. 1. Family history. 2. Age greater than 55 years. 3. Gender (men more likely than women). 4. Prior TIA. 5. Race, with Hispanics and African Americans at higher risk. C. Lifestyle factors. 1. Cigarette smoking. 2. Physical inactivity. 3. Poor diet. 4. Excessive alcohol intake. 5. Illicit drug use. 6. Oral contraceptive use. Subjective Data A. Common complaints/symptoms—the types of com-plaints a person would have depends on the area of the brain that is affected. In general, there are three main classifications of TIA/CVA based on circulation patterns. 1. Anterior circulation symptoms. a. Carotid artery: Contralateral motor and sensory loss to arm/leg. b. Anterior cerebral artery: Confusion, personality changes, motor, or sensory loss in leg. c. Middle cerebral artery (majority of TIAs/CVAs): Face asymmetry, motor or sensory loss in arm, slurred speech, or aphasia. 2. Posterior circulation symptoms. a. Contralateral motor or sensory loss. b. Ipsilateral visual field loss. c. Cortical blindness. d. Dysarthria. e. Dysphagia. f. Diplopia. g. Quadriparesis. 3. Vertebrobasilar circulation symptoms. a. Confusion. b. Slurred speech. c. Blurry vision or blindness. d. Weakness of both arms or legs. e. Difficulty walking, ataxia. f. Paresthesias. B. Common/typical scenario—a typical event is described as happening all of the sudden. One moment the person is fine, the next moment the symptoms occur. In the majority of the cases, the symptoms resolve within 10 minutes and the person is back to his or her previous self. C. Family and social history. 1. A family history of stroke can raise the risk of stroke, especially if before the age of 65. 2. Smoking, physical inactivity, alcoholism, illicit drug use, and poor diet are all important factors to document. D. Review of systems—typically all symptoms will have resolved by the time of the interview, but it is important to document which systems were affected. 1. Visual fields—blurry vision, double vision, loss of vision, and/or sense of a curtain being pulled down over one eye (amaurosis fugax). 2. Language—slurred speech, difficulty speaking, inabil-ity to find words, and/or inability to understand others. 3. Extremities—weakness, numbness, tingling, and/or strange sensations. Physical Examination A. Cranial nerve testing—smile, stick out tongue, raise eye-brows, extraocular movements, and/or visual fields. B. Motor strength. C. Sensory testing. D. Gait and posture—walking heel to toe and/or finger to nose test. Diagnostic Tests A. CT head. B. MRI brain within 24 hours. C. Carotid Doppler—to assess for carotid disease. D. ECG—to assess for atrial fibrillation. E. T ransthoracic echocardiogram (TTE) to rule out any car-dioembolic source. F. Lab tests—glucose, chemistry profile, lipid panel. 1. Consider hypercoagulable workup if younger than 40 years of age or based on history. 2. Consider alcohol levels based on history. Differential Diagnosis A. Ischemic stroke. B. Hemorrhagic stroke. C. Migraine. D. Bell's palsy. E. Seizure. Transient Ischemia Attack

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156 F. Hypoglycemic/hyperglycemia episode. G. Sepsis. H. Vertigo. I. Neuromuscular or neurodegenerative disease. J. Brain tumor. K. Meningitis. L. Syncope. Evaluation and Management Plan A. General plan. 1. Obtain results from diagnostic tests. 2. Prevent further stroke from modification of risk fac-tors. 3. Manage blood pressure. 4. Initiate lipid control. 5. Maximize blood glucose control. B. Patient/family teaching points. 1. Assess family baseline understanding of TIAs/CVAs. 2. Educate on risk factor modification. 3. Educate on the role of diet/exercise in preventing future TIAs/CVAs. 4. Educate on role of pharmacotherapy and adverse effects. 5. Provide pamphlets and educational materials. 6. Introduce smoking cessation plan if indicated. 7. Introduce weight loss program if indicated. C. Pharmacotherapy. 1. Antiplatelet drugs—low dose aspirin or clopidogrel should be initiated as soon as intracranial hemorrhage has been ruled out. a. Aspirin 81 to 325 mg. b. Clopidogrel. 2. Anticoagulants—prescribed only if there is an increased cardioembolic risk as determined by the CHA 2DS2-VAS c Score (see Table 6. 4). 3. Thrombolytics—not indicated if there is resolution of symptoms. D. Surgical intervention. 1. Carotid endarterectomy if person is symptomatic with severe carotid stenosis (70%-99% blockage). E. Discharge instructions. 1. Warning signs of stroke. 2. What to do if person suspects a stroke: Call 911. 3. Possible Medic Alert bracelet if taking a blood thinner. Follow-Up A. Follow-up with primary care provider within 2 weeks. Consultation/Referral A. Refer all patients to neurology team. TABLE 6. 4 CHA2DS2-VASc Score Criteria Condition No. of Points Congestive heart failure 1 Hypertension 1 Age≥75 y 2 Diabetes mellitus 1 CVA/TIA/Thromboembolic event 2 Vascular disease (prior MI, peripheral artery disease, aortic plaque)1 Age 65-74 1 Female 1 Note: 0 points: No need for antiplatelet or anticoagulants; 1 point: None OR aspirin OR anticoagulant, depending on situation; ≥2 points: Start anticoagulant. CVA, cerebrovascular accident; MI, myocardial infarction; TIA, transient ischemic attack. Source: Lip, G. Y., & Halperin, J. L. (2010, June). Improving stroke risk stratification in atrial fibrillation. American Journal of Medicine, 123 (6), 484-488. doi:10. 1016/j. amjmed. 2009. 12. 013 Special/Geriatric Considerations A. Hypercoagulopathy can occur secondary to cancer, preg-nancy, and in sickle cell disease. Patients under the age of 40 who present with TIA should undergo a hypercoagulable workup. Bibliography Easton, J. D., Saver, J. L., Albers, G. W., Alberts, M. J., Chaturvedi, S., Feldmann, E.,... Sacco, R. L. (2009). Definition and evalua-tion of transient ischemic attack: A scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council, Council on Cardiovascular Surgery and Anesthesia: Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease, The American Academy of Neurology affirms the value of this statement as an educational tool for neurologist. Stroke, 40, 2276-2293. doi:10. 1161/STROKEAHA. 108. 192218 Giles, M. F., & Rothwell, P. M. (2007). Risk of stroke early after transient ischemic attack: A systematic review and meta-analysis. Lancet Neurol-ogy, 6 (12), 1063-1072. doi:10. 1016/S1474-4422(07)70274-0 Johnston, S. C. (2002). T ransient ischemic attack. New England Journal of Medicine, 347, 1687-1692. doi:10. 1056/NEJMcp020891 Kernan, W. N., Ovbiagele, B., Black, H. R., Bravata, D. M., Chimowitz, M. I., Ezekowitz, M. D.,... Wilson, J. A. (2014). Guidelines for the pre-vention of stroke in patients with stroke and transient ischemic attack: A guideline for healthcare professionals from the American Heart Associa-tion/American Stroke Association. Stroke, 45, 2160. doi:10. 1161/STR. 0000000000000024 Lip, G. Y., & Halperin, J. L. (2010, June). Improving stroke risk stratifica-tion in atrial fibrillation. American Journal of Medicine, 123 (6), 484-488. doi:10. 1016/j. amjmed. 2009. 12. 0136. Neurology Guidelines

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157 7Targeted Temperature Management Guidelines Sarah L. Livesay, Kiffon M. Keigher, Monique Lambert, Christina Shin, and Danielle Zielinski Fever Management Sarah L. Livesay, Kiffon M. Keigher, Monique Lambert, Christina Shin, and Danielle Zielinski Definition A. Therapeutic hypothermia, also called targeted tempera-ture management (TTM), consists of intervention(s) for the management of fever and includes the use of antipyretic med-ications, surface cooling, and intravascular devices to reduce temperature. B. Fever is defined by at least one core temperature measure-ment of ≥38. 3∘C on two consecutive days. C. High fever is defined by one or more measurement of core temperature of ≥39. 5∘C. D. Fevers of acute brain injury (either traumatic or vascular in nature) are independently associated with worse outcomes, which are associated with temperatures greater than 37. 3∘C in a number of studies. 1. Fever control is important because it contributes to cerebral ischemia and possible worsening of cere-bral edema, leads to increased intracranial pressures, and results in decreased levels of consciousness. Incidence A. The incidence of fever with traumatic brain injury (TBI) is difficult to quantify because targeted therapies are often initiated within hours of onset. However, it is estimated that there are approximately 1. 4 million cases of TBI in the United States annually. B. Patients with subarachnoid hemorrhage (SAH) have been shown to have a high incidence of fever development; SAH occurs in as many as 72% of patients diagnosed with SAH. C. Patients with intracranial hemorrhage (ICH) have up to a 53% risk of fever development in some studies, and this risk increases to as much as 83% with patients who also have intraventricular hemorrhage (IVH). Pathogenesis A. Noninfectious, or central, fever is the physiological loss of ability to autoregulate body temperature. In ICUs, fever with a noninfectious source has been shown to have an ear-lier onset (within 72 hours of admission) than fever with an infectious source. B. Infectious fevers occur in response to infection. Fever is associated with sepsis in up to 74% of hospitalized patients and as many as 90% of those with severe sepsis. C. Heat shock proteins are induced by fever. These are criti-cal for anti-inflammatory effects and cellular survival during stress. D. Patients with neurological injury are at risk for both infec-tious and noninfectious fevers. Predisposing Factors A. Infectious processes. 1. Bacterial. a. Urinary tract infection. b. Upper respiratory infection. i. Pneumonia. ii. Bronchitis. iii. Sinusitis. c. Central line infection. d. Bloodstream infection. e. Cerebrospinal fluid (CSF) infection. i. Ventriculitis. ii. Meningitis. f. Cellulitis. g. Clostridium difficile enteritis. 2. Fungal. 3. Viral. a. Influenza. b. Meningitis. c. Shingles. d. HIV/AIDS. e. Mumps/measles/rubella. f. Infectious mononucleosis. g. Herpes. B. Surgical incisions, which should be monitored for signs and symptoms of infection. C. Invasive lines and devices, which may predispose patients to infection. 1. Foley catheters. 2. Endotracheal tubes/tracheostomies. 3. External ventricular drains/ventriculoperitoneal shunts/lumbar drains. 4. Gastrostomy tubes. 5. Central lines, arterial lines, pulmonary artery catheters, peripherally inserted central catheters, intra-venous lines. D. Some medications. 1. Steroids. 2. Antibiotics. 3. Serotonergic drugs, which may lead to serotonin syn-dromes. 4. Anesthetics, specifically volatile anesthetic agents, which are associated with malignant hyperthermia. 5. Anticholinergic agents. 6. Sympathomimetic agents. E. Deep vein thrombosis (DVT). F. Blood transfusion reactions. Fever Management

