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A 39-year-old man was admitted to the hospital due to hematemesis and melena for 2 wk, with a new episode lasting 1 d.\nTwo weeks before admission, the patient had hematemesis and melena without obvious known causes. He vomited light red fluids 4-5 times/d and passed tarry stools 3-4 times/d; these events were accompanied by epigastric pain, abdominal distension, and fatigue. He had no dizziness or syncope. He was hospitalized at a local hospital where examinations showed a hemoglobin (Hb) level of 86 g/L. Esophagogastroduodenoscopy (EGD) showed fresh blood in the descending part of the duodenum but did not show a clear bleeding site. The patient was treated with blood transfusion, acid blockers, and intravenous (IV) fluid and discharged from the hospital after no recurrence of hematemesis or melena was observed.\nOne day before admission to our hospital, the patient vomited bright red blood once and was admitted to the local hospital. Bedside EGD showed no obvious bleeding in the upper gastrointestinal tract. During his hospitalization, the patient had repeated hematemesis and hematochezia 4-5 times/d accompanied by left upper abdominal pain and fatigue. His minimum Hb level was 42 g/L. After treatment with blood transfusion, IV fluid, acid blockers, and hemostasis, he was transferred to our hospital for emergency admission.\nThe patient had a history of chronic pancreatitis. He denied chronic diseases such as hypertension, coronary heart disease, and diabetes, a history of abdominal surgery and trauma, and a history of food and drug allergy.\nThe patient denied a history of smoking and drinking and any history of diseases in family members.\nOn admission, the patient had a body temperature of 37.2 °C, a pulse of 102 beats/min, a respiratory rate of 19 times/min, a blood pressure of 117/91 mmHg, and an oxygen saturation of 98%. The patient had manifestations of anemia and pale conjunctiva. His abdomen was soft with upper abdominal tenderness. No rebound tenderness was noted. No abdominal mass was palpable. No other obvious abnormality was noted.\nThe complete blood count on admission was as follows: White blood cell count, 8.00 × 109/L; red blood cell count, 2.34 × 109/L; Hb, 66 g/L; hematocrit, 0.192; platelet count, 108 × 109/L; total amylase, 198 U/L; D-dimer, 6060 µg/L; hypersensitive C-reactive protein, 40.1 mg/L; procalcitonin, 0.12 ng/mL; and serum albumin, 24 g/L (Table ). Coagulation function, alanine aminotransferase, aspartate aminotransferase, total bilirubin, alkaline phosphatase, glutamyl transpeptidase, urinalysis results, stool analysis, tumor marker expression, troponin I, and electrocardiogram results were all within normal limits.\nA noncontrast-enhanced computed tomography (CT) scan of the abdomen and pelvis showed pancreatic swelling, uneven density, vague edges, multiple spots of calcifications, and hyperintense opacities in the pancreatic head and body, indicating chronic pancreatitis and pancreatic head hemorrhage.\nSubsequent contrast-enhanced CT of the abdomen showed isointense, rounded opacities with a diameter of approximately 41 mm in the pancreatic head that were enhanced with contrast in the arterial phase and were closely related to the gastroduodenal artery, indicating pseudoaneurysm (Figure ). Furthermore, digital subtraction angiography performed via the celiac trunk showed the formation of pseudoaneurysms at the proximal gastroduodenal artery; the remaining blood vessels were unremarkable (Figure , Video 1A).

A 55-year-old male diagnosed case of ethanol-related chronic pancreatitis presented with frequent episodes of melena associated with paroxysms of abdominal pain. He was given blood transfusions elsewhere for severe anemia. As patient had persistent GI bleeding with repeated drop in hemoglobin, he was referred for further evaluation and management. On clinical examination, he had profuse sweating, hypotension, tachycardia, severe pallor and mild tenderness in the epigastrium. His laboratory investigations revealed hemoglobin of 7.1 g% and hematocrit of 22%, mild renal failure and increased serum triglycerides. Contrast-enhanced computed tomography of the abdomen showed evidence of chronic calcifying pancreatitis (). Esophagogastroduodenoscopy with a standard scope and colonoscopy were normal. Repeat esophagogastroduodenoscopy with a standard scope after an episode of melena showed active bleeding from the ampulla (). Angiographic study could not localize the site of bleeding. Endoscopic ultrasound showed chronic pancreatitis with a heterogeneous inflammatory lesion in the body of the pancreas (). As the bleeding source could not be localized and the patient had ongoing melena and drop in hemoglobin, emergency exploratory laparotomy was performed after initial hemodynamic stabilization. Pancreas was seen adherent to splenic vessels and hilum. There was evidence of splenic vein rupturing into the main pancreatic duct. Distal pancreatectomy with splenectomy was performed. The patient had an uneventful recovery postoperatively. Postoperative histology demonstrated chronic calcifying pancreatitis (), lymphnodes with reactive hyperplasia and congested spleen (). He was discharged in a hemodynamically stable condition and there was no further recurrence of GI bleeding after 6 months of follow up.

Write a detailed clinical case vignette based on the following key phrases: Gastrointestinal bleeding, Pseudoaneurysm, Chronic pancreatitis

A 39-year-old man was admitted to the hospital due to hematemesis and melena for 2 wk, with a new episode lasting 1 d.\nTwo weeks before admission, the patient had hematemesis and melena without obvious known causes. He vomited light red fluids 4-5 times/d and passed tarry stools 3-4 times/d; these events were accompanied by epigastric pain, abdominal distension, and fatigue. He had no dizziness or syncope. He was hospitalized at a local hospital where examinations showed a hemoglobin (Hb) level of 86 g/L. Esophagogastroduodenoscopy (EGD) showed fresh blood in the descending part of the duodenum but did not show a clear bleeding site. The patient was treated with blood transfusion, acid blockers, and intravenous (IV) fluid and discharged from the hospital after no recurrence of hematemesis or melena was observed.\nOne day before admission to our hospital, the patient vomited bright red blood once and was admitted to the local hospital. Bedside EGD showed no obvious bleeding in the upper gastrointestinal tract. During his hospitalization, the patient had repeated hematemesis and hematochezia 4-5 times/d accompanied by left upper abdominal pain and fatigue. His minimum Hb level was 42 g/L. After treatment with blood transfusion, IV fluid, acid blockers, and hemostasis, he was transferred to our hospital for emergency admission.\nThe patient had a history of chronic pancreatitis. He denied chronic diseases such as hypertension, coronary heart disease, and diabetes, a history of abdominal surgery and trauma, and a history of food and drug allergy.\nThe patient denied a history of smoking and drinking and any history of diseases in family members.\nOn admission, the patient had a body temperature of 37.2 °C, a pulse of 102 beats/min, a respiratory rate of 19 times/min, a blood pressure of 117/91 mmHg, and an oxygen saturation of 98%. The patient had manifestations of anemia and pale conjunctiva. His abdomen was soft with upper abdominal tenderness. No rebound tenderness was noted. No abdominal mass was palpable. No other obvious abnormality was noted.\nThe complete blood count on admission was as follows: White blood cell count, 8.00 × 109/L; red blood cell count, 2.34 × 109/L; Hb, 66 g/L; hematocrit, 0.192; platelet count, 108 × 109/L; total amylase, 198 U/L; D-dimer, 6060 µg/L; hypersensitive C-reactive protein, 40.1 mg/L; procalcitonin, 0.12 ng/mL; and serum albumin, 24 g/L (Table ). Coagulation function, alanine aminotransferase, aspartate aminotransferase, total bilirubin, alkaline phosphatase, glutamyl transpeptidase, urinalysis results, stool analysis, tumor marker expression, troponin I, and electrocardiogram results were all within normal limits.\nA noncontrast-enhanced computed tomography (CT) scan of the abdomen and pelvis showed pancreatic swelling, uneven density, vague edges, multiple spots of calcifications, and hyperintense opacities in the pancreatic head and body, indicating chronic pancreatitis and pancreatic head hemorrhage.\nSubsequent contrast-enhanced CT of the abdomen showed isointense, rounded opacities with a diameter of approximately 41 mm in the pancreatic head that were enhanced with contrast in the arterial phase and were closely related to the gastroduodenal artery, indicating pseudoaneurysm (Figure ). Furthermore, digital subtraction angiography performed via the celiac trunk showed the formation of pseudoaneurysms at the proximal gastroduodenal artery; the remaining blood vessels were unremarkable (Figure , Video 1A).

A 67-year-old Caucasian man was admitted with diffuse abdominal pain, vomiting, diarrhea, and 4 kg weight loss within a couple of weeks. He had a history of alcohol abuse but further medical history was negative. There was no significant abdominal tenderness, no abdominal palpable mass or flank-knocking tenderness. Laboratory studies showed mild anemia with a hemoglobin level of 10.0 g/dL. An abdominal ultrasound (US) scan showed a partially inverted flow in the portal vein with a small cirrhotic liver, ascites, and a small spleen. Abdominal computed tomography (CT) revealed a large pseudoaneurysm between the SMA and coeliac trunk with a diameter of 77 × 53 × 59 mm. Just below this pseudoaneurysm lay the pancreas with calcifications due to chronic pancreatitis. CT angiography revealed an arterioportal fistula between the pseudoaneurysm and portal vein. Due to this pseudoaneurysm, there was compression of the superior mesenteric vein. Ascites around the liver and spleen were seen, probably due to portal hypertension. There was an increase of the pseudoaneurysm diameter compared to the abdominal CT scan made 5 days earlier, with a maximal diameter of 81 mm (Fig. ). Digital angiography revealed a pseudoaneurysm arising from the proximal superior mesenteric artery with fistulization to the portal vein. The pseudoaneurysm was filled via a large defect in the top of the superior mesenteric artery (Fig. ).\nFrom a technical point of view, covered stenting of the SMA was preferred over embolization of the pseudoaneurysm. A 6 French LIMA sheath was placed in the superior mesenteric artery using a femoral approach. Next, a balloon-expandable covered stent (Bentley Begraft® diameter 8 mm, length 37 mm; Bentley, Hechingen, Germany) was deployed in the SMA. Control angiography showed refilling of the pseudoaneurysm via the common hepatic artery (CHA) through the right gastric and gastroduodenal arteries (Fig. ). Since there was no filling of the CHA from the coeliac trunk, it is probable that the CHA originated from the SMA as a normal variant and was separated from its origin, possibly due to the pancreatitis (Fig. ). After catheterization of the CHA via the left and then the right gastric artery, selective embolization was performed with a 2.7 Fr Progreat® microcatheter (Terumo Medical Corp., Somerset, NY, USA) using multiple Hilal microcoils (3, 4, and 5 mm wide and 3 and 6 cm long; Cook Medical, Bloomington, IN, USA), covering the origin of the GDA (Fig. ). The residual perfusion of the liver is only supplied by the right gastric artery from the left gastric artery.\nPostoperatively, the patient was given clopidogrel therapy for 6 weeks and lifelong acetylsalicylic acid.\nHe was discharged on the eighth postoperative day. Follow-up after 6 months revealed no recurrent abdominal symptoms. The pseudoaneurysm was no longer detectable on control CT angiography (Fig. ).

Write a detailed clinical case vignette based on the following key phrases: Gastrointestinal bleeding, Pseudoaneurysm, Chronic pancreatitis

A 39-year-old man was admitted to the hospital due to hematemesis and melena for 2 wk, with a new episode lasting 1 d.\nTwo weeks before admission, the patient had hematemesis and melena without obvious known causes. He vomited light red fluids 4-5 times/d and passed tarry stools 3-4 times/d; these events were accompanied by epigastric pain, abdominal distension, and fatigue. He had no dizziness or syncope. He was hospitalized at a local hospital where examinations showed a hemoglobin (Hb) level of 86 g/L. Esophagogastroduodenoscopy (EGD) showed fresh blood in the descending part of the duodenum but did not show a clear bleeding site. The patient was treated with blood transfusion, acid blockers, and intravenous (IV) fluid and discharged from the hospital after no recurrence of hematemesis or melena was observed.\nOne day before admission to our hospital, the patient vomited bright red blood once and was admitted to the local hospital. Bedside EGD showed no obvious bleeding in the upper gastrointestinal tract. During his hospitalization, the patient had repeated hematemesis and hematochezia 4-5 times/d accompanied by left upper abdominal pain and fatigue. His minimum Hb level was 42 g/L. After treatment with blood transfusion, IV fluid, acid blockers, and hemostasis, he was transferred to our hospital for emergency admission.\nThe patient had a history of chronic pancreatitis. He denied chronic diseases such as hypertension, coronary heart disease, and diabetes, a history of abdominal surgery and trauma, and a history of food and drug allergy.\nThe patient denied a history of smoking and drinking and any history of diseases in family members.\nOn admission, the patient had a body temperature of 37.2 °C, a pulse of 102 beats/min, a respiratory rate of 19 times/min, a blood pressure of 117/91 mmHg, and an oxygen saturation of 98%. The patient had manifestations of anemia and pale conjunctiva. His abdomen was soft with upper abdominal tenderness. No rebound tenderness was noted. No abdominal mass was palpable. No other obvious abnormality was noted.\nThe complete blood count on admission was as follows: White blood cell count, 8.00 × 109/L; red blood cell count, 2.34 × 109/L; Hb, 66 g/L; hematocrit, 0.192; platelet count, 108 × 109/L; total amylase, 198 U/L; D-dimer, 6060 µg/L; hypersensitive C-reactive protein, 40.1 mg/L; procalcitonin, 0.12 ng/mL; and serum albumin, 24 g/L (Table ). Coagulation function, alanine aminotransferase, aspartate aminotransferase, total bilirubin, alkaline phosphatase, glutamyl transpeptidase, urinalysis results, stool analysis, tumor marker expression, troponin I, and electrocardiogram results were all within normal limits.\nA noncontrast-enhanced computed tomography (CT) scan of the abdomen and pelvis showed pancreatic swelling, uneven density, vague edges, multiple spots of calcifications, and hyperintense opacities in the pancreatic head and body, indicating chronic pancreatitis and pancreatic head hemorrhage.\nSubsequent contrast-enhanced CT of the abdomen showed isointense, rounded opacities with a diameter of approximately 41 mm in the pancreatic head that were enhanced with contrast in the arterial phase and were closely related to the gastroduodenal artery, indicating pseudoaneurysm (Figure ). Furthermore, digital subtraction angiography performed via the celiac trunk showed the formation of pseudoaneurysms at the proximal gastroduodenal artery; the remaining blood vessels were unremarkable (Figure , Video 1A).

A 38-year-old male complaining of recurrent episodes of melena for the past 2 weeks was admitted to the emergency department of our hospital. Two days before the hospital visit, the patient had complained of the presence of blood in vomiting and had a history of recurrent complaints of upper abdominal pain often radiating to the back. His previous medical history revealed that he had suffered from chronic pancreatitis for 3 years before present admission, possibly due to alcohol abuse. He was resuscitated with the blood and intravenous fluid for melena during present admission. Ultrasonography (USG) whole abdomen revealed a moderately enlarged liver (18.5 cm × 12.3 cm) with heterogeneous echotexture, with a prominent portal vein, of size 1.3 cm; hepatic and splenic hilar collaterals were suggestive of portal hypertension. The presence of mild ascites was documented. Transabdominal USG showed echogenic pancreas with multiple, small, hyperechoic, nonshadowing foci in the pancreas suggestive of fibrotic changes. There was evidence of irregular dilated main pancreatic duct with pancreatic and intraductal calculi. These features were consistent with chronic pancreatitis. The findings were suggestive of alcoholic liver disease with portal hypertension and chronic obstructive pancreatitis. After resuscitation, upper GI endoscopy was performed on two different occasions that showed bleeding from the second part of the duodenum with an abnormal tortuous vessel at the ampulla of Vater. This was diagnosed as hemosuccus pancreaticus, which might have caused the bleeding []. Serendipitously during the endoscopy, a worm was also found penetrating the mucosa of the duodenum. The worm was retrieved and referred to the laboratory for identification. It was a single intact live worm (size 12.3 mm × 0.3 mm) reddish pink, with head bent in the same direction of the body curvature with a spine at the posterior end []. The buccal capsule had six teeth (four hook-like on ventral surface and two knob-like on dorsal surface) []. The live worm was seen to lay eggs while examining under the microscope []. Three consecutive stool samples of the patients were examined. The stool sample was dark-colored, semi-solid in consistency without any parasitic elements. Wet mount examination of stool revealed nonbile-stained ova (60– 65 μm in length, 40– 45 μm in width) with transparent hyaline shell membrane containing blastomeres. The above morphological features of the worm and micrometry of the ova were consistent with Ancylostoma duodenale. For further confirmation and to exclude the probability of mixed infection with Strongyloides stercoralis, the modified Harada– Mori nematode larval culture method[] was performed, and larva of hookworm was retrieved after 1 week of incubation at ambient room temperature. However, duodenal biopsy could not be done to rule out this possibility.\nThe patient was a chronic alcoholic and had deranged liver functions. Other laboratory test revealed low hemoglobin (5.6 g/dL), elevated total leukocyte count (12,300/μl) with increased eosinophils (neutrophils - 54%, lymphocytes – 24%, eosinophils – 16%, and monocytes – 6%), hyperbilirubinemia (total serum bilirubin 12.5 mg% and conjugated bilirubin 11.7 mg%), alanine transaminase/aspartate transaminase (87.7/90 IU), serum alkaline phosphatase (827 IU/L), hypoalbuminemia (2.3 g%), and raised serum globulin (3.9 g%) with reversal of albumin:globulin ratio. Blood and urine cultures were bacteriologically sterile. Peripheral blood smear examination showed microcytic, hypochromic anemia, with the absence of any hemoparasites. The patient was planned for contrast-enhanced computed tomography (CECT) abdomen, but the course of illness was rapidly fatal, and he succumbed to the illness within 48 h of admission, hindering further investigative course. The cause of death was unexplained shock secondary to upper GI bleeding precipitated by chronic, alcoholic liver disease with chronic pancreatitis and portal hypertension.

Write a detailed clinical case vignette based on the following key phrases: Gastrointestinal bleeding, Pseudoaneurysm, Chronic pancreatitis

A 47-year-old male, nonsmoker with no significant medical history initially presented with sudden onset right-sided chest pain, fever, and shortness of breath. After a hemorrhagic pleural tap and chest x-ray demonstrating large retro cardiac soft tissue density, gross right pleural effusion, and right lower lobe lung collapse the patient was referred to our center with a working diagnosis of thoracic malignancy and large lung carcinoma with hemorrhagic pleural effusion.\nThe patient was admitted to our center for further workup. Immediately after, the patient experienced severe respiratory distress; oxygen saturation (SpO2) was 74% on two liters of oxygen. The patient was transferred to the intensive care unit (ICU) with pulse: 102 beats per minute and regular, blood pressure: 95/79 mm Hg, respiratory rate: 22/minute, temperature: 97°F, and SpO2: 100% on high-flow oxygen. Glasgow Coma Scale (GCS) was 15/15, and on examination of the chest, there was decreased air entry on the right side. A right-sided chest drain was placed; 1300 ml of hemorrhagic fluid was drained by the end of the day. Total leukocyte count (TLC) then was 21710/mm^3. A blood and sputum culture was obtained. The sputum sample demonstrated Klebsiella pneumonia, which was managed accordingly, normalizing the counts on the days to come. Whole blood was transfused during the ICU stay as required. After three days the patient was shifted to the general ward with the drain holding 50 ml of blood and stable vital signs.\nCECT chest performed on the fifth day of admission demonstrated a large lesion involving the subcarinal region with intensely enhancing focus adjacent to right bronchus intermedius likely pseudoaneurysm with associated hematoma, collapse of basal right-lower lobe, and collection in the right pleural space (Figure ). The plan for the trucut biopsy of the lung was deferred, and a bronchial angiogram with embolization for bronchial artery pseudoaneurysm was planned. The right common femoral artery was accessed with a 5 French gauge (Fr) vascular sheath, a diagnostic angiographic catheter (Shepherd catheter 5 Fr, Cook Medical, USA) aided in cannulating the right bronchial artery. A selective angiogram revealed a pseudoaneurysm with patent distal flow (Figure ). After the introduction of the 2.1 Fr microcatheter (Artec microcatheter, Japan) the distal normal arterial lumen was reached and coiled with a 2 mm x 2 mm pushable coil (Cook Medical, USA). Similarly, a 2 mm x 2 mm pushable coil was used to trap the front door/proximal part of the right bronchial artery. Post coil embolization, angiogram after 15 minutes showed reduced flow to the sac; however, complete thrombosis was not seen (Figure ). Another permanent embolizing agent Glue mixed with lipiodol (1:7 ratio) was used to achieve complete embolization endpoint. The final angiogram revealed complete thrombosis of the pseudoaneurysm sac and the right bronchial artery (Figure ). No immediate complications were noted. Hemostasis was achieved at the groin by manual compression. After a few days, the chest tube was removed due to a minimal drain.\nFollow-up CT angiography showed coils in the subcarinal region without obvious abnormal enhancement suggestive of adequate embolization and a slight decrease in the size of hematoma at the subcarinal region. The patient was hemodynamically stable and symptomatically better, thus was discharged after one week of hospital stay. The patient was re-evaluated after three weeks by a CECT chest, which showed a significant interval decrease in the lesion at the subcarinal region, subsegmental collapse of a basal segment of the right lower lung, and a significant decrease in the pleural collection (Figure ).

A 55-year-old male diagnosed case of ethanol-related chronic pancreatitis presented with frequent episodes of melena associated with paroxysms of abdominal pain. He was given blood transfusions elsewhere for severe anemia. As patient had persistent GI bleeding with repeated drop in hemoglobin, he was referred for further evaluation and management. On clinical examination, he had profuse sweating, hypotension, tachycardia, severe pallor and mild tenderness in the epigastrium. His laboratory investigations revealed hemoglobin of 7.1 g% and hematocrit of 22%, mild renal failure and increased serum triglycerides. Contrast-enhanced computed tomography of the abdomen showed evidence of chronic calcifying pancreatitis (). Esophagogastroduodenoscopy with a standard scope and colonoscopy were normal. Repeat esophagogastroduodenoscopy with a standard scope after an episode of melena showed active bleeding from the ampulla (). Angiographic study could not localize the site of bleeding. Endoscopic ultrasound showed chronic pancreatitis with a heterogeneous inflammatory lesion in the body of the pancreas (). As the bleeding source could not be localized and the patient had ongoing melena and drop in hemoglobin, emergency exploratory laparotomy was performed after initial hemodynamic stabilization. Pancreas was seen adherent to splenic vessels and hilum. There was evidence of splenic vein rupturing into the main pancreatic duct. Distal pancreatectomy with splenectomy was performed. The patient had an uneventful recovery postoperatively. Postoperative histology demonstrated chronic calcifying pancreatitis (), lymphnodes with reactive hyperplasia and congested spleen (). He was discharged in a hemodynamically stable condition and there was no further recurrence of GI bleeding after 6 months of follow up.

Write a detailed clinical case vignette based on the following key phrases: Gastrointestinal bleeding, Pseudoaneurysm, Chronic pancreatitis

A 47-year-old male, nonsmoker with no significant medical history initially presented with sudden onset right-sided chest pain, fever, and shortness of breath. After a hemorrhagic pleural tap and chest x-ray demonstrating large retro cardiac soft tissue density, gross right pleural effusion, and right lower lobe lung collapse the patient was referred to our center with a working diagnosis of thoracic malignancy and large lung carcinoma with hemorrhagic pleural effusion.\nThe patient was admitted to our center for further workup. Immediately after, the patient experienced severe respiratory distress; oxygen saturation (SpO2) was 74% on two liters of oxygen. The patient was transferred to the intensive care unit (ICU) with pulse: 102 beats per minute and regular, blood pressure: 95/79 mm Hg, respiratory rate: 22/minute, temperature: 97°F, and SpO2: 100% on high-flow oxygen. Glasgow Coma Scale (GCS) was 15/15, and on examination of the chest, there was decreased air entry on the right side. A right-sided chest drain was placed; 1300 ml of hemorrhagic fluid was drained by the end of the day. Total leukocyte count (TLC) then was 21710/mm^3. A blood and sputum culture was obtained. The sputum sample demonstrated Klebsiella pneumonia, which was managed accordingly, normalizing the counts on the days to come. Whole blood was transfused during the ICU stay as required. After three days the patient was shifted to the general ward with the drain holding 50 ml of blood and stable vital signs.\nCECT chest performed on the fifth day of admission demonstrated a large lesion involving the subcarinal region with intensely enhancing focus adjacent to right bronchus intermedius likely pseudoaneurysm with associated hematoma, collapse of basal right-lower lobe, and collection in the right pleural space (Figure ). The plan for the trucut biopsy of the lung was deferred, and a bronchial angiogram with embolization for bronchial artery pseudoaneurysm was planned. The right common femoral artery was accessed with a 5 French gauge (Fr) vascular sheath, a diagnostic angiographic catheter (Shepherd catheter 5 Fr, Cook Medical, USA) aided in cannulating the right bronchial artery. A selective angiogram revealed a pseudoaneurysm with patent distal flow (Figure ). After the introduction of the 2.1 Fr microcatheter (Artec microcatheter, Japan) the distal normal arterial lumen was reached and coiled with a 2 mm x 2 mm pushable coil (Cook Medical, USA). Similarly, a 2 mm x 2 mm pushable coil was used to trap the front door/proximal part of the right bronchial artery. Post coil embolization, angiogram after 15 minutes showed reduced flow to the sac; however, complete thrombosis was not seen (Figure ). Another permanent embolizing agent Glue mixed with lipiodol (1:7 ratio) was used to achieve complete embolization endpoint. The final angiogram revealed complete thrombosis of the pseudoaneurysm sac and the right bronchial artery (Figure ). No immediate complications were noted. Hemostasis was achieved at the groin by manual compression. After a few days, the chest tube was removed due to a minimal drain.\nFollow-up CT angiography showed coils in the subcarinal region without obvious abnormal enhancement suggestive of adequate embolization and a slight decrease in the size of hematoma at the subcarinal region. The patient was hemodynamically stable and symptomatically better, thus was discharged after one week of hospital stay. The patient was re-evaluated after three weeks by a CECT chest, which showed a significant interval decrease in the lesion at the subcarinal region, subsegmental collapse of a basal segment of the right lower lung, and a significant decrease in the pleural collection (Figure ).

A 67-year-old Caucasian man was admitted with diffuse abdominal pain, vomiting, diarrhea, and 4 kg weight loss within a couple of weeks. He had a history of alcohol abuse but further medical history was negative. There was no significant abdominal tenderness, no abdominal palpable mass or flank-knocking tenderness. Laboratory studies showed mild anemia with a hemoglobin level of 10.0 g/dL. An abdominal ultrasound (US) scan showed a partially inverted flow in the portal vein with a small cirrhotic liver, ascites, and a small spleen. Abdominal computed tomography (CT) revealed a large pseudoaneurysm between the SMA and coeliac trunk with a diameter of 77 × 53 × 59 mm. Just below this pseudoaneurysm lay the pancreas with calcifications due to chronic pancreatitis. CT angiography revealed an arterioportal fistula between the pseudoaneurysm and portal vein. Due to this pseudoaneurysm, there was compression of the superior mesenteric vein. Ascites around the liver and spleen were seen, probably due to portal hypertension. There was an increase of the pseudoaneurysm diameter compared to the abdominal CT scan made 5 days earlier, with a maximal diameter of 81 mm (Fig. ). Digital angiography revealed a pseudoaneurysm arising from the proximal superior mesenteric artery with fistulization to the portal vein. The pseudoaneurysm was filled via a large defect in the top of the superior mesenteric artery (Fig. ).\nFrom a technical point of view, covered stenting of the SMA was preferred over embolization of the pseudoaneurysm. A 6 French LIMA sheath was placed in the superior mesenteric artery using a femoral approach. Next, a balloon-expandable covered stent (Bentley Begraft® diameter 8 mm, length 37 mm; Bentley, Hechingen, Germany) was deployed in the SMA. Control angiography showed refilling of the pseudoaneurysm via the common hepatic artery (CHA) through the right gastric and gastroduodenal arteries (Fig. ). Since there was no filling of the CHA from the coeliac trunk, it is probable that the CHA originated from the SMA as a normal variant and was separated from its origin, possibly due to the pancreatitis (Fig. ). After catheterization of the CHA via the left and then the right gastric artery, selective embolization was performed with a 2.7 Fr Progreat® microcatheter (Terumo Medical Corp., Somerset, NY, USA) using multiple Hilal microcoils (3, 4, and 5 mm wide and 3 and 6 cm long; Cook Medical, Bloomington, IN, USA), covering the origin of the GDA (Fig. ). The residual perfusion of the liver is only supplied by the right gastric artery from the left gastric artery.\nPostoperatively, the patient was given clopidogrel therapy for 6 weeks and lifelong acetylsalicylic acid.\nHe was discharged on the eighth postoperative day. Follow-up after 6 months revealed no recurrent abdominal symptoms. The pseudoaneurysm was no longer detectable on control CT angiography (Fig. ).

Write a detailed clinical case vignette based on the following key phrases: Gastrointestinal bleeding, Pseudoaneurysm, Chronic pancreatitis

A 47-year-old male, nonsmoker with no significant medical history initially presented with sudden onset right-sided chest pain, fever, and shortness of breath. After a hemorrhagic pleural tap and chest x-ray demonstrating large retro cardiac soft tissue density, gross right pleural effusion, and right lower lobe lung collapse the patient was referred to our center with a working diagnosis of thoracic malignancy and large lung carcinoma with hemorrhagic pleural effusion.\nThe patient was admitted to our center for further workup. Immediately after, the patient experienced severe respiratory distress; oxygen saturation (SpO2) was 74% on two liters of oxygen. The patient was transferred to the intensive care unit (ICU) with pulse: 102 beats per minute and regular, blood pressure: 95/79 mm Hg, respiratory rate: 22/minute, temperature: 97°F, and SpO2: 100% on high-flow oxygen. Glasgow Coma Scale (GCS) was 15/15, and on examination of the chest, there was decreased air entry on the right side. A right-sided chest drain was placed; 1300 ml of hemorrhagic fluid was drained by the end of the day. Total leukocyte count (TLC) then was 21710/mm^3. A blood and sputum culture was obtained. The sputum sample demonstrated Klebsiella pneumonia, which was managed accordingly, normalizing the counts on the days to come. Whole blood was transfused during the ICU stay as required. After three days the patient was shifted to the general ward with the drain holding 50 ml of blood and stable vital signs.\nCECT chest performed on the fifth day of admission demonstrated a large lesion involving the subcarinal region with intensely enhancing focus adjacent to right bronchus intermedius likely pseudoaneurysm with associated hematoma, collapse of basal right-lower lobe, and collection in the right pleural space (Figure ). The plan for the trucut biopsy of the lung was deferred, and a bronchial angiogram with embolization for bronchial artery pseudoaneurysm was planned. The right common femoral artery was accessed with a 5 French gauge (Fr) vascular sheath, a diagnostic angiographic catheter (Shepherd catheter 5 Fr, Cook Medical, USA) aided in cannulating the right bronchial artery. A selective angiogram revealed a pseudoaneurysm with patent distal flow (Figure ). After the introduction of the 2.1 Fr microcatheter (Artec microcatheter, Japan) the distal normal arterial lumen was reached and coiled with a 2 mm x 2 mm pushable coil (Cook Medical, USA). Similarly, a 2 mm x 2 mm pushable coil was used to trap the front door/proximal part of the right bronchial artery. Post coil embolization, angiogram after 15 minutes showed reduced flow to the sac; however, complete thrombosis was not seen (Figure ). Another permanent embolizing agent Glue mixed with lipiodol (1:7 ratio) was used to achieve complete embolization endpoint. The final angiogram revealed complete thrombosis of the pseudoaneurysm sac and the right bronchial artery (Figure ). No immediate complications were noted. Hemostasis was achieved at the groin by manual compression. After a few days, the chest tube was removed due to a minimal drain.\nFollow-up CT angiography showed coils in the subcarinal region without obvious abnormal enhancement suggestive of adequate embolization and a slight decrease in the size of hematoma at the subcarinal region. The patient was hemodynamically stable and symptomatically better, thus was discharged after one week of hospital stay. The patient was re-evaluated after three weeks by a CECT chest, which showed a significant interval decrease in the lesion at the subcarinal region, subsegmental collapse of a basal segment of the right lower lung, and a significant decrease in the pleural collection (Figure ).

A 38-year-old male complaining of recurrent episodes of melena for the past 2 weeks was admitted to the emergency department of our hospital. Two days before the hospital visit, the patient had complained of the presence of blood in vomiting and had a history of recurrent complaints of upper abdominal pain often radiating to the back. His previous medical history revealed that he had suffered from chronic pancreatitis for 3 years before present admission, possibly due to alcohol abuse. He was resuscitated with the blood and intravenous fluid for melena during present admission. Ultrasonography (USG) whole abdomen revealed a moderately enlarged liver (18.5 cm × 12.3 cm) with heterogeneous echotexture, with a prominent portal vein, of size 1.3 cm; hepatic and splenic hilar collaterals were suggestive of portal hypertension. The presence of mild ascites was documented. Transabdominal USG showed echogenic pancreas with multiple, small, hyperechoic, nonshadowing foci in the pancreas suggestive of fibrotic changes. There was evidence of irregular dilated main pancreatic duct with pancreatic and intraductal calculi. These features were consistent with chronic pancreatitis. The findings were suggestive of alcoholic liver disease with portal hypertension and chronic obstructive pancreatitis. After resuscitation, upper GI endoscopy was performed on two different occasions that showed bleeding from the second part of the duodenum with an abnormal tortuous vessel at the ampulla of Vater. This was diagnosed as hemosuccus pancreaticus, which might have caused the bleeding []. Serendipitously during the endoscopy, a worm was also found penetrating the mucosa of the duodenum. The worm was retrieved and referred to the laboratory for identification. It was a single intact live worm (size 12.3 mm × 0.3 mm) reddish pink, with head bent in the same direction of the body curvature with a spine at the posterior end []. The buccal capsule had six teeth (four hook-like on ventral surface and two knob-like on dorsal surface) []. The live worm was seen to lay eggs while examining under the microscope []. Three consecutive stool samples of the patients were examined. The stool sample was dark-colored, semi-solid in consistency without any parasitic elements. Wet mount examination of stool revealed nonbile-stained ova (60– 65 μm in length, 40– 45 μm in width) with transparent hyaline shell membrane containing blastomeres. The above morphological features of the worm and micrometry of the ova were consistent with Ancylostoma duodenale. For further confirmation and to exclude the probability of mixed infection with Strongyloides stercoralis, the modified Harada– Mori nematode larval culture method[] was performed, and larva of hookworm was retrieved after 1 week of incubation at ambient room temperature. However, duodenal biopsy could not be done to rule out this possibility.\nThe patient was a chronic alcoholic and had deranged liver functions. Other laboratory test revealed low hemoglobin (5.6 g/dL), elevated total leukocyte count (12,300/μl) with increased eosinophils (neutrophils - 54%, lymphocytes – 24%, eosinophils – 16%, and monocytes – 6%), hyperbilirubinemia (total serum bilirubin 12.5 mg% and conjugated bilirubin 11.7 mg%), alanine transaminase/aspartate transaminase (87.7/90 IU), serum alkaline phosphatase (827 IU/L), hypoalbuminemia (2.3 g%), and raised serum globulin (3.9 g%) with reversal of albumin:globulin ratio. Blood and urine cultures were bacteriologically sterile. Peripheral blood smear examination showed microcytic, hypochromic anemia, with the absence of any hemoparasites. The patient was planned for contrast-enhanced computed tomography (CECT) abdomen, but the course of illness was rapidly fatal, and he succumbed to the illness within 48 h of admission, hindering further investigative course. The cause of death was unexplained shock secondary to upper GI bleeding precipitated by chronic, alcoholic liver disease with chronic pancreatitis and portal hypertension.

