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162,700 |
3744718-1
| 23,960,457 |
noncomm/PMC003xxxxxx/PMC3744718.xml
|
Intramedullary Spinal Cord Metastasis in Renal Cell Carcinoma: A Case Report of the Surgical Experience
|
A 44-yr-old male was diagnosed with renal cell carcinoma on the left kidney with lung metastasis and was treated by molecular target agent therapy (Sunitinib, 37.5 mg/day, per oral, 4/2 week scheduled) without surgery (). After 6 months later from a diagnosis of RCC, he presented rapid progressive paraparesis and both leg numbness. His motor power of both hip flexion was 3/5 (0; none, 5; normal) and other distal lower extremity was 4/5.\nMagnetic resonance image (MRI) of the spine revealed intramedullary mass lesion on T12 level (). This lesion showed iso-signal intensity (SI) on T1 weighted images (T1WI) and high-SI on T2 weighted images (T2WI) with significant rim enhancement after gadolinium based contrast agent injection. Extensive edematous infiltration on intramedullary space which shows high SI on T2WI was checked up to the upper thoracic level.\nFocal radiotherapy on the spine was initiated due to his refusal for surgery. Over the following 10 days during radiotherapy, his neurological deficit rapidly progressed to 2-3/5 on the right lower extremity and 0-1/5 on the left lower extremity. Under the umbilicus level (sensory dermatome level T10), all components of sensory, including pain, touch, vibration and temperature, were decreased and painful paresthesia on both lower extremities was checked. He also complained of urinary incontinence and decreased anal sphincter tone was checked on the neurological examination.\nFor the rapid progression of neurological deficit, emergency surgery was performed. Under the neural integrity monitoring (NIM-SPINE, Medtronic Sofamor Danek, USA), laminectomy of T10, T11, and T12 was performed. Under the intra-operative ultrasonographic view, mass lesion was confirmed near the T12 pedicle. After midline dural incision, arachnoid membrane was opened. For abnormal lesion was not checked on the surface of the spinal cord, posterior myelotomy through midline posterior sulcus was performed. After gentle dissection, soft and grayish colored tumor lesion distinguishable on microscopic view was checked. Microsurgical removal of the tumor with the use of Cavitron Ultrasonic Aspirator (CUSA, Valleylab, USA) was performed. On the neural integrity monitoring, no abnormal signal change was checked during the whole operation.\nAfter surgery, painful paresthesia of both lower extremities was immediately improved on the visual analogue scale (VAS) from 7 to 2. Significant improvement of motor power to self-ambulation with walking stick was checked on an outpatient follow-up after 2 months later from surgery. Follow up MRI imaging after 2 months later from surgery, enhancing mass lesion was nearly total removed and edematous infiltration on T2WI was significantly reduced ().\nOn a histological examination, it was composed of nests of clear tumor cells with intermediate nuclear grade vascular meshwork and showed a strong cytoplasmic reaction within tumor cells in immunohistochemical staining for both cytokeratin and vimentin ().\nOn the neurological examination of 6 months from surgery, the motor power of both lower limbs was improved to 3-4/5, and he could walk by himself with the assistant of a walking stick.
|
[[44.0, 'year']]
|
M
|
{'11583203': 1, '4346871': 1, '8857717': 1, '3659245': 1, '11154816': 1, '30069434': 1, '33051797': 1, '16778676': 1, '614063': 1, '32637205': 2, '8876713': 1, '4052974': 1, '6260415': 1, '30258759': 1, '15526223': 1, '30643818': 1, '84065': 1, '23960457': 2}
|
{'7332509-1': 1}
|
162,701 |
3744719-1
| 23,960,458 |
noncomm/PMC003xxxxxx/PMC3744719.xml
|
Therapeutic Hypothermia Following Emergent Coronary Artery Bypass Grafting After Failed Percutaneous Coronary Intervention in a Comatose Post-Cardiac Arrest Patient
|
A 60-yr-old female without a significant past medical history presented to the emergency department (ED) with cardiac arrest on March 14, 2012. A security guard found her at her apartment and called for the emergency medical services (EMS). EMS personnel transported her to the ED without patient monitoring or basic life support for 10 min. She had collapsed 25 min before ED arrival and was in asystole. Return of spontaneous circulation (ROSC) was achieved after 14 min of advanced life support, including the application of 3 shocks, orotracheal intubation, and the administration of 4 mg adrenaline and 300 mg amiodarone. Her initial blood pressure was 68/49 mmHg, her pulse was 90 beats per minute, and her tympanic temperature was 36℃. The patient was comatose (Glasgow coma scale score E1VTM2=4) with a pupillary light reflex and self-respiration. The initial electrocardiogram showed atrial fibrillation with ST-segment elevation in leads V5-6, II, III, and aVF, indicating STEMI (). A blood gas analysis was significant for severe acidosis (pH 6.97; lactate 6.1 mM/L; BE -10.8). A 2D-echocardiogram performed by a cardiologist in the ED revealed moderate left ventricle systolic dysfunction, an ejection fraction of 30%-40% and akinesis of the basal-apical inferolateral wall and lateral wall. At 55 min after ROSC, she underwent PCI, which failed because the guide wire could not pass the lesion of completely occluded left proximal circumflex artery (LCx) due to extreme angulation. She also had 70% diffuse stenosis of the proximal and middle left anterior descending coronary artery on coronary angiogram. An intra-aortic balloon pump was applied because of her unstable vital signs, and she was transferred to the operating room for an emergent CABG at approximately 4 hr after ROSC. A hard segment in the proximal area of the LCx was observed in the heart, and the aortocoronary saphenous vein graft (SVG) was anastomosed to the second obtuse marginal branch of the LCx. The CABG was finished in 6 hr 20 min. She was brought to the intensive care unit (ICU) at 10 hr 25 min after ROSC. On arrival in the ICU her rectal temperature was 34.6℃. For cerebral protection, TH was initiated using an endovascular cooling system (Alsius Corp., Irvine, CA) with sedative and neuromuscular blocker infusion despite the risk of hypothermia-induced coagulation abnormalities after CABG. At 2 hr after TH initiation, her body temperature reached the target rectal temperature of 34℃, which was maintained for 12 hr. The patient was actively rewarmed to 36.5℃ at a rate of 0.25℃/hr (). During the maintenance of TH, her 12-hr postoperative blood loss was approximately 1,060 mL, and blood products, including 4 U of fresh-frozen plasma, 1 U of packed red blood cells and 1 U of single-donor platelets, were required to stabilise the patient. During TH, several coagulation parameters were altered, including prothrombin time (PT, 15.3-50.6 sec; reference range, 10-14 sec), international normalised ratio (INR, 1.36-4.23; reference range, 0.85-1.5), and activated partial thromboplastin time (aPPT, 46.2->120 sec; reference range, 23-35 sec). No complications were associated with hypothermia, except for coagulation abnormalities. On day 2, amplitude-integrated electroencephalography showed continuous normal voltage, and somatosensory-evoked potential showed bilateral N20 peaks. The patient regained consciousness at 36 hr after ROSC and was successfully extubated on day 5. Her mental state continued to show improvement to baseline despite a minor calculation disorder. She suffered pneumonia and pancreatitis during her stay in the ward and was discharged home with a cerebral performance category scale (CPC) score of 1 six weeks later.
|
[[60.0, 'year']]
|
F
|
{'11568036': 1, '20559755': 1, '21320342': 1, '20956225': 1, '21155925': 1, '18379264': 1, '19327421': 1, '21823388': 1, '19602732': 1, '22172748': 1, '10921704': 1, '19535947': 1, '17467430': 1, '25514569': 1, '17074288': 1, '18194725': 1, '18834816': 1, '23960458': 2}
|
{}
|
162,702 |
3744737-1
| 23,964,296 |
noncomm/PMC003xxxxxx/PMC3744737.xml
|
Intercoronary Communication between the Circumflex and Right Coronary Arteries Coexisted with Coronary Vasospasm
|
A 45-year-old male presented with chest pain that was aggravated in early morning. He was a current smoker with 20 pack-years and used to have chest pain on exertion intermittently. Electrocardiogram showed ST elevation on leads from V 1-3, and chest X-ray was normal. Laboratory findings revealed mildly elevated cardiac enzyme; creatine kinase-MB and troponin I level were 6.9 ng/mL (0.0-5.0) and 0.3 ng/mL (0.00-0.16), respectively. Transthoracic echocardiography demonstrated hypokinetic mid anteroseptum with preserved left ventricular global systolic function. Coronary angiography was performed and revealed no significant luminal narrowing or occlusion of coronary arteries. However, selective injection of left coronary artery showed retrograde filling of the distal right coronary artery (RCA) from distal left circumflex artery (LCX), and right coronary injection visualized RCA and distal and mid portion of LCX simultaneously visualized (). Retrograde filling was not related to collaterals, but to a bidirectional intercoronary communication.\nWhen ergonovine was administered intravenously in a dose of 50 ug, the significant spasm of proximal left anterior descending artery (LAD) was provoked with chest pain (). The spasm and chest pain subsided promptly after intracoronary injection of 200 ug of nitroglycerin ().
|
[[45.0, 'year']]
|
M
|
{'14563300': 1, '12067937': 1, '16844248': 1, '21200121': 1, '21646842': 1, '20967149': 2, '26885496': 1, '2208265': 1, '28496514': 2, '7879964': 1, '31105760': 1, '16518672': 1, '2914314': 1, '23964296': 2}
|
{'2957636-1': 1, '5424847-1': 1}
|
162,703 |
3744738-1
| 23,964,297 |
noncomm/PMC003xxxxxx/PMC3744738.xml
|
Spontaneous Coronary Artery Dissection Mimicking Coronary Spasm Diagnosed by Intravascular Ultrasonography
|
A 35-year-old woman was transferred to the emergency room with acute onset chest pain radiating to the neck. She was a teacher of mathematics and her symptoms initially developed during a lecture. She had no past medical history of collagen tissue disease or blunt trauma to the chest, was not on any medication and had a family history of hypercholesterolemia. She reported no autoimmune disease, was not pregnant or in the early post-partum period, nor did she take an oral contraceptive pill or report any history of drug abuse. She was also not menstruating at time of admission. Risk factors for coronary artery disease were not found. At presentation, her blood pressure was 116/70 mm Hg and her heart rate was 75 beats/min. Her physical examination results were within normal limits without murmurs, rubs or gallops. There were no manifestations of connective tissue disease and the hematologic, renal parameters were normal. The initial electrocardiogram showed nonspecific T wave inversion in leads III, aVF () and the initial chest X-ray was normal without cardiomegaly or pulmonary edema. Cardiac enzymes were elevated with initial serum troponin T of 0.07 mcg/L (normal <0.014 mcg/L), creatinine kinase (CK) of 138 U/L (normal <215 U/L) and CK-MB of 8.49 mcg/L (normal <3.77 mcg/L). The total cholesterol, triglyceride, high density lipoprotein-cholesterol and low density lipoprotein-cholesterol results were 162 mg/dL (139-230 mg/dL), 33 mg/dL (48-177 mg/dL), 64 mg/dL (40-81 mg/dL) and 106 mg/dL (64-160 mg/dL), respectively. Transthoracic echocardiography demonstrated normal left ventricular systolic function, with an ejection fraction of 73% and no regional wall motion abnormalities. We performed coronary angiography under suspicion of myocardial infarction. The right coronary artery (RCA) and left circumflex artery images were normal, but there was diffuse stenotic lesion of the mid left anterior descending artery (LAD) with up to 80% luminal narrowing. The lesion slightly improved after intracoronary injection of nitroglycerine (). To evaluate the etiology of the stenotic lesion, in terms of spasm, atherosclerosis or other cause, intravascular ultrasound (IVUS, Boston scientific Co., CA, USA) was performed. IVUS showed an isolated dissection flap composed of all of the intima and media, including the internal elastic lamina and external elastic lamina, compressed by hematoma in the false lumen at the bifurcation edge of the mid LAD and diagonal branch. The dissection entry tear site to the false lumen was not detected on angiogram. Furthermore, this site was not clearly detected even on IVUS, and there was no communication between the false and true lumen (). Atherosclerotic change was not detected in this vessel (LAD) on the IVUS. 3.0×28 and 2.5×23 mm sized two Xience Prime stents (Abbott Vascular, Santa Clara, CA, USA) were deployed over the dissection from the distal portion of the mid LAD for preventing any subsequent propagation of the dissection. Subsequent angiography revealed no residual stenosis without secondary dissection and restoration of Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow (). Subsequent IVUS demonstrated a fully covered dissection lesion ().\nThe patient had a favorable clinical course and was discharged on aspirin, clopidogrel, beta blocker and statin. She remained asymptomatic without any complications at six month follow-up.
|
[[35.0, 'year']]
|
F
|
{'9093522': 1, '2522724': 1, '19046896': 1, '10025069': 1, '16179173': 1, '20104464': 1, '11696840': 1, '21744151': 1, '15298035': 1, '25774346': 1, '21127744': 2, '18513437': 2, '8172069': 1, '7091163': 1, '11835932': 1, '30546665': 1, '30546631': 1, '22800851': 1, '20440039': 1, '32850088': 2, '19496145': 1, '22442833': 1, '21041853': 1, '23964297': 2}
|
{'2995159-1': 1, '2429898-1': 1, '2429898-2': 1, '2429898-3': 1, '2429898-4': 1, '7427437-1': 1}
|
162,704 |
3744739-1
| 23,964,298 |
noncomm/PMC003xxxxxx/PMC3744739.xml
|
Pulmonary Alveolar Hemorrhage after Clopidogrel Use for ST Elevation Myocardial Infarction
|
A 62-year-old man was transferred to our hospital because of chest pain. The patient had a medical history of hypertension and had been a heavy smoker for 40 pack-years. On arrival, his blood pressure was 114/70 mm Hg, heart rate was 75 bpm, respiratory rate was 16/minute, and body temperature was 36.5℃. White blood cell count was 13930/mm3, hemoglobin was 14.2 g/dL, and platelets were 294000/mm3. Aspartate aminotransferase was 79 U/L and alanine aminotransferase was 104 U/L. Blood urea nitrogen, creatinine, and electrolytes were all within normal limits. Electrocardiogram showed an ST elevation in the V 1 through V 6 leads, and ST depression in the II, III and aVF leads. The patient was diagnosed as having ST elevation myocardial infarction. After the patient had taken 300 mg aspirin and 600 mg clopidogrel, he underwent primary PCI. Coronary angiograms showed 99% stenosis of the mid-left anterior descending artery (). Therefore, a coronary stent (Endeavor®, Zotarolimus-Eluting Coronary Stent, 3.0×26 mm, Medtronic) was implanted (). The patient was admitted to the coronary care unit (CCU) and triple antiplatelet therapy was started.\nOn the third day after admission, the patient coughed up bloody sputum and had a fever. The chest radiograph showed mild infiltration of both upper lung fields (). We diagnosed pneumonia and administered piperacillin/tazobactam. The patient's vital signs, symptoms, and cardiac markers improved; then the patient was transferred to the general ward.\nOn the sixth day after admission, the patient complained of dyspnea and continuous bloody sputum. Chest computed tomography with enhancement showed patchy areas of ground-glass opacity in a central distribution in both upper lobes (). The findings were consistent with diffuse alveolar hemorrhage. We considered triple antiplatelet therapy as the most likely cause. We discontinued cilostazol and carried out a study to discriminate between alveolar hemorrhage caused by antiplatelet therapy and alveolar hemorrhage due to a different disease. Anti-phospholipid antibody, anti-cardiolipin antibody, P-antinuclear and antineutrophil cytoplasmic autoantibodies (ANCA), C-ANCA, ANA, complement 3, complement 4, anti-ds deoxyribonucleic acid antibody, anti-Leptospira antibody were all negative. The patient's platelet count was 257000/mm3.\nOn the eleventh day after admission, the patient suddenly fell into acute respiratory failure and was transferred to the CCU. We intubated the patient. The chest radiograph showed diffuse infiltration in both lung fields (). Bronchoscopy revealed diffuse hemorrhage of the bronchial walls in the bilateral lung fields. We discontinued clopidogrel on the ninth day after admission.\nOn the seventeenth day after admission, his symptoms improved and we extubated the patient. The chest radiograph showed decreased infiltration of both the lung fields (). The patient was transferred to the general ward. The patient wanted to be transferred to another hospital. On the third day after the transfer, the patient died of ventricular fibrillation at the hospital to which he had been transferred.
|
[[62.0, 'year']]
|
M
|
{'19942100': 1, '12042732': 1, '20837828': 1, '20817281': 1, '15313956': 1, '32166033': 2, '34285493': 2, '27044406': 1, '16751677': 1, '14504182': 1, '27843786': 2, '28154663': 1, '21514251': 1, '11435642': 1, '16908769': 1, '23964298': 2}
|
{'8285274-1': 1, '7060896-1': 1, '5100679-1': 1}
|
162,705 |
3744740-1
| 23,964,299 |
noncomm/PMC003xxxxxx/PMC3744740.xml
|
A Delayed, Unusual Non-Cardiogenic Pulmonary Edema after Intravascular Administration of Non-Ionic, Low Osmolar Radiocontrast Media for Coronary Angiography
|
A 56-year-old male was admitted to the outpatient clinic with a 6-day history of chest pain on exertion lasting for over 10 minutes per episode. The patient has been treated for hypertension and diabetes mellitus at our hospital since 2009. He had no history of allergies. On admission, his blood pressure and pulse rate were 95/55 mm Hg and 70 bpm, respectively. The electrocardiogram showed ST-segment elevation with Q-wave formation in II, III, and aVF, and reciprocal ST-segment depression in I, aVL, and V 4-6 (). His troponin-T level was elevated to 3.03 ng/mL (reference range: 0-0.100 ng/mL), while creatine kinase-MB was within the normal limit. His initial chest radiography showed no pulmonary edema and no cardiomegaly (). Echocardiography showed hypokinesia from the base to the mid-inferior wall with preserved left ventricle (LV) systolic function (Ejection fraction=56% by Biplane modified Simpson's formula). He was diagnosed with recent myocardial infarction. Coronary angiography demonstrated a critical stenosis in the mid right coronary artery (RCA) with thrombolysis in myocardial infarction grade I flow () and an insignificant stenosis in the left coronary artery. He underwent stent placement (a 4.0×18 mm Everolimus-eluting stent) in the mid RCA (). The patient was given 200 mL of iopamidol (Isovue-300, Dongkook pharmaceuticals, Seoul, Korea), a non-ionic, low osmolar (616 mOsm/kg water) RCM. About 3 hours after the procedure, he developed a fever of above 38℃. However, the patient was not experiencing a rash, itching, angioedema, rales or wheezing in the lung field. The patient did not complain of any other symptoms, such as dyspnea, and his vital signs were stable. We decided to observe him; we took his bacterial and viral cultures. The next day, high fever persisted and the patient started to complain of mild dyspnea. Chest radiography showed diffuse bilateral alveolar infiltrates (). Arterial blood gas analysis revealed a pH of 7.436, a PCO2 of 30.2 mm Hg, a PO2 of 75.9 mm Hg, and an oxygen saturation of 95.7%, while receiving nasal cannula oxygen at a flow rate of 5 L/min. The patient's white blood cell count was 9400/mm3, but eosinophil levels were not raised. Follow-up echocardiography revealed preserved LV systolic function without interval change, in comparison with the initial study. The elevated troponin-T level was on the decline from baseline. We did not perform invasive hemodynamic monitoring of Swan-Ganz catheterization or central line insertion. At first, we dealt the patient's condition as cardiogenic pulmonary edema due to fluid or osmolar overload. The patient received intravenous furosemide and antibiotics. However, he was still febrile (up to 40℃) and pulmonary edema became progressively worse despite negative volume balance (). Subsequently, the patient was diagnosed with NCPE manifesting as a delayed reaction to RCM despite some limitations, such as the absence of eosinophilia and pulmonary wedge pressure monitoring. The patient was promptly given intravenous hydrocortisone and antihistamine. We cut his dosage of diuretics and discontinued antibiotic treatment after 48 hours when all of his cultures were negative. The patient's fever stopped and the pulmonary edema started to improve one day after the initiation of steroid injection (). The patient was discharged from the hospital 7 days after the index procedure with complete recovery from pulmonary edema ().
|
[[56.0, 'year']]
|
M
|
{'12130948': 1, '15647034': 1, '19563991': 1, '7499690': 1, '9498876': 1, '21779853': 1, '28321244': 1, '11305580': 1, '7583844': 1, '16001811': 1, '19805846': 1, '8915300': 1, '29942165': 2, '11937188': 1, '12541128': 1, '16688432': 1, '11550775': 1, '23964299': 2}
|
{'6005305-1': 1}
|
162,706 |
3744741-1
| 23,964,300 |
noncomm/PMC003xxxxxx/PMC3744741.xml
|
Severe Pulmonary Hypertension in Primary Sjögren's Syndrome
|
A 65-year-old female was presented with dyspnea on exertion (New York Heart Association, NYHA class III) for over a period of 1 year. For 5 years, she had complained of dry mouth, intermittent dry eye, and gritty feeling under the eyelids. However, she did not have Raynaud's phenomenon or parotid swelling. She denied taking anorexiants or other drugs. Further, she did not have any sort of family history.\nBlood pressure, pulse rate, and respiration rate were 114/78 mm Hg, 92 per minute, and 24 per minute, respectively. Cardiovascular examination revealed a grade 2/6 systolic murmur in the left low parasternal area, a more accentuated P2 than A2, and both jugular veins that are both slightly distended.\nLaboratory exam disclosed polyclonal hypergammaglobulinemia identified by slightly increased total protein (8.2 g/dL, normal 6.5-8.1 g/dL) and gamma globulin (22.4%, normal 11.1-18.8%). Autoantibody tests showed positive results for anti-nuclear antibodies (1 : 640, speckled, anticytoplasmic antibody: positive), rheumatoid factors (57.10 IU/mL, normal <14 IU/mL), and anti-Ro (SSA) antibodies (3+), while anti-neutrophil cytoplasmic antibodies (ANCA), antibodies to La (SSB), double stranded DNA, Sm, ribonucleoprotein (RNP), topoisomerase-I (Scl-70), histidyl-tRNA synthetase (Jo-1) were negative. Antibodies to cardiolipin and lupus anticoagulant were also negative. Serum complements protein levels were all slightly decreased (C3 87.0 mg/dL, normal 90-180 mg/dL; C4 7.2 mg/dL, normal 10-40 mg/dL; CH50 21.6 U/mL, normal 34-71 U/mL). Anti-human immunodeficiency virus antibodies, hepatitis B virus antigen and antibodies, and anti-hepatitis C antibodies were all negative. Erythrocyte sedimentation rate was increased (42 mm/hour, normal 0-20 mm/hour). Hemoglobin, white blood cell and platelet counts, and urine test were within normal limits. N-terminal pro B-type natriuretic peptide level was 1469.1 pg/mL (normal 0-125 pg/mL). Creatinine kinase-MB and troponin-I were also within normal limits. Arterial blood gas analysis in room air showed pH 7.44, pO2 78 mm Hg, and pCO2 34 mm Hg.\nPulmonary function test revealed normal ventilatory pattern with normal CO diffusion capacity. Chest X-ray demonstrated grossly normal lung fields with a mildly enlarged right ventricle. Electrocar-diogram showed tall, peak P waves in lead II, III, and aVF, suggesting right atrial enlargement. Transthoracic echocardiography showed a mildly enlarged and thick right ventricle, hypokinetic right ventricular free wall, grade II tricuspid regurgitation, and peak tricuspid regurgitation jet velocity of 4.64 m/s with an estimated right ventricular systolic pressure (RVSP) of 91.1 mm Hg (). Transthoracic and transesophageal echocardiography excluded any other congenital, valvular, and myocardial diseases. Right heart catheterization also revealed severe PH. Pulmonary artery pressure was 74/27 mm Hg (mean 46 mm Hg) with a pulmonary capillary wedge pressure of 7 mm Hg (). Cardiac index was calculated as 2.27 L/min/m2 and pulmonary vascular resistance was 11 Wood units. Elevated pulmonary artery pressure was not significantly decreased with adenosine infusion. Chest computed tomography and lung perfusion scan did not show abnormal findings compatible with pulmonary embolism. Schirmer's test was positive. Salivary gland scintigraphy disclosed severely decreased tracer uptakes in both parotid and submandibular glands.\nConsidering her clinical, laboratory, cardiologic, imaging findings and the Revised International Classification Criteria for Sjögren's Syndrome by the American-European Consensus Group, she was clearly diagnosed with severe PH associated with primary Sjögren's syndrome. She was treated with 62.5 mg endothelin receptor antagonist (Bosentan®) twice a day for the initial month and 125 mg twice a day for the following months, 200 mg hydroxychloroquine twice a day, 50 mg azathioprine twice a day, and topical corticosteroid and sodium hyaluronidate eye drops. A follow-up transthoracic echocardiography after 6 months of treatment showed somewhat improved right ventricle contractility and decreased estimated RVSP (65.5 mm Hg) compared to the initial exam (). Equally, her dyspnea symptom was much improved and uneventfully, she is being followed up at an outpatient clinic.
|
[[65.0, 'year']]
|
F
|
{'20692541': 1, '14714969': 1, '7294510': 1, '6148159': 1, '16980719': 1, '16014687': 1, '8110261': 1, '17873760': 1, '6374900': 1, '8432515': 1, '10325906': 1, '16840400': 1, '14995003': 1, '12006334': 1, '6859087': 1, '34616495': 1, '848800': 1, '11859694': 1, '15226160': 1, '23964300': 2}
|
{}
|
162,707 |
3744784-1
| 23,619,485 |
noncomm/PMC003xxxxxx/PMC3744784.xml
|
Ocular toxoplasmosis associated with scleritis
|
A 26-year-old woman presented with complaints of sudden onset of severe pain, redness, and defective vision in her right eye since 10 days. There was no history of trauma or any prior symptoms in the affected eye. There was no history suggestive of any other systemic illness. She denied any history of intravenous or other drug use.\nShe gave history of being treated with oral medications, for decreased vision in her left eye, 5 years earlier.\nHer best corrected visual acuity was 20/200 in OD and 20/20 in OS. Intraocular pressure was normal in both eyes. Anterior segment examination of her right eye showed a diffuse non-necrotizing scleritis, localized inferiorly []. There were few fresh granulomatous keratic precipitates on the inferior cornea and 2+ cells and flare in the anterior chamber. Lens was clear. The anterior vitreous had 3+ cells. Anterior segment examination of the left eye was within normal limits.\nOcular fundus examination of the right eye revealed a 3+ vitreous haze suggestive of intense vitritis. Through the haze the disc was barely seen, but the characteristic “Headlight in Fog” appearance of macular retinochoroiditis was lacking. The inferior periphery, however, showed a circumferentially oriented large yellow lesion involving the inferonasal quadrant, with the posterior extent till the equator. Another similar lesion was noted in the superonasal periphery, discontinuous with the main lesion. Her left ocular fundus showed multiple confluent pigmented chorioretinal scars, starting in the periphery of the nasal to the inferotemporal quadrants, with tongue-shaped extensions posteriorly, beyond the equator. There were two round scars around one disc diameter in size above the superotemporal arcade [Figs. and ].\nB scan Ultrasonography of right eye revealed associated posterior scleritis, but without any evidence of retinal detachment [].\nIn view of intense vitritis with confluent peripheral retinitis in one eye of an otherwise healthy woman with similar location of scars in the other eye, a provisional diagnosis of acute retinal necrosis with scleritis was made. A vitreous tap was performed under aseptic precautions through the inferotemporal quadrant, avoiding the area of scleritis. She was empirically started on oral valacyclovir in the recommended dose. Topical Dexamethasone drops were started 6th hourly along with Homatropine eye drops instilled 12th hourly in the right eye. Oral steroids were added after 48 h of starting oral antivirals. The complete blood picture was normal; a purified protein derivative (PPD) test dose given on presentation was negative. Her chest X-ray was normal and systemic examination by a physician did not reveal any evidence of systemic tuberculosis or Diabetes mellitus.\nSerology for syphilis and Human immunodeficiency virus were negative.\nThe vitreous sample subjected to multiplex polymerase chain reaction (PCR) test, revealed the presence of Toxoplasma. The sample was negative for Herpes simplex virus, Herpes zoster virus, and Mycobacterium tuberculosis. She was started on oral trimethoprim/sulfamethoxazole (160 mg/800 mg b.i.d.) and Azithromycin (500 mg o.d.), along with oral steroids in the recommended doses. The antiviral, which had shown no response for 3 days, was stopped.\nOn review after a week, she was tolerating her treatment well and showing signs of improvement. At the end of 3 weeks, her visual acuity had improved to 20/30 in the affected eye.\nThe scleritis had completely resolved, and the areas of peripheral retinochoroiditis were scarring with pigmentation. She completed the course of antitoxoplasma treatment, and is currently asymptomatic.
|
[[26.0, 'year']]
|
F
|
{'11202921': 1, '12441842': 1, '32823398': 1, '12140026': 1, '15791166': 1, '3226688': 1, '18400917': 1, '14644206': 1, '23619485': 2}
|
{}
|
162,708 |
3744785-1
| 23,803,483 |
noncomm/PMC003xxxxxx/PMC3744785.xml
|
Periorbital dirofilariasis—Clinical and imaging findings: Live worm on ultrasound
|
A 2-year-old female child presented with acute onset of periorbital edema in right eye. She was initially diagnosed as preseptal cellulitis and treated with systemic antibiotics. There was mild resolution of edema, but a cystic swelling was apparent in the right upper eyelid.\nUltrasound was performed with high-resolution probe (8MHz) and showed a well-defined cyst approximately 2.5×1.5 cm in the lateral part of right upper eyelid. The cyst showed within it a coiled structure with parallel echogenic walls []. It showed continuous movement which represents the live worm. MRI was done to know any deep intraorbital extension and exclude other intraorbital abnormalities. MRI of orbits showed a cyst in the lateral part of upper eyelid which showed hyperintense signal on coronal short-tau inversion recovery image [], hypointense signal on coronal T1 image [] and revealed rim enhancement on post-contrast T1-weighted fat saturated images [ (coronal) and (sagittal)]. The cyst was confined to the upper lid. Ill-defined intermediate signal intensity was seen on STIR images [] within the cyst which may represent the worm.\nSurgical excision of the parasitic cyst was done through an upper lid crease incision. The cyst was adherent to the levator palpebrae superioris muscle. It contained a live motile worm measuring about 9 cm in length []. Histopathological examination [] showed a worm with thick cuticle, muscle coat, longitudinal and transverse striations and double uterus. Based on histopathological appearance, the worm was identified as D.repens.\nPost-operatively, the child was asymptomatic except for a mild residual ptosis which was improving.
|
[[2.0, 'year']]
|
F
|
{'8778658': 1, '30567586': 1, '12583426': 1, '2607577': 1, '12082307': 1, '10094355': 1, '11556571': 1, '20090252': 1, '26846596': 1, '12502905': 1, '24492509': 1, '34790837': 2, '27134918': 1, '2644857': 1, '11243759': 1, '16505560': 1, '6650744': 1, '18579995': 2, '27266512': 2, '23803483': 2}
|
{'8592590-1': 1, '4895828-1': 1, '2636165-1': 1}
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162,709 |
3744787-1
| 23,571,247 |
noncomm/PMC003xxxxxx/PMC3744787.xml
|
Serpiginous choroiditis and acute retinal necrosis occurring in the same patient
|
A 23-year-old male presented with the complaint of decreased vision in the right eye since 3 months. He had been treated elsewhere for right eye choroiditis with intravenous methyl prednisone acetate (IVMP) 1 g/day for 3 days followed by oral steroids and Tab Azathioprine. At presentation, he was taking Tab Prednisone 50 mg/day and Tab Azathioprine 125 mg/day. Best corrected visual acuities (BCVA) were 20/200 and 20/20 in the right and left eyes, respectively. Left eye was essentially normal on examination. Right eye revealed quiet anterior chamber and quiet vitreous cavity with a yellowish area of active choroiditis with geographic borders involving the macula in serpiginous pattern. Fundus fluorescein angiography confirmed the findings. He was diagnosed as a case of active macular serpiginous choroiditis. After obtaining physician's clearance, we prescribed Tab Prednisone 60 mg/day (1 mg/kg body weight), Tab Azathioprine 50 mg thrice a day, Tab Cyclosporine 150 mg twice a day, with antacid and calcium supplements. QuantiFERON-TB Gold test was found to be negative. On regular follow-up visits, the choroiditis lesions were noted to heal over a period of 3 months, and treatment was gradually tapered.\nAfter 3 months, patient complained of redness, pain and blurring of vision in the left eye. At this point of time, he was on Tab Prednisone 7.5 mg/day, Tab Azathioprine 50 mg/day and Tab Cyclosporine 200 mg/day. BCVA were 20/400 and 20/20 partial in the right and left eyes, respectively. Right eye examination revealed a quiet eye with healed lesions of macular serpiginous choroiditis []. Left eye had 2+ anterior chamber cells, severe vitritis, and an area of retinal whitening suggestive of necrotizing retinitis in the inferonasal periphery. A clinical diagnosis of acute retinal necrosis was made. Tab Cyclosporine and Tab Azathioprine were stopped, Tab Prednisone was hiked to 60 mg/day, and intravenous Aciclovir 500 mg thrice a day was started under monitoring. Serum ELISA for Human immunodeficiency virus (HIV) was negative. On regular examinations, vitreous haze decreased markedly and the lesion showed signs of healing []. After 1 week, intravenous Aciclovir was stopped and the patient was prescribed Tab Valaciclovir 1 g thrice a day, and Tab Prednisone to be tapered at 10 mg/week. As on last visit after 2 months, anterior chamber was quiet and retinitis had resolved significantly. The patient is under regular follow-up.