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158 G. Mechanical ventilation, which puts patients at increased risk for developing ventilator-associated infections. H. Chronic medical illnesses, which may result in compro-mised immune systems and/or autoimmune disorders. Subjective Data A. Common complaints/symptoms. Patients with brain injuries may not be alert enough to reliably provide subjective complaints. Spinal cord injured patients may not be able to describe pain in detail due to sensory or thermoregulatory loss. 1. Warm or overheated feeling. 2. Chills. 3. Generalized body aches. 4. Sweating. 5. Palpitations or fluttering of heart. 6. Headache. B. Other signs and symptoms. 1. Decreased level of consciousness or altered mental sta-tus. 2. Tachycardia. 3. Tachypnea. 4. Hypotension or hypertension. 5. Increased intracranial pressure. 6. Vasospasm in patients with SAH as evidenced by trending transcranial Doppler velocities and/or digital subtraction angiography (DSA), computed tomography angiogram (CTA), or magnetic resonance angiography (MRA) imaging. 7. Positive cultures: Blood, CSF, pleural fluid, urine. 8. Abnormal lab results: Elevated white blood cell (WBC) count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP). C. Review of systems. 1. Assess patient for fever or symptoms suggesting fever prior to hospital admission. 2. Inquire about any recent or current known infec-tions, cold/influenza symptoms, or abnormal rashes/skin lesions. 3. Evaluate for any chills, shivering, or other symptoms suggestive of fever. 4. Assess for loss of appetite, weight loss, dehydration, or nausea or vomiting or other gastrointestinal (GI) upset. Physical Examination A. Check blood pressure, pulse, respirations, and tempera-ture. 1. Temperature monitoring methods are essential in order to obtain accurate and reliable measurements. Con-tinuous monitoring is ideal, but if this is not possible, patients' temperatures should be checked on an hourly basis using core methods. a. The most accurate source of core temperature monitoring is using a pulmonary artery catheter. b. Other core methods of temperature monitoring include intravesicular (bladder), esophageal, and rec-tal. c. Peripheral methods of temperature monitoring include tympanic membrane, axillary, and oral. B. Look for any lines or drains that may be a nidus for infec-tion. 1. Urinary Foley catheter. 2. Central venous catheters, arterial lines. 3. Lumbar drain, ventricular drain. 4. Any other surgical lines or drains. 5. Lines for mechanical ventilation. C. Examine skin thoroughly. 1. Check for cellulitis. 2. Recent surgical wounds. 3. Any skin breakdown. D. Auscultate heart and lungs. 1. Listen for murmurs or consolidation. E. Perform a neurological exam as appropriate for the patient's diagnosis. Diagnostic Tests A. All tests and imaging should be directed at ruling out infectious causes of fever as well as venous thromboembolism, transfusion reaction, drug fever, adrenal insufficiency, thy-roid storm, and any other noninfectious, noncentral etiolo-gies. Tests should be ordered with discretion and with the individual patient in mind. B. Laboratory tests. 1. Complete blood count with differential. a. Acute neurological injury can cause a rise in inflammatory markers, similar to an infectious response. The percentage of neutrophils, however, is likely higher in patients with infectious fever. 2. Basic metabolic panel. 3. Liver function tests and bilirubin. 4. Amylase and lipase. 5. ESR/CRP. 6. Cortisol. 7. Thyroid-stimulating hormone (TSH), triiodothyro-nine (T3), and thyroxine (T4). 8. Procalcitonin. C. Microbiology. 1. HIV antibody. 2. Heterophile antibody. 3. Hepatitis serologies. 4. Urine culture. 5. Blood culture. 6. CSF culture. 7. Tuberculin skin test. D. Imaging. 1. Chest radiograph. 2. CT of chest and abdomen. 3. Ultrasonography. Evaluation and Management Plan A. If the fever is caused by an infectious source, source con-trol is the priority, which involves removing any related lines or drains as well as choosing an effective antimicrobial agent. B. If the fever is caused by a noninfectious, noncentral con-dition, it will need to be addressed accordingly. Possible causes are: 1. Venous thromboembolism. 2. Transfusion reaction. 3. Drug fever. 4. Adrenal insufficiency. 5. Thyroid storm. C. If other etiologies of fever have been ruled out and the most likely cause of a patient's fever is central and due to neu-rological injury, the following treatments can be used. 1. Pharmacologic methods. a. Antipyretic agents: Acetaminophen, aspirin, or nonsteroidal anti-inflammatory drugs (NSAIDs). i. These agents are likely to be ineffective in brain-injured patients with impaired temperature regulatory mechanisms. 7. Targeted Temperature Management Guidelines

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159 ii. Acetaminophen is the preferred agent because aspirin and NSAIDs have undesirable side effects such as platelet dysfunction and GI upset. b. Steroids: Not used because of multiple side effects. 2. External cooling. a. Evaporation. i. Water or alcohol sponge baths. b. Conduction. i. Ice packs. ii. Immersion in cold water. iii. Water-circulating cooling blankets or pads. Improved accuracy with newer technology pro-vides constant monitoring of temperature and adjustment of circulating water to maintain desired body temperature. c. Convection. i. Fans. ii. Ambient air temperature control. iii. Air-circulating cooling blankets. d. Radiation. i. Skin exposure. 3. Invasive cooling. a. Cold saline boluses. b. Intravascular catheters. D. Complications. Many serious complications arise from induction of hypothermia as opposed to normothermia in a patient. Most of these adverse effects are not problematic until core body temperatures are 35∘C or lower. However, a number of complications may occur when attempting maintenance of normal temperatures. 1. Hepatic and renal toxicity. 2. Catheter-related thrombosis and infection. 3. Skin breakdown. a. Surface cooling may predispose to skin lesions due to its intrinsic mechanism of action via contact with skin. b. This risk may be low depending on the type of material used, the temperature of the material, and the length of time of intense cooling. c. Skin should be monitored for blistering, bruising, or sign of breakdown from prolonged cold exposure. d. Circulating water temperature should be moni-tored continuously, and prolonged periods of cold cir-culating water should be avoided. 4. Subsequent infections. 5. Shivering. a. The metabolic effects of shivering can be consider-able, resulting from increased energy expenditure. b. Shivering can produce heat, which is counterpro-ductive. c. The implications and management of shivering are extensive (see the following section “Shivering During Targeted Temperature Management”). Follow-Up A. There are no special follow-up needs for central fevers, because they are generally related to the initial neurological insult. B. Follow-up and postdischarge monitoring is related to the patient's admission diagnosis as well as new issues that may have occurred during hospitalization. Consultation/Referral A. Inpatient consults are relevant to the diagnosis of each patient. B. Examples of consults for noncentral fevers. 1. Infectious disease. 2. Wound/ostomy. 3. Hematology. 4. Endocrinology. 5. Pharmacy. 6. Others related to fever etiology. C. Pastoral care. Special/Geriatric Considerations A. Geriatric individuals often have unique presentations and require special considerations when gathering a history and physical. B. Treatment methods may also vary slightly due to multiple comorbidities and less reserve. 1. The elderly are more prone to ICU delirium and men-tal status changes while hospitalized, making history and physical examination challenging at times. 2. Skin breakdown is a regular concern in geriatric patients, because mobility and skin caliber are lower in these individuals, particularly with external cooling methods. 3. Geriatric patients may not always mount a febrile response to infection. They can become hypothermic in an infected state. 4. The effectiveness of different cooling methods increase with advanced age secondary to slower counterregula-tory response to small temperature changes, decreased metabolism, decreased vascular response (and as a result, vasoconstriction), and often a lower body mass index (BMI). 5. Medications may need to be adjusted more frequently in the elderly, whether because of hepatic/renal function or low BMI. Fever Management Bibliography Aiyagari, V., & Diringer, M. N. (2007). Fever control and its impact on out-comes: What is the evidence? Journal of the Neurological Sciences, 261 (1), 39-46. doi:10. 1016/j. jns. 2007. 04. 030 Badjatia, N. (2009). Hyperthermia and fever control in brain injury. Critical Care Medicine, 37 (37),S250-S257. doi:10. 1097/ccm. 0b013e3181aa5e8d Bor, D. H. (2018). Approach to the adult with fever of unknown origin. In A. Bloom (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/ contents/approach-to-the-adult-with-fever-of-unknown-origin Commichau, C., Scarmeas, N., & Mayer, S. A. (2003). Risk factors for fever in the neurologic intensive care unit. Neurology, 60 (5),837-841. doi:10. 1212/01. WNL. 0000047344. 28843. EB Fernandez, A., Schmidt, J. M., Claassen, J., Pavlicova, M., Huddleston, D., Kreiter, K. T., & Mayer, S. A. (2007). Fever after subarachnoid hemor-rhage: Risk factors and impact on outcome. Neurology, 68 (13), 1013-1019. doi:10. 1212/01. wnl. 0000258543. 45879. f5 Geri, G., Champigneulle, B., Bougouin, W., Arnaout, M., & Cariou, A. (2015). Common physiological response during TTM. BMC Emergency Medicine, 15 (Suppl. 1), A14. doi:10. 1186/1471-227X-15-S1-A14 Hocker, S. E., Tian, L., Li, G., Steckelberg, J. M., Mandrekar, J. N., & Rabinstein, A. A. (2013). Indicators of central fever in the neurologic intensive care unit. JAMA Neurology, 70 (12), 1499-1504. doi:10. 1001/ jamaneurol. 2013. 4354 Hossmann, K.-A. (2012). The two pathophysiologies of focal brain ischemia: Implications for translational stroke research. Journal of Cerebral Blood Flow & Metabolism, 32 (7), 1310-1316. doi:10. 1038/jcbfm. 2011. 186 Laupland, K. B. (2009). Fever in the critically ill medical patient. Critical Care Medicine, 37 (7), S273-S278. doi:10. 1097/CCM. 0b013e3181aa6117