Write a detailed clinical case vignette based on the following key phrases: Gastrointestinal bleeding, Pseudoaneurysm, Chronic pancreatitis

A 67-year-old Caucasian man was admitted with diffuse abdominal pain, vomiting, diarrhea, and 4 kg weight loss within a couple of weeks. He had a history of alcohol abuse but further medical history was negative. There was no significant abdominal tenderness, no abdominal palpable mass or flank-knocking tenderness. Laboratory studies showed mild anemia with a hemoglobin level of 10.0 g/dL. An abdominal ultrasound (US) scan showed a partially inverted flow in the portal vein with a small cirrhotic liver, ascites, and a small spleen. Abdominal computed tomography (CT) revealed a large pseudoaneurysm between the SMA and coeliac trunk with a diameter of 77 × 53 × 59 mm. Just below this pseudoaneurysm lay the pancreas with calcifications due to chronic pancreatitis. CT angiography revealed an arterioportal fistula between the pseudoaneurysm and portal vein. Due to this pseudoaneurysm, there was compression of the superior mesenteric vein. Ascites around the liver and spleen were seen, probably due to portal hypertension. There was an increase of the pseudoaneurysm diameter compared to the abdominal CT scan made 5 days earlier, with a maximal diameter of 81 mm (Fig. ). Digital angiography revealed a pseudoaneurysm arising from the proximal superior mesenteric artery with fistulization to the portal vein. The pseudoaneurysm was filled via a large defect in the top of the superior mesenteric artery (Fig. ).\nFrom a technical point of view, covered stenting of the SMA was preferred over embolization of the pseudoaneurysm. A 6 French LIMA sheath was placed in the superior mesenteric artery using a femoral approach. Next, a balloon-expandable covered stent (Bentley Begraft® diameter 8 mm, length 37 mm; Bentley, Hechingen, Germany) was deployed in the SMA. Control angiography showed refilling of the pseudoaneurysm via the common hepatic artery (CHA) through the right gastric and gastroduodenal arteries (Fig. ). Since there was no filling of the CHA from the coeliac trunk, it is probable that the CHA originated from the SMA as a normal variant and was separated from its origin, possibly due to the pancreatitis (Fig. ). After catheterization of the CHA via the left and then the right gastric artery, selective embolization was performed with a 2.7 Fr Progreat® microcatheter (Terumo Medical Corp., Somerset, NY, USA) using multiple Hilal microcoils (3, 4, and 5 mm wide and 3 and 6 cm long; Cook Medical, Bloomington, IN, USA), covering the origin of the GDA (Fig. ). The residual perfusion of the liver is only supplied by the right gastric artery from the left gastric artery.\nPostoperatively, the patient was given clopidogrel therapy for 6 weeks and lifelong acetylsalicylic acid.\nHe was discharged on the eighth postoperative day. Follow-up after 6 months revealed no recurrent abdominal symptoms. The pseudoaneurysm was no longer detectable on control CT angiography (Fig. ).

A 55-year-old male diagnosed case of ethanol-related chronic pancreatitis presented with frequent episodes of melena associated with paroxysms of abdominal pain. He was given blood transfusions elsewhere for severe anemia. As patient had persistent GI bleeding with repeated drop in hemoglobin, he was referred for further evaluation and management. On clinical examination, he had profuse sweating, hypotension, tachycardia, severe pallor and mild tenderness in the epigastrium. His laboratory investigations revealed hemoglobin of 7.1 g% and hematocrit of 22%, mild renal failure and increased serum triglycerides. Contrast-enhanced computed tomography of the abdomen showed evidence of chronic calcifying pancreatitis (). Esophagogastroduodenoscopy with a standard scope and colonoscopy were normal. Repeat esophagogastroduodenoscopy with a standard scope after an episode of melena showed active bleeding from the ampulla (). Angiographic study could not localize the site of bleeding. Endoscopic ultrasound showed chronic pancreatitis with a heterogeneous inflammatory lesion in the body of the pancreas (). As the bleeding source could not be localized and the patient had ongoing melena and drop in hemoglobin, emergency exploratory laparotomy was performed after initial hemodynamic stabilization. Pancreas was seen adherent to splenic vessels and hilum. There was evidence of splenic vein rupturing into the main pancreatic duct. Distal pancreatectomy with splenectomy was performed. The patient had an uneventful recovery postoperatively. Postoperative histology demonstrated chronic calcifying pancreatitis (), lymphnodes with reactive hyperplasia and congested spleen (). He was discharged in a hemodynamically stable condition and there was no further recurrence of GI bleeding after 6 months of follow up.

Write a detailed clinical case vignette based on the following key phrases: Gastrointestinal bleeding, Pseudoaneurysm, Chronic pancreatitis

A 55-year-old male diagnosed case of ethanol-related chronic pancreatitis presented with frequent episodes of melena associated with paroxysms of abdominal pain. He was given blood transfusions elsewhere for severe anemia. As patient had persistent GI bleeding with repeated drop in hemoglobin, he was referred for further evaluation and management. On clinical examination, he had profuse sweating, hypotension, tachycardia, severe pallor and mild tenderness in the epigastrium. His laboratory investigations revealed hemoglobin of 7.1 g% and hematocrit of 22%, mild renal failure and increased serum triglycerides. Contrast-enhanced computed tomography of the abdomen showed evidence of chronic calcifying pancreatitis (). Esophagogastroduodenoscopy with a standard scope and colonoscopy were normal. Repeat esophagogastroduodenoscopy with a standard scope after an episode of melena showed active bleeding from the ampulla (). Angiographic study could not localize the site of bleeding. Endoscopic ultrasound showed chronic pancreatitis with a heterogeneous inflammatory lesion in the body of the pancreas (). As the bleeding source could not be localized and the patient had ongoing melena and drop in hemoglobin, emergency exploratory laparotomy was performed after initial hemodynamic stabilization. Pancreas was seen adherent to splenic vessels and hilum. There was evidence of splenic vein rupturing into the main pancreatic duct. Distal pancreatectomy with splenectomy was performed. The patient had an uneventful recovery postoperatively. Postoperative histology demonstrated chronic calcifying pancreatitis (), lymphnodes with reactive hyperplasia and congested spleen (). He was discharged in a hemodynamically stable condition and there was no further recurrence of GI bleeding after 6 months of follow up.

A 38-year-old male complaining of recurrent episodes of melena for the past 2 weeks was admitted to the emergency department of our hospital. Two days before the hospital visit, the patient had complained of the presence of blood in vomiting and had a history of recurrent complaints of upper abdominal pain often radiating to the back. His previous medical history revealed that he had suffered from chronic pancreatitis for 3 years before present admission, possibly due to alcohol abuse. He was resuscitated with the blood and intravenous fluid for melena during present admission. Ultrasonography (USG) whole abdomen revealed a moderately enlarged liver (18.5 cm × 12.3 cm) with heterogeneous echotexture, with a prominent portal vein, of size 1.3 cm; hepatic and splenic hilar collaterals were suggestive of portal hypertension. The presence of mild ascites was documented. Transabdominal USG showed echogenic pancreas with multiple, small, hyperechoic, nonshadowing foci in the pancreas suggestive of fibrotic changes. There was evidence of irregular dilated main pancreatic duct with pancreatic and intraductal calculi. These features were consistent with chronic pancreatitis. The findings were suggestive of alcoholic liver disease with portal hypertension and chronic obstructive pancreatitis. After resuscitation, upper GI endoscopy was performed on two different occasions that showed bleeding from the second part of the duodenum with an abnormal tortuous vessel at the ampulla of Vater. This was diagnosed as hemosuccus pancreaticus, which might have caused the bleeding []. Serendipitously during the endoscopy, a worm was also found penetrating the mucosa of the duodenum. The worm was retrieved and referred to the laboratory for identification. It was a single intact live worm (size 12.3 mm × 0.3 mm) reddish pink, with head bent in the same direction of the body curvature with a spine at the posterior end []. The buccal capsule had six teeth (four hook-like on ventral surface and two knob-like on dorsal surface) []. The live worm was seen to lay eggs while examining under the microscope []. Three consecutive stool samples of the patients were examined. The stool sample was dark-colored, semi-solid in consistency without any parasitic elements. Wet mount examination of stool revealed nonbile-stained ova (60– 65 μm in length, 40– 45 μm in width) with transparent hyaline shell membrane containing blastomeres. The above morphological features of the worm and micrometry of the ova were consistent with Ancylostoma duodenale. For further confirmation and to exclude the probability of mixed infection with Strongyloides stercoralis, the modified Harada– Mori nematode larval culture method[] was performed, and larva of hookworm was retrieved after 1 week of incubation at ambient room temperature. However, duodenal biopsy could not be done to rule out this possibility.\nThe patient was a chronic alcoholic and had deranged liver functions. Other laboratory test revealed low hemoglobin (5.6 g/dL), elevated total leukocyte count (12,300/μl) with increased eosinophils (neutrophils - 54%, lymphocytes – 24%, eosinophils – 16%, and monocytes – 6%), hyperbilirubinemia (total serum bilirubin 12.5 mg% and conjugated bilirubin 11.7 mg%), alanine transaminase/aspartate transaminase (87.7/90 IU), serum alkaline phosphatase (827 IU/L), hypoalbuminemia (2.3 g%), and raised serum globulin (3.9 g%) with reversal of albumin:globulin ratio. Blood and urine cultures were bacteriologically sterile. Peripheral blood smear examination showed microcytic, hypochromic anemia, with the absence of any hemoparasites. The patient was planned for contrast-enhanced computed tomography (CECT) abdomen, but the course of illness was rapidly fatal, and he succumbed to the illness within 48 h of admission, hindering further investigative course. The cause of death was unexplained shock secondary to upper GI bleeding precipitated by chronic, alcoholic liver disease with chronic pancreatitis and portal hypertension.

Write a detailed clinical case vignette based on the following key phrases: Gastrointestinal bleeding, Pseudoaneurysm, Chronic pancreatitis

A 67-year-old Caucasian man was admitted with diffuse abdominal pain, vomiting, diarrhea, and 4 kg weight loss within a couple of weeks. He had a history of alcohol abuse but further medical history was negative. There was no significant abdominal tenderness, no abdominal palpable mass or flank-knocking tenderness. Laboratory studies showed mild anemia with a hemoglobin level of 10.0 g/dL. An abdominal ultrasound (US) scan showed a partially inverted flow in the portal vein with a small cirrhotic liver, ascites, and a small spleen. Abdominal computed tomography (CT) revealed a large pseudoaneurysm between the SMA and coeliac trunk with a diameter of 77 × 53 × 59 mm. Just below this pseudoaneurysm lay the pancreas with calcifications due to chronic pancreatitis. CT angiography revealed an arterioportal fistula between the pseudoaneurysm and portal vein. Due to this pseudoaneurysm, there was compression of the superior mesenteric vein. Ascites around the liver and spleen were seen, probably due to portal hypertension. There was an increase of the pseudoaneurysm diameter compared to the abdominal CT scan made 5 days earlier, with a maximal diameter of 81 mm (Fig. ). Digital angiography revealed a pseudoaneurysm arising from the proximal superior mesenteric artery with fistulization to the portal vein. The pseudoaneurysm was filled via a large defect in the top of the superior mesenteric artery (Fig. ).\nFrom a technical point of view, covered stenting of the SMA was preferred over embolization of the pseudoaneurysm. A 6 French LIMA sheath was placed in the superior mesenteric artery using a femoral approach. Next, a balloon-expandable covered stent (Bentley Begraft® diameter 8 mm, length 37 mm; Bentley, Hechingen, Germany) was deployed in the SMA. Control angiography showed refilling of the pseudoaneurysm via the common hepatic artery (CHA) through the right gastric and gastroduodenal arteries (Fig. ). Since there was no filling of the CHA from the coeliac trunk, it is probable that the CHA originated from the SMA as a normal variant and was separated from its origin, possibly due to the pancreatitis (Fig. ). After catheterization of the CHA via the left and then the right gastric artery, selective embolization was performed with a 2.7 Fr Progreat® microcatheter (Terumo Medical Corp., Somerset, NY, USA) using multiple Hilal microcoils (3, 4, and 5 mm wide and 3 and 6 cm long; Cook Medical, Bloomington, IN, USA), covering the origin of the GDA (Fig. ). The residual perfusion of the liver is only supplied by the right gastric artery from the left gastric artery.\nPostoperatively, the patient was given clopidogrel therapy for 6 weeks and lifelong acetylsalicylic acid.\nHe was discharged on the eighth postoperative day. Follow-up after 6 months revealed no recurrent abdominal symptoms. The pseudoaneurysm was no longer detectable on control CT angiography (Fig. ).

A 38-year-old male complaining of recurrent episodes of melena for the past 2 weeks was admitted to the emergency department of our hospital. Two days before the hospital visit, the patient had complained of the presence of blood in vomiting and had a history of recurrent complaints of upper abdominal pain often radiating to the back. His previous medical history revealed that he had suffered from chronic pancreatitis for 3 years before present admission, possibly due to alcohol abuse. He was resuscitated with the blood and intravenous fluid for melena during present admission. Ultrasonography (USG) whole abdomen revealed a moderately enlarged liver (18.5 cm × 12.3 cm) with heterogeneous echotexture, with a prominent portal vein, of size 1.3 cm; hepatic and splenic hilar collaterals were suggestive of portal hypertension. The presence of mild ascites was documented. Transabdominal USG showed echogenic pancreas with multiple, small, hyperechoic, nonshadowing foci in the pancreas suggestive of fibrotic changes. There was evidence of irregular dilated main pancreatic duct with pancreatic and intraductal calculi. These features were consistent with chronic pancreatitis. The findings were suggestive of alcoholic liver disease with portal hypertension and chronic obstructive pancreatitis. After resuscitation, upper GI endoscopy was performed on two different occasions that showed bleeding from the second part of the duodenum with an abnormal tortuous vessel at the ampulla of Vater. This was diagnosed as hemosuccus pancreaticus, which might have caused the bleeding []. Serendipitously during the endoscopy, a worm was also found penetrating the mucosa of the duodenum. The worm was retrieved and referred to the laboratory for identification. It was a single intact live worm (size 12.3 mm × 0.3 mm) reddish pink, with head bent in the same direction of the body curvature with a spine at the posterior end []. The buccal capsule had six teeth (four hook-like on ventral surface and two knob-like on dorsal surface) []. The live worm was seen to lay eggs while examining under the microscope []. Three consecutive stool samples of the patients were examined. The stool sample was dark-colored, semi-solid in consistency without any parasitic elements. Wet mount examination of stool revealed nonbile-stained ova (60– 65 μm in length, 40– 45 μm in width) with transparent hyaline shell membrane containing blastomeres. The above morphological features of the worm and micrometry of the ova were consistent with Ancylostoma duodenale. For further confirmation and to exclude the probability of mixed infection with Strongyloides stercoralis, the modified Harada– Mori nematode larval culture method[] was performed, and larva of hookworm was retrieved after 1 week of incubation at ambient room temperature. However, duodenal biopsy could not be done to rule out this possibility.\nThe patient was a chronic alcoholic and had deranged liver functions. Other laboratory test revealed low hemoglobin (5.6 g/dL), elevated total leukocyte count (12,300/μl) with increased eosinophils (neutrophils - 54%, lymphocytes – 24%, eosinophils – 16%, and monocytes – 6%), hyperbilirubinemia (total serum bilirubin 12.5 mg% and conjugated bilirubin 11.7 mg%), alanine transaminase/aspartate transaminase (87.7/90 IU), serum alkaline phosphatase (827 IU/L), hypoalbuminemia (2.3 g%), and raised serum globulin (3.9 g%) with reversal of albumin:globulin ratio. Blood and urine cultures were bacteriologically sterile. Peripheral blood smear examination showed microcytic, hypochromic anemia, with the absence of any hemoparasites. The patient was planned for contrast-enhanced computed tomography (CECT) abdomen, but the course of illness was rapidly fatal, and he succumbed to the illness within 48 h of admission, hindering further investigative course. The cause of death was unexplained shock secondary to upper GI bleeding precipitated by chronic, alcoholic liver disease with chronic pancreatitis and portal hypertension.

Write a detailed clinical case vignette based on the following key phrases: Gastrointestinal bleeding, Pseudoaneurysm, Chronic pancreatitis

A 55-year-old obese woman was first examined in March 2006 complaining of diplopia and unilateral exophthalmos in the left eye (). She reported a 2.5-year long history of TAO in the context of Graves disease, poorly responsive to intravenous methylprednisolone regimens.\nShe returned 3 years later with a recent onset of symptoms in the previously not involved right eye. She was particularly concerned about the emergence of a soft “lump” in the outer part of the recently involved right eye. Exophthalmos, eyelid retraction and the presence of a soft lump under the eyelid protruding above the lateral canthus were noted in the right eye (). The lesion was soft upon palpation and persisted unchanged after a 7-month follow-up time despite gradual stabilization of thyroid levels. An orbit MRI showed orbital fat prolapsing anteriorly, anterior bowing of the orbital septum and lateral displacement of the lacrimal gland which looked smaller in the involved orbit as opposed to normal size and appearance of the lacrimal gland in the contralateral left orbit ().

A 72-year-old man presented in November 2008 with pronounced ocular misalignment and a conjunctival protrusion under both upper eyelids. He had been diagnosed with autoimmune hyperthyroidism 8 years before. Orbit MRI showed anterior herniation of orbital fat with the lacrimal gland identified at the normal position and size (). The patient declined strabismus surgery and has been followed for 20 months with no change in the clinical picture.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 68-year-old male presented in May 2006 complaining of a visible “mass” protruding under the lateral part of his mildly swollen right upper eyelid and intermittent diplopia.\nThe “mass” had a yellowish purple hue and was soft and non tender upon palpation. Upper eyelid retraction and restriction of elevation was noted in the right eye (). A systemic work-up for autoimmune dysthyroidism revealed euthyroid status and borderline elevation of anti-TSH receptor antibodies: 8.8 (nl <9, sensitivity 0.8). The diagnosis of euthyroid Graves orbitopathy was established based on the typical constellation of ipsilateral proptosis, eyelid retraction, lid and conjunctival edema as well as tendon sparing enlargement of right inferior and medial rectus muscles. An orbit MRI outlined anterior herniation of intraorbital fat () with slight displacement of the lacrimal gland temporally in the involved right orbit as opposed to normal appearance of the lacrimal gland on the left side.\nHe was treated with intravenous and oral steroids with partial resolution of exophthalmos and diplopia. The prolapse did not cause any symptoms and remained unchanged after 44 months of follow-up time.

A 55-year-old obese woman was first examined in March 2006 complaining of diplopia and unilateral exophthalmos in the left eye (). She reported a 2.5-year long history of TAO in the context of Graves disease, poorly responsive to intravenous methylprednisolone regimens.\nShe returned 3 years later with a recent onset of symptoms in the previously not involved right eye. She was particularly concerned about the emergence of a soft “lump” in the outer part of the recently involved right eye. Exophthalmos, eyelid retraction and the presence of a soft lump under the eyelid protruding above the lateral canthus were noted in the right eye (). The lesion was soft upon palpation and persisted unchanged after a 7-month follow-up time despite gradual stabilization of thyroid levels. An orbit MRI showed orbital fat prolapsing anteriorly, anterior bowing of the orbital septum and lateral displacement of the lacrimal gland which looked smaller in the involved orbit as opposed to normal size and appearance of the lacrimal gland in the contralateral left orbit ().

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 55-year-old obese woman was first examined in March 2006 complaining of diplopia and unilateral exophthalmos in the left eye (). She reported a 2.5-year long history of TAO in the context of Graves disease, poorly responsive to intravenous methylprednisolone regimens.\nShe returned 3 years later with a recent onset of symptoms in the previously not involved right eye. She was particularly concerned about the emergence of a soft “lump” in the outer part of the recently involved right eye. Exophthalmos, eyelid retraction and the presence of a soft lump under the eyelid protruding above the lateral canthus were noted in the right eye (). The lesion was soft upon palpation and persisted unchanged after a 7-month follow-up time despite gradual stabilization of thyroid levels. An orbit MRI showed orbital fat prolapsing anteriorly, anterior bowing of the orbital septum and lateral displacement of the lacrimal gland which looked smaller in the involved orbit as opposed to normal size and appearance of the lacrimal gland in the contralateral left orbit ().

A 71-year-old man presented in November 2007 complaining of a “mass” like protrusion under the lateral part of both upper eyelids for the last several months (). He had previously undergone orbit decompression and strabismus surgery in both eyes elsewhere for TAO diagnosed 5 years before, confirmed with past orbit MRI scans. The lesion had a light purple-yellow hue () and was soft and non tender upon palpation.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 55-year-old obese woman was first examined in March 2006 complaining of diplopia and unilateral exophthalmos in the left eye (). She reported a 2.5-year long history of TAO in the context of Graves disease, poorly responsive to intravenous methylprednisolone regimens.\nShe returned 3 years later with a recent onset of symptoms in the previously not involved right eye. She was particularly concerned about the emergence of a soft “lump” in the outer part of the recently involved right eye. Exophthalmos, eyelid retraction and the presence of a soft lump under the eyelid protruding above the lateral canthus were noted in the right eye (). The lesion was soft upon palpation and persisted unchanged after a 7-month follow-up time despite gradual stabilization of thyroid levels. An orbit MRI showed orbital fat prolapsing anteriorly, anterior bowing of the orbital septum and lateral displacement of the lacrimal gland which looked smaller in the involved orbit as opposed to normal size and appearance of the lacrimal gland in the contralateral left orbit ().

A 72-year-old man presented in October 2008 complaining of a yellowish bulge protruding under the upper eyelid of both eyes for the past 6 months and a gradually worsening “swelling” of his eyes. Clinical and paraclinical testing revealed hyperthyroidism and signs of Graves orbitopathy. An orbit MRI revealed excess orbital fat herniating anteriorly (). The lacrimal gland on either side was identified in place and was of normal size. He was followed for 15 months, during that time thyroid levels stabilized, without an improvement in the size of the lesion.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 55-year-old obese woman was first examined in March 2006 complaining of diplopia and unilateral exophthalmos in the left eye (). She reported a 2.5-year long history of TAO in the context of Graves disease, poorly responsive to intravenous methylprednisolone regimens.\nShe returned 3 years later with a recent onset of symptoms in the previously not involved right eye. She was particularly concerned about the emergence of a soft “lump” in the outer part of the recently involved right eye. Exophthalmos, eyelid retraction and the presence of a soft lump under the eyelid protruding above the lateral canthus were noted in the right eye (). The lesion was soft upon palpation and persisted unchanged after a 7-month follow-up time despite gradual stabilization of thyroid levels. An orbit MRI showed orbital fat prolapsing anteriorly, anterior bowing of the orbital septum and lateral displacement of the lacrimal gland which looked smaller in the involved orbit as opposed to normal size and appearance of the lacrimal gland in the contralateral left orbit ().

A 65-year-old woman presented in October 2010 for evaluation of a melanocytic lesion on her right upper eyelid. She reported a long history of hypothyroidism and bilateral exophthalmos, upon remission at the time of presentation. Asymmetric bilateral subconjunctival temporal protrusions were noted () which by history had emerged shortly after the onset of TAO. There was no change in the clinical picture after 5 months’ follow-up time.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 68-year-old male presented in May 2006 complaining of a visible “mass” protruding under the lateral part of his mildly swollen right upper eyelid and intermittent diplopia.\nThe “mass” had a yellowish purple hue and was soft and non tender upon palpation. Upper eyelid retraction and restriction of elevation was noted in the right eye (). A systemic work-up for autoimmune dysthyroidism revealed euthyroid status and borderline elevation of anti-TSH receptor antibodies: 8.8 (nl <9, sensitivity 0.8). The diagnosis of euthyroid Graves orbitopathy was established based on the typical constellation of ipsilateral proptosis, eyelid retraction, lid and conjunctival edema as well as tendon sparing enlargement of right inferior and medial rectus muscles. An orbit MRI outlined anterior herniation of intraorbital fat () with slight displacement of the lacrimal gland temporally in the involved right orbit as opposed to normal appearance of the lacrimal gland on the left side.\nHe was treated with intravenous and oral steroids with partial resolution of exophthalmos and diplopia. The prolapse did not cause any symptoms and remained unchanged after 44 months of follow-up time.

A 72-year-old man presented in November 2008 with pronounced ocular misalignment and a conjunctival protrusion under both upper eyelids. He had been diagnosed with autoimmune hyperthyroidism 8 years before. Orbit MRI showed anterior herniation of orbital fat with the lacrimal gland identified at the normal position and size (). The patient declined strabismus surgery and has been followed for 20 months with no change in the clinical picture.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 71-year-old man presented in November 2007 complaining of a “mass” like protrusion under the lateral part of both upper eyelids for the last several months (). He had previously undergone orbit decompression and strabismus surgery in both eyes elsewhere for TAO diagnosed 5 years before, confirmed with past orbit MRI scans. The lesion had a light purple-yellow hue () and was soft and non tender upon palpation.

A 72-year-old man presented in November 2008 with pronounced ocular misalignment and a conjunctival protrusion under both upper eyelids. He had been diagnosed with autoimmune hyperthyroidism 8 years before. Orbit MRI showed anterior herniation of orbital fat with the lacrimal gland identified at the normal position and size (). The patient declined strabismus surgery and has been followed for 20 months with no change in the clinical picture.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 72-year-old man presented in October 2008 complaining of a yellowish bulge protruding under the upper eyelid of both eyes for the past 6 months and a gradually worsening “swelling” of his eyes. Clinical and paraclinical testing revealed hyperthyroidism and signs of Graves orbitopathy. An orbit MRI revealed excess orbital fat herniating anteriorly (). The lacrimal gland on either side was identified in place and was of normal size. He was followed for 15 months, during that time thyroid levels stabilized, without an improvement in the size of the lesion.

A 72-year-old man presented in November 2008 with pronounced ocular misalignment and a conjunctival protrusion under both upper eyelids. He had been diagnosed with autoimmune hyperthyroidism 8 years before. Orbit MRI showed anterior herniation of orbital fat with the lacrimal gland identified at the normal position and size (). The patient declined strabismus surgery and has been followed for 20 months with no change in the clinical picture.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 72-year-old man presented in November 2008 with pronounced ocular misalignment and a conjunctival protrusion under both upper eyelids. He had been diagnosed with autoimmune hyperthyroidism 8 years before. Orbit MRI showed anterior herniation of orbital fat with the lacrimal gland identified at the normal position and size (). The patient declined strabismus surgery and has been followed for 20 months with no change in the clinical picture.

A 65-year-old woman presented in October 2010 for evaluation of a melanocytic lesion on her right upper eyelid. She reported a long history of hypothyroidism and bilateral exophthalmos, upon remission at the time of presentation. Asymmetric bilateral subconjunctival temporal protrusions were noted () which by history had emerged shortly after the onset of TAO. There was no change in the clinical picture after 5 months’ follow-up time.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 68-year-old male presented in May 2006 complaining of a visible “mass” protruding under the lateral part of his mildly swollen right upper eyelid and intermittent diplopia.\nThe “mass” had a yellowish purple hue and was soft and non tender upon palpation. Upper eyelid retraction and restriction of elevation was noted in the right eye (). A systemic work-up for autoimmune dysthyroidism revealed euthyroid status and borderline elevation of anti-TSH receptor antibodies: 8.8 (nl <9, sensitivity 0.8). The diagnosis of euthyroid Graves orbitopathy was established based on the typical constellation of ipsilateral proptosis, eyelid retraction, lid and conjunctival edema as well as tendon sparing enlargement of right inferior and medial rectus muscles. An orbit MRI outlined anterior herniation of intraorbital fat () with slight displacement of the lacrimal gland temporally in the involved right orbit as opposed to normal appearance of the lacrimal gland on the left side.\nHe was treated with intravenous and oral steroids with partial resolution of exophthalmos and diplopia. The prolapse did not cause any symptoms and remained unchanged after 44 months of follow-up time.

A 71-year-old man presented in November 2007 complaining of a “mass” like protrusion under the lateral part of both upper eyelids for the last several months (). He had previously undergone orbit decompression and strabismus surgery in both eyes elsewhere for TAO diagnosed 5 years before, confirmed with past orbit MRI scans. The lesion had a light purple-yellow hue () and was soft and non tender upon palpation.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 68-year-old male presented in May 2006 complaining of a visible “mass” protruding under the lateral part of his mildly swollen right upper eyelid and intermittent diplopia.\nThe “mass” had a yellowish purple hue and was soft and non tender upon palpation. Upper eyelid retraction and restriction of elevation was noted in the right eye (). A systemic work-up for autoimmune dysthyroidism revealed euthyroid status and borderline elevation of anti-TSH receptor antibodies: 8.8 (nl <9, sensitivity 0.8). The diagnosis of euthyroid Graves orbitopathy was established based on the typical constellation of ipsilateral proptosis, eyelid retraction, lid and conjunctival edema as well as tendon sparing enlargement of right inferior and medial rectus muscles. An orbit MRI outlined anterior herniation of intraorbital fat () with slight displacement of the lacrimal gland temporally in the involved right orbit as opposed to normal appearance of the lacrimal gland on the left side.\nHe was treated with intravenous and oral steroids with partial resolution of exophthalmos and diplopia. The prolapse did not cause any symptoms and remained unchanged after 44 months of follow-up time.

A 72-year-old man presented in October 2008 complaining of a yellowish bulge protruding under the upper eyelid of both eyes for the past 6 months and a gradually worsening “swelling” of his eyes. Clinical and paraclinical testing revealed hyperthyroidism and signs of Graves orbitopathy. An orbit MRI revealed excess orbital fat herniating anteriorly (). The lacrimal gland on either side was identified in place and was of normal size. He was followed for 15 months, during that time thyroid levels stabilized, without an improvement in the size of the lesion.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 68-year-old male presented in May 2006 complaining of a visible “mass” protruding under the lateral part of his mildly swollen right upper eyelid and intermittent diplopia.\nThe “mass” had a yellowish purple hue and was soft and non tender upon palpation. Upper eyelid retraction and restriction of elevation was noted in the right eye (). A systemic work-up for autoimmune dysthyroidism revealed euthyroid status and borderline elevation of anti-TSH receptor antibodies: 8.8 (nl <9, sensitivity 0.8). The diagnosis of euthyroid Graves orbitopathy was established based on the typical constellation of ipsilateral proptosis, eyelid retraction, lid and conjunctival edema as well as tendon sparing enlargement of right inferior and medial rectus muscles. An orbit MRI outlined anterior herniation of intraorbital fat () with slight displacement of the lacrimal gland temporally in the involved right orbit as opposed to normal appearance of the lacrimal gland on the left side.\nHe was treated with intravenous and oral steroids with partial resolution of exophthalmos and diplopia. The prolapse did not cause any symptoms and remained unchanged after 44 months of follow-up time.

A 65-year-old woman presented in October 2010 for evaluation of a melanocytic lesion on her right upper eyelid. She reported a long history of hypothyroidism and bilateral exophthalmos, upon remission at the time of presentation. Asymmetric bilateral subconjunctival temporal protrusions were noted () which by history had emerged shortly after the onset of TAO. There was no change in the clinical picture after 5 months’ follow-up time.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 72-year-old man presented in October 2008 complaining of a yellowish bulge protruding under the upper eyelid of both eyes for the past 6 months and a gradually worsening “swelling” of his eyes. Clinical and paraclinical testing revealed hyperthyroidism and signs of Graves orbitopathy. An orbit MRI revealed excess orbital fat herniating anteriorly (). The lacrimal gland on either side was identified in place and was of normal size. He was followed for 15 months, during that time thyroid levels stabilized, without an improvement in the size of the lesion.

A 71-year-old man presented in November 2007 complaining of a “mass” like protrusion under the lateral part of both upper eyelids for the last several months (). He had previously undergone orbit decompression and strabismus surgery in both eyes elsewhere for TAO diagnosed 5 years before, confirmed with past orbit MRI scans. The lesion had a light purple-yellow hue () and was soft and non tender upon palpation.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 65-year-old woman presented in October 2010 for evaluation of a melanocytic lesion on her right upper eyelid. She reported a long history of hypothyroidism and bilateral exophthalmos, upon remission at the time of presentation. Asymmetric bilateral subconjunctival temporal protrusions were noted () which by history had emerged shortly after the onset of TAO. There was no change in the clinical picture after 5 months’ follow-up time.

A 71-year-old man presented in November 2007 complaining of a “mass” like protrusion under the lateral part of both upper eyelids for the last several months (). He had previously undergone orbit decompression and strabismus surgery in both eyes elsewhere for TAO diagnosed 5 years before, confirmed with past orbit MRI scans. The lesion had a light purple-yellow hue () and was soft and non tender upon palpation.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 72-year-old man presented in October 2008 complaining of a yellowish bulge protruding under the upper eyelid of both eyes for the past 6 months and a gradually worsening “swelling” of his eyes. Clinical and paraclinical testing revealed hyperthyroidism and signs of Graves orbitopathy. An orbit MRI revealed excess orbital fat herniating anteriorly (). The lacrimal gland on either side was identified in place and was of normal size. He was followed for 15 months, during that time thyroid levels stabilized, without an improvement in the size of the lesion.

A 65-year-old woman presented in October 2010 for evaluation of a melanocytic lesion on her right upper eyelid. She reported a long history of hypothyroidism and bilateral exophthalmos, upon remission at the time of presentation. Asymmetric bilateral subconjunctival temporal protrusions were noted () which by history had emerged shortly after the onset of TAO. There was no change in the clinical picture after 5 months’ follow-up time.

Write a detailed clinical case vignette based on the following key phrases: Graves disease, Thyroid-associated orbitopathy (TAO), Orbital fat prolapse

A 38-year-old female patient presented to our fast-track ENT clinic with persistent left-sided throat discomfort and pain for several months. The throat pain lateralised to the left and radiated to her left ear. She also reported positive reflux symptoms with heartburn. At the time of review, medical management had been implemented (with high-dose oral proton pump inhibitor and raft-forming alginate); however, this yielded no symptomatic relief. Voice Handicap Index (VHI) was 11 and Eating Assessment Tool (EAT-10) score was 1. She was a non-smoker, and her past medical history was insignificant.\nOffice examination of the neck, oral cavity and oropharynx was unremarkable. Flexible nasendoscopy was performed, which revealed some post-cricoid oedema consistent with laryngopharyngeal reflux (Figure ). A contrast-enhanced magnetic resonance imaging (MRI) scan of the neck was normal. As symptoms continued to persist, a transnasal oesophagoscopy (TNO) under local anaesthetic was performed as an office procedure where a proximal oesophageal lesion was identified (Figure ). The lesion appeared small (approximately 3 mm in diameter), exophytic, non-ulcerating and papillomatous. It was located on the left side of the upper oesophageal mucosa, 23 cm from the nasal sill. Multiple punch biopsies were taken.\nHistological examination of the specimen revealed squamous cell papilloma of benign appearance with prominent papillae and acanthotic stratified squamous epithelium without cellular atypia. The specimen tested positive for human papilloma virus (HPV). Oesophageal manometry and 24-hour oesophageal pH monitoring indicated borderline pathological reflux with some proximal penetration (DeMeester score [DMS] = 15.9).\nThe patient then underwent complete endoscopic excision of the lesion. Histology confirmed HPV-positive squamous papilloma. Anti-reflux treatment, including lifestyle changes, was continued. Following excision, the patient’s symptoms resolved and a yearly follow-up confirmed their complete remission. It is yet uncertain whether symptomatic relief was a result of excision, continued anti-reflux treatment, or even a placebo effect associating the procedure.

A 53-year-old male with history of alcohol abuse presented with new-onset seizure/syncope, six painless maroon stools, and coffee-ground emesis. The patient admitted to frequent diclofenac use and ketorolac injections. He did not have a history of varices. Vital signs demonstrated tachycardia (heart rate 111 beats/min) and hypotension (79/59 mmHg). Physical exam revealed pale conjunctiva, dry mucous membranes, and maroon colored stool. He was found to be anemic with a hemoglobin of 7.9 G/dL and had an elevated INR of 1.2. He was transfused two units of packed red blood cells and was started on a pantoprazole drip.\nOnce stabilized, initial EGD revealed an island of tissue growth in the mid-esophagus and a bleeding duodenal ulcer that was injected with epinephrine, cauterized with gold probe and clipped. Biopsy of the esophageal lesion was deferred to outpatient follow-up given the severity of the patient's presenting condition. He had no further signs of gastrointestinal bleeding. Two weeks later, a repeat EGD was performed. Biopsies were taken of the stomach mucosa and mid-esophageal mass (see ). Gastric biopsy demonstrated mild chronic gastritis without dysplastic changes or Helicobacter pylori. Esophageal biopsy demonstrated findings consistent with squamous papilloma (see Figures and ).

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 53-year-old male with history of alcohol abuse presented with new-onset seizure/syncope, six painless maroon stools, and coffee-ground emesis. The patient admitted to frequent diclofenac use and ketorolac injections. He did not have a history of varices. Vital signs demonstrated tachycardia (heart rate 111 beats/min) and hypotension (79/59 mmHg). Physical exam revealed pale conjunctiva, dry mucous membranes, and maroon colored stool. He was found to be anemic with a hemoglobin of 7.9 G/dL and had an elevated INR of 1.2. He was transfused two units of packed red blood cells and was started on a pantoprazole drip.\nOnce stabilized, initial EGD revealed an island of tissue growth in the mid-esophagus and a bleeding duodenal ulcer that was injected with epinephrine, cauterized with gold probe and clipped. Biopsy of the esophageal lesion was deferred to outpatient follow-up given the severity of the patient's presenting condition. He had no further signs of gastrointestinal bleeding. Two weeks later, a repeat EGD was performed. Biopsies were taken of the stomach mucosa and mid-esophageal mass (see ). Gastric biopsy demonstrated mild chronic gastritis without dysplastic changes or Helicobacter pylori. Esophageal biopsy demonstrated findings consistent with squamous papilloma (see Figures and ).