|
[[23.0, 'year']]
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M
|
{'12854034': 1, '12355692': 1, '12441719': 1, '8172275': 1, '17504853': 1, '10966948': 1, '6757060': 1, '20385534': 1, '20172069': 1, '23571247': 2}
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{}
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162,710 |
3744788-1
| 23,571,241 |
noncomm/PMC003xxxxxx/PMC3744788.xml
|
Choroidal neovascularization secondary to choroidal nevus simulating an inflammatory lesion
|
A 16-year-old girl was referred to our clinic with a diagnosis of neuroretinitis or juxtapapillary chorioretinitis. The patient had a 3-week history of decreased vision and metamorphopsia in her left eye. Her medical and family history were unremarkable. There was no history of trauma or high myopia. Before referral, systemic work-up for tuberculosis, sarcoidosis, syphilis, Lyme disease, brucellosis, and toxoplasmosis was negative. At our initial visit, best-corrected visual acuity was 20/20 in the right eye and counting fingers in the left eye. There was a mild relative afferent pupillary defect in the left eye. Biomicroscopic examination was within normal limits. There was no cellular reaction in the anterior chamber or vitreous cavity. The intraocular pressure was 16 mmHg in both eyes. Fundus examination of the left eye revealed a juxtapapillary, elevated, white chorioretinal lesion consistent with CNV that was associated with exudation and retinal edema []. The juxtapapillary choroidal nevus underlying CNV was not visible with color fundus photography [], but we were able to detect it with the brightest illumination of the indirect ophthalmoscope. Fundus fluorescein angiography (FFA) demonstrated extrafoveal, juxtapapillary CNV, and late diffuse hyperfluorescence superior to this lesion. Optic disc was normal in all phases of the angiography [Fig. –]. Optic coherence tomography (OCT) confirmed CNV with overlying intraretinal cysts and minimal subretinal fluid. A diagnosis of juxtapapillary CNV associated with a choroidal nevus was made. After a written informed consent was obtained, three consecutive monthly intravitreal bevacizumab (1.25 mg/0.05 ml) injections were performed. After treatment, best-corrected visual acuity improved to 20/50. CNV appeared inactive and smaller in size with complete resolution of exudation exposing an underlying choroidal nevus with 6 × 6 × 2.6 mm in dimensions []. OCT demonstrated gradual resolution of subretinal fluid and intraretinal cysts []. FFA revealed burnt-out fibrotic CNV with late staining and juxtapapillary hypofluorescence due to underlying choroidal nevus []. The lesion was still inactive and final visual acuity was stable throughout 2 years of follow-up.
|
[[16.0, 'year']]
|
F
|
{'19969359': 1, '7685589': 1, '12967828': 1, '12093647': 1, '15629316': 1, '25606040': 2, '23571241': 2}
|
{'4296248-1': 1}
|
162,711 |
3744789-1
| 23,571,263 |
noncomm/PMC003xxxxxx/PMC3744789.xml
|
Orbital malignant melanoma associated with nevus of Ota
|
A 45-year-old male, who had a history of diabetes, presented to our department with the complaint of swelling of left eye (LE). He had noticed a gradual increase in the swelling for the last 6-8 months. On examination, LE revealed loss of perception of light, edema of lids, and bluish black pigmentation in the periorbital region and conjunctiva []. Ocular motility was restricted in all directions. An irregular mass could be felt through the upper lid, which was fixed to deeper structures. Scar of orbitotomy was seen on the left side. On retraction of the lids, the left eyeball was shrunken and pushed upward by the mass. Only a part of the cornea was visible []. He was using scleral shell prosthesis for cosmetic correction. The right eye was normal with a visual acuity of 6/9. Ophthalmoscopic examination of right eye showed few microaneurysms in the macular area. Patient revealed history of bluish black discolouration around the LE, since childhood. Approximately 13 years back, he had noticed protrusion of LE and was diagnosed elsewhere as orbital malignant melanoma. It was managed with lateral orbitotomy for excision biopsy followed by external beam radiotherapy. Later,cosmetic correction with scleral shell prosthesis was given elsewhere, over the phthisical LE. Four years back, in 2005, he attended the Oncology department of Amala Institute of Medical Sciences, for check up. Computerized tomography (CT) scan and magnetic resonance imaging (MRI) of left orbit showed orbital lesion and he was given Cobalt-60 teletherapy. There was no bony metastasis or extraorbital extension of the lesion as per records.\nIn late 2008, he was referred to us with recurrence of left orbit swelling which gradually increased in size. Repeat CT showed recurrent malignant melanoma in left orbit with extension into the optic canal and lateral wall of orbit []. The orbit was filled by the pigmented tumor with infiltration into the orbital tissues and periorbita. Histopathology showed a mass of brownish soft tissue measuring 3.5 × 3 × 1.5 cm behind the eyeball. Serial sectioning of the eyeball showed atrophic eyeball. Microscopic examination showed cellular neoplasm arranged in a fascicular pattern composed of spindle cells having prominent nuclei and eosinophilic cytoplasm []. Mitotic figures were frequent and cells were laden with dark brown melanin pigment. The eyeball was distorted by the neoplasm. There was infiltration into the optic nerve, orbital muscles, and retrobulbar fibroadipose tissue. In view of the extensive spread of the tumor locally, a modified exenteration with frontal flap repair was done on the left side. Adjuvant chemotherapy was given after wound healing. During follow-up, prosthesis for LE was given []. After 1 year of follow-up, the patient did not have any recurrence or metastasis.
|
[[45.0, 'year']]
|
M
|
{'29326884': 1, '16234467': 1, '14673306': 1, '26265645': 2, '2730864': 1, '3349013': 1, '32900269': 1, '12045961': 1, '19850543': 1, '23571263': 2}
|
{'4550988-1': 1}
|
162,712 |
3744790-1
| 23,803,484 |
noncomm/PMC003xxxxxx/PMC3744790.xml
|
Pseudomonas aeruginosa endophthalmitis masquerading as chronic uveitis
|
A 65-year-old male presented with decreased vision in the left eye of 15-day duration which was gradual in onset, progressive in nature, and associated with pain and redness. The patient had undergone an uneventful cataract surgery in another center, 10 months back, with good visual recovery. He had had similar episodes during the past 4–5 months and had been treated with steroids (topical and systemic) elsewhere for chronic uveitis. As his symptoms worsened with steroids this particular time, the patient was referred to us. He had lost vision in his right eye due to trauma 20 years back.\nOn examination of the left eye, his vision was perception of hand movements. Anterior segment findings included circumcorneal congestion and mild corneal haziness with keratic precipitates and pigments over the endothelium. The anterior chamber showed cells and flare 2+. The pupil was irregular in shape and dilated. The posterior chamber intraocular lens (IOL) was in situ with pigment dispersion on the IOL and yellowish exudates behind it. Details of the fundus were not visualized except for a yellow glow []. B-scan ultrasonography showed multiple dot like echoes with low to moderate reflectivity in the vitreous suggestive of inflammatory debris []. All other systemic investigations were normal except for a low hemoglobin level of 8mg/dL.\nAn aqueous tap was done and subjected to potassium hydroxide (KOH), Gram stain, and culture/sensitivity, followed by intravitreal antibiotics (ceftazidime 2.25 mg/0.1 mL and vancomycin 1 mg/0.1 mL). Aqueous tap revealed P.aeruginosa sensitive to ciprofloxacin. The patient was then started on systemic (tablet 750 mg twice a day) and intravitreal ciprofloxacin (0.2 mg/0.1 mL). As there was clinical improvement with this treatment regimen, repeat intravitreal injections of ciprofloxacin and vancomycin were given on two occasions subsequently. Once the exudates cleared, the patient was restarted on systemic steroids with one dose of intravitreal dexamethasone (400 μg/0.1 mL). The patient improved symptomatically and on the last follow-up at two months, his vision was counting fingers at three meters. Examination of the fundus revealed clearing media with the disc and third-order blood vessels well seen [].
|
[[65.0, 'year']]
|
M
|
{'11781270': 1, '30930672': 1, '19304082': 1, '9642602': 1, '17038190': 1, '20379462': 2, '20404450': 1, '14736778': 1, '24881621': 1, '12383826': 1, '23803484': 2}
|
{'2850999-1': 1}
|
162,713 |
3744858-1
| 23,961,301 |
noncomm/PMC003xxxxxx/PMC3744858.xml
|
A Complication During Femoral Broaching in Total Hip Arthroplasty: \nA Case Report
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A 60 year old male was scheduled for THA for left primary end-stage hip osteoarthritis (OA). (Fig. ) In the operating room, a spinal-epidural anesthesia was administered. After positioning for posterior-approach THA, an 8 cm incision was placed over the left hip. The short external rotators were indentified, released and tagged with stitches. Elevation of the gluteus minimus exposed the capsule which was subsequently incised and tagged. The hip was dislocated, the neck cut and the femoral head removed. The acetabulum was prepared in the usual fashion and a size #58 no-hole shell (R3, smith&nephew, Memphis, TN) was press-fitted.\nTo start the preparation of the proximal femoral canal, a box osteotome was used to open the canal. After reaming for a size #14 stem (Synergy, smith&nephew, Memphis, TN), the femur was broached for a size #14 stem. Trial reduction with a standard offset neck and a plus eight head showed restoration of the lesser trochanter-to-center distance (LTC) and the femoral offset.\nAfter trial reduction, an attempt to remove the broach failed, and despite using a heavy mallet and ultimately a removal slap hammer it was not possible to remove the broach. After trying to remove the broach for 30 minutes, flexible osteotoms were utilized to carefully loosen up the proximal part. After one and half hours of repeated extraction attempts, we decided to stop.\nConsidering the configuration of the proximal femoral canal, it was assumed that the broach got hung up distally. Therefore, the decision for a second incision was made to release the broach distally. The exact length of a #14 broach was measured and an 8 cm skin incision was placed proximal to the distal tip of the implant. After dissection of the vastus lateralis, a drill was placed on the posterior aspect of the femur distal to the broach tip which was confirmed by an intraoperative radiograph (Fig. ).\nMidway between the neck cut and the distal tip, a second posterior drill hole was placed, leaving 5-6 cm of bone proximally. Using an oscillating saw, the two drill holes were connected. After completing the posterior femoral split, the broach could now easily be extract.\nHereafter, a total of 6 Dall-Miles cables (Stryker, Mahwah, NJ) were applied: one just proximal and distal to the lesser trochanter (LT); two along the osteotomy line; and one at the tip of the implant and one distal. The cable wires were tightened and after over reaming the distal canal the same broach was re-inserted. Trial reduction showed restoration of the lesser trochanter to center distance and the femoral offset.\nAt this time, the broach could be smoothly removed and a size #14 stem was impacted achieving excellent press-fit. A +8, #36 head (Oxinium, smith&nephew, Memphis, TN) was added and the hip was reduced.\nThe patient was instructed partial weight bearing 20% for 4 weeks, before weight bearing as tolerated was initiated.\nAt the 6-week and 12-week routine follow-up appointments, the femoral implant was found to be stable with no focal lucencies (Fig. ).
|
[[60.0, 'year']]
|
M
|
{'3416526': 1, '14565592': 1, '18534482': 1, '3720113': 1, '1991771': 1, '22570223': 1, '16457913': 1, '11764371': 1, '28199936': 1, '3326881': 1, '4737675': 1, '34327165': 2, '34466637': 1, '19504161': 1, '19487522': 1, '8363862': 1, '9195321': 1, '1634574': 1, '3416522': 1, '23961301': 2}
|
{'8310626-1': 1}
|
162,714 |
3745098-1
| 23,960,318 |
noncomm/PMC003xxxxxx/PMC3745098.xml
|
Rare case of nasolacrimal duct opening into face
|
A 22-year-old male presented with pinkish looking pit lateral to the left ala of nose with history of repeated purulent discharge with intermittent conjunctivitis since birth []. History of intermittent mild pain and tenderness in the left cheek improved with antibiotics. There was no history of excessive lacrimation from left eye. On clinical examination, a pinkish opening about 5 mm in diameter was seen inferolateral to the base of left ala, and on palpation there was no bony indentation or notching on the nasolacrimal and infraorbital region. However on moderate pressure over the lateral wall of nose there was increased discharge from the opening. The patient otherwise had a normally developed face with no evidence of any cleft. Injecting saline into this opening showed exit of saline from the punctum of inferior canaliculus confirming the nasolacrimal duct []. All the routine investigations were within normal limits. CT scan or MRI was not done because of resource constrains and the diagnosis was confirmed by injecting saline into the duct.\nThe patient was operated under general anesthesia. We cannulated the lower end of the nasolacrimal duct with no. 5 infant feeding tube. The alar facial groove was marked with methylene blue and infiltrated with 1:20000 adrenaline solution. A circular incision was placed around the swelling which was extended superiorly in the alar-facial groove taking care not to injure the nasolacrimal duct with the feeding tube in place as a guide The lower third of the duct was dissected circumferentially []. The lower part of the incision was deepened till the mucosa lining the lateral wall of nose so as to reach the inferior meatus. The distal opening of the nasolacrimal duct was cut 2 mm on the medial side and sutured with the opening in the nasal mucosa with 4.0 catgut. The incision was closed with 6.0 Prolene []. Patient was on intravenous ceftriaxone 1 g IV followed by oral cefixime for five days, Gentamicin eye drop for two weeks. The stent and the sutures were removed after five days. Patient was asymptomatic three months later when followed up.
|
[[22.0, 'year']]
|
M
|
{'3964482': 1, '8196943': 1, '12919073': 1, '12867406': 1, '2393773': 1, '23960318': 2}
|
{}
|
162,715 |
3745099-1
| 23,960,319 |
noncomm/PMC003xxxxxx/PMC3745099.xml
|
Gluteal flap for omphalocele repair in a case of epigastric heteropagus: A novel approach for surgical management
|
A 2-day-old male was referred to us as a case of conjoined twins. The baby was a full-term normal vaginal delivery, first in birth order, born out of non-consanguineous marriage. The mother was 25 years old, not registered for antenatal care and with no antenatal ultrasound scans done.\nOn examination, there was an incomplete parasitic twin attached to the epigastrium of the auto-site with an omphalocele above. The parasitic twin had well-developed lower limbs, a penis with urethra, which was blind beyond its root, a poorly developed scrotum without testes and an anal dimple without an anal opening []. The auto-site had an omphalocele, the contents of which were liver and intestine. No other obvious congenital anomalies were noticed. On auscultation, a pan systolic murmur was audible, and the second heart sound was loud.\nOn investigating, the haematogical profile was normal. Radiographs showed normally developed bones in both lower limbs and pelvis of the parasite. 2D-echocardiography (2D-ECHO) revealed multiple cardiac anomalies (atrial septum defect [ASD], ventricular septum defect [VSD], patent ductus arteriosus [PDA], overriding of aorta, and peripheral pulmonic stenosis). Ultrasonography with Doppler showed the parasitic twin being supplied by a single vascular pedicle arising from the epigastric region. The omphalocele contained right lobe of liver and bowel loops. The patient was taken up for surgery after the complete work-up.\nOperative management consisted of the removal of the parasitic twin and covering the omphalocele with the gluteal skin flap secured from the parasitic twin. The gluteal skin flap was based on the cutaneous branches of the superficial epigastric vessels of the auto-site and superior gluteal perforating artery of the parasite. During removal of the parasitic twin, a large section of skin and fat (flap) was raised by making an incision parallel to the iliac crest [Figures and ]. The fat on the superolateral aspect of the flap was dissected down to the level of the deep fascia covering thr gluteus maximus muscle. This flap was then used to cover the omphalocele of auto-site [].\nPost-operative course was uneventful, except for infection along the edges of the skin flaps, which was managed conservatively. Patient is asymptomatic after 6 months of follow-up.
|
[[2.0, 'day']]
|
M
|
{'26023494': 2, '21292102': 1, '14700156': 1, '1552454': 1, '22666802': 2, '3421755': 1, '16034774': 1, '8340868': 1, '34467432': 1, '11240507': 1, '23960319': 2}
|
{'4420321-1': 1, '3351264-1': 1, '3351264-2': 1}
|
162,716 |
3745101-1
| 23,960,321 |
noncomm/PMC003xxxxxx/PMC3745101.xml
|
Retrograde vascularisation of fibula free flap in composite oro-mandibular reconstruction
|
A 64-year-old gentleman with a post radiation recurrent squamous carcinoma of the left lower alveolus was posted for composite resection and reconstruction with fibula free flap by simultaneous two team approach. The left fibula was selected and after flap harvest, the left neck vessels (superior thyroid and facial) were assessed for the volume and character of the flow and were found to be good. The bone defect was extending from midline anteriorly to proximal ramus posteriorly and the soft-tissue defect was confined to the oral cavity []. The flap was designed in a manner so that the superior thyroid vessels were to be used as donor vessels as they were away from the previous zone of irradiation and the blood flow was also good after dissecting them and dividing to look for the volume and adequacy of blood flow. After osteotomy and preliminary intra oral in setting of the skin paddle, and during the time of anastomosis, it was found that the flow in the superior thyroid artery was inadequate after initial good flow. Routine measures such as application of warm saline, xylocaine solution and later papaverine did not improve the flow and in such a situation, the options available were\nTo open the right neck and use vessels from that side either directly or with a vein graft To use a vein graft and anastomose with the facial artery on the same (left) side as the flow in this vessel was good To use the distal end of the flap pedicle vessels for anastomosis with left facial artery, so as to establish the vascular flow in a retrograde manner. This was because the clipped distal ends of the peroneal pedicle vessels were near to the left facial artery.\nBefore exploring the opposite neck or harvesting a vein graft, a decision was made to attempt retrograde vascularisation of the flap via the distal end of the peroneal vessels. First, the arterial anastomosis was completed between the distal end of the peroneal artery and left facial artery (end-to-end) and the flow was checked. The arterial flow was good as evidenced by the pulsations of the donor and recipient vessels and with the venous outflow from the distal end of the peroneal venae commitantes. This was followed by venous anastomosis between the distal end of the peroneal venae commitantes and a tributary of the left internal jugular vein (end to end). The skin paddle bleeding was also good with a sterile needle prick. Thus, the vascularity was restored with retrograde flow and was well established by the time the intra oral inset was completed []. The neck was then closed and post-op period was uneventful. After 6 weeks, a computed tomography (CT) angiogram revealed good establishment of blood flow to the neo mandible [Figures and ].
|
[[64.0, 'year']]
|
M
|
{'22754154': 1, '10566577': 1, '20368871': 2, '21713209': 1, '22190800': 1, '22438088': 1, '21217976': 1, '11149769': 1, '22531521': 1, '23960321': 2}
|
{'2845378-1': 1}
|
162,717 |
3745102-1
| 23,960,322 |
noncomm/PMC003xxxxxx/PMC3745102.xml
|
Management of bi-canalicular block: A novel technique
|
A 45-year-old male presented to us with complaint of epiphora in the left eye and a scar at medial canthus following a road traffic accident 1 year ago, with injury to the left upper and lower eyelid involving both the canaliculi. Primary repair of laceration was performed elsewhere, with no canalicular repair. On examination, left medial canthal dystopia of 4 mm and a scar near the canalicular region was noted. Syringing was performed, which revealed proximal lower canalicular obstruction 3 mm from the punctum and 2 mm obstruction from the upper punctum. The rest of ophthalmic examination was normal.\nDuring the surgical procedure, skin incision site was marked for medial canthoplasty in the form of Z. External DCR through subciliary incision was performed. Lacrimal sac was opened and the common ostium was visualised. The stent of silicon tube, ends of which were bent at right angle, were passed retrogradely into the common internal opening and through the lower canaliculus. The tip of probe was palpable near the eyelid margin, distal to the obstruction, and a no. 15 Bard Parker's blade was used to cut down onto the probe tip, thereby creating pseudopunctum []. Similar procedure was performed for the upper eyelid. Silicone intubation was performed through common ostium, out through the lower pseudopunctum and returned through the upper pseudopunctum down through common ostium into the nose []. DCR was then completed in usual way. Monopedicle flap from the upper eyelid containing skin and orbicularis was created. The medial canthal tendon was sutured to periostium of medial orbital rim at the desired location. Upper eyelid monopedicle flap was transposed to the lower eyelid defect, created after suturing the medial canthal tendon.\nTube was removed 3 months post-operatively and on last follow-up (6 months); patient was symptom free with a patent canaliculus on syringing and good cosmesis.
|
[[45.0, 'year']]
|
M
|
{'20054416': 1, '10599666': 1, '14288913': 1, '1951585': 1, '23960322': 2}
|
{}
|
162,718 |
3745104-1
| 23,960,324 |
noncomm/PMC003xxxxxx/PMC3745104.xml
|
Penile replantation
|
A 70-year-old male with a history of psychiatric disorder presented to the casualty with a self-inflicted traumatic amputation of his penis, which he accomplished with a sharp vegetable-cutting knife in an attempted suicide. The penis was cut about 1.5 cm from the base. All but a skin-bridge of 0.5 cm width was transected in a clean-cut and the organ was ischemic and insensate [Figures and ]. The patient had no other co-morbidities.\nIn the casualty the penis was thoroughly washed with normal saline. Initially the wound was bound with a dressing and tetanus prophylaxis was administered.\nUnder general anesthesia hematoma was evacuated with 1% sodium heparin solution irrigation and gentle pressure. Nonviable tissue was debrided. Tourniquet was applied to the stump. Dissection under magnification was done and deep dorsal vein, dorsal nerves, and arteries were identified on either side. We also took special care to dissect out the cavernosal arteries on both sides.\nA 16 F Foley's catheter was inserted in a retrograde manner through the severed penile portion extending inward through the penile remnant and passed into the bladder. Urethra was spatulated and sutured over the catheter [] and corpus spongiosum was repaired using interrupted 6-0 synthetic absorbable suture. Both cavernosal arteries were anastomosed using 10-0 nylon. The cavernous bodies were reconstructed by suturing the tunica albuginea of each corpus cavernosum to the proximal corresponding segment using 4-0 polyglactic acid sutures. The dorsal vein and two arteries were anastomosed under a microscope with interrupted 9-0 identified [] and nylon sutures. Dorsal nerves were re-approximated and sutured with 10-0 nylon [].\nVascularity was reestablished within 7 hours after the amputation. The fascia and skin were sutured loosely. After releasing the tourniquet the arterial pulse and venous return were detected, the superficial penile veins displayed normal turgor.\nPostoperatively the patient was put on broad-spectrum antibiotics and heparin infusion for 5 days. Psychiatric consultation was provided. The suture-line got healed in 7 days after which dressings were discontinued []. Urethral catheter was left in-situ for 3 weeks. Cosmetic appearance of the penis was fair after two post-operative weeks. The patient was reviewed at an interval of 3 months. After 1 year patient had maintained a normal urinary flow. Since the patient was 70-year old and had psychiatric illness, the erection and sensation in the glans could not reliably be recorded.
|
[[70.0, 'year']]
|
M
|
{'20027564': 1, '6614331': 1, '22399258': 1, '26955545': 2, '32744990': 1, '19601940': 1, '17701923': 1, '33082932': 2, '22196008': 1, '834785': 1, '2073234': 1, '31143674': 1, '23960324': 2}
|
{'4733009-1': 1, '7542248-1': 1}
|
162,719 |
3745130-1
| 23,960,313 |
noncomm/PMC003xxxxxx/PMC3745130.xml
|
Surgical management of scalp arterio-venous malformation and scalp venous malformation: An experience of eleven cases
|
An 8-month-old male child presented with a 9 × 11 cm swelling in mid-frontal region extending more to the right up to the supra-orbital region. Swelling increased in size during cry and prone position of the baby, and it was compressible and non pulsatile. There was no other prominent vessel on face and scalp. The right orbit was a little downward and outward placed. Right half of his face was little hypoplastic. CT scan of brain showed extra-calvarial soft tissue mass in frontal region, and there was no apparent bony gap infront of anterior fontanel. CT angiogram showed soft tissue mass was vascular lesion connected with SSS through emissary veins and intracranial dural sinuses including SSS were normal. There were no prominent veins of face or scalp connected with vascular lesion. The lesion was excised completely by elevation of a bi-frontal flap through a post-hairline bi-coronal incision. Connecting emissary veins were coagulated and cut to remove the lesion. The lesion was well-defined capsulated without septation and filled with venous blood. Histopathology reported venous malformation-sinus pericranii. The patient recovered uneventfully (Figures and ) and has remained asymptomatic for last 5 years (until the last follow-up).
|
[[8.0, 'month']]
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M
|
{'18688142': 1, '1271098': 1, '29492122': 2, '10845298': 1, '33330007': 1, '15336874': 1, '18291475': 1, '1885982': 1, '32934937': 2, '17307602': 1, '7596493': 1, '2366088': 1, '8956889': 1, '8193859': 1, '19338409': 1, '12021881': 1, '4682507': 1, '1185217': 1, '19687460': 1, '27917332': 2, '5158779': 1, '29623485': 1, '17379525': 1, '4679742': 1, '8692383': 1, '28715722': 1, '2798886': 1, '22639692': 2, '32072087': 1, '15626838': 1, '23960313': 2}
|
{'3745130-2': 2, '7482528-1': 1, '3358958-1': 1, '5099298-1': 1, '5820896-1': 1}
|
162,720 |
3745130-2
| 23,960,313 |
noncomm/PMC003xxxxxx/PMC3745130.xml
|
Surgical management of scalp arterio-venous malformation and scalp venous malformation: An experience of eleven cases
|
A 43-years-old male patient presented with right-sided pulsatile, progressively increasing fronto-parieto-temporal swelling measuring about 15 × 19 cm. He had headache and tinnitus. The swelling was diffusely serpentine. There was skin changes (ulceration and healed ulcerated areas). He had a history of surgery 5 years back in another institution. According to the patient, the lesion progressively increased in size after the operation. He also had recurrent attack of haemorrhage from the ulcerated area but none were of serious nature to cause shock and were controlled by pressure dressings. CT scan showed large soft tissue swelling [] and the bony windows showed multiple erosions and prominent vascular marking. Right-sided common carotid artery and ECA angiogram showed huge dilatation of branches (occipital artery, posterior auricular artery, superficial temporal artery and maxillary artery and its branches, including meningeal and middle temporal arteries) of ECA supplying the AVM. Left ECA angiogram showed enlargement and tortuousity of left occipital, posterior auricular and superficial temporal arteries supplying the AVM crossing the midline. Both internal carotid artery (ICA) angiograms showed prominent ophthalmic and supraorbital and supratrochlear arteries supplying the AVM. ACA, middle cerebral (MCA) and vertebro-basilar arterial systems were normal and intracranial venous drainage system seemed to be normal []. Right-sided ECA was ligated at the beginning of operation through a neck incision (During ligation, partial rupture of ECA occurred, which was immediately controlled). Then, AVM was excised completely with some part of skin (ulcerated and infected area). At the posterior part of AVM, there was some intracranial venous connection through bony erosion. There was also some significant pericranial component of AVM. Wound was closed with a transposition scalp flap. Postoperatively, there was minor wound infection that was controlled by regular dressing and antibiotic. Cosmetic appearance improved after 2 months []. The patient has remained free of recurrence of AVM for last 1.5 years (until the last follow-up).
|
[[43.0, 'year']]
|
M
|
{'18688142': 1, '1271098': 1, '29492122': 2, '10845298': 1, '33330007': 1, '15336874': 1, '18291475': 1, '1885982': 1, '32934937': 2, '17307602': 1, '7596493': 1, '2366088': 1, '8956889': 1, '8193859': 1, '19338409': 1, '12021881': 1, '4682507': 1, '1185217': 1, '19687460': 1, '27917332': 2, '5158779': 1, '29623485': 1, '17379525': 1, '4679742': 1, '8692383': 1, '28715722': 1, '2798886': 1, '22639692': 2, '32072087': 1, '15626838': 1, '23960313': 2}
|
{'3745130-1': 2, '7482528-1': 1, '3358958-1': 1, '5099298-1': 1, '5820896-1': 1}
|
162,721 |
3745288-1
| 23,966,800 |
noncomm/PMC003xxxxxx/PMC3745288.xml
|
Warfarin-induced calciphylaxis: a case report and review of literature
|
A 56-year-old female patient presented after a fall, with worsening lower extremity edema. She was found to have acute-on-chronic kidney injury (7.46 mg/dL on baseline creatinine of 2.42 mg/dL). Past medical history was significant for diabetes mellitus type II and diabetic neuropathy, morbid obesity (body mass index = 48 kg/m2), deep venous thrombosis, and pulmonary embolism, receiving warfarin for 2 years and 9 months, dyslipidemia, hypertension, chronic kidney disease stage I V, and peripheral vascular disease status post-amputation of the left toe 5 months earlier. Workup for acute kidney injury (AKI) was conducted, excluding post obstructive, prerenal, vasculitis, and multiple myeloma. The patient had a drop in hemoglobin; warfarin was withheld for 4 days on suspicion of blood loss and then restarted on day 6 (international normalized ratio [INR] = 1.6 reaching 1.3) after placement of an Ash catheter and initiation of dialysis with INR target in the range of 2–3, which was maintained throughout the entire hospital stay.\nThe patient developed a right foot blister on day 7 and bilateral thigh blisters on day 10 () that were attributed initially to volume overload. Laboratory values were as follows: serum calcium (Ca) 7.4 mg/dL, albumin 2.9 g/dL, inorganic phosphorus 10.3 mg/dL, creatinine 7.68 mg/dL, blood urea nitrogen (BUN) 98 mg/dL, erythrocyte sedimentation rate (ESR) 122 mm/hr, intact parathyroid hormone (PTH) 368 pg/mL, glucose 109 mg/dL. The patient had significant proteinuria of 8,456 mg/g, attributed to diabetic nephropathy (glycated hemoglobin [HbA1c] 5.2%). Total bilirubin was 0.5 mg/dL, alkaline phosphatase was 65 IU/L, aspartate aminotransferase (AST) was 15 IU/L, and alanine aminotransferase (ALT) was 24 IU/L.\nThe skin became mottled and the lesions worsened progressively over 3 days to become necrotic eschars (). Similar lesions developed over the lower extremities, flanks, and lower abdomen (). Extended workup for vasculitis, autoimmune disorders, and coagulopathies was conducted and all were negative: anti-nuclear antibodies (ANA), anti-smith antibodies, anti-double-stranded DNA (dsDNA), anti-ribonucleoprotein (RNP) antibody, anti-neutrophil cytoplasmic antibodies (ANCA) (proteinase-3 AB and myeloperoxidase AB), Sjögren A and Sjögren B antibodies, C3 and C4 complement level, immunoglobulin (Ig)G anti-platelet factor (PF)-4, lupus anticoagulant, anti-cardiolipin IgG and IgM, anti-phospholipid IgM IgG antibodies, β2 glycoprotein I IgG IgM IgA antibodies, hepatitis serologies for hepatitis C and B virus, and workup for multiple myeloma. Protein C function was 33%, expected secondary to Coumadin therapy. Protein S activity, antithrombin III, IgA-IgM-IgG levels were all normal.\nThe patient became septic, with persistent leukocytosis and low-grade fever, along with worsening of skin lesions (), with white blood count of 26 TH/mm3, platelet count of 264 TH/mm3, albumin of 1 g/dL, AST of 38 IU/L, ALT of 37 IU/L, total bilirubin (Tbil) of 0.5 mg/dL, and alkaline phosphatase of 124 IU/L.\nThe patient had eschar lesions on the right lower extremity (75 × 20 cm), the left lower extremity (75 × 20 cm), and an abdominal lesion (10 × 5 × 5 cm) (). The burn specialist provided care and the patient underwent skin debridement and wound care; however, all resuscitation efforts failed on day 42.\nA skin biopsy was performed and showed a portion of skin and subcutaneous tissue with diffuse necrosis and focal acute inflammation as well as multiple small arteries showing calcification of the tunica media. This pattern is strongly suggestive of calciphylaxis (). Autopsy confirmed our diagnosis, with diffuse calcification of the splanchnic and renal arteries media.\nWISN usually appears 3–10 days after starting warfarin, but can occur after many months to 15 years. WISN and calciphylaxis shares similar clinical findings and only biopsy of the skin can differentiate between the two conditions, showing a thrombotic occlusion in dermal, subcutaneous vasculature with hemorrhage. WISN lesions predominate in areas where there is relatively greater adipose tissue, for example, the breasts, thighs, hips, and buttock region.\nAll workup for AKI and skin necrosis was conducted and vasculitis, multiple myeloma, coagulation disorder, heparin-induced thrombocytopenia, and cryoglobulinemia were excluded. The skin biopsy confirmed our diagnosis and excluded disseminated intravascular coagulation and other microthrombotic etiologies.\nThe pathogenesis of calciphylaxis is not well-known. It is related to many conditions such as malignancies, cirrhosis, primary hyperparathyroidism, and secondary hyperparathyroidism as a result of short-bowel syndrome and Crohn’s disease. Previous observational studies have suggested several risk factors, including hyperphosphatemia, hypercalcemia, low serum albumin levels, female gender, obesity, diabetes mellitus, calcium content of the skin, warfarin therapy,,,, systemic corticosteroid use, and elevation in alkaline phosphatase. Clarifying the causality relationship of many coexistent conditions in end-stage renal disease is challenging.\nHayashi et al conducted a multivariate analysis and found that there was a 10.1-fold higher risk of calciphylaxis with warfarin therapy.\nCases of calciphylaxis have been reported as occurring in the absence of hyperparathyroidism and renal failure.,, These findings support the view of calciphylaxis as a final common endpoint of an independent pathway. Calciphylaxis is believed to occur as a product of culminating conditions and stimuli via a final common pathway involving the nuclear factor kappa–beta activation, leading to vascular calcification.\nDescriptive cross-sectional data in humans as well as experimental data in rodents report a positive correlation of vitamin K antagonists and vascular calcification, leading to wide concern regarding the use of warfarin in cardiovasculopathic patients, and the viewing of this disease as partly iatrogenic when it is not a well-known natural sequel of chronic kidney disease (such as renal bone disease or renal hypertension or renal anemia).\nWarfarin therapy provokes an unbalanced pro- and anti-calcification factors, by inhibiting a matrix G1A protein responsible for inhibiting the mineralization of tissues. Matrix G1A protein is an 84 amino acid vitamin K dependent that is activated by carboxylation of glutamate residues.,, In rat models, the disruption of this protein led to extensive vascular calcification,, and this possibly occurs in patients receiving long-term warfarin therapy. Retrospectively, vitamin K supplementation can lead to suppression of the calcification tendency.\nThere are two subtypes of vitamin K: vitamin K1 is the most important for the activation of hepatic clotting factors, and vitamin K2 is involved in the inhibition of calcium deposition in the vasculature. Genetic variation and differential gamma-carboxylation at the glutamate residues is thought to be responsible for the varying phenotypes and susceptibility to vascular calcification.–\nAs this is a multifactorial disease, multifactorial treatment may be a successful intervention tool.,\nSupportive treatment includes wound and pain management. Some success has been achieved with hyperbaric oxygen and intravenous sodium thiosulfate therapy. Correction of hypercalcemia and hyperphosphatemia is essential for treatment. Parathyroidectomy may benefit patients with refractory hyperphosphatemia.\nWe hypothesize that the reintroduction of warfarin creates an imbalance favoring calcification in the vessels in previously sensitized conditions, which set our patient up for a catastrophic acceleration of vascular calcification.\nUnderstanding the pathophysiology of this process will certainly enhance our treatment approach and reduce the morbidity and mortality of this devastating condition.