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160 Laupland, K. B., Shahpori, R., Kirkpatrick, A. W., Ross, T., Gregson, D. B., & Stelfox, H. T. (2008). Occurrence and outcome of fever in critically ill adults. Critical Care Medicine, 36 (5), 1531-1535. doi:10. 1097/CCM. 0b013e318170efd3 Lopez, G. A. (2016). Temperature management in the neurointen-sive care unit. Current Treatment Options in Neurology, 18 (3), 12. doi:10. 1007/s11940-016-0393-6 Luscombe, M., & Andrzejowski, J. C. (2006). Clinical applications of induced hyperthermia. Continuing Education in Anesthesia, Critical Care & Pain, 6, 23-27. Retrieved from https://academic. oup. com/bjaed/ article/6/1/23/347011/Clinical-applications-of-induced-hypothermia Mac Laren, G., & Spelman, D. (2018). Fever in the intensive care unit. In G. Finlay (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/ contents/fever-in-the-intensive-care-unit Mc Intyre, L. A., Fergusson, D. A., H ́ebert, P. C., Moher, D., & Hutchison, J. S. (2003). Prolonged therapeutic hypothermia after traumatic brain injury in adults: A systematic review. Journal of the American Medical Association, 289 (22), 2992-2999. doi:10. 1001/jama. 289. 22. 2992 Mc Kinley, W., Mc Namee, S., Meade, M., Kandra, K., & Abdul, N. (2006). Incidence, etiology, and risk factors for fever following acute spinal cord injury. The Journal of Spinal Cord Medicine, 29 (5), 501-506. doi:10. 1080/10790268. 2006. 11753899 Mrozek, S., Vardon, F., & Geeraerts, T. (2012). Brain temperature: Physiol-ogy and pathophysiology after brain injury. Anesthesiology Research and Practice, 2012, 13. doi:10. 1155/2012/989487 O'Grady, N. P., Barie, P. S., Bartlett, J. G., Bleck, T., Carroll, K., Kalil, A. C., & Masur, H. (2008). Guidelines for evaluation of new fever in critically ill adult patients: 2008 update from the American College of Critical Care Medicine and the Infectious Diseases Society of Amer-ica. Critical Care Medicine, 36 (4), 1330-1349. doi:10. 1097/CCM. 0b013e318169eda9 Rabinstein, A. A., & Sandhu, K. (2007). Non-infectious fever in the neu-rological intensive care unit: Incidence, causes and predictors. Journal of Neurology, Neurosurgery & Psychiatry, 78 (11), 1278-1280. doi:10. 1136/ jnnp. 2006. 112730 Ryan, M., & Levy, M. M. (2003). Clinical review: Fever in intensive care unit patients. Critical Care, 7 (3), 221. doi:10. 1186/cc1879 Scaravilli, V., Tinchero, G., & Citerio, G. (2011). Fever management in SAH. Neurocritical Care, 15, 287. doi:10. 1007/s12028-011-9588-6 Schwarz, S., Häfner, K., Aschoff, A., & Schwab, S. (2000). Incidence and prognostic significance of fever following intracerebral hemorrhage. Neurology, 54 (2), 354-361. doi:10. 1212/WNL. 54. 2. 354 Walter, E. J., Hanna-Jumma, S., Carraretto, M., & Forni, L. (2016). The pathophysiological basis and consequences of fever. Critical Care, 20 (1), 200. doi:10. 1186/s13054-016-1375-5 Yenari, M. A., & Hemmen, T. M. (2010). Therapeutic hypothermia for brain ischemia. Stroke, 41 (10 Suppl. 1), S72-S74. doi:10. 1161/ STROKEAHA. 110. 595371 Hypothermia or Targeted Temperature Management After Cardiac Arrest Definition A. Hypothermia after cardiac arrest is the application of therapeutic cooling of the body for a prescribed period of time after cardiac arrest. Incidence A. Approximately 326,000 people in the United States experienced an out-of-hospital cardiac arrest in 2011, and approximately 11% of those who experienced a cardiac arrest survived to hospital discharge. B. Approximately 209,000 people experienced an in-hospital cardiac arrest. C. Survival statistics after in-hospital cardiac arrest are gen-erally lower than out-of-hospital cardiac arrest. Pathogenesis A. Neuronal injury occurs as a consequence of the hypoxia-ischemia and reperfusion that occurs with cardiac arrest andreturn of circulation. When this cascade of injury results in altered consciousness or coma, it's often referred to as hypoxic-ischemic encephalopathy (HIE). However, there are multiple causes of HIE in addition to cardiac arrest. B. Hypothermia or targeted temperature management (TTM) starts in the hours after return of spontaneous circulation (ROSC) decreases cerebral metabolism, inter-rupting multiple inflammatory pathways, and suppressing nitric oxide formation and suppressing programmed cell death. Predisposing Factors A. Coronary artery disease and other comorbid illnesses (such as diabetes, chronic kidney disease). Subjective Data A. The patient's history, functional status, and symptoms at the time of arrest may help determine the arrest etiology and assess if the patient or decision maker would want TTM as a postarrest intervention. B. Criteria for TTM. 1. Initial cardiac rhythm at time of arrest. a. TTM is indicated for patients who do not awaken after successful resuscitation with ROSC after an arrest with an initial rhythm of ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT). b. While the strongest evidence supports TTM in patients with VT or VF initial rhythm, the therapy may be considered for patients with asystole or pulse-less electrical activity (PEA) initial rhythms. C. Common complaints/symptoms. 1. Patients with HIE demonstrate impaired neuro-logical function and should receive a complete neuro-logical examination, including assessment of level of consciousness, brainstem function, motor function, respiratory pattern, and the presence of cranial nerve deficits. Impaired neurological function includes decreased level of arousal, inappropriate response to stimuli such as withdrawing from pain or decorticate or decerebrate posturing, and abnormal cranial nerve responses. D. Other signs and symptoms. 1. Other signs and symptoms depend on the cause of cardiac arrest and the timing from the arrest to ROSC, in addition to the comorbidities of individual patients. Physical Examination A. Check vital signs and perform telemetry monitoring. B. Monitor for hypotension with possible compensatory tachycardia and signs of heart failure, including adventitious lung sounds, peripheral edema, or jugular venous distension. C. Temperature. D. Perfusion. 1. Peripheral pulses may be weak, and there may be poor capillary refill. E. Oxygenation status on ventilator, O2saturation. F. Cardiac examination: Murmurs, rubs, or gallops, S4. 1. New murmur may suggest papillary muscle dysfunc-tion or septal rupture. G. Neurological examination: Assessment of level of con-sciousness, brainstem function, motor function, respiratory pattern, and the presence of cranial nerve deficits. Diagnostic Tests A. Routine diagnostic tests include: 1. EKG. 7. Targeted Temperature Management Guidelines Porat, R., & Dinarello, C. A. (2018). Pathophysiology and treatment of fever in adults. In A. Bloom (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/pathophysiology-and-treatment-of-fever-in-adults