A 61-year-old female with history of uncontrolled diabetes mellitus type 2 complicated by gastroparesis, prior esophageal dilation, and ileostomy was being evaluated with endoscopy as outpatient for worsening dysphagia. EGD was significant for a small nodule in the proximal esophagus (see ), normal GEJ (gastroesophageal junction), mild gastritis, and normal duodenum. Gastric biopsy demonstrated mild chronic gastritis without dysplastic changes or Helicobacter pylori. Esophageal biopsy demonstrated findings consistent with squamous papilloma.

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 67-year-old Caucasian man visited his primary care physician with complaints of hematemesis and continuous dysphagia. He had history of cigarette smoking and social alcohol consumption. Previous medical history included hypertension and hyperlipidemia. An initial EGD showed multiple verrucous lesions extending from 30 cm to 39 cm from his incisors. Pathological examination of the multiple biopsies showed squamous papillomatosis.\nThe patient was referred for evaluation at our hospital and a new EGD showed the same extensive verrucous lesions with three large growths on the distal esophagus causing significant stenosis. He repeated the biopsies and maintained the previous histological diagnosis. A thoracoabdominal CT-Scan revealed large esophageal lesions apparently superficial with thickening of the esophageal wall. Endoscopic Ultrasound showed that these changes were almost all limited to the mucosa and submucosa except in one area where they appeared to penetrate deeper.\nAt this time, the patient’s dysphagia got worse and there was substantial suspicion of potential malignancy. After a multidisciplinary discussion, he was proposed for surgery. He underwent a minimally invasive Ivor-Lewis Esophagectomy (laparoscopy + right lateral thoracoscopy) with a mechanical termino-lateral esophago-gastric upper thoracic anastomosis (at approximately 24/25 cm from the incisors) (Figs. , ). The postoperative (PO) period was uneventful and the patient was discharged at the 9th PO day.\nThe examination of esophagectomy specimen () showed a squamous cell carcinoma in situ (verrucous type) of the distal esophagus with areas of high dysplasia and extensive diffuse squamous papillomatosis. There were no signs of lymphatic or perineural invasion and margins were clear. The eighteen lymph nodes excised were all negative for malignancy. The TNM stage (8th edition) was Tis N0. One year later, at the follow-up consultation, there were no signs of recurrence.

A 53-year-old male with history of alcohol abuse presented with new-onset seizure/syncope, six painless maroon stools, and coffee-ground emesis. The patient admitted to frequent diclofenac use and ketorolac injections. He did not have a history of varices. Vital signs demonstrated tachycardia (heart rate 111 beats/min) and hypotension (79/59 mmHg). Physical exam revealed pale conjunctiva, dry mucous membranes, and maroon colored stool. He was found to be anemic with a hemoglobin of 7.9 G/dL and had an elevated INR of 1.2. He was transfused two units of packed red blood cells and was started on a pantoprazole drip.\nOnce stabilized, initial EGD revealed an island of tissue growth in the mid-esophagus and a bleeding duodenal ulcer that was injected with epinephrine, cauterized with gold probe and clipped. Biopsy of the esophageal lesion was deferred to outpatient follow-up given the severity of the patient's presenting condition. He had no further signs of gastrointestinal bleeding. Two weeks later, a repeat EGD was performed. Biopsies were taken of the stomach mucosa and mid-esophageal mass (see ). Gastric biopsy demonstrated mild chronic gastritis without dysplastic changes or Helicobacter pylori. Esophageal biopsy demonstrated findings consistent with squamous papilloma (see Figures and ).

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 44-year-old woman visited the outpatient clinic with reports of EGD examination showing a GEJ polyp. EGD had been performed as part of a health promotion screening, and the patient denied having any subjective symptom or past medical history including smoking and alcohol consumption. She looked generally healthy. Physical examination and laboratory test revealed that all values were within the normal reference range.\nEGD examination revealed that the polyp was located just on the squamocolumnar junction of the GEJ and presented as a 1.5-cm protruding polypoid mass with an irregular and nodular surface (). Forceps biopsy was performed to exclude malignant tumor. Microscopic examination revealed squamous papilloma showing papillary squamous epithelium with a fibrovascular core. Squamous epithelial cells of the papilloma showed koilocytosis with irregular nuclear membrane and perinuclear halo, which histologically confirmed the presence of human papillomavirus infection ().\nAfter obtaining informed consent from the patient, endoscopic mucosal resection was performed to remove the whole papilloma at the GEJ to avoid a possible increase in the size of the tumor. Histological examination of the resected specimen revealed a nodular mass with papillary growth consisting of squamous cell epithelium with a well-structured inner fibrovascular core, which was compatible with squamous papilloma. The specimen showed complete and curative resection, without involvement of the lateral or vertical margin.\nTwo years later, the patient revisited our clinic for esophageal reflux symptoms. Follow-up EGD incidentally revealed a polyp at the GEJ at the exact spot of the previously removed papilloma. The polyp measured approximately 1.0 cm and had a morphology similar to that of the previous papilloma (), suggesting recurrence. Although the polyp was smaller than that detected 2 years previously, endoscopic submucosal dissection was performed owing to fibrotic scarring and non-lifting sign at the anal side of the polyp (). The polyp was removed en bloc and completely, without marginal involvement. Microscopic examination revealed nodular mass with papillary growth. Histologic examination revealed usual papilloma showing papillary squamous epithelium, with a well-developed fibrovascular core. However, multifocal severe squamous atypia was observed throughout the mucosal epithelium, compatible with squamous cell carcinoma in situ (). The patient was finally diagnosed with squamous cell carcinoma in situ arising from esophageal squamous papilloma.

A 53-year-old male with history of alcohol abuse presented with new-onset seizure/syncope, six painless maroon stools, and coffee-ground emesis. The patient admitted to frequent diclofenac use and ketorolac injections. He did not have a history of varices. Vital signs demonstrated tachycardia (heart rate 111 beats/min) and hypotension (79/59 mmHg). Physical exam revealed pale conjunctiva, dry mucous membranes, and maroon colored stool. He was found to be anemic with a hemoglobin of 7.9 G/dL and had an elevated INR of 1.2. He was transfused two units of packed red blood cells and was started on a pantoprazole drip.\nOnce stabilized, initial EGD revealed an island of tissue growth in the mid-esophagus and a bleeding duodenal ulcer that was injected with epinephrine, cauterized with gold probe and clipped. Biopsy of the esophageal lesion was deferred to outpatient follow-up given the severity of the patient's presenting condition. He had no further signs of gastrointestinal bleeding. Two weeks later, a repeat EGD was performed. Biopsies were taken of the stomach mucosa and mid-esophageal mass (see ). Gastric biopsy demonstrated mild chronic gastritis without dysplastic changes or Helicobacter pylori. Esophageal biopsy demonstrated findings consistent with squamous papilloma (see Figures and ).

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 53-year-old male with history of alcohol abuse presented with new-onset seizure/syncope, six painless maroon stools, and coffee-ground emesis. The patient admitted to frequent diclofenac use and ketorolac injections. He did not have a history of varices. Vital signs demonstrated tachycardia (heart rate 111 beats/min) and hypotension (79/59 mmHg). Physical exam revealed pale conjunctiva, dry mucous membranes, and maroon colored stool. He was found to be anemic with a hemoglobin of 7.9 G/dL and had an elevated INR of 1.2. He was transfused two units of packed red blood cells and was started on a pantoprazole drip.\nOnce stabilized, initial EGD revealed an island of tissue growth in the mid-esophagus and a bleeding duodenal ulcer that was injected with epinephrine, cauterized with gold probe and clipped. Biopsy of the esophageal lesion was deferred to outpatient follow-up given the severity of the patient's presenting condition. He had no further signs of gastrointestinal bleeding. Two weeks later, a repeat EGD was performed. Biopsies were taken of the stomach mucosa and mid-esophageal mass (see ). Gastric biopsy demonstrated mild chronic gastritis without dysplastic changes or Helicobacter pylori. Esophageal biopsy demonstrated findings consistent with squamous papilloma (see Figures and ).

A 54-year-old female with history of fibromyalgia, chronic opioid dependency, cyanocobalamin deficiency, vitamin D deficiency, and GERD with previously noted Los Angeles class C esophagitis was being evaluated with endoscopy as outpatient for dysphagia and abdominal pain. EGD was significant for an exophytic wart-like growth in the distal esophagus, minimally irregular Z-line noted at GEJ, mild gastritis without ulcers, and normal duodenum. GEJ biopsy demonstrated focal intestinal metaplasia suggestive of Barrett's esophagus without dysplastic changes. Esophageal biopsy demonstrated findings consistent with squamous papilloma (see Figures and ).

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 38-year-old female patient presented to our fast-track ENT clinic with persistent left-sided throat discomfort and pain for several months. The throat pain lateralised to the left and radiated to her left ear. She also reported positive reflux symptoms with heartburn. At the time of review, medical management had been implemented (with high-dose oral proton pump inhibitor and raft-forming alginate); however, this yielded no symptomatic relief. Voice Handicap Index (VHI) was 11 and Eating Assessment Tool (EAT-10) score was 1. She was a non-smoker, and her past medical history was insignificant.\nOffice examination of the neck, oral cavity and oropharynx was unremarkable. Flexible nasendoscopy was performed, which revealed some post-cricoid oedema consistent with laryngopharyngeal reflux (Figure ). A contrast-enhanced magnetic resonance imaging (MRI) scan of the neck was normal. As symptoms continued to persist, a transnasal oesophagoscopy (TNO) under local anaesthetic was performed as an office procedure where a proximal oesophageal lesion was identified (Figure ). The lesion appeared small (approximately 3 mm in diameter), exophytic, non-ulcerating and papillomatous. It was located on the left side of the upper oesophageal mucosa, 23 cm from the nasal sill. Multiple punch biopsies were taken.\nHistological examination of the specimen revealed squamous cell papilloma of benign appearance with prominent papillae and acanthotic stratified squamous epithelium without cellular atypia. The specimen tested positive for human papilloma virus (HPV). Oesophageal manometry and 24-hour oesophageal pH monitoring indicated borderline pathological reflux with some proximal penetration (DeMeester score [DMS] = 15.9).\nThe patient then underwent complete endoscopic excision of the lesion. Histology confirmed HPV-positive squamous papilloma. Anti-reflux treatment, including lifestyle changes, was continued. Following excision, the patient’s symptoms resolved and a yearly follow-up confirmed their complete remission. It is yet uncertain whether symptomatic relief was a result of excision, continued anti-reflux treatment, or even a placebo effect associating the procedure.

A 61-year-old female with history of uncontrolled diabetes mellitus type 2 complicated by gastroparesis, prior esophageal dilation, and ileostomy was being evaluated with endoscopy as outpatient for worsening dysphagia. EGD was significant for a small nodule in the proximal esophagus (see ), normal GEJ (gastroesophageal junction), mild gastritis, and normal duodenum. Gastric biopsy demonstrated mild chronic gastritis without dysplastic changes or Helicobacter pylori. Esophageal biopsy demonstrated findings consistent with squamous papilloma.

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 38-year-old female patient presented to our fast-track ENT clinic with persistent left-sided throat discomfort and pain for several months. The throat pain lateralised to the left and radiated to her left ear. She also reported positive reflux symptoms with heartburn. At the time of review, medical management had been implemented (with high-dose oral proton pump inhibitor and raft-forming alginate); however, this yielded no symptomatic relief. Voice Handicap Index (VHI) was 11 and Eating Assessment Tool (EAT-10) score was 1. She was a non-smoker, and her past medical history was insignificant.\nOffice examination of the neck, oral cavity and oropharynx was unremarkable. Flexible nasendoscopy was performed, which revealed some post-cricoid oedema consistent with laryngopharyngeal reflux (Figure ). A contrast-enhanced magnetic resonance imaging (MRI) scan of the neck was normal. As symptoms continued to persist, a transnasal oesophagoscopy (TNO) under local anaesthetic was performed as an office procedure where a proximal oesophageal lesion was identified (Figure ). The lesion appeared small (approximately 3 mm in diameter), exophytic, non-ulcerating and papillomatous. It was located on the left side of the upper oesophageal mucosa, 23 cm from the nasal sill. Multiple punch biopsies were taken.\nHistological examination of the specimen revealed squamous cell papilloma of benign appearance with prominent papillae and acanthotic stratified squamous epithelium without cellular atypia. The specimen tested positive for human papilloma virus (HPV). Oesophageal manometry and 24-hour oesophageal pH monitoring indicated borderline pathological reflux with some proximal penetration (DeMeester score [DMS] = 15.9).\nThe patient then underwent complete endoscopic excision of the lesion. Histology confirmed HPV-positive squamous papilloma. Anti-reflux treatment, including lifestyle changes, was continued. Following excision, the patient’s symptoms resolved and a yearly follow-up confirmed their complete remission. It is yet uncertain whether symptomatic relief was a result of excision, continued anti-reflux treatment, or even a placebo effect associating the procedure.

A 67-year-old Caucasian man visited his primary care physician with complaints of hematemesis and continuous dysphagia. He had history of cigarette smoking and social alcohol consumption. Previous medical history included hypertension and hyperlipidemia. An initial EGD showed multiple verrucous lesions extending from 30 cm to 39 cm from his incisors. Pathological examination of the multiple biopsies showed squamous papillomatosis.\nThe patient was referred for evaluation at our hospital and a new EGD showed the same extensive verrucous lesions with three large growths on the distal esophagus causing significant stenosis. He repeated the biopsies and maintained the previous histological diagnosis. A thoracoabdominal CT-Scan revealed large esophageal lesions apparently superficial with thickening of the esophageal wall. Endoscopic Ultrasound showed that these changes were almost all limited to the mucosa and submucosa except in one area where they appeared to penetrate deeper.\nAt this time, the patient’s dysphagia got worse and there was substantial suspicion of potential malignancy. After a multidisciplinary discussion, he was proposed for surgery. He underwent a minimally invasive Ivor-Lewis Esophagectomy (laparoscopy + right lateral thoracoscopy) with a mechanical termino-lateral esophago-gastric upper thoracic anastomosis (at approximately 24/25 cm from the incisors) (Figs. , ). The postoperative (PO) period was uneventful and the patient was discharged at the 9th PO day.\nThe examination of esophagectomy specimen () showed a squamous cell carcinoma in situ (verrucous type) of the distal esophagus with areas of high dysplasia and extensive diffuse squamous papillomatosis. There were no signs of lymphatic or perineural invasion and margins were clear. The eighteen lymph nodes excised were all negative for malignancy. The TNM stage (8th edition) was Tis N0. One year later, at the follow-up consultation, there were no signs of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 38-year-old female patient presented to our fast-track ENT clinic with persistent left-sided throat discomfort and pain for several months. The throat pain lateralised to the left and radiated to her left ear. She also reported positive reflux symptoms with heartburn. At the time of review, medical management had been implemented (with high-dose oral proton pump inhibitor and raft-forming alginate); however, this yielded no symptomatic relief. Voice Handicap Index (VHI) was 11 and Eating Assessment Tool (EAT-10) score was 1. She was a non-smoker, and her past medical history was insignificant.\nOffice examination of the neck, oral cavity and oropharynx was unremarkable. Flexible nasendoscopy was performed, which revealed some post-cricoid oedema consistent with laryngopharyngeal reflux (Figure ). A contrast-enhanced magnetic resonance imaging (MRI) scan of the neck was normal. As symptoms continued to persist, a transnasal oesophagoscopy (TNO) under local anaesthetic was performed as an office procedure where a proximal oesophageal lesion was identified (Figure ). The lesion appeared small (approximately 3 mm in diameter), exophytic, non-ulcerating and papillomatous. It was located on the left side of the upper oesophageal mucosa, 23 cm from the nasal sill. Multiple punch biopsies were taken.\nHistological examination of the specimen revealed squamous cell papilloma of benign appearance with prominent papillae and acanthotic stratified squamous epithelium without cellular atypia. The specimen tested positive for human papilloma virus (HPV). Oesophageal manometry and 24-hour oesophageal pH monitoring indicated borderline pathological reflux with some proximal penetration (DeMeester score [DMS] = 15.9).\nThe patient then underwent complete endoscopic excision of the lesion. Histology confirmed HPV-positive squamous papilloma. Anti-reflux treatment, including lifestyle changes, was continued. Following excision, the patient’s symptoms resolved and a yearly follow-up confirmed their complete remission. It is yet uncertain whether symptomatic relief was a result of excision, continued anti-reflux treatment, or even a placebo effect associating the procedure.

A 44-year-old woman visited the outpatient clinic with reports of EGD examination showing a GEJ polyp. EGD had been performed as part of a health promotion screening, and the patient denied having any subjective symptom or past medical history including smoking and alcohol consumption. She looked generally healthy. Physical examination and laboratory test revealed that all values were within the normal reference range.\nEGD examination revealed that the polyp was located just on the squamocolumnar junction of the GEJ and presented as a 1.5-cm protruding polypoid mass with an irregular and nodular surface (). Forceps biopsy was performed to exclude malignant tumor. Microscopic examination revealed squamous papilloma showing papillary squamous epithelium with a fibrovascular core. Squamous epithelial cells of the papilloma showed koilocytosis with irregular nuclear membrane and perinuclear halo, which histologically confirmed the presence of human papillomavirus infection ().\nAfter obtaining informed consent from the patient, endoscopic mucosal resection was performed to remove the whole papilloma at the GEJ to avoid a possible increase in the size of the tumor. Histological examination of the resected specimen revealed a nodular mass with papillary growth consisting of squamous cell epithelium with a well-structured inner fibrovascular core, which was compatible with squamous papilloma. The specimen showed complete and curative resection, without involvement of the lateral or vertical margin.\nTwo years later, the patient revisited our clinic for esophageal reflux symptoms. Follow-up EGD incidentally revealed a polyp at the GEJ at the exact spot of the previously removed papilloma. The polyp measured approximately 1.0 cm and had a morphology similar to that of the previous papilloma (), suggesting recurrence. Although the polyp was smaller than that detected 2 years previously, endoscopic submucosal dissection was performed owing to fibrotic scarring and non-lifting sign at the anal side of the polyp (). The polyp was removed en bloc and completely, without marginal involvement. Microscopic examination revealed nodular mass with papillary growth. Histologic examination revealed usual papilloma showing papillary squamous epithelium, with a well-developed fibrovascular core. However, multifocal severe squamous atypia was observed throughout the mucosal epithelium, compatible with squamous cell carcinoma in situ (). The patient was finally diagnosed with squamous cell carcinoma in situ arising from esophageal squamous papilloma.

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 38-year-old female patient presented to our fast-track ENT clinic with persistent left-sided throat discomfort and pain for several months. The throat pain lateralised to the left and radiated to her left ear. She also reported positive reflux symptoms with heartburn. At the time of review, medical management had been implemented (with high-dose oral proton pump inhibitor and raft-forming alginate); however, this yielded no symptomatic relief. Voice Handicap Index (VHI) was 11 and Eating Assessment Tool (EAT-10) score was 1. She was a non-smoker, and her past medical history was insignificant.\nOffice examination of the neck, oral cavity and oropharynx was unremarkable. Flexible nasendoscopy was performed, which revealed some post-cricoid oedema consistent with laryngopharyngeal reflux (Figure ). A contrast-enhanced magnetic resonance imaging (MRI) scan of the neck was normal. As symptoms continued to persist, a transnasal oesophagoscopy (TNO) under local anaesthetic was performed as an office procedure where a proximal oesophageal lesion was identified (Figure ). The lesion appeared small (approximately 3 mm in diameter), exophytic, non-ulcerating and papillomatous. It was located on the left side of the upper oesophageal mucosa, 23 cm from the nasal sill. Multiple punch biopsies were taken.\nHistological examination of the specimen revealed squamous cell papilloma of benign appearance with prominent papillae and acanthotic stratified squamous epithelium without cellular atypia. The specimen tested positive for human papilloma virus (HPV). Oesophageal manometry and 24-hour oesophageal pH monitoring indicated borderline pathological reflux with some proximal penetration (DeMeester score [DMS] = 15.9).\nThe patient then underwent complete endoscopic excision of the lesion. Histology confirmed HPV-positive squamous papilloma. Anti-reflux treatment, including lifestyle changes, was continued. Following excision, the patient’s symptoms resolved and a yearly follow-up confirmed their complete remission. It is yet uncertain whether symptomatic relief was a result of excision, continued anti-reflux treatment, or even a placebo effect associating the procedure.

A 54-year-old female with history of fibromyalgia, chronic opioid dependency, cyanocobalamin deficiency, vitamin D deficiency, and GERD with previously noted Los Angeles class C esophagitis was being evaluated with endoscopy as outpatient for dysphagia and abdominal pain. EGD was significant for an exophytic wart-like growth in the distal esophagus, minimally irregular Z-line noted at GEJ, mild gastritis without ulcers, and normal duodenum. GEJ biopsy demonstrated focal intestinal metaplasia suggestive of Barrett's esophagus without dysplastic changes. Esophageal biopsy demonstrated findings consistent with squamous papilloma (see Figures and ).

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 67-year-old Caucasian man visited his primary care physician with complaints of hematemesis and continuous dysphagia. He had history of cigarette smoking and social alcohol consumption. Previous medical history included hypertension and hyperlipidemia. An initial EGD showed multiple verrucous lesions extending from 30 cm to 39 cm from his incisors. Pathological examination of the multiple biopsies showed squamous papillomatosis.\nThe patient was referred for evaluation at our hospital and a new EGD showed the same extensive verrucous lesions with three large growths on the distal esophagus causing significant stenosis. He repeated the biopsies and maintained the previous histological diagnosis. A thoracoabdominal CT-Scan revealed large esophageal lesions apparently superficial with thickening of the esophageal wall. Endoscopic Ultrasound showed that these changes were almost all limited to the mucosa and submucosa except in one area where they appeared to penetrate deeper.\nAt this time, the patient’s dysphagia got worse and there was substantial suspicion of potential malignancy. After a multidisciplinary discussion, he was proposed for surgery. He underwent a minimally invasive Ivor-Lewis Esophagectomy (laparoscopy + right lateral thoracoscopy) with a mechanical termino-lateral esophago-gastric upper thoracic anastomosis (at approximately 24/25 cm from the incisors) (Figs. , ). The postoperative (PO) period was uneventful and the patient was discharged at the 9th PO day.\nThe examination of esophagectomy specimen () showed a squamous cell carcinoma in situ (verrucous type) of the distal esophagus with areas of high dysplasia and extensive diffuse squamous papillomatosis. There were no signs of lymphatic or perineural invasion and margins were clear. The eighteen lymph nodes excised were all negative for malignancy. The TNM stage (8th edition) was Tis N0. One year later, at the follow-up consultation, there were no signs of recurrence.

A 61-year-old female with history of uncontrolled diabetes mellitus type 2 complicated by gastroparesis, prior esophageal dilation, and ileostomy was being evaluated with endoscopy as outpatient for worsening dysphagia. EGD was significant for a small nodule in the proximal esophagus (see ), normal GEJ (gastroesophageal junction), mild gastritis, and normal duodenum. Gastric biopsy demonstrated mild chronic gastritis without dysplastic changes or Helicobacter pylori. Esophageal biopsy demonstrated findings consistent with squamous papilloma.

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 44-year-old woman visited the outpatient clinic with reports of EGD examination showing a GEJ polyp. EGD had been performed as part of a health promotion screening, and the patient denied having any subjective symptom or past medical history including smoking and alcohol consumption. She looked generally healthy. Physical examination and laboratory test revealed that all values were within the normal reference range.\nEGD examination revealed that the polyp was located just on the squamocolumnar junction of the GEJ and presented as a 1.5-cm protruding polypoid mass with an irregular and nodular surface (). Forceps biopsy was performed to exclude malignant tumor. Microscopic examination revealed squamous papilloma showing papillary squamous epithelium with a fibrovascular core. Squamous epithelial cells of the papilloma showed koilocytosis with irregular nuclear membrane and perinuclear halo, which histologically confirmed the presence of human papillomavirus infection ().\nAfter obtaining informed consent from the patient, endoscopic mucosal resection was performed to remove the whole papilloma at the GEJ to avoid a possible increase in the size of the tumor. Histological examination of the resected specimen revealed a nodular mass with papillary growth consisting of squamous cell epithelium with a well-structured inner fibrovascular core, which was compatible with squamous papilloma. The specimen showed complete and curative resection, without involvement of the lateral or vertical margin.\nTwo years later, the patient revisited our clinic for esophageal reflux symptoms. Follow-up EGD incidentally revealed a polyp at the GEJ at the exact spot of the previously removed papilloma. The polyp measured approximately 1.0 cm and had a morphology similar to that of the previous papilloma (), suggesting recurrence. Although the polyp was smaller than that detected 2 years previously, endoscopic submucosal dissection was performed owing to fibrotic scarring and non-lifting sign at the anal side of the polyp (). The polyp was removed en bloc and completely, without marginal involvement. Microscopic examination revealed nodular mass with papillary growth. Histologic examination revealed usual papilloma showing papillary squamous epithelium, with a well-developed fibrovascular core. However, multifocal severe squamous atypia was observed throughout the mucosal epithelium, compatible with squamous cell carcinoma in situ (). The patient was finally diagnosed with squamous cell carcinoma in situ arising from esophageal squamous papilloma.

A 61-year-old female with history of uncontrolled diabetes mellitus type 2 complicated by gastroparesis, prior esophageal dilation, and ileostomy was being evaluated with endoscopy as outpatient for worsening dysphagia. EGD was significant for a small nodule in the proximal esophagus (see ), normal GEJ (gastroesophageal junction), mild gastritis, and normal duodenum. Gastric biopsy demonstrated mild chronic gastritis without dysplastic changes or Helicobacter pylori. Esophageal biopsy demonstrated findings consistent with squamous papilloma.

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 54-year-old female with history of fibromyalgia, chronic opioid dependency, cyanocobalamin deficiency, vitamin D deficiency, and GERD with previously noted Los Angeles class C esophagitis was being evaluated with endoscopy as outpatient for dysphagia and abdominal pain. EGD was significant for an exophytic wart-like growth in the distal esophagus, minimally irregular Z-line noted at GEJ, mild gastritis without ulcers, and normal duodenum. GEJ biopsy demonstrated focal intestinal metaplasia suggestive of Barrett's esophagus without dysplastic changes. Esophageal biopsy demonstrated findings consistent with squamous papilloma (see Figures and ).

A 61-year-old female with history of uncontrolled diabetes mellitus type 2 complicated by gastroparesis, prior esophageal dilation, and ileostomy was being evaluated with endoscopy as outpatient for worsening dysphagia. EGD was significant for a small nodule in the proximal esophagus (see ), normal GEJ (gastroesophageal junction), mild gastritis, and normal duodenum. Gastric biopsy demonstrated mild chronic gastritis without dysplastic changes or Helicobacter pylori. Esophageal biopsy demonstrated findings consistent with squamous papilloma.

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 44-year-old woman visited the outpatient clinic with reports of EGD examination showing a GEJ polyp. EGD had been performed as part of a health promotion screening, and the patient denied having any subjective symptom or past medical history including smoking and alcohol consumption. She looked generally healthy. Physical examination and laboratory test revealed that all values were within the normal reference range.\nEGD examination revealed that the polyp was located just on the squamocolumnar junction of the GEJ and presented as a 1.5-cm protruding polypoid mass with an irregular and nodular surface (). Forceps biopsy was performed to exclude malignant tumor. Microscopic examination revealed squamous papilloma showing papillary squamous epithelium with a fibrovascular core. Squamous epithelial cells of the papilloma showed koilocytosis with irregular nuclear membrane and perinuclear halo, which histologically confirmed the presence of human papillomavirus infection ().\nAfter obtaining informed consent from the patient, endoscopic mucosal resection was performed to remove the whole papilloma at the GEJ to avoid a possible increase in the size of the tumor. Histological examination of the resected specimen revealed a nodular mass with papillary growth consisting of squamous cell epithelium with a well-structured inner fibrovascular core, which was compatible with squamous papilloma. The specimen showed complete and curative resection, without involvement of the lateral or vertical margin.\nTwo years later, the patient revisited our clinic for esophageal reflux symptoms. Follow-up EGD incidentally revealed a polyp at the GEJ at the exact spot of the previously removed papilloma. The polyp measured approximately 1.0 cm and had a morphology similar to that of the previous papilloma (), suggesting recurrence. Although the polyp was smaller than that detected 2 years previously, endoscopic submucosal dissection was performed owing to fibrotic scarring and non-lifting sign at the anal side of the polyp (). The polyp was removed en bloc and completely, without marginal involvement. Microscopic examination revealed nodular mass with papillary growth. Histologic examination revealed usual papilloma showing papillary squamous epithelium, with a well-developed fibrovascular core. However, multifocal severe squamous atypia was observed throughout the mucosal epithelium, compatible with squamous cell carcinoma in situ (). The patient was finally diagnosed with squamous cell carcinoma in situ arising from esophageal squamous papilloma.

A 67-year-old Caucasian man visited his primary care physician with complaints of hematemesis and continuous dysphagia. He had history of cigarette smoking and social alcohol consumption. Previous medical history included hypertension and hyperlipidemia. An initial EGD showed multiple verrucous lesions extending from 30 cm to 39 cm from his incisors. Pathological examination of the multiple biopsies showed squamous papillomatosis.\nThe patient was referred for evaluation at our hospital and a new EGD showed the same extensive verrucous lesions with three large growths on the distal esophagus causing significant stenosis. He repeated the biopsies and maintained the previous histological diagnosis. A thoracoabdominal CT-Scan revealed large esophageal lesions apparently superficial with thickening of the esophageal wall. Endoscopic Ultrasound showed that these changes were almost all limited to the mucosa and submucosa except in one area where they appeared to penetrate deeper.\nAt this time, the patient’s dysphagia got worse and there was substantial suspicion of potential malignancy. After a multidisciplinary discussion, he was proposed for surgery. He underwent a minimally invasive Ivor-Lewis Esophagectomy (laparoscopy + right lateral thoracoscopy) with a mechanical termino-lateral esophago-gastric upper thoracic anastomosis (at approximately 24/25 cm from the incisors) (Figs. , ). The postoperative (PO) period was uneventful and the patient was discharged at the 9th PO day.\nThe examination of esophagectomy specimen () showed a squamous cell carcinoma in situ (verrucous type) of the distal esophagus with areas of high dysplasia and extensive diffuse squamous papillomatosis. There were no signs of lymphatic or perineural invasion and margins were clear. The eighteen lymph nodes excised were all negative for malignancy. The TNM stage (8th edition) was Tis N0. One year later, at the follow-up consultation, there were no signs of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 67-year-old Caucasian man visited his primary care physician with complaints of hematemesis and continuous dysphagia. He had history of cigarette smoking and social alcohol consumption. Previous medical history included hypertension and hyperlipidemia. An initial EGD showed multiple verrucous lesions extending from 30 cm to 39 cm from his incisors. Pathological examination of the multiple biopsies showed squamous papillomatosis.\nThe patient was referred for evaluation at our hospital and a new EGD showed the same extensive verrucous lesions with three large growths on the distal esophagus causing significant stenosis. He repeated the biopsies and maintained the previous histological diagnosis. A thoracoabdominal CT-Scan revealed large esophageal lesions apparently superficial with thickening of the esophageal wall. Endoscopic Ultrasound showed that these changes were almost all limited to the mucosa and submucosa except in one area where they appeared to penetrate deeper.\nAt this time, the patient’s dysphagia got worse and there was substantial suspicion of potential malignancy. After a multidisciplinary discussion, he was proposed for surgery. He underwent a minimally invasive Ivor-Lewis Esophagectomy (laparoscopy + right lateral thoracoscopy) with a mechanical termino-lateral esophago-gastric upper thoracic anastomosis (at approximately 24/25 cm from the incisors) (Figs. , ). The postoperative (PO) period was uneventful and the patient was discharged at the 9th PO day.\nThe examination of esophagectomy specimen () showed a squamous cell carcinoma in situ (verrucous type) of the distal esophagus with areas of high dysplasia and extensive diffuse squamous papillomatosis. There were no signs of lymphatic or perineural invasion and margins were clear. The eighteen lymph nodes excised were all negative for malignancy. The TNM stage (8th edition) was Tis N0. One year later, at the follow-up consultation, there were no signs of recurrence.

A 54-year-old female with history of fibromyalgia, chronic opioid dependency, cyanocobalamin deficiency, vitamin D deficiency, and GERD with previously noted Los Angeles class C esophagitis was being evaluated with endoscopy as outpatient for dysphagia and abdominal pain. EGD was significant for an exophytic wart-like growth in the distal esophagus, minimally irregular Z-line noted at GEJ, mild gastritis without ulcers, and normal duodenum. GEJ biopsy demonstrated focal intestinal metaplasia suggestive of Barrett's esophagus without dysplastic changes. Esophageal biopsy demonstrated findings consistent with squamous papilloma (see Figures and ).

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 44-year-old woman visited the outpatient clinic with reports of EGD examination showing a GEJ polyp. EGD had been performed as part of a health promotion screening, and the patient denied having any subjective symptom or past medical history including smoking and alcohol consumption. She looked generally healthy. Physical examination and laboratory test revealed that all values were within the normal reference range.\nEGD examination revealed that the polyp was located just on the squamocolumnar junction of the GEJ and presented as a 1.5-cm protruding polypoid mass with an irregular and nodular surface (). Forceps biopsy was performed to exclude malignant tumor. Microscopic examination revealed squamous papilloma showing papillary squamous epithelium with a fibrovascular core. Squamous epithelial cells of the papilloma showed koilocytosis with irregular nuclear membrane and perinuclear halo, which histologically confirmed the presence of human papillomavirus infection ().\nAfter obtaining informed consent from the patient, endoscopic mucosal resection was performed to remove the whole papilloma at the GEJ to avoid a possible increase in the size of the tumor. Histological examination of the resected specimen revealed a nodular mass with papillary growth consisting of squamous cell epithelium with a well-structured inner fibrovascular core, which was compatible with squamous papilloma. The specimen showed complete and curative resection, without involvement of the lateral or vertical margin.\nTwo years later, the patient revisited our clinic for esophageal reflux symptoms. Follow-up EGD incidentally revealed a polyp at the GEJ at the exact spot of the previously removed papilloma. The polyp measured approximately 1.0 cm and had a morphology similar to that of the previous papilloma (), suggesting recurrence. Although the polyp was smaller than that detected 2 years previously, endoscopic submucosal dissection was performed owing to fibrotic scarring and non-lifting sign at the anal side of the polyp (). The polyp was removed en bloc and completely, without marginal involvement. Microscopic examination revealed nodular mass with papillary growth. Histologic examination revealed usual papilloma showing papillary squamous epithelium, with a well-developed fibrovascular core. However, multifocal severe squamous atypia was observed throughout the mucosal epithelium, compatible with squamous cell carcinoma in situ (). The patient was finally diagnosed with squamous cell carcinoma in situ arising from esophageal squamous papilloma.

A 54-year-old female with history of fibromyalgia, chronic opioid dependency, cyanocobalamin deficiency, vitamin D deficiency, and GERD with previously noted Los Angeles class C esophagitis was being evaluated with endoscopy as outpatient for dysphagia and abdominal pain. EGD was significant for an exophytic wart-like growth in the distal esophagus, minimally irregular Z-line noted at GEJ, mild gastritis without ulcers, and normal duodenum. GEJ biopsy demonstrated focal intestinal metaplasia suggestive of Barrett's esophagus without dysplastic changes. Esophageal biopsy demonstrated findings consistent with squamous papilloma (see Figures and ).

Write a detailed clinical case vignette based on the following key phrases: Esophageal lesions, Squamous papilloma, Endoscopy

A 75-year-old male presented at our emergency department with painful swelling of his left leg for 12 hours without prior trauma history (). He also complained of numbness and weakness of the left lower leg and foot. His medical history was notable for hypertension and hyperlipidemia. On physical examination, the entire leg showed purplish discolorization and left femoral and dorsalis pedis artery pulses were detectable by hand-held Doppler. Duplex ultrasound (DUS) revealed left ilio-femoro-popliteal DVT (). Intravenous heparin was immediately administered and an emergent venous thrombectomy was performed under local anesthesia (), which provided pain relief. The next day, the left leg color was normalized () and motor and sensory defects were fully recovered. Anticoagulation therapy was prescribed for 6 months and follow-up computed tomography (CT) at 6 months revealed no residual thrombus ().