|
[[56.0, 'year']]
|
F
|
{'20677545': 1, '27069859': 1, '23581997': 1, '23254751': 1, '20627839': 1, '31048656': 1, '24740885': 1, '22344774': 1, '18419610': 1, '22121234': 1, '20019019': 1, '27507694': 1, '24772252': 1, '21652561': 1, '30834840': 2, '33391959': 2, '26816477': 2, '32294899': 1, '23966800': 2}
|
{'4714392-1': 1, '7767840-1': 1, '6864595-1': 1}
|
162,722 |
3745295-1
| 23,966,768 |
noncomm/PMC003xxxxxx/PMC3745295.xml
|
Hyperautofluorescent ring in eyes with macular holes
|
A 62-year-old woman was referred to our department with a diagnosis of MH in her left eye. She had not noticed the decrease in her central vision until it was pointed out by an optometrist. At presentation, her decimal best-corrected visual acuity (BCVA) was 1.0 in the right eye and 0.08 in the left eye. Fundus photographs and fundus autofluorescence images were taken with the Optos® 200Tx (Optos, Scotland, United Kingdom), and optical coherence tomography was performed with the Cirrus™ HD OCT (Carl Zeiss Meditec Japan, Tokyo, Japan). The left eye had a large MH with an operculum ( and ). The minimal and maximal diameters of the MH were 864 μm and 1,345 μm, respectively, and a depigmented ring was observed surrounding the area of the fluid cuff ( and ). Fundus autofluorescence showed a hyperautofluorescent ring corresponding to the depigmented ring ( and ).\nCombined phacoemulsification and vitrectomy with a 25-gauge system was performed on the left eye under local anesthesia. Core vitrectomy following the creation of posterior vitreous detachment was performed with an ultrahigh-speed cutter (5,000 cycles per minute, Alcon Laboratories Inc, Fort Worth, TX, USA). The internal limiting membrane was stained with 0.025% Brilliant Blue G and peeled within the vascular arcade. The peripheral retina was examined for 360 degrees with scleral indentation to search for any retinal breaks. The vitreous cavity was filled with 20% sulfur hexafluoride, and the patient was instructed to maintain a prone position for as long as possible.\nAn anatomic closure of the MH was not achieved. She did not want any additional treatment, and the MH remained open for 6 months after the vitrectomy ( and ). Fundus autofluorescence at this time showed the same size hyperautofluorescent ring as the preoperative one in spite of a decrease in the postoperative size of the opened MH (). The decimal BCVA of the left eye 6 months after the vitrectomy was poor at 0.08.
|
[[62.0, 'year']]
|
F
|
{'19576500': 1, '20075976': 1, '7890502': 1, '7785690': 1, '11382645': 1, '18507731': 1, '21234585': 1, '9640179': 1, '15126174': 1, '7993209': 1, '17460593': 1, '16490523': 1, '20970106': 1, '19666736': 1, '17435683': 1, '21909053': 1, '16829804': 1, '12485276': 1, '8233393': 1, '3174041': 1, '22320413': 1, '20541263': 1, '18412595': 1, '7612549': 1, '19028741': 1, '23966768': 2}
|
{'3745295-2': 2, '3745295-3': 2}
|
162,723 |
3745295-2
| 23,966,768 |
noncomm/PMC003xxxxxx/PMC3745295.xml
|
Hyperautofluorescent ring in eyes with macular holes
|
A 69-year-old woman was referred to our department with a diagnosis of MH in her right eye. She reported that her central vision had decreased 13 years earlier, and her doctor informed her that no treatment was available to close the MH at that time. At our initial examination, her decimal BCVA was 0.1 in the right eye and 1.0 in the left eye. The minimal and maximal diameter of the MH were 681 μm and 1,555 μm, respectively ( and ). Optical coherence tomography showed disruptions of the photoreceptor inner and outer segment junction (IS/OS) line and the external limiting membrane line at the edge of the cuff of subretinal fluid (). A depigmented ring was seen surrounding the area of the fluid cuff, and fundus autofluorescence showed a hyperautofluorescent ring corresponding to the depigmented ring ( and ).\nCombined phacoemulsification and vitrectomy was performed with a 25-gauge ultrahigh-speed cutter on the right eye under local anesthesia. After core vitrectomy followed by the creation of posterior vitreous detachment, peripheral vitrectomy and 360 degree vitreous shaving with scleral indentation was performed. The internal limiting membrane within the vascular arcade was peeled assisted by Brilliant Blue G staining. The vitreous cavity was filled with 12% perfluoropropane. She was instructed to maintain a prone position for as long as possible.\nThe MH was anatomically closed but the optical coherence tomography images did not show any recovery of the IS/OS line or the external limiting membrane line 6 months after vitrectomy ( and ). Fundus autofluorescence showed the same size of hyperautofluorescent ring as seen preoperatively despite the MH being closed (). The decimal BCVA of the right eye 6 months after the vitrectomy was 0.2.
|
[[69.0, 'year']]
|
F
|
{'19576500': 1, '20075976': 1, '7890502': 1, '7785690': 1, '11382645': 1, '18507731': 1, '21234585': 1, '9640179': 1, '15126174': 1, '7993209': 1, '17460593': 1, '16490523': 1, '20970106': 1, '19666736': 1, '17435683': 1, '21909053': 1, '16829804': 1, '12485276': 1, '8233393': 1, '3174041': 1, '22320413': 1, '20541263': 1, '18412595': 1, '7612549': 1, '19028741': 1, '23966768': 2}
|
{'3745295-1': 2, '3745295-3': 2}
|
162,724 |
3745295-3
| 23,966,768 |
noncomm/PMC003xxxxxx/PMC3745295.xml
|
Hyperautofluorescent ring in eyes with macular holes
|
A 71-year-old woman was referred to our department with a diagnosis of MH in her right eye. She reported that her central vision had decreased 15 years earlier, and her doctor informed her that no treatment was available to close the MH at that time. At our initial examination, her decimal BCVA was 0.1 in the right eye and 0.8 in the left eye. The minimal and maximal diameter of the MH was 818 μm and 1,494 μm, respectively ( and ). Optical coherence tomography showed disruptions of the IS/OS line and the external limiting membrane line at the edge of the cuff of subretinal fluid (). A depigmented ring and corresponding hyperautofluorescent ring were observed ( and ).\nCombined phacoemulsification and vitrectomy was performed on the right eye with a 25-gauge ultrahigh-speed cutter under local anesthesia. After core vitrectomy followed by the creation of posterior vitreous detachment, peripheral vitrectomy and 360 degree vitreous shaving was performed. The inverted internal limiting membrane flap technique assisted by Brilliant Blue G staining was performed. The vitreous cavity was filled with 20% sulfur hexafluoride, and she was instructed to maintain a prone position for as long as possible.\nPostoperatively, the MH was anatomically closed but a recovery of both the IS/OS line and the external limiting membrane line was not seen 6 months after vitrectomy ( and ). Fundus autofluorescence showed the same size of hyperautofluorescent ring as seen preoperatively despite the MH being closed (). The decimal BCVA of the right eye 6 months after the vitrectomy was 0.2.
|
[[71.0, 'year']]
|
F
|
{'19576500': 1, '20075976': 1, '7890502': 1, '7785690': 1, '11382645': 1, '18507731': 1, '21234585': 1, '9640179': 1, '15126174': 1, '7993209': 1, '17460593': 1, '16490523': 1, '20970106': 1, '19666736': 1, '17435683': 1, '21909053': 1, '16829804': 1, '12485276': 1, '8233393': 1, '3174041': 1, '22320413': 1, '20541263': 1, '18412595': 1, '7612549': 1, '19028741': 1, '23966768': 2}
|
{'3745295-1': 2, '3745295-2': 2}
|
162,725 |
3745633-1
| 23,961,255 |
noncomm/PMC003xxxxxx/PMC3745633.xml
|
Focal FDG Uptake in Lung Parenchyma Without Structural Alterations on CT
|
A 48-year-old female, under surveillance following surgery for gastric cancer was referred for control evaluation by the F-18 FDG PET/CT study. F-18 FDG PET/CT images demonstrated an area of increased FDG uptake in the right lung middle lobe parenchyma, without any structural abnormality on CT []. A repeat F-18 FDG PET/CT scan was performed after a brief interval of 4 days of the first study did not reveal any abnormality; the previously noted intense focus of FDG avidity having been completely resolved []; the latter suggesting the benign nature of the lung abnormality. On the basis of clinical presentation and imaging studies a final diagnosis of iatrogenic microembolism was made.
|
[[48.0, 'year']]
|
F
|
{'17418153': 1, '33623519': 2, '30678651': 1, '915099': 1, '17895795': 1, '21611073': 2, '21498287': 1, '32351270': 1, '19452248': 1, '29142360': 1, '12928963': 1, '23961255': 2}
|
{'7875025-1': 1, '7875025-2': 1, '3097806-1': 1}
|
162,726 |
3745634-1
| 23,961,256 |
noncomm/PMC003xxxxxx/PMC3745634.xml
|
A Rare Case of Suprahepatic Gall Bladder with Phocomelia and Pancytopenia: Detected by Tc-99m Mebrofenin Scintigraphy
|
A 25-year-old female presented to the Department of Nuclear Medicine for hepatobiliary scintigraphy with complaints of recurrent epigastric pain, abdominal distention, and recurrent episodes of jaundice in the past and with the suspicion of a functional gallbladder pathology. The patient gave history of bleeding gums, skin rashes, menorrhagia, and epistaxis of 1 year duration. She was being treated as a case of pancytopenia with hypersplenism. The patient was born out of a non-consanguineous marriage, normal delivery, and was second in birth order. Developmental history did not reveal any delay in achieving milestones except for an absent right hand below elbow since birth. There was no family history suggestive of any congenital disorders like absent limbs, bleeding disorders, etc., On physical examination, there was no jaundice, pallor, loss of hair, or any muscle wasting. There were multiple purple spots which did not fade on pressure on both upper limbs. The right hand was absent below elbow. Abdominal examination revealed splenomegaly with the spleen palpable to 6 cm below the costal margin. Laboratory investigations showed decreased hemoglobin (7.3 gm/dl), Total Leukocyte Count (3.01 × 103/uL), platelets (23 × 103/uL), and mean cell volume (67). Kidney function tests were normal. Liver function tests showed elevated serum bilirubin (1.50 mg/dl), alanine aminotransferase (123 IU/l), and normal alkaline phosphatase (300 U/l). Serum amylase was normal. Hepatitis profile (Hepatits B surface Antigen, Hepatits B core Antigen, HepatitsC virus) was negative. Upper gastrointestinal endoscopy showed two small chronic pyloric ulcers. An USG abdomen done 2 years back had revealed contracted gallbladder with splenomegaly and left ovarian cyst; a repeat abdominal USG done 2 months prior to the hepatobiliary scan could not locate the gallbladder in its normal anatomical location.\nA 90-min dynamic Tc-99m Mebrofenin hepatobiliary study was performed using an intravenous dose of 7 mCi (259 MBq) Tc-99m Mebrofenin. The patient was placed in a supine position under a large field-of-view dual-head gamma camera using low-energy all-purpose parallel-hole collimator and 20% energy window centered at 140 keV. Ninety dynamic frames of 1 min duration each for the dynamic study (matrix size 128 × 128) followed by two static frames of 3 min duration each at 90 min and 3 h (matrix size 256 × 256) were acquired using a single detector (anterior).\nThe scan showed an intense focus of tracer uptake in relation to the upper border of the right lobe of the liver [], which became visible within 15 min of Tc-99m Mebrofenin injection. At 15 min post injection, the patient was given standard fatty meal (half and half milk 8 oz/70 kg) orally. The intensity of the focal uptake decreased gradually, and by the completion of 90 min, uptake in the suprahepatic region had markedly decreased. The liver showed uniform tracer uptake with small-sized right lobe. Liver to bowel transit time was normal (45 min). Gallbladder emptying (ejection fraction) was also calculated. Emptying was 90% at 90 min and 100% at 3 h. A diagnosis of an ectopic (suprahepatic) gallbladder with normal ejection fraction, and right hepatic lobe hypoplasia was made. A Tc99-m sulfur colloid SPECT transverse section showed gallbladder in suprahepatic location []. A subsequent MRCP [Figures and ] confirmed the scintigraphic diagnosis of suprahepatic gallbladder. On MRCP, the axial HASTE [] and coronal TRUFI [] images demonstrated a suprahepatic gallbladder located superior to segment VIII, hypoplasia of the right hepatic lobe with compensatory hypertrophy of the left hepatic lobe, and gross splenomegaly. A 3.5 M Hz routine abdominal USG was done which revealed an ectopic gallbladder (right subphrenic) with small right hepatic lobe and hypertrophied left hepatic lobe [], which was previously reported as normal [].
|
[[25.0, 'year']]
|
F
|
{'5650100': 1, '13171532': 1, '3871152': 1, '22174525': 2, '14524168': 1, '6611951': 1, '34045393': 2, '25761535': 1, '8192016': 1, '20065577': 1, '7377967': 1, '14220636': 1, '23961256': 2}
|
{'8270044-1': 1, '3237217-1': 1}
|
162,727 |
3745635-1
| 23,961,257 |
noncomm/PMC003xxxxxx/PMC3745635.xml
|
18F-FDG PET-CT for Staging of Conjunctival Melanoma
|
A 34-year-old male patient was referred to our hospital with a six-month history of a progressive pigmented nodule in the palpebral conjunctiva of the left eye. The patient reported a previous pigmented lesion detected years before. Full ophthalmologic examination revealed a pigmented lesion encompassing both palpebral margins of the left eye, in the bulbar and palpebral conjunctiva. A firm, preauricular node was detected by physical examination. No conjunctival pigmented lesion was detected in the right eye. Systemic examination was unremarkable.\nMagnetic resonance imaging (MRI) revealed thickening of the conjunctiva, with a heterogeneous signal at T1 and short time inversion - recovery (STIR), and positive enhancement with gadolinium. The lesion involved the anterior portion of the ocular globe. There was no evidence of metastatic disease.\nConjunctival biopsy showed atypical melanocytosis, compatible with malignant melanoma in situ of the conjunctiva, with 2 mm of intraepithelial extension.\nCT with intravenous contrast revealed two nodules at the superior lobe of the left lung and one nodule at the inferior lobe of the left lung. A fine needle aspiration biopsy of the preauricular lymph node was positive for malignancy.\nTo restage the patient for planning of treatment, a PET-CT scan with 18F-FDG was performed. This study revealed increased tracer uptake at the primary ocular lesion [] and at the preauricular node []. The scan was negative for systemic spread of the disease.
|
[[34.0, 'year']]
|
M
|
{'19095158': 1, '18287273': 1, '11952577': 1, '31939615': 1, '25580155': 1, '19173134': 1, '20531189': 1, '18369064': 1, '27321895': 1, '32892167': 1, '19412870': 1, '34830847': 1, '23961257': 2}
|
{}
|
162,728 |
3745636-1
| 23,961,258 |
noncomm/PMC003xxxxxx/PMC3745636.xml
|
Excessive Hepatic Arterial-portal Venous Shunting May Predict Failure of Microparticle Localization in Hepatocellular Carcinomas
|
A 58-year-old gentleman with a history of hepatitis C was detected to have an asymptomatic arterial enhancing right liver lobe mass on CT imaging, measuring approximately 6 × 8 cm in the longest cross-sectional diameter in liver segments 7/8, with evidence of branch portal vein thrombosis. His alpha fetoprotein levels were elevated as well. The results were in keeping with a hepatocellular carcinoma. He was subsequently referred for consideration of Y-90 SIRT using SIR-Spheres®. Biochemical evidence of underlying liver dysfunction was noted [albumin: 29 G/L, bilirubin: 26 umol/L, aspartate aminotransferase (AST): 164 U/L, alanine transaminase (ALT): 57 U/L, and prothrombin time (PT): 12.1 seconds], but values were still within acceptable limits for Y-90 SIRT.\nA hepatic angiogram was performed. A 5F Cobra catheter was advanced into the hepatic artery proper, and selective angiogram followed by an intra-arterial catheter CT angiogram was performed. The CT angiogram demonstrated good vascular blush in liver segments 7/8, corresponding to the tumor seen on prior CT imaging. However, subsequent portal venous enhancement was noted, indicating hepatic arterial-portal venous shunting [].\nFive millicuries of Tc-99m-MAA was subsequently administered slowly under manual hand control, and the patient underwent SPECT/CT imaging of the liver within one hour of administration of MAA.\nSPECT/CT imaging revealed minimal accumulation of MAA in the tumor in liver segment 7/8, with conversely more intense tracer localization in the surrounding liver parenchyma, resulting in an ‘inverse’-type localization of microspheres within the liver [].\nBased on the findings of the Tc99m-MAA SPECT/CT, the calculated TNR by partition dosimetry model was 0.18 with a liver lung shunting value of 19%. With a calculated dose limit to the normal liver parenchyma of 70 Gy, the radiation dose to the tumor was 36 Gy and to the lung was 15Gy. Based on assessment by partition modeling, the patient was deemed not a suitable candidate for Y-90 SIRT.
|
[[58.0, 'year']]
|
M
|
{'7947110': 1, '8271063': 1, '2766018': 1, '16923973': 1, '3174978': 1, '1327493': 1, '8130973': 1, '2549567': 1, '26097416': 1, '16904840': 1, '8753684': 1, '7931662': 1, '20598004': 1, '23961258': 2}
|
{}
|
162,729 |
3745662-1
| 23,828,750 |
noncomm/PMC003xxxxxx/PMC3745662.xml
|
Rectal Cap Polyposis Masquerading as Ulcerative Colitis with Pseudopolyposis and Presenting as Chronic Anemia: A Case Study with Review of Literature
|
A 27-year-old man visited another hospital with chief complaints of generalised weakness, pallor and intermittent rectal bleeding for 2 years prior to his presentation. Physical examination was unremarkable. His haematological profile showed low haemoglobin levels (8.5 g/dl). The rest of the laboratory parameters including total serum protein and erythrocyte sedimentation rate were within normal limits. Stool culture was negative for pathogenic organisms. Colonoscopy revealed pseudopolyps along with multiple erythematous and eroded mucosal lesions in the rectum []. He was diagnosed clinically as ulcerative colitis for which he received oral aminosalicylic acid followed by prednisolone for 6 months. However, the patient was non-responsive to this medical therapy. He was also transfused blood on two separate occasions along with hematenimics because of persistently low hemoglobin. One year after the initial treatment he was admitted to our hospital because of worsening of symptoms, which were now accompanied by mucous diarrhoea, straining at defecation and rectal prolapse (feeling of mass protruding out from rectum). Laboratory data at the time of present admission also revealed low hemoglobin (8.0 g/dl) however, remaining hematological investigations were within normal limits. On digital rectal examination, multiple soft elevated lesions were palpable. Contrast enhanced computed tomography of the lower abdomen and pelvis showed multiple rectal polyps and thickening of the rectal wall with a maximum wall thickness of 12 mm along with its abnormal inferior descent [].\nAs the patient was non-responsive to medical therapy, low anterior resection of the rectum was done. Intra-operatively, multiple sessile polyps were noted in the rectum along with erythema of the surrounding mucosa. An intra-operative diagnosis of inflammatory polyposis was considered. The post operative course of the patient was uneventful.\nGross examination of the resected specimen revealed multiple sessile rectal polyps, ranging in size from 0.3 cm to 3.0 cm in maximum diameter. The surface of these polyps was ulcerated and was covered with a yellow white fibrinous exudate. The surrounding colonic mucosa showed mild erythema while the intervening colonic mucosa was unremarkable []. Histologically, the surface of these polyps had “caps” of inflammatory granulation tissue and exudate while the base had hyperplastic and cystically dilated crypts. The lamina propria contained a large number of lymphomononuclear cells as well as mucin lakes. Hemosiderin laden macrophages were also observed at places. There was no evidence of adenomatous change or malignancy []. The histopathological findings were consistent with the diagnosis of inflammatory CP.\nThree months post-operatively the hemoglobin levels had improved to 11.3 g/dl.
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[[27.0, 'year']]
|
M
|
{'8491408': 1, '22816031': 1, '15164251': 1, '22333383': 1, '29774225': 1, '12443720': 1, '15785885': 1, '20405375': 1, '20431770': 1, '20874796': 1, '29971597': 2, '10950064': 1, '16099801': 1, '21869875': 1, '24733565': 1, '23828750': 2}
|
{'6029993-1': 1}
|
162,730 |
3745678-1
| 23,961,447 |
noncomm/PMC003xxxxxx/PMC3745678.xml
|
Human subcutaneous dirofilariasis in Assam
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A 43-year-old woman from Sibsagar district of Assam reported with a gradually increasing swelling (2 cm × 1 cm) for one year on the chest wall over the sternum. There was no associated itching, pain or discharge from the swelling. She gave a history of getting a course of oral antibiotic once without improvement. On surgical excision of the nodule, a partially disintegrated white, thread like a worm of 5 cm in length was extracted []. Patient's blood was checked for microfilaremia, but no microfilaria was detected in her blood.
|
[[43.0, 'year']]
|
F
|
{'15949193': 1, '11686084': 1, '7218805': 1, '9564568': 1, '5764050': 1, '20090252': 1, '12235915': 1, '24783097': 1, '12583426': 1, '14651660': 1, '7708440': 1, '17374975': 1, '9802101': 1, '15926098': 1, '15937374': 1, '20966580': 1, '21623126': 1, '10774712': 1, '30693219': 1, '23358737': 1, '8778658': 1, '15829752': 1, '30996536': 1, '19891881': 1, '8758146': 1, '17216316': 1, '16505560': 1, '23961447': 2}
|
{'3745678-2': 2, '3745678-3': 2}
|
162,731 |
3745678-2
| 23,961,447 |
noncomm/PMC003xxxxxx/PMC3745678.xml
|
Human subcutaneous dirofilariasis in Assam
|
A 30-year-old man attended a private hospital in Dibrugarh district with a gradually increasing swelling of 2 cm × 2 cm size for one year on the right cheek. He gave a history of periodical redness, pain and itching for which he was treated symptomatically. The swelling was attached to buccinator muscle underneath and on excision a live, intact, thin, white worm of 12 cm in length came out []. Patient was checked for microfilaremia and was found to be negative.
|
[[30.0, 'year']]
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M
|
{'15949193': 1, '11686084': 1, '7218805': 1, '9564568': 1, '5764050': 1, '20090252': 1, '12235915': 1, '24783097': 1, '12583426': 1, '14651660': 1, '7708440': 1, '17374975': 1, '9802101': 1, '15926098': 1, '15937374': 1, '20966580': 1, '21623126': 1, '10774712': 1, '30693219': 1, '23358737': 1, '8778658': 1, '15829752': 1, '30996536': 1, '19891881': 1, '8758146': 1, '17216316': 1, '16505560': 1, '23961447': 2}
|
{'3745678-1': 2, '3745678-3': 2}
|
162,732 |
3745678-3
| 23,961,447 |
noncomm/PMC003xxxxxx/PMC3745678.xml
|
Human subcutaneous dirofilariasis in Assam
|
A 21-year-old male reported to the surgery out patient department of a teaching hospital with a swelling in the right side of the lower abdomen since 2 months. It started as a small swelling of 1 cm × 1 cm but gradually increased in size to 2 cm × 3 cm with history of periodical itching. On examination, a small movable cystic swelling was found in the right lower quadrant of the anterior abdominal wall. On surgical excision, the cyst was found to be subcutaneous with no attachment to the underlying tissue. On opening the cyst, a live, 12 cm long, white thin worm was found []. The patient was tested for microfilaremia, which was found to be negative.\nThe worms were fixed in formalin and cleared in glycerine for proper viewing of the structures. The worms were white, elongated, 0.5 mm thick and 5 cm to 12 cm in length. The two ends of the intact worms were comparatively thin. The multi layered cuticle showed distinct longitudinal ridges [] and transverse striations []. The cuticle of the first worm was disintegrated at places. The spaces between the ridges were equal to the length of the ridges themselves. The muscle cells were well developed []. The genus Dirofilaria was identified by its thick, multi layered cuticle with ridging and transverse striations, large muscle cells and prominent lateral cord. The paired uteri and the intestinal tube were seen in two of the worms []. Based on size, cuticular and internal morphologic features the second and the third worm were identified as adult female of D. repens while speciation of the first worm could not be done though it was identified as Dirofilaria.
|
[[21.0, 'year']]
|
M
|
{'15949193': 1, '11686084': 1, '7218805': 1, '9564568': 1, '5764050': 1, '20090252': 1, '12235915': 1, '24783097': 1, '12583426': 1, '14651660': 1, '7708440': 1, '17374975': 1, '9802101': 1, '15926098': 1, '15937374': 1, '20966580': 1, '21623126': 1, '10774712': 1, '30693219': 1, '23358737': 1, '8778658': 1, '15829752': 1, '30996536': 1, '19891881': 1, '8758146': 1, '17216316': 1, '16505560': 1, '23961447': 2}
|
{'3745678-1': 2, '3745678-2': 2}
|
162,733 |
3745697-1
| 23,960,287 |
noncomm/PMC003xxxxxx/PMC3745697.xml
|
Ogilvie's syndrome following posterior spinal arthrodesis for scoliosis
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A 12 years and 8 months old female presented with a double structural thoracic and lumbar scoliosis associated with Arnold-Chiari 1 malformation and an extensive cervicothoracic syringomyelia. At age 11 years and 11 months she developed acute weakness affecting both hands and feet with associated pins and needles down the arms and legs, as well as altered sensation affecting the right upper limb below the elbow while her bladder and bowel function was normal. The patient underwent an urgent cranio-cervical decompression including a posterior fossa craniotomy and C5/C6 laminectomy with syringostomy and placement of a syringopleural shunt to drain the syrinx []. She recovered well following surgery and there were no residual neurological signs or symptoms at the time of presentation in our clinic.\nOn clinical examination at age 12 years and 8 months, she had a progressive thoracic and lumbar scoliosis extending from T5 to T10 measuring 60° and T10 to L3 measuring 50° respectively. Neurological examination was normal. The patient had normal function including sport activities. She was skeletally immature and pre-menarche with Risser grade 1. An MRI of the whole spine demonstrated adequate decompression of the cranio-cervical junction and a small residual cervical syrinx which was considered to require no further treatment at the time by our neurosurgical colleagues.\nThe patient underwent posterior spinal arthrodesis extending from T4 to L3 at age 12 years and 10 months with the use of segmental pedicle screw and rod instrumentation and autologous iliac crest bone graft []. Spinal cord monitoring was performed during the procedure recording motor and sensory (cortical and cervical) evoked potentials which remained stable throughout. Postoperative neurological examination was normal. The patient had 3 doses of intravenous (IV) cefuroxime; one at induction to anaesthesia, and 2 after surgery at 8-hourly intervals.\nIn the postoperative period, the patient developed prolonged abdominal distension without pain which was considered to be due to paralytic ileus as the result of the major spinal operation, as well as the effect of narcotic analgesic agents delivered during and after surgery. There was no nausea or vomiting and the bowel sounds were preserved but reduced. She had no electrolyte abnormalities and her blood tests were normal other than an expected small reduction in haemoglobin. The spinal wound healed uneventfully and the patient mobilized out of bed on postoperative day 2.\nAt the end of the first week following surgery the abdominal distension began to increase and she started having generalized abdominal pain with associated tenderness in the right iliac fossa. She had no vomiting and no bowel movements. Repeat blood tests showed marginal leukocytosis coinciding with the onset of abdominal pain while the remaining parameters including electrolytes, kidney and liver function tests were within normal limits. She was initially managed conservatively maintaining fluid and electrolyte balance and placing a nasogastric tube for aspiration of gastric contents. Repeat ultrasounds and a CT scan of the abdomen did not demonstrate evidence of mechanical obstruction, congenital anomaly (such as a fibrous band or a malrotated bowel), or cecal/sigmoid volvulus []. During the whole postoperative period our patient was under regular review by our general surgical colleagues.\nDue to aggravation of the patient's abdominal distension and absence of clear signs of peritonitis pain a laparoscopy was decided on postoperative day 16 followed by an exploratory laparotomy. At that stage no definitive diagnosis was made. The laparotomy showed the cecum and ascending colon to be grossly inflamed with multiple ragged perforations, no dilatation and gross contamination of the abdomen. Multiple loops of small bowel were adherent to the anterior abdominal wall in the right iliac fossa. The remainder of the transverse, descending and sigmoid colon was found to be entirely normal. A limited right hemi-colectomy and ileocecal anastomosis was performed and the patient returned to the intensive care with nasogastric aspirations. She remained intubated for 7 days and was treated with meropenem and vancomycin for 2 weeks as the peritoneal cultures showed a mixed growth of Enterococcus and E. coli. This was changed to ciprofloxacin for an additional period of 3 weeks. She made gradual recovery with good bowel function, returned to feedings over a period of 2 weeks and was discharged on postoperative day 32.\nThe surgical specimen sent for histopathology included 3 cm of terminal ileum, 5.5 cm appendix and 12 cm of colon. A single large defect was identified at the cecum and multiple defects in the ascending colon above the ileocecal valve. The microscopic examination of the small bowel and appendix were normal. Sections from the colon and cecum showed ulcerations and perforation with organized fibrinous peritonitis. There were no features of Crohn's disease, ulcerative colitis or vascular abnormality. The surgical findings combined with the clinical picture and the pathology report confirmed the diagnosis of Ogilvie's syndrome.\nAt latest followup, 3.2 years after scoliosis surgery our patient was skeletally mature (Risser 5), had no abdominal complaints and was on a normal diet. Spinal radiographs showed maintenance of an excellent correction of her scoliosis and no signs of infection, instrumentation failure or nonunion. She had normal activities including sports and no complaints of her back.
|
[[12.0, 'year'], [8.0, 'month']]
|
F
|
{'16510828': 1, '17873816': 1, '12486363': 1, '22131898': 1, '10676594': 1, '22159323': 1, '15905772': 1, '3180976': 1, '21216326': 1, '11578068': 1, '25214851': 2, '11176241': 1, '10403850': 1, '439361': 1, '3753674': 1, '11714568': 1, '30179219': 2, '19830099': 2, '17260618': 1, '1555081': 1, '18886657': 1, '1588406': 1, '3877425': 1, '26692695': 1, '23960287': 2}
|
{'6146187-1': 1, '4157003-1': 1, '2726477-1': 1}
|
162,734 |
3745698-1
| 23,960,288 |
noncomm/PMC003xxxxxx/PMC3745698.xml
|
Conjoined legs: Sirenomelia or caudal regression syndrome?