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161 2. Full range of blood tests, including complete metabolic panel, complete blood count, cardiac enzymes, arterial blood gas, coagulation studies, and liver function tests. a. Evaluate for infection, bleeding risk, oxygenation status, and cardiac enzyme elevation. 3. Chest x-ray. a. Evaluate for pulmonary edema. 4. Transthoracic echocardiogram. a. May help identify the etiology of cardiac arrest or determine if urgent surgical repair is needed (e. g., aortic dissection, papillary muscle rupture, sep-tal rupture, cardiac tamponade, wall rupture). B. Patients must be assessed to determine if the benefit of TTM outweighs the risk. Generally speaking, patients are the best candidates for TTM if they meet the following criteria. 1. Patient is unconscious, generally defined as a Glasgow Coma Score less than 8. 2. Cardiac arrest is cardiac in origin. a. Patient must achieve ROSC after basic or advanced life support interventions. b. Cardiac arrest and resuscitation efforts were not prolonged (generally <30-50 minutes in clinical tri-als). c. As mentioned, the best evidence supports TTM in patients with an initial cardiac rhythm of VT or VF, which is usually cardiac in origin. TTM may be considered in other arrest etiologies as well. However, the outcome improvement is not as robust. 3. Patients with any of the following conditions were not included in clinical trials and the risk of TTM may out-weigh the benefit. a. Pregnancy. b. Intracranial hemorrhage or stroke. c. Bleeding diathesis. d. Active infection: Greater than 6 hours since ROSC. e. Systolic blood pressure (SBP) less than 80 mm Hg despite fluid resuscitation, vasopressor agents, or advanced cardiac interventions (e. g., intra-aortic bal-loon pump). Evaluation and Management Plan A. General goal: To evaluate patient for TTM and initiate as quickly as possible after ROSC. 1. Target temperature. a. Initial trials in hypothermia after cardiac arrest established a target temperature of 33∘C for 24 hours. A recent trial compared 33∘C to 36∘C and found there was no difference in outcomes between the two temperatures. Therefore, either temperature may be used as the target for TTM (Nielsen et al., 2013). b. Certain patient criteria may cause the clinician to choose one temperature over another. For example, a higher temperature may be preferred in patients with bleeding or infection risk whereas a lower temperature may be helpful for patients with seizures or cerebral edema. B. Hemodynamic goals. 1. Avoid hypotension (SBP <90 mm Hg, mean arterial pressure [MAP] <65 mm Hg). Most published protocols titrate vasopressors to a MAP greater than 65 mm Hg. 2. Monitor arterial oxygen saturation, venous oxygen saturation, and urine output to determine end organ per-fusion and titrate therapies accordingly. C. Stages of TTM. 1. Generally divided into three stages: Induction, main-tenance, and rewarming. a. Induction. i. Induction of TTM should begin as quickly as possible after the patient is determined to be a can-didate for therapy. ii. A smooth and well-coordinated induction includes coordination of medication adminis-tration, diagnostic tests, and application of the cooling device aimed at rapid reduction of tem-perature to goal. b. Maintenance at target temperature for 24 hours. c. Rewarming. i. After 24 hours at the target temperature, rewarming is started. Rewarming should occur slowly, particularly for patients who are cooled to 33∘C, at a rate no faster than 0. 1∘C to 0. 3∘C. ii. Quick rewarming may precipitate rebound cerebral edema and elevated intracranial pressure, as well as other systemic complications. 2. Post-rewarming, a fourth stage: Often discussed related to ongoing fever prevention and prognostication. a. After the patient returns to normal body tem-perature, interventions to prevent fever should be continued. b. Prognostication post-TTM may take additional time compared to patients after cardiac arrest who do not receive TTM. 3. Cooling techniques. a. TTM is best implemented with advanced temper-ature technology. b. Cooling blankets and intravascular devices are available. There are benefits and drawbacks to each type of technology. Technology should be reviewed for accuracy and degree of temperature control. i. Surface cooling is easily applied by the nursing staff, leading to quick induction. Compli-cations may include skin burns if the water tem-perature is allowed to be very cold for prolonged periods. ii. Intravascular cooling may decrease the occur-rence of shivering. The intravascular line must be placed by a qualified practitioner, and this must be considered in the induction workflow. Intravas-cular catheters are associated with higher rates of deep venous thrombosis (DVT). D. Complications. 1. Cardiac. a. Bradycardia is often seen in hypothermia, usu-ally at colder temperatures compared to warmer ones. Cardiac intervals (PR, QRS, QTc) can lengthen. This is generally well tolerated by the patient and resolves once rewarming has occurred. b. Central venous pressure (CVP) may increase due to vasoconstriction from cold temperatures. 2. Pulmonary. a. Patients are at high risk for pulmonary edema fol-lowing cardiac arrest, particularly if they received fluid for resuscitation or to induce TTM. Treatment should be individualized and commonly involves diuretics and oxygen support. Patients undergoing TTM at a lower temperature often experience a cold diuresis and will mobilize the excess fluid. b. During TTM, there is an increased solubility of O2and CO2, which leads to a decrease in Pa O2and Hypothermia or Targeted Temperature Management

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162 Pa CO 2and a left shift of the oxygen-hemoglobin dissociation curve. Ventilators may require fre-quent setting changes during induction of cooling. Arterial blood gas values should be corrected for temperature. c. Normocarbia (end-tidal CO2of 30-40 mm Hg or Pa CO2of 35-45 mm Hg) is a reasonable goal during TTM. 3. Endocrine. a. In critically ill patients, tight control of low nor-mal serum glucose levels is associated with increased frequency of hypoglycemic episodes. No one range is recommended for postcardiac arrest patients in guide-lines. It is reasonable to avoid wide fluctuations in serum glucose. b. At lower body temperature, there is a decreased production of insulin by the pancreas and decreased insulin sensitivity, resulting in higher exogenous insulin needs during hypothermia at lower target tem-peratures. c. Hyperglycemia during HIE is associated with worse outcomes and should be avoided. d. Increased lactate and ketone levels may be noted in blood or urine samples drawn during TTM to lower target temperatures. 4. Hypokalemia, hyperkalemia, and electrolyte imbal-ances. a. As body temperature drops, serum potas-sium moves intracellularly, resulting in a serum hypokalemia that must be monitored with frequent lab checks and potassium supplementation. However, when the body rewarms, intracellular potassium then shifts extracellularly. Potassium replacement should be less aggressive toward the end of the maintenance period and during rewarming. Rewarming should be slow and controlled to minimize excessive potassium shifts. b. Fluctuations in additional electrolytes such as cal-cium and magnesium may be seen and should be fre-quently monitored during TTM. 5. Neurological. a. Seizures are estimated to occur in 12% to 22% of patients who are comatose after cardiac arrest. Clinical signs of seizures may be obscured by coma or sedatives and paralytics administered during TTM. Therefore, seizure activity may be subclinical and the only evi-dence on EEG monitoring. b. The available evidence does not support prophy-lactic treatment and no specific antiseizure medica-tion is identified as superior in this setting. It is reasonable to undergo frequent or continuous EEG monitoring in patients during TTM to identify sub-clinical seizures or status epilepticus. 6. Renal. a. During TTM, particularly targeting a lower tem-perature, patients often experience a cold diuresis, or increased urine output during the induction period. This results as hypothermia increases venous return secondary to venous constriction. This, combined with an increase in atrial natriuretic peptide (ANP), decreased antidiuretic hormone (ADH), and tubular dysfunction from the cardiac arrest, may lead to large volume diuresis. b. If uncorrected, this may lead to hypovolemia and hemoconcentration. 7. Hepatic and gastrointestinal. a. The cardiac arrest and reperfusion of ROSC often results in decreased hepatic clearance, decreased hep-atic blood flow, and decreased speed of enzymatic reactions. This may result in an increased amount of plasma drug levels and effects. This must be consid-ered because many patients are on continuous vaso-pressors and receiving sedatives and analgesics during TTM. b. During TTM, the gastrointestinal system demon-strates decreased motility and delayed gastric emp-tying. Patients may be at risk for developing gas-tric stress ulcers and should receive prophylaxis as indicated. c. Postcardiac arrest, liver function testing should be monitored, and increased levels of amylase may occur even without acute pancreatitis. Patients may have ele-vated liver enzymes, and these should be monitored during TTM and therapy adjusted as necessary. 8. Hematological. a. TTM results in platelet and neutrophil inhibition, particularly at lower target temperatures and longer duration. Patients are at risk for bleeding and infec-tion. b. In addition to neutrophil dysfunction, patients are at risk for infection as vasoconstriction may lead to decreased white blood cell (WBC) migration to the site of infection and a decreased inflammatory response. E. Shivering during TTM. 1. Definition. a. Shivering is an involuntary, rhythmic tremor that consists of oscillatory movements of various skeletal muscle groups. The act of shivering is both an antici-pated consequence as well as an adverse effect of ther-apeutic hypothermia. b. Shivering is usually greatest at temperatures between 34∘C and 36∘C. 2. Pathogenesis. a. Core temperature is tightly regulated within the range of 36∘C to 37∘C. In healthy humans, peripheral vasoconstriction is triggered at 36. 5∘C and shivering typically starts at 35. 5∘C. b. In patients with brain injury, peripheral vasocon-striction and shivering thresholds are often higher; thus, thermoregulatory defenses vigorously respond to drops in core temperature. Elderly patients also experience shivering at higher temperatures than those who are younger. Additional risk factors include male sex, and electrolyte derangement such as hypo-magnesemia. 3. Consequence of shivering. a. Increase in systemic and cerebral energy consump-tion. b. Increase in metabolic demand. c. Increase in oxygen and carbon dioxide production. d. Increases in intraocular and in intracranial pres-sure. e. Precipitation of hemodynamic changes including heart rate, respiratory rate, and blood pressure. f. Hindering the process of cooling as heat is trans-ferred from the core to the periphery. g. Possible increased pain or bodily discomfort. 7. Targeted Temperature Management Guidelines