A 74-year-old man presented to the emergency department after a motorcycle accident. He had a deformity in the right leg. His comorbidities were chronic obstructive pulmonary disease, ischemic cardiomyopathy due to myocardial infarction, atrial fibrillation, hypertension, and dyslipidemia. His medications included aspirin and clopidogrel. Following investigations in this admission, a brain computed tomography (CT) revealed that he had acute traumatic subdural hematoma that was managed with nonoperative treatment. His right leg was broken, which was diagnosed as a closed fracture of the tibia and fibula, and was managed conservatively. He had fractures at the left iliac crest and the left superior pubic rami. The neurovascular conditions were normal. During admission, he had acute dyspnea with desaturation but no chest pain at ten days after admission. On examination, his blood pressure was 102/78 mmHg, pulse rate was 100/min, respiratory rate was 24/min, and blood oxygen saturation (SpO2) was 90% in room air, which was not corrected with oxygen supplement. He had crepitation at his left lower lung but no wheezing. CT angiography of the chest was performed and showed acute PEs at the right superior and inferior trunk. He was found to have acute respiratory failure and hypotension after the chest CT angiography was finished. He was scheduled for an emergency operation for surgical pulmonary embolectomy.\nOn the next day at the surgical intensive care unit (ICU), he developed progressive left leg edema with cyanosis. He had no fever and he could still move his leg, but his pain could not be evaluated since he was delirious. On examination, his left lower limb exhibited discoloration at his left foot without any ulcer or bleb, moist skin, or pitting edema, and the left dorsalis pedis and posterior tibial pulse could be palpated (1+) but were diminished (). The motor functions remained intact. Doppler ultrasonography was performed and revealed an uncompressible vein along the midsuperior femoral vein to the popliteal vein. His laboratory investigation showed that the leukocytosis and creatinine level rose from 1.04 mg% to 1.62 mg% and creatinine phosphokinase (CPK) was 322 U/L. He was diagnosed with PCD at the left femoral vein. The intervention radiologist attempted a catheter-directed thrombectomy, but it failed because the guider could not pass through the intraluminal clot. The patient was scheduled for emergency operation again for surgical thrombectomy with fasciotomy of the left leg (). The operative finding was a thrombus in the femoral vein that was 10 cm in length (). The compartment pressures before performing the fasciotomy at the anterior, lateral, and superficial posterior compartments were 43 mmHg, 37 mmHg, and 47 mmHg, respectively. The deep posterior compartment pressure was not measured. After the operation, his pain was relieved and the left dorsalis pedis and posterior tibial pulse were normal. He continued on wound dressings and the fasciotomy was closed by split-thickness skin graft. He continued on oral anticoagulant drugs for six months and underwent elective ray amputation at five months after the PCD for a dry gangrenous left big toe.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A Hispanic 58-year-old female with a past medical history of gastritis arrived into the emergency room (ER) with acute onset severe pain on the left leg associated with discoloration of the leg. According to the patient, approximately three hours prior to her arrival to the ER, she was walking when, suddenly, she started experiencing sharp pain in her left leg which rapidly progressed. The physical examination was remarkable for left lower extremity pain, discoloration, edema, associated with tenderness to touch, diminished distal pulses, and reduce sensation and mobility throughout the leg, which can be appreciated below (Figure ).\nWithin the first 30 min after her arrival to the hospital, a pressure Doppler was performed where extensive deep vein thrombosis (DVT) (left femoral-popliteal venous thrombosis) (Figure ) diagnosis was made and within the subsequent 60 min, a computed tomography angiography (CTA) aorto-ilio-femoral runoff with delayed phase was performed, showing delayed opacification of arterial segments below the knee level (Figure ), confirming the diagnosis. A bolus of heparin was given, followed by an infusion. Thrombolysis was offered to the patient, however, she refused due to concern for side effects.\nAfter one hour of starting heparin infusion, blood flow to the leg was regained and the patient recovered full sensation and movement in the leg; coloration returned to normal in the affected leg. The patient was admitted for continued observation and discharged later on direct oral anticoagulants (DOACs) without any recurrence of DVT so far.\nThe patient denied recent flights, a sedentary lifestyle, surgery, trauma, alcohol, tobacco, and drug use. There was neither a previous episode nor a family history of similar symptoms to her knowledge. Age-appropriate oncology screening was negative; mammogram from June 2020 was normal; colonoscopy four years before the presentation was also negative; Pap smears as well. Thrombophilia workup done by the Hematology/Oncology service was unrevealing, leading to a diagnosis of unprovoked DVT.\nThe curious part of the case is that even though thrombolysis and thrombectomy are considered the gold standard in the treatment of PCD, this patient had a spontaneous recovery only with heparin which serves as the only purpose to prevent the propagation of the thrombus. This specific patient according to Rutherford limb ischemia classification [] was a IIb which granted surgical intervention. Still, it remains unclear how such an extensive DVT improved in so quick fashion without thrombectomy/thrombolysis but seems that early use of heparin might have played an important role in the evolution of this patient's case and that early use of heparin might decrease the need for surgical intervention in some patients.

A 75-year-old male presented at our emergency department with painful swelling of his left leg for 12 hours without prior trauma history (). He also complained of numbness and weakness of the left lower leg and foot. His medical history was notable for hypertension and hyperlipidemia. On physical examination, the entire leg showed purplish discolorization and left femoral and dorsalis pedis artery pulses were detectable by hand-held Doppler. Duplex ultrasound (DUS) revealed left ilio-femoro-popliteal DVT (). Intravenous heparin was immediately administered and an emergent venous thrombectomy was performed under local anesthesia (), which provided pain relief. The next day, the left leg color was normalized () and motor and sensory defects were fully recovered. Anticoagulation therapy was prescribed for 6 months and follow-up computed tomography (CT) at 6 months revealed no residual thrombus ().

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 75-year-old male presented at our emergency department with painful swelling of his left leg for 12 hours without prior trauma history (). He also complained of numbness and weakness of the left lower leg and foot. His medical history was notable for hypertension and hyperlipidemia. On physical examination, the entire leg showed purplish discolorization and left femoral and dorsalis pedis artery pulses were detectable by hand-held Doppler. Duplex ultrasound (DUS) revealed left ilio-femoro-popliteal DVT (). Intravenous heparin was immediately administered and an emergent venous thrombectomy was performed under local anesthesia (), which provided pain relief. The next day, the left leg color was normalized () and motor and sensory defects were fully recovered. Anticoagulation therapy was prescribed for 6 months and follow-up computed tomography (CT) at 6 months revealed no residual thrombus ().

A 49-year-old woman presented with acute coronary syndrome for which she received aspirin, clopidogrel, atorvastatin, enoxaparin, and tenecteplase at another facility. She was then transferred to our institute for further management. She underwent coronary angiography which was suggestive of triple vessel disease. As the patient was in acute congestive heart failure (Killip IV) with pulmonary edema, she was intubated and mechanically ventilated. She underwent coronary artery bypass grafting surgery the following day where she received 20,000U of unfractionated heparin.\nOn postoperative day (POD) 6, the patient developed right pedal edema with cyanosis. Bilateral lower limbs Arterial Doppler was normal. Venous Doppler of the right lower limb was suggestive of thrombosis of the right Common Femoral, Superficial Femoral, Popliteal, and Great Saphenous Veins. She also had progressively worsening thrombocytopenia in which the platelet count dropped from 297 × 109/L on day 1 of postenoxaparin exposure to a nadir of 20 × 109/L on day 8. With a suspicion of HIT and thrombosis (HITT), enoxaparin was replaced with fondaparinux on POD 7. She tested positive for HIT type 2 antibodies on day 10. Her platelets started improving by POD 11 [].\nOn POD 13, two-dimensional echocardiography done was suggestive of a left ventricular thrombus (with an ejection fraction of 25%) which resolved completely by POD 44 with anticoagulation. Fondaparinux was bridged with oral Vitamin K Antagonist-Acenocoumarol for HITT and PCD. Once there was a line of demarcation for gangrene, she underwent a right forefoot amputation on POD 34.\nThe patient was discharged on POD 47 with medications for cardiac failure along with acenocoumarol.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 75-year-old male presented at our emergency department with painful swelling of his left leg for 12 hours without prior trauma history (). He also complained of numbness and weakness of the left lower leg and foot. His medical history was notable for hypertension and hyperlipidemia. On physical examination, the entire leg showed purplish discolorization and left femoral and dorsalis pedis artery pulses were detectable by hand-held Doppler. Duplex ultrasound (DUS) revealed left ilio-femoro-popliteal DVT (). Intravenous heparin was immediately administered and an emergent venous thrombectomy was performed under local anesthesia (), which provided pain relief. The next day, the left leg color was normalized () and motor and sensory defects were fully recovered. Anticoagulation therapy was prescribed for 6 months and follow-up computed tomography (CT) at 6 months revealed no residual thrombus ().

An 88-year-old man was admitted to our facility with altered mental status, hypotension (blood pressure range: 71-84/47-57 mmHg in the right arm supine position), fever (104oF), and tachycardia (heart rate: 140-150 beats/min) on arrival at the emergency room. Prior to admission, he was on hemodialysis for the past three months for end-stage renal disease secondary to rapidly progressive glomerulonephritis (has a right permacath). He was receiving intermittent heparin flushes along with dialysis to maintain the patency of the extracorporeal circuit. Other significant past medical history included a splenectomy in 2007. Clinical manifestations, imaging tests, and blood cultures suggested septic shock secondary to Streptococcal pneumonia. The patient was started on meropenem and vancomycin. A left internal jugular catheter and arterial line (in the right upper extremity) were placed for fluid resuscitation and blood pressure monitoring, respectively, and the patient was managed per surviving sepsis guidelines. On day three of hospitalization, the patient started to complain about a right-hand pain at the site of the arterial catheter. The physical examination was remarkable for a swollen and cyanotic right upper extremity, especially the second and third fingers (Figure ), with a barely palpable radial pulse compared to the left side. Arterial Doppler of the upper extremities was obtained, with findings indicative of significant right-sided arterial insufficiency. Further evaluation by venous duplex ultrasound identified a massive thrombus in the axillary, brachial, and basilic veins of the right arm with the solely spared ulna vein being hugely engorged (Figures -).\nWe considered the possibility of catheter-induced venous thrombosis, sepsis-associated disseminated intravascular coagulation and heparin-induced thrombocytopenia as working diagnoses. Given the suspicion of heparin-induced thrombocytopenia, we discontinued heparin immediately while the patient’s peripheral smear and coagulation cascade were investigated. Although the patient had low platelets (Table ), prolonged prothrombin time (16 (normal: 11-13 sec)), activated partial thromboplastin time (63 (normal: 25-35 sec)), elevated fibrin degradation products (>40 (normal: <10 mcg/ml)), which were suspicious for sepsis-related disseminated intravascular coagulation; normal factor VII (77 (normal: 50-150%)), high VIII levels (192 (normal: 50-150%)), normal haptoglobin (163 (normal: 36-195 mg/dl)), mildly decreased hemoglobulin (range: 12.1-12.9 (normal:13.5-17.5 g/dl)), and the presence of very few schistiocytes (<0.5%) on a peripheral smear made disseminated intravascular coagulation less likely. Laboratory data were remarkable for a significant drop in the platelet count from 234*109/L (on initiation of hemodialysis) to 44*109/L (the day of hospital admission) over the past three months. Based on the 4T score, heparin-induced thrombocytopenia was highly suspected and argatroban was initiated at 1 mg/kg/min. Vascular surgery consultation was obtained to address the gangrene in the second and third digits of the right upper extremity. However, considering his critically septic situation with multiple morbidities, a decision was made not to proceed with invasive maneuvers. On hospital day four, heparin-platelet factor 4 (PF4) antibodies (1.67 (normal: <0.4), heparin inhibition: >50%), and serotonin release assays returned positive (using enzyme-linked immunosorbent assay), confirming heparin-induced thrombocytopenia. On hospital day eight, repeated venous duplex demonstrated normal compressibility and spontaneous flow in the vein of the right upper extremity. The platelet count recovered and no further thrombotic complications were observed. Though we were able to manage the patient’s advanced gangrene with argatroban, his second and third fingers were amputated in the end.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 75-year-old male presented at our emergency department with painful swelling of his left leg for 12 hours without prior trauma history (). He also complained of numbness and weakness of the left lower leg and foot. His medical history was notable for hypertension and hyperlipidemia. On physical examination, the entire leg showed purplish discolorization and left femoral and dorsalis pedis artery pulses were detectable by hand-held Doppler. Duplex ultrasound (DUS) revealed left ilio-femoro-popliteal DVT (). Intravenous heparin was immediately administered and an emergent venous thrombectomy was performed under local anesthesia (), which provided pain relief. The next day, the left leg color was normalized () and motor and sensory defects were fully recovered. Anticoagulation therapy was prescribed for 6 months and follow-up computed tomography (CT) at 6 months revealed no residual thrombus ().

A 64-year-old man with a history of obesity (BMI 38 Kg/m^2), arterial hypertension, atrial fibrillation, type 2 diabetes, chronic kidney disease, obstructive sleep apnea, and chronic venous insufficiency presented to the Emergency Department complaining of dyspnea, fever, and chest pain which started 7 days before. The patient was hypoxemic in room air (SpO2 80% and PaO2 43 mmHg). Inferior limbs appeared normal. A molecular swab formalized diagnosis of SARS-CoV2-related pneumonia. Respiratory distress progressed despite non-invasive-ventilation and hemodynamic instability requiring vasoactive support ensued. The patient was intubated and transferred to the ICU. The patient received invasive protective ventilation and hemodynamic support with noradrenaline. Gas exchange progressively worsened to a PaO2/FiO2 ratio of 70 mmHg. He developed a shock, and his lower limbs started to appear mottled. Lung and cardiac ultrasound were compatible with severe interstitial pneumonia and with no signs of pressure overload of the right heart. His coagulation profile was highly altered, as both aPTT and INR were elevated (respectively 2.28 seconds and 6.42), platelets were 164,000/mm3, and D-dimer was 117,521 UI/ml. Coagulation parameters continually worsened (), and treatment with one unit of fresh frozen plasma and vitamin K was required. Inferior limbs’ color progressively worsened, becoming frankly cyanotic, while pulses were still normal. Doppler ultrasound showed bilateral thrombosis of tibial and small saphenous veins. A continuous infusion of iloprost was started, as PCD was suspected (). Continuous infusion of unfractionated heparin was instituted, at a dose of 500-1000 IU per hour, according to aPTT, as well as continuous veno-venous hemodiafiltration as the patient developed acute kidney injury. The patient’s general conditions worsened (), and despite maximal treatment, he passed away after eight days of ICU care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 21-year-old female college student presented to the emergency department (ED) with severe pain in her left hip, thigh, and calf. The pain started suddenly when she was playing basketball a few hours earlier. She twisted her torso to shoot the ball and heard a “pop” in her left hip with immediate onset of pain, and she subsequently fell to her knees. She was initially able to ambulate but had worsening pain and rapid progression of swelling and mottling in the left leg from her hip to her ankle. She denied any pain or swelling in that extremity prior to the injury during the basketball game. With the exception of oral contraceptive use, she had no significant medical or family history.\nOn examination her left extremity was mottled, dusky, and cool to the touch from the hip to the toes and she had decreased dorsalis pedis and posterior tibial pulses when compared with the right extremity. The leg was markedly tender to palpation and sensation to light touch was diminished. Passive range of motion of the hip, knee, and ankle elicited severe pain.\nPOCUS was performed at the bedside to evaluate for arterial blood flow and deep venous thrombosis. This demonstrated normal color flow in the femoral and popliteal arteries (), but echogenic material was noted within the left common femoral vein extending distally to the popliteal vein and the veins were non-compressible (). Vascular surgery was immediately consulted, and while awaiting their arrival to the ED the patient was sent for an emergent computed tomography (CT) angiogram, which confirmed arterial patency and extensive deep venous thrombosis in the left popliteal, femoral, and iliac veins (). A heparin bolus was given and the patient was then taken to interventional radiology where she underwent partial thrombectomy, catheter-directed tissue plasminogen activator (tPA) treatment, and placement of an inferior vena cava (IVC) filter. By the next morning her leg was noted to be well-perfused, non-tender, and without swelling, and her pain had resolved. A workup for hypercoagulable states revealed heterozygosity for the Factor V Leiden mutation. She was discharged one week later on warfarin after bridging from enoxaparin.

A 75-year-old male presented at our emergency department with painful swelling of his left leg for 12 hours without prior trauma history (). He also complained of numbness and weakness of the left lower leg and foot. His medical history was notable for hypertension and hyperlipidemia. On physical examination, the entire leg showed purplish discolorization and left femoral and dorsalis pedis artery pulses were detectable by hand-held Doppler. Duplex ultrasound (DUS) revealed left ilio-femoro-popliteal DVT (). Intravenous heparin was immediately administered and an emergent venous thrombectomy was performed under local anesthesia (), which provided pain relief. The next day, the left leg color was normalized () and motor and sensory defects were fully recovered. Anticoagulation therapy was prescribed for 6 months and follow-up computed tomography (CT) at 6 months revealed no residual thrombus ().

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 75-year-old male presented at our emergency department with painful swelling of his left leg for 12 hours without prior trauma history (). He also complained of numbness and weakness of the left lower leg and foot. His medical history was notable for hypertension and hyperlipidemia. On physical examination, the entire leg showed purplish discolorization and left femoral and dorsalis pedis artery pulses were detectable by hand-held Doppler. Duplex ultrasound (DUS) revealed left ilio-femoro-popliteal DVT (). Intravenous heparin was immediately administered and an emergent venous thrombectomy was performed under local anesthesia (), which provided pain relief. The next day, the left leg color was normalized () and motor and sensory defects were fully recovered. Anticoagulation therapy was prescribed for 6 months and follow-up computed tomography (CT) at 6 months revealed no residual thrombus ().

A 66-year-old female presented to the emergency department with three days of acute LLE swelling, pain, cyanosis, inability to bear weight, dyspnea, and hypoxemia (Figure ). She denied recent travel, hormone replacement, or a history of DVT/pulmonary embolism (PE). Her medical history was notable for systemic lupus erythematosus, CREST (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome, Sjogren’s syndrome, and local invasive anal squamous cell carcinoma. Doppler ultrasound revealed LLE thrombus extending from the greater saphenous vein to the popliteal vein. She was admitted to the intensive care unit (ICU) and started on an unfractionated heparin drip.\nThe vascular surgery team was consulted for surgical intervention. After further review of her case, the vascular surgery team elected for an endovascular approach with CDT of LLE. Initial venogram demonstrated extensive clotting of the tibial, popliteal, and femoral venous systems extending into the iliac system (Figures , ). From a tibial approach, a guidewire was advanced up to the common iliac, but a chronic occlusion of the left common iliac vein was found, which could not be crossed. A venous collateral circulation system in communication with the right iliac venous system was identified. In order to decrease the overall clot burden, two 50-cm EKOS endovascular catheters were placed in the left external iliac vein and collateral system. Repeat venogram at 24 hours post-CDT showed significant improvement of the overall clot burden with almost complete resolution of the clot in the LLE; however, the chronic occlusion remained (Figure ). A 20 x 80 mm Boston Scientific Wallstent™ (endoprosthesis stent) was advanced across the total chronic total occlusion and deployed. Post-operative venogram demonstrated significant improvement in flow in the system, with all flow going through the iliac system, and no flow further through the previously seen collaterals. Intravascular ultrasound was advanced through the area, which showed severe compression of the stent. A 12x 40 mm Atlas® dilatation catheter (Bard Peripheral Vascular Inc., Tempe, AZ, USA) was used for angioplasty. Repeat intravascular ultrasound showed persistent compression of the area. A 8 x 40 mm Boston Scientific Mustang™ dilatation catheter (high-pressure balloon) was used to re-attempt angioplasty; however, compression was still noted (Figure ). Regardless, outflow improved throughout the left common iliac system, and no further interventions were performed. The patient returned to the ICU and transitioned to direct oral anticoagulation without any further complications. She was subsequently transferred to a medicine ward for further care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 75-year-old male presented at our emergency department with painful swelling of his left leg for 12 hours without prior trauma history (). He also complained of numbness and weakness of the left lower leg and foot. His medical history was notable for hypertension and hyperlipidemia. On physical examination, the entire leg showed purplish discolorization and left femoral and dorsalis pedis artery pulses were detectable by hand-held Doppler. Duplex ultrasound (DUS) revealed left ilio-femoro-popliteal DVT (). Intravenous heparin was immediately administered and an emergent venous thrombectomy was performed under local anesthesia (), which provided pain relief. The next day, the left leg color was normalized () and motor and sensory defects were fully recovered. Anticoagulation therapy was prescribed for 6 months and follow-up computed tomography (CT) at 6 months revealed no residual thrombus ().

A 49-year-old Chinese man sustained severe knife trauma and was referred to a local hospital. An exploratory laparotomy showed traumatic rupture of his left external iliac vein with massive intraperitoneal bleeding, but his iliac artery was intact. To rescue him, the proximal and distal parts of his injured external iliac vein were ligated (there was no vascular surgeon in the local hospital); however, his left leg quickly became severely swollen, cyanotic and pulseless. Two hours after the first operation, he was transferred to the emergency department of our university hospital with endotracheal tube intubation. On physical examination, he was tachycardic (142 beats per minute), hypotensive (86/50mmHg). His left lower extremity was markedly edematous, cyanotic, mottled (Figure \na) and had no palpable pulse, but his right lower extremity was normal. He was diagnosed with posttraumatic PCD. Considering the high risk of pulmonary embolism during the next surgical procedure, an OptEase® retrievable vena cava filter (Cordis Corp., New Brunswick, NJ, USA) was placed in his inferior vena cava via his right femoral vein under digital subtraction angiography (Figure \n). His abdomen was immediately reopened while his left leg was also prepared for treatment.During the second emergent laparotomy, there was less blood in his pelvic cavity. No active bleeding was identified. His left iliac vein and artery were exposed and his entire iliac artery appeared normal and without rupture. His external iliac vein was ligated but not transected, connected only by the posterior wall, and the caudal part of his iliac vein was significantly dilated. By replacing the vascular clamp in the proximal and distal parts of the rupture, the ligations on both sides of the venous rupture were resolved. A wedge-shaped rupture was revealed, approximately 4cm in length, on the anterolateral side of his left external iliac vein. The edges of the venous rupture were smooth as a result of the knife trauma. Although the ligated parts of his iliac vein appeared congested, the lumen was smooth and contained no clot. The damaged vein was repaired with continuous 4-0 Prolene sutures (Ethicon, Inc, Somerville, NJ, USA) after the patient was systemically heparinized with 5000 units heparin. Before the sutures were finally ligated, the clamp at the cranial aspect was removed and the caudal clamp was left in place. After the backflow was clear of thrombotic debris, the clamp on his caudal iliac vein was removed and the clamp at the cranial aspect left in place. The left leg was gently massaged from calf to thigh; as a result, some thrombi in the caudal part of the vein were flushed out with the venous blood flow, and the sutures were finally ligated until the venous blood was free of thrombus. His iliac vein, although narrower after repair, was patent (Figure \n).\nAfter the operation, the patient was sent to the surgical intensive care unit with mechanical ventilation. Despite the fact that his left leg showed some signs of compartment syndrome with blisters in his calf, fasciotomy was not performed. He received systemic anticoagulation, initially with low-molecular-weight heparin, then with warfarin, titrating to an international normalized ratio (INR) between 2.0 and 2.5.Three days postoperatively, mechanical ventilation was discontinued and his signs and symptoms improved dramatically. Pulses in his left lower extremity became palpable on postoperative day 5, and the swelling and discoloration decreased. On postoperative day 30, he was taken off the OptEase® filter and the venogram showed a small amount of residual thrombus in his left external iliac vein (Figure \n). The inferior vena cava was patent, with no residual defects around the filter and no thrombus in the filter. He was discharged from the hospital in a stable condition, with full resolution of symptoms, on postoperative day 35 (Figure \nb). He was mostly asymptomatic at a recent 3-month follow-up visit except for slight edema in his left leg after walking. He continues on warfarin, maintaining an INR between 2.0 and 2.5, and wears elastic compression stockings.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

The patient is a 78-year-old woman who presented to emergency department with 2 days of gradually worsening right lower extremity (RLE) swelling, pain, and paresthesia that was limiting mobility. She was independent with a clinical frailty score of 2. Her past medical history was significant for diabetes mellitus with Hgb a1c 10.5 and a provoked left lower extremity DVT 30 years earlier treated with a course of warfarin and permanent IVC filter placement. She denied prior hypercoagulability workup and reported that her first episode of thrombosis followed a prolonged airplane ride. She was not anticoagulated at the time of presentation. She denied a history of dysrhythmias, prior embolic events, recent travel, injury, surgery, illness, or known exposure to COVID-19. She denied a family history of blood clots or hypercoagulability.\nPhysical examination revealed an RLE that was severely taut with cyanosis with nonpalpable peripheral pulses and multiphasic signaling on Doppler and tenderness to the mid-thigh. The contralateral limb was soft, nontender with color appropriate of ethnicity and palpable peripheral pulses. An RLE venous duplex ultrasound scan was performed with noncompressible veins and loss of spontaneous flow from the right popliteal vein extending to the right common femoral vein consistent with DVT. On presentation, she did not display hemodynamic instability nor complained of cardiopulmonary symptoms.\nBecause of progressive symptoms concerning for PCD and imminent development of venous gangrene in a patient with good functional status, she was admitted directly to the angiography suite for CDT and pharmacomechanical thrombectomy with tissue plasminogen activator (tPA) and heparin. Angiogram revealed thrombus extending proximal to the IVC filter in the mid-IVC (). She was transferred to the intensive care unit for continued CDT with tPA (1 mg/h) and heparin (500 u/h) through a Uni∗Fuse catheter. tPA was discontinued overnight for a fibrinogen of 82 mg/dL. The next morning, she reported subjective improvement of symptoms and return of palpable peripheral pulses with resolution of pain. She returned to the angiography suite for catheter removal and completion venogram that revealed persistent thrombus burden, and the decision to remove the remainder of the clot was made to decrease the risk of recurrence. Using the Penumbra Indigo CAT8 system (Penumbra, Alameda, Calif), mechanical suction thrombectomy, and balloon venoplasty were performed with successful recanalization (). She was transferred to the floor, heparin was discontinued, and rivaroxaban initiated.\nOn postoperative day 2, she was noted to have expressive aphasia and left-sided hemiplegia. A noncontrast computed tomography and computed tomography angiogram of the head and neck were performed without evidence of a hemorrhage or significant carotid or aortic arch atherosclerotic disease. International normalized ratio was therapeutic at 2.0. Given the concern for stroke, a diffusion-weighted magnetic resonance imaging of the brain was obtained () and was notable for the focal area of restricted diffusion within the right thalamus. Because of recent anticoagulation and thrombolysis, she was not a candidate for systemic tPA. Heparin was not reinitiated because of therapeutic international normalized ratio on rivaroxaban. She was transferred to a tertiary center with neurological and neurosurgical capabilities where she underwent a transesophageal echocardiogram with bubble study that revealed a PFO with an atrial septal aneurysm and left-to-right flow noted with color Doppler and a moderate right-to-left shunt during bubble study but no left atrial mass or thrombus. Rivaroxaban was continued and her neurological status improved. She was discharged to a rehabilitation facility with improved left-sided weakness on postoperative day 3. After 2 weeks of rehabilitation, the patient was discharged with a modified Rankin score of 1. Patency of the RLE veins was unknown at the time of discharge, but a repeat duplex ultrasound scan at 8 months after initial presentation showed chronic thrombus in the right common femoral vein, but the RLE venous system remained patent.\nBecause of multiple episodes of thrombosis, she was placed on lifelong anticoagulation with apixaban. Hypercoagulable disorder was suspected but was deferred by her hematologist as diagnosis would not change plan for management.

A 75-year-old male presented at our emergency department with painful swelling of his left leg for 12 hours without prior trauma history (). He also complained of numbness and weakness of the left lower leg and foot. His medical history was notable for hypertension and hyperlipidemia. On physical examination, the entire leg showed purplish discolorization and left femoral and dorsalis pedis artery pulses were detectable by hand-held Doppler. Duplex ultrasound (DUS) revealed left ilio-femoro-popliteal DVT (). Intravenous heparin was immediately administered and an emergent venous thrombectomy was performed under local anesthesia (), which provided pain relief. The next day, the left leg color was normalized () and motor and sensory defects were fully recovered. Anticoagulation therapy was prescribed for 6 months and follow-up computed tomography (CT) at 6 months revealed no residual thrombus ().

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 74-year-old man presented to the emergency department after a motorcycle accident. He had a deformity in the right leg. His comorbidities were chronic obstructive pulmonary disease, ischemic cardiomyopathy due to myocardial infarction, atrial fibrillation, hypertension, and dyslipidemia. His medications included aspirin and clopidogrel. Following investigations in this admission, a brain computed tomography (CT) revealed that he had acute traumatic subdural hematoma that was managed with nonoperative treatment. His right leg was broken, which was diagnosed as a closed fracture of the tibia and fibula, and was managed conservatively. He had fractures at the left iliac crest and the left superior pubic rami. The neurovascular conditions were normal. During admission, he had acute dyspnea with desaturation but no chest pain at ten days after admission. On examination, his blood pressure was 102/78 mmHg, pulse rate was 100/min, respiratory rate was 24/min, and blood oxygen saturation (SpO2) was 90% in room air, which was not corrected with oxygen supplement. He had crepitation at his left lower lung but no wheezing. CT angiography of the chest was performed and showed acute PEs at the right superior and inferior trunk. He was found to have acute respiratory failure and hypotension after the chest CT angiography was finished. He was scheduled for an emergency operation for surgical pulmonary embolectomy.\nOn the next day at the surgical intensive care unit (ICU), he developed progressive left leg edema with cyanosis. He had no fever and he could still move his leg, but his pain could not be evaluated since he was delirious. On examination, his left lower limb exhibited discoloration at his left foot without any ulcer or bleb, moist skin, or pitting edema, and the left dorsalis pedis and posterior tibial pulse could be palpated (1+) but were diminished (). The motor functions remained intact. Doppler ultrasonography was performed and revealed an uncompressible vein along the midsuperior femoral vein to the popliteal vein. His laboratory investigation showed that the leukocytosis and creatinine level rose from 1.04 mg% to 1.62 mg% and creatinine phosphokinase (CPK) was 322 U/L. He was diagnosed with PCD at the left femoral vein. The intervention radiologist attempted a catheter-directed thrombectomy, but it failed because the guider could not pass through the intraluminal clot. The patient was scheduled for emergency operation again for surgical thrombectomy with fasciotomy of the left leg (). The operative finding was a thrombus in the femoral vein that was 10 cm in length (). The compartment pressures before performing the fasciotomy at the anterior, lateral, and superficial posterior compartments were 43 mmHg, 37 mmHg, and 47 mmHg, respectively. The deep posterior compartment pressure was not measured. After the operation, his pain was relieved and the left dorsalis pedis and posterior tibial pulse were normal. He continued on wound dressings and the fasciotomy was closed by split-thickness skin graft. He continued on oral anticoagulant drugs for six months and underwent elective ray amputation at five months after the PCD for a dry gangrenous left big toe.

A Hispanic 58-year-old female with a past medical history of gastritis arrived into the emergency room (ER) with acute onset severe pain on the left leg associated with discoloration of the leg. According to the patient, approximately three hours prior to her arrival to the ER, she was walking when, suddenly, she started experiencing sharp pain in her left leg which rapidly progressed. The physical examination was remarkable for left lower extremity pain, discoloration, edema, associated with tenderness to touch, diminished distal pulses, and reduce sensation and mobility throughout the leg, which can be appreciated below (Figure ).\nWithin the first 30 min after her arrival to the hospital, a pressure Doppler was performed where extensive deep vein thrombosis (DVT) (left femoral-popliteal venous thrombosis) (Figure ) diagnosis was made and within the subsequent 60 min, a computed tomography angiography (CTA) aorto-ilio-femoral runoff with delayed phase was performed, showing delayed opacification of arterial segments below the knee level (Figure ), confirming the diagnosis. A bolus of heparin was given, followed by an infusion. Thrombolysis was offered to the patient, however, she refused due to concern for side effects.\nAfter one hour of starting heparin infusion, blood flow to the leg was regained and the patient recovered full sensation and movement in the leg; coloration returned to normal in the affected leg. The patient was admitted for continued observation and discharged later on direct oral anticoagulants (DOACs) without any recurrence of DVT so far.\nThe patient denied recent flights, a sedentary lifestyle, surgery, trauma, alcohol, tobacco, and drug use. There was neither a previous episode nor a family history of similar symptoms to her knowledge. Age-appropriate oncology screening was negative; mammogram from June 2020 was normal; colonoscopy four years before the presentation was also negative; Pap smears as well. Thrombophilia workup done by the Hematology/Oncology service was unrevealing, leading to a diagnosis of unprovoked DVT.\nThe curious part of the case is that even though thrombolysis and thrombectomy are considered the gold standard in the treatment of PCD, this patient had a spontaneous recovery only with heparin which serves as the only purpose to prevent the propagation of the thrombus. This specific patient according to Rutherford limb ischemia classification [] was a IIb which granted surgical intervention. Still, it remains unclear how such an extensive DVT improved in so quick fashion without thrombectomy/thrombolysis but seems that early use of heparin might have played an important role in the evolution of this patient's case and that early use of heparin might decrease the need for surgical intervention in some patients.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 74-year-old man presented to the emergency department after a motorcycle accident. He had a deformity in the right leg. His comorbidities were chronic obstructive pulmonary disease, ischemic cardiomyopathy due to myocardial infarction, atrial fibrillation, hypertension, and dyslipidemia. His medications included aspirin and clopidogrel. Following investigations in this admission, a brain computed tomography (CT) revealed that he had acute traumatic subdural hematoma that was managed with nonoperative treatment. His right leg was broken, which was diagnosed as a closed fracture of the tibia and fibula, and was managed conservatively. He had fractures at the left iliac crest and the left superior pubic rami. The neurovascular conditions were normal. During admission, he had acute dyspnea with desaturation but no chest pain at ten days after admission. On examination, his blood pressure was 102/78 mmHg, pulse rate was 100/min, respiratory rate was 24/min, and blood oxygen saturation (SpO2) was 90% in room air, which was not corrected with oxygen supplement. He had crepitation at his left lower lung but no wheezing. CT angiography of the chest was performed and showed acute PEs at the right superior and inferior trunk. He was found to have acute respiratory failure and hypotension after the chest CT angiography was finished. He was scheduled for an emergency operation for surgical pulmonary embolectomy.\nOn the next day at the surgical intensive care unit (ICU), he developed progressive left leg edema with cyanosis. He had no fever and he could still move his leg, but his pain could not be evaluated since he was delirious. On examination, his left lower limb exhibited discoloration at his left foot without any ulcer or bleb, moist skin, or pitting edema, and the left dorsalis pedis and posterior tibial pulse could be palpated (1+) but were diminished (). The motor functions remained intact. Doppler ultrasonography was performed and revealed an uncompressible vein along the midsuperior femoral vein to the popliteal vein. His laboratory investigation showed that the leukocytosis and creatinine level rose from 1.04 mg% to 1.62 mg% and creatinine phosphokinase (CPK) was 322 U/L. He was diagnosed with PCD at the left femoral vein. The intervention radiologist attempted a catheter-directed thrombectomy, but it failed because the guider could not pass through the intraluminal clot. The patient was scheduled for emergency operation again for surgical thrombectomy with fasciotomy of the left leg (). The operative finding was a thrombus in the femoral vein that was 10 cm in length (). The compartment pressures before performing the fasciotomy at the anterior, lateral, and superficial posterior compartments were 43 mmHg, 37 mmHg, and 47 mmHg, respectively. The deep posterior compartment pressure was not measured. After the operation, his pain was relieved and the left dorsalis pedis and posterior tibial pulse were normal. He continued on wound dressings and the fasciotomy was closed by split-thickness skin graft. He continued on oral anticoagulant drugs for six months and underwent elective ray amputation at five months after the PCD for a dry gangrenous left big toe.