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A 12-year-old boy presented with fusion of lower legs above the ankle joint. Bilateral femur and upper two-third of tibia and fibula were separated. There was fusion of both legs in the lower one third of leg []. The boy weighed 23 kgs at the time of admission. The parents were nonconsanguineous. There was no history of maternal diabetes and patient had a breach presentation with immediate birth cry. Both knees had flexion deformities (right: 10° and left: 25° as measured by 180° goniometer). Both legs were short (left shorter than right). Both feet were rudimentary. The right foot had a valgus rocker-bottom deformity. All toes were present but rudimentary. The left foot showed absence of all toes. Physical examination showed left tibia vara. The chest evaluation in sitting revealed pigeon chest and elevated right shoulder. There was expansion of 2, 3, and 3 cm in axilla, nipple, and xiphisternum levels, respectively. Posterior examination of the trunk showed thoracic scoliosis with convexity to right. He was having no other physical anomalies in the skull, face, and lumbar region.\nMagnetic resonance imaging of spine showed no abnormality in soft tissue planes that is expected from CRS or sirenomelia-like blunted sharp ending of spinal cord or hypoplastic sacrum. Ultrasound of abdomen and pelvis ruled out any visceral anomalies. Color Doppler imaging for both lower limbs showed that anterior tibial, posterior tibial, and peroneal arteries were small in caliber and nontraceable throughout their extent but showed normal triphasic flow pattern in visualized segments. Bilateral external iliac, common femoral, superficial femoral, profunda femoris, and popliteal arteries were normal in caliber and blood flow.\nThe superficial and deep veins were competent in both sides and showed spontaneous phasic flow with adequate response to valsalva and augmentation. There was no evidence of deep venous thrombosis (DVT), arterial venous malformation (AVM) and aneurysm.\nA multidisciplinary surgical team, composed of a plastic surgeon, a vascular surgeon, and an orthopedic surgeon, achieved complete separation of the lower limbs. The typical zigzag incisions were marked between the limbs, Z-plasty of skin was performed [] with independent vascular and nerve supplies. The vascular surgeon identified the anteriortibial, posterior tibial, and peroneal arteries on both the limbs. Intraoperatively, it was found that femurs, tibias, and fibulas were normally represented. Muscles seemed to be present and tonic. After separation, the left side tibia was found to be posterolaterally angulated for which a corrective osteotomy was done and fixed with K-wire to make the feet plantigrade []. Pulse oximeters were helpful during the surgical procedure to assess the viability of the separated limb. Wound closure was performed with split thickness skin grafting from anterolateral thigh. The skin-graft donor site was closed with absorbable sutures. A generous amount of antibiotic ointment was directly applied to the skin graft, and the incisions were followed by a nonadherent dressing material. Dressing was changed after 72 h. The boy had two separate legs with a good aesthetic and functional result [].\nPostoperative physiotherapy consisted of active movements after the skin grafts had settled in by 6 days. The child was instructed to massage the scars to soften them. Once the scar was well established, a cast was applied to stretch the knee flexion contracture which was mostly of soft tissue origin. Strengthening exercises, balance retraining, and gait reeducation were also introduced as part of therapy.\nAfter the surgery, the child demonstrated grade 3 muscle strength in bilateral quadriceps. The arm span was 141 cm but the child measured only 114 cm in total vertical height The hip range of motion was within normal limits and the child was able to stand on both feet and was able to walk with prosthesis []. The prosthesis prescribed was partial type prosthesis for right side and Syme's type of prosthesis for left side along with distal weight bearing socket having soft lining and ethaflex extension for foot and a pair of normal shoes. Anterior strap with pad was given above the bulbous end for suspension.\nAt 6 months’ followup after the operation, the child presented with excellent general condition and good state of healing of the skin scars at the lower extremities, without any evidence of skin retraction. At the time of this writing, the boy was 13-year-old and growing normally. The parents were instructed to go for a detailed assessment to rule out the possibility of any urologic, congenital heart defects and any neuroblastoma that might have coexisted.
|
[[12.0, 'year']]
|
M
|
{'1849924': 1, '10333372': 1, '26061294': 1, '11782287': 1, '12369674': 1, '2651695': 1, '8827914': 1, '16575365': 1, '11271050': 1, '3238607': 1, '3142930': 1, '26023368': 1, '11896527': 1, '1802847': 1, '26670448': 1, '4812361': 1, '26023366': 2, '8815138': 1, '14695398': 1, '1960198': 1, '18360750': 1, '12813764': 1, '16752437': 1, '23960288': 2}
|
{'4420302-1': 1}
|
162,735 |
3745699-1
| 23,960,289 |
noncomm/PMC003xxxxxx/PMC3745699.xml
|
Spontaneous resolution of postoperative lumbar pseudomeningoceles: A report of four cases
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A 17-year-old boy underwent posterior instrumentation from L2-S1 vertebra and anteriorcolumn reconstruction for an unstable burst fracture of L4 vertebra. Intraoperatively, the left L4 nerve root was avulsed with a dural defect. A fat graft was used to seal the CSF leak at the time of wound closure. The patient had complete motor and sensory loss in left L4 root distribution which remained unchanged postoperatively. Postoperatively, the patient was put on routine antibiotics for gram positive and negative coverage and analgesics. He was catheterized and advised strict bed rest. On the 5th postoperative day, when the patient was mobilized, a fluctuant swelling of approximately 12 × 8 cm was noticed at the operated site. Since the patient remained asymptomatic and the wound healed uneventfully, he was discharged after suture removal and was observed closely. At 3 months followup, the swelling had resolved completely both clinically and radiologically [].
|
[[17.0, 'year']]
|
M
|
{'29709844': 1, '28658870': 1, '25296539': 1, '32399352': 2, '31663047': 1, '34268167': 2, '31768293': 2, '19292403': 1, '34113681': 1, '20383537': 1, '15347231': 1, '32189874': 1, '34840902': 1, '15965222': 1, '33097586': 1, '7024283': 1, '28966827': 1, '16859266': 1, '20302667': 1, '30210814': 1, '25711914': 1, '15305842': 1, '23960289': 2}
|
{'3745699-2': 2, '3745699-3': 2, '3745699-4': 2, '8244681-1': 1, '7213667-1': 1, '6826298-1': 1, '6826298-2': 1}
|
162,736 |
3745699-2
| 23,960,289 |
noncomm/PMC003xxxxxx/PMC3745699.xml
|
Spontaneous resolution of postoperative lumbar pseudomeningoceles: A report of four cases
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A 24-year-old male presented to us 4 months following a right L4-L5 fenestration and discectomy, with a fluctuant swelling of about 5 × 4 cms at the operated site. He had grade 4 power in right long toe extensors which remained the same after surgery. He was otherwise asymptomatic. He was advised exploration and repair, but he declined. He was followed-up and at 6 months postoperatively, the pseudomeningocele was found to have resolved completely both clinically and radiologically [].
|
[[24.0, 'year']]
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M
|
{'29709844': 1, '28658870': 1, '25296539': 1, '32399352': 2, '31663047': 1, '34268167': 2, '31768293': 2, '19292403': 1, '34113681': 1, '20383537': 1, '15347231': 1, '32189874': 1, '34840902': 1, '15965222': 1, '33097586': 1, '7024283': 1, '28966827': 1, '16859266': 1, '20302667': 1, '30210814': 1, '25711914': 1, '15305842': 1, '23960289': 2}
|
{'3745699-1': 2, '3745699-3': 2, '3745699-4': 2, '8244681-1': 1, '7213667-1': 1, '6826298-1': 1, '6826298-2': 1}
|
162,737 |
3745699-3
| 23,960,289 |
noncomm/PMC003xxxxxx/PMC3745699.xml
|
Spontaneous resolution of postoperative lumbar pseudomeningoceles: A report of four cases
|
A 61-year-old lady who underwent posterior instrumentation, debridement, and fusion of L5-S1 vertebra for tuberculous spondylodiscitis. She presented after 18 months postoperatively with fluctuant swelling of approximately 9 × 6 cm at the operated site. She did not have any neurological deficit she had taken antitubercular course for 9 months. She had noticed the swelling 2 months after surgery but did not seek any medical attention as it was completely asymptomatic. She had completed a 9-month course of anti tubercular regime. The diagnosis of a large pseudomeningocele was confirmed on a magnetic resonance imaging (MRI). She was advised exploration and repair but she declined. She returned for followup 3 years later and the lesion was found to have resolved completely both clinically and radiologically [].
|
[[61.0, 'year']]
|
F
|
{'29709844': 1, '28658870': 1, '25296539': 1, '32399352': 2, '31663047': 1, '34268167': 2, '31768293': 2, '19292403': 1, '34113681': 1, '20383537': 1, '15347231': 1, '32189874': 1, '34840902': 1, '15965222': 1, '33097586': 1, '7024283': 1, '28966827': 1, '16859266': 1, '20302667': 1, '30210814': 1, '25711914': 1, '15305842': 1, '23960289': 2}
|
{'3745699-1': 2, '3745699-2': 2, '3745699-4': 2, '8244681-1': 1, '7213667-1': 1, '6826298-1': 1, '6826298-2': 1}
|
162,738 |
3745699-4
| 23,960,289 |
noncomm/PMC003xxxxxx/PMC3745699.xml
|
Spontaneous resolution of postoperative lumbar pseudomeningoceles: A report of four cases
|
A 26-year-old male, who underwent a left sided L4-L5 fenestration and discectomy, presented 10 days later with a fluctuant swelling over the back. His neurological status was normal. His radicular symptoms were relieved but had occasional postural headache. He was planned for surgical exploration and repair of the dural defect. During the waiting period for surgery, as he showed spontaneous regression, the surgery was deferred and it was decided to observe the patient closely. At 3 months, he showed complete resolution of the swelling which was further confirmed on the MRI [].
|
[[26.0, 'year']]
|
M
|
{'29709844': 1, '28658870': 1, '25296539': 1, '32399352': 2, '31663047': 1, '34268167': 2, '31768293': 2, '19292403': 1, '34113681': 1, '20383537': 1, '15347231': 1, '32189874': 1, '34840902': 1, '15965222': 1, '33097586': 1, '7024283': 1, '28966827': 1, '16859266': 1, '20302667': 1, '30210814': 1, '25711914': 1, '15305842': 1, '23960289': 2}
|
{'3745699-1': 2, '3745699-2': 2, '3745699-3': 2, '8244681-1': 1, '7213667-1': 1, '6826298-1': 1, '6826298-2': 1}
|
162,739 |
3745700-1
| 23,960,290 |
noncomm/PMC003xxxxxx/PMC3745700.xml
|
Replantation of a circumferentially degloved ring finger by venous arterializations
|
A 41-year-old woman sustained a complete degloving injury of her right ring fingers by a roller machine in January 2011. The finger was denuded of skin and subcutaneous tissue from the middle part of the proximal phalanx to as far as the nail plate, leaving bones, tendons and the nail bed intact [Figure and ]. The degloved skin was preserved except for a 5 cm longitudinal strip on the dorsum of the finger. The nail demonstrated brisk bleeding. The function of flexor and extensor tendon was preserved. The vessels were cautiously located in the subcutaneous layer under microscopy. The neurovascular bundles remained in good condition in the denuded finger. There were numerous good-caliber (one mm diameter or greater) superficial veins in the palmar and dorsal aspects of the peeled skin. Vein arterialization was determined as a blood supply to the avulsed skin. After the digital Allen test to the ring finger was confirmed intact, the ulnar digital artery was transected. The proximal artery was anastomosed with a distal vein in the palmar aspect of the avulsed skin without tension. Two dorsal veins were anastomosed for outflow. The skin was loosely closed with 5/0 nylon. The finger turned pink. Dextran (500 mL daily) was infused for 5 days to enhance microcirculation. Swelling and congestion appeared for 3 days after the operation, but these findings subsided and the finger survived uneventfully. After 3 months, the patient returned to her previous job. At 1 year followup, the active range of motion of at the metarcarpalophalangeal joint was 0°-90°, at the proximal interphalangeal joint 0°-110° and at the distal interphalangeal joint 10°-40°. Light-touch sensation of the ring finger was intact and she scored a value of 9 mm on static 2-point discrimination testing. She did not complain of any cold intolerance of the ring finger. She was satisfied with the appearance and function of the digit [Figure -].
|
[[41.0, 'year']]
|
F
|
{'30078904': 1, '25114435': 1, '19897322': 1, '3986426': 1, '9583485': 1, '14646649': 1, '22022033': 1, '20878729': 1, '20878731': 1, '9339278': 1, '17667410': 1, '17826561': 1, '23960290': 2}
|
{}
|
162,740 |
3745701-1
| 23,960,291 |
noncomm/PMC003xxxxxx/PMC3745701.xml
|
Posttraumatic osteonecrosis and nonunion of distal pole of scaphoid
|
A 30 year old male presented to the outpatient department in January 2010 with complaints of increasing pain and stiffness in the left wrist for the last 2 years following a fall on outstretched hand. He took treatment in form of massage for two and half months and no radiological investigations were done for his injury. He returned to stitching clothes, his profession, after two and a half months. His wrist pain increased progressively along with restriction of movements to such an extent that he had to discontinue his job. On examination his left wrist (non-dominant) showed gross restriction of motion with just 10 degrees of dorsiflexion and 15 degrees of palmar flexion. There was mild tenderness on radial side of wrist, which was more marked in the anatomical snuffbox. Radiographs showed a nonunion of scaphoid with avascular necrosis of distal pole with no evidence of radiocarpal arthritis []. The lateral intrascaphoid angle as observed in the lateral view was 60° indicating a mild humpback deformity; however, luno-capitate angle was 0°, indicating absence of carpal instability. There was no loss of carpal height. The carpal height ratio was 50% (45-60%), ruling out a carpal collapse. Computed tomographic (CT) scan of right wrist showed the distinct fracture line in the scaphoid with cystic changes in the adjacent region of bony fragments and a sclerotic distal fragment [].\nAn open reduction and internal fixation of the nonunion with k-wires supplemented with a pronator quadratus muscle pedicle bone graft was planned. The scaphoid was exposed through a standard palmar approach after extending the incision beyond the distal palmer crease by 2 cm []. Nonunion was exposed and fractured surfaces cleared of fibrous tissue. The distal fragment was retrieved, which was approximately 1 × 0.5 cm in size. No bleeding could be observed in the distal fragment on curettage of its fractured surface, confirming avascular distal fragment as preoperative MRI was not done in this patient for assessing avascularity. The nonunion was reduced and a 2.0 mm k-wire was passed across the fracture site from distal to proximal fragment, under fluoroscopic guidance. We had planned fixation with Herbert's screw, however, because of the fear of crushing the small sized distal fragment, we preferred k-wire. The pronator quadratus muscle pedicle bone graft was harvested and transposed to the nonunion site. A second k-wire was now introduced, which held the graft in position and supplemented the fixation of the fracture []. The wound was closed in layers with a suction drain in place. The wrist was immobilized in a below elbow plaster of paris cast in neutral flexion The postoperative radiographs showed a reduction in the lateral intrascaphoid angle to 46° from a preoperative 60° []. The pop cast was continued for 12 weeks followed by gradual mobilization and range of motion exercises. At 6 months, sound union at the fracture site was observed radiographically and was confirmed by CT scan [Figure and ]. He returned to (stitching clothes) job at 4 months and resumed his part time farming activities after k-wire removal at 6 months, postoperatively. At 2 years followup, he was able to perform all activities of daily living and had attained his pre-injury functional level. He still experiences mild pain after heavy work and has restriction of terminal 10° of palmar flexion []. His Disabilities of the arm, Shoulder and Hand (DASH) Score was 4.25, which is consistent with good hand function. The magnetic resonance imaging (MRI) scan of the left wrist showed evidence of revascularization 2 years post-injury suggesting successful incorporation of pronator quadratus muscle pedicle bone graft [].
|
[[30.0, 'year']]
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M
|
{'3100997': 1, '11210969': 1, '15271549': 1, '6844937': 1, '11775472': 1, '26330781': 1, '1400550': 1, '6996886': 1, '21430877': 2, '7430591': 1, '6693468': 1, '12063324': 1, '3284681': 1, '23960291': 2}
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{'3051129-1': 1}
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162,741 |
3746042-1
| 24,010,107 |
noncomm/PMC003xxxxxx/PMC3746042.xml
|
Life-Threatening Lower Gastrointestinal Hemorrhage in Pediatric Crohn's Disease
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A 13 years old boy was admitted to the hospital because of gross hematochezia. There was nothing significant in the patient's past medical history over the past 6 months. He reported suffering from intermittent diarrhea and abdominal pain. Also, he went from 47 kg to 40 kg during the course of 3 months. He was initially believed to have hematochezia and therefore a colonoscopy was performed. After the colonoscopy, he was sent to our hospital with suspicion of inflammatory bowel disease. At his first visit, his blood pressure, pulse rate, respiratory rate, body temperature, height and body weight were 110/65 mm/Hg, 90/min, 20/min, 36.5℃, 164.2 cm (25-50 p) and 40 kg (5-10 p), respectively. He appeared chronically ill and was pale. The physical examination upon admission showed slight pain and tenderness at the peri-umbilical region without muscular guarding. His bowel sounds were normal and the rectal examination revealed an empty ampulla with no other peculiar symptoms regarding peri-anal abscess or fistula. The laboratory investigations during the first exam were as follows: erythrocyte sedimentation rate (ESR) 84 mm/h, C-reactive protein 106 mg/L (normal 0-8 mg/L), albumin 2.8 g/dL, prothrombin time 11.5 sec, partial thromboplastin time 28.1 sec, hemoglobin 10.4 g/dL, leucocytes 9.8×109/L with normal leukocyte differentiation, and thrombocytes 489×109/L. A stool occult blood test was also performed and found to be positive. The colonoscopy showed an inflammatory bowel with multiple linear deep ulcerations, cobble stone appearances and pseudo-polyps (). In addition, in the MRI enterography, a diffuse bowel wall thickening was observed at the distal to terminal ileum, cecum and rectosigmoid colon. Accordingly, he was diagnosed with Crohn's disease. His Pediatric Crohn's disease Activity Index (PCDAI) score was 68. Initially, induction therapy was performed with oral steroids (30 mg/day) and Azathioprine (100 mg/day). He was also given 8weeks of EEN with a polymeric formula (Monowell 2,000 mL daily). After medical therapy, the abdominal pain has declined slightly and the ESR and C-reactive protein (CRP) was reduced but intermittent mild bloody stools were still observed. After the 10th day of hospitalization, approximately 1,000 mL of a fresh bloody stool and dizziness with about a 10-second loss of consciousness had occurred. At this time, his blood pressure had dropped to 80/40 mmHg. In addition, his hemoglobin levels dropped from 10.4 g/dL to 7.6 g/dL. Accordingly, 6 units blood transfusion was performed over a 24 hour time period. After the blood transfusion, his vital signs had stabilized. Based on the patient's past history and the colonoscopy data, we presumed that this gastrointestinal hemorrhage was caused by Crohn's disease. At that point, oral steroid treatment was changed to intravenous steroids and the patient was placed under conservative care. However, even after 10 days, due to over 500 mL of continuous massive hematochezia and repetitive hemoglobin drop, blood transfusion was needed. Thus, a bleeding focus evaluation was performed. From the GI bleeding scintigraphy, the radiotracer was found to be up taken in the mid to left upper quadrant in the abdomen and no abnormal signs were observed in the abdomen CT. A duodenal ulcer was observed in the upper endoscopy but no other acute findings were made. A colonoscopy was then performed and multiple active ulcerations in the distal ileum and inflammatory polyps and cobble stone appearance were found (). Ulcers and bleeding was also expected to be found; however, current active bleeding was not observed and no other bleeding focus was present. For 3 weeks, even with steroid induction and azathioprine therapy, mucosal healing was not successful. The PCDAI score was also 60, which was indicative of continued severe disease activity. Since steroid therapy was ineffective, infliximab infusion (5 mg/kg) was initiated. On the 21st day, a superior mesenteric angiography was performed. In this test, no active bleeding was observed; however, a hypervascular blush, which caused by inflammatory changes, was observed near the proximal ascending colon and ileocecal (IC) valve. To account for this, 2 superior mesenteric arteries were selected using a microcatheter and gel foam arterial embolization was successfully performed ( and ). A hematochezia was found nowhere and the PCDAI score had decreased by 20 points. Starting on the 27th day, mucosal healing and bleeding was thought to be well managed from infliximab infusion and embolization and maintenance therapy was performed using mesalazine (4,000 mg/day). 2 weeks after the first infliximab injection, which corresponded to the 34th day of hospitalization, valve, a second infusion of infliximab (5 mg/kg) was done. However, 650 mL of massive hematochezia was observed on the 35th day of hospitalization. For the first 24 hours, the patient was given 2 units of blood. However, even with active transfusion, the massive rectal hemorrhage continued and his hemoglobin levels dropped from 12.6 gm/dL to 11.6 gm/dL. At this point, we deemed it necessary to perform surgery. To examine the precise operation scale, a second angiography was performed before the operation. The superior mesenteric artery angiography showed a hypervascular blush near the proximal ascending colon and IC valve; however, no active bleeding was observed (). On the 36th day of hospitalization, an ileocecectomy and hand sewn end to side anastomosis were performed. During the operation, wall edema and inflammation was found on the IC valve which was about 30 cm deep into the terminal ileum. An ileostomy was initiated to observe the inside of the lumen and a cobble like appearance, mucosal ulceration and dark blood clot was found. The lumen of the cecum was relatively clean and inflammation was not severe. Although a single bleeding point was not identified, the hemorrhage presumably originated from the diffusely multifocal ulcerated ileal mucosa. Approximately 30 cm of the terminal ileum and cecum together were cut and an ileocecectomy was performed as well as a hand swen end to side anastomosis (). According to the pathologic examination, the ileocecum was erythematous and multiple ulceration, transmural inflammation with perforation and small non-caseating granuloma were observed, a condition that was compatible with Crohn's disease. No colonic diverticula were identified. After the ileocecectomy, the patient's bleeding promptly ceased and he did not require additional blood transfusions. On the 6th postoperative day, a clear liquid diet was started and on the 7th postoperative day, a dark brown colored stool was evident; however, no more hemorrhage episodes occurred and the abdominal pain was managed, which resulted in a steady increase in food consumption. The daily dose of prednisolone was set at 30 mg/day initially and was decreased according to the clinical activity of the disease. On the 12th postoperative day, the PCDAI score was 15 and the wound had cleared; therefore, the patient was discharged. Currently, the patient is in maintenance therapy and receives only infliximab. After the hospitalization, the PCDAI score remained below 10 and disease activity was controlled. The patient has no recurrence of bleeding or evidence of Crohn's disease and is currently in good condition.
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[[13.0, 'year']]
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M
|
{'22457862': 1, '22387837': 1, '4198183': 1, '414598': 1, '20222123': 1, '19696538': 1, '17560414': 1, '15564805': 1, '21122547': 1, '18668673': 1, '7813353': 1, '17973582': 1, '33885977': 1, '15365422': 1, '16378180': 1, '24010107': 2}
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{}
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162,742 |
3746049-1
| 24,010,108 |
noncomm/PMC003xxxxxx/PMC3746049.xml
|
Epstein-Barr Virus Infection with Acute Pancreatitis Associated with Cholestatic Hepatitis
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An 11-year-old female was admitted to the emergency center of another hospital with a 1-day history of left upper quadrant abdominal pain, nausea and vomiting. Laboratory data revealed amylase at 1,200 U/L (normal range, 0-220), lipase at 2,000 U/L (normal range, 13.8-110), aspartate aminotransferase (AST) at 724 U/L (normal range, 3-38), and alanine aminotransferase (ALT) at 815 U/L (normal range, 4-44). Computed tomography (CT) finding of the abdomen showed swelling of the pancreas with peripancreatic fluid accumulation compatible with acute pancreatitis. She was transferred to our hospital with a preliminary diagnosis of acute hepatitis and pancreatitis.\nShe had no past history of abdominal trauma, surgery or cholecystitis. She had not received any medications known to cause pancreatitis. She did not report any familial history of pancreatitis or gallstone.\nOn physical examination she appeared sick with icteric sclera. Tenderness on left upper quadrant of abdomen without rebound tenderness was noticed. Exudative pharyngotonsillitis, cervical lymphadenopathy, and hepatosplenomegaly were not present.\nLaboratory investigation revealed hemoglobin of 13.6 g/dL, hematocrit of 39.5%, platelet of 356,000/mm3, white blood cell count of 8,540/mm3 (neutrophil 72%, monocyte 2.7%, lymphocyte 19%). Atypical lymphocyte was absent on peripheral blood smear. Blood chemistry showed AST of 465 U/L, ALT of 657 U/L, total/direct bilirubin of 4.0/1.9 mg/dL (normal range, total bilirubin 0.2-1.2, direct bilirubin 0-0.4). Serum amylase and lipase were elevated to 4,010 U/L and 4,941 U/L respectively (). Alkaline phosphatase was raised to 1,056 U/L (normal range, 104-338) and gamma-glutamyltransferase was raised to 456 U/L (normal range, 16-73). Diagnosis was acute cholestatic hepatitis concurrent with pancreatitis. Other laboratory data showed prothrombin time-international normalized ratio of 1.02, serum total protein of 7.7 g/dL, serum albumin of 4.5 g/dL, blood urea nitrogen of 7 mg/dL, creatinine of 0.7 mg/dL.\nViral hepatitis profiles results including HBsAg, anti-HAV IgM, anti-HCV, anti-HEV IgM/IgG were all negative. Laboratory results for various infectious agent for pancreatitis and hepatitis including anti-mycoplasma IgM, anti-cytomegalovirus IgM, anti-mumps IgM, anti-rubella IgM, anti-measles IgM, leptospira antibody, Clonorchis sinensis antibody were all negative. Serum antinuclear antibody result to evaluate autoimmune disease was negative. Stool smear test for parasites was also negative.\nAlthough the peripheral blood smear did not show atypical lymphocytes, a diagnosis of reactivated EBV infection was made by the positive result of viral capsid antigen (VCA) IgM, VCA IgG and Epstein-Barr nuclear antigen. Heterophile antibody converted from initial negative result to positive in repeated serologic test on 9th day of hospitalization.\nOn radiologic examination, the plain radiographs of abdomen were found unremarkable. Magnetic resonance cholangiopancreatography was performed, which did not show choledochal cyst, pancreatic divisum or a pancreatic duct anomaly.\nThe patient was treated with conservative management with fasting and total parenteral nutrition. On 2nd day of hospitalization, blood chemistry was improved as amylase of 996 U/L, lipase of 516 U/L, AST of 178 U/L, ALT of 440 U/L, total bilirubin of 3.1 mg/dL, direct bilirubin of 1.2 mg/dL. Gastrointestinal symptom such as abdominal pain or vomiting improved also, and she started a regular diet on 4th day when amylase and lipase were normalized (). On 11th day of hospitalization, rapid normalization of biochemical results was observed on follow up laboratory tests. The results were amylase of 223 U/L, lipase of 63 U/L, AST of 31 U/L, ALT of 18 U/L, total bilirubin of 0.4 mg/dL, direct bilirubin of 0.2 mg/dL (). During the 20-month-follow up in the outpatient clinic, she remained in good condition without any sign of relapse of the hepatitis or pancreatitis.
|
[[11.0, 'year']]
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F
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{'21238898': 1, '17963301': 1, '5765134': 1, '16038753': 1, '6169587': 1, '16354962': 1, '5940698': 1, '18437090': 1, '17913534': 1, '6286529': 1, '31732544': 1, '10445566': 1, '6310536': 1, '32064430': 2, '24010108': 2}
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{'7012545-1': 1}
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162,743 |
3746057-1
| 24,010,098 |
noncomm/PMC003xxxxxx/PMC3746057.xml
|
Acute Pancreatitis Induced by Azathioprine and 6-mercaptopurine Proven by Single and Low Dose Challenge Testing in a Child with Crohn Disease
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A 14-year-old boy who had been diagnosed with Crohn disease was admitted suffering from high fever and epigastric pain for 5 days. High fever and epigastric pain developed after 34 days of mesalazine and 15 days of azathioprine, after completion of initial treatment with antibiotics and steroid tapering.\nPrior to 40 days before admission, the patient had been admitted suffering from intermittent hematochezia, diarrhea and weight loss for 3 months. Colonoscopy and biopsy had diagnosed Crohn disease. Pediatric Crohn Disease Activity Index score was 57 as moderate/severe degree. The patient had initially been administered antibiotics and steroid, followed by mesalazine (1,500 mg/day) first and later switching this to azathioprine (75 mg/day) only, allowing overlapping period of the two medications before reaching azathioprine-only regimen. No family history of IBD or pancreatitis was identified. Parity was unremarkable. The patient had been born full term with a birth weight of 3,400 g by normal vaginal delivery.\nThe patient's vital sign was 110/60 mmHg of blood pressure, 98/min of heart rate, 20/min of respiratory rate, and body temperature of 39.1℃. The patient showed mild dehydration, soft and non-distended abdomen, and there was no hepatosplenomegaly. Epigastric and periumbilical area tenderness were evident, but no rebound tenderness. Hemoglobin was 11.1 g/dL, hematocrit was 31.5%, white blood cell count was 11,660/mm3 (neutrophil 86%, lymphocyte 8%), platelet was 312,000/mm3. Serum sodium was 138 mEq/L, potassium 3.6 mEq/L, aspartate aminotransferase/alanine aminotransferase 15/7 U/L, total/direct bilirubin 0.9/0.3 mg/dL, calcium 8.6 mg/dL, and phosphorus 3.3 mg/dL. Erythrocyte sedimentation rate was elevated to 54/26 mm/hr, C-reactive protein to 13.32 mg/dL, and amylase and lipase to 227 U/L (normal range, 0-220) and 363 U/L (normal range, 3-110). Anti-nuclear antibody, lupus anticoagulant antibody, rheumatoid factor, anti-smooth antibody, anti-microsomal antibody, antineutrophil cytoplasmic autoantibodies profile were all negative, and serum IgG was 813.96 mg/dL (normal range, 800-1,700). Abdominal ultrasonography showed mild swelling of the pancreas with no demonstrable pancreatic fluid collection.\nThe patient was diagnosed with acute pancreatitis and received supportive care, but the fever and abdominal pain continued. Two days later after admission, amylase and lipase was more elevated as 1,080 U/L and 1,912 U/L, abdominal ultrasonography showed aggravated pancreatitis with marked swelling. Drug-induced pancreatitis was presumed, and mesalazine and azathioprine were discontinued. The patient was fasted and was given total parenteral nutrition. Two days later after drug discontinuance, the fever and epigastric pain subsided, and 4 days after drug discontinuance, amylase and lipase had decreased (93 U/L and 150 U/L, respectively).\nAt that time, the biological medication for Crohn disease in children was not included in the approved lists of Korean Medical Insurance. Therefore, we had to confirm exactly the relationship between prescribed medications and pancreatitis. When we had a plan ahead of a medication challenge test, we were also afraid of serious adverse reaction of pancreatitis in an ethical aspect for the patient. However, the benefits from the challenge test thought to be overweight the possible risks in the aspect of deciding the patient's present and future treatment regimen.\nTherefore, single and low dose challenge tests were performed to confirm the relationship of drug adverse drug reactions and acute pancreatitis (). Before the challenge tests, amylase and lipase values were 132 U/L and 110 U/L, respectively. Two hours after a single administration of azathioprine (50 mg), the patient developed epigastric pain without vomiting. Seven hours after the single administration, the symptom had subsided. Six hours after the challenge test, amylase and lipase values were markedly increased (303 U/L and 443 U/L, respectively) and were further elevated (458 U/L and 909 U/L, respectively) 18 hours later. Three days following the challenge test, the amylase and lipase values had normalized. One day later, the challenge test was repeated with a single administration of 6-mercaptopurine (25 mg) to select an alternative drug. Before the challenge test, amylase and lipase values were 114 U/L and 83 U/L, respectively. Six hours later, the patient developed epigastric pain without vomiting. The symptom had subsided 12 hours later. Six hours later from the challenge test, the amylase and lipase values were increased (155 U/L and 156 U/L, respectively). Eighteen hours later, the amylase and lipase values were further increased (161 U/L and 193 U/L, respectively). Two days from the challenge test, the amylase and lipase values had normalized.\nAfter 1-month steroid maintenance therapy, the mesalazine challenge test was done. The challenge test with a single administration of mesalazine (500 mg) did not elicit vomiting or epigastric pain. Before the test, amylase and lipase values were 139 U/L and 48 U/L, respectively. Twelve hours later, the amylase and lipase values were 114 U/L and 41 U/L, respectively, and were 110 U/L and 39 U/L, respectively, 18 hours later. This was interpreted as a negative response.\nThe patient was administered solely with mesalazine. Despite regular medication for 1 year, Crohn disease relapsed as intermittent perianal abscess and diarrhea with hematochezia. Symptoms subsided after administration of infliximab. Presently, the patient is symptom-free and is being followed-up on an outpatient basis.