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163 TABLE 7. 1 The Bedside Shivering Assessment Scale Score Definition 0None: No shivering noted on palpation of the masseter,neck, or chest wall. 1Mild:Shiveringislocalizedtotheneckand/orthorax only. 2Moderate: Shivering involves grossmovement of the upper extremities(in addition to the neck and thorax). 3Severe:Shivering involves grossmovements of the trunk and upper and lower extremities. Source:Badjatia,N.,Strongilis,E.,Gordon,E.,Prescutti,M.,Fernandez,L., Fernandez,A.,... Mayer,S. A. (2012). Metabolicimpactofshiveringduring therapeutic temperaturemodulation: The Bedside Shivering Assessment Scale. Stroke, 39, 3242-3247. doi:10. 1161/STROKEAHA. 108. 523654 4. Assessment. a. The most common and only validated tool for the assessment of shivering is the Bedside Shivering Assessment Scale (see Table 7. 1). i. This scale measures the degree of shivering during induced hypothermia. ii. It assists in determining the efficacy of non-pharmacological and pharmacological interven-tions. 5. Management. a. Goals of therapy. i. Stopping or suppressing the vigorous central thermoregulatory reflex versus treating skeletal muscle contractions. ii. Using a multimodal approach to counter the effects of shivering, which includes both nonphar-macological and pharmacological therapy. b. Nonpharmacological agents. i. Skin counter-warming aims to reduce vaso-constriction by decreasing the shivering threshold by 1∘C for every 4∘C increase in mean skin tem-perature. ii. An air circulating blanket is an example of a device poised to counter the metabolic impact of shivering. iii. Focal hand warming has been proven suc-cessful in the reduction of shivering, while facial rewarming has conflicting data to support use in the treatment of shivering. c. Pharmacological agents. i. Sedatives and hypnotics. 1)Propofol, dexmedetomidine, midazolam, and diazepam are agents utilized to reduce the shivering threshold. 2)Propofol is also recommended as a con-tinuous infusion for induced hypothermia. However, the risks associated with use include hypotension. Several pharmacokinetic stud-ies have identified increased plasma concen-trations during hypothermia. The practitioner must take caution in the titration of this potent sedative to avoid untoward effects. 3)Dexmedetomidine has proven to be effec-tive in countering shivering. The limiting factor may be related to the high cost of med-ication delivery. 4)Diazepam IV at high doses (20 mg) has proven to successfully reduce core body tem-perature, and avoid unnecessary increases in oxygen consumption caused by discomfort. ii. Analgesics and opioids. 1)Meperidine has proven to be most benefi-cial in the reduction of the shiver threshold. 2)Precautions include respiratory depres-sion, nausea and vomiting, and increased seizure potential with prolonged drug admin-istration. 3)Combination therapies tend to have a syn-ergistic effect as in the case of meperidine and buspirone improving the effect of lowering the shivering threshold. 4)Fentanyl and morphine are frequently used analgesics post cardiac arrest and induced hypothermia. Both effectively reduce the shiver threshold. However, caution must be used with morphine as it has a higher prob-ability for hypotension. iii. Alpha-agonists. 1)Clonidine is the most widely used alpha-agonist during induced hypothermia, as well as the most researched. 2)A single dose has demonstrated to be as effective as meperidine in lowering the shiver-ing threshold. Caution must be taken because clonidine can induce bradycardia and exacer-bate bradycardia from induced hypothermia. iv. N-methyl-D-aspartate (NMDA) antagonists. v. Magnesium. 1)Use of magnesium sulfate to control shivering has both neuroprotective qualities for brain-injured patients and acts to guard against hypomagnesemia, which is a common finding during induced hypothermic states. 2)Often used in combination with meperi-dine for its thermoregulatory effect to reduce shivering, shorten time to target temperature, and improve overall patient comfort. vi. Neuromuscular blocking agents (NMBAs). 1)Agents such as dantrolene, methylphenidate, and doxapram control the skeletal muscle contractions associated with shivering. However, they are often left as the last therapeutic option. 2)Caution must be taken with NMBAs because induced hypothermia reduces clear-ance of NMBAs and may prolong paralysis well after normothermia has been reached. 6. Conclusions. a. Shivering left untreated adversely affects the patient, and it may negate the benefit of induced hypothermia and create unintended hemodynamic instability and life-threatening metabolic derange-ments. b. Shivering management can be successfully imple-mented with a multimodal approach utilizing both nonpharmacological and pharmacological interven-tions with no adverse events. Consultation/Referral A. Consult with cardiology to determine the etiology of car-diac arrest, perform acute interventions, and manage any dys-rhythmias. Hypothermia or Targeted Temperature Management

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164 B. Consult with neurology and/or neurocritical care for the critical management of the patient during TTM and prog-nostication post-TTM. C. Consult with critical care (or neurocritical care) as needed for critical management. Special/Geriatric Considerations A. Because liver and kidney impairment may be present fol-lowing cardiac arrest, older patients are at further risk for adverse events and impaired drug metabolism. The medica-tions identified as high risk in elderly patients (Beers criteria) should be avoided when possible. B. Older patients may cool more quickly due to thinner skin and less body fat, which may also precipitate vasoconstriction and shivering. For these same reasons, these patients are at higher risk for skin breakdown. Bibliography American Geriatrics Society 2015 Beers Criteria Update Expert Panel. (2015). American Geriatrics Society 2015 updated Beers Criteria for potentially inappropriate medication use in older adults. Journal of the American Geriatrics Society, 63, 2227-2246. Andresen, M., Gazmuri, J. T., Marín, A., Regueira, T., & Rovegno, M. (2015). Therapeutic hypothermia for acute brain injuries. Scandina-vian Journal of Trauma, Resuscitation and Emergency Medicine, 23 (1), 42. doi:10. 1186/s13049-015-0121-3 Badjatia, N. (2012). Shivering: Scores and protocols. Critical Care, 16(Suppl. 2), A9. Retrieved from https://www. ncbi. nlm. nih. gov/pmc/ articles/PMC3389469 Badjatia, N., Strongilis, E., Gordon, E., Prescutti, M., Fernandez, L., Fer-nandez, A.,... Mayer, S. A. (2012). Metabolic impact of shivering dur-ing therapeutic temperature modulation: The Bedside Shivering Assess-ment Scale. Stroke, 39, 3242-3247. doi:10. 1161/STROKEAHA. 108. 523654 Boddicker, K. A., Zhang, Y., Zimmerman, M. B., Davies, L. R., & Kerber, R. E. (2005). Hypothermia improves defibrillation success and resuscita-tion outcomes from ventricular fibrillation. Circulation, 111 (24), 3195-3201. doi:10. 1161/CIRCULATIONAHA. 104. 492108 Callaway, C. W., Donnino, M. W., Fink, E. L., Geocadin, R. G., Golan, E., Kern, K. B.,... Zimmerman, J. Z. (2015). Part 8: Post-cardiac arrest care: 2015 American Heart Association guidelines update for cardiopul-monary resuscitation and emergency cardiovascular care. Circulation, 132(18 Suppl. 2), S456-S482. doi:10. 1161/CIR. 0000000000000262 Choi, H. A., Ko, S.-B., Presciutti, M., Fernandez, L., Carpenter, A. M., Lesch, C., & Badjatia, N. (2011). Prevention of shivering during thera-peutic temperature modulation: The Columbia anti-shivering protocol. Neurocritical Care, 14, 389-394. doi:10. 1007/s12028-010-9474-7 Geri, G., Champigneulle, B., Bougouin, W., Arnaout, M., & Cariou, A. (2015). Common physiological response during TTM. BMC Emergency Medicine, 15, A14. doi:10. 1186/1471-227X-15-S1-A14. Retrieved from https://www. ncbi. nlm. nih. gov/pmc/articles/PMC4480975/Logan, A. S., Sangkachand, P., & Funk, M. (2011). Optimal management of shivering during therapeutic hypothermia after cardiac arrest. Critical Care Nurse, 31 (6), e18-e30. doi:10. 4037/ccn2011618 Lopez, G. A. (2016). Temperature management in the neurointensive care unit. Current Treatment Options in Neurology, 18, 12. doi:10. 1007/ s11940-016-0393-6 Luscombe, M., & Andrzejowski, J. C. (2006). Clinical applications of induced hyperthermia. Continuing Education in Anesthesia, Critical Care & Pain, 6, 23-27. Retrieved from https://academic. oup. com/bjaed/ article/6/1/23/347011/Clinical-applications-of-induced-hypothermia Mozaffarian, D., Benjamin, E. J., Go, A. S., Arnett, D. K., Blaha, M. J., Cushman, M., & Turner, M. B. (2015). Heart disease and stroke statistics—2015 update. Circulation, 131, e29-e322. doi:10. 1161/CIR. 0000000000000152 Nielsen, N., Wetterslev, J., Cronberg, T., Erlinge, D., Gasche, Y., Has-sager, C., & Friberg, H. (2013). Targeted temperature management at 33∘C versus 36∘C after cardiac arrest. New England Journal of Medicine, 369(23), 2197-2206. doi:10. 1056/NEJMoa1310519 Polderman, K. H., & Herold, I. (2009). Therapeutic hypothermia and con-trolled normothermia in the intensive care unit: Practical considerations, side effects, and cooling methods. Critical Care Medicine, 37 (3), 1101-1120. doi:10. 1097/ccm. 0b013e3181962ad5 Povlishock, J. T., Buki, A., Koiziumi, H., Stone, J., & Okonkwo, D. O. (1999). Initiating mechanisms involved in the pathobiology of trau-matically induced axonal injury and interventions targeted at blunt-ing their progression. In A. Baethmann, N. Plesnila, F. Ringel, & J. Eriskat (Eds. ), Current progress in the understanding of secondary brain damage from trauma (vol. 73, pp. 15-20). Vienna, Austria: Springer. doi:10. 1007/978-3-7091-6391-7_3 Sandroni, C., & Geocadin, C. S. (2015). Neurological prognostication after cardiac arrest. Current Opinion Critical Care, 21, 209-214. doi:10. 1097/MCC. 0000000000000202 Scirica, B. M. (2013). Therapeutic hypothermia after cardiac arrest. Circula-tion, 127, 244-250. doi:10. 1161/CIRCULATIONAHA. 111. 076851 Taccone, F. S., Cronberg, T., Friberg, H., Greer, D., Horn, J., Oddo, M., & Vincent, J.-L. (2014). How to assess prognosis after cardiac arrest and therapeutic hypothermia. Critical Care, 18, 202. doi:10. 1186/cc13696 Van Poucke, S., Stevens, K., Marcus, A. E., & Lanc ́e, M. (2014). Hypother-mia: Effects on platelet functioning hemostasis. Thrombosis Journal, 12, 31. doi:10. 1186/s12959-014-0031-z Weant, K. A., Martin, J. E., Humphries, R. L., & Cook, A. M. (2010). Pharmacologic options for reducing the shivering response to therapeu-tic hypothermia. Pharmacotherapy, 30, 830-841. doi:10. 1592/phco. 30. 8. 830 Wijdicks, E. F., Hijdra, A., Young, G. B., Bassetti, C. L., & Wiebe, S. A. (2006). Practice parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review). Neurol-ogy, 67, 203-210. doi:10. 1212/01. wnl. 0000227183. 21314. cd7. Targeted Temperature Management Guidelines Liu-De Ryke, X., & Rhoney, D. H. (2008, April 4). Pharmacological management of therapeutic hypothermia-induced shivering. Retrieved from http://www. sccm. org/Communications/Critical-Connections/ Archives/Pages/Pharmacological-Management-of-Therapeutic-Hypothermia-Induced-Shivering. aspx