A 49-year-old woman presented with acute coronary syndrome for which she received aspirin, clopidogrel, atorvastatin, enoxaparin, and tenecteplase at another facility. She was then transferred to our institute for further management. She underwent coronary angiography which was suggestive of triple vessel disease. As the patient was in acute congestive heart failure (Killip IV) with pulmonary edema, she was intubated and mechanically ventilated. She underwent coronary artery bypass grafting surgery the following day where she received 20,000U of unfractionated heparin.\nOn postoperative day (POD) 6, the patient developed right pedal edema with cyanosis. Bilateral lower limbs Arterial Doppler was normal. Venous Doppler of the right lower limb was suggestive of thrombosis of the right Common Femoral, Superficial Femoral, Popliteal, and Great Saphenous Veins. She also had progressively worsening thrombocytopenia in which the platelet count dropped from 297 × 109/L on day 1 of postenoxaparin exposure to a nadir of 20 × 109/L on day 8. With a suspicion of HIT and thrombosis (HITT), enoxaparin was replaced with fondaparinux on POD 7. She tested positive for HIT type 2 antibodies on day 10. Her platelets started improving by POD 11 [].\nOn POD 13, two-dimensional echocardiography done was suggestive of a left ventricular thrombus (with an ejection fraction of 25%) which resolved completely by POD 44 with anticoagulation. Fondaparinux was bridged with oral Vitamin K Antagonist-Acenocoumarol for HITT and PCD. Once there was a line of demarcation for gangrene, she underwent a right forefoot amputation on POD 34.\nThe patient was discharged on POD 47 with medications for cardiac failure along with acenocoumarol.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 74-year-old man presented to the emergency department after a motorcycle accident. He had a deformity in the right leg. His comorbidities were chronic obstructive pulmonary disease, ischemic cardiomyopathy due to myocardial infarction, atrial fibrillation, hypertension, and dyslipidemia. His medications included aspirin and clopidogrel. Following investigations in this admission, a brain computed tomography (CT) revealed that he had acute traumatic subdural hematoma that was managed with nonoperative treatment. His right leg was broken, which was diagnosed as a closed fracture of the tibia and fibula, and was managed conservatively. He had fractures at the left iliac crest and the left superior pubic rami. The neurovascular conditions were normal. During admission, he had acute dyspnea with desaturation but no chest pain at ten days after admission. On examination, his blood pressure was 102/78 mmHg, pulse rate was 100/min, respiratory rate was 24/min, and blood oxygen saturation (SpO2) was 90% in room air, which was not corrected with oxygen supplement. He had crepitation at his left lower lung but no wheezing. CT angiography of the chest was performed and showed acute PEs at the right superior and inferior trunk. He was found to have acute respiratory failure and hypotension after the chest CT angiography was finished. He was scheduled for an emergency operation for surgical pulmonary embolectomy.\nOn the next day at the surgical intensive care unit (ICU), he developed progressive left leg edema with cyanosis. He had no fever and he could still move his leg, but his pain could not be evaluated since he was delirious. On examination, his left lower limb exhibited discoloration at his left foot without any ulcer or bleb, moist skin, or pitting edema, and the left dorsalis pedis and posterior tibial pulse could be palpated (1+) but were diminished (). The motor functions remained intact. Doppler ultrasonography was performed and revealed an uncompressible vein along the midsuperior femoral vein to the popliteal vein. His laboratory investigation showed that the leukocytosis and creatinine level rose from 1.04 mg% to 1.62 mg% and creatinine phosphokinase (CPK) was 322 U/L. He was diagnosed with PCD at the left femoral vein. The intervention radiologist attempted a catheter-directed thrombectomy, but it failed because the guider could not pass through the intraluminal clot. The patient was scheduled for emergency operation again for surgical thrombectomy with fasciotomy of the left leg (). The operative finding was a thrombus in the femoral vein that was 10 cm in length (). The compartment pressures before performing the fasciotomy at the anterior, lateral, and superficial posterior compartments were 43 mmHg, 37 mmHg, and 47 mmHg, respectively. The deep posterior compartment pressure was not measured. After the operation, his pain was relieved and the left dorsalis pedis and posterior tibial pulse were normal. He continued on wound dressings and the fasciotomy was closed by split-thickness skin graft. He continued on oral anticoagulant drugs for six months and underwent elective ray amputation at five months after the PCD for a dry gangrenous left big toe.

An 88-year-old man was admitted to our facility with altered mental status, hypotension (blood pressure range: 71-84/47-57 mmHg in the right arm supine position), fever (104oF), and tachycardia (heart rate: 140-150 beats/min) on arrival at the emergency room. Prior to admission, he was on hemodialysis for the past three months for end-stage renal disease secondary to rapidly progressive glomerulonephritis (has a right permacath). He was receiving intermittent heparin flushes along with dialysis to maintain the patency of the extracorporeal circuit. Other significant past medical history included a splenectomy in 2007. Clinical manifestations, imaging tests, and blood cultures suggested septic shock secondary to Streptococcal pneumonia. The patient was started on meropenem and vancomycin. A left internal jugular catheter and arterial line (in the right upper extremity) were placed for fluid resuscitation and blood pressure monitoring, respectively, and the patient was managed per surviving sepsis guidelines. On day three of hospitalization, the patient started to complain about a right-hand pain at the site of the arterial catheter. The physical examination was remarkable for a swollen and cyanotic right upper extremity, especially the second and third fingers (Figure ), with a barely palpable radial pulse compared to the left side. Arterial Doppler of the upper extremities was obtained, with findings indicative of significant right-sided arterial insufficiency. Further evaluation by venous duplex ultrasound identified a massive thrombus in the axillary, brachial, and basilic veins of the right arm with the solely spared ulna vein being hugely engorged (Figures -).\nWe considered the possibility of catheter-induced venous thrombosis, sepsis-associated disseminated intravascular coagulation and heparin-induced thrombocytopenia as working diagnoses. Given the suspicion of heparin-induced thrombocytopenia, we discontinued heparin immediately while the patient’s peripheral smear and coagulation cascade were investigated. Although the patient had low platelets (Table ), prolonged prothrombin time (16 (normal: 11-13 sec)), activated partial thromboplastin time (63 (normal: 25-35 sec)), elevated fibrin degradation products (>40 (normal: <10 mcg/ml)), which were suspicious for sepsis-related disseminated intravascular coagulation; normal factor VII (77 (normal: 50-150%)), high VIII levels (192 (normal: 50-150%)), normal haptoglobin (163 (normal: 36-195 mg/dl)), mildly decreased hemoglobulin (range: 12.1-12.9 (normal:13.5-17.5 g/dl)), and the presence of very few schistiocytes (<0.5%) on a peripheral smear made disseminated intravascular coagulation less likely. Laboratory data were remarkable for a significant drop in the platelet count from 234*109/L (on initiation of hemodialysis) to 44*109/L (the day of hospital admission) over the past three months. Based on the 4T score, heparin-induced thrombocytopenia was highly suspected and argatroban was initiated at 1 mg/kg/min. Vascular surgery consultation was obtained to address the gangrene in the second and third digits of the right upper extremity. However, considering his critically septic situation with multiple morbidities, a decision was made not to proceed with invasive maneuvers. On hospital day four, heparin-platelet factor 4 (PF4) antibodies (1.67 (normal: <0.4), heparin inhibition: >50%), and serotonin release assays returned positive (using enzyme-linked immunosorbent assay), confirming heparin-induced thrombocytopenia. On hospital day eight, repeated venous duplex demonstrated normal compressibility and spontaneous flow in the vein of the right upper extremity. The platelet count recovered and no further thrombotic complications were observed. Though we were able to manage the patient’s advanced gangrene with argatroban, his second and third fingers were amputated in the end.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 74-year-old man presented to the emergency department after a motorcycle accident. He had a deformity in the right leg. His comorbidities were chronic obstructive pulmonary disease, ischemic cardiomyopathy due to myocardial infarction, atrial fibrillation, hypertension, and dyslipidemia. His medications included aspirin and clopidogrel. Following investigations in this admission, a brain computed tomography (CT) revealed that he had acute traumatic subdural hematoma that was managed with nonoperative treatment. His right leg was broken, which was diagnosed as a closed fracture of the tibia and fibula, and was managed conservatively. He had fractures at the left iliac crest and the left superior pubic rami. The neurovascular conditions were normal. During admission, he had acute dyspnea with desaturation but no chest pain at ten days after admission. On examination, his blood pressure was 102/78 mmHg, pulse rate was 100/min, respiratory rate was 24/min, and blood oxygen saturation (SpO2) was 90% in room air, which was not corrected with oxygen supplement. He had crepitation at his left lower lung but no wheezing. CT angiography of the chest was performed and showed acute PEs at the right superior and inferior trunk. He was found to have acute respiratory failure and hypotension after the chest CT angiography was finished. He was scheduled for an emergency operation for surgical pulmonary embolectomy.\nOn the next day at the surgical intensive care unit (ICU), he developed progressive left leg edema with cyanosis. He had no fever and he could still move his leg, but his pain could not be evaluated since he was delirious. On examination, his left lower limb exhibited discoloration at his left foot without any ulcer or bleb, moist skin, or pitting edema, and the left dorsalis pedis and posterior tibial pulse could be palpated (1+) but were diminished (). The motor functions remained intact. Doppler ultrasonography was performed and revealed an uncompressible vein along the midsuperior femoral vein to the popliteal vein. His laboratory investigation showed that the leukocytosis and creatinine level rose from 1.04 mg% to 1.62 mg% and creatinine phosphokinase (CPK) was 322 U/L. He was diagnosed with PCD at the left femoral vein. The intervention radiologist attempted a catheter-directed thrombectomy, but it failed because the guider could not pass through the intraluminal clot. The patient was scheduled for emergency operation again for surgical thrombectomy with fasciotomy of the left leg (). The operative finding was a thrombus in the femoral vein that was 10 cm in length (). The compartment pressures before performing the fasciotomy at the anterior, lateral, and superficial posterior compartments were 43 mmHg, 37 mmHg, and 47 mmHg, respectively. The deep posterior compartment pressure was not measured. After the operation, his pain was relieved and the left dorsalis pedis and posterior tibial pulse were normal. He continued on wound dressings and the fasciotomy was closed by split-thickness skin graft. He continued on oral anticoagulant drugs for six months and underwent elective ray amputation at five months after the PCD for a dry gangrenous left big toe.

A 64-year-old man with a history of obesity (BMI 38 Kg/m^2), arterial hypertension, atrial fibrillation, type 2 diabetes, chronic kidney disease, obstructive sleep apnea, and chronic venous insufficiency presented to the Emergency Department complaining of dyspnea, fever, and chest pain which started 7 days before. The patient was hypoxemic in room air (SpO2 80% and PaO2 43 mmHg). Inferior limbs appeared normal. A molecular swab formalized diagnosis of SARS-CoV2-related pneumonia. Respiratory distress progressed despite non-invasive-ventilation and hemodynamic instability requiring vasoactive support ensued. The patient was intubated and transferred to the ICU. The patient received invasive protective ventilation and hemodynamic support with noradrenaline. Gas exchange progressively worsened to a PaO2/FiO2 ratio of 70 mmHg. He developed a shock, and his lower limbs started to appear mottled. Lung and cardiac ultrasound were compatible with severe interstitial pneumonia and with no signs of pressure overload of the right heart. His coagulation profile was highly altered, as both aPTT and INR were elevated (respectively 2.28 seconds and 6.42), platelets were 164,000/mm3, and D-dimer was 117,521 UI/ml. Coagulation parameters continually worsened (), and treatment with one unit of fresh frozen plasma and vitamin K was required. Inferior limbs’ color progressively worsened, becoming frankly cyanotic, while pulses were still normal. Doppler ultrasound showed bilateral thrombosis of tibial and small saphenous veins. A continuous infusion of iloprost was started, as PCD was suspected (). Continuous infusion of unfractionated heparin was instituted, at a dose of 500-1000 IU per hour, according to aPTT, as well as continuous veno-venous hemodiafiltration as the patient developed acute kidney injury. The patient’s general conditions worsened (), and despite maximal treatment, he passed away after eight days of ICU care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 21-year-old female college student presented to the emergency department (ED) with severe pain in her left hip, thigh, and calf. The pain started suddenly when she was playing basketball a few hours earlier. She twisted her torso to shoot the ball and heard a “pop” in her left hip with immediate onset of pain, and she subsequently fell to her knees. She was initially able to ambulate but had worsening pain and rapid progression of swelling and mottling in the left leg from her hip to her ankle. She denied any pain or swelling in that extremity prior to the injury during the basketball game. With the exception of oral contraceptive use, she had no significant medical or family history.\nOn examination her left extremity was mottled, dusky, and cool to the touch from the hip to the toes and she had decreased dorsalis pedis and posterior tibial pulses when compared with the right extremity. The leg was markedly tender to palpation and sensation to light touch was diminished. Passive range of motion of the hip, knee, and ankle elicited severe pain.\nPOCUS was performed at the bedside to evaluate for arterial blood flow and deep venous thrombosis. This demonstrated normal color flow in the femoral and popliteal arteries (), but echogenic material was noted within the left common femoral vein extending distally to the popliteal vein and the veins were non-compressible (). Vascular surgery was immediately consulted, and while awaiting their arrival to the ED the patient was sent for an emergent computed tomography (CT) angiogram, which confirmed arterial patency and extensive deep venous thrombosis in the left popliteal, femoral, and iliac veins (). A heparin bolus was given and the patient was then taken to interventional radiology where she underwent partial thrombectomy, catheter-directed tissue plasminogen activator (tPA) treatment, and placement of an inferior vena cava (IVC) filter. By the next morning her leg was noted to be well-perfused, non-tender, and without swelling, and her pain had resolved. A workup for hypercoagulable states revealed heterozygosity for the Factor V Leiden mutation. She was discharged one week later on warfarin after bridging from enoxaparin.

A 74-year-old man presented to the emergency department after a motorcycle accident. He had a deformity in the right leg. His comorbidities were chronic obstructive pulmonary disease, ischemic cardiomyopathy due to myocardial infarction, atrial fibrillation, hypertension, and dyslipidemia. His medications included aspirin and clopidogrel. Following investigations in this admission, a brain computed tomography (CT) revealed that he had acute traumatic subdural hematoma that was managed with nonoperative treatment. His right leg was broken, which was diagnosed as a closed fracture of the tibia and fibula, and was managed conservatively. He had fractures at the left iliac crest and the left superior pubic rami. The neurovascular conditions were normal. During admission, he had acute dyspnea with desaturation but no chest pain at ten days after admission. On examination, his blood pressure was 102/78 mmHg, pulse rate was 100/min, respiratory rate was 24/min, and blood oxygen saturation (SpO2) was 90% in room air, which was not corrected with oxygen supplement. He had crepitation at his left lower lung but no wheezing. CT angiography of the chest was performed and showed acute PEs at the right superior and inferior trunk. He was found to have acute respiratory failure and hypotension after the chest CT angiography was finished. He was scheduled for an emergency operation for surgical pulmonary embolectomy.\nOn the next day at the surgical intensive care unit (ICU), he developed progressive left leg edema with cyanosis. He had no fever and he could still move his leg, but his pain could not be evaluated since he was delirious. On examination, his left lower limb exhibited discoloration at his left foot without any ulcer or bleb, moist skin, or pitting edema, and the left dorsalis pedis and posterior tibial pulse could be palpated (1+) but were diminished (). The motor functions remained intact. Doppler ultrasonography was performed and revealed an uncompressible vein along the midsuperior femoral vein to the popliteal vein. His laboratory investigation showed that the leukocytosis and creatinine level rose from 1.04 mg% to 1.62 mg% and creatinine phosphokinase (CPK) was 322 U/L. He was diagnosed with PCD at the left femoral vein. The intervention radiologist attempted a catheter-directed thrombectomy, but it failed because the guider could not pass through the intraluminal clot. The patient was scheduled for emergency operation again for surgical thrombectomy with fasciotomy of the left leg (). The operative finding was a thrombus in the femoral vein that was 10 cm in length (). The compartment pressures before performing the fasciotomy at the anterior, lateral, and superficial posterior compartments were 43 mmHg, 37 mmHg, and 47 mmHg, respectively. The deep posterior compartment pressure was not measured. After the operation, his pain was relieved and the left dorsalis pedis and posterior tibial pulse were normal. He continued on wound dressings and the fasciotomy was closed by split-thickness skin graft. He continued on oral anticoagulant drugs for six months and underwent elective ray amputation at five months after the PCD for a dry gangrenous left big toe.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 74-year-old man presented to the emergency department after a motorcycle accident. He had a deformity in the right leg. His comorbidities were chronic obstructive pulmonary disease, ischemic cardiomyopathy due to myocardial infarction, atrial fibrillation, hypertension, and dyslipidemia. His medications included aspirin and clopidogrel. Following investigations in this admission, a brain computed tomography (CT) revealed that he had acute traumatic subdural hematoma that was managed with nonoperative treatment. His right leg was broken, which was diagnosed as a closed fracture of the tibia and fibula, and was managed conservatively. He had fractures at the left iliac crest and the left superior pubic rami. The neurovascular conditions were normal. During admission, he had acute dyspnea with desaturation but no chest pain at ten days after admission. On examination, his blood pressure was 102/78 mmHg, pulse rate was 100/min, respiratory rate was 24/min, and blood oxygen saturation (SpO2) was 90% in room air, which was not corrected with oxygen supplement. He had crepitation at his left lower lung but no wheezing. CT angiography of the chest was performed and showed acute PEs at the right superior and inferior trunk. He was found to have acute respiratory failure and hypotension after the chest CT angiography was finished. He was scheduled for an emergency operation for surgical pulmonary embolectomy.\nOn the next day at the surgical intensive care unit (ICU), he developed progressive left leg edema with cyanosis. He had no fever and he could still move his leg, but his pain could not be evaluated since he was delirious. On examination, his left lower limb exhibited discoloration at his left foot without any ulcer or bleb, moist skin, or pitting edema, and the left dorsalis pedis and posterior tibial pulse could be palpated (1+) but were diminished (). The motor functions remained intact. Doppler ultrasonography was performed and revealed an uncompressible vein along the midsuperior femoral vein to the popliteal vein. His laboratory investigation showed that the leukocytosis and creatinine level rose from 1.04 mg% to 1.62 mg% and creatinine phosphokinase (CPK) was 322 U/L. He was diagnosed with PCD at the left femoral vein. The intervention radiologist attempted a catheter-directed thrombectomy, but it failed because the guider could not pass through the intraluminal clot. The patient was scheduled for emergency operation again for surgical thrombectomy with fasciotomy of the left leg (). The operative finding was a thrombus in the femoral vein that was 10 cm in length (). The compartment pressures before performing the fasciotomy at the anterior, lateral, and superficial posterior compartments were 43 mmHg, 37 mmHg, and 47 mmHg, respectively. The deep posterior compartment pressure was not measured. After the operation, his pain was relieved and the left dorsalis pedis and posterior tibial pulse were normal. He continued on wound dressings and the fasciotomy was closed by split-thickness skin graft. He continued on oral anticoagulant drugs for six months and underwent elective ray amputation at five months after the PCD for a dry gangrenous left big toe.

A 66-year-old female presented to the emergency department with three days of acute LLE swelling, pain, cyanosis, inability to bear weight, dyspnea, and hypoxemia (Figure ). She denied recent travel, hormone replacement, or a history of DVT/pulmonary embolism (PE). Her medical history was notable for systemic lupus erythematosus, CREST (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome, Sjogren’s syndrome, and local invasive anal squamous cell carcinoma. Doppler ultrasound revealed LLE thrombus extending from the greater saphenous vein to the popliteal vein. She was admitted to the intensive care unit (ICU) and started on an unfractionated heparin drip.\nThe vascular surgery team was consulted for surgical intervention. After further review of her case, the vascular surgery team elected for an endovascular approach with CDT of LLE. Initial venogram demonstrated extensive clotting of the tibial, popliteal, and femoral venous systems extending into the iliac system (Figures , ). From a tibial approach, a guidewire was advanced up to the common iliac, but a chronic occlusion of the left common iliac vein was found, which could not be crossed. A venous collateral circulation system in communication with the right iliac venous system was identified. In order to decrease the overall clot burden, two 50-cm EKOS endovascular catheters were placed in the left external iliac vein and collateral system. Repeat venogram at 24 hours post-CDT showed significant improvement of the overall clot burden with almost complete resolution of the clot in the LLE; however, the chronic occlusion remained (Figure ). A 20 x 80 mm Boston Scientific Wallstent™ (endoprosthesis stent) was advanced across the total chronic total occlusion and deployed. Post-operative venogram demonstrated significant improvement in flow in the system, with all flow going through the iliac system, and no flow further through the previously seen collaterals. Intravascular ultrasound was advanced through the area, which showed severe compression of the stent. A 12x 40 mm Atlas® dilatation catheter (Bard Peripheral Vascular Inc., Tempe, AZ, USA) was used for angioplasty. Repeat intravascular ultrasound showed persistent compression of the area. A 8 x 40 mm Boston Scientific Mustang™ dilatation catheter (high-pressure balloon) was used to re-attempt angioplasty; however, compression was still noted (Figure ). Regardless, outflow improved throughout the left common iliac system, and no further interventions were performed. The patient returned to the ICU and transitioned to direct oral anticoagulation without any further complications. She was subsequently transferred to a medicine ward for further care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 74-year-old man presented to the emergency department after a motorcycle accident. He had a deformity in the right leg. His comorbidities were chronic obstructive pulmonary disease, ischemic cardiomyopathy due to myocardial infarction, atrial fibrillation, hypertension, and dyslipidemia. His medications included aspirin and clopidogrel. Following investigations in this admission, a brain computed tomography (CT) revealed that he had acute traumatic subdural hematoma that was managed with nonoperative treatment. His right leg was broken, which was diagnosed as a closed fracture of the tibia and fibula, and was managed conservatively. He had fractures at the left iliac crest and the left superior pubic rami. The neurovascular conditions were normal. During admission, he had acute dyspnea with desaturation but no chest pain at ten days after admission. On examination, his blood pressure was 102/78 mmHg, pulse rate was 100/min, respiratory rate was 24/min, and blood oxygen saturation (SpO2) was 90% in room air, which was not corrected with oxygen supplement. He had crepitation at his left lower lung but no wheezing. CT angiography of the chest was performed and showed acute PEs at the right superior and inferior trunk. He was found to have acute respiratory failure and hypotension after the chest CT angiography was finished. He was scheduled for an emergency operation for surgical pulmonary embolectomy.\nOn the next day at the surgical intensive care unit (ICU), he developed progressive left leg edema with cyanosis. He had no fever and he could still move his leg, but his pain could not be evaluated since he was delirious. On examination, his left lower limb exhibited discoloration at his left foot without any ulcer or bleb, moist skin, or pitting edema, and the left dorsalis pedis and posterior tibial pulse could be palpated (1+) but were diminished (). The motor functions remained intact. Doppler ultrasonography was performed and revealed an uncompressible vein along the midsuperior femoral vein to the popliteal vein. His laboratory investigation showed that the leukocytosis and creatinine level rose from 1.04 mg% to 1.62 mg% and creatinine phosphokinase (CPK) was 322 U/L. He was diagnosed with PCD at the left femoral vein. The intervention radiologist attempted a catheter-directed thrombectomy, but it failed because the guider could not pass through the intraluminal clot. The patient was scheduled for emergency operation again for surgical thrombectomy with fasciotomy of the left leg (). The operative finding was a thrombus in the femoral vein that was 10 cm in length (). The compartment pressures before performing the fasciotomy at the anterior, lateral, and superficial posterior compartments were 43 mmHg, 37 mmHg, and 47 mmHg, respectively. The deep posterior compartment pressure was not measured. After the operation, his pain was relieved and the left dorsalis pedis and posterior tibial pulse were normal. He continued on wound dressings and the fasciotomy was closed by split-thickness skin graft. He continued on oral anticoagulant drugs for six months and underwent elective ray amputation at five months after the PCD for a dry gangrenous left big toe.

A 49-year-old Chinese man sustained severe knife trauma and was referred to a local hospital. An exploratory laparotomy showed traumatic rupture of his left external iliac vein with massive intraperitoneal bleeding, but his iliac artery was intact. To rescue him, the proximal and distal parts of his injured external iliac vein were ligated (there was no vascular surgeon in the local hospital); however, his left leg quickly became severely swollen, cyanotic and pulseless. Two hours after the first operation, he was transferred to the emergency department of our university hospital with endotracheal tube intubation. On physical examination, he was tachycardic (142 beats per minute), hypotensive (86/50mmHg). His left lower extremity was markedly edematous, cyanotic, mottled (Figure \na) and had no palpable pulse, but his right lower extremity was normal. He was diagnosed with posttraumatic PCD. Considering the high risk of pulmonary embolism during the next surgical procedure, an OptEase® retrievable vena cava filter (Cordis Corp., New Brunswick, NJ, USA) was placed in his inferior vena cava via his right femoral vein under digital subtraction angiography (Figure \n). His abdomen was immediately reopened while his left leg was also prepared for treatment.During the second emergent laparotomy, there was less blood in his pelvic cavity. No active bleeding was identified. His left iliac vein and artery were exposed and his entire iliac artery appeared normal and without rupture. His external iliac vein was ligated but not transected, connected only by the posterior wall, and the caudal part of his iliac vein was significantly dilated. By replacing the vascular clamp in the proximal and distal parts of the rupture, the ligations on both sides of the venous rupture were resolved. A wedge-shaped rupture was revealed, approximately 4cm in length, on the anterolateral side of his left external iliac vein. The edges of the venous rupture were smooth as a result of the knife trauma. Although the ligated parts of his iliac vein appeared congested, the lumen was smooth and contained no clot. The damaged vein was repaired with continuous 4-0 Prolene sutures (Ethicon, Inc, Somerville, NJ, USA) after the patient was systemically heparinized with 5000 units heparin. Before the sutures were finally ligated, the clamp at the cranial aspect was removed and the caudal clamp was left in place. After the backflow was clear of thrombotic debris, the clamp on his caudal iliac vein was removed and the clamp at the cranial aspect left in place. The left leg was gently massaged from calf to thigh; as a result, some thrombi in the caudal part of the vein were flushed out with the venous blood flow, and the sutures were finally ligated until the venous blood was free of thrombus. His iliac vein, although narrower after repair, was patent (Figure \n).\nAfter the operation, the patient was sent to the surgical intensive care unit with mechanical ventilation. Despite the fact that his left leg showed some signs of compartment syndrome with blisters in his calf, fasciotomy was not performed. He received systemic anticoagulation, initially with low-molecular-weight heparin, then with warfarin, titrating to an international normalized ratio (INR) between 2.0 and 2.5.Three days postoperatively, mechanical ventilation was discontinued and his signs and symptoms improved dramatically. Pulses in his left lower extremity became palpable on postoperative day 5, and the swelling and discoloration decreased. On postoperative day 30, he was taken off the OptEase® filter and the venogram showed a small amount of residual thrombus in his left external iliac vein (Figure \n). The inferior vena cava was patent, with no residual defects around the filter and no thrombus in the filter. He was discharged from the hospital in a stable condition, with full resolution of symptoms, on postoperative day 35 (Figure \nb). He was mostly asymptomatic at a recent 3-month follow-up visit except for slight edema in his left leg after walking. He continues on warfarin, maintaining an INR between 2.0 and 2.5, and wears elastic compression stockings.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

The patient is a 78-year-old woman who presented to emergency department with 2 days of gradually worsening right lower extremity (RLE) swelling, pain, and paresthesia that was limiting mobility. She was independent with a clinical frailty score of 2. Her past medical history was significant for diabetes mellitus with Hgb a1c 10.5 and a provoked left lower extremity DVT 30 years earlier treated with a course of warfarin and permanent IVC filter placement. She denied prior hypercoagulability workup and reported that her first episode of thrombosis followed a prolonged airplane ride. She was not anticoagulated at the time of presentation. She denied a history of dysrhythmias, prior embolic events, recent travel, injury, surgery, illness, or known exposure to COVID-19. She denied a family history of blood clots or hypercoagulability.\nPhysical examination revealed an RLE that was severely taut with cyanosis with nonpalpable peripheral pulses and multiphasic signaling on Doppler and tenderness to the mid-thigh. The contralateral limb was soft, nontender with color appropriate of ethnicity and palpable peripheral pulses. An RLE venous duplex ultrasound scan was performed with noncompressible veins and loss of spontaneous flow from the right popliteal vein extending to the right common femoral vein consistent with DVT. On presentation, she did not display hemodynamic instability nor complained of cardiopulmonary symptoms.\nBecause of progressive symptoms concerning for PCD and imminent development of venous gangrene in a patient with good functional status, she was admitted directly to the angiography suite for CDT and pharmacomechanical thrombectomy with tissue plasminogen activator (tPA) and heparin. Angiogram revealed thrombus extending proximal to the IVC filter in the mid-IVC (). She was transferred to the intensive care unit for continued CDT with tPA (1 mg/h) and heparin (500 u/h) through a Uni∗Fuse catheter. tPA was discontinued overnight for a fibrinogen of 82 mg/dL. The next morning, she reported subjective improvement of symptoms and return of palpable peripheral pulses with resolution of pain. She returned to the angiography suite for catheter removal and completion venogram that revealed persistent thrombus burden, and the decision to remove the remainder of the clot was made to decrease the risk of recurrence. Using the Penumbra Indigo CAT8 system (Penumbra, Alameda, Calif), mechanical suction thrombectomy, and balloon venoplasty were performed with successful recanalization (). She was transferred to the floor, heparin was discontinued, and rivaroxaban initiated.\nOn postoperative day 2, she was noted to have expressive aphasia and left-sided hemiplegia. A noncontrast computed tomography and computed tomography angiogram of the head and neck were performed without evidence of a hemorrhage or significant carotid or aortic arch atherosclerotic disease. International normalized ratio was therapeutic at 2.0. Given the concern for stroke, a diffusion-weighted magnetic resonance imaging of the brain was obtained () and was notable for the focal area of restricted diffusion within the right thalamus. Because of recent anticoagulation and thrombolysis, she was not a candidate for systemic tPA. Heparin was not reinitiated because of therapeutic international normalized ratio on rivaroxaban. She was transferred to a tertiary center with neurological and neurosurgical capabilities where she underwent a transesophageal echocardiogram with bubble study that revealed a PFO with an atrial septal aneurysm and left-to-right flow noted with color Doppler and a moderate right-to-left shunt during bubble study but no left atrial mass or thrombus. Rivaroxaban was continued and her neurological status improved. She was discharged to a rehabilitation facility with improved left-sided weakness on postoperative day 3. After 2 weeks of rehabilitation, the patient was discharged with a modified Rankin score of 1. Patency of the RLE veins was unknown at the time of discharge, but a repeat duplex ultrasound scan at 8 months after initial presentation showed chronic thrombus in the right common femoral vein, but the RLE venous system remained patent.\nBecause of multiple episodes of thrombosis, she was placed on lifelong anticoagulation with apixaban. Hypercoagulable disorder was suspected but was deferred by her hematologist as diagnosis would not change plan for management.

A 74-year-old man presented to the emergency department after a motorcycle accident. He had a deformity in the right leg. His comorbidities were chronic obstructive pulmonary disease, ischemic cardiomyopathy due to myocardial infarction, atrial fibrillation, hypertension, and dyslipidemia. His medications included aspirin and clopidogrel. Following investigations in this admission, a brain computed tomography (CT) revealed that he had acute traumatic subdural hematoma that was managed with nonoperative treatment. His right leg was broken, which was diagnosed as a closed fracture of the tibia and fibula, and was managed conservatively. He had fractures at the left iliac crest and the left superior pubic rami. The neurovascular conditions were normal. During admission, he had acute dyspnea with desaturation but no chest pain at ten days after admission. On examination, his blood pressure was 102/78 mmHg, pulse rate was 100/min, respiratory rate was 24/min, and blood oxygen saturation (SpO2) was 90% in room air, which was not corrected with oxygen supplement. He had crepitation at his left lower lung but no wheezing. CT angiography of the chest was performed and showed acute PEs at the right superior and inferior trunk. He was found to have acute respiratory failure and hypotension after the chest CT angiography was finished. He was scheduled for an emergency operation for surgical pulmonary embolectomy.\nOn the next day at the surgical intensive care unit (ICU), he developed progressive left leg edema with cyanosis. He had no fever and he could still move his leg, but his pain could not be evaluated since he was delirious. On examination, his left lower limb exhibited discoloration at his left foot without any ulcer or bleb, moist skin, or pitting edema, and the left dorsalis pedis and posterior tibial pulse could be palpated (1+) but were diminished (). The motor functions remained intact. Doppler ultrasonography was performed and revealed an uncompressible vein along the midsuperior femoral vein to the popliteal vein. His laboratory investigation showed that the leukocytosis and creatinine level rose from 1.04 mg% to 1.62 mg% and creatinine phosphokinase (CPK) was 322 U/L. He was diagnosed with PCD at the left femoral vein. The intervention radiologist attempted a catheter-directed thrombectomy, but it failed because the guider could not pass through the intraluminal clot. The patient was scheduled for emergency operation again for surgical thrombectomy with fasciotomy of the left leg (). The operative finding was a thrombus in the femoral vein that was 10 cm in length (). The compartment pressures before performing the fasciotomy at the anterior, lateral, and superficial posterior compartments were 43 mmHg, 37 mmHg, and 47 mmHg, respectively. The deep posterior compartment pressure was not measured. After the operation, his pain was relieved and the left dorsalis pedis and posterior tibial pulse were normal. He continued on wound dressings and the fasciotomy was closed by split-thickness skin graft. He continued on oral anticoagulant drugs for six months and underwent elective ray amputation at five months after the PCD for a dry gangrenous left big toe.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A Hispanic 58-year-old female with a past medical history of gastritis arrived into the emergency room (ER) with acute onset severe pain on the left leg associated with discoloration of the leg. According to the patient, approximately three hours prior to her arrival to the ER, she was walking when, suddenly, she started experiencing sharp pain in her left leg which rapidly progressed. The physical examination was remarkable for left lower extremity pain, discoloration, edema, associated with tenderness to touch, diminished distal pulses, and reduce sensation and mobility throughout the leg, which can be appreciated below (Figure ).\nWithin the first 30 min after her arrival to the hospital, a pressure Doppler was performed where extensive deep vein thrombosis (DVT) (left femoral-popliteal venous thrombosis) (Figure ) diagnosis was made and within the subsequent 60 min, a computed tomography angiography (CTA) aorto-ilio-femoral runoff with delayed phase was performed, showing delayed opacification of arterial segments below the knee level (Figure ), confirming the diagnosis. A bolus of heparin was given, followed by an infusion. Thrombolysis was offered to the patient, however, she refused due to concern for side effects.\nAfter one hour of starting heparin infusion, blood flow to the leg was regained and the patient recovered full sensation and movement in the leg; coloration returned to normal in the affected leg. The patient was admitted for continued observation and discharged later on direct oral anticoagulants (DOACs) without any recurrence of DVT so far.\nThe patient denied recent flights, a sedentary lifestyle, surgery, trauma, alcohol, tobacco, and drug use. There was neither a previous episode nor a family history of similar symptoms to her knowledge. Age-appropriate oncology screening was negative; mammogram from June 2020 was normal; colonoscopy four years before the presentation was also negative; Pap smears as well. Thrombophilia workup done by the Hematology/Oncology service was unrevealing, leading to a diagnosis of unprovoked DVT.\nThe curious part of the case is that even though thrombolysis and thrombectomy are considered the gold standard in the treatment of PCD, this patient had a spontaneous recovery only with heparin which serves as the only purpose to prevent the propagation of the thrombus. This specific patient according to Rutherford limb ischemia classification [] was a IIb which granted surgical intervention. Still, it remains unclear how such an extensive DVT improved in so quick fashion without thrombectomy/thrombolysis but seems that early use of heparin might have played an important role in the evolution of this patient's case and that early use of heparin might decrease the need for surgical intervention in some patients.