|
[[14.0, 'year']]
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M
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{'38178': 1, '34064706': 1, '10952399': 1, '15986855': 1, '26594832': 1, '19381059': 1, '10192201': 1, '18513380': 1, '19077517': 1, '20227028': 1, '29305366': 1, '26939974': 1, '27465323': 1, '16105163': 1, '16306770': 1, '18159175': 1, '16082282': 1, '33204673': 1, '24010098': 2}
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{}
|
162,744 |
3746058-1
| 24,010,097 |
noncomm/PMC003xxxxxx/PMC3746058.xml
|
A Case of Small Bowel Ulcer Associated with Helicobacter pylori
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11-year-old girl\nEpigastric pain and nonbilous vomiting\nAn 11-year-old girl presented with a history of stabbing epigastric pain every 10 minutes and nonbilous vomiting more than 10 times a day. She did not have fever or diarrhea.\nShe had undergone a gastrotomy and removal of an 8 cm trichobezoar 6 years previously. She ate hair on the floor at that time habitually. She had not been administered medication during the past 3 months.\nShe was 140 cm (25-50th percentile) in height and 34 kg (25-50th percentile) in weight, and her vital signs were: blood pressure, 100/60 mmHg; pulse, 88 beats per minute; respiratory rate, 20 breaths per minute; and temperature, 36.2℃. On admission, she had a clear mental status but seemed acutely ill. Neither conjunctiva were pale, and both sclera were icteric. Respiratory and heart sounds were normal. Abdominal distention was not observed, but bowel sounds were mildly activated. She complained of severe tenderness in the epigastric area with no rebound tenderness. No hepatosplenomegaly or other abdominal mass was detected on abdominal palpation. There was no patchy baldness or abnormalities of the skin or mucosa.\nOn admission, initial laboratory tests showed hemoglobin, 13.2 g/dL; hematocrit, 38.3%; white blood cell count, 13,260/mm3 (neutrophils 88.5%); platelet count, 272,000/mm3; erythrocyte sedimentation rate, 9 mm/hr; and C-reactive protein, 1.6 mg/L. The biochemical profile consisted of serum protein, 6.7 g/dL; albumin, 4.7 g/dL; total bilirubin, 0.5 mg/dL; direct bilirubin, 0.2 mg/dL; aspartate aminotransferase, 17 IU/L; alanine aminotransferase, 11 IU/L; blood urea nitrogen, 6.8 mg/dL; creatinine, 0.5 mg/dL; and amylase, 55 U/mL. A blood coagulation test showed a prothrombin time-internationalized normal ratio, 1.17; and activated partial thromboplastin time, 27.0 sec. Urine analysis showed specific gravity, 1.025; pH, 6.0; negative for protein, glucose, blood, urobilinogen, bilirubin, and nitrite, but positive for ketone bodies. No white blood cells or red blood cells were observed in the urine.\nA simple abdominal X-ray was unremarkable at admission. Abdominal computed tomography (CT) revealed a 4 cm sized low attenuating mass-like lesion in the stomach (). We performed esophagogastroduodenoscopy (EGD) for identifying a recurrence of trichobezoar (). Mucosal erythema was observed in the gastric antrum, but no ulcerative lesions were found in the stomach. A scar, which was considered a gastrotomy suture line, and a duodenal bulb with structural deformity were noted. We suspected transition of the mass below the stomach, so we inserted a longer endoscopic fiber using a CF-Q260AL (Olympus, Tokyo, Japan). We inserted the fiber 60 cm from the incisor without kinking and approached the proximal jejunum. We found multiple longitudinal ulcerative lesions from the duodenal bulb to the proximal jejunum, although there was no trichobezoar or mass causing a mechanical bowel obstruction. We performed a small bowel series after marking the endoscopic approach level using clips () and found normal contrast transition without obstruction or abnormal findings near the mass. Partial hypertrophy of the bowel mucosal fold was noted, but no abnormality was found in the ileocecal portion. The rapid urease test in the duodenal bulb was negative.\nChronic inflammation with lymphoid follicles was noted on pathological examination of the ulcerative lesion ().\nSerum gastrin level and the autoimmune antibody test were performed to determine the cause for the small bowel ulcer. The laboratory findings showed serum gastrin, 57.0 pg/mL; negative anti-neutrophil cytoplasm antibodies and anti-Saccaromyces cerevisiae antibodies; and negative Tb-polymerase chain reaction of the bowel mucosa tissue. The patient received lansoprazole (15 mg/dose, twice a day). On the day of discharge, 4 days after admission, the epigastric pain improved, and she returned to a normal diet. After discharge, she received H. pylori eradication therapy, including lansoprazole (15 mg/dose, twice per day), amoxicillin (50 mg/kg/day in two divided doses), and clarithromycin (30 mg/kg/day in two divided doses) for 2 weeks. She took additional lansoprazole (15 mg/dose, once per day) for 4 weeks, subsequently. Eight weeks after stopping the medication, the urea breath test was negative. The patient has not had any specific symptoms for 18 months.
|
[[11.0, 'year']]
|
F
|
{'19654540': 1, '2051269': 1, '10638564': 1, '17072972': 1, '9840123': 1, '15184762': 1, '6588497': 1, '6134060': 1, '7853632': 1, '22171147': 1, '25552229': 1, '17003940': 1, '21199512': 1, '27421288': 1, '24010097': 2}
|
{}
|
162,745 |
3746147-1
| 23,964,339 |
noncomm/PMC003xxxxxx/PMC3746147.xml
|
A Large-Sized Phytobezoar Located on the Rare Site of the Gastrointestinal Tract
|
A 71-year-old male, who 8 years previously had undergone subtotal gastrectomy with gastroduodenostomy because of early gastric cancer, came to the Department of Emergency with severe epigastric discomfort, abdominal pain and vomiting of 3 days' duration. He had a history of diabetes mellitus for 14 years and was using 12 IU of insulin daily. Despite using insulin, his blood glucose level was not strictly controlled, usually ranging from 250 to 300 mg/dL. The latest hemoglobin A1c level checked 6 months earlier was 7.3%. He had also been diagnosed with end-stage renal disease (ESRD) 6 years previously and had hemodialysis three times a week since then.\nOn clinical examination, he was drowsy with disorientation. His vital signs were within the normal range. Chest and cardiac findings were unremarkable. The abdomen was not distended, and no mass was palpable. Laboratory test results showed a hemoglobin concentration of 10.4 g/dL, a leukocyte count of 6.4×103 g/µL, and a platelet count of 85×103/µL. His serum creatinine was 8.48 mg/dL and urea nitrogen was 45 mg/dL, which had not increased since the previous lab results obtained 1 month earlier. Amylase and lipase were increased up to 848 and 272 U/L, respectively. The serum glucose level was only 38 mg/dL. After immediate intravenous glucose solution infusion, his mental status improved. The rest of his biological examination results were normal.\nAbdominal radiography showed a normal bowel gas pattern and no significant abnormalities. The patient underwent an abdominal pelvic computed tomography (CT) scan to evaluate the cause of his gastrointestinal symptoms. The CT scan revealed 7×8 cm-sized well-defined duodenal mass including gas bubble inside (). Mild pancreatic duct dilatation was also observed. An esophagogastroduodenoscopy was then performed to obtain accurate diagnosis. The anastomosis site was intact without any stricture; however, directly under the anastomosis site, a huge, dark greenish bezoar was confirmed in the duodenum (). There were also many small ulcers on the periphery of the bezoar. We attempted to pull the bezoar out into the gastric cavity for fragmentation by lithotripsy, which was failed because it was tightly adhering to the lumen of the duodenum. Therefore, we injected 50 mL of Coca-Cola directly to the bezoar in order to reduce its size and soften its consistency. Thirty minutes after the Coca-Cola injection, we attempted to move the bezoar using an alligator forceps (FG-47L-1; Olympus, Tokyo, Japan) and a snare (MTW Endoskopie, Wesel, Germany), which failed again. The patient was admitted to the General Ward from the Emergency Room for further treatment. Three nasogastric lavages were performed using 1.5 L of Coca-Cola every 12 hours with a proton pump inhibitor injection and glucose control by insulin. The next endoscopy demonstrated that the bezoar had become smaller and softer. It could finally be pulled out into the gastric cavity using an alligator forceps and was broken into small pieces by lithotripsy (Lithotriptor handle; Medi-globe, Hachenmuhle, Germany) (). The fragmented pieces were successfully removed using a snare and a basket (MTW Endoskopie). Inspection demonstrated that the removed bezoar was a phytobezoar ().\nAbdominal radiography performed just after the complete endoscopic removal showed no evidence of bowel obstruction. With appropriate intravenous nutritional support using insulin, the patient's serum glucose level was maintained within the normal range. Three days after the complete endoscopic removal, the patient was examined again through second-look endoscopy. No residual bezoar was seen, although small ulcers caused by local pressure on the duodenal wall were observed (). The patient was discharged with instructions to maintain sufficiently soft diet. Since his discharge, he has had no subsequent episode of abdominal pain or vomiting. On follow-up endoscopy performed 3 months later, no recurrence of a bezoar was noted and his ulcers were completely healed ().
|
[[71.0, 'year']]
|
M
|
{'16330268': 1, '26473129': 2, '12612525': 1, '16545170': 1, '19437568': 1, '5029071': 1, '17875133': 1, '21921383': 1, '28149129': 1, '27403434': 1, '34947946': 2, '18552481': 1, '28943577': 1, '23964339': 2}
|
{'4604284-1': 1, '8703957-1': 1, '8703957-2': 1}
|
162,746 |
3746148-1
| 23,964,340 |
noncomm/PMC003xxxxxx/PMC3746148.xml
|
Successful Treatment of Duodenal Variceal Bleeding by Endoscopic Clipping
|
A 49-year-old male patient presented with hematemesis and hematochezia. He had been diagnosed with alcoholic liver cirrhosis 14 years ago, and had hyperthyroidism and diabetes.\nAt the time of admission the patient's blood pressure was 60/30 mm Hg, pulse rate was 122 per minute, and respiratory rate was 20 per minute. Basal body temperature was 36℃ and blood glucose level was 257 mmol/L. Physical examination showed acutely ill appearance with mild confusion. The patient had conjunctival pallor, no scleral icterus and no abnormalities on chest auscultation. The abdomen was soft to palpation but was distended, and there was tenderness to palpation at the epigastrium without rebound tenderness.\nLaboratory findings showed hemoglobin concentration of 7.9 g/dL, leukocytes 12,060/mm3 (neutrophils 86.7%), and platelets 101,000/mm3. Serum biochemistry showed the total protein concentration to be 4.9 g/dL, albumin concentration 2.0 g/dL, total bilirubin 0.52 mg/dL, blood urea nitrogen 15.4 mg/dL, creatinine 0.9 mg/dL, aspartate aminotransferase/alanine aminotransferase 31/51, alkaline phosphatase 93 IU/L, prothrombin time 14.4 seconds (international normalised ratio, 1.21), while all of hepatitis B surface antigen, hepatitis B surface antibody, and antihepatitis C virus were negative.\nAn emergency upper gastrointestinal endoscopy was performed on the day of the patient's admission. It showed a varix (F3, Lm, Cb, RC-) without red color sign from all along the mid to lower esophagus. Apart from signs of congestive gastropathy, there were no other lesions suggestive of bleeding. Along the entire wall of the duodenal bulb was a pulsating blue dumbbell-shaped varix and stigma on the surface of this varix (). This was considered to be a bleeding focus, so the efferent vein and afferent vein were ligated using hemoclips, and hemostasis was achieved following hemoclips placement directly on the visible vessel ().\nThree dimensional (3D) computed tomographic (CT) angiography was performed to verify the duodenal varix and the collateral pathways which showed a broad collateral varix around the duodenum and the head of the pancreas due to thrombosis of the main portal vein and the splenic vein (). Following 3D CT angiography, somatostatin intravenous injection and blood transfusion were given along with other conservative management. Although the patient had large amounts of melena, his vital signs were stabilized. A follow-up endoscopy 3 days after he procedure showed no signs of bleeding and two hemoclips were fixed on the varix (). The vital signs were stable, without any more melena, and the patient was discharged from the hospital 14 days after his first admission. Repeat endoscopy 3 months later revealed persistent duodenal varix but of a reduced size and absence of the stigmata of recent bleeding (). Since then, the patient has not had any rebleeding episodes and is being followed up on an outpatient basis.
|
[[49.0, 'year']]
|
M
|
{'8813517': 1, '9219810': 1, '31650032': 1, '21170835': 1, '2785068': 1, '29142527': 1, '28242804': 2, '12364992': 1, '3498234': 1, '10486613': 1, '9755256': 1, '17905019': 1, '28203136': 2, '9260811': 1, '34484536': 2, '887749': 1, '9732183': 1, '19513934': 1, '23964340': 2}
|
{'5337649-1': 1, '5301088-1': 1, '8403701-1': 1}
|
162,747 |
3746149-1
| 23,964,341 |
noncomm/PMC003xxxxxx/PMC3746149.xml
|
A Case of Squamous Metaplasia of the Stomach
|
A 79-year-old man had undergone an endoscopic submucosal dissection for a gastric adenoma with low grade dysplasia 3 years ago. The final histological diagnosis was low grade dysplasia, equal to the preresectional diagnosis. Then he underwent surveillance endoscopy annually. There was no abnormal finding on first and second follow-ups. However, at the third visit, a conventional endoscopy revealed a whitish flat lesion in the lesser curvature of cardiac region of the stomach (), the lesion which was away from the scar area which occurred after the endoscopic resection of the adenoma. In addition, the whitish lesion was distinctly away from the normal esophageal mucosa, but its appearance looked like normal esophageal mucosa. Therefore, chromoendoscopy using Lugol's iodine solution was performed to make sure whether the lesion was squamous mucosa or not. When Lugol's iodine solution was applied, the lesion was stained brown in the same way as normal esophageal mucosa (). The endoscopic biopsy from the whitish lesion revealed stratified squamous epithelial mucosa (). The final diagnosis was gastric squamous metaplasia.
|
[[79.0, 'year']]
|
M
|
{'3430744': 1, '10935797': 1, '26465909': 1, '191328': 1, '21113875': 1, '1282115': 1, '25505726': 2, '33612676': 1, '14254074': 1, '6045404': 1, '23964341': 2}
|
{'4260108-1': 1}
|
162,748 |
3746150-1
| 23,964,342 |
noncomm/PMC003xxxxxx/PMC3746150.xml
|
Superior Mesenteric Artery Syndrome Diagnosed with Linear Endoscopic Ultrasound (with Video) in a Patient with Normal Body Mass Index
|
A 61-year-old female visited the emergency room complaining of sudden abdominal pain and nausea after overeating. She visited a local clinic where she underwent abdominal CT and was prescribed an analgesic, but the pain did not subside, so she visited our hospital. Her medical and social histories were noncontributory. At admission, her blood pressure was 120/80 mm Hg, pulse rate 68 per minute, respiratory rate 18 per minute, body temperature 36.9℃, height 157 cm, weight 50 kg, and BMI 20.3. She denied a history of weight loss. The physical examination revealed an acutely ill-looking appearance with epigastric tenderness. The complete blood count showed leukocytes 10,600/µL, hemoglobin 13.3 g/dL, and platelet count 208,000/µL. The blood chemistry showed total bilirubin 0.5 mg/dL, aspartate aminotransferase 18 U/L, alanine aminotransferase 13 U/L, amylase 106 U/L, blood urea nitrogen 23 mg/dL, creatinine 0.67 mg/dL, and C-reactive protein 0.26 mg/dL.\nThe initial abdominal X-ray revealed a large amount of food distending the stomach and mild gas accumulation in the small and large bowel (). An abdominal CT taken at the local clinic showed a hugely distended stomach and duodenum (). The aortomesenteric distance on CT was 7.4 mm which was decreased than normal mean aortomesenteric distance of 10 to 28 mm in healthy people. Conventional barium studies, which still play an important role for diagnosis of SMA syndrome, could not be performed because of severe gastroptosis and distended stomach. Then we performed esophagogastroduodenoscopy (EGD) and EUS to rule out intestinal intraluminal obstruction and gastric or duodenal ulcer disease that might be secondary to reflux or that might constitute a primary pathology mimicking SMA syndrome. EGD revealed a huge amount of food in the stomach (). Since that EUS could give us more information about surrounding organs which can directly compress the duodenum, we performed linear EUS (EG3870-UTK; Pentax, Tokyo, Japan). This did not show any abnormality of the gallbladder, common bile duct or pancreas. However, it showed the SMA running almost parallel to the abdominal aorta, with an aortomesenteric angle of 10° (normal range, 38° to 65°), confirming the diagnosis of SMA syndrome (, Supplementary Video 1 [available online at ]). The patient was managed conservatively with bowel rest and intravenous fluids. The abdominal pain and nausea were relieved and the patient started a soft diet on day 5 of admission and was discharged on day 7 of admission without any symptoms.
|
[[61.0, 'year']]
|
F
|
{'3183134': 1, '20195969': 1, '20579827': 1, '20014467': 1, '32721914': 1, '6733420': 1, '30081961': 2, '17476104': 1, '6496852': 1, '18810558': 1, '13411383': 1, '18030215': 1, '14634981': 1, '10881780': 1, '17062207': 1, '12203080': 1, '16707974': 1, '3631039': 1, '11518108': 1, '23964342': 2}
|
{'6091179-1': 1}
|
162,749 |
3746151-1
| 23,964,343 |
noncomm/PMC003xxxxxx/PMC3746151.xml
|
Endoscopic Treatment of a Symptomatic Ileal Lipoma with Recurrent Ileocolic Intussusceptions by Using Cap-Assisted Colonoscopy
|
A 73-year-old woman presented with intermittent abdominal pain and weight loss of 15 kg for the past 2 years. Her pain was frequently accompanied by nausea and/or diarrhea and tended to be aggravated by food intake. Her past medical and familial histories were unremarkable. On examination, vital signs were stable but she appeared a little chronically ill. Her abdomen was soft with no palpable mass; bowel sounds were somewhat increased and mild tenderness was noted in the right lower quadrant (RLQ). Initial laboratory blood tests were normal.\nColonoscopy revealed an erythematous polypoid mass at the proximal ascending colon and it seemed to have a huge stalk thicker than the mass itself (). With air being inflated during colonoscopy, it was not seen in the colonic lumen and abruptly disappeared. As the endoscope was advanced through the ICV, there was a polypoid mass in the terminal ileum and multiple tiny hemorrhagic spots on the ileal mucosa; the mass intussuscepted into the colon through the ICV had reverted back to its original site in the terminal ileum (). The thick stalk must have been an intussusceptum of the terminal ileum with the mass as a lead point. In its original position in the ileum, a short stalk was identified on the base of the polypoid mass. Additionally, abdominal computed tomography (CT) scan revealed a well-demarcated pedunculated subepithelial mass with fat attenuation indicating a lipoma of the terminal ileum ().\nThis ileal lipoma was thought to have been responsible for her abdominal pain and weight loss on account of repeated ileocolic intussusceptions causing intermittent intestinal obstructions. Because the patient strongly refused surgical treatment, we planned to endoscopically remove her ileal lipoma considering potential sequelae of ileal resection. In order to perform endoscopic procedure in the spacious colonic lumen, we tried to retract the mass into the colonic lumen through the ICV but unfortunately failed. Therefore, to keep a clear visual field within the narrow lumen of the ileum, a cap-assisted colonoscopy technique was used. After submucosal injection into the base of the mass, a snare polypectomy was performed within the ileum (). And then, three clips were placed to prevent delayed hemorrhage or perforation (). There were no immediate complications after the polypectomy. The histopathology report confirmed a 2.6×2.7 cm subepithelial lipoma. At 2 days of fasting after the procedure, oral intake was started and the patient complained of no symptoms related to food intake. Since resection of the lipoma, her body weight has gradually restored.
|
[[73.0, 'year']]
|
F
|
{'19152443': 1, '9402125': 1, '33898899': 1, '3596141': 1, '9074370': 1, '3284624': 1, '15788588': 1, '13934160': 1, '23964343': 2}
|
{}
|
162,750 |
3746152-1
| 23,964,344 |
noncomm/PMC003xxxxxx/PMC3746152.xml
|
Endoscopic Removal of a Proximally Migrated Metal Stent during Balloon Sweeping after Stent Trimming
|
A 74-year-old woman was admitted due to jaundice and epigastric pain which lasted for 7 days. Laboratory tests revealed the following: white blood cell count, 5.84×109/L (reference range, 4.0 to 10.8×109/L); aspartate aminotransferase, 123 IU/L; alanine aminotransferase, 144 IU/L; total bilirubin, 5.2 mg/dL; alkaline phosphatase, 488 IU/L; amylase, 315 U/L; lipase, 689 U/L; carbohydrate antigen 19-9, 35.86 U/mL; and carcinoembryonic antigen, 1.65 ng/mL. An abdominal computed tomography scan showed a ~2.1-cm low-attenuated mass lesion abutting on the superior mesenteric vein with dilatation of the intrahepatic bile duct, common bile duct (CBD) and pancreatic duct (PD), which suggested pancreas neoplasm. Subsequent endoscopic retrograde cholangiopancreatography (ERCP) showed short segmental distal CBD narrowing and diffuse irregular narrowing of the PD with marked upstream ductal dilatation (). After a 5-Fr single pigtail 7-cm-long stent was inserted into the PD following brushing cytology and an 8.5-Fr Tannenbaum, 7-cm-long (Cook Endoscopy, Winston-Salem, NC, USA) stent was inserted into the CBD, her symptoms improved and the obstructive jaundice resolved. Finally, we diagnosed her as a pancreas adenocarcinoma with CBD obstruction.\nTwo months later, she underwent repeat ERCP for stent exchange using a 60-mm-long, 10-mm diameter cSEMS (Bonastent; Standard Sci Tech Inc., Seoul, Korea), because she refused surgical operation. However, she was readmitted in 2 months due to epigastric pain, fever, and jaundice. A subsequent endoscopy showed a partial distally migrated cSEMS that was impossible to access and revise through the migrated stent. We decided to remove the stent but failed with forceps and a snare.\nThus, stent trimming was performed with an APC system (ERBE Elektromedizin GmbH, Tübingen, Germany). The power setting was 60 W, and the argon gas flow was set to 2 L/min. The amputated stump margin was set about 10 mm from the papilla. Stent amputation progressed in a circumferential manner until it was completely cut after 10 minutes (). The stent fragment was removed with a retrieval net. Then, a retrieval balloon was used to remove the clogging sludge following insertion of a guidewire through the remnant fragmented stent. However, while moving the balloon back and forth, the remnant stent migrated proximally very abruptly and floated to the dilated CBD. Immediate retrieval of the stent was not attempted because of the sharp cutting plane edge. Two 7-Fr double pigtail stents (9- and 10-cm long, respectively; Cook Endoscopy) were inserted in both intrahepatic bile ducts through the proximally migrated metal stent (). However, the patient was readmitted twice because of cholangitis and obstructive jaundice after 1 month, so removal of the proximally migrated metal stent was planned. Following removal of the double pigtail stent with rat tooth forceps, the stricture was dilated to 8 mm with a balloon catheter (Hurricane biliary balloon dilatation catheter; Boston Scientific, Natick, MA, USA). The proximal end of the floating metal stent was captured with a basket, rotated 180° in the CBD, and then removed successfully (, ). No procedure related complications occurred during the removal of the migrated stent, and then a uSEMS was inserted successfully. Since then, no complications have been observed for 5 months.
|
[[74.0, 'year']]
|
F
|
{'9270926': 1, '18226706': 1, '30766947': 1, '27030246': 1, '10863921': 1, '19267200': 1, '12244508': 1, '1281903': 1, '10570336': 1, '19542849': 1, '33204918': 1, '21677835': 1, '15472699': 1, '16848800': 1, '17163328': 1, '32273895': 2, '21299614': 1, '9473549': 1, '15844021': 1, '15812404': 1, '16301035': 1, '23964344': 2}
|
{'7136765-1': 1}
|
162,751 |
3746224-1
| 23,960,394 |
noncomm/PMC003xxxxxx/PMC3746224.xml
|
Keratosis Follicularis Spinulosa Decalvans: A Rare Cause of Scarring Alopecia in Two Young Indian Girls
|
A 8-year-old female came to the clinic with complaints of hair loss over the scalp since 6 years with sparse eye brows. Hair loss was progressive in spite of trying Ayurvedic medicine and homeopathy. On examination hair density was reduced over the scalp with vellus and terminal hairs. Multiple follicular papules were seen giving roughness to the scalp [Figures and ]. Similar lesions were seen all over the back, chest wall, extensor aspects of limbs. There was no history of photophobia and ophthalmic examination showed no evidence of conjunctival/corneal involvement. Punch biopsies were taken and submitted for histopathological examination. Her 5 year old sister had similar complaints. Both the siblings were normal at birth, the above symptoms started from the age of 2 years. However, biopsy was not taken from the younger sibling. Histopathologic examination revealed hyperkeratosis and mild acanthosis of epidermis with follicular plugging and dilated infundibulum []. The dermis revealed perifollicular lymphocytic infiltrate with eccentric epithelial atrophy, polytrichia, and perifollicular fibrosis []. Periodicacid Schiffs (PAS) stain done did not show any fungal organisms. Considering family history and clinical features, a diagnosis of KFSD was offered.
|
[[8.0, 'year']]
|
F
|
{'20952906': 1, '15965418': 1, '1550124': 1, '28954108': 1, '12399750': 1, '6336927': 1, '16778532': 1, '21508573': 1, '18280351': 1, '9598732': 1, '23960394': 2}
|
{}
|
162,752 |
3746225-1
| 23,960,395 |
noncomm/PMC003xxxxxx/PMC3746225.xml
|
Bullous Pilomatricoma: A Rare Variant Resembling Bouncy Ball
|
A 17-year-old girl presented with a solitary reddish semi-transparent blister over her right upper arm since 3 months. Initially, the lesion started as a solid pin-head sized papule, which gradually progressed to form a semi-transparent blister with a hard nodule inside. No history of local trauma or insect bite. No history of similar lesions in the past or in family members.\nOn examination, single 2 cm sized erythematous semi-transparent bullae with a white nodule was seen on the medial aspect of the right upper arm [Figure and ]. The appearance of this resembled a bouncy ball []. On palpation, the bullae had a jelly like consistency and the nodule underneath was hard. On puncturing the lesion, it oozed a jelly like material. Systemic examination was normal. We considered a differential diagnosis of infected sebaceous cyst and dermatofibroma.\nRoutine investigations were normal and excision biopsy was carried out []. Histopathology revealed islands of basaloid cells with central abrupt keratinization and dilated lymphatics with dermal edema [Figures and ]. Ghost cells (shadow cells) [], foreign body giant cell reaction [], and small foci of calcification were also seen []. With these findings, diagnosis of bullous pilomatricoma was made.
|
[[17.0, 'year']]
|
F
|
{'12974707': 1, '25473249': 1, '15268712': 1, '9046744': 1, '10192393': 1, '6863619': 1, '11558887': 1, '17519628': 1, '10640845': 1, '686751': 1, '8170843': 1, '21506983': 1, '22772621': 1, '23960395': 2}
|
{}
|
162,753 |
3746226-1
| 23,960,396 |
noncomm/PMC003xxxxxx/PMC3746226.xml
|
Trichothiodystrophy in a Child with Occult Learning Disorder
|
A 13-month-old girl presented with hair fragility and hair loss since age of 3 months. The mother had an uncomplicated antenatal history with first trimester vaginal bleeding. She was born at term, of non-consanguineous parents. At birth, she was encased in a collodion membrane, which was shed after 2 weeks. There was no photosensitivity and sweating was normal. An initial impression of self-healing collodion baby was made.\nPhysical examination revealed a prematurely aged appearance, frontal bossing [], sparse scalp hair [], knotted area on right scalp, absent eyebrows, brittle finger and toe nails with onychoschizia [], and normal sweating. The skin showed mild xerosis with eczema on the trunk.\nLight microscopy of haircuts showed trichorrhexis nodosa, trichoschisis []. On polarized microscopy, the hair shafts exhibited light and dark banding in a tiger-tail pattern []. Karyotype was 46XX. Full blood count, electrolytes, renal, liver function, serum immunoglobulin, and lymphocyte subsets were normal.\n2D echocardiogram revealed a moderate atrial septal defect, mild pulmonary valve stenosis, and tricuspid valve regurgitation. Ultrasound of the head was performed to investigate macrocephaly. This showed asymmetry of the lateral ventricles with left frontal horn dilatation. She was found to have global developmental delay, particularly in the gross motor skills. She started rolling on her stomach at 8 months, and by 14 months, she was not crawling, showed poor dynamic sitting balance and oro-motor delay with poor chewing and feeding skills.\nThe clinical features and hair microscopy findings were consistent with a diagnosis of TTD. The patient was followed up closely with dermatologists, cardiologists, and neurologists. She received physiotherapy for motor skill improvement, and was enrolled in “Rainbow Centre,” a school with special facilities catering to children with learning disability.
|
[[13.0, 'month']]
|
F
|
{'7458366': 1, '9758621': 1, '11369901': 1, '8453147': 1, '9496800': 1, '18603627': 1, '19681155': 1, '9012405': 1, '5120162': 1, '15220921': 1, '23960396': 2}
|
{}
|
162,754 |
3746227-1
| 23,960,397 |
noncomm/PMC003xxxxxx/PMC3746227.xml
|
Trichotillomania in a Case of Vascular Dementia
|
A 79-year-old right-handed Hindu Indian male retired engineer was referred by his family physician to the psychiatry outpatient division of our private clinic. He presented with progressive cognitive and mental deterioration, involving memory impairment and executive dysfunction (difficulties in planning, sequencing, abstraction, and goal-directed behavior). This was coupled with behavioral and personality changes that began 3 years prior to the memory impairments and cognitive deterioration. His wife (main caregiver) reported deterioration in personal hygiene, an abandonment of personal interests and apathy with a lack of will to do anything. The patient just lay in bed all day long, locked up in his room. His magnetic resonance imaging brain revealed multiple infarcts in subcortical and cortical areas of the brain. The patient was diagnosed as having vascular dementia. The patient was started on Donepezil 10 mg per day and multivitamins were prescribed, with a 20% improvement in cognitive symptoms over a 4 week period. During the 3rd week of treatment he began pulling out his scalp hair throughout the day and multiple times. The patient gave no explanation for this act, and denied any feeling of tension prior to the act or deriving any pleasure from the act. He reported no pain, and had no insight regarding its compulsive nature or the potential harmful consequences to his skin. There was no evidence of any delusional beliefs or psychotic features related to his hair-pulling behavior. No history of similar symptoms, obsessive compulsive disorder or dementia in the family was present. The trichotillomania persisted despite treatment with several selective serotonin reuptake inhibitors (SSRIs) like Sertraline, Fluoxetine, Escitalopram, and Fluvoxamine (all separately in divided doses) and Mirtazapine with no improvement with any of the drugs. The patient had a mini mental status examination score of 16. The patient's informal neuropsychological exam showed marked memory deficits, executive dysfunction, and apraxia. No language deficits were noted except slowness in speech. A metabolic workup for treatable causes of dementia revealed no abnormalities that could contribute to his cognitive deficits. The patient followed-up for a few months and did not follow-up thereafter.
|
[[79.0, 'year']]
|
M
|
{'19428495': 1, '22641961': 1, '27840761': 2, '19926375': 1, '9255863': 1, '22138231': 1, '11427250': 1, '17403968': 1, '29769783': 2, '21797657': 1, '19692854': 1, '18318881': 1, '20533371': 1, '23960397': 2}
|
{'5093278-1': 1, '5939009-1': 1}
|
162,755 |
3746228-1
| 23,960,398 |
noncomm/PMC003xxxxxx/PMC3746228.xml
|
Zinc Deficiency Associated with Hypothyroidism: An Overlooked Cause of Severe Alopecia
|
A 28-year-old woman presented with weakness, lack of appetite, diffuse hair loss, and asymptomatic scaly skin lesions of 2 months duration. There was no history suggestive of connective tissue disease or malabsorption. On physical examination, the patient appeared depressed. She had pallor and puffiness of the upper part of the face. There was diffuse, dry scaling over the face and extremities, along with annular, erythematous, scaly patches over the nape of the neck. The notable finding on the scalp was profound diffuse alopecia [] with marked hair loss over the occipital area []. There was also severe thinning of the hair of the eyebrows and eyelashes []. A hair pull test done from five different sites on the scalp was positive. Light microscopic examination of the hair revealed telogen type hair roots without any hair shaft abnormalities. Thyroid function tests were as follows: T3 70 ng/dl (normal 80-200), T4 2 mcg/dl (normal 4-12), and Thyroid Stimulating Hormone 64 IU/ml (normal 0.30-4.5). All routine investigations including antinuclear antibody profile were within normal limits, except for a low hemoglobin level of 9 g/dl. Histopathological examination of an annular scaly lesion showed minimal epidermal hyperplasia with a mild perivascular inflammatory infiltrate.\nThyroid hormone supplements were started, but the scaly lesions persisted and there was no detectable improvement in the hair loss. Since a definite diagnosis of the annular scaly lesions could not be made, plasma zinc level was estimated, which was 62 mcg/dl (normal 66-144 mcg/dl and optimal levels 90-150 mcg/dl).[] Zinc monohydrate 140 mg capsules containing 50 mg of elemental zinc was given twice a day, along with other multivitamins. One month later, the skin lesions had cleared completely, and there was such a remarkable improvement in her mental depression and facial puffiness, that her facies was totally unrecognizable when compared to her previous appearance []. Subsequent follow-up demonstrated complete regrowth of hair over a course of 4 months [].
|
[[28.0, 'year']]
|
F
|
{'30671883': 1, '10201332': 1, '28417080': 1, '31056723': 1, '26734478': 1, '11285315': 1, '27881965': 1, '29546054': 1, '28217478': 1, '34944304': 1, '22223987': 1, '31810194': 1, '2142391': 1, '22565422': 1, '107785': 1, '18049926': 1, '17618180': 1, '22483512': 1, '16255843': 1, '23960398': 2}
|
{}
|
162,756 |
3746229-1
| 23,960,399 |
noncomm/PMC003xxxxxx/PMC3746229.xml
|
Allergic Contact Dermatitis to Superglue
|
A 28-year-old man who was using wig for androgenic alopecia presented with itchy, oozy erythematous plaque on the anterior hair line since 3 months []. Patient used superglue to fix the wig to the scalp. The lesions were restricted to the area where adhesive was used to fix the wig. A diagnosis of allergic contact dermatitis to superglue was made.\nThe patient was patch tested with Indian Standard Series, Dental series (Chemotechnique Diagnostics, Vellinge, Sweden) which contained the acrylates series. An open patch test with the superglue was done to the patient. The readings were taken at 48 and 72 h. He developed a positive (1+) allergic reaction to 2-hydroxyethyl methaacrylate [] in dental series and superglue. Biopsy showed evidence of chronic lymphocytic spongiotic dermatitis. The patient was advised to abstain from using the wig and treated with topical steroids. The lesions subsided after 2 weeks.
|
[[28.0, 'year']]
|
M
|
{'3427950': 1, '3782172': 1, '8508628': 1, '28492024': 1, '28492045': 1, '20920413': 1, '18503683': 1, '23960399': 2}
|
{}
|
162,757 |
3746230-1
| 23,960,400 |
noncomm/PMC003xxxxxx/PMC3746230.xml
|
Short Anagen Hair Syndrome
|
A healthy Hispanic 3-year-old girl presented with a history of short hair since birth. The mother reported that there was excessive shedding and poor hair growth, and that the girl had never needed a haircut. Family history was negative for hair loss or hair diseases. Aggravating factors were denied and the past medical history was uneventful. Upon examination the patient was well- developed and did not present any abnormality except for short, dark, and thin hair [Figures and ]. The pull test was positive. Body hair was normal, as was the rest of the physical examination.\nDermoscopy of pulled hairs showed 4.7 cm long telogen hairs with tipped points, which indicates that the hair had never been cut. A diagnosis of SAS was established through clinical and dermoscopic parameters.
|
[[3.0, 'year']]
|
F
|
{'3828219': 1, '28791288': 1, '20546972': 1, '14576690': 1, '10971339': 1, '16021162': 1, '21545502': 1, '20553398': 1, '23158639': 1, '23960400': 2}
|
{}
|
162,758 |
3746231-1
| 23,960,401 |
noncomm/PMC003xxxxxx/PMC3746231.xml
|
Alopecia Areata Treated with Phenolisation and Intravenous Dexamethasone Pulses
|
A 13 year old girl presented to us with diffuse hair loss over the scalp involving more than 50% of the scalp [] for the past 6 months. She had consulted many dermatologists in the past 6 months since the onset of her complains, but none of the treatment brought relief. Therefore, it was not only the disease entity that we needed to consider but also the financial and psychosocial impact on the patient. She had no associated hair loss over any other body site. There was no history suggestive of any associated complaints. Her nails were normal on examination. There was no history of similar complains in the family. After taking a prior informed consent, phenolisation was done over the bald patches with 88% phenol until a uniform ivory white frost appeared. Phenol was applied all over the bald patches, covering more than 50% of scalp surface; 1 ml of phenol was taken in a container and applied to the scalp by dipping a bud in phenol. We assume that out of 1 ml, some amount of phenol was left in the bud. Thus, the total application of phenol was below the safe limit. No neutralization was done. The patient did complain of burning sensation and was given 5 mg diazepam orally. She underwent 5 such sittings at an interval of 15 days each. She was also given dexamethasone pulse therapy for 4 months. Dexamethasone was given in the dose of 60 mg intravenously in 5% dextrose. She was given dexamethasone and phenolisation at an interval of 15 days. She began to show response to therapy after the 2nd sitting when vellus hair regrowth was evident diffusely all over the bald patches. After five sessions done with 88% phenolisation and 4 pulses of dexamethasone intravenous therapy, she showed marked improvement with well-marked hair growth over the patches. Phenolisation is painful and therefore she was given intravenous diazepam prior to the procedure. There were no reported side effects in the present case.
|
[[13.0, 'year']]
|
F
|
{'8274789': 1, '19281605': 1, '8850047': 1, '20885062': 1, '23960401': 2}
|
{}
|
162,759 |
3746232-1
| 23,960,402 |
noncomm/PMC003xxxxxx/PMC3746232.xml
|
Colocalization of Vitiligo and Alopecia Areata: Coincidence or Consequence?
|
A 12-year-old boy presented to the skin outpatient department with history of depigmented areas on the scalp, face, neck, arms and legs for 5 years. He also gave a history of development of patchy loss of hair over some of these lesions for 3 years. There was no previous history of any trauma or medications. Family history was not relevant. On examination, there were depigmented macules over the scalp, forehead, eyebrows, periorbital, perioral, preauricular regions, neck, elbows, hands, feet, shins, nose, chin, hands, knees and feet [Figures and ]. Patches of hair loss were seen, limited to some of these depigmented areas over the vertex and occipital region of the scalp and eyebrows []. Other body areas were not affected by patchy hair loss. Clinically, the diagnosis of vitiligo with AA was made. On histopathological examination [] of the skin biopsy specimen obtained from the scalp, dense peribulbar infiltrate was seen in the dermis. Other features were in keeping with the diagnosis of AA. Additionally, the basal layer of the epidermis was almost devoid of pigment, [] confirming the diagnosis of vitiligo over the same site.