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165 8 Endocrine Guidelines Catherine Harris Adrenal Insufficiency Kathryn Evans Kreider Definition A. Insufficient production of glucocorticoids and/or miner-alocorticoids and adrenal androgens as a result of primary adrenal failure or failure of the pituitary or hypothalamus. Cortisol and mineralocorticoids are essential to life because of their role in energy and fluid homeostasis. B. Primary adrenal insufficiency (PAI). 1. Also known as Addison's disease. 2. Deficiency in adrenal hormones as a result of direct injury to the adrenal glands. C. Secondary adrenal insufficiency (SAI). 1. Insufficient adrenal hormones due to lack of pituitary stimulation. D. Tertiary adrenal insufficiency (TAI). 1. Insufficient adrenal hormones due to lack of hypotha-lamic stimulation on the pituitary. E. Adrenal crisis (AC). 1. Potentially fatal condition that occurs when there is heightened need for cortisol in response to stress in the presence of adrenal insufficiency (AI). 2. May be the initial presentation of AI. Incidence A. The prevalence of primary AI is 100 to 140 cases per million. 1. Women more often affected. 2. Peak age 30 to 50 years. B. The prevalence of secondary AI is 150 to 280 cases per million. 1. Women more often affected. 2. Peak age around 60 years. C. The risk of AC in patients with existing AI is 6. 3% per patient year. Pathogenesis A. PAI is caused by destruction of the adrenal cortex, most often by antiadrenal antibodies. 1. Hormone deficiency occurs when 90% of the cortex is lost. 2. All adrenal hormones may be affected, including min-eralocorticoids (aldosterone) and adrenal androgens. B. Central AI includes SAI and TAI. 1. SAI is a result of deficient ACTH from the pituitary gland leading to decreased adrenal stimulation. 2. TAI involves disruption of corticotropin-releasing hormone (CRH), vasopressin, or both, from the hypotha-lamus, resulting in decreased stimulation of the pituitary gland and reduced ACTH. 3. The hypothalamic-pituitary axis (HPA) is impaired. 4. Production of aldosterone and adrenal androgens is unaffected. Predisposing Factors A. Primary AI. 1. Presence of other autoimmune conditions (e. g., autoimmune thyroid disease, type 1 diabetes mellitus, autoimmune polyendocrinopathy syndromes). 2. Disseminated infection (e. g., tuberculosis, HIV, cytomegalovirus, fungal infections). 3. Adrenal hemorrhage, metastases, or infiltration. 4. Various genetic disorders (e. g., congenital adrenal hyperplasia, adrenoleukodystrophy). 5. Use of medications associated with drug-induced AI (e. g., fluconazole, etomidate, phenobarbital, rifampin). B. Secondary AI. 1. Pituitary tumor or trauma. 2. Infections or infiltrative processes (e. g., tuberculosis, meningitis, sarcoidosis). 3. Pituitary surgery. C. Tertiary AI. 1. Most common cause: Long-term use of exogenous glucocorticoids. 2. Hypothalamic dysfunction secondary to tumors or infiltrative processes. D. AC. 1. Abrupt cessation of glucocorticoid use. 2. Acute physiologic stress in the presence of AI. 3. Previous AC. 4. Risk increased if significant comorbidity present. Subjective Data A. Common complaints/symptoms. 1. Tends to be nonspecific with an insidious onset, including: a. Weakness and fatigue. b. Anorexia and weight loss. B. Common/typical scenario. 1. History of the present illness. a. Elicit information about onset, duration, and severity of symptoms. b. Obtain a detailed medical history. c. Inquire about recent illness, injury, trauma, surgery, and procedures. d. Evaluate for history of glucocorticoid use. Adrenal Insufficiency

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166 2. Other signs and symptoms. a. AI. i. Abdominal pain. ii. Myalgia or arthralgia. iii. Depression or anxiety. iv. Dizziness or postural hypotension. v. Salt craving. vi. Skin hyperpigmentation. vii. Decreased libido in women (if androgen defi-cient). viii. Loss of pubic and axillary hair in females (if androgen deficient). ix. Electrolyte imbalances including hypona-tremia and hyperkalemia. x. Hypoglycemia. b. AC. i. Severe weakness. ii. Syncope. iii. Abdominal pain, nausea, and vomiting. iv. Back pain. v. Confusion. Physical Examination A. Vital signs. 1. Orthostatic hypotension in AI. 2. Hypotension in AC. B. Skin. 1. Hyperpigmentation, particularly sun-exposed areas, skin creases, mucous membranes, scars, and breast are-olas. 2. In females, pubic and/or axillary hair loss. C. Signs of dehydration. D. Cardiovascular examination. E. Mental status examination. 1. Altered consciousness and delirium in AC. Diagnostic Tests A. Diagnostic testing for AI should be performed in any hospitalized patient with symptoms suggestive of AI that are otherwise unexplained. B. AI is usually diagnosed by a low morning (8 a. m. ) serum cortisol level and a low stimulated cortisol level. 1. Cortisol levels are usually at their highest levels in the morning; low levels should raise suspicion of AI. 2. The diagnosis of AI is likely if the morning cortisol level is less than 5 mcg/d L, and less than 3 mcg/d L is highly suggestive. 3. A low serum cortisol level ( <5 mcg/d L) in addition to a high ACTH level ( >66 pmol/L) is highly predictive of AI. a. ACTH twice the upper limit of normal of the reference range is consistent with PAI. 4. A high ACTH with a normal cortisol level may be an early indicator of AI. C. The most common stimulation test is the corticotropin stimulation test (“cort-stim”), also known as the ACTH test or cosyntropin test. 1. This test is the gold standard for diagnosing primary (not secondary) AI. 2. Cosyntropin is synthetic ACTH given to patients intramuscularly (IM) to stimulate the adrenal glands to produce cortisol. 3. Cosyntropin testing can be done at any time of day. a. Testing is often done early morning (8 a. m. ) so morning cortisol levels can be drawn simultaneously. 4. Steps for performing the cort-stim test include:a. Draw baseline lab tests, including serum cortisol and ACTH. b. Administer 250 mcg of cosyntropin IM or intra-venous (IV). c. After 30 or 60 minutes, draw peak serum cortisol level. 5. Peak serum cortisol levels less than 18 mcg/d L indi-cate AI. a. Certain conditions can alter cortisol measurements (alter cortisol-binding globulin [CBG]). i. Estrogen-containing contraceptives can falsely increase cortisol. ii. Patients with nephrotic syndrome, liver dis-ease, or those with critical illness may have low CBG values and falsely low cortisol levels. 6. High ACTH levels (often >300 ng/L) are character-istic of PAI. 7. Renin and aldosterone should be measured to assess mineralocorticoid deficiency if there is a concern for PAI. a. PAI is associated with loss of the part of the adrenal gland that produces mineralocorticoid hormones. i. Elevated plasma renin and low or inappropri-ately normal aldosterone is typical. 8. If SAI or TAI is suspected (pituitary or hypothalamus dysfunction), it is recommended that an endocrinologist be consulted to assist with biochemical testing and con-firmatory testing. Differential Diagnosis A. Malnutrition. B. Gastrointestinal (GI) dysfunction. C. Malignancy. D. Failure to thrive. E. Hyperthyroidism. Evaluation and Management Plan A. General plan: Replacement of glucocorticoid with physi-ologic dosing; hemodynamic stability. B. Pharmacotherapy. 1. If AI is diagnosed in the hospital and the patient is acutely ill/decompensating, stress-dose steroids should be used immediately and continued until the patient show signs of recovery. 2. If AI or adrenal crisis is suspected in a hospitalized patient who is acutely ill, start stress-dose steroids prior to receiving results of diagnostic testing. a. Example: Hydrocortisone 50 mg IV q6h. b. Alternative: Hydrocortisone 100 mg IV given immediately, followed by 200 mg hydrocortisone given over 24 hours (continuous IV or intermittent injections). 3. Stress dosing of steroids should be used for patients with previously diagnosed AI who present to the hospital with acute illness or injury. 4. Patients should also be given a bolus of IV fluids for acute adrenal crisis. a. 1,000 m L saline or 5% dextrose in saline given within the first hour. 5. If AI is diagnosed in the hospital and the patient is not acutely ill or demonstrating signs of AC, physiologic dosing may be started with careful consideration to other comorbid conditions and patient acuity. 6. All patients with confirmed PAI require lifelong glu-cocorticoid therapy. a. Options—may be dosed based on body mass index or weight. 8. Endocrine Guidelines