A 49-year-old woman presented with acute coronary syndrome for which she received aspirin, clopidogrel, atorvastatin, enoxaparin, and tenecteplase at another facility. She was then transferred to our institute for further management. She underwent coronary angiography which was suggestive of triple vessel disease. As the patient was in acute congestive heart failure (Killip IV) with pulmonary edema, she was intubated and mechanically ventilated. She underwent coronary artery bypass grafting surgery the following day where she received 20,000U of unfractionated heparin.\nOn postoperative day (POD) 6, the patient developed right pedal edema with cyanosis. Bilateral lower limbs Arterial Doppler was normal. Venous Doppler of the right lower limb was suggestive of thrombosis of the right Common Femoral, Superficial Femoral, Popliteal, and Great Saphenous Veins. She also had progressively worsening thrombocytopenia in which the platelet count dropped from 297 × 109/L on day 1 of postenoxaparin exposure to a nadir of 20 × 109/L on day 8. With a suspicion of HIT and thrombosis (HITT), enoxaparin was replaced with fondaparinux on POD 7. She tested positive for HIT type 2 antibodies on day 10. Her platelets started improving by POD 11 [].\nOn POD 13, two-dimensional echocardiography done was suggestive of a left ventricular thrombus (with an ejection fraction of 25%) which resolved completely by POD 44 with anticoagulation. Fondaparinux was bridged with oral Vitamin K Antagonist-Acenocoumarol for HITT and PCD. Once there was a line of demarcation for gangrene, she underwent a right forefoot amputation on POD 34.\nThe patient was discharged on POD 47 with medications for cardiac failure along with acenocoumarol.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A Hispanic 58-year-old female with a past medical history of gastritis arrived into the emergency room (ER) with acute onset severe pain on the left leg associated with discoloration of the leg. According to the patient, approximately three hours prior to her arrival to the ER, she was walking when, suddenly, she started experiencing sharp pain in her left leg which rapidly progressed. The physical examination was remarkable for left lower extremity pain, discoloration, edema, associated with tenderness to touch, diminished distal pulses, and reduce sensation and mobility throughout the leg, which can be appreciated below (Figure ).\nWithin the first 30 min after her arrival to the hospital, a pressure Doppler was performed where extensive deep vein thrombosis (DVT) (left femoral-popliteal venous thrombosis) (Figure ) diagnosis was made and within the subsequent 60 min, a computed tomography angiography (CTA) aorto-ilio-femoral runoff with delayed phase was performed, showing delayed opacification of arterial segments below the knee level (Figure ), confirming the diagnosis. A bolus of heparin was given, followed by an infusion. Thrombolysis was offered to the patient, however, she refused due to concern for side effects.\nAfter one hour of starting heparin infusion, blood flow to the leg was regained and the patient recovered full sensation and movement in the leg; coloration returned to normal in the affected leg. The patient was admitted for continued observation and discharged later on direct oral anticoagulants (DOACs) without any recurrence of DVT so far.\nThe patient denied recent flights, a sedentary lifestyle, surgery, trauma, alcohol, tobacco, and drug use. There was neither a previous episode nor a family history of similar symptoms to her knowledge. Age-appropriate oncology screening was negative; mammogram from June 2020 was normal; colonoscopy four years before the presentation was also negative; Pap smears as well. Thrombophilia workup done by the Hematology/Oncology service was unrevealing, leading to a diagnosis of unprovoked DVT.\nThe curious part of the case is that even though thrombolysis and thrombectomy are considered the gold standard in the treatment of PCD, this patient had a spontaneous recovery only with heparin which serves as the only purpose to prevent the propagation of the thrombus. This specific patient according to Rutherford limb ischemia classification [] was a IIb which granted surgical intervention. Still, it remains unclear how such an extensive DVT improved in so quick fashion without thrombectomy/thrombolysis but seems that early use of heparin might have played an important role in the evolution of this patient's case and that early use of heparin might decrease the need for surgical intervention in some patients.

An 88-year-old man was admitted to our facility with altered mental status, hypotension (blood pressure range: 71-84/47-57 mmHg in the right arm supine position), fever (104oF), and tachycardia (heart rate: 140-150 beats/min) on arrival at the emergency room. Prior to admission, he was on hemodialysis for the past three months for end-stage renal disease secondary to rapidly progressive glomerulonephritis (has a right permacath). He was receiving intermittent heparin flushes along with dialysis to maintain the patency of the extracorporeal circuit. Other significant past medical history included a splenectomy in 2007. Clinical manifestations, imaging tests, and blood cultures suggested septic shock secondary to Streptococcal pneumonia. The patient was started on meropenem and vancomycin. A left internal jugular catheter and arterial line (in the right upper extremity) were placed for fluid resuscitation and blood pressure monitoring, respectively, and the patient was managed per surviving sepsis guidelines. On day three of hospitalization, the patient started to complain about a right-hand pain at the site of the arterial catheter. The physical examination was remarkable for a swollen and cyanotic right upper extremity, especially the second and third fingers (Figure ), with a barely palpable radial pulse compared to the left side. Arterial Doppler of the upper extremities was obtained, with findings indicative of significant right-sided arterial insufficiency. Further evaluation by venous duplex ultrasound identified a massive thrombus in the axillary, brachial, and basilic veins of the right arm with the solely spared ulna vein being hugely engorged (Figures -).\nWe considered the possibility of catheter-induced venous thrombosis, sepsis-associated disseminated intravascular coagulation and heparin-induced thrombocytopenia as working diagnoses. Given the suspicion of heparin-induced thrombocytopenia, we discontinued heparin immediately while the patient’s peripheral smear and coagulation cascade were investigated. Although the patient had low platelets (Table ), prolonged prothrombin time (16 (normal: 11-13 sec)), activated partial thromboplastin time (63 (normal: 25-35 sec)), elevated fibrin degradation products (>40 (normal: <10 mcg/ml)), which were suspicious for sepsis-related disseminated intravascular coagulation; normal factor VII (77 (normal: 50-150%)), high VIII levels (192 (normal: 50-150%)), normal haptoglobin (163 (normal: 36-195 mg/dl)), mildly decreased hemoglobulin (range: 12.1-12.9 (normal:13.5-17.5 g/dl)), and the presence of very few schistiocytes (<0.5%) on a peripheral smear made disseminated intravascular coagulation less likely. Laboratory data were remarkable for a significant drop in the platelet count from 234*109/L (on initiation of hemodialysis) to 44*109/L (the day of hospital admission) over the past three months. Based on the 4T score, heparin-induced thrombocytopenia was highly suspected and argatroban was initiated at 1 mg/kg/min. Vascular surgery consultation was obtained to address the gangrene in the second and third digits of the right upper extremity. However, considering his critically septic situation with multiple morbidities, a decision was made not to proceed with invasive maneuvers. On hospital day four, heparin-platelet factor 4 (PF4) antibodies (1.67 (normal: <0.4), heparin inhibition: >50%), and serotonin release assays returned positive (using enzyme-linked immunosorbent assay), confirming heparin-induced thrombocytopenia. On hospital day eight, repeated venous duplex demonstrated normal compressibility and spontaneous flow in the vein of the right upper extremity. The platelet count recovered and no further thrombotic complications were observed. Though we were able to manage the patient’s advanced gangrene with argatroban, his second and third fingers were amputated in the end.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A Hispanic 58-year-old female with a past medical history of gastritis arrived into the emergency room (ER) with acute onset severe pain on the left leg associated with discoloration of the leg. According to the patient, approximately three hours prior to her arrival to the ER, she was walking when, suddenly, she started experiencing sharp pain in her left leg which rapidly progressed. The physical examination was remarkable for left lower extremity pain, discoloration, edema, associated with tenderness to touch, diminished distal pulses, and reduce sensation and mobility throughout the leg, which can be appreciated below (Figure ).\nWithin the first 30 min after her arrival to the hospital, a pressure Doppler was performed where extensive deep vein thrombosis (DVT) (left femoral-popliteal venous thrombosis) (Figure ) diagnosis was made and within the subsequent 60 min, a computed tomography angiography (CTA) aorto-ilio-femoral runoff with delayed phase was performed, showing delayed opacification of arterial segments below the knee level (Figure ), confirming the diagnosis. A bolus of heparin was given, followed by an infusion. Thrombolysis was offered to the patient, however, she refused due to concern for side effects.\nAfter one hour of starting heparin infusion, blood flow to the leg was regained and the patient recovered full sensation and movement in the leg; coloration returned to normal in the affected leg. The patient was admitted for continued observation and discharged later on direct oral anticoagulants (DOACs) without any recurrence of DVT so far.\nThe patient denied recent flights, a sedentary lifestyle, surgery, trauma, alcohol, tobacco, and drug use. There was neither a previous episode nor a family history of similar symptoms to her knowledge. Age-appropriate oncology screening was negative; mammogram from June 2020 was normal; colonoscopy four years before the presentation was also negative; Pap smears as well. Thrombophilia workup done by the Hematology/Oncology service was unrevealing, leading to a diagnosis of unprovoked DVT.\nThe curious part of the case is that even though thrombolysis and thrombectomy are considered the gold standard in the treatment of PCD, this patient had a spontaneous recovery only with heparin which serves as the only purpose to prevent the propagation of the thrombus. This specific patient according to Rutherford limb ischemia classification [] was a IIb which granted surgical intervention. Still, it remains unclear how such an extensive DVT improved in so quick fashion without thrombectomy/thrombolysis but seems that early use of heparin might have played an important role in the evolution of this patient's case and that early use of heparin might decrease the need for surgical intervention in some patients.

A 64-year-old man with a history of obesity (BMI 38 Kg/m^2), arterial hypertension, atrial fibrillation, type 2 diabetes, chronic kidney disease, obstructive sleep apnea, and chronic venous insufficiency presented to the Emergency Department complaining of dyspnea, fever, and chest pain which started 7 days before. The patient was hypoxemic in room air (SpO2 80% and PaO2 43 mmHg). Inferior limbs appeared normal. A molecular swab formalized diagnosis of SARS-CoV2-related pneumonia. Respiratory distress progressed despite non-invasive-ventilation and hemodynamic instability requiring vasoactive support ensued. The patient was intubated and transferred to the ICU. The patient received invasive protective ventilation and hemodynamic support with noradrenaline. Gas exchange progressively worsened to a PaO2/FiO2 ratio of 70 mmHg. He developed a shock, and his lower limbs started to appear mottled. Lung and cardiac ultrasound were compatible with severe interstitial pneumonia and with no signs of pressure overload of the right heart. His coagulation profile was highly altered, as both aPTT and INR were elevated (respectively 2.28 seconds and 6.42), platelets were 164,000/mm3, and D-dimer was 117,521 UI/ml. Coagulation parameters continually worsened (), and treatment with one unit of fresh frozen plasma and vitamin K was required. Inferior limbs’ color progressively worsened, becoming frankly cyanotic, while pulses were still normal. Doppler ultrasound showed bilateral thrombosis of tibial and small saphenous veins. A continuous infusion of iloprost was started, as PCD was suspected (). Continuous infusion of unfractionated heparin was instituted, at a dose of 500-1000 IU per hour, according to aPTT, as well as continuous veno-venous hemodiafiltration as the patient developed acute kidney injury. The patient’s general conditions worsened (), and despite maximal treatment, he passed away after eight days of ICU care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A Hispanic 58-year-old female with a past medical history of gastritis arrived into the emergency room (ER) with acute onset severe pain on the left leg associated with discoloration of the leg. According to the patient, approximately three hours prior to her arrival to the ER, she was walking when, suddenly, she started experiencing sharp pain in her left leg which rapidly progressed. The physical examination was remarkable for left lower extremity pain, discoloration, edema, associated with tenderness to touch, diminished distal pulses, and reduce sensation and mobility throughout the leg, which can be appreciated below (Figure ).\nWithin the first 30 min after her arrival to the hospital, a pressure Doppler was performed where extensive deep vein thrombosis (DVT) (left femoral-popliteal venous thrombosis) (Figure ) diagnosis was made and within the subsequent 60 min, a computed tomography angiography (CTA) aorto-ilio-femoral runoff with delayed phase was performed, showing delayed opacification of arterial segments below the knee level (Figure ), confirming the diagnosis. A bolus of heparin was given, followed by an infusion. Thrombolysis was offered to the patient, however, she refused due to concern for side effects.\nAfter one hour of starting heparin infusion, blood flow to the leg was regained and the patient recovered full sensation and movement in the leg; coloration returned to normal in the affected leg. The patient was admitted for continued observation and discharged later on direct oral anticoagulants (DOACs) without any recurrence of DVT so far.\nThe patient denied recent flights, a sedentary lifestyle, surgery, trauma, alcohol, tobacco, and drug use. There was neither a previous episode nor a family history of similar symptoms to her knowledge. Age-appropriate oncology screening was negative; mammogram from June 2020 was normal; colonoscopy four years before the presentation was also negative; Pap smears as well. Thrombophilia workup done by the Hematology/Oncology service was unrevealing, leading to a diagnosis of unprovoked DVT.\nThe curious part of the case is that even though thrombolysis and thrombectomy are considered the gold standard in the treatment of PCD, this patient had a spontaneous recovery only with heparin which serves as the only purpose to prevent the propagation of the thrombus. This specific patient according to Rutherford limb ischemia classification [] was a IIb which granted surgical intervention. Still, it remains unclear how such an extensive DVT improved in so quick fashion without thrombectomy/thrombolysis but seems that early use of heparin might have played an important role in the evolution of this patient's case and that early use of heparin might decrease the need for surgical intervention in some patients.

A 21-year-old female college student presented to the emergency department (ED) with severe pain in her left hip, thigh, and calf. The pain started suddenly when she was playing basketball a few hours earlier. She twisted her torso to shoot the ball and heard a “pop” in her left hip with immediate onset of pain, and she subsequently fell to her knees. She was initially able to ambulate but had worsening pain and rapid progression of swelling and mottling in the left leg from her hip to her ankle. She denied any pain or swelling in that extremity prior to the injury during the basketball game. With the exception of oral contraceptive use, she had no significant medical or family history.\nOn examination her left extremity was mottled, dusky, and cool to the touch from the hip to the toes and she had decreased dorsalis pedis and posterior tibial pulses when compared with the right extremity. The leg was markedly tender to palpation and sensation to light touch was diminished. Passive range of motion of the hip, knee, and ankle elicited severe pain.\nPOCUS was performed at the bedside to evaluate for arterial blood flow and deep venous thrombosis. This demonstrated normal color flow in the femoral and popliteal arteries (), but echogenic material was noted within the left common femoral vein extending distally to the popliteal vein and the veins were non-compressible (). Vascular surgery was immediately consulted, and while awaiting their arrival to the ED the patient was sent for an emergent computed tomography (CT) angiogram, which confirmed arterial patency and extensive deep venous thrombosis in the left popliteal, femoral, and iliac veins (). A heparin bolus was given and the patient was then taken to interventional radiology where she underwent partial thrombectomy, catheter-directed tissue plasminogen activator (tPA) treatment, and placement of an inferior vena cava (IVC) filter. By the next morning her leg was noted to be well-perfused, non-tender, and without swelling, and her pain had resolved. A workup for hypercoagulable states revealed heterozygosity for the Factor V Leiden mutation. She was discharged one week later on warfarin after bridging from enoxaparin.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A Hispanic 58-year-old female with a past medical history of gastritis arrived into the emergency room (ER) with acute onset severe pain on the left leg associated with discoloration of the leg. According to the patient, approximately three hours prior to her arrival to the ER, she was walking when, suddenly, she started experiencing sharp pain in her left leg which rapidly progressed. The physical examination was remarkable for left lower extremity pain, discoloration, edema, associated with tenderness to touch, diminished distal pulses, and reduce sensation and mobility throughout the leg, which can be appreciated below (Figure ).\nWithin the first 30 min after her arrival to the hospital, a pressure Doppler was performed where extensive deep vein thrombosis (DVT) (left femoral-popliteal venous thrombosis) (Figure ) diagnosis was made and within the subsequent 60 min, a computed tomography angiography (CTA) aorto-ilio-femoral runoff with delayed phase was performed, showing delayed opacification of arterial segments below the knee level (Figure ), confirming the diagnosis. A bolus of heparin was given, followed by an infusion. Thrombolysis was offered to the patient, however, she refused due to concern for side effects.\nAfter one hour of starting heparin infusion, blood flow to the leg was regained and the patient recovered full sensation and movement in the leg; coloration returned to normal in the affected leg. The patient was admitted for continued observation and discharged later on direct oral anticoagulants (DOACs) without any recurrence of DVT so far.\nThe patient denied recent flights, a sedentary lifestyle, surgery, trauma, alcohol, tobacco, and drug use. There was neither a previous episode nor a family history of similar symptoms to her knowledge. Age-appropriate oncology screening was negative; mammogram from June 2020 was normal; colonoscopy four years before the presentation was also negative; Pap smears as well. Thrombophilia workup done by the Hematology/Oncology service was unrevealing, leading to a diagnosis of unprovoked DVT.\nThe curious part of the case is that even though thrombolysis and thrombectomy are considered the gold standard in the treatment of PCD, this patient had a spontaneous recovery only with heparin which serves as the only purpose to prevent the propagation of the thrombus. This specific patient according to Rutherford limb ischemia classification [] was a IIb which granted surgical intervention. Still, it remains unclear how such an extensive DVT improved in so quick fashion without thrombectomy/thrombolysis but seems that early use of heparin might have played an important role in the evolution of this patient's case and that early use of heparin might decrease the need for surgical intervention in some patients.

A 66-year-old female presented to the emergency department with three days of acute LLE swelling, pain, cyanosis, inability to bear weight, dyspnea, and hypoxemia (Figure ). She denied recent travel, hormone replacement, or a history of DVT/pulmonary embolism (PE). Her medical history was notable for systemic lupus erythematosus, CREST (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome, Sjogren’s syndrome, and local invasive anal squamous cell carcinoma. Doppler ultrasound revealed LLE thrombus extending from the greater saphenous vein to the popliteal vein. She was admitted to the intensive care unit (ICU) and started on an unfractionated heparin drip.\nThe vascular surgery team was consulted for surgical intervention. After further review of her case, the vascular surgery team elected for an endovascular approach with CDT of LLE. Initial venogram demonstrated extensive clotting of the tibial, popliteal, and femoral venous systems extending into the iliac system (Figures , ). From a tibial approach, a guidewire was advanced up to the common iliac, but a chronic occlusion of the left common iliac vein was found, which could not be crossed. A venous collateral circulation system in communication with the right iliac venous system was identified. In order to decrease the overall clot burden, two 50-cm EKOS endovascular catheters were placed in the left external iliac vein and collateral system. Repeat venogram at 24 hours post-CDT showed significant improvement of the overall clot burden with almost complete resolution of the clot in the LLE; however, the chronic occlusion remained (Figure ). A 20 x 80 mm Boston Scientific Wallstent™ (endoprosthesis stent) was advanced across the total chronic total occlusion and deployed. Post-operative venogram demonstrated significant improvement in flow in the system, with all flow going through the iliac system, and no flow further through the previously seen collaterals. Intravascular ultrasound was advanced through the area, which showed severe compression of the stent. A 12x 40 mm Atlas® dilatation catheter (Bard Peripheral Vascular Inc., Tempe, AZ, USA) was used for angioplasty. Repeat intravascular ultrasound showed persistent compression of the area. A 8 x 40 mm Boston Scientific Mustang™ dilatation catheter (high-pressure balloon) was used to re-attempt angioplasty; however, compression was still noted (Figure ). Regardless, outflow improved throughout the left common iliac system, and no further interventions were performed. The patient returned to the ICU and transitioned to direct oral anticoagulation without any further complications. She was subsequently transferred to a medicine ward for further care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A Hispanic 58-year-old female with a past medical history of gastritis arrived into the emergency room (ER) with acute onset severe pain on the left leg associated with discoloration of the leg. According to the patient, approximately three hours prior to her arrival to the ER, she was walking when, suddenly, she started experiencing sharp pain in her left leg which rapidly progressed. The physical examination was remarkable for left lower extremity pain, discoloration, edema, associated with tenderness to touch, diminished distal pulses, and reduce sensation and mobility throughout the leg, which can be appreciated below (Figure ).\nWithin the first 30 min after her arrival to the hospital, a pressure Doppler was performed where extensive deep vein thrombosis (DVT) (left femoral-popliteal venous thrombosis) (Figure ) diagnosis was made and within the subsequent 60 min, a computed tomography angiography (CTA) aorto-ilio-femoral runoff with delayed phase was performed, showing delayed opacification of arterial segments below the knee level (Figure ), confirming the diagnosis. A bolus of heparin was given, followed by an infusion. Thrombolysis was offered to the patient, however, she refused due to concern for side effects.\nAfter one hour of starting heparin infusion, blood flow to the leg was regained and the patient recovered full sensation and movement in the leg; coloration returned to normal in the affected leg. The patient was admitted for continued observation and discharged later on direct oral anticoagulants (DOACs) without any recurrence of DVT so far.\nThe patient denied recent flights, a sedentary lifestyle, surgery, trauma, alcohol, tobacco, and drug use. There was neither a previous episode nor a family history of similar symptoms to her knowledge. Age-appropriate oncology screening was negative; mammogram from June 2020 was normal; colonoscopy four years before the presentation was also negative; Pap smears as well. Thrombophilia workup done by the Hematology/Oncology service was unrevealing, leading to a diagnosis of unprovoked DVT.\nThe curious part of the case is that even though thrombolysis and thrombectomy are considered the gold standard in the treatment of PCD, this patient had a spontaneous recovery only with heparin which serves as the only purpose to prevent the propagation of the thrombus. This specific patient according to Rutherford limb ischemia classification [] was a IIb which granted surgical intervention. Still, it remains unclear how such an extensive DVT improved in so quick fashion without thrombectomy/thrombolysis but seems that early use of heparin might have played an important role in the evolution of this patient's case and that early use of heparin might decrease the need for surgical intervention in some patients.

A 49-year-old Chinese man sustained severe knife trauma and was referred to a local hospital. An exploratory laparotomy showed traumatic rupture of his left external iliac vein with massive intraperitoneal bleeding, but his iliac artery was intact. To rescue him, the proximal and distal parts of his injured external iliac vein were ligated (there was no vascular surgeon in the local hospital); however, his left leg quickly became severely swollen, cyanotic and pulseless. Two hours after the first operation, he was transferred to the emergency department of our university hospital with endotracheal tube intubation. On physical examination, he was tachycardic (142 beats per minute), hypotensive (86/50mmHg). His left lower extremity was markedly edematous, cyanotic, mottled (Figure \na) and had no palpable pulse, but his right lower extremity was normal. He was diagnosed with posttraumatic PCD. Considering the high risk of pulmonary embolism during the next surgical procedure, an OptEase® retrievable vena cava filter (Cordis Corp., New Brunswick, NJ, USA) was placed in his inferior vena cava via his right femoral vein under digital subtraction angiography (Figure \n). His abdomen was immediately reopened while his left leg was also prepared for treatment.During the second emergent laparotomy, there was less blood in his pelvic cavity. No active bleeding was identified. His left iliac vein and artery were exposed and his entire iliac artery appeared normal and without rupture. His external iliac vein was ligated but not transected, connected only by the posterior wall, and the caudal part of his iliac vein was significantly dilated. By replacing the vascular clamp in the proximal and distal parts of the rupture, the ligations on both sides of the venous rupture were resolved. A wedge-shaped rupture was revealed, approximately 4cm in length, on the anterolateral side of his left external iliac vein. The edges of the venous rupture were smooth as a result of the knife trauma. Although the ligated parts of his iliac vein appeared congested, the lumen was smooth and contained no clot. The damaged vein was repaired with continuous 4-0 Prolene sutures (Ethicon, Inc, Somerville, NJ, USA) after the patient was systemically heparinized with 5000 units heparin. Before the sutures were finally ligated, the clamp at the cranial aspect was removed and the caudal clamp was left in place. After the backflow was clear of thrombotic debris, the clamp on his caudal iliac vein was removed and the clamp at the cranial aspect left in place. The left leg was gently massaged from calf to thigh; as a result, some thrombi in the caudal part of the vein were flushed out with the venous blood flow, and the sutures were finally ligated until the venous blood was free of thrombus. His iliac vein, although narrower after repair, was patent (Figure \n).\nAfter the operation, the patient was sent to the surgical intensive care unit with mechanical ventilation. Despite the fact that his left leg showed some signs of compartment syndrome with blisters in his calf, fasciotomy was not performed. He received systemic anticoagulation, initially with low-molecular-weight heparin, then with warfarin, titrating to an international normalized ratio (INR) between 2.0 and 2.5.Three days postoperatively, mechanical ventilation was discontinued and his signs and symptoms improved dramatically. Pulses in his left lower extremity became palpable on postoperative day 5, and the swelling and discoloration decreased. On postoperative day 30, he was taken off the OptEase® filter and the venogram showed a small amount of residual thrombus in his left external iliac vein (Figure \n). The inferior vena cava was patent, with no residual defects around the filter and no thrombus in the filter. He was discharged from the hospital in a stable condition, with full resolution of symptoms, on postoperative day 35 (Figure \nb). He was mostly asymptomatic at a recent 3-month follow-up visit except for slight edema in his left leg after walking. He continues on warfarin, maintaining an INR between 2.0 and 2.5, and wears elastic compression stockings.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A Hispanic 58-year-old female with a past medical history of gastritis arrived into the emergency room (ER) with acute onset severe pain on the left leg associated with discoloration of the leg. According to the patient, approximately three hours prior to her arrival to the ER, she was walking when, suddenly, she started experiencing sharp pain in her left leg which rapidly progressed. The physical examination was remarkable for left lower extremity pain, discoloration, edema, associated with tenderness to touch, diminished distal pulses, and reduce sensation and mobility throughout the leg, which can be appreciated below (Figure ).\nWithin the first 30 min after her arrival to the hospital, a pressure Doppler was performed where extensive deep vein thrombosis (DVT) (left femoral-popliteal venous thrombosis) (Figure ) diagnosis was made and within the subsequent 60 min, a computed tomography angiography (CTA) aorto-ilio-femoral runoff with delayed phase was performed, showing delayed opacification of arterial segments below the knee level (Figure ), confirming the diagnosis. A bolus of heparin was given, followed by an infusion. Thrombolysis was offered to the patient, however, she refused due to concern for side effects.\nAfter one hour of starting heparin infusion, blood flow to the leg was regained and the patient recovered full sensation and movement in the leg; coloration returned to normal in the affected leg. The patient was admitted for continued observation and discharged later on direct oral anticoagulants (DOACs) without any recurrence of DVT so far.\nThe patient denied recent flights, a sedentary lifestyle, surgery, trauma, alcohol, tobacco, and drug use. There was neither a previous episode nor a family history of similar symptoms to her knowledge. Age-appropriate oncology screening was negative; mammogram from June 2020 was normal; colonoscopy four years before the presentation was also negative; Pap smears as well. Thrombophilia workup done by the Hematology/Oncology service was unrevealing, leading to a diagnosis of unprovoked DVT.\nThe curious part of the case is that even though thrombolysis and thrombectomy are considered the gold standard in the treatment of PCD, this patient had a spontaneous recovery only with heparin which serves as the only purpose to prevent the propagation of the thrombus. This specific patient according to Rutherford limb ischemia classification [] was a IIb which granted surgical intervention. Still, it remains unclear how such an extensive DVT improved in so quick fashion without thrombectomy/thrombolysis but seems that early use of heparin might have played an important role in the evolution of this patient's case and that early use of heparin might decrease the need for surgical intervention in some patients.

The patient is a 78-year-old woman who presented to emergency department with 2 days of gradually worsening right lower extremity (RLE) swelling, pain, and paresthesia that was limiting mobility. She was independent with a clinical frailty score of 2. Her past medical history was significant for diabetes mellitus with Hgb a1c 10.5 and a provoked left lower extremity DVT 30 years earlier treated with a course of warfarin and permanent IVC filter placement. She denied prior hypercoagulability workup and reported that her first episode of thrombosis followed a prolonged airplane ride. She was not anticoagulated at the time of presentation. She denied a history of dysrhythmias, prior embolic events, recent travel, injury, surgery, illness, or known exposure to COVID-19. She denied a family history of blood clots or hypercoagulability.\nPhysical examination revealed an RLE that was severely taut with cyanosis with nonpalpable peripheral pulses and multiphasic signaling on Doppler and tenderness to the mid-thigh. The contralateral limb was soft, nontender with color appropriate of ethnicity and palpable peripheral pulses. An RLE venous duplex ultrasound scan was performed with noncompressible veins and loss of spontaneous flow from the right popliteal vein extending to the right common femoral vein consistent with DVT. On presentation, she did not display hemodynamic instability nor complained of cardiopulmonary symptoms.\nBecause of progressive symptoms concerning for PCD and imminent development of venous gangrene in a patient with good functional status, she was admitted directly to the angiography suite for CDT and pharmacomechanical thrombectomy with tissue plasminogen activator (tPA) and heparin. Angiogram revealed thrombus extending proximal to the IVC filter in the mid-IVC (). She was transferred to the intensive care unit for continued CDT with tPA (1 mg/h) and heparin (500 u/h) through a Uni∗Fuse catheter. tPA was discontinued overnight for a fibrinogen of 82 mg/dL. The next morning, she reported subjective improvement of symptoms and return of palpable peripheral pulses with resolution of pain. She returned to the angiography suite for catheter removal and completion venogram that revealed persistent thrombus burden, and the decision to remove the remainder of the clot was made to decrease the risk of recurrence. Using the Penumbra Indigo CAT8 system (Penumbra, Alameda, Calif), mechanical suction thrombectomy, and balloon venoplasty were performed with successful recanalization (). She was transferred to the floor, heparin was discontinued, and rivaroxaban initiated.\nOn postoperative day 2, she was noted to have expressive aphasia and left-sided hemiplegia. A noncontrast computed tomography and computed tomography angiogram of the head and neck were performed without evidence of a hemorrhage or significant carotid or aortic arch atherosclerotic disease. International normalized ratio was therapeutic at 2.0. Given the concern for stroke, a diffusion-weighted magnetic resonance imaging of the brain was obtained () and was notable for the focal area of restricted diffusion within the right thalamus. Because of recent anticoagulation and thrombolysis, she was not a candidate for systemic tPA. Heparin was not reinitiated because of therapeutic international normalized ratio on rivaroxaban. She was transferred to a tertiary center with neurological and neurosurgical capabilities where she underwent a transesophageal echocardiogram with bubble study that revealed a PFO with an atrial septal aneurysm and left-to-right flow noted with color Doppler and a moderate right-to-left shunt during bubble study but no left atrial mass or thrombus. Rivaroxaban was continued and her neurological status improved. She was discharged to a rehabilitation facility with improved left-sided weakness on postoperative day 3. After 2 weeks of rehabilitation, the patient was discharged with a modified Rankin score of 1. Patency of the RLE veins was unknown at the time of discharge, but a repeat duplex ultrasound scan at 8 months after initial presentation showed chronic thrombus in the right common femoral vein, but the RLE venous system remained patent.\nBecause of multiple episodes of thrombosis, she was placed on lifelong anticoagulation with apixaban. Hypercoagulable disorder was suspected but was deferred by her hematologist as diagnosis would not change plan for management.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 49-year-old woman presented with acute coronary syndrome for which she received aspirin, clopidogrel, atorvastatin, enoxaparin, and tenecteplase at another facility. She was then transferred to our institute for further management. She underwent coronary angiography which was suggestive of triple vessel disease. As the patient was in acute congestive heart failure (Killip IV) with pulmonary edema, she was intubated and mechanically ventilated. She underwent coronary artery bypass grafting surgery the following day where she received 20,000U of unfractionated heparin.\nOn postoperative day (POD) 6, the patient developed right pedal edema with cyanosis. Bilateral lower limbs Arterial Doppler was normal. Venous Doppler of the right lower limb was suggestive of thrombosis of the right Common Femoral, Superficial Femoral, Popliteal, and Great Saphenous Veins. She also had progressively worsening thrombocytopenia in which the platelet count dropped from 297 × 109/L on day 1 of postenoxaparin exposure to a nadir of 20 × 109/L on day 8. With a suspicion of HIT and thrombosis (HITT), enoxaparin was replaced with fondaparinux on POD 7. She tested positive for HIT type 2 antibodies on day 10. Her platelets started improving by POD 11 [].\nOn POD 13, two-dimensional echocardiography done was suggestive of a left ventricular thrombus (with an ejection fraction of 25%) which resolved completely by POD 44 with anticoagulation. Fondaparinux was bridged with oral Vitamin K Antagonist-Acenocoumarol for HITT and PCD. Once there was a line of demarcation for gangrene, she underwent a right forefoot amputation on POD 34.\nThe patient was discharged on POD 47 with medications for cardiac failure along with acenocoumarol.

An 88-year-old man was admitted to our facility with altered mental status, hypotension (blood pressure range: 71-84/47-57 mmHg in the right arm supine position), fever (104oF), and tachycardia (heart rate: 140-150 beats/min) on arrival at the emergency room. Prior to admission, he was on hemodialysis for the past three months for end-stage renal disease secondary to rapidly progressive glomerulonephritis (has a right permacath). He was receiving intermittent heparin flushes along with dialysis to maintain the patency of the extracorporeal circuit. Other significant past medical history included a splenectomy in 2007. Clinical manifestations, imaging tests, and blood cultures suggested septic shock secondary to Streptococcal pneumonia. The patient was started on meropenem and vancomycin. A left internal jugular catheter and arterial line (in the right upper extremity) were placed for fluid resuscitation and blood pressure monitoring, respectively, and the patient was managed per surviving sepsis guidelines. On day three of hospitalization, the patient started to complain about a right-hand pain at the site of the arterial catheter. The physical examination was remarkable for a swollen and cyanotic right upper extremity, especially the second and third fingers (Figure ), with a barely palpable radial pulse compared to the left side. Arterial Doppler of the upper extremities was obtained, with findings indicative of significant right-sided arterial insufficiency. Further evaluation by venous duplex ultrasound identified a massive thrombus in the axillary, brachial, and basilic veins of the right arm with the solely spared ulna vein being hugely engorged (Figures -).\nWe considered the possibility of catheter-induced venous thrombosis, sepsis-associated disseminated intravascular coagulation and heparin-induced thrombocytopenia as working diagnoses. Given the suspicion of heparin-induced thrombocytopenia, we discontinued heparin immediately while the patient’s peripheral smear and coagulation cascade were investigated. Although the patient had low platelets (Table ), prolonged prothrombin time (16 (normal: 11-13 sec)), activated partial thromboplastin time (63 (normal: 25-35 sec)), elevated fibrin degradation products (>40 (normal: <10 mcg/ml)), which were suspicious for sepsis-related disseminated intravascular coagulation; normal factor VII (77 (normal: 50-150%)), high VIII levels (192 (normal: 50-150%)), normal haptoglobin (163 (normal: 36-195 mg/dl)), mildly decreased hemoglobulin (range: 12.1-12.9 (normal:13.5-17.5 g/dl)), and the presence of very few schistiocytes (<0.5%) on a peripheral smear made disseminated intravascular coagulation less likely. Laboratory data were remarkable for a significant drop in the platelet count from 234*109/L (on initiation of hemodialysis) to 44*109/L (the day of hospital admission) over the past three months. Based on the 4T score, heparin-induced thrombocytopenia was highly suspected and argatroban was initiated at 1 mg/kg/min. Vascular surgery consultation was obtained to address the gangrene in the second and third digits of the right upper extremity. However, considering his critically septic situation with multiple morbidities, a decision was made not to proceed with invasive maneuvers. On hospital day four, heparin-platelet factor 4 (PF4) antibodies (1.67 (normal: <0.4), heparin inhibition: >50%), and serotonin release assays returned positive (using enzyme-linked immunosorbent assay), confirming heparin-induced thrombocytopenia. On hospital day eight, repeated venous duplex demonstrated normal compressibility and spontaneous flow in the vein of the right upper extremity. The platelet count recovered and no further thrombotic complications were observed. Though we were able to manage the patient’s advanced gangrene with argatroban, his second and third fingers were amputated in the end.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 49-year-old woman presented with acute coronary syndrome for which she received aspirin, clopidogrel, atorvastatin, enoxaparin, and tenecteplase at another facility. She was then transferred to our institute for further management. She underwent coronary angiography which was suggestive of triple vessel disease. As the patient was in acute congestive heart failure (Killip IV) with pulmonary edema, she was intubated and mechanically ventilated. She underwent coronary artery bypass grafting surgery the following day where she received 20,000U of unfractionated heparin.\nOn postoperative day (POD) 6, the patient developed right pedal edema with cyanosis. Bilateral lower limbs Arterial Doppler was normal. Venous Doppler of the right lower limb was suggestive of thrombosis of the right Common Femoral, Superficial Femoral, Popliteal, and Great Saphenous Veins. She also had progressively worsening thrombocytopenia in which the platelet count dropped from 297 × 109/L on day 1 of postenoxaparin exposure to a nadir of 20 × 109/L on day 8. With a suspicion of HIT and thrombosis (HITT), enoxaparin was replaced with fondaparinux on POD 7. She tested positive for HIT type 2 antibodies on day 10. Her platelets started improving by POD 11 [].\nOn POD 13, two-dimensional echocardiography done was suggestive of a left ventricular thrombus (with an ejection fraction of 25%) which resolved completely by POD 44 with anticoagulation. Fondaparinux was bridged with oral Vitamin K Antagonist-Acenocoumarol for HITT and PCD. Once there was a line of demarcation for gangrene, she underwent a right forefoot amputation on POD 34.\nThe patient was discharged on POD 47 with medications for cardiac failure along with acenocoumarol.