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[[12.0, 'year']]
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M
|
{'33911306': 1, '21712899': 2, '9125754': 1, '10571834': 1, '14870990': 1, '19040503': 1, '19320739': 1, '14043621': 1, '478074': 1, '2355182': 1, '14582666': 1, '11712689': 1, '34604326': 1, '8170863': 1, '23960402': 2}
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{'3107954-1': 1}
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162,760 |
3746233-1
| 23,960,403 |
noncomm/PMC003xxxxxx/PMC3746233.xml
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Monilethrix with Variable Expressivity
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A 32-year-old male presented with decreased hair over the scalp and body since childhood. Patient was asymptomatic, and there was no history suggestive of impaired psychomotor development. He did not give any history of similar illness in his family members. Examination showed diffuse hair loss with short and brittle hairs over scalp, predominantly over the occipital region []. The moustache and pubic area also showed short broken hairs. Beard, axillary and body hairs were absent []. Follicular keratotic papules were seen over the occiput, nape of neck and extensor arms []. The eyes, nails and teeth were normal. Light microscopy of hair showed beaded appearance with elliptical nodes separated by narrower internodes thus establishing the diagnosis of monilethrix [].
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[[32.0, 'year']]
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M
|
{'10504448': 1, '15744029': 1, '6627730': 1, '20948138': 1, '16575393': 1, '23960403': 2}
|
{}
|
162,761 |
3746308-1
| 23,960,430 |
noncomm/PMC003xxxxxx/PMC3746308.xml
|
Pseudocyesis: A complication of antipsychotic-induced increased prolactin levels and weight gain
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Mrs. X, a 46-year-old woman presented with an acute onset illness, continuous in course of 2-month duration, which started about 2 months after the death of her only son in a road traffic accident, characterized by liability of effect, delusion of persecution, visual hallucinations, regressed behavior, restlessness, irritability, disorganized behavior, muttering to self, decreased sleep, decreased appetite and poor self-care. There was no history of first rank symptoms, grandiosity, core depressive symptoms, any substance abuse, head injury, seizures, loss of consciousness and cognitive disturbances. There was no family history of mental illness, and premorbidly the patient had histrionic traits. Initially, a diagnosis of Acute and Transient Psychotic Disorder (acute polymorphic psychotic disorder without symptoms of schizophrenia) (as per ICD-10) was considered and she was started on risperidone up to 3 mg/day, but her condition kept worsening resulting in hospitalization. At the initial evaluation her weight was 83 kilograms, height was 158 cm and waist circumference was 102.5 cm. Routine investigations and computed tomography of the brain did not reveal any abnormality. In view of non-response to 4 weeks of therapy, risperidone was stopped and she was started on olanzapine up to 20 mg/day, with which she initially showed response, and was discharged after 5 weeks. However, within 2 weeks she had worsening of symptoms leading to re-admission. Due to the florid symptoms, she was started on electroconvulsive therapy and antipsychotic was changed to trifluperazine 15 mg/day. A diagnostic possibility of psychosis (not otherwise specified) (as per ICD-10) was considered. Her psychotic symptoms stabilized with trifluperazine and ECT, but she developed depressive symptoms after stoppage of ECT, amounting to moderate depressive episode without somatic features (as per ICD-10) and required treatment with sertraline 100 mg/day. With this combination she remained well for 14 months. Although she did not achieve her premorbid self, her residual negative symptoms did not interfere much with her level of functioning. During the stable phase, her body weight, waist circumference, lipid profile and fasting blood sugar levels remained stable. However, initially reported irregular menstrual cycles and later developed amenorrhea and galactorrhea on investigation was found to have significant increase in serum prolactin levels (150 ng/ml). Tab trifluperazine was crossed tapered with tab quetiapine, which was increased to 300 mg/day. With starting of quetiapine, she started gaining weight and her waist circumference increased significantly. While cross-tapering was being done, she started having relapse of symptoms of psychosis. The symptoms kept on worsening despite increase in the dose of quetiapine to 600 mg/day along with clonazepam 6 mg/day with good compliance. The relapse also coincided with the death anniversary of her son. The symptomatology of the current episode was very similar to the previous episode, but additionally she had delusion of pregnancy. She reported that she is pregnant, is able to perceive the movements of the fetus and is shortly going to deliver a male child. When anybody tried to tell her against the same, she would become irritable and violent. Persistence of symptoms with quetiapine led to third admission. On mental status examination, she held the belief of being pregnant firmly and could not be convinced against the same. While in the hospital at times she reported pain in the abdomen and would say that she was having labor pain and is going to give birth to a male child. She would also go to pass urine frequently, would demand for healthy food traditionally given to pregnant mothers and would walk by protruding her abdomen.\nAt this time, her body weight was 96 kilograms and waist circumference was 138 cm. Her lipid profile revealed raised triglyceride levels and reduced high density lipoprotein levels. Ultrasound abdomen revealed bulky uterus with multiple fibroids with no fetal sac and repeat serum prolactin levels were 89.5 ng/ml and 76.55 ng/ml on 2 different occasions 2 weeks apart. All other investigations including urine pregnancy test, thyroid function test and serum cortisol levels were done in consultation with the gynecologist and endocrinologist, which were found to be within normal limits. During the hospital stay, she very firmly held the belief that she is pregnant even though she had her menstrual periods. She would often ask the treating team to shift her to the maternity ward. She was initially managed with tab ziprasidone up to 120 mg/day along with electroconvulsive therapy. Although she showed some improvement in her positive symptoms with this treatment, delusion of pregnancy persisted at the same intensity. Increase in dose of ziprasidone to 140 mg/day led to changes in the electrocardiogram and resultantly it was stopped. After giving all the available options, patient's husband opted for clozapine. After proper evaluation, she was started on clozapine and the dose was gradually increased to 200 mg/day, with which she achieved remission with no further increase in body weight and waist circumference over the period of 12 weeks of therapy. Remission was also accompanied with normalization of serum prolactin levels. After remission, she acknowledged that she had false belief of being pregnant.
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[[46.0, 'year']]
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F
|
{'19096992': 1, '5540348': 1, '1773250': 1, '25133144': 1, '12890303': 1, '30405270': 1, '33927534': 1, '18354070': 1, '23960430': 2}
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{}
|
162,762 |
3746309-1
| 23,960,431 |
noncomm/PMC003xxxxxx/PMC3746309.xml
|
Additive effect of propofol and fentanyl precipitating cardiogenic shock
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A 34-year-old woman presented with complaints of umbilical hernia and had no secondary infection on clinical examination. The surgery was performed under conscious sedation and analgesia procedure which is routinely preferred by the anesthetists for minor surgeries. The patient experienced sudden, severe hemodynamic deterioration after undergoing this minor surgical procedure. Spontaneous breathing was maintained by continuous infusion of propofol at a rate of 100 μg/kg/min to achieve conscious sedation after administering fentanyl 100 μg intravenously. During surgery, the patient remained hemodynamically stable. Patient had nausea and vomiting in the early postoperative period, which were treated with 4 mg of intravenous ondansetron. A few minutes later, the patient experienced hemodynamic instability with sinus tachycardia and hypotension. Her heart rate was 122 regular beats/minute, and the blood pressure was 50/30 mmHg. The oxygen saturation had decreased to 80% as recorded by pulse oximetry, despite oxygen supply through face mask. She was immediately treated with intravenous dopamine and dobutamine as well as with ventilator support due to acute respiratory failure. The arterial gasometry showed oxygen pressure 40 mmHg and carbon dioxide pressure 49 mmHg; the electrocardiogram monitor showed sinus tachycardia. The signs of heart failure (HF) were found in the bedside digital X-ray of chest and emergency transthoracic echocardiography (TTE) revealed severe biventricular dysfunction with global hypokinesia. The LVEF was 42%. Coronary angiography showed no coronary lesions. An intra-aortic balloon pump was introduced for counterpulsation. The repeat TTE revealed LVEF 32% and a left ventricular extracorporeal membrane oxygenation (ECMO) device was inserted to assist the impaired clinical course of the patient. The LVEF gradually improved and on the 5th postoperative day the ventilatory support and circulatory perfusion assistance were removed. Troponin T and C reactive protein levels remained within normal limits. The other routine investigations like chemistry panel, complete blood cell count, and coagulation profile were within normal limits. The serology battery for myocarditis, blood cultures, urine cultures, and cytotoxic antibodies were found insignificant. An endomyocardial biopsy was not performed because of its low diagnostic yield. Three weeks later, a new TTE showed a non-dilated left ventricle, absence of segmental contractility alterations, and an LVEF in the normal range. She was reviewed for 6 months in out-patient department and was found asymptomatic and required no further treatment.
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[[34.0, 'year']]
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F
|
{'21464061': 1, '19092649': 1, '19577484': 1, '21824313': 1, '21297474': 1, '21510576': 1, '24250216': 1, '18312523': 1, '20412475': 1, '20412350': 1, '21536364': 1, '21804711': 1, '12441012': 1, '21751687': 1, '23960431': 2}
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{}
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162,763 |
3746448-1
| 23,960,383 |
noncomm/PMC003xxxxxx/PMC3746448.xml
|
Small bowel obstruction in percutaneous fixation of traumatic pelvic fractures
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A 51-year-old man, with no medical history of note, was in a motorcycle accident. In the emergency room, he presented with hemodynamic instability due to a pelvic fracture and a concomitant catastrophic soft tissue injury involving the scrotum, perineum, and anus with absence of the anal reflex. The extended EcoFast showed no fluid collection in the abdomen and no pneumothorax. The pelvis X-ray showed ischiopubic and ileopubic fractures associated with symphyseal disruption (anterior posterior fracture APII, see Young and Burgess). After the resuscitation phase, the patient underwent full-body computed tomography (CT) [] and was subsequently transferred to the operating theater. His pelvis was fixed with external screws [].\nAn exploratory laparotomy was performed to exclude abdominal organ damage, and a loop colostomy was performed for the anal incompetence. Then, the patient was admitted to our intensive care unit (ICU), where no bowel function was observed for the first 6 post-operative (PO) days. On PO day 7, the patient presented with abdominal distension, elevated inflammatory indices, and fever, so we performed abdominal CT with oral and intravenous contrast looking for signs of intestinal obstruction.\nThe clinical hypothesis of obstruction was confirmed by the presence of numerous dilated small bowel loops with air/fluid levels; CT showed an ileum segment trapped in the sacral fracture [].\nThe patient underwent an exploratory laparotomy that confirmed the cause of the obstruction; a small bowel resection and an end-to-end manual anastomosis were thus performed.\nThe second post-operative period was uneventful, and the patient was discharged from the ICU to a ward. An evaluation of the rectal sphincter showed normal function; therefore, after the peroneal wound healed, the colostomy was closed.
|
[[51.0, 'year']]
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M
|
{'17495062': 1, '18288016': 1, '26815683': 1, '16309680': 1, '6418021': 1, '10052792': 1, '23960383': 2}
|
{}
|
162,764 |
3746449-1
| 23,960,384 |
noncomm/PMC003xxxxxx/PMC3746449.xml
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Hypothermic overdose, not all bad?
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A 51-year-old woman presented to the emergency department (ED) in the evening following an intentional overdose of alcohol and her psychiatric medication and was not seen for the previous 24 h. She was found unresponsive at home on the kitchen floor by her parents who had been trying to contact her who then called the ambulance service to her flat. She was lying with her face down and had blood on her face and it was presumed by the paramedics that she had fallen and may have rolled on the floor as there was blood smears on the floor. She was supine on the floor and surrounded by empty packets of medication and two empty wine bottles. It was estimated from the dates on the packets and missing pills that she had taken 5800 mg of quetiapine and 240 mg of citalopram. Paramedics reported that they read the thermostat in her flat read 10°C.\nParamedics brought the patient to the ED and her Glascow Coma Scale as eight with agonal respirations, pulse of 56/min, blood pressure of 55/35 mmHg, and a core temperature of 24°C. Her ears, nose, and mouth were covered with blood from her nose. There were no other external injuries and the remainder of the exam was unremarkable.\nArterial blood gas demonstrated a pH-7.05, pCO2-55 mmHg, pO2-107 mmHg, Bicarb - 15 mmol/L, and Lactate - 11 mmol/L. Full blood count and electrolytes were unremarkable. Cardiac enzymes were not performed. The electrocardiogram (ECG) demonstrated multiple axis changes with increased QRS, prolonged QTc, ventricular ectopic beats, and Osborne (J) waves []. Chest X-ray demonstrated right lower lobe infiltrate suggesting aspiration. Toxicology showed an ethanol concentration of 21 mmol/L and paracetamol of < 30 μmol/L. computed tomography (CT) scans of her head and c-spine were normal.\nIn the ED, the patient was intubated and ventilated with warmed humidified oxygen. An orogastric tube was inserted and 200 ml of blood was aspirated, likely from swallowed blood as there was no other evidence of gastrointestinal bleeding or internal injury found during her hospital course. She was given 200 mmols of sodium bicarbonate, 2 g of magnesium sulfate, 4.4 mmols of calcium gluconate, and a low-dose adrenaline infusion of 0.5 mg/h. Management of hypothermia included removal of clothing, warming blanket, active warming with warmed intravenous normal saline and warmed bladder, and gastric lavage. An indwelling rectal thermometer was placed and her core temperature rose approximately 0.5°C an hour until it reached 38°C.\nA Her body temperature returned to normal over the next day and her vital signs returned to normal. She was extubated 24 h later and was treated for aspiration pneumonia. She recovered completely except for numbness in her left leg. She was transferred to the psychiatric ward after 72 h of medical admission as she had admitted to this being a suicide attempt.
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[[51.0, 'year']]
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F
|
{'15845138': 1, '16096514': 1, '11132243': 1, '16564768': 1, '20210726': 1, '18606348': 1, '12098179': 1, '25666953': 1, '10665270': 1, '22114630': 1, '11391127': 1, '11856793': 1, '23960384': 2}
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{}
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162,765 |
3746782-1
| 23,976,844 |
noncomm/PMC003xxxxxx/PMC3746782.xml
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Valproic acid-associated low fibrinogen and delayed intracranial hemorrhage: case report and mini literature review
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A 41-year-old male had suffered from gradual hearing loss in his right ear for 2 years. Head computed tomography and magnetic resonance imaging scans showed a neoplasm in the cerebellopontine angle region, which was suspected to be acoustic neurilemmoma. Preoperative routine coagulation tests of APTT, PT, thrombin time, Fbg, and platelet count (Plt) were within the normal ranges, and he had no history of bleeding since birth. Clinical examination, biochemistry analysis, and kidney function were normal. The echocardiogram showed normal sinus rhythm. The patient had a history of hepatitis B 20 years before; however, liver enzymes and synthesis function were normal before surgery.\nResection of the neoplasm was successfully performed and blood loss was not excessive during the operation. The results of the pathological examination confirmed the diagnosis of acoustic neurilemmoma. VPA was administered at 20 mg/kg/day to prevent seizures after surgery. Twelve days after surgery, the patient reported headache and examination suggested suspected re-bleeding from the surgical site. This was confirmed in the second surgery. He was treated by decompressive craniotomy to relieve the high pressure.\nAfter the second surgery, a drainage tube was inserted in the incision, since interim bleeding was present (). He received daily transfusions of fresh plasma and cryoprecipitate to improve coagulation function, but the volume of drainage from surgical lesions remained about 30 mL/d. His coagulation function was again tested and he was found to have normal PT, APTT, TT, D-dimer, coagulation factors, and Plt, but a low Fbg level (0.8–1.6 g/L; reference value, 2–4 g/L), high tissue-type plasminogen activator (t-PA) activity (5,400 U/mL; reference value, 300–600 U/mL), and high fibrinogen/fibrin degradation product (FDP) level (60 mg/L; reference value, <10 mg/L). Meanwhile, his biochemistry results, kidney function, and liver function remained normal.\nThe patient was referred to the Department of Hematology for further management on 30 days following his first surgery. With a supplement of daily Fbg (3 g/d) and use of antifibrinolytic agents for 5 days, the amount of bleeding from the drainage tube decreased gradually and the patient felt his headache relieved without VPA. Coagulation was tested daily and results showed that the Fbg gradually returned to normal within 5 days: from 0.8 g/L on the first day to 1.2 g/L on the second day of treatment, 1.8 g/L on the third day, 2.3 g/L on the fourth day, and 3.5 g/L on the fifth. Coagulation parameters were maintained at normal levels in a week without Fbg transfusion.\nFollowing this, the patient was referred again to the Department of Neurosurgery and VPA treatment was resumed. Amazingly, his Fbg level decreased over time, reaching the minimum level of 0.53 g/L on the fifth day of VPA re-administration. Fortunately, the patient had no bleeding symptoms or manifestation. VPA-associated hypofibrinogenemia was suspected, so the treatment discontinued. Following this, his Fbg level returned to normal and remained stable. The drainage tube was removed 61 days after his first surgery. At follow-up at 6 months, the patient’s hemostatic parameters including Fbg were normal and no symptoms of bleeding were found.
|
[[41.0, 'year']]
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M
|
{'19482838': 1, '21472635': 1, '8603633': 1, '16886976': 1, '11913569': 1, '8614514': 1, '8733899': 1, '25214766': 2, '18600085': 1, '33376233': 1, '16608372': 1, '7512905': 1, '22363677': 1, '19404518': 1, '16787750': 1, '20798865': 1, '78084': 1, '15013052': 1, '8280448': 1, '23976844': 2}
|
{'4159221-1': 1}
|
162,766 |
3746942-1
| 23,970,922 |
noncomm/PMC003xxxxxx/PMC3746942.xml
|
Global coronary arteries spasm in a young patient
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A 42-year-old smoker man without history of cardiac problem and no other cardiac risk factors presented with one episode syncope and was referred to our cardiology clinic for work-up. His syncope was sudden, with no triggered factor, tongue biting, abnormal movement, lower limb weakness and blurred vision and chest pain. He had negative T inversion in anterior leads, therefore we admitted him in our ward.\nOn admission, heart rate was 56 beats/min, blood pressure was 110/70 mmHg, and he was breathing at a rate of 12 per minute, with oxygen saturations around 95% on room air. Cardiovascular examination was normal. There was not orthostatic change. Blood chemistry was normal including cholesterol levels. Asymptomatic episodes of ST-segment elevation were revealed in the 24-hour Holter monitoring and we decided to perform coronary angiography. Echocardiogram was normal. His coronary angiogram showed diffuse significant narrowing of proximal left anterior descending artery (LAD), 90% osteal stenosis of large obtuse marginal (OM), 90% diffuse narrowing of proximal right coronary artery (RCA) ( and ).\nWe decided to perform multivessel percutaneous coronary intervention (PCI) for him, but after intra-coronary injection of nitrate, amazingly his angiogram became completely normal ( and ). There was no organic coronary stenosis. Patient symptoms were completely resolved and he discharged on diltiazem and nitroglycerine, one month later he presented with sudden cardiac death.
|
[[42.0, 'year']]
|
M
|
{'14434946': 1, '11988204': 1, '29942338': 2, '23970922': 2}
|
{'6011852-1': 1}
|
162,767 |
3747023-1
| 23,976,859 |
noncomm/PMC003xxxxxx/PMC3747023.xml
|
Increased biogenic catecholamine and metabolite levels in two patients with malignant catatonia
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The patient was an 18-year-old man with bipolar disorder. At age 14 years, he began to exhibit repeated episodes of mania followed by depression in approximately one-month cycles. His mental state was stabilized with lithium carbonate (dose 1,300 mg/day, blood concentration 0.74 mEq/L). After remaining mentally stable for 2 years, the dosage was tapered and finally discontinued. Three months after discontinuing lithium therapy, he experienced a depressive state lasting approximately 10 days. Lithium carbonate 600 mg/day was restarted, but the depressive state persisted throughout June and July. In August, the dosage was increased to 800 mg/day, but when the depressive state recurred, he was admitted to our hospital on August 12. His psychiatric condition shifted to a hypomanic state the next day, but subsided on August 30. On September 9, he suddenly became stuporous, and his temperature increased to 37.8°C. Because he was unable to eat or drink independently, he received intravenous fluid replacement, and the course of his condition was observed without administering any drugs. Blood analysis revealed a slight increase in the level of serum creatine kinase to 88 IU/L (normal range 13–70 IU/L), and an increased white blood cell count (14,000/mm3). On September 10, the patient’s body temperature was 37.8°C, and rose to 38°C on September 11–13. An antipyretic (indomethacin 50 mg) was administered intrarectally on two occasions, but did not appear to reduce the patient’s fever. An antibiotic was administered intravenously. Because his C-reactive protein level (0.006 mg/dL) on September 13 did not indicate infection, administration of the antibiotic was discontinued. He had severe diaphoresis and urinary incontinence, and his entire body trembled sporadically. At the same time, his systolic blood pressure increased to 180–190 mmHg, and his pulse rate was 100–120 beats per minute. Antihypertensive drugs such as alpha or beta blockers were not administered. On September 16, he had a fever of 38.4°C. He exhibited increased muscle tone but no muscle rigidity. On September 18, no abnormal findings were found on lumbar puncture or on abdominal computed tomography and echography. His fever persisted in the range of 37.0°C–37.8°C until October 4. His stupor improved spontaneously thereafter.\nOn September 29, a 24-hour urine sample revealed high levels of adrenaline (91.1 μg/day; normal range 3–15 μg/day), noradrenaline (168.7 μg/day; normal range 26–121 μg/day), and vanillylmandelic acid (6.5 mg/day; normal range 1.4–5.1 mg/day). On October 11, he appeared to have recovered, and levels of adrenaline (10.7 μg/day), noradrenaline (46.7 μg/day), and vanillylmandelic acid (3.1 mg/day) returned to within normal range.
|
[[18.0, 'year']]
|
M
|
{'17541044': 1, '12832234': 1, '3732257': 1, '6114644': 1, '4815341': 1, '22038451': 1, '11941111': 1, '1959190': 1, '19566780': 1, '16959907': 1, '9169979': 1, '19884605': 1, '8679789': 1, '7908547': 1, '7647836': 1, '8719118': 1, '1420647': 1, '6126826': 1, '23976859': 2}
|
{'3747023-2': 2}
|
162,768 |
3747023-2
| 23,976,859 |
noncomm/PMC003xxxxxx/PMC3747023.xml
|
Increased biogenic catecholamine and metabolite levels in two patients with malignant catatonia
|
A 44-year-old man who had been diagnosed with schizophrenia at 23 years of age was admitted with symptoms of psychomotor agitation, auditory hallucinations, and emotional instability. He was prescribed chlorpromazine 150 mg/day, haloperidol 9 mg/day, biperiden 6 mg/day, carbamazepine 600 mg/day, and lithium carbonate 600 mg/day. A few months later, his psychiatric symptoms had improved, and his mood had become stable. However, on February 1, his psychiatric symptoms suddenly worsened. He developed restlessness, excitation, and paranoid thoughts. An increased dose of antipsychotics and frequent intramuscular injections of chlorpromazine and haloperidol did not improve his psychotic symptoms. He exhibited recurring episodes of stupor and excitement. On February 15, his body temperature increased to 39.5°C, his systolic blood pressure increased to 170 mmHg, his pulse rate was 120 beats per minute, and he exhibited diaphoresis. Blood analysis on February 17 revealed a serum creatine kinase level of 10,110 IU/L (normal range 46–210 IU/L) and a white blood cell count of 8,100/mm3. All antipsychotics were stopped, and fluid replacement and dantrolene 40 mg/day were started. On February 18, he was transferred to our hospital. On admission, a cerebrospinal fluid examination revealed no abnormal findings. His body temperature was 39.4°C, and he had labile blood pressure (systolic blood pressure 130–170 mmHg). He exhibited marked diaphoresis but no muscle rigidity. His serum creatine kinase value was 2,744 IU/L and his white blood cell count was 9,600/mm3. The patient received intravenous fluids and administration of dantrolene was continued.\nFrom the night of February 18, the patient showed intermittent excitement; however, repeated injections of intravenous diazepam 10 mg were ineffective. Therefore, electroconvulsive therapy was started on February 23. On March 3, after completion of five electroconvulsive therapy sessions, his psychiatric and physical symptoms resolved.\nHis catecholamine levels were not determined in 24-hour urine samples because his high level of excitement made this impractical. However, plasma catecholamine levels were measured on the morning of February 18 when he was transferred to our hospital. This measurement revealed high levels of adrenaline (102.0 pg/mL; normal morning range <100.0 pg/mL), noradrenaline (1,672.0 pg/mL; normal morning range 100–450 pg/mL), and dopamine (128.0 pg/mL; normal morning range <20.0 pg/mL).
|
[[44.0, 'year']]
|
M
|
{'17541044': 1, '12832234': 1, '3732257': 1, '6114644': 1, '4815341': 1, '22038451': 1, '11941111': 1, '1959190': 1, '19566780': 1, '16959907': 1, '9169979': 1, '19884605': 1, '8679789': 1, '7908547': 1, '7647836': 1, '8719118': 1, '1420647': 1, '6126826': 1, '23976859': 2}
|
{'3747023-1': 2}
|
162,769 |
3747847-1
| 23,983,453 |
noncomm/PMC003xxxxxx/PMC3747847.xml
|
Retinal vein occlusion during flare of multicentric Castleman’s disease
|
A 63-year-old active male cyclist with HIV (CD4 377/viral load <48 copies/mL) presented with blurred vision and light sensitivity in his left eye for several days while experiencing a flare of MCD disease with fever, tender lymphadenopathy, and profound fatigue. The patient had a history of right eye central retinal vein occlusion with vitreous hemorrhage resulting in significant permanent vision loss 4 years previously. Near that time he initially developed recurrent fevers, he also had cytopenias, hepatosplenomegaly, and tender lymphadenopathy that eventually led to diagnosis of MCD confirmed by lymph node biopsy. The patient declined recommended therapy with rituximab due to share of cost and prolonged remissions between flares. Initiation of valganciclovir 1-year ago resulted in attenuation and reduced frequency of MCD flares. On examination, his visual acuity was 20/200 in the right eye and 20/100 in the left eye. Intraocular pressure in both eyes and blood pressure were normal. Retinal examination in the right eye showed macular atrophy and laser burns after panretinal photocoagulation. The fundus exam of the left eye revealed optic nerve swelling, tortuous veins, cotton-wool spots, and intraretinal hemorrhages, a few of which were white-centered Roth spots (white arrows on ). Fluorescein angiography and spectral-domain optical coherence tomography (SD-OCT) showed delayed perfusion times and macular edema in the left eye, respectively. SD-OCT showed subretinal fluid extending from the optic disc to the fovea (). Hypercoagulability workup demonstrated only mildly increased anti-cardiolipin antibody; there was no evidence of a lupus anticoagulant, prothrombin, or factor V Leiden mutation and the patient had normal antithrombin, protein C, and S. His left eye was treated with intravitreal injection of bevacizumab 1.25 mg in 0.05 mL. After a single injection there was a rapid improvement in visual acuity in his eye. At the last visit 6 months after treatment his visual acuity remained at 20/20 with normal retinal findings (). He also initially received the recommended systemic therapy with rituximab followed by high dose zidovudine with valganciclovir; this resulted in the longest remission to date of systemic MCD flare (>12 months to date).
|
[[63.0, 'year']]
|
M
|
{'20954588': 1, '25391075': 1, '21678090': 1, '23198204': 2, '25391074': 1, '20532148': 2, '10482111': 1, '11812439': 1, '33389938': 2, '16365797': 1, '13356266': 1, '16141865': 1, '34171004': 2, '23983453': 2}
|
{'7149248-1': 1, '3502791-1': 1, '2882085-1': 1, '7802104-1': 1}
|
162,770 |
3748632-1
| 23,977,657 |
noncomm/PMC003xxxxxx/PMC3748632.xml
|
Tuberculous dactylitis (spina ventosa) with concomitant ipsilateral axillary scrofuloderma in an immunocompetent child: A rare presentation of skeletal tuberculosis
|
An 8-year-old destitute girl was brought by members of an internationally acclaimed humanitarian organization, with complaints of pain and swelling in the left index finger of five month's duration. On examination, she had features of a draining abscess on the dorso-ulnar aspect of the proximal phalanx of the left index finger []. On detailed medical history, she admitted having low-grade fever and significant weight loss over the last four months. Her general examination revealed emaciation with pallor and three small scantily draining axillary ulcers with accompanying axillary lymphadenopathy and an additional satellite ulcer in the midaxillary line near the anterior axillary fold []. Rest of her general and systemic examination was unremarkable. The radiograph showed features of osteomyelitis in the proximal phalanx distal to the physis []. Chest X-ray was normal but tuberculin test was strongly positive about 12 mm. Sedimentation rate was 73 mm/first hour. Aspirate from the small abscess around the sinus of the index finger showed no acid fast bacilli (AFB) on Ziehl Neelsen (ZN) staining and no pyogenic bacteria grew on culture. Fine needle aspirate from the ipsilateral axillary lymph node however, showed granulomatous inflammation with necrosis and additional slide subsequently came positive for AFB on ZN staining. Abdominal ultrasonography was normal. A diagnosis of tuberculous osteomyelitis of the second proximal phalanx, with disseminated tuberculosis in the form of axillary (lymph node origin) scrofuloderma was made. The patient was started on a four drug regimen (isoniazid + rifampicin + pyrazinamide + ethambutol for the first two months followed by isoniazid + rifampin for a total of seven months) as per DOT guidelines. Attention was also given to improve on her nutrition including high protein diet with zinc, calcium, vitamin D supplements and hematinics. The patient was given no splint immobilization for the index finger and active range of motion exercises was encouraged early. The patient was doing better with progressive healing of the bony lesion without any surgery []. The axillary scrofulodermic sinuses were healing, as well and patient was consistently gaining weight and hemoglobin level over months. We have not come across any literature showing concomitant presence of tuberculous dactylitis, axillary scrofuloderma suggesting active disseminated tuberculosis in an immunocompetent child above 6 years age.
|
[[8.0, 'year']]
|
F
|
{'26904449': 2, '21491177': 1, '27358553': 1, '16036148': 1, '15502464': 1, '7065732': 1, '9265892': 1, '3084774': 1, '11861245': 1, '34262359': 2, '16398085': 1, '22431957': 2, '20396659': 2, '19180687': 1, '23977657': 2}
|
{'8273899-1': 1, '2853045-1': 1, '4738515-1': 1, '3296115-1': 1}
|
162,771 |
3748639-1
| 23,977,656 |
noncomm/PMC003xxxxxx/PMC3748639.xml
|
Colloid milium
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A 38-year-old driver man from Ahvaz, Fitzpatrick skin type III, in otherwise good health was referred to our hospital for asymptomatic papules on dorsal of the hands of 3-year duration. These lesions developed within 3 years and were increasing in summer and decreasing in winter but none of them resolved.\nPhysical examination disclosed numerous small papules 2-3 mm in diameter, yellowish brown on dorsal of the hands [Figures -].\nHe had no other current or past medical problems. His medical history was negative for photosensitizing medications and disorders. Familial history was negative.\nA biopsy was taken from one of these lesions, and diagnosis of colloid milium was confirmed.\nHistologic exam by hematoxylin and eosin staining revealed deposition of pale eosinophilic homogenous material containing artifactual fissures in dermal papillae [].
|
[[38.0, 'year']]
|
M
|
{'2582010': 1, '11807456': 1, '16637813': 1, '11069478': 1, '11896771': 1, '4112715': 1, '1220808': 1, '422871': 1, '26236412': 1, '12359620': 1, '8403474': 1, '621374': 1, '6853793': 1, '16581569': 1, '23977656': 2}
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{}
|
162,772 |
3748640-1
| 23,977,662 |
noncomm/PMC003xxxxxx/PMC3748640.xml
|
Case report of the extramedullary hematopoiesis presented as a hypervascular intracranial mass
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A 34-year-old man presented with progressive headache and epileptic condition for the last 10 months. He was known to have intermediate B-thalassemia. He experienced severe nausea, vomiting, and growing loss of vision. He was admitted in the neurosurgery ward of Alzahra Hospital, Isfahan, Iran.\nOn the day of admission, he was anemic and received transfusion therapy for the first time, after he became a candidate for surgery. On lateral skull X-ray showed thickening of diploic space []. Non-contrast and contrast-enhanced brain computed tomography scan (CT) in bony and soft tissue window revealed external and internal skull Tables and diploic space thickening and one hyperdense enhancible left paraventricular mass with peripheral edema [Figures -]. On axial T1-W and T2-W brain magnetic resonance imaging (MRI), a hyper- and hypointense paraventricular mass with peripheral edema was identified [Figures and ]. After injection of gadolinium, sagittal T1-W images showed intense and homogeneous enhancement [Figures -]. A surgical biopsy showed infi ltration by megakaryocytes, erythroblasts, and myeloid cells corresponding to EMH.