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167 i. Hydrocortisone 15 to 20 mg in the morning and 5 to 10 mg in the afternoon (12-4 p. m. ). ii. Prednisolone 3 to 5 mg/d total in 1 to 2 daily doses. b. Patients may occasionally be given glucocorticoid divided into three daily doses. c. Dexamethasone should generally be avoided due to potential for Cushing-like features and overreplace-ment. 7. Mineralocorticoid replacement should be initiated in all patients who exhibit aldosterone deficiency. a. Fludrocortisone should be initiated at doses of 50 to 100 mg/d. b. Salt intake should not be restricted. 8. Response should be measured clinically for both glu-cocorticoid and mineralocorticoid replacement (blood pressure [BP], weight, energy levels, and signs of glu-cocorticoid excess; salt craving, postural hypotension, edema). a. Electrolytes should be measured to confirm correct mineralocorticoid replacement. b. Other biochemical tests are not recommended. C. Discharge instructions. 1. Patient should be counseled on signs and symptoms of under-and overreplacement of cortisol. 2. Patients require a steroid emergency card and a med-ical alert bracelet. 3. Patient should be counseled extensively on “sick day rules. ” a. Home management of illness with fever: Patients should double or triple home steroid dose for 2 to 3 days or until recovery; increase electrolyte-containing fluids. b. Management of GI-related illness: Patient should inject 100 mg hydrocortisone IM if unable to tolerate oral administration. c. Minor to moderate surgical stress: Double or triple home dosing until event is over. 4. Patients should have a prescription for IM hydrocortisone in case they are unable to take PO steroids. 5. Patients with mineralocorticoid deficiency should be counseled to increase salt intake on days of excess heat, sweating, or physical activity. Follow-Up A. Patients should follow-up with an outpatient provider every 3 to 6 months until clinically stable, with appointments every 6 to 12 months reasonable thereafter. B. Patients should be evaluated at each clinical visit for signs and symptoms of over-and underreplacement. 1. Signs of overreplacement may include insomnia, weight gain, peripheral edema, or hypertension. 2. Signs of underreplacement are similar to the signs and symptoms of AI. C. Patients should receive periodic clinical and biochemical evaluation to screen for other autoimmune conditions. 1. Type 1 diabetes. 2. Autoimmune thyroid disease. 3. Pernicious anemia. 4. Celiac disease. 5. Premature ovarian failure. Consultation/Referral A. Referral to an endocrinologist is recommended to assist with long-term steroid management. Special/Geriatric Considerations A. Pregnant patients should be evaluated at least once per trimester. 1. A glucocorticoid dose increase may be required in the third trimester. 2. Stress-dose steroids are required during labor. Bibliography Bornstein, S. R., Allolio, B., Arlt, W., Barthel, A., Don-Wauchope, A., Hammer, G. D.,... Torpy, D. J. (2016). Diagnosis and treatment of primary adrenal insufficiency: An endocrine society clinical practice guideline. Journal of Clinical Endocrinology and Metabolism, 101 (2), 364-389. doi:10. 1210/jc. 2015-1710 Charmandari, E., Nicolaides, N. C., & Chrousos, G. P. (2014). Adrenal insufficiency. The Lancet, 383 (9935), 2152-2167. doi:10. 1016/S0140-6736(13)61684-0 Husebye, E. S., Allolio, B., Arlt, W., Badenhopp, K., Bensing, S., Betterle, C.,... Pearce, S. H. (2014). Consensus statement on the diagnosis, treatment and follow-up of patients with primary adrenal insufficiency. Journal of Internal Medicine, 275 (2), 104-115. doi:10. 1111/joim. 12162 Smans, L. C., Van der Valk, E. S., Hermus, A. R., & Zelissen, P. M. (2016). Incidence of adrenal crisis in patients with adrenal insufficiency. Clinical Endocrinology, 84, 17-22. doi:10. 1111/cen. 12865 Diabetes Mellitus—Type 1 Julie Stone Definition A. Due to autoimmune destruction of the pancreatic beta cells. B. Previously referred to as insulin-dependent diabetes or juvenile-onset diabetes. C. Further divided into two subgroups based on patho-genesis. 1. Immune-mediated diabetes. a. Autoimmune-mediated destruction of pancreatic beta cells. b. Often have other autoimmune disorders such as Hashimoto's thyroiditis, Graves' disease, Addison's disease, celiac disease, vitiligo, autoimmune hepatitis, myasthenia gravis, and pernicious anemia. 2. Idiopathic type 1 diabetes. a. No known etiologies. b. Permanent insulinopenia and prone to ketosis. c. No evidence of autoimmunity. d. African or Asian ancestry. e. Strongly inherited; no human leukocyte antigen association. Incidence A. In 2012, approximately 1. 25 million American children and adults had type 1 diabetes. B. Worldwide incidence is increasing by approximately 3% per year. Pathogenesis A. Autoimmune destruction of pancreatic beta cells; 85% of type 1 diabetes patients have detectable circulating anti-bodies. B. Rate of beta cell destruction can vary. 1. Rapid in infants and children. 2. Slow in adults. Predisposing Factors A. Presence of other autoimmune diseases. B. Family history of diabetes. Diabetes Mellitus—Type 1

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168 C. Viruses. D. Environmental toxins. Subjective Data A. Common complaints/symptoms. 1. Polyuria (96%). 2. Polydipsia. 3. Weight loss. 4. Fatigue. B. Common/typical scenario. 1. Patients frequently complain of fatigue and weakness. They may have muscle cramps, blurred vision, and signif-icant polyuria, polydipsia, and polyphagia. 2. Weight loss occurs over time despite normal or increased appetite. C. Family and social history. 1. Ask about family history since there is a strong link to family history. 2. Ask about type of occupation, if the person is a shift worker, use of alcohol, smoking, or recreational drug use. 3. Review how much exercise the person gets. D. Review of symptoms. 1. HEENT. a. Dental issues. Periodontal disease is associated with diabetes. 2. Psychologic. a. Depression. b. Anxiety. c. Disordered eating. d. Psychosocial barriers/support. e. Barriers to self-management. 3. Microvascular complications. a. Neuropathy. b. Nephropathy. c. Retinopathy. 4. Macrovascular complications. a. Coronary artery disease. b. Cerebrovascular disease. c. Peripheral arterial disease. Physical Examination A. Height, weight, body mass index (BMI), waist circumfer-ence. B. Vital signs. C. Funduscopic examination. D. Thyroid palpation. E. Skin examination. 1. Acanthosis nigricans (see Figure 8. 1). 2. Lipohypertrophy. 3. Diabetic dermopathy. 4. Skin tags. F. Foot examination. 1. Inspection, noting mycotic changes to nail or skin. 2. Vascular examination. a. Hair patterns or lack of hair growth. b. Pulses (dorsalis pedis and posterior tibial). c. Temperature/color. 3. Reflexes. a. Patellar. b. Achilles. 4. Proprioception, vibration, and monofilament sensa-tion. Diagnostic Tests A. Glycosylated hemoglobin (Hgb A1C), fasting glucose, random glucose, or 2-hour glucose tolerance test to diagnose. 1. Hgb A1C greater than 6. 5%. 2. Fasting glucose greater than 126 mg/d L. 3. Random glucose greater than 200 mg/d L with classic symptoms of hyperglycemia. 4. 2-hour glucose tolerance test greater than 200 mg/d L. B. Antibodies to check at time of diagnosis. 1. Glutamic acid decarboxylase (GAD). 2. Islet cell antibodies. 3. Zinc antibodies. C. Hgb A1C on admission to hospital if no result available for past 3 months. D. Yearly lab work. 1. Fasting lipid panel. 2. Liver function tests. 3. Urine albumin-to-creatinine ratio. 4. Serum creatinine and estimated glomerular filtration rate (GFR). 5. Thyroid-stimulating hormone. E. C-peptide and random glucose to determine insulin pro-duction by beta cells. Differential Diagnosis A. Steroid-induced diabetes. B. Pancreatitis. C. Cushing's disease. D. Pancreatic endocrine tumor. E. Gestational diabetes. F. MODY type diabetes. G. Latent autoimmune diabetes in adults (LADA). H. Type 2 diabetes. I. Cystic fibrosis-related diabetes. J. Posttransplant diabetes. K. Postpancreatectomy diabetes. Evaluation and Management Plan A. General plan. The recommended outpatient comprehen-sive treatment plan for type 1 diabetes according to the American Association of Diabetes Educators consists of the following seven self-care behaviors. 1. Healthy eating: The patient should see a registered dietician for medical nutrition therapy counseling. 2. Being active: At least 150 minutes of moderate to vig-orous intensity physical activity spread out over a week is required. This can include resistance exercises and flexi-bility exercises. 3. Monitoring: It is recommended to test glucose before meals and bedtime (more if needed). 4. Medications (insulin). a. Delivery method options: Pens, vial and syringe, pump. b. Regimen choices (premixed insulin vs. basal and prandial). c. Proper storage of insulin. d. Preparation, administration, and site rotation of insulin injection. e. Disposal of sharps. f. Hypoglycemia symptoms. 5. Problem solving. 6. Healthy coping. 7. Reducing risks. B. Patient/family teaching points. 1. Inpatient education focuses on survival skills only. a. Checking glucose. b. Taking medications. c. Diet. d. Hypoglycemia treatment. 8. Endocrine Guidelines