A 64-year-old man with a history of obesity (BMI 38 Kg/m^2), arterial hypertension, atrial fibrillation, type 2 diabetes, chronic kidney disease, obstructive sleep apnea, and chronic venous insufficiency presented to the Emergency Department complaining of dyspnea, fever, and chest pain which started 7 days before. The patient was hypoxemic in room air (SpO2 80% and PaO2 43 mmHg). Inferior limbs appeared normal. A molecular swab formalized diagnosis of SARS-CoV2-related pneumonia. Respiratory distress progressed despite non-invasive-ventilation and hemodynamic instability requiring vasoactive support ensued. The patient was intubated and transferred to the ICU. The patient received invasive protective ventilation and hemodynamic support with noradrenaline. Gas exchange progressively worsened to a PaO2/FiO2 ratio of 70 mmHg. He developed a shock, and his lower limbs started to appear mottled. Lung and cardiac ultrasound were compatible with severe interstitial pneumonia and with no signs of pressure overload of the right heart. His coagulation profile was highly altered, as both aPTT and INR were elevated (respectively 2.28 seconds and 6.42), platelets were 164,000/mm3, and D-dimer was 117,521 UI/ml. Coagulation parameters continually worsened (), and treatment with one unit of fresh frozen plasma and vitamin K was required. Inferior limbs’ color progressively worsened, becoming frankly cyanotic, while pulses were still normal. Doppler ultrasound showed bilateral thrombosis of tibial and small saphenous veins. A continuous infusion of iloprost was started, as PCD was suspected (). Continuous infusion of unfractionated heparin was instituted, at a dose of 500-1000 IU per hour, according to aPTT, as well as continuous veno-venous hemodiafiltration as the patient developed acute kidney injury. The patient’s general conditions worsened (), and despite maximal treatment, he passed away after eight days of ICU care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 21-year-old female college student presented to the emergency department (ED) with severe pain in her left hip, thigh, and calf. The pain started suddenly when she was playing basketball a few hours earlier. She twisted her torso to shoot the ball and heard a “pop” in her left hip with immediate onset of pain, and she subsequently fell to her knees. She was initially able to ambulate but had worsening pain and rapid progression of swelling and mottling in the left leg from her hip to her ankle. She denied any pain or swelling in that extremity prior to the injury during the basketball game. With the exception of oral contraceptive use, she had no significant medical or family history.\nOn examination her left extremity was mottled, dusky, and cool to the touch from the hip to the toes and she had decreased dorsalis pedis and posterior tibial pulses when compared with the right extremity. The leg was markedly tender to palpation and sensation to light touch was diminished. Passive range of motion of the hip, knee, and ankle elicited severe pain.\nPOCUS was performed at the bedside to evaluate for arterial blood flow and deep venous thrombosis. This demonstrated normal color flow in the femoral and popliteal arteries (), but echogenic material was noted within the left common femoral vein extending distally to the popliteal vein and the veins were non-compressible (). Vascular surgery was immediately consulted, and while awaiting their arrival to the ED the patient was sent for an emergent computed tomography (CT) angiogram, which confirmed arterial patency and extensive deep venous thrombosis in the left popliteal, femoral, and iliac veins (). A heparin bolus was given and the patient was then taken to interventional radiology where she underwent partial thrombectomy, catheter-directed tissue plasminogen activator (tPA) treatment, and placement of an inferior vena cava (IVC) filter. By the next morning her leg was noted to be well-perfused, non-tender, and without swelling, and her pain had resolved. A workup for hypercoagulable states revealed heterozygosity for the Factor V Leiden mutation. She was discharged one week later on warfarin after bridging from enoxaparin.

A 49-year-old woman presented with acute coronary syndrome for which she received aspirin, clopidogrel, atorvastatin, enoxaparin, and tenecteplase at another facility. She was then transferred to our institute for further management. She underwent coronary angiography which was suggestive of triple vessel disease. As the patient was in acute congestive heart failure (Killip IV) with pulmonary edema, she was intubated and mechanically ventilated. She underwent coronary artery bypass grafting surgery the following day where she received 20,000U of unfractionated heparin.\nOn postoperative day (POD) 6, the patient developed right pedal edema with cyanosis. Bilateral lower limbs Arterial Doppler was normal. Venous Doppler of the right lower limb was suggestive of thrombosis of the right Common Femoral, Superficial Femoral, Popliteal, and Great Saphenous Veins. She also had progressively worsening thrombocytopenia in which the platelet count dropped from 297 × 109/L on day 1 of postenoxaparin exposure to a nadir of 20 × 109/L on day 8. With a suspicion of HIT and thrombosis (HITT), enoxaparin was replaced with fondaparinux on POD 7. She tested positive for HIT type 2 antibodies on day 10. Her platelets started improving by POD 11 [].\nOn POD 13, two-dimensional echocardiography done was suggestive of a left ventricular thrombus (with an ejection fraction of 25%) which resolved completely by POD 44 with anticoagulation. Fondaparinux was bridged with oral Vitamin K Antagonist-Acenocoumarol for HITT and PCD. Once there was a line of demarcation for gangrene, she underwent a right forefoot amputation on POD 34.\nThe patient was discharged on POD 47 with medications for cardiac failure along with acenocoumarol.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 49-year-old woman presented with acute coronary syndrome for which she received aspirin, clopidogrel, atorvastatin, enoxaparin, and tenecteplase at another facility. She was then transferred to our institute for further management. She underwent coronary angiography which was suggestive of triple vessel disease. As the patient was in acute congestive heart failure (Killip IV) with pulmonary edema, she was intubated and mechanically ventilated. She underwent coronary artery bypass grafting surgery the following day where she received 20,000U of unfractionated heparin.\nOn postoperative day (POD) 6, the patient developed right pedal edema with cyanosis. Bilateral lower limbs Arterial Doppler was normal. Venous Doppler of the right lower limb was suggestive of thrombosis of the right Common Femoral, Superficial Femoral, Popliteal, and Great Saphenous Veins. She also had progressively worsening thrombocytopenia in which the platelet count dropped from 297 × 109/L on day 1 of postenoxaparin exposure to a nadir of 20 × 109/L on day 8. With a suspicion of HIT and thrombosis (HITT), enoxaparin was replaced with fondaparinux on POD 7. She tested positive for HIT type 2 antibodies on day 10. Her platelets started improving by POD 11 [].\nOn POD 13, two-dimensional echocardiography done was suggestive of a left ventricular thrombus (with an ejection fraction of 25%) which resolved completely by POD 44 with anticoagulation. Fondaparinux was bridged with oral Vitamin K Antagonist-Acenocoumarol for HITT and PCD. Once there was a line of demarcation for gangrene, she underwent a right forefoot amputation on POD 34.\nThe patient was discharged on POD 47 with medications for cardiac failure along with acenocoumarol.

A 66-year-old female presented to the emergency department with three days of acute LLE swelling, pain, cyanosis, inability to bear weight, dyspnea, and hypoxemia (Figure ). She denied recent travel, hormone replacement, or a history of DVT/pulmonary embolism (PE). Her medical history was notable for systemic lupus erythematosus, CREST (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome, Sjogren’s syndrome, and local invasive anal squamous cell carcinoma. Doppler ultrasound revealed LLE thrombus extending from the greater saphenous vein to the popliteal vein. She was admitted to the intensive care unit (ICU) and started on an unfractionated heparin drip.\nThe vascular surgery team was consulted for surgical intervention. After further review of her case, the vascular surgery team elected for an endovascular approach with CDT of LLE. Initial venogram demonstrated extensive clotting of the tibial, popliteal, and femoral venous systems extending into the iliac system (Figures , ). From a tibial approach, a guidewire was advanced up to the common iliac, but a chronic occlusion of the left common iliac vein was found, which could not be crossed. A venous collateral circulation system in communication with the right iliac venous system was identified. In order to decrease the overall clot burden, two 50-cm EKOS endovascular catheters were placed in the left external iliac vein and collateral system. Repeat venogram at 24 hours post-CDT showed significant improvement of the overall clot burden with almost complete resolution of the clot in the LLE; however, the chronic occlusion remained (Figure ). A 20 x 80 mm Boston Scientific Wallstent™ (endoprosthesis stent) was advanced across the total chronic total occlusion and deployed. Post-operative venogram demonstrated significant improvement in flow in the system, with all flow going through the iliac system, and no flow further through the previously seen collaterals. Intravascular ultrasound was advanced through the area, which showed severe compression of the stent. A 12x 40 mm Atlas® dilatation catheter (Bard Peripheral Vascular Inc., Tempe, AZ, USA) was used for angioplasty. Repeat intravascular ultrasound showed persistent compression of the area. A 8 x 40 mm Boston Scientific Mustang™ dilatation catheter (high-pressure balloon) was used to re-attempt angioplasty; however, compression was still noted (Figure ). Regardless, outflow improved throughout the left common iliac system, and no further interventions were performed. The patient returned to the ICU and transitioned to direct oral anticoagulation without any further complications. She was subsequently transferred to a medicine ward for further care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 49-year-old woman presented with acute coronary syndrome for which she received aspirin, clopidogrel, atorvastatin, enoxaparin, and tenecteplase at another facility. She was then transferred to our institute for further management. She underwent coronary angiography which was suggestive of triple vessel disease. As the patient was in acute congestive heart failure (Killip IV) with pulmonary edema, she was intubated and mechanically ventilated. She underwent coronary artery bypass grafting surgery the following day where she received 20,000U of unfractionated heparin.\nOn postoperative day (POD) 6, the patient developed right pedal edema with cyanosis. Bilateral lower limbs Arterial Doppler was normal. Venous Doppler of the right lower limb was suggestive of thrombosis of the right Common Femoral, Superficial Femoral, Popliteal, and Great Saphenous Veins. She also had progressively worsening thrombocytopenia in which the platelet count dropped from 297 × 109/L on day 1 of postenoxaparin exposure to a nadir of 20 × 109/L on day 8. With a suspicion of HIT and thrombosis (HITT), enoxaparin was replaced with fondaparinux on POD 7. She tested positive for HIT type 2 antibodies on day 10. Her platelets started improving by POD 11 [].\nOn POD 13, two-dimensional echocardiography done was suggestive of a left ventricular thrombus (with an ejection fraction of 25%) which resolved completely by POD 44 with anticoagulation. Fondaparinux was bridged with oral Vitamin K Antagonist-Acenocoumarol for HITT and PCD. Once there was a line of demarcation for gangrene, she underwent a right forefoot amputation on POD 34.\nThe patient was discharged on POD 47 with medications for cardiac failure along with acenocoumarol.

A 49-year-old Chinese man sustained severe knife trauma and was referred to a local hospital. An exploratory laparotomy showed traumatic rupture of his left external iliac vein with massive intraperitoneal bleeding, but his iliac artery was intact. To rescue him, the proximal and distal parts of his injured external iliac vein were ligated (there was no vascular surgeon in the local hospital); however, his left leg quickly became severely swollen, cyanotic and pulseless. Two hours after the first operation, he was transferred to the emergency department of our university hospital with endotracheal tube intubation. On physical examination, he was tachycardic (142 beats per minute), hypotensive (86/50mmHg). His left lower extremity was markedly edematous, cyanotic, mottled (Figure \na) and had no palpable pulse, but his right lower extremity was normal. He was diagnosed with posttraumatic PCD. Considering the high risk of pulmonary embolism during the next surgical procedure, an OptEase® retrievable vena cava filter (Cordis Corp., New Brunswick, NJ, USA) was placed in his inferior vena cava via his right femoral vein under digital subtraction angiography (Figure \n). His abdomen was immediately reopened while his left leg was also prepared for treatment.During the second emergent laparotomy, there was less blood in his pelvic cavity. No active bleeding was identified. His left iliac vein and artery were exposed and his entire iliac artery appeared normal and without rupture. His external iliac vein was ligated but not transected, connected only by the posterior wall, and the caudal part of his iliac vein was significantly dilated. By replacing the vascular clamp in the proximal and distal parts of the rupture, the ligations on both sides of the venous rupture were resolved. A wedge-shaped rupture was revealed, approximately 4cm in length, on the anterolateral side of his left external iliac vein. The edges of the venous rupture were smooth as a result of the knife trauma. Although the ligated parts of his iliac vein appeared congested, the lumen was smooth and contained no clot. The damaged vein was repaired with continuous 4-0 Prolene sutures (Ethicon, Inc, Somerville, NJ, USA) after the patient was systemically heparinized with 5000 units heparin. Before the sutures were finally ligated, the clamp at the cranial aspect was removed and the caudal clamp was left in place. After the backflow was clear of thrombotic debris, the clamp on his caudal iliac vein was removed and the clamp at the cranial aspect left in place. The left leg was gently massaged from calf to thigh; as a result, some thrombi in the caudal part of the vein were flushed out with the venous blood flow, and the sutures were finally ligated until the venous blood was free of thrombus. His iliac vein, although narrower after repair, was patent (Figure \n).\nAfter the operation, the patient was sent to the surgical intensive care unit with mechanical ventilation. Despite the fact that his left leg showed some signs of compartment syndrome with blisters in his calf, fasciotomy was not performed. He received systemic anticoagulation, initially with low-molecular-weight heparin, then with warfarin, titrating to an international normalized ratio (INR) between 2.0 and 2.5.Three days postoperatively, mechanical ventilation was discontinued and his signs and symptoms improved dramatically. Pulses in his left lower extremity became palpable on postoperative day 5, and the swelling and discoloration decreased. On postoperative day 30, he was taken off the OptEase® filter and the venogram showed a small amount of residual thrombus in his left external iliac vein (Figure \n). The inferior vena cava was patent, with no residual defects around the filter and no thrombus in the filter. He was discharged from the hospital in a stable condition, with full resolution of symptoms, on postoperative day 35 (Figure \nb). He was mostly asymptomatic at a recent 3-month follow-up visit except for slight edema in his left leg after walking. He continues on warfarin, maintaining an INR between 2.0 and 2.5, and wears elastic compression stockings.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 49-year-old woman presented with acute coronary syndrome for which she received aspirin, clopidogrel, atorvastatin, enoxaparin, and tenecteplase at another facility. She was then transferred to our institute for further management. She underwent coronary angiography which was suggestive of triple vessel disease. As the patient was in acute congestive heart failure (Killip IV) with pulmonary edema, she was intubated and mechanically ventilated. She underwent coronary artery bypass grafting surgery the following day where she received 20,000U of unfractionated heparin.\nOn postoperative day (POD) 6, the patient developed right pedal edema with cyanosis. Bilateral lower limbs Arterial Doppler was normal. Venous Doppler of the right lower limb was suggestive of thrombosis of the right Common Femoral, Superficial Femoral, Popliteal, and Great Saphenous Veins. She also had progressively worsening thrombocytopenia in which the platelet count dropped from 297 × 109/L on day 1 of postenoxaparin exposure to a nadir of 20 × 109/L on day 8. With a suspicion of HIT and thrombosis (HITT), enoxaparin was replaced with fondaparinux on POD 7. She tested positive for HIT type 2 antibodies on day 10. Her platelets started improving by POD 11 [].\nOn POD 13, two-dimensional echocardiography done was suggestive of a left ventricular thrombus (with an ejection fraction of 25%) which resolved completely by POD 44 with anticoagulation. Fondaparinux was bridged with oral Vitamin K Antagonist-Acenocoumarol for HITT and PCD. Once there was a line of demarcation for gangrene, she underwent a right forefoot amputation on POD 34.\nThe patient was discharged on POD 47 with medications for cardiac failure along with acenocoumarol.

The patient is a 78-year-old woman who presented to emergency department with 2 days of gradually worsening right lower extremity (RLE) swelling, pain, and paresthesia that was limiting mobility. She was independent with a clinical frailty score of 2. Her past medical history was significant for diabetes mellitus with Hgb a1c 10.5 and a provoked left lower extremity DVT 30 years earlier treated with a course of warfarin and permanent IVC filter placement. She denied prior hypercoagulability workup and reported that her first episode of thrombosis followed a prolonged airplane ride. She was not anticoagulated at the time of presentation. She denied a history of dysrhythmias, prior embolic events, recent travel, injury, surgery, illness, or known exposure to COVID-19. She denied a family history of blood clots or hypercoagulability.\nPhysical examination revealed an RLE that was severely taut with cyanosis with nonpalpable peripheral pulses and multiphasic signaling on Doppler and tenderness to the mid-thigh. The contralateral limb was soft, nontender with color appropriate of ethnicity and palpable peripheral pulses. An RLE venous duplex ultrasound scan was performed with noncompressible veins and loss of spontaneous flow from the right popliteal vein extending to the right common femoral vein consistent with DVT. On presentation, she did not display hemodynamic instability nor complained of cardiopulmonary symptoms.\nBecause of progressive symptoms concerning for PCD and imminent development of venous gangrene in a patient with good functional status, she was admitted directly to the angiography suite for CDT and pharmacomechanical thrombectomy with tissue plasminogen activator (tPA) and heparin. Angiogram revealed thrombus extending proximal to the IVC filter in the mid-IVC (). She was transferred to the intensive care unit for continued CDT with tPA (1 mg/h) and heparin (500 u/h) through a Uni∗Fuse catheter. tPA was discontinued overnight for a fibrinogen of 82 mg/dL. The next morning, she reported subjective improvement of symptoms and return of palpable peripheral pulses with resolution of pain. She returned to the angiography suite for catheter removal and completion venogram that revealed persistent thrombus burden, and the decision to remove the remainder of the clot was made to decrease the risk of recurrence. Using the Penumbra Indigo CAT8 system (Penumbra, Alameda, Calif), mechanical suction thrombectomy, and balloon venoplasty were performed with successful recanalization (). She was transferred to the floor, heparin was discontinued, and rivaroxaban initiated.\nOn postoperative day 2, she was noted to have expressive aphasia and left-sided hemiplegia. A noncontrast computed tomography and computed tomography angiogram of the head and neck were performed without evidence of a hemorrhage or significant carotid or aortic arch atherosclerotic disease. International normalized ratio was therapeutic at 2.0. Given the concern for stroke, a diffusion-weighted magnetic resonance imaging of the brain was obtained () and was notable for the focal area of restricted diffusion within the right thalamus. Because of recent anticoagulation and thrombolysis, she was not a candidate for systemic tPA. Heparin was not reinitiated because of therapeutic international normalized ratio on rivaroxaban. She was transferred to a tertiary center with neurological and neurosurgical capabilities where she underwent a transesophageal echocardiogram with bubble study that revealed a PFO with an atrial septal aneurysm and left-to-right flow noted with color Doppler and a moderate right-to-left shunt during bubble study but no left atrial mass or thrombus. Rivaroxaban was continued and her neurological status improved. She was discharged to a rehabilitation facility with improved left-sided weakness on postoperative day 3. After 2 weeks of rehabilitation, the patient was discharged with a modified Rankin score of 1. Patency of the RLE veins was unknown at the time of discharge, but a repeat duplex ultrasound scan at 8 months after initial presentation showed chronic thrombus in the right common femoral vein, but the RLE venous system remained patent.\nBecause of multiple episodes of thrombosis, she was placed on lifelong anticoagulation with apixaban. Hypercoagulable disorder was suspected but was deferred by her hematologist as diagnosis would not change plan for management.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

An 88-year-old man was admitted to our facility with altered mental status, hypotension (blood pressure range: 71-84/47-57 mmHg in the right arm supine position), fever (104oF), and tachycardia (heart rate: 140-150 beats/min) on arrival at the emergency room. Prior to admission, he was on hemodialysis for the past three months for end-stage renal disease secondary to rapidly progressive glomerulonephritis (has a right permacath). He was receiving intermittent heparin flushes along with dialysis to maintain the patency of the extracorporeal circuit. Other significant past medical history included a splenectomy in 2007. Clinical manifestations, imaging tests, and blood cultures suggested septic shock secondary to Streptococcal pneumonia. The patient was started on meropenem and vancomycin. A left internal jugular catheter and arterial line (in the right upper extremity) were placed for fluid resuscitation and blood pressure monitoring, respectively, and the patient was managed per surviving sepsis guidelines. On day three of hospitalization, the patient started to complain about a right-hand pain at the site of the arterial catheter. The physical examination was remarkable for a swollen and cyanotic right upper extremity, especially the second and third fingers (Figure ), with a barely palpable radial pulse compared to the left side. Arterial Doppler of the upper extremities was obtained, with findings indicative of significant right-sided arterial insufficiency. Further evaluation by venous duplex ultrasound identified a massive thrombus in the axillary, brachial, and basilic veins of the right arm with the solely spared ulna vein being hugely engorged (Figures -).\nWe considered the possibility of catheter-induced venous thrombosis, sepsis-associated disseminated intravascular coagulation and heparin-induced thrombocytopenia as working diagnoses. Given the suspicion of heparin-induced thrombocytopenia, we discontinued heparin immediately while the patient’s peripheral smear and coagulation cascade were investigated. Although the patient had low platelets (Table ), prolonged prothrombin time (16 (normal: 11-13 sec)), activated partial thromboplastin time (63 (normal: 25-35 sec)), elevated fibrin degradation products (>40 (normal: <10 mcg/ml)), which were suspicious for sepsis-related disseminated intravascular coagulation; normal factor VII (77 (normal: 50-150%)), high VIII levels (192 (normal: 50-150%)), normal haptoglobin (163 (normal: 36-195 mg/dl)), mildly decreased hemoglobulin (range: 12.1-12.9 (normal:13.5-17.5 g/dl)), and the presence of very few schistiocytes (<0.5%) on a peripheral smear made disseminated intravascular coagulation less likely. Laboratory data were remarkable for a significant drop in the platelet count from 234*109/L (on initiation of hemodialysis) to 44*109/L (the day of hospital admission) over the past three months. Based on the 4T score, heparin-induced thrombocytopenia was highly suspected and argatroban was initiated at 1 mg/kg/min. Vascular surgery consultation was obtained to address the gangrene in the second and third digits of the right upper extremity. However, considering his critically septic situation with multiple morbidities, a decision was made not to proceed with invasive maneuvers. On hospital day four, heparin-platelet factor 4 (PF4) antibodies (1.67 (normal: <0.4), heparin inhibition: >50%), and serotonin release assays returned positive (using enzyme-linked immunosorbent assay), confirming heparin-induced thrombocytopenia. On hospital day eight, repeated venous duplex demonstrated normal compressibility and spontaneous flow in the vein of the right upper extremity. The platelet count recovered and no further thrombotic complications were observed. Though we were able to manage the patient’s advanced gangrene with argatroban, his second and third fingers were amputated in the end.

A 64-year-old man with a history of obesity (BMI 38 Kg/m^2), arterial hypertension, atrial fibrillation, type 2 diabetes, chronic kidney disease, obstructive sleep apnea, and chronic venous insufficiency presented to the Emergency Department complaining of dyspnea, fever, and chest pain which started 7 days before. The patient was hypoxemic in room air (SpO2 80% and PaO2 43 mmHg). Inferior limbs appeared normal. A molecular swab formalized diagnosis of SARS-CoV2-related pneumonia. Respiratory distress progressed despite non-invasive-ventilation and hemodynamic instability requiring vasoactive support ensued. The patient was intubated and transferred to the ICU. The patient received invasive protective ventilation and hemodynamic support with noradrenaline. Gas exchange progressively worsened to a PaO2/FiO2 ratio of 70 mmHg. He developed a shock, and his lower limbs started to appear mottled. Lung and cardiac ultrasound were compatible with severe interstitial pneumonia and with no signs of pressure overload of the right heart. His coagulation profile was highly altered, as both aPTT and INR were elevated (respectively 2.28 seconds and 6.42), platelets were 164,000/mm3, and D-dimer was 117,521 UI/ml. Coagulation parameters continually worsened (), and treatment with one unit of fresh frozen plasma and vitamin K was required. Inferior limbs’ color progressively worsened, becoming frankly cyanotic, while pulses were still normal. Doppler ultrasound showed bilateral thrombosis of tibial and small saphenous veins. A continuous infusion of iloprost was started, as PCD was suspected (). Continuous infusion of unfractionated heparin was instituted, at a dose of 500-1000 IU per hour, according to aPTT, as well as continuous veno-venous hemodiafiltration as the patient developed acute kidney injury. The patient’s general conditions worsened (), and despite maximal treatment, he passed away after eight days of ICU care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

An 88-year-old man was admitted to our facility with altered mental status, hypotension (blood pressure range: 71-84/47-57 mmHg in the right arm supine position), fever (104oF), and tachycardia (heart rate: 140-150 beats/min) on arrival at the emergency room. Prior to admission, he was on hemodialysis for the past three months for end-stage renal disease secondary to rapidly progressive glomerulonephritis (has a right permacath). He was receiving intermittent heparin flushes along with dialysis to maintain the patency of the extracorporeal circuit. Other significant past medical history included a splenectomy in 2007. Clinical manifestations, imaging tests, and blood cultures suggested septic shock secondary to Streptococcal pneumonia. The patient was started on meropenem and vancomycin. A left internal jugular catheter and arterial line (in the right upper extremity) were placed for fluid resuscitation and blood pressure monitoring, respectively, and the patient was managed per surviving sepsis guidelines. On day three of hospitalization, the patient started to complain about a right-hand pain at the site of the arterial catheter. The physical examination was remarkable for a swollen and cyanotic right upper extremity, especially the second and third fingers (Figure ), with a barely palpable radial pulse compared to the left side. Arterial Doppler of the upper extremities was obtained, with findings indicative of significant right-sided arterial insufficiency. Further evaluation by venous duplex ultrasound identified a massive thrombus in the axillary, brachial, and basilic veins of the right arm with the solely spared ulna vein being hugely engorged (Figures -).\nWe considered the possibility of catheter-induced venous thrombosis, sepsis-associated disseminated intravascular coagulation and heparin-induced thrombocytopenia as working diagnoses. Given the suspicion of heparin-induced thrombocytopenia, we discontinued heparin immediately while the patient’s peripheral smear and coagulation cascade were investigated. Although the patient had low platelets (Table ), prolonged prothrombin time (16 (normal: 11-13 sec)), activated partial thromboplastin time (63 (normal: 25-35 sec)), elevated fibrin degradation products (>40 (normal: <10 mcg/ml)), which were suspicious for sepsis-related disseminated intravascular coagulation; normal factor VII (77 (normal: 50-150%)), high VIII levels (192 (normal: 50-150%)), normal haptoglobin (163 (normal: 36-195 mg/dl)), mildly decreased hemoglobulin (range: 12.1-12.9 (normal:13.5-17.5 g/dl)), and the presence of very few schistiocytes (<0.5%) on a peripheral smear made disseminated intravascular coagulation less likely. Laboratory data were remarkable for a significant drop in the platelet count from 234*109/L (on initiation of hemodialysis) to 44*109/L (the day of hospital admission) over the past three months. Based on the 4T score, heparin-induced thrombocytopenia was highly suspected and argatroban was initiated at 1 mg/kg/min. Vascular surgery consultation was obtained to address the gangrene in the second and third digits of the right upper extremity. However, considering his critically septic situation with multiple morbidities, a decision was made not to proceed with invasive maneuvers. On hospital day four, heparin-platelet factor 4 (PF4) antibodies (1.67 (normal: <0.4), heparin inhibition: >50%), and serotonin release assays returned positive (using enzyme-linked immunosorbent assay), confirming heparin-induced thrombocytopenia. On hospital day eight, repeated venous duplex demonstrated normal compressibility and spontaneous flow in the vein of the right upper extremity. The platelet count recovered and no further thrombotic complications were observed. Though we were able to manage the patient’s advanced gangrene with argatroban, his second and third fingers were amputated in the end.

A 21-year-old female college student presented to the emergency department (ED) with severe pain in her left hip, thigh, and calf. The pain started suddenly when she was playing basketball a few hours earlier. She twisted her torso to shoot the ball and heard a “pop” in her left hip with immediate onset of pain, and she subsequently fell to her knees. She was initially able to ambulate but had worsening pain and rapid progression of swelling and mottling in the left leg from her hip to her ankle. She denied any pain or swelling in that extremity prior to the injury during the basketball game. With the exception of oral contraceptive use, she had no significant medical or family history.\nOn examination her left extremity was mottled, dusky, and cool to the touch from the hip to the toes and she had decreased dorsalis pedis and posterior tibial pulses when compared with the right extremity. The leg was markedly tender to palpation and sensation to light touch was diminished. Passive range of motion of the hip, knee, and ankle elicited severe pain.\nPOCUS was performed at the bedside to evaluate for arterial blood flow and deep venous thrombosis. This demonstrated normal color flow in the femoral and popliteal arteries (), but echogenic material was noted within the left common femoral vein extending distally to the popliteal vein and the veins were non-compressible (). Vascular surgery was immediately consulted, and while awaiting their arrival to the ED the patient was sent for an emergent computed tomography (CT) angiogram, which confirmed arterial patency and extensive deep venous thrombosis in the left popliteal, femoral, and iliac veins (). A heparin bolus was given and the patient was then taken to interventional radiology where she underwent partial thrombectomy, catheter-directed tissue plasminogen activator (tPA) treatment, and placement of an inferior vena cava (IVC) filter. By the next morning her leg was noted to be well-perfused, non-tender, and without swelling, and her pain had resolved. A workup for hypercoagulable states revealed heterozygosity for the Factor V Leiden mutation. She was discharged one week later on warfarin after bridging from enoxaparin.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

An 88-year-old man was admitted to our facility with altered mental status, hypotension (blood pressure range: 71-84/47-57 mmHg in the right arm supine position), fever (104oF), and tachycardia (heart rate: 140-150 beats/min) on arrival at the emergency room. Prior to admission, he was on hemodialysis for the past three months for end-stage renal disease secondary to rapidly progressive glomerulonephritis (has a right permacath). He was receiving intermittent heparin flushes along with dialysis to maintain the patency of the extracorporeal circuit. Other significant past medical history included a splenectomy in 2007. Clinical manifestations, imaging tests, and blood cultures suggested septic shock secondary to Streptococcal pneumonia. The patient was started on meropenem and vancomycin. A left internal jugular catheter and arterial line (in the right upper extremity) were placed for fluid resuscitation and blood pressure monitoring, respectively, and the patient was managed per surviving sepsis guidelines. On day three of hospitalization, the patient started to complain about a right-hand pain at the site of the arterial catheter. The physical examination was remarkable for a swollen and cyanotic right upper extremity, especially the second and third fingers (Figure ), with a barely palpable radial pulse compared to the left side. Arterial Doppler of the upper extremities was obtained, with findings indicative of significant right-sided arterial insufficiency. Further evaluation by venous duplex ultrasound identified a massive thrombus in the axillary, brachial, and basilic veins of the right arm with the solely spared ulna vein being hugely engorged (Figures -).\nWe considered the possibility of catheter-induced venous thrombosis, sepsis-associated disseminated intravascular coagulation and heparin-induced thrombocytopenia as working diagnoses. Given the suspicion of heparin-induced thrombocytopenia, we discontinued heparin immediately while the patient’s peripheral smear and coagulation cascade were investigated. Although the patient had low platelets (Table ), prolonged prothrombin time (16 (normal: 11-13 sec)), activated partial thromboplastin time (63 (normal: 25-35 sec)), elevated fibrin degradation products (>40 (normal: <10 mcg/ml)), which were suspicious for sepsis-related disseminated intravascular coagulation; normal factor VII (77 (normal: 50-150%)), high VIII levels (192 (normal: 50-150%)), normal haptoglobin (163 (normal: 36-195 mg/dl)), mildly decreased hemoglobulin (range: 12.1-12.9 (normal:13.5-17.5 g/dl)), and the presence of very few schistiocytes (<0.5%) on a peripheral smear made disseminated intravascular coagulation less likely. Laboratory data were remarkable for a significant drop in the platelet count from 234*109/L (on initiation of hemodialysis) to 44*109/L (the day of hospital admission) over the past three months. Based on the 4T score, heparin-induced thrombocytopenia was highly suspected and argatroban was initiated at 1 mg/kg/min. Vascular surgery consultation was obtained to address the gangrene in the second and third digits of the right upper extremity. However, considering his critically septic situation with multiple morbidities, a decision was made not to proceed with invasive maneuvers. On hospital day four, heparin-platelet factor 4 (PF4) antibodies (1.67 (normal: <0.4), heparin inhibition: >50%), and serotonin release assays returned positive (using enzyme-linked immunosorbent assay), confirming heparin-induced thrombocytopenia. On hospital day eight, repeated venous duplex demonstrated normal compressibility and spontaneous flow in the vein of the right upper extremity. The platelet count recovered and no further thrombotic complications were observed. Though we were able to manage the patient’s advanced gangrene with argatroban, his second and third fingers were amputated in the end.

A 66-year-old female presented to the emergency department with three days of acute LLE swelling, pain, cyanosis, inability to bear weight, dyspnea, and hypoxemia (Figure ). She denied recent travel, hormone replacement, or a history of DVT/pulmonary embolism (PE). Her medical history was notable for systemic lupus erythematosus, CREST (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome, Sjogren’s syndrome, and local invasive anal squamous cell carcinoma. Doppler ultrasound revealed LLE thrombus extending from the greater saphenous vein to the popliteal vein. She was admitted to the intensive care unit (ICU) and started on an unfractionated heparin drip.\nThe vascular surgery team was consulted for surgical intervention. After further review of her case, the vascular surgery team elected for an endovascular approach with CDT of LLE. Initial venogram demonstrated extensive clotting of the tibial, popliteal, and femoral venous systems extending into the iliac system (Figures , ). From a tibial approach, a guidewire was advanced up to the common iliac, but a chronic occlusion of the left common iliac vein was found, which could not be crossed. A venous collateral circulation system in communication with the right iliac venous system was identified. In order to decrease the overall clot burden, two 50-cm EKOS endovascular catheters were placed in the left external iliac vein and collateral system. Repeat venogram at 24 hours post-CDT showed significant improvement of the overall clot burden with almost complete resolution of the clot in the LLE; however, the chronic occlusion remained (Figure ). A 20 x 80 mm Boston Scientific Wallstent™ (endoprosthesis stent) was advanced across the total chronic total occlusion and deployed. Post-operative venogram demonstrated significant improvement in flow in the system, with all flow going through the iliac system, and no flow further through the previously seen collaterals. Intravascular ultrasound was advanced through the area, which showed severe compression of the stent. A 12x 40 mm Atlas® dilatation catheter (Bard Peripheral Vascular Inc., Tempe, AZ, USA) was used for angioplasty. Repeat intravascular ultrasound showed persistent compression of the area. A 8 x 40 mm Boston Scientific Mustang™ dilatation catheter (high-pressure balloon) was used to re-attempt angioplasty; however, compression was still noted (Figure ). Regardless, outflow improved throughout the left common iliac system, and no further interventions were performed. The patient returned to the ICU and transitioned to direct oral anticoagulation without any further complications. She was subsequently transferred to a medicine ward for further care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

An 88-year-old man was admitted to our facility with altered mental status, hypotension (blood pressure range: 71-84/47-57 mmHg in the right arm supine position), fever (104oF), and tachycardia (heart rate: 140-150 beats/min) on arrival at the emergency room. Prior to admission, he was on hemodialysis for the past three months for end-stage renal disease secondary to rapidly progressive glomerulonephritis (has a right permacath). He was receiving intermittent heparin flushes along with dialysis to maintain the patency of the extracorporeal circuit. Other significant past medical history included a splenectomy in 2007. Clinical manifestations, imaging tests, and blood cultures suggested septic shock secondary to Streptococcal pneumonia. The patient was started on meropenem and vancomycin. A left internal jugular catheter and arterial line (in the right upper extremity) were placed for fluid resuscitation and blood pressure monitoring, respectively, and the patient was managed per surviving sepsis guidelines. On day three of hospitalization, the patient started to complain about a right-hand pain at the site of the arterial catheter. The physical examination was remarkable for a swollen and cyanotic right upper extremity, especially the second and third fingers (Figure ), with a barely palpable radial pulse compared to the left side. Arterial Doppler of the upper extremities was obtained, with findings indicative of significant right-sided arterial insufficiency. Further evaluation by venous duplex ultrasound identified a massive thrombus in the axillary, brachial, and basilic veins of the right arm with the solely spared ulna vein being hugely engorged (Figures -).\nWe considered the possibility of catheter-induced venous thrombosis, sepsis-associated disseminated intravascular coagulation and heparin-induced thrombocytopenia as working diagnoses. Given the suspicion of heparin-induced thrombocytopenia, we discontinued heparin immediately while the patient’s peripheral smear and coagulation cascade were investigated. Although the patient had low platelets (Table ), prolonged prothrombin time (16 (normal: 11-13 sec)), activated partial thromboplastin time (63 (normal: 25-35 sec)), elevated fibrin degradation products (>40 (normal: <10 mcg/ml)), which were suspicious for sepsis-related disseminated intravascular coagulation; normal factor VII (77 (normal: 50-150%)), high VIII levels (192 (normal: 50-150%)), normal haptoglobin (163 (normal: 36-195 mg/dl)), mildly decreased hemoglobulin (range: 12.1-12.9 (normal:13.5-17.5 g/dl)), and the presence of very few schistiocytes (<0.5%) on a peripheral smear made disseminated intravascular coagulation less likely. Laboratory data were remarkable for a significant drop in the platelet count from 234*109/L (on initiation of hemodialysis) to 44*109/L (the day of hospital admission) over the past three months. Based on the 4T score, heparin-induced thrombocytopenia was highly suspected and argatroban was initiated at 1 mg/kg/min. Vascular surgery consultation was obtained to address the gangrene in the second and third digits of the right upper extremity. However, considering his critically septic situation with multiple morbidities, a decision was made not to proceed with invasive maneuvers. On hospital day four, heparin-platelet factor 4 (PF4) antibodies (1.67 (normal: <0.4), heparin inhibition: >50%), and serotonin release assays returned positive (using enzyme-linked immunosorbent assay), confirming heparin-induced thrombocytopenia. On hospital day eight, repeated venous duplex demonstrated normal compressibility and spontaneous flow in the vein of the right upper extremity. The platelet count recovered and no further thrombotic complications were observed. Though we were able to manage the patient’s advanced gangrene with argatroban, his second and third fingers were amputated in the end.