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[[34.0, 'year']]
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M
|
{'8113103': 1, '15162237': 1, '8192010': 1, '14520481': 1, '19252807': 1, '8131005': 1, '14694310': 1, '15682407': 1, '15580341': 1, '21857583': 1, '17134026': 1, '23977662': 2}
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{}
|
162,773 |
3748642-1
| 23,977,655 |
noncomm/PMC003xxxxxx/PMC3748642.xml
|
Delayed cerebellar ataxia: A rare self limiting complication of plasmodium falciparum malaria
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A 23-year-old pre-morbid healthy male patient was referred to our hospital with complaints of giddiness and loss of balance while walking since 1 month associated with mild, throbbing, generalized headache. There was no history of nausea, vomiting, seizure, syncope, preceding head injury or any addictions. About 1 month back, patient was admitted to a local hospital with complaints of fever with chills, for which patient was treated with Ceftriaxone and Amikacin for 3 days. No history of patient having received anti-malarial in any form. Patient's fever did subside but then he developed giddiness and started requiring support for walking. Patient received symptomatic treatment but had no symptom relief hence a CT scan of head was done, which was apparently normal. There was no drug-history suggestive of cause for his ataxia. Due to persistence of symptoms the patient was referred to our center for further management. On admission to our hospital, his pulse was 72/min, blood pressure 100/70 mm of Hg, respiratory rate 18 cycles/min, afebrile, pallor was present; no icterus, cyanosis, clubbing, edema; jugular venous pressure was normal. There was no evidence of any neurocutaneous markers. Cardiovascular and respiratory systems’ examination were unremarkable. Per abdomen examination was suggestive of splenomegaly (palpable 2 cm below the left costal margin), no hepatomegaly. On neurological examination, he was fully alert, conscious and oriented to time, place and person. On higher mental examination only attention span was reduced. All cranial nerves and sensory system were normal. On motor system examination, he had hypotonia in all limbs. All superficial reflexes were normal with bilateral plantars flexors. Deep tendon reflexes were normal in upper limbs and exaggerated in lower limbs with pendular knee jerks in both the lower limbs. Finger-Nose Test, Knee-Heel test, Dysdiadokokinesis, Tandem Gait were bilaterally impaired. Nystagmus-Absent. There were no signs of meningeal irritation. His laboratory investigations were as follows: Hb-9.9 G%, WBC-5800 cumm of blood, Polymorphs-70% Lymphocytes-26%, Monocytes-1%, Eosinophils-3%, Platelet Count-1.8 lakh. Erythrocyte sedimentation rate 110 mm at the end of 1 h.\nPeripheral smear showed gametes and rings of plasmodium falciparum malaria with parasitic index-2.8%. Random blood sugar-83 mg/dl, blood urea-22 mg/dl, serum creatinine-1.2 mg/dl, serum sodium-136 mEq/L, serum potassium-3.8 mEq/L.\nMRI Brain-Normal study.\nCerebrospinal Fluid Analysis-Normal study.\nSerum Vitamin B12 levels-Within normal limits.\nSerum Thiamine levels-Within normal limits.\nChest X-Ray PA View-Within normal limits.\nECG 12 Leads-Within normal limits.\nUSG (Abdomen + Pelvis)-Splenomegaly (16 cms).\nHe was started on quinine sulphate orally, along with pyrimethamine and sulfadoxine on doses recommended by WHO 2010 guidelines for treatment of malaria. His cerebellar signs showed a complete recovery in 14 days with waxing and waning phenomenon. He did not require any steroids. He was discharged after 14 days in a hemodynamically stable condition and with no neurodeficit.
|
[[23.0, 'year']]
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M
|
{'32067632': 1, '34457209': 1, '27335053': 1, '1440767': 1, '9251340': 1, '25192715': 1, '10402329': 1, '7931448': 1, '30367650': 2, '12038655': 1, '8324845': 1, '3109603': 1, '23977655': 2}
|
{'6204022-1': 1, '6204022-2': 1, '6204022-3': 1, '6204022-4': 1}
|
162,774 |
3748649-1
| 23,983,567 |
noncomm/PMC003xxxxxx/PMC3748649.xml
|
Mycetoma foot
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A 60-year-old male living in a village about 90 km from Pune presented to our hospital with a history of generalized swelling of the left foot of about 11 months’ duration. The initial lesion had started as a single nodule over the dorsum of the foot and was followed by a second nodule that appeared two months later and a few more nodules subsequently. These lesions, mainly distributed over the dorsum of the foot [], then burst to develop sinuses from which there was intermittent discharge of yellow colored granules. Over a period of three months, the patient developed pain in the foot that made walking difficult The left foot was grossly swollen to the ankle with healed sinuses. The clinical findings at this point were suggestive of mycetoma.\nOsteomyelitic changes involving the left calcaneum were seen. Since there was no discharging sinus at the time of presentation, biopsy was done from the site under ultrasound guidance and the specimen sent for staining and culture. Non-acid fast gram-positive narrow filamentous branching bacilli were seen [Figures and ]. Culture in plain Sabourauds’ dextrose agar showed growths of Nocardia species.\nThe patient was started on Trimethoprim-sulphamethoxazole (14 mg/kg, twice daily) along with Dapsone (1.5 mg/kg, twice daily) and Rifampicin (600 mg/day). The swelling decreased in size following surgical debridement of one large painful nodule. The patient has been followed up for a period of three months so far and the medication will be continued for a total period of six months or until cure is achieved.
|
[[60.0, 'year']]
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M
|
{'6376380': 1, '17007542': 1, '1752637': 1, '29641691': 1, '11880433': 1, '19398458': 1, '30532253': 1, '19112799': 1, '8669179': 1, '25207000': 1, '23983567': 2}
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{}
|
162,775 |
3748667-1
| 23,977,663 |
noncomm/PMC003xxxxxx/PMC3748667.xml
|
Cancer problem in Peutz–Jeghers syndrome
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In 2003, a 40-year-old woman consulted a doctor because of feeling a palpable mass in the right breast and bleeding discharge from both breasts. Mammography was taken and revealed bilateral mass with infiltrating margins. Excisional biopsy was performed on both breasts. In histopatholgical examination, grossly; the right side showed a nonencapsulated mass with 5.0 × 4.0 × 1.0 cm size as well as relatively dense consistency and the left one showed the same mass with 6.0 × 3.0 × 2.0 cm size. In microscopic examination it was showed carcinoma in atypical sclerosing papilloma of both breasts [].\nOne month later bilateral modified radical mastectomy and axillary lymph nodes dissection were performed. In microscopic examination there was no residual of primary tumor and the only abnormality is atypical ductal hyperplasia. Lymph-nodes, skin, and nipple were free. Three months later a colonoscopy was performed and multiple polyps were found in the large bowel. Biopsy was taken and the result was hamartomatous polyp [].\nTwo years later in 2005, she was referred to the hospital again because of abnormal uterine bleeding (menometrorrhagia). Pelvic ultrasound showed increased endometrial thickness with normal adnexal regions. Bilateral salpingo-oophorectomy was performed. In histopathological examination, grossly, the uterus was measured 10.0 × 8.0 × 3.0 cm. The right ovary was measured 4.0 × 2.0 × 1.0 cm and the left one 4.0 × 3.0 × 1.0 cm. The cut surface of both ovaries showed nonhomogenous appearance with no obvious lesion. In microscopic examination, both ovaries showed sharply circumscribed rounded epithelial nests composed of ring-shaped tubules encircling the hyalinized basement membrane-like material. The nests have two basic patterns: The simple pattern is that of a single tubule encircling a central rounded hyaline mass, and the complex pattern is characterized by communicating tubules encircling multiple hyaline masses. These features are compatible with sex cord tumor with annular tubules that are usually associated with Peutz–Jeghers syndrome []. Except simple hyperplasia of endometrium; no any pathologic feature was found in the endometrium.
|
[[40.0, 'year']]
|
F
|
{'1117595': 1, '7104978': 1, '20181116': 2, '11039077': 1, '17344176': 1, '21837607': 1, '26337050': 1, '21503748': 1, '2599445': 1, '21617985': 1, '8912836': 1, '22040664': 1, '21856304': 1, '21503746': 1, '12144681': 1, '11950848': 1, '16474908': 1, '24306927': 1, '15398245': 1, '10408777': 1, '10353780': 1, '9672254': 1, '11113065': 1, '8188091': 1, '9428765': 1, '14662533': 1, '15323138': 1, '22067184': 1, '21941977': 1, '23977663': 2}
|
{'2830979-1': 1}
|
162,776 |
3748684-1
| 23,983,288 |
noncomm/PMC003xxxxxx/PMC3748684.xml
|
Kounis syndrome resulting from anaphylaxis to diclofenac
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A 64-year-old man was admitted for surgical correction following fracture of both bones of the left leg. During pre-anaesthetic check-up, his blood pressure was recorded as 134/86 mmHg and pulse rate was 70/min. The patient was not a known smoker or alcoholic. There was no history of allergy, bronchial asthma or any previous surgeries. His functional capacity was 7 metabolic equivalents. His airway was graded as Mallampatti class 2. Systemic examination was normal. All investigations, including kidney function, haemogram, urine, random blood sugar, electrocardiogram and chest X-ray, were within normal limits. He was accepted for anaesthesia under ASA physical status class I.\nIn the ward, the patient complained of severe pain and was given diclofenac sodium 50 mg intramuscular in the gluteal region. Ten minutes thereafter, the patient developed chest pain and pruritus over the lip along with redness and wheal over the site of injection. His blood pressure was found to be 70/54 mm of Hg with a heart rate of 104 beats per minute. Electrocardiography (ECG) showed ST-segment elevation in leads II, III and avF. An ST-segment elevation myocardial infarction (STEMI) of inferior wall was diagnosed and, following primary management, the patient was immediately shifted to the intensive care unit and cardiology consultation was sought. Detailed physical examination of the patient revealed diffuse erythema and rash primarily over the trunk, allergic etiology of the cardiac event was considered in view of the clinical history and temporal relationship with intramuscular diclofenac sodium injection.\nTreatment was started with 0.1 mg adrenaline (1 in 10,000) and 10 mg chlorpheniramine maleate IV, along with 125 mg of methyl prednisolone. Intravenous administration of fluid was continued. Emergent coronary angiography revealed normal coronary vessels. The troponin T level was found to be elevated, but levels of creatine kinase (56 units/L) and creatine kinase-MB (3 units/L) fractions remained normal.\nThe patient's blood pressure by this time was 104/68 mmHg. The rashes disappeared completely over the next 2–3 h and the electrocardiographic findings returned to normal. Serum tryptase however was found to be elevated, which was done before shifting the patient to the cath lab and also 2 h after the coronary event. The patient was discharged to home after conservative management for the fracture and asked to come for surgery at a later date.
|
[[64.0, 'year']]
|
M
|
{'25538414': 1, '20461972': 1, '16249041': 1, '15364808': 1, '11692116': 1, '16476189': 1, '1793697': 1, '15330009': 1, '26813799': 2, '12032577': 1, '17498056': 1, '28781470': 1, '15632231': 1, '23983288': 2}
|
{'4714393-1': 1}
|
162,777 |
3748686-1
| 23,983,290 |
noncomm/PMC003xxxxxx/PMC3748686.xml
|
Dexmedetomidine overdosage: An unusual presentation
|
A 3-year-old male child, weighing 11 kg and 87 cm in height diagnosed with pyogenic meningitis, was being treated at our facility with intra-venous ceftriaxone and dexamethasone. He was responding well to the treatment. As a result of a clerical error, he was accidentally administered 100 mcg of dexmedetomidine as an intra-venous bolus. Within minutes, he became unconscious, heart rate: 65/min, respiratory rate (RR): 8-10/min, blood pressure: 70/40 mm of Hg, oxygen saturation (SpO2) was 85% and constricted pupils with normal eye reflex []. Auscultation of the chest was unremarkable.\nWith oxygen supplementation by Venturi mask (FiO2 of 0.5), in the next 10 min [] his SpO2 improved to 98% and his RR increased to 14-16/min. As the incident occurred early in the morning, the child was in a fasting state and so deemed at a low risk for aspiration. Considering this and his improved respiratory parameters, endotracheal intubation was deferred. When the patient did not respond to two intra-venous 100 ml bolus of normal saline (10 ml/kg), he was then started on intra-venous infusion of adrenaline 0.04 mcg/kg/min, which was gradually increased to 0.08 mcg/kg/min. His blood pressure gradually improved in the next 1 h to 106/70 mm of Hg and heart rate to 80/min. The dose of adrenaline could be gradually tapered and was finally stopped after 7 h of the dexmedetomidine injection.\nHis blood glucose measured soon after injection of dexmedetomidine was 96 mg/dl and it continued to remain within normal limits.\nSize of the pupils observed in ambient light was found to be 0.5-1 mm approximately. The direct light reflex and consensual light reflex were normal bilaterally. The pupillary size had normalised to 2-2.5 mm by 2 h.\nPatient, unconscious since the bolus injection of dexmedetomidine, started responding to painful stimuli after 3 h. After 4 h, the child started responding to calling by name and after 7 h he became conscious and oriented.
|
[[3.0, 'year']]
|
M
|
{'1361311': 1, '12594584': 1, '20144378': 1, '9728818': 1, '15039474': 1, '11167662': 1, '19232941': 1, '16389294': 1, '15987381': 1, '16369581': 1, '10886121': 1, '20885920': 2, '23983290': 2}
|
{'2946583-1': 1}
|
162,778 |
3748687-1
| 23,983,291 |
noncomm/PMC003xxxxxx/PMC3748687.xml
|
Anaesthetic management of a neonate with Kasabach-Merritt syndrome
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A 2.5 kg 1-month-old boy, delivered at term, afflicted with KMS presented for excision and split skin grafting of a giant haemangioma over the left thigh, extending from the inguinal region to the knee, with a circumferential girth of 32.5 cm []. Patient had received intravenous propranolol[] and prednisolone[] for 10 days and intralesional bleomycin injection once, which produced a slight, but insignificant reduction in the size of haemangioma. Apart from pallor, examination was unremarkable and there were no other co-morbidities. The patient had been transfused 150 mL of packed RBCs, 250 mL platelet concentrates and 110 mL of fresh frozen plasma but the anaemia, thrombocytopenia and coagulopathy persisted. Pre-operative haemoglobin was 7.6 g/dL, platelets 19,000/cumm, bleeding time 9 min and international normalized ratio (INR) was 1.6. Other biochemical investigations including arterial blood gas analysis were all within normal limits. Appropriate radiological investigations were carried out to rule out haemangioma in other visceral organs.\nIntravenous access was secured with two 24 G intravenous cannulae. The neonate was pre-medicated with injection hydrocortisone 10 mg IV and injection fentanyl 2.5 μg IV. After standard induction using sevoflurane and atracurium, an uncuffed endotracheal tube, size 3.0 mm ID was inserted. Paracetamol 70 mg suppository was administered for post-operative analgesia. Normothermia was maintained with the use of Mediprema® Infant Operating Table and HOTLINE® Blood and Fluid Warmer. Since, the application of a conventional tourniquet was technically impossible in an attempt to minimize blood loss, we requested the surgeon to tie a Foley's catheter around the proximal most part of thigh (tourniquet time 35 min). The haemangioma was excised and raw area was covered with a skin graft taken from the excised haemangioma itself, in an attempt to further decrease the blood loss. Intraoperative blood loss was 300 mL and was appropriately replaced with 150 mL packed cells, 50 mL fresh frozen plasma and 50 mL platelet concentrates. Patient was haemodynamically stable throughout the procedure and had adequate urine output. Arterial blood gas analysis and serum electrolytes performed prior to extubation were within normal limits. Recovery from anaesthesia was smooth and uneventful. In the post-operative period, patient received additional 200 ml of packed cells and 50 mL of platelet concentrates. On the second post-operative day, the haemoglobin was 9.9 g/dL, platelets had increased to 64,000 cells/cumm and INR had improved to 1.3. Further post-operative course was uneventful.
|
[[1.0, 'month']]
|
M
|
{'25738066': 1, '19207911': 1, '27829366': 2, '11298580': 1, '25624555': 1, '18577262': 2, '22648868': 1, '23983291': 2}
|
{'2438320-1': 1, '5101728-1': 1}
|
162,779 |
3748688-1
| 23,983,292 |
noncomm/PMC003xxxxxx/PMC3748688.xml
|
Anaesthetic management of previously non-diagnosed phaeochromocytoma: Clinical vigilance, the ultimate saviour of anaesthesiologist
|
A 39-year-old male, a case of von Hippel Lindau (VHL) syndrome and follow-up case of renal cell carcinoma (right) post radical nephrectomy and right adrenalectomy 2 weeks ago, was planned for left radical adrenalectomy for left adrenal mass and radiofrequency ablation (RFA) of left renal tumour. A preoperative assessment revealed the patient to be a known hypertensive, diabetic (on insulin) with a post coronary artery bypass graft (CABG) status (2005) on β-blocker (Tab. Metoprolol). Aspirin was stopped 5 days ago. Clinical history revealed episodes of headache, dizziness on change to erect posture, palpitations, recent episode of retrosternal chest pain with radiation to epigastrium and functional capacity of 2-3 metabolic equivalents. Clinical examination revealed an afebrile, averagely built and nourished patient with blood pressure (BP) of 130-170/80-90 mm Hg and pulse rate of 70-78/min. Airway assessment showed Mallampati airway class II, adequate mouth opening, thyromental distance >3 finger breadth and normal range of neck movements. Systemic examination did not reveal any significant findings..\nInvestigations were within normal limits except capillary blood glucose (CBG) which ranged between 178 and 266 mg/dl. Cardiological evaluation showed ischaemic changes in electrocardiogram (ECG) for inferior and basal regions, dobutamine stress echocardiography (DSE) positive for provocable ischaemia in anterior, mid and basal lateral walls, echocardiography revealing akinetic inferior wall in mid and basal region and mid posterior wall with partial thickness scar, left ventricular ejection fraction (LVEF)=50% and mild mitral regurgitation with grade I diastolic dysfunction. Urinary catecholamine levels,including values of 24 hours collection were within normal limits(metanephrines-58 ng/ml, and 284.2 μg/day, epinephrine-1.86 pg/ml and norepinephrine-48.3μg/day). Histopathological examination of previously excised adrenal tumour was suggestive of adrenocortical carcinoma. Glycaemic control was achieved with insulin as per sliding scale. Patient was accepted under ASA class III with high-risk consent. Two units of packed red blood cells (PRBC) were kept ready.\nOn the morning of surgery, patient was shifted to OT and connected to monitors – noninvasive blood pressure (NIBP), SpO2 and ECG. Initial recordings displayed BP=220/100 mm Hg, heart rate (HR)=82/min and SpO2=100%. Midazolam 2.0 mg IV was administered. Before induction, a thoracic epidural catheter was placed, followed by a 20-G arterial line over left radial artery and a 7-Fr triple-lumen central line over right internal jugular vein. A 7-Fr Swan Ganz pulmonary artery (PA) catheter was inserted under local anaesthesia, keeping in mind the findings of cardiological evaluation. PA catheter showed value of 26/13 mm Hg. Post-intubation, patient was mechanically ventilated in volume control mode with end-tidal carbon dioxide (ETCO2) and minimum alveolar concentration (MAC) monitoring. No haemodynamic disturbances were observed during or after induction/intubation. Patient was catheterised. Insulin infusion was started for glycaemic control. Dexmedetomidine infusion was added to supplement depth of anaesthesia. A baseline arterial blood gas (ABG) and CBG were done post-induction. DJ stenting (left) was done in lithotomy position.\nThe patient was then transported on C-circuit to the Department of Radiology for computed tomography (CT)-guided RFA. Patient was placed in prone position in the CT gantry. Ventilation was managed with ventilator using oxygen only. Anaesthesia was managed with increased infusion rates of dexmedetomidine and periodic boluses of propofol, fentanyl and rocuronium. At the end of the 3-h procedure, patient was transported back to the operation theatre and radical adrenalectomy was started in the right lateral decubitus position. Blood loss was estimated to be approximately 1500 ml. PA wedge pressure (PAWP) was found to be 3-4 mm Hg, while central venous pressure (CVP) was 2-6 cm H2O. Fluid resuscitation was carried out with crystalloids and colloids, the total intraoperative volumes being 3500 ml and 2000 ml, respectively. Two units of PRBC were also transfused intraoperatively. During tumour handling, massive fluctuations in haemodynamics were noted with BP shooting up to 208/110 mmHg and HR upto 125/min. SpO2 and EtCO2 were within normal limits. Immediately sodium nitroprusside (SNP) infusion was started and vitals were restored. Following tumour removal, blood pressure dropped drastically to 70/32 mm Hg, which prompted us to start an infusion of noradrenaline and adrenaline. SNP infusion was discontinued. Hydrocortisone 200 mg IV was administered. Sodium bicarbonate was administered as serial ABGs showed progressive metabolic acidosis. Urine output was 2700 ml intraoperatively.\nAnalgesia was maintained with boluses of IV fentanyl, and IV tramadol. Approximately 30 min before closure, IV ondansetron was administered. Post-extubation, patient was comfortable with stable haemodynamics and satisfactory visual analogue scale (VAS) score. Patient was shifted to surgical intensive care unit (ICU) for postoperative monitoring and evaluation. Postoperative tenure was uneventful and patient was discharged on 27 March 2012. Postoperatively, histopathological evaluation of the adrenal tumour revealed it to be a phaeochromocytoma and a renal cell carcinoma (RCC) from the biopsy of renal tumour prior to the RFA. The slide of previously excised adrenal tumour was re-evaluated and found to be a phaeochromocytoma too.
|
[[39.0, 'year']]
|
M
|
{'6141233': 1, '18617683': 1, '6453259': 1, '2665275': 1, '25386452': 1, '27994341': 1, '23983292': 2}
|
{}
|
162,780 |
3748690-1
| 23,983,294 |
noncomm/PMC003xxxxxx/PMC3748690.xml
|
Fibrodysplasia of maxilla: A difficult airway
|
A 22-year-old boy weighing 38 kg, presented with a huge swelling on the left side of the face, which extended partly on to the right side also. The swelling had increased to present size over 7 years as in .\nExamination revealed swelling on both sides of face extending from infraorbital region (left > right) involving the maxillary and mandibular area along with the upper part of the lip. Anatomy of the nose was distorted along with the deviation of upper lip. Pre-operative evaluation was carried out thoroughly with routine investigations. Airway assessment revealed Mallampati class I, thyromental distance - 6 cm with adequate mouth opening and upper lip bite test – grade III.[]\nRadiological finding showed involvement of maxillary, mandibular and nasal bone causing total blockade of left posterior nare with narrowing of the right.\nMallampati grading did not suggest difficult airway, but the upper lip bite test along with the extent of the tumour distorting the anatomy both externally and internally made us still think of difficulty in intubation along with difficult mask ventilation. The size and extent of swelling was defined carefully to plan for mask holding and to avoid soft-tissue trauma during intubation. As difficult mask ventilation and intubation was anticipated, a difficult airway cart was kept ready containing laryngeal mask airway of size 3, McCoy blade size 3 and 4 and bougie. Written informed consent was obtained.\nPriority of our anaesthetic plan was to achieve mask ventilation. If it was not possible, we planned to do awake fibroptic intubation with local blocks through oral route as posterior nares were almost blocked, remote possibility of tracheostomy was thought of and ENT surgeon was kept informed to be available.\nThe boy was pre-medicated with injection midazolam 0.02 mg/kg and fentanyl 2 μg/kg. As adequate mask ventilation was not possible due to inability of the biggest mask to close the nostrils and mouth, we adopted the following steps to achieve adequate mask ventilation: Both nostrils were closed using cotton balls after explaining the patient same. It did not cause any inconvenience as left posterior nare was blocked completely with narrowing of the right nare. Then the mask was held on to the oral cavity. As the swelling involved upper part of the lip, there occurred leak, which was covered with gauze, but still adequate seal was not achieved. Hence, we planned to hold the mask by two pairs of hands by two persons, which made us achieve adequate bag filling successfully. The boy was induced with injection propofol 2 mg/kg and sevoflurane (2-6%). Mask ventilation was possible only with two persons holding the mask. Even after apnoea, we were able to mask ventilate with adequate chest expansion. Then we decided to perform a trial laryngoscopy to assess the ease of intubation. There was difficulty in introducing the direct laryngoscope as the left side of upper lip was involved by swelling. McIntosh laryngoscope with no. 3 blade was used through, which we could visualize only epiglottis with CL grading of III.[] As mask ventilation was achieved with two persons adequately we decided to give succinylcholine 1.5 mg/kg in order to facilitate the better visualization of the glottis on direct laryngoscopy. To facilitate the same we further decided to use McCoy blade of size 3. With all these precautions, our laryngoscopy with McCoy blade revealed CL grade IIIa.[] As there was no improvement in CL grading following relaxation and with McCoy blade, we decided to introduce the bougie and thread the tube over it and the same was accomplished with single attempt as in . Following uneventful intraoperative period, boy was extubated at the end of surgery on the table (in view of anatomy of the tumour not impinging on the upper airway post-operative airway oedema was not anticipated and this opinion to extubate patient on the table was in consensus with the operating surgeons), shifted to intensive care unit and to ward, the next day.
|
[[22.0, 'year']]
|
M
|
{'10671848': 1, '20532087': 1, '27051379': 2, '19923516': 1, '24700924': 1, '10709889': 1, '25885089': 1, '23983294': 2}
|
{'4799620-1': 1}
|
162,781 |
3748691-1
| 23,983,295 |
noncomm/PMC003xxxxxx/PMC3748691.xml
|
Anaesthetic management of an unrecognized cerebral arteriovenous malformation bleed in a 45-day old baby
|
A 45-day-old male baby (weight 4 kg) was admitted with a history of poor feeding and an irritable cry. On examination, the anterior fontanelle was full with a head circumference of 36 cm. The child's Glasgow Coma Scale (GCS) score was 10/15 (E3V2M5). There was scissoring of the legs with an ill-sustained clonus. Routine blood investigations were within normal limits except for low hemoglobin (Hb) of 8 g/dl. The partial thromboplastin time (PTT) was 44, while the prothrombin time (PT) was 19.3 with the International Normalized Ratio (INR) being 1.6. Computerized tomography (CT) of brain (plain) showed a left frontoparietal hematoma measuring 6 × 4.5 cm with a midline shift of 13 mm [].\nA clinical diagnosis of hemorrhagic diseases of the new born was considered. As the child had a large hematoma associated with midline shift, it was decided to evacuate the hematoma after correcting the PT, PTT, and Hb. After correcting the PT, PTT, and Hb with 150 ml of fresh frozen plasma (FFP) and 100 ml of packed red cells, the child was taken to the operating room (OR).\nIn the OR, electrocardiography (ECG), non-invasive blood pressure (NiBP) and pulse oximetry (SPO2) were established. The child was induced with 2 μg/kg of fentanyl, 5 mg/kg of thiopentone and was paralysed with atracurium (0.5 mg/kg). The airway was secured with a 4 mm uncuffed endotracheal tube (ETT). Anaesthesia was maintained with air, oxygen (FiO2-40%) and isoflurane (MAC 0.9-1). Left femoral arterial line (20 Gauge) and a right-sided 5F triple lumen femoral venous catheter were inserted. Baseline PPV (10-12) and central venous pressure (7-8 cm of H2O) were noted. Intraoperative fluid administration was guided by the PPV (Philips IntelliVue MP 70™).\nAs there was a significant blood loss during craniotomy, blood transfusion was started from the beginning of surgery. Durotomy was associated with significant bleeding and drop in blood pressure from 90/55 to 45/25 mm of Hg, with a heart rate of 120/min. This was initially treated with fluid and ephedrine (0.5 mg) boluses. Since there was an ongoing blood loss, low dose adrenaline (0.03 μg/kg/min) was started to support the circulation while resuscitating with blood, FFP. After the durotomy, a large AVM was identified. As there was bleeding from the AVM, surgeon decided to go ahead with excision of the AVM. While resecting the AVM, the child lost more than 2.75 times the blood volume (>850 ml), which was replaced with packed cell, FFP, cryoprecipitate and platelet in the ratio of 1.5:1:1:1. Serial Hb, coagulation profiles (PT, PTT, platelets, fibrinogen), arterial blood gas (ABG), electrolytes were done intraoperatively []. After 1.5 times of blood volume loss, a single bolus dose (10 mg/kg) of Tranexamic Acid (TA) was given.\nDuring the intraoperative period, the PPV varied from 10 to 13. However, during the period of sudden blood loss associated with hypotension, the PPV reached a maximum of up to 25-30. During these episodes, 50-60 ml of fluid was given, which brought down the PPV to less than 13. We did not measure CVP during the intraoperative period as the CVP port was used for administration of adrenaline. The other two lumens were used for giving blood products. Adrenaline infusion was tapered and stopped once the hemostasis was achieved. Normothermia (36-37°C) was maintained using a warm blanket (Bair Hugger™505) and warmed fluids (fluid warmer - Animec AM2S™) during the procedure. The urine output was >30 ml/h throughout the surgery. Postoperatively, the child was ventilated for 48 h and then extubated. Biopsy of the specimen was consistent with vascular malformation. At the 12 months follow-up period; the child had no delay in milestones or deficits.