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169 FIGURE 8. 1 Acanthosis nigricans is a dark, velvety, hyperpigmentation of the skin, often found at the skin folds. Source: Lyons, F., & Ousley, L. (2015). Dermatology for the advanced practice nurse (p. 55). New York, NY: Springer Publishing Company. 2. Outpatient education is more comprehensive and uses guidelines by the American Association of Diabetes Edu-cators to direct the education. The patient should be referred to outpatient diabetes education at the time of diagnosis, yearly thereafter, and as needed or if therapy changes. C. Pharmacotherapy. 1. Insulin: Mainstay of therapy. a. Initiate therapy using a 0. 3 units/kg/d total daily dose. b. Follow 50/50 rule. i. Give one-half of the total daily dose as basal insulin (long-acting insulin). ii. Give one-half of the total daily dose as pran-dial insulin divided evenly between three meals (usually rapid-acting or short-acting insulin). iii. Add a gentle correction scale using the same rapid or short-acting insulin in number 2. Use 1 unit for every 50 points glucose is above 150 mg/d L. c. In the outpatient setting, the patient should learn carbohydrate counting, and then prandial insulin can be dosed as a ratio of 1 unit insulin to number of grams of carbohydrates. d. Consider insulin pump therapy at some point in the future. 2. Pramlintide. a. Delays gastric emptying, blunts secretion of glucagon, and enhances satiety. b. Food and Drug Administration (FDA) approved for use in adults with type 1 diabetes; most helpful in treating these patients. c. Helps with weight loss and reduces insulin dose. D. Discharge instructions. 1. Verify the patient's understanding of how to take med-ications as prescribed. a. Dose. b. Route. c. Frequency. d. Relationship to meals. e. Proper disposal of sharps. f. Rotation of sites for subcutaneous insulin injec-tions. g. Need for refrigeration. 2. Make sure the patient is familiar with dietary restric-tions. a. The patient should aim for consistent amounts of carbohydrates per meal at first. Then the goal will be to learn to dose insulin to the amount of carbohydrates using carbohydrate counting. 3. Be sure the patient knows when glucose monitoring is important. a. Before meals and bedtime. b. Before and after exercise. c. Before driving. d. More often as needed. Follow-Up A. Recommend annual eye examination and podiatry exam-ination. B. Recommend outpatient education if appropriate. C. Follow-up with endocrinologist or primary care provider. Specify how soon patient should be seen. Specify when to call provider. D. Outline hypoglycemia treatment. 1. Rule of 15: 15 g of simple carbohydrates every 15 minutes until glucose is above 70 mg/d L (e. g., 1/2 cup juice, 1/2 cup pop, glucose gel, glucose tablets). 2. Carry glucose tablets or gel at all times. 3. Instruct the patient to carry a glucagon kit that can be administered by a friend or family member if the patient is unresponsive. Consultation/Referral A. Refer the patient to endocrinology for new diagnosis, uncontrolled Hgb A1C, multiple complications of diabetes, or comorbid conditions affecting the diabetes control. B. Refer the patient to nephrology for nephropathy. C. Refer the patient to ophthalmology for yearly eye exami-nation. D. Refer the patient to podiatry for issues and/or yearly examination. E. Refer the patient to a dentist (periodontal check, dental cleaning twice a year). F. Refer the patient to psychology for coping with chronic disease. Diabetes Mellitus—Type 1

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170 Special/Geriatric Considerations A. Pregnancy. 1. Retinopathy risk: Counsel patient on the risk of development or progression of retinopathy. Dilated eye examination should ideally occur preconception, each trimester, and 1 year postpartum. 2. Potentially teratogenic medications should be stopped. 3. Measurements of fasting and postprandial glucose are recommended. 4. Hgb A1C is lower during pregnancy. Target in preg-nancy is 6% to 6. 5%. 5. Glycemic targets. a. Fasting 95 mg/d L or lower. b. 1-hour postprandial 140 mg/d L or lower. c. 2-hour postprandial 120 mg/d L or lower. 6. Changes in insulin requirements (see Table 8. 1). a. First trimester. b. Second trimester. c. Third trimester. 7. Labor and delivery: Use regular insulin intravenous infusion and immediate postpartum until glucose is stable. 8. Postpartum care. a. Insulin sensitivity increases with delivery and returns to prepregnancy levels over 1 to 2 weeks. b. Prevent hypoglycemia with breastfeeding, erratic sleep, and eating that occurs postpartum. B. Geriatric. 1. Determine glycemic goals based on expected life span, comorbid conditions, and ability of patient to self-manage disease. 2. Use hypoglycemia prevention. Bibliography Cefalu, W. T. (2017). Standards of medical care in diabetes-2017. Diabetes Care, 40 (Suppl. 1), s1-s135. doi:10. 2337/dc17-S003 Lyons, F., & Ousley, L. (2015). Dermatology for the advanced practice nurse (p. 55). New York, NY: Springer Publishing Company. Menke, A., Orchard, T., Imperatore, G., Bullard, K., Mayer-Davis, E., & Cowie, C. (2013). The prevalence of type 1 diabetes in the United States. Epidemiology, 24, 773-774. doi:10. 1097/EDE. 0b013e31829ef01a Mensing, C. (2011). The art and science of diabetes self-management education desk reference (2nd ed). Chicago, IL: American Association of Diabetes Educators. Statistics About Diabetes. (n. d. ). Retrieved from http://www. diabetes. org/ diabetes-basics/statistics/ Diabetes Mellitus—Type 2 Julie Stone Definition A. Relative (rather than absolute) insulin deficiency and peripheral insulin resistance. B. Previously referred to as non-insulin-dependent diabetes or adult-onset diabetes. Incidence A. Accounts for 90% to 95% of all cases of diabetes. B. According to the 2017 Centers for Disease Control and Prevention's National Diabetes Statistics Report, an esti-mated 30. 3 million Americans or 9. 4% of the population had diabetes in 2015 (see Table 8. 2). C. In 2015, an estimated 1. 5 million new cases of diabetes was diagnosed among U. S. adults older than 18 years. D. Diabetes was the seventh leading cause of death in 2015. E. Prevalence varies among different ethnicities (see Table 8. 3). Pathogenesis A. Specific etiologies are not known. There is no autoim-mune destruction of beta cells. B. Excess weight causes insulin resistance. Most patients with type 2 diabetes are overweight or obese. C. Abdominal obesity contributes to increased risk. D. Ketoacidosis seldom occurs. E. Hyperglycemia develops gradually; it is often undiag-nosed for years before the official diagnosis is made. F. Insulin secretion is defective and unable to compensate for increased insulin resistance. Predisposing Factors A. Age; risk is higher as age increases. B. Obesity, with body mass index (BMI) greater than or equal to 25 kg/m2. C. Lack of physical activity. D. Women with prior gestational diabetes. E. History of prediabetes. F. History of metabolic syndrome. G. Comorbidities of hypertension and dyslipidemia. H. Higher rates in certain ethnic populations. 1. African Americans. 2. American Indian. 3. Hispanic/Latino. 4. Asian American. I. Strong genetic predisposition. J. Medications. 1. Glucocorticoids. 2. Thiazide diuretics. 3. Atypical antipsychotics. Subjective Data A. Common complaints/symptoms. 1. Polyuria. 2. Blurred vision. 3. Polydipsia. 4. Malaise/fatigue. TABLE 8. 1 Changing Insulin Requirements During Pregnancy Trimester First Second Third Insulin requirements Woman often has decrease in total daily insulin requirements. May experience increased hypoglycemia. Woman often has rapidly increasing insulin resistance with need for weekly insulin dose adjustments. Woman often has a leveling off of insulin requirements or a small decrease. 8. Endocrine Guidelines

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