|
[[45.0, 'day']]
|
M
|
{'21876453': 1, '17822565': 1, '22113930': 1, '11907171': 1, '14705722': 1, '20390324': 1, '10795888': 1, '23983295': 2}
|
{}
|
162,782 |
3748692-1
| 23,983,296 |
noncomm/PMC003xxxxxx/PMC3748692.xml
|
Anaesthesia with and without dexmedetomidine for a child with multiple congenital anomalies posted for bilateral cataract extraction
|
A 5-month-old, 3.67 kg, male baby presented with bilateral mature congenital cataracts and was posted for sequential bilateral eye lens excision and anterior vitrectomy under general anaesthesia.\nThe baby was delivered as a full-term baby by normal delivery and his low birth weight (1.8 kg), fever, jaundice with hepatosplenomegaly necessitated neonatal intensive care unit (ICU) admission for 15 days. He was investigated for congenital rubella syndrome, but serology was not supportive. Atrial septal defect (ASD) was identified preoperatively by clinical examination and echocardiography. Echocardiography revealed mild pulmonary hypertension with, secundum type of ASD (4 mm) with left to right flow. Baby had right sided cleft lip and palate, bilateral mature cataracts, no signs of cyanosis, and infection or congestive cardiac failure. The baby had normal heart rate (HR) (140/min, regular) and respiratory rate (40/min) maintaining good oxygen saturation (99%) on room air. However, icterus was evident.\nLungs were clear. An ejection systolic murmur was heard, which was most prominent over the pulmonary area of the precordium. On per abdominal examination, hepatosplenomegaly was palpable. The child was irritable, but neurologically normal.\nHis routine pre-operative haematological and biochemical investigations were normal. C reactive proteins were negative. However, high reticulocyte count (4.7%), with unconjugated hyperbilirubinemia (total 18.2 mg%, direct 3.1 mg%, indirect 15.1 mg%) was suggestive of pre-hepatic jaundice.[]\nX-ray chest depicted cardiomegaly with normal airway and lung fields. Electrocardiogram (ECG) revealed right axis deviation and incomplete right bundle branch block.\nThe child was kept nil by mouth for 4 h prior to the surgery. The child was pre-medicated with oral midazolam 1.5 mg 45 min before surgery and intravenous glycopyrrolate 15 μg 10 min before surgery.\nIn the operating room, monitoring included heart rate (HR), mean arterial pressure, pulse oximetry, ECG and end-tidal carbon dioxide monitoring (EtCO2) carried out throughout both operations. While IOP was measured (using Schioetz tonometer) before and after giving pre-medication, before administration of succinylcholine, immediately after intubation, and then every 2 min for 6 min before starting both the surgeries.\nAnaesthesia was induced with thiopentone sodium (20 mg, in two 10 mg doses) and suxamethonium (10 mg) was injected for muscle relaxation after ability to mask-ventilate the patient was confirmed. Intubation was achieved using No. 3 sized plain endotracheal tube. Pressure-controlled ventilation was used manually with 250 ml bag attached to Ayres T piece to maintain mild hypocarbia. Anaesthesia was maintained with oxygen, nitrous oxide (50:50) and sevoflurane (2-4%), and atracurium. Dextrose with 0.33% saline was infused at the rate of 2.5cc/min (total 150 cc) with the help of infusion pump. Patient was haemodynamically stable throughout the intra-operative period. At the end of surgery, neuromuscular blockade was reversed with neostigmine 0.2 mg and glycopyrrolate 30 μg. On recovery of vital reflexes, baby was extubated. Dexamethasone 0.5 mg was given intravenously before shifting the baby to paediatric ICU.\nPost-operative course was uneventful except the emergence agitation, which was partially alleviated by tramadol suppository (12.5 mg) and presence of his mother in paediatric ICU.\nHe was rescheduled for surgery of the other eye after 10 days. Second time Dexmedetomidine 0.5 μg was given intravenously over 10 minutes in addition to other premedicants. Rest of the anaesthetic management was similar and uneventful.\nFor second surgery, there was 50% reduction in the dose of thiopentone sodium and concentration of sevoflurane required to keep adequate depth of anaesthesia was 3%. Maximum drop in HR was 10% of baseline during the first operation while it was 22% during the second operation. Succinylcholine and intubation increased IOP during both the operations. However, during the second operation, after premedication with dexmedetomidine, the IOP rise was not different from the baseline value (before premedication) and was significantly lower than that of the first surgery. After the second surgery, the child was awake, but quiet.
|
[[5.0, 'month']]
|
M
|
{'3137318': 1, '16324031': 1, '11207355': 1, '14693585': 1, '16790625': 1, '1351736': 1, '18285392': 1, '17273114': 1, '23983296': 2}
|
{}
|
162,783 |
3748693-1
| 23,983,297 |
noncomm/PMC003xxxxxx/PMC3748693.xml
|
Aphonia following tracheal intubation: An unanticipated post-operative complication
|
A 32-year-old male patient with Mallampati (MP) I airway was posted for elective laparotomy for excision of hepatic flexure mass. Patient was intubated with 8.5 mm internal diameter (ID) ETT in first attempt. Hoarseness of voice was noted 3 h after extubation and indirect laryngoscopy (IDL) revealed right vocal cord palsy. There was spontaneous resolution of the condition in 40 days.
|
[[32.0, 'year']]
|
M
|
{'7453467': 1, '7936678': 1, '17341543': 1, '31559208': 1, '1185065': 1, '27601749': 1, '33884139': 1, '6824152': 1, '5107366': 1, '8064954': 1, '23983297': 2}
|
{'3748693-2': 2, '3748693-3': 2}
|
162,784 |
3748693-2
| 23,983,297 |
noncomm/PMC003xxxxxx/PMC3748693.xml
|
Aphonia following tracheal intubation: An unanticipated post-operative complication
|
A 38-year-old male patient with MP II airway was posted for surgery with multiple fractures of right upper limb and soft-tissue injuries on the scalp and face. Patient was intubated with 9 mm ID ETT in first attempt. Patient could not phonate after extubation and IDL revealed wavy distortion of both vocal cords. Patient regained normal voice over 60 days.
|
[[38.0, 'year']]
|
M
|
{'7453467': 1, '7936678': 1, '17341543': 1, '31559208': 1, '1185065': 1, '27601749': 1, '33884139': 1, '6824152': 1, '5107366': 1, '8064954': 1, '23983297': 2}
|
{'3748693-1': 2, '3748693-3': 2}
|
162,785 |
3748693-3
| 23,983,297 |
noncomm/PMC003xxxxxx/PMC3748693.xml
|
Aphonia following tracheal intubation: An unanticipated post-operative complication
|
A 42-year-old obese female patient with MP III and short neck received general anaesthesia for incisional hernia repair and was intubated with 7 mm ID ETT after three attempts. She had a sore throat in the post-operative period and on the third day, developed loss of voice. IDL revealed slight bowing of left vocal cord and she regained normal voice over 26 days.\nThere was no history indicative of pre-existing pathology including hormonal disorders (thyroid, parathyroid), metabolic (diabetes mellitus and autonomic neuropathy) or arthritic disorders in any of the patients. Portex® ETTs were used in all patients and cuff was inflated with air and cuff pressure was not monitored.
|
[[42.0, 'year']]
|
F
|
{'7453467': 1, '7936678': 1, '17341543': 1, '31559208': 1, '1185065': 1, '27601749': 1, '33884139': 1, '6824152': 1, '5107366': 1, '8064954': 1, '23983297': 2}
|
{'3748693-1': 2, '3748693-2': 2}
|
162,786 |
3749082-1
| 23,983,483 |
noncomm/PMC003xxxxxx/PMC3749082.xml
|
Comorbidity of Kawasaki disease and group a streptococcal pleural effusion in a healthy child: a case report
|
A 3-year-old female patient presented with a 5-day history of fever, sore throat, and cough, but no rash. Past medical history was unremarkable, as was family history. Immunizations were up to date for age. On admission to the ward, her vital signs were: temperature 39.5°C; pulse 130 beats per minute; blood pressure 100/70 mmHg, respiratory rate 50 per minute; oxygen saturation 90% on oxygen 2/L per minute via nasal cannula; weight 13.8 kg (50th percentile); and length 94 cm (48th percentile). Her skin had normal texture, with no rashes, hypopigmentation, or hyperpigmentation, her capillary refill was around 3 seconds, and the oral mucosa was mildly dry. The patient had decreased air entry and coarse crackles in the right lower and middle zones of the lung. The throat was erythematous and there was no cervical lymphadenopathy. The rest of the physical examination was unremarkable.\nInitial laboratory results were: white blood cells 24,000/μL (neutrophils 60.2%, lymphocytes 35.4%, monocytes 4.3%, basophils 0.1%), hemoglobin 10.3 g/dL, and platelets 206,000/μL. C-reactive protein was 100 mg/L, erythrocyte sedimentation rate was 65 mm/hour, albumin was 18 g/L, creatinine was 66 μmol/L, aspartate aminotransferase was 100 U/L, and alanine aminotransferase was 60 U/L. Serum glucose, blood urea nitrogen, calcium, sodium, chloride, and potassium were normal. Venous blood gas was pH 7.2, pCO2 44 mmHg, pO2 29 mmHg, and HCO3 17 meq/L, with a base excess of 11. Anteroposterior chest radiographs showed a right middle and lower lobar consolidation with moderate pleural effusion.\nThe patient was started on intravenous normal saline 20 mL/kg due to dehydration. She was then transferred to the pediatric intensive care unit due to increased oxygen requirement. A chest tube was inserted and 200 mL of pus was drained. The pleural fluid culture yielded GAS. The patient was started on intravenous cefuroxime and clindamycin. Nasopharyngeal and throat swabs, blood culture, and a Mantoux skin test were all negative.\nOn the eighth hospital day, there was no clinical response to antibiotics, and fever persisted, with new onset of abdominal pain, diarrhea, and slight tachycardia at a heart rate of 150 beats per minute.\nA repeat blood count showed a significant white cell count of 30,000/μL, hemoglobin 7.7 g/dL, platelets 600,000/μL, aspartate aminotransferase 180 U/L, alanine aminotransferase 120 U/L, and albumin 18 g/L, with a rise in erythrocyte sedimentation rate and C-reactive protein.\nThe differential diagnosis included bacterial resistance to antibiotics, nonbacterial etiologies such as a virus or aspiration of a foreign body, bronchiolitis obliterans, hypersensitivity pneumonitis, atypical Kawasaki disease, eosinophilic pneumonia, Wegener’s granulomatosis, pulmonary sequestration, and cystic adenomatoid malformation.\nSince atypical Kawasaki disease was in the differential diagnosis, an echocardiogram was ordered which showed a prominent of left anterior descending artery (0.26 cm, z-score 3.2) and left main coronary artery (0.35 cm, z-score 3.2), with no vegetations or pericardial effusion. Our team decided to give one dose of intravenous immunoglobulin 2 g/kg, and high-dose aspirin (80 mg/kg/day) was started. The fever resolved in 24 hours and the patient’s general condition improved, but desquamation developed on the hands and feet. The diagnosis of atypical Kawasaki disease was confirmed.\nThe patient was discharged home in a stable condition on oral antibiotics for 2 weeks and on an antiplatelet dose of aspirin. She was seen in the outpatient clinic in good condition, and a repeat echocardiogram at 6 weeks was normal.
|
[[3.0, 'year']]
|
F
|
{'21738542': 1, '19430379': 1, '15574639': 1, '23281308': 1, '16938766': 1, '19116718': 1, '22474462': 1, '15295233': 1, '26975816': 1, '28101385': 2, '22745623': 1, '17039750': 1, '12833488': 1, '31760956': 2, '22057395': 1, '22348488': 1, '19038400': 1, '23565324': 1, '20664742': 1, '22318812': 1, '17471041': 1, '15870671': 1, '12072892': 1, '14500320': 1, '23983483': 2}
|
{'6876070-1': 1, '5215141-1': 1}
|
162,787 |
3750890-1
| 23,739,713 |
noncomm/PMC003xxxxxx/PMC3750890.xml
|
Epidermoid carcinoma of the skin mimicking breast\ncancer
|
A 55-year-old female patient presented a lesion on the right breast for two years and\nstated that initially it was only a small sore that did not heal. The lesion enlarged\nslowly during the two following years and rapidly in the past three months. At first,\nthe patient did not seek medical attention because of hesitation. When she presented to\nthe department, she had already undergone a biopsy of the lesion which revealed an\nundifferentiated carcinoma. Subsequently a mastectomy was planned, as it was considered\nas a breast cancer case. On physical examination, a large 15x10cm ulcerated lesion was\nobserved on the right breast, extending from the upper portion of the junction of the\nupper quadrants to an area near the right clavicle, without evidence of invasion of the\nbreast parenchyma ( and ). The axilla and the supraclavicular fossa had no\nsuspected lymph nodes. Because of the clinical history, a diagnosis of breast skin\ncarcinoma was considered, which was confirmed by a histopathological examination\nrevealing epidermoid carcinoma T4N2M0. Chest radiography and abdominal ultrasound were\nunremarkable. Afterwards, a wide excision of the lesion with a 2cm margin was performed.\nA defect at the surgical field was left open for subsequent tissue grafting because of\nan infection observed intraoperatively. She had a good immediate postoperative course,\nand the skin grafting was scheduled. The definitive histopathological examination\nconfirmed a moderately differentiated epidermoid carcinoma with free surgical margins.\nSix months later, she presented with a defective, but complete cicatrization. Currently,\nfive years after surgery, she remains without evidence of ongoing disease.
|
[[55.0, 'year']]
|
F
|
{'19660023': 1, '19575067': 1, '21031073': 2, '20565942': 2, '15871330': 1, '23739713': 2}
|
{'2907399-1': 1, '2956953-1': 1}
|
162,788 |
3750891-1
| 23,739,706 |
noncomm/PMC003xxxxxx/PMC3750891.xml
|
Dermoscopy of lichen aureus
|
A 54-year-old woman, living in Rio de Janeiro since age 15, reported the appearance of a\nasymptomatic golden-brown macule on her left ankle, initially (9 months previously)\nmeasuring one centimeter and increasing in size over that period ().\nDermoscopy showed coppery-red pigmentation on background, permeated by dark brown\nnetwork. In addition, linear vessels in the central portion of the lesion accompanied by\npunctate vessels and of peculiar circular conformation, especially in the periphery of\nthe lesion ( and ).\nSkin biopsy and histopathological examination showed vacuolization of the basal layer of\nthe epidermis, lichenoid infiltrate in the dermis, extravasation of red blood cells and\nhemossiderin within macrophages ().\nOcclusive therapy with 0.05% clobetasol propionate was performed for three months,\nresulting in little improvement
|
[[54.0, 'year']]
|
F
|
{'29606831': 1, '3978038': 1, '15492206': 1, '31997996': 1, '9551337': 1, '33768022': 1, '27828629': 1, '29166512': 2, '18794462': 1, '32477970': 1, '30066773': 1, '31544096': 2, '23739706': 2}
|
{'5674707-1': 1, '6743400-1': 1}
|
162,789 |
3750892-1
| 23,739,703 |
noncomm/PMC003xxxxxx/PMC3750892.xml
|
Rosai-Dorfman disease presenting with extensive cutaneous\nmanifestation - Case report
|
A 43-year-old woman, mulatto, reported the appearance of an asymptomatic tumor on her\nright thigh, which she had had for about 11 months. No comorbidities were reported.\nThe examination revealed an indurated hyper-pigmented plaque with reddish-yellow\nnodules, on her right thigh, measuring 15 cm in diameter (). An erythematous nodule was presented on her right buttock (). The patient reported that these lesions\nwere painless. A painless inguinal lymph node on the same side of the skin lesions was\nalso revealed upon examination.\nThe histopathology of the skin lesion exhibited a slightly acanthotic epidermis, dermis\nand hypodermis with a diffuse infiltrate, consisting of lymphocytes, plasma cells and\nneutrophils (). Occasional histiocytes\ncontaining intact inflammatory cells within the cytoplasm (emperipolesis) were also seen\n(). Immunohistochemical studies\nrevealed histiocytes with positivity for S100 and CD68 and negativity for CD1a. The\nhistopathology of the inguinal lymph node showed dilated nodal sinuses with large\nnumbers of histiocytes exhibiting emperipolesis ().\nLaboratory finds were microcytic anemia and polyclonal hypergammaglobulinemia. The image\ntests (ultrasound and CT) showed a marked thickening of the skin and the subcutaneous\ntissue located in the anterolateral region of the right thigh; enlarged lymph nodes up\nto 2cm long located in the right inguinal chain; a normal-sized liver with the rare\npresence of homogeneous cysts of 0.5cm. The myelogram was normal.\nThe patient was referred to the oncology service for surgical treatment.
|
[[43.0, 'year']]
|
F
|
{'18211480': 1, '12361136': 1, '12121554': 1, '19668942': 1, '16618860': 1, '19451502': 1, '12492979': 1, '16433797': 1, '12558621': 1, '23739703': 2}
|
{}
|
162,790 |
3750893-1
| 23,739,691 |
noncomm/PMC003xxxxxx/PMC3750893.xml
|
American tegumentary leishmaniasis: an uncommon clinical\nand histopathological presentation
|
In September 2010, a 42-year-old male patient from a rural area in Ceará noticed the\nonset of a nodule on his ear. Over the ensuing months, there was a minimal swelling of\nthe lesion. Treatment with topical steroids and antibiotics produced no improvement.\nPhysical examination revealed an erythematous nodule of fibrous-elastic tissue on the\nright ear lobe with no purulent discharge. The patient, with no history of local trauma,\ndid not experience localized pain, itching or constitutional symptoms ().\nThe patient´s blood glucose was normal and the VDRL test was nonreactive. Serologic\ntests for HIV were not undertaken. A biopsy was carried out about six months after the\nonset of the clinical condition.\nThe histological sections showed epithelial atrophy, and Grenz's zone in the dermis,\nwith a dense superficial and deep lymphoplasmacytic and histiocytic infiltrate. A large\nnumber of structures consistent with Leishmania sp. amastigotes was\nobserved in macrophages. The results of the Leishmanin skin test (LST) were positive,\nwith 10 mm of induration ( and ).\nThe patient missed follow-up but returned three months later with no changes on the\nlesion. Since no abnormalities were found in the general laboratory tests, treatment was\nstarted with meglumine antimoniate (15mg/kg) over 20 days. Two months after the end of\ntherapy the lesions showed clear signs of regression ().
|
[[42.0, 'year']]
|
M
|
{'21437523': 1, '27007563': 2, '7569614': 1, '19563944': 1, '30022292': 1, '18937655': 1, '19755742': 1, '21738967': 1, '15663657': 1, '17664781': 1, '23739691': 2}
|
{'4804557-1': 1}
|
162,791 |
3750894-1
| 23,739,711 |
noncomm/PMC003xxxxxx/PMC3750894.xml
|
Non Hodgkin T cell lymphoma: an atypical clinical\npresentation
|
We describe a 46-year-old, black male patient, born in Cape Verde. He first noted,\nmonths prior to presentation, a dermatosis that almost exclusively involved his face and\ntrunk consisting of multiple small monomorphic papules with an erythematous smooth\nsurface. The patient reported dysesthesia at the distal ends of both feet and\nparoxistical difficulty in mobilizing both feet. These symptoms suggested the existence\nof a sensory motor polyneuropathy.A cutaneous biopsy was performed motivated by these\nfindings. The histopathological evaluation revealed perivascular and periadnexal\ninflammatory infiltration of nerve bundles with lymphocytic permeation which, with\nsimultaneous findings of cutaneous involvement and sensory motor polyneuropathy, could\nbe consistent with the diagnosis of leprosy. The patient was therefore referred for a\nconsultation at the hospital regarding the possibility of Hansen's disease. The physical\nexamination revealed a dermatosis involving the face and the upper torso that consisted\nof multiple infracentimetric monomorphic papules and plaques with a smooth erythematous\nsurface ( and ). There was no hypoesthesia in relation to skin lesions.\nExamination of ganglionic chains revealed several adenopathies below the chin and in\naxillary chains. The adenopathies that were found were over one centimeter in diameter,\nwith a hard consistency. Palpation of the abdomen revealed no masses or organomegaly.\nThe neurological examination did not reveal thickening or pain upon palpation of the\nnerve roots. There was slight hypoesthesia at the distal end of both feet, with\ndiminished thermal, tactile and pain sensitivity.\nThe patient also reported weight loss of 12 kg(>10%) during the past year which had\nnever been taken into consideration. The patient denied any other constitutional\nsymptoms, including fever, anorexia and malaise.\nThe supplementary study revealed: normocytic normochromic anemia(10.4 g/dL), white blood\ncell count with lymphocytosis(3500) and thrombocytopenia (94000),VS 71mm in 1st hour,\nβ2-microglobulin(8.0 mg/dL) and LDH(689 U/L) and negative results for HIV, HTLV, EBV.\nPCR applied to a biopsy performed from the synovial tissue proved negative for\nM. leprae.\nBody axial tomography showed severe ganglion involvement of the axillary and inguinal\nlymph nodes and mild splenomegaly with multiple small parenchymal nodules. The skin\nbiopsy revealed diffuse lymphoid infiltration in the dermis composed of CD3, CD4\npositive T-cells, some of which had CD8 positivity (, and ). The axillary lymph node biopsy identified a lymphocytic\nproliferation composed of small cells with CD2, CD3 positive cells and CD7, CD8, CD20\nnegative cells, and TIA expression allowing the diagnosis of T-cell lymphoma with\ncytotoxic expression (). The study of\nT-cell receptors rearrangement by PCR confirmed the monoclonality of the cell population\nbased on the analysis of gamma genes.The absence of typical clinical lesions and the\ntypical histological markers of Hansen's disease, the successively negative nasal smears\nand skin swabs, together with the PCR detection technique for M. leprae,\nallowed for the exclusion of a Hansen's disease diagnosis. The evaluation by a\nneurologist allowed a correlation between lymphoma and demyelinating neuropathy to be\ncharacterized as a rare paraneoplastic syndrome.\nThe patient was started on chemotherapy with CHOP (cyclophosphamide, doxorubicin,\nvincristine and prednisolone), which led to partial remission of the cutaneous lesions\n() but with subsequent loss of\nresponse. Second line therapeutic management with ESHAP (etoposide, methylprednisolone,\ncytarabine and cisplatin ) was then initiated with no noticeable clinical response. The\npatient was then started on a CMOPP chemotherapy regimen (cyclophosphamide,\nmechlorethamine, vincristine, procarbazine and prednisolone), but at 12 months follow-up\nthere was invariable progression of the systemic disease, resulting in the patient´s\ndeath.
|
[[46.0, 'year']]
|
M
|
{'16225594': 1, '21753698': 1, '15543550': 1, '10830738': 1, '15166664': 1, '20925471': 1, '20196721': 1, '15531460': 1, '21801133': 1, '23739711': 2}
|
{}
|
162,792 |
3750895-1
| 23,739,714 |
noncomm/PMC003xxxxxx/PMC3750895.xml
|
Nail apparatus melanoma: a diagnostic opportunity
|
17-year-old female student from Manaus (Amazonas State), Fitzpatrick's phototype III,\npresented at the dermatology clinic with two ulcerated lesions. These were consistent\nwith leishmaniasis, both clinically and by lab (presence of Leshmania\nsp. amatigotes pattern on direct examination). Pentavalent antimonial was\nprescribed. During clinic follow-up, it was noted that the patient had a longitudinal\nmelanonychia on the right thumb (). On\nquestioning, she informed that this had been present for approximately one year. She\nalso reported family history of melanoma (great-aunt). Dermatoscopic examination\nrevealed lines varying in color from light brown to black, with different sizes, width\nand distances, with the most proximal area being more intense and thicker than the\ndistal area, forming a triangular shape (). Ungual matrix biopsy was performed by shaving. Histopathology was compatible\nwith melanoma in situ ().\nSurgical management involved excision of ungual apparatus up to periosteal region.\nFollowing histopathology no neoplasm showed in the 40 cuts made. Clinical staging was\nTisN0M0 (Stage 0). Patient followed up for 11 months without recurrence ().
|
[[17.0, 'year']]
|
F
|
{'33937480': 1, '25396092': 1, '20016126': 1, '21531039': 1, '21175755': 1, '10642684': 1, '20404227': 1, '28492005': 1, '17320240': 1, '19922528': 1, '23739714': 2}
|
{}
|
162,793 |
3750897-1
| 23,739,700 |
noncomm/PMC003xxxxxx/PMC3750897.xml
|
Lymphangiectatic Kaposi's sarcoma in a patient with\nAIDS
|
In 2001, a 32-year-old male was referred to the department of dermatology reporting a\nhistory of lesions in the proximal right thigh. A skin biopsy was performed and\nsuggested diagnosis of KS. A partial improvement was noted when antiretroviral therapy\n(TARV) was started, but the patient was lost to follow-up. At diagnosis, CD4+ T-cell\ncount was 409 cells/mm3 and viral load 76,000 copies/mm. In 2010, the patient returned with a worsening clinical status, including an\nincreased number of lesions and edema around the right lower limb. Dermatological\nexamination revealed isolated and confluent erythematousviolaceous tuberous lesions of\nvarying sizes as well as a vegetating tumor on the inner right thigh ( and ). Histopathological examination revealed inter-cellular epidermal edema,\nproliferation of spindle cells, neoangiogenesis and large dilated intratumoral and\nperitumoral thin-walled lymphatic vessels (). Magnetic resonance imaging showed a volumetric increase in the diameter of\nthe entire right thigh associated with severe edema of the entire subcutaneous tissue\nand a heterogeneous, hypodense area in the proximal right thigh (). Lymphangiocintigraphy revealed bilateral retention of the\nradiotracer, which was more pronounced in the right lower limb, with signs of lymphatic\nleakage (). CT scan of the skull and chest\nshowed no abnormalities and the endoscopy was normal. The patient was referred to a\nspecialized cancer treatment center, where he resumed chemotherapy with paclitaxel, with\npartial reduction of edema and lesions.
|
[[32.0, 'year']]
|
M
|
{'19439884': 1, '22253598': 1, '18655700': 1, '16922960': 1, '18226270': 2, '10863237': 1, '10749966': 1, '3901851': 1, '15334644': 1, '23739700': 2}
|
{'2275292-1': 1, '2275292-2': 1}
|
162,794 |
3750898-1
| 23,739,715 |
noncomm/PMC003xxxxxx/PMC3750898.xml
|
Marshall's syndrome
|
A 6-year-old boy, phototype IV, from Rio de Janeiro, Brazil, arrived at the Pediatric\nDermatology Service with infiltrated, well circumscribed erythematous and edematous\nplaques with polycyclic configuration, on his face, back and extremities for two months,\nassociated with episodes of fever ( and\n). He had not taken any medication. Laboratory\nstudies revealed normal blood count values (except for a high eosinophils rate - 7%).\nSerological reactions for syphilis (VDRL), HIV and baciloscopy were negative. Serum\nα1antitrypsin was not available. A biopsy specimen obtained from one of the infiltrated\nplaques showed a neutrophilic disease with edema of the dermal papillae and dense\nneutrophilic dermal infiltrate ().\nTreatment with Dapsone (1mg/Kg/day) and Prednisone (0.5mg/Kg/day) was initiated. All\ninflammatory plaques resolved slowly and left atrophic, wrinkled areas, causing a\npremature aging appearance (). A biopsy\nspecimen of the atrophic cutaneous areas showed decreased thickness of the reticular\ndermis. Acid orcein staining showed marked decrease in the number of elastic fibers in\nthe reticular dermis. The existing fibers were shortened and fragmented, but collagen\nappeared normal (). The patient evolved\nwith other recurrent episodes and, as a result, new wrinkled areas every time he failed\nto follow treatment recommendations.
|
[[6.0, 'year']]
|
M
|
{'2745999': 1, '7826089': 1, '15569023': 1, '34807425': 1, '1148114': 1, '92145': 1, '5926113': 1, '5555855': 1, '2298964': 1, '15280835': 1, '5835325': 1, '23739715': 2}
|
{}
|
162,795 |
3750899-1
| 23,739,718 |
noncomm/PMC003xxxxxx/PMC3750899.xml
|
Cutaneous leukocytoclastic vasculitis in the presence of\nmethimazole therapy
|
Female patient, 33-years-old, black, host to GD for over 6 years, using MTM since the\nonset of symptoms. Patient was advised to seek dermatology assistance due to the\nemergence of superficial skin lesions in the lower limbs over a period of 20 days,\nassociated with fever, joint pain and tremor of the extremities. The dermatological exam\nexposed erythematous purpuric lesions on the dorsum of the feet and plantar cavus tense\nblisters with hemorrhagic content in the malleolar region which spread to large necrotic\nareas. (, and ).\nThe chest x-ray and renal function tests failed to detect significant changes. The\nabsence of hematuria was also noted. Laboratory data is presented in\nA biopsy of the superficial skin lesion was in addition performed in the right lateral\nmalleolus region. Histopathological examination revealed neutrophilic leukocytoclastic\nvasculitis of small vessels ().\nIn view of the tests feedback, we decided to discontinue MTM and start therapy with\nprednisone (1mg/kg). We were able to observe continuous improvement after 7 days ().
|
[[33.0, 'year']]
|
F
|
{'31008018': 2, '12353714': 1, '20061292': 1, '17086001': 1, '15745981': 1, '19494377': 1, '17435868': 1, '12727967': 1, '9920055': 1, '31762745': 2, '23739718': 2}
|
{'6873099-1': 1, '6470634-1': 1}
|
162,796 |
3750903-1
| 23,739,708 |
noncomm/PMC003xxxxxx/PMC3750903.xml
|
Case for diagnosis
|
A 67-year-old woman, without remarkable medical or family background, presented with a\n6month history of a pruritic sclerotic lesion on her abdomen. The sclerotic lesion had\nbeen accompanied by a blister on the back of the right foot for 4 months and there had\nbeen no previous trauma. Physical examination revealed several 2-4 cm, ivory colored,\nshiny, sclerotic lesion on the abdomen ()\nand soft plaque on the back of the right foot (). There were no other lesions on her body. An incision-al biopsy specimen\nrevealed hyperkeratosis, atrophy of the epidermis, marked edema in the upper dermis\nresulting in a subepidermal blister and homogenization of collagen in the papillary\ndermis ().\nAfter the diagnosis of Bullous lichen sclerosus et atrophicus was made, we started\ntreatment with topical corticosteroid and achieved stabilization and slight improvement.
|
[[67.0, 'year']]
|
F
|
{'20854400': 1, '22068779': 1, '19018788': 1, '9738793': 1, '26312692': 2, '23739708': 2}
|
{'4540526-1': 1}
|
162,797 |
3750904-1
| 23,739,716 |
noncomm/PMC003xxxxxx/PMC3750904.xml
|
Case for diagnosis
|
A 27 year-old-man with no known history of personal or familial illnesses was referred\nto our clinic with a 10 year history of cervical telangiectasias with no associated\nsymptoms. The patient denied any preceding or simultaneous episodes of disease with this\ndermatosis, as well as concomitant or recent use of any medication. We found no changes\non his physical exam, except the presence of groups of blancheable, erythematous\nmacules, of a bright red tone, with a Blaschko lines distribution and localized only on\nthe right lateral aspect of the neck (\nand ). Blood work did not reveal any changes,\nnamely in liver enzymes or infectious serologies. What is your diagnosis?
|
[[27.0, 'year']]
|
M
|
{'6824361': 1, '18388386': 1, '21308321': 1, '15459535': 1, '434856': 1, '6853780': 1, '19061602': 1, '21635824': 1, '23739716': 2}
|
{}
|
162,798 |
3750905-1
| 23,739,690 |
noncomm/PMC003xxxxxx/PMC3750905.xml
|
Do you know this syndrome?
|
The case of a 13-year-old female patient is here described. Frontal and temporal lesions\nappeared at 4 years of age, followed by smaller malar and chin lesions since age 5. Her\nmother referred hypochromic maculae on dorsum present from birth. In childhood, she had\none episode of seizure associated with fever, with normal EEG. There was no family\nhistory of similar skin lesions.\nIn CT of the skull, multiple amorphous subependimary calcifications were present. In\nthoracic and lumbar spine CT, partial defect in fusion of the posterior neural arch was\nfound at the T11, T12, S1 and L5 levels.\nOn examination, she had multiple pinkish-brown, shiny papules, about 2 mm in diameter in\nthe malar region and chin, brownish frontal and pre-auricular plaques and multiple\nhypochromic stains on the trunk, including ash leaf spots (, and ). The frontal and pre-auricular lesions are\nprobably fibrous plaques, classified as angiofibromas; the patient did not allow a\nbiopsy, so other possible diagnosis such as melanocytic naevi, verrucous naevi and even\nShagreen patch with unusual localization should be considered.
|
[[13.0, 'year']]
|
F
|
{'22250258': 1, '21931059': 1, '19715644': 1, '21182496': 1, '17637444': 1, '18722871': 1, '22068806': 1, '23739690': 2}
|
{}
|
162,799 |
3751027-1
| 23,722,429 |
noncomm/PMC003xxxxxx/PMC3751027.xml
|
Feasibility of remote magnetic navigation for epicardial ablation
|
A 78-year-old male with chronic ischaemic heart disease was referred for recurrent episodes of VT treated by implantable cardioverter defibrillator (ICD) discharges. He had previously undergone an endocardial VT ablation. His recent CAG showed a chronic total right coronary artery occlusion with good collateral flow and no progression over time. Under treatment with bisoprolol, amiodarone, phenytoin, and lidocaine the clinical VT with a cycle length of 430 ms was reproducibly induced during the invasive EP study. Endocardial and epicardial mapping indentified a substrate in the inferior scar of myocardial infarction.\nThirty-three RF pulses were applied with a mean energy of 34 W from both epicardial and endocardial access in order to obtain scar homogenisation. At the conclusion of the procedure the VT was no longer inducible. There was no significant pericardial bleeding during and after the procedure. The patient was discharged home on oral bisoprolol, amiodarone, and phenytoin. At 3-month follow-up the patient was free of sustained ventricular arrhythmias.
|
[[78.0, 'year']]
|
M
|
{'21841191': 1, '23959847': 1, '20434589': 1, '21744697': 1, '24155102': 1, '19602023': 1, '21508006': 1, '27722835': 1, '22006012': 1, '22653815': 1, '17296855': 1, '15851176': 1, '24710865': 2, '16731472': 1, '21149511': 1, '16847159': 1, '20974761': 1, '26215291': 1, '22719063': 1, '22702255': 1, '22554147': 1, '18955400': 1, '10807445': 1, '19789687': 1, '16784438': 1, '24399322': 1, '23722429': 2}
|
{'3751027-2': 2, '3751027-3': 2, '4016330-1': 1, '4016330-2': 1}
|
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