A 49-year-old Chinese man sustained severe knife trauma and was referred to a local hospital. An exploratory laparotomy showed traumatic rupture of his left external iliac vein with massive intraperitoneal bleeding, but his iliac artery was intact. To rescue him, the proximal and distal parts of his injured external iliac vein were ligated (there was no vascular surgeon in the local hospital); however, his left leg quickly became severely swollen, cyanotic and pulseless. Two hours after the first operation, he was transferred to the emergency department of our university hospital with endotracheal tube intubation. On physical examination, he was tachycardic (142 beats per minute), hypotensive (86/50mmHg). His left lower extremity was markedly edematous, cyanotic, mottled (Figure \na) and had no palpable pulse, but his right lower extremity was normal. He was diagnosed with posttraumatic PCD. Considering the high risk of pulmonary embolism during the next surgical procedure, an OptEase® retrievable vena cava filter (Cordis Corp., New Brunswick, NJ, USA) was placed in his inferior vena cava via his right femoral vein under digital subtraction angiography (Figure \n). His abdomen was immediately reopened while his left leg was also prepared for treatment.During the second emergent laparotomy, there was less blood in his pelvic cavity. No active bleeding was identified. His left iliac vein and artery were exposed and his entire iliac artery appeared normal and without rupture. His external iliac vein was ligated but not transected, connected only by the posterior wall, and the caudal part of his iliac vein was significantly dilated. By replacing the vascular clamp in the proximal and distal parts of the rupture, the ligations on both sides of the venous rupture were resolved. A wedge-shaped rupture was revealed, approximately 4cm in length, on the anterolateral side of his left external iliac vein. The edges of the venous rupture were smooth as a result of the knife trauma. Although the ligated parts of his iliac vein appeared congested, the lumen was smooth and contained no clot. The damaged vein was repaired with continuous 4-0 Prolene sutures (Ethicon, Inc, Somerville, NJ, USA) after the patient was systemically heparinized with 5000 units heparin. Before the sutures were finally ligated, the clamp at the cranial aspect was removed and the caudal clamp was left in place. After the backflow was clear of thrombotic debris, the clamp on his caudal iliac vein was removed and the clamp at the cranial aspect left in place. The left leg was gently massaged from calf to thigh; as a result, some thrombi in the caudal part of the vein were flushed out with the venous blood flow, and the sutures were finally ligated until the venous blood was free of thrombus. His iliac vein, although narrower after repair, was patent (Figure \n).\nAfter the operation, the patient was sent to the surgical intensive care unit with mechanical ventilation. Despite the fact that his left leg showed some signs of compartment syndrome with blisters in his calf, fasciotomy was not performed. He received systemic anticoagulation, initially with low-molecular-weight heparin, then with warfarin, titrating to an international normalized ratio (INR) between 2.0 and 2.5.Three days postoperatively, mechanical ventilation was discontinued and his signs and symptoms improved dramatically. Pulses in his left lower extremity became palpable on postoperative day 5, and the swelling and discoloration decreased. On postoperative day 30, he was taken off the OptEase® filter and the venogram showed a small amount of residual thrombus in his left external iliac vein (Figure \n). The inferior vena cava was patent, with no residual defects around the filter and no thrombus in the filter. He was discharged from the hospital in a stable condition, with full resolution of symptoms, on postoperative day 35 (Figure \nb). He was mostly asymptomatic at a recent 3-month follow-up visit except for slight edema in his left leg after walking. He continues on warfarin, maintaining an INR between 2.0 and 2.5, and wears elastic compression stockings.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

An 88-year-old man was admitted to our facility with altered mental status, hypotension (blood pressure range: 71-84/47-57 mmHg in the right arm supine position), fever (104oF), and tachycardia (heart rate: 140-150 beats/min) on arrival at the emergency room. Prior to admission, he was on hemodialysis for the past three months for end-stage renal disease secondary to rapidly progressive glomerulonephritis (has a right permacath). He was receiving intermittent heparin flushes along with dialysis to maintain the patency of the extracorporeal circuit. Other significant past medical history included a splenectomy in 2007. Clinical manifestations, imaging tests, and blood cultures suggested septic shock secondary to Streptococcal pneumonia. The patient was started on meropenem and vancomycin. A left internal jugular catheter and arterial line (in the right upper extremity) were placed for fluid resuscitation and blood pressure monitoring, respectively, and the patient was managed per surviving sepsis guidelines. On day three of hospitalization, the patient started to complain about a right-hand pain at the site of the arterial catheter. The physical examination was remarkable for a swollen and cyanotic right upper extremity, especially the second and third fingers (Figure ), with a barely palpable radial pulse compared to the left side. Arterial Doppler of the upper extremities was obtained, with findings indicative of significant right-sided arterial insufficiency. Further evaluation by venous duplex ultrasound identified a massive thrombus in the axillary, brachial, and basilic veins of the right arm with the solely spared ulna vein being hugely engorged (Figures -).\nWe considered the possibility of catheter-induced venous thrombosis, sepsis-associated disseminated intravascular coagulation and heparin-induced thrombocytopenia as working diagnoses. Given the suspicion of heparin-induced thrombocytopenia, we discontinued heparin immediately while the patient’s peripheral smear and coagulation cascade were investigated. Although the patient had low platelets (Table ), prolonged prothrombin time (16 (normal: 11-13 sec)), activated partial thromboplastin time (63 (normal: 25-35 sec)), elevated fibrin degradation products (>40 (normal: <10 mcg/ml)), which were suspicious for sepsis-related disseminated intravascular coagulation; normal factor VII (77 (normal: 50-150%)), high VIII levels (192 (normal: 50-150%)), normal haptoglobin (163 (normal: 36-195 mg/dl)), mildly decreased hemoglobulin (range: 12.1-12.9 (normal:13.5-17.5 g/dl)), and the presence of very few schistiocytes (<0.5%) on a peripheral smear made disseminated intravascular coagulation less likely. Laboratory data were remarkable for a significant drop in the platelet count from 234*109/L (on initiation of hemodialysis) to 44*109/L (the day of hospital admission) over the past three months. Based on the 4T score, heparin-induced thrombocytopenia was highly suspected and argatroban was initiated at 1 mg/kg/min. Vascular surgery consultation was obtained to address the gangrene in the second and third digits of the right upper extremity. However, considering his critically septic situation with multiple morbidities, a decision was made not to proceed with invasive maneuvers. On hospital day four, heparin-platelet factor 4 (PF4) antibodies (1.67 (normal: <0.4), heparin inhibition: >50%), and serotonin release assays returned positive (using enzyme-linked immunosorbent assay), confirming heparin-induced thrombocytopenia. On hospital day eight, repeated venous duplex demonstrated normal compressibility and spontaneous flow in the vein of the right upper extremity. The platelet count recovered and no further thrombotic complications were observed. Though we were able to manage the patient’s advanced gangrene with argatroban, his second and third fingers were amputated in the end.

The patient is a 78-year-old woman who presented to emergency department with 2 days of gradually worsening right lower extremity (RLE) swelling, pain, and paresthesia that was limiting mobility. She was independent with a clinical frailty score of 2. Her past medical history was significant for diabetes mellitus with Hgb a1c 10.5 and a provoked left lower extremity DVT 30 years earlier treated with a course of warfarin and permanent IVC filter placement. She denied prior hypercoagulability workup and reported that her first episode of thrombosis followed a prolonged airplane ride. She was not anticoagulated at the time of presentation. She denied a history of dysrhythmias, prior embolic events, recent travel, injury, surgery, illness, or known exposure to COVID-19. She denied a family history of blood clots or hypercoagulability.\nPhysical examination revealed an RLE that was severely taut with cyanosis with nonpalpable peripheral pulses and multiphasic signaling on Doppler and tenderness to the mid-thigh. The contralateral limb was soft, nontender with color appropriate of ethnicity and palpable peripheral pulses. An RLE venous duplex ultrasound scan was performed with noncompressible veins and loss of spontaneous flow from the right popliteal vein extending to the right common femoral vein consistent with DVT. On presentation, she did not display hemodynamic instability nor complained of cardiopulmonary symptoms.\nBecause of progressive symptoms concerning for PCD and imminent development of venous gangrene in a patient with good functional status, she was admitted directly to the angiography suite for CDT and pharmacomechanical thrombectomy with tissue plasminogen activator (tPA) and heparin. Angiogram revealed thrombus extending proximal to the IVC filter in the mid-IVC (). She was transferred to the intensive care unit for continued CDT with tPA (1 mg/h) and heparin (500 u/h) through a Uni∗Fuse catheter. tPA was discontinued overnight for a fibrinogen of 82 mg/dL. The next morning, she reported subjective improvement of symptoms and return of palpable peripheral pulses with resolution of pain. She returned to the angiography suite for catheter removal and completion venogram that revealed persistent thrombus burden, and the decision to remove the remainder of the clot was made to decrease the risk of recurrence. Using the Penumbra Indigo CAT8 system (Penumbra, Alameda, Calif), mechanical suction thrombectomy, and balloon venoplasty were performed with successful recanalization (). She was transferred to the floor, heparin was discontinued, and rivaroxaban initiated.\nOn postoperative day 2, she was noted to have expressive aphasia and left-sided hemiplegia. A noncontrast computed tomography and computed tomography angiogram of the head and neck were performed without evidence of a hemorrhage or significant carotid or aortic arch atherosclerotic disease. International normalized ratio was therapeutic at 2.0. Given the concern for stroke, a diffusion-weighted magnetic resonance imaging of the brain was obtained () and was notable for the focal area of restricted diffusion within the right thalamus. Because of recent anticoagulation and thrombolysis, she was not a candidate for systemic tPA. Heparin was not reinitiated because of therapeutic international normalized ratio on rivaroxaban. She was transferred to a tertiary center with neurological and neurosurgical capabilities where she underwent a transesophageal echocardiogram with bubble study that revealed a PFO with an atrial septal aneurysm and left-to-right flow noted with color Doppler and a moderate right-to-left shunt during bubble study but no left atrial mass or thrombus. Rivaroxaban was continued and her neurological status improved. She was discharged to a rehabilitation facility with improved left-sided weakness on postoperative day 3. After 2 weeks of rehabilitation, the patient was discharged with a modified Rankin score of 1. Patency of the RLE veins was unknown at the time of discharge, but a repeat duplex ultrasound scan at 8 months after initial presentation showed chronic thrombus in the right common femoral vein, but the RLE venous system remained patent.\nBecause of multiple episodes of thrombosis, she was placed on lifelong anticoagulation with apixaban. Hypercoagulable disorder was suspected but was deferred by her hematologist as diagnosis would not change plan for management.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 21-year-old female college student presented to the emergency department (ED) with severe pain in her left hip, thigh, and calf. The pain started suddenly when she was playing basketball a few hours earlier. She twisted her torso to shoot the ball and heard a “pop” in her left hip with immediate onset of pain, and she subsequently fell to her knees. She was initially able to ambulate but had worsening pain and rapid progression of swelling and mottling in the left leg from her hip to her ankle. She denied any pain or swelling in that extremity prior to the injury during the basketball game. With the exception of oral contraceptive use, she had no significant medical or family history.\nOn examination her left extremity was mottled, dusky, and cool to the touch from the hip to the toes and she had decreased dorsalis pedis and posterior tibial pulses when compared with the right extremity. The leg was markedly tender to palpation and sensation to light touch was diminished. Passive range of motion of the hip, knee, and ankle elicited severe pain.\nPOCUS was performed at the bedside to evaluate for arterial blood flow and deep venous thrombosis. This demonstrated normal color flow in the femoral and popliteal arteries (), but echogenic material was noted within the left common femoral vein extending distally to the popliteal vein and the veins were non-compressible (). Vascular surgery was immediately consulted, and while awaiting their arrival to the ED the patient was sent for an emergent computed tomography (CT) angiogram, which confirmed arterial patency and extensive deep venous thrombosis in the left popliteal, femoral, and iliac veins (). A heparin bolus was given and the patient was then taken to interventional radiology where she underwent partial thrombectomy, catheter-directed tissue plasminogen activator (tPA) treatment, and placement of an inferior vena cava (IVC) filter. By the next morning her leg was noted to be well-perfused, non-tender, and without swelling, and her pain had resolved. A workup for hypercoagulable states revealed heterozygosity for the Factor V Leiden mutation. She was discharged one week later on warfarin after bridging from enoxaparin.

A 64-year-old man with a history of obesity (BMI 38 Kg/m^2), arterial hypertension, atrial fibrillation, type 2 diabetes, chronic kidney disease, obstructive sleep apnea, and chronic venous insufficiency presented to the Emergency Department complaining of dyspnea, fever, and chest pain which started 7 days before. The patient was hypoxemic in room air (SpO2 80% and PaO2 43 mmHg). Inferior limbs appeared normal. A molecular swab formalized diagnosis of SARS-CoV2-related pneumonia. Respiratory distress progressed despite non-invasive-ventilation and hemodynamic instability requiring vasoactive support ensued. The patient was intubated and transferred to the ICU. The patient received invasive protective ventilation and hemodynamic support with noradrenaline. Gas exchange progressively worsened to a PaO2/FiO2 ratio of 70 mmHg. He developed a shock, and his lower limbs started to appear mottled. Lung and cardiac ultrasound were compatible with severe interstitial pneumonia and with no signs of pressure overload of the right heart. His coagulation profile was highly altered, as both aPTT and INR were elevated (respectively 2.28 seconds and 6.42), platelets were 164,000/mm3, and D-dimer was 117,521 UI/ml. Coagulation parameters continually worsened (), and treatment with one unit of fresh frozen plasma and vitamin K was required. Inferior limbs’ color progressively worsened, becoming frankly cyanotic, while pulses were still normal. Doppler ultrasound showed bilateral thrombosis of tibial and small saphenous veins. A continuous infusion of iloprost was started, as PCD was suspected (). Continuous infusion of unfractionated heparin was instituted, at a dose of 500-1000 IU per hour, according to aPTT, as well as continuous veno-venous hemodiafiltration as the patient developed acute kidney injury. The patient’s general conditions worsened (), and despite maximal treatment, he passed away after eight days of ICU care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 66-year-old female presented to the emergency department with three days of acute LLE swelling, pain, cyanosis, inability to bear weight, dyspnea, and hypoxemia (Figure ). She denied recent travel, hormone replacement, or a history of DVT/pulmonary embolism (PE). Her medical history was notable for systemic lupus erythematosus, CREST (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome, Sjogren’s syndrome, and local invasive anal squamous cell carcinoma. Doppler ultrasound revealed LLE thrombus extending from the greater saphenous vein to the popliteal vein. She was admitted to the intensive care unit (ICU) and started on an unfractionated heparin drip.\nThe vascular surgery team was consulted for surgical intervention. After further review of her case, the vascular surgery team elected for an endovascular approach with CDT of LLE. Initial venogram demonstrated extensive clotting of the tibial, popliteal, and femoral venous systems extending into the iliac system (Figures , ). From a tibial approach, a guidewire was advanced up to the common iliac, but a chronic occlusion of the left common iliac vein was found, which could not be crossed. A venous collateral circulation system in communication with the right iliac venous system was identified. In order to decrease the overall clot burden, two 50-cm EKOS endovascular catheters were placed in the left external iliac vein and collateral system. Repeat venogram at 24 hours post-CDT showed significant improvement of the overall clot burden with almost complete resolution of the clot in the LLE; however, the chronic occlusion remained (Figure ). A 20 x 80 mm Boston Scientific Wallstent™ (endoprosthesis stent) was advanced across the total chronic total occlusion and deployed. Post-operative venogram demonstrated significant improvement in flow in the system, with all flow going through the iliac system, and no flow further through the previously seen collaterals. Intravascular ultrasound was advanced through the area, which showed severe compression of the stent. A 12x 40 mm Atlas® dilatation catheter (Bard Peripheral Vascular Inc., Tempe, AZ, USA) was used for angioplasty. Repeat intravascular ultrasound showed persistent compression of the area. A 8 x 40 mm Boston Scientific Mustang™ dilatation catheter (high-pressure balloon) was used to re-attempt angioplasty; however, compression was still noted (Figure ). Regardless, outflow improved throughout the left common iliac system, and no further interventions were performed. The patient returned to the ICU and transitioned to direct oral anticoagulation without any further complications. She was subsequently transferred to a medicine ward for further care.

A 64-year-old man with a history of obesity (BMI 38 Kg/m^2), arterial hypertension, atrial fibrillation, type 2 diabetes, chronic kidney disease, obstructive sleep apnea, and chronic venous insufficiency presented to the Emergency Department complaining of dyspnea, fever, and chest pain which started 7 days before. The patient was hypoxemic in room air (SpO2 80% and PaO2 43 mmHg). Inferior limbs appeared normal. A molecular swab formalized diagnosis of SARS-CoV2-related pneumonia. Respiratory distress progressed despite non-invasive-ventilation and hemodynamic instability requiring vasoactive support ensued. The patient was intubated and transferred to the ICU. The patient received invasive protective ventilation and hemodynamic support with noradrenaline. Gas exchange progressively worsened to a PaO2/FiO2 ratio of 70 mmHg. He developed a shock, and his lower limbs started to appear mottled. Lung and cardiac ultrasound were compatible with severe interstitial pneumonia and with no signs of pressure overload of the right heart. His coagulation profile was highly altered, as both aPTT and INR were elevated (respectively 2.28 seconds and 6.42), platelets were 164,000/mm3, and D-dimer was 117,521 UI/ml. Coagulation parameters continually worsened (), and treatment with one unit of fresh frozen plasma and vitamin K was required. Inferior limbs’ color progressively worsened, becoming frankly cyanotic, while pulses were still normal. Doppler ultrasound showed bilateral thrombosis of tibial and small saphenous veins. A continuous infusion of iloprost was started, as PCD was suspected (). Continuous infusion of unfractionated heparin was instituted, at a dose of 500-1000 IU per hour, according to aPTT, as well as continuous veno-venous hemodiafiltration as the patient developed acute kidney injury. The patient’s general conditions worsened (), and despite maximal treatment, he passed away after eight days of ICU care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 64-year-old man with a history of obesity (BMI 38 Kg/m^2), arterial hypertension, atrial fibrillation, type 2 diabetes, chronic kidney disease, obstructive sleep apnea, and chronic venous insufficiency presented to the Emergency Department complaining of dyspnea, fever, and chest pain which started 7 days before. The patient was hypoxemic in room air (SpO2 80% and PaO2 43 mmHg). Inferior limbs appeared normal. A molecular swab formalized diagnosis of SARS-CoV2-related pneumonia. Respiratory distress progressed despite non-invasive-ventilation and hemodynamic instability requiring vasoactive support ensued. The patient was intubated and transferred to the ICU. The patient received invasive protective ventilation and hemodynamic support with noradrenaline. Gas exchange progressively worsened to a PaO2/FiO2 ratio of 70 mmHg. He developed a shock, and his lower limbs started to appear mottled. Lung and cardiac ultrasound were compatible with severe interstitial pneumonia and with no signs of pressure overload of the right heart. His coagulation profile was highly altered, as both aPTT and INR were elevated (respectively 2.28 seconds and 6.42), platelets were 164,000/mm3, and D-dimer was 117,521 UI/ml. Coagulation parameters continually worsened (), and treatment with one unit of fresh frozen plasma and vitamin K was required. Inferior limbs’ color progressively worsened, becoming frankly cyanotic, while pulses were still normal. Doppler ultrasound showed bilateral thrombosis of tibial and small saphenous veins. A continuous infusion of iloprost was started, as PCD was suspected (). Continuous infusion of unfractionated heparin was instituted, at a dose of 500-1000 IU per hour, according to aPTT, as well as continuous veno-venous hemodiafiltration as the patient developed acute kidney injury. The patient’s general conditions worsened (), and despite maximal treatment, he passed away after eight days of ICU care.

A 49-year-old Chinese man sustained severe knife trauma and was referred to a local hospital. An exploratory laparotomy showed traumatic rupture of his left external iliac vein with massive intraperitoneal bleeding, but his iliac artery was intact. To rescue him, the proximal and distal parts of his injured external iliac vein were ligated (there was no vascular surgeon in the local hospital); however, his left leg quickly became severely swollen, cyanotic and pulseless. Two hours after the first operation, he was transferred to the emergency department of our university hospital with endotracheal tube intubation. On physical examination, he was tachycardic (142 beats per minute), hypotensive (86/50mmHg). His left lower extremity was markedly edematous, cyanotic, mottled (Figure \na) and had no palpable pulse, but his right lower extremity was normal. He was diagnosed with posttraumatic PCD. Considering the high risk of pulmonary embolism during the next surgical procedure, an OptEase® retrievable vena cava filter (Cordis Corp., New Brunswick, NJ, USA) was placed in his inferior vena cava via his right femoral vein under digital subtraction angiography (Figure \n). His abdomen was immediately reopened while his left leg was also prepared for treatment.During the second emergent laparotomy, there was less blood in his pelvic cavity. No active bleeding was identified. His left iliac vein and artery were exposed and his entire iliac artery appeared normal and without rupture. His external iliac vein was ligated but not transected, connected only by the posterior wall, and the caudal part of his iliac vein was significantly dilated. By replacing the vascular clamp in the proximal and distal parts of the rupture, the ligations on both sides of the venous rupture were resolved. A wedge-shaped rupture was revealed, approximately 4cm in length, on the anterolateral side of his left external iliac vein. The edges of the venous rupture were smooth as a result of the knife trauma. Although the ligated parts of his iliac vein appeared congested, the lumen was smooth and contained no clot. The damaged vein was repaired with continuous 4-0 Prolene sutures (Ethicon, Inc, Somerville, NJ, USA) after the patient was systemically heparinized with 5000 units heparin. Before the sutures were finally ligated, the clamp at the cranial aspect was removed and the caudal clamp was left in place. After the backflow was clear of thrombotic debris, the clamp on his caudal iliac vein was removed and the clamp at the cranial aspect left in place. The left leg was gently massaged from calf to thigh; as a result, some thrombi in the caudal part of the vein were flushed out with the venous blood flow, and the sutures were finally ligated until the venous blood was free of thrombus. His iliac vein, although narrower after repair, was patent (Figure \n).\nAfter the operation, the patient was sent to the surgical intensive care unit with mechanical ventilation. Despite the fact that his left leg showed some signs of compartment syndrome with blisters in his calf, fasciotomy was not performed. He received systemic anticoagulation, initially with low-molecular-weight heparin, then with warfarin, titrating to an international normalized ratio (INR) between 2.0 and 2.5.Three days postoperatively, mechanical ventilation was discontinued and his signs and symptoms improved dramatically. Pulses in his left lower extremity became palpable on postoperative day 5, and the swelling and discoloration decreased. On postoperative day 30, he was taken off the OptEase® filter and the venogram showed a small amount of residual thrombus in his left external iliac vein (Figure \n). The inferior vena cava was patent, with no residual defects around the filter and no thrombus in the filter. He was discharged from the hospital in a stable condition, with full resolution of symptoms, on postoperative day 35 (Figure \nb). He was mostly asymptomatic at a recent 3-month follow-up visit except for slight edema in his left leg after walking. He continues on warfarin, maintaining an INR between 2.0 and 2.5, and wears elastic compression stockings.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

The patient is a 78-year-old woman who presented to emergency department with 2 days of gradually worsening right lower extremity (RLE) swelling, pain, and paresthesia that was limiting mobility. She was independent with a clinical frailty score of 2. Her past medical history was significant for diabetes mellitus with Hgb a1c 10.5 and a provoked left lower extremity DVT 30 years earlier treated with a course of warfarin and permanent IVC filter placement. She denied prior hypercoagulability workup and reported that her first episode of thrombosis followed a prolonged airplane ride. She was not anticoagulated at the time of presentation. She denied a history of dysrhythmias, prior embolic events, recent travel, injury, surgery, illness, or known exposure to COVID-19. She denied a family history of blood clots or hypercoagulability.\nPhysical examination revealed an RLE that was severely taut with cyanosis with nonpalpable peripheral pulses and multiphasic signaling on Doppler and tenderness to the mid-thigh. The contralateral limb was soft, nontender with color appropriate of ethnicity and palpable peripheral pulses. An RLE venous duplex ultrasound scan was performed with noncompressible veins and loss of spontaneous flow from the right popliteal vein extending to the right common femoral vein consistent with DVT. On presentation, she did not display hemodynamic instability nor complained of cardiopulmonary symptoms.\nBecause of progressive symptoms concerning for PCD and imminent development of venous gangrene in a patient with good functional status, she was admitted directly to the angiography suite for CDT and pharmacomechanical thrombectomy with tissue plasminogen activator (tPA) and heparin. Angiogram revealed thrombus extending proximal to the IVC filter in the mid-IVC (). She was transferred to the intensive care unit for continued CDT with tPA (1 mg/h) and heparin (500 u/h) through a Uni∗Fuse catheter. tPA was discontinued overnight for a fibrinogen of 82 mg/dL. The next morning, she reported subjective improvement of symptoms and return of palpable peripheral pulses with resolution of pain. She returned to the angiography suite for catheter removal and completion venogram that revealed persistent thrombus burden, and the decision to remove the remainder of the clot was made to decrease the risk of recurrence. Using the Penumbra Indigo CAT8 system (Penumbra, Alameda, Calif), mechanical suction thrombectomy, and balloon venoplasty were performed with successful recanalization (). She was transferred to the floor, heparin was discontinued, and rivaroxaban initiated.\nOn postoperative day 2, she was noted to have expressive aphasia and left-sided hemiplegia. A noncontrast computed tomography and computed tomography angiogram of the head and neck were performed without evidence of a hemorrhage or significant carotid or aortic arch atherosclerotic disease. International normalized ratio was therapeutic at 2.0. Given the concern for stroke, a diffusion-weighted magnetic resonance imaging of the brain was obtained () and was notable for the focal area of restricted diffusion within the right thalamus. Because of recent anticoagulation and thrombolysis, she was not a candidate for systemic tPA. Heparin was not reinitiated because of therapeutic international normalized ratio on rivaroxaban. She was transferred to a tertiary center with neurological and neurosurgical capabilities where she underwent a transesophageal echocardiogram with bubble study that revealed a PFO with an atrial septal aneurysm and left-to-right flow noted with color Doppler and a moderate right-to-left shunt during bubble study but no left atrial mass or thrombus. Rivaroxaban was continued and her neurological status improved. She was discharged to a rehabilitation facility with improved left-sided weakness on postoperative day 3. After 2 weeks of rehabilitation, the patient was discharged with a modified Rankin score of 1. Patency of the RLE veins was unknown at the time of discharge, but a repeat duplex ultrasound scan at 8 months after initial presentation showed chronic thrombus in the right common femoral vein, but the RLE venous system remained patent.\nBecause of multiple episodes of thrombosis, she was placed on lifelong anticoagulation with apixaban. Hypercoagulable disorder was suspected but was deferred by her hematologist as diagnosis would not change plan for management.

A 64-year-old man with a history of obesity (BMI 38 Kg/m^2), arterial hypertension, atrial fibrillation, type 2 diabetes, chronic kidney disease, obstructive sleep apnea, and chronic venous insufficiency presented to the Emergency Department complaining of dyspnea, fever, and chest pain which started 7 days before. The patient was hypoxemic in room air (SpO2 80% and PaO2 43 mmHg). Inferior limbs appeared normal. A molecular swab formalized diagnosis of SARS-CoV2-related pneumonia. Respiratory distress progressed despite non-invasive-ventilation and hemodynamic instability requiring vasoactive support ensued. The patient was intubated and transferred to the ICU. The patient received invasive protective ventilation and hemodynamic support with noradrenaline. Gas exchange progressively worsened to a PaO2/FiO2 ratio of 70 mmHg. He developed a shock, and his lower limbs started to appear mottled. Lung and cardiac ultrasound were compatible with severe interstitial pneumonia and with no signs of pressure overload of the right heart. His coagulation profile was highly altered, as both aPTT and INR were elevated (respectively 2.28 seconds and 6.42), platelets were 164,000/mm3, and D-dimer was 117,521 UI/ml. Coagulation parameters continually worsened (), and treatment with one unit of fresh frozen plasma and vitamin K was required. Inferior limbs’ color progressively worsened, becoming frankly cyanotic, while pulses were still normal. Doppler ultrasound showed bilateral thrombosis of tibial and small saphenous veins. A continuous infusion of iloprost was started, as PCD was suspected (). Continuous infusion of unfractionated heparin was instituted, at a dose of 500-1000 IU per hour, according to aPTT, as well as continuous veno-venous hemodiafiltration as the patient developed acute kidney injury. The patient’s general conditions worsened (), and despite maximal treatment, he passed away after eight days of ICU care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 21-year-old female college student presented to the emergency department (ED) with severe pain in her left hip, thigh, and calf. The pain started suddenly when she was playing basketball a few hours earlier. She twisted her torso to shoot the ball and heard a “pop” in her left hip with immediate onset of pain, and she subsequently fell to her knees. She was initially able to ambulate but had worsening pain and rapid progression of swelling and mottling in the left leg from her hip to her ankle. She denied any pain or swelling in that extremity prior to the injury during the basketball game. With the exception of oral contraceptive use, she had no significant medical or family history.\nOn examination her left extremity was mottled, dusky, and cool to the touch from the hip to the toes and she had decreased dorsalis pedis and posterior tibial pulses when compared with the right extremity. The leg was markedly tender to palpation and sensation to light touch was diminished. Passive range of motion of the hip, knee, and ankle elicited severe pain.\nPOCUS was performed at the bedside to evaluate for arterial blood flow and deep venous thrombosis. This demonstrated normal color flow in the femoral and popliteal arteries (), but echogenic material was noted within the left common femoral vein extending distally to the popliteal vein and the veins were non-compressible (). Vascular surgery was immediately consulted, and while awaiting their arrival to the ED the patient was sent for an emergent computed tomography (CT) angiogram, which confirmed arterial patency and extensive deep venous thrombosis in the left popliteal, femoral, and iliac veins (). A heparin bolus was given and the patient was then taken to interventional radiology where she underwent partial thrombectomy, catheter-directed tissue plasminogen activator (tPA) treatment, and placement of an inferior vena cava (IVC) filter. By the next morning her leg was noted to be well-perfused, non-tender, and without swelling, and her pain had resolved. A workup for hypercoagulable states revealed heterozygosity for the Factor V Leiden mutation. She was discharged one week later on warfarin after bridging from enoxaparin.

A 66-year-old female presented to the emergency department with three days of acute LLE swelling, pain, cyanosis, inability to bear weight, dyspnea, and hypoxemia (Figure ). She denied recent travel, hormone replacement, or a history of DVT/pulmonary embolism (PE). Her medical history was notable for systemic lupus erythematosus, CREST (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome, Sjogren’s syndrome, and local invasive anal squamous cell carcinoma. Doppler ultrasound revealed LLE thrombus extending from the greater saphenous vein to the popliteal vein. She was admitted to the intensive care unit (ICU) and started on an unfractionated heparin drip.\nThe vascular surgery team was consulted for surgical intervention. After further review of her case, the vascular surgery team elected for an endovascular approach with CDT of LLE. Initial venogram demonstrated extensive clotting of the tibial, popliteal, and femoral venous systems extending into the iliac system (Figures , ). From a tibial approach, a guidewire was advanced up to the common iliac, but a chronic occlusion of the left common iliac vein was found, which could not be crossed. A venous collateral circulation system in communication with the right iliac venous system was identified. In order to decrease the overall clot burden, two 50-cm EKOS endovascular catheters were placed in the left external iliac vein and collateral system. Repeat venogram at 24 hours post-CDT showed significant improvement of the overall clot burden with almost complete resolution of the clot in the LLE; however, the chronic occlusion remained (Figure ). A 20 x 80 mm Boston Scientific Wallstent™ (endoprosthesis stent) was advanced across the total chronic total occlusion and deployed. Post-operative venogram demonstrated significant improvement in flow in the system, with all flow going through the iliac system, and no flow further through the previously seen collaterals. Intravascular ultrasound was advanced through the area, which showed severe compression of the stent. A 12x 40 mm Atlas® dilatation catheter (Bard Peripheral Vascular Inc., Tempe, AZ, USA) was used for angioplasty. Repeat intravascular ultrasound showed persistent compression of the area. A 8 x 40 mm Boston Scientific Mustang™ dilatation catheter (high-pressure balloon) was used to re-attempt angioplasty; however, compression was still noted (Figure ). Regardless, outflow improved throughout the left common iliac system, and no further interventions were performed. The patient returned to the ICU and transitioned to direct oral anticoagulation without any further complications. She was subsequently transferred to a medicine ward for further care.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 21-year-old female college student presented to the emergency department (ED) with severe pain in her left hip, thigh, and calf. The pain started suddenly when she was playing basketball a few hours earlier. She twisted her torso to shoot the ball and heard a “pop” in her left hip with immediate onset of pain, and she subsequently fell to her knees. She was initially able to ambulate but had worsening pain and rapid progression of swelling and mottling in the left leg from her hip to her ankle. She denied any pain or swelling in that extremity prior to the injury during the basketball game. With the exception of oral contraceptive use, she had no significant medical or family history.\nOn examination her left extremity was mottled, dusky, and cool to the touch from the hip to the toes and she had decreased dorsalis pedis and posterior tibial pulses when compared with the right extremity. The leg was markedly tender to palpation and sensation to light touch was diminished. Passive range of motion of the hip, knee, and ankle elicited severe pain.\nPOCUS was performed at the bedside to evaluate for arterial blood flow and deep venous thrombosis. This demonstrated normal color flow in the femoral and popliteal arteries (), but echogenic material was noted within the left common femoral vein extending distally to the popliteal vein and the veins were non-compressible (). Vascular surgery was immediately consulted, and while awaiting their arrival to the ED the patient was sent for an emergent computed tomography (CT) angiogram, which confirmed arterial patency and extensive deep venous thrombosis in the left popliteal, femoral, and iliac veins (). A heparin bolus was given and the patient was then taken to interventional radiology where she underwent partial thrombectomy, catheter-directed tissue plasminogen activator (tPA) treatment, and placement of an inferior vena cava (IVC) filter. By the next morning her leg was noted to be well-perfused, non-tender, and without swelling, and her pain had resolved. A workup for hypercoagulable states revealed heterozygosity for the Factor V Leiden mutation. She was discharged one week later on warfarin after bridging from enoxaparin.

A 49-year-old Chinese man sustained severe knife trauma and was referred to a local hospital. An exploratory laparotomy showed traumatic rupture of his left external iliac vein with massive intraperitoneal bleeding, but his iliac artery was intact. To rescue him, the proximal and distal parts of his injured external iliac vein were ligated (there was no vascular surgeon in the local hospital); however, his left leg quickly became severely swollen, cyanotic and pulseless. Two hours after the first operation, he was transferred to the emergency department of our university hospital with endotracheal tube intubation. On physical examination, he was tachycardic (142 beats per minute), hypotensive (86/50mmHg). His left lower extremity was markedly edematous, cyanotic, mottled (Figure \na) and had no palpable pulse, but his right lower extremity was normal. He was diagnosed with posttraumatic PCD. Considering the high risk of pulmonary embolism during the next surgical procedure, an OptEase® retrievable vena cava filter (Cordis Corp., New Brunswick, NJ, USA) was placed in his inferior vena cava via his right femoral vein under digital subtraction angiography (Figure \n). His abdomen was immediately reopened while his left leg was also prepared for treatment.During the second emergent laparotomy, there was less blood in his pelvic cavity. No active bleeding was identified. His left iliac vein and artery were exposed and his entire iliac artery appeared normal and without rupture. His external iliac vein was ligated but not transected, connected only by the posterior wall, and the caudal part of his iliac vein was significantly dilated. By replacing the vascular clamp in the proximal and distal parts of the rupture, the ligations on both sides of the venous rupture were resolved. A wedge-shaped rupture was revealed, approximately 4cm in length, on the anterolateral side of his left external iliac vein. The edges of the venous rupture were smooth as a result of the knife trauma. Although the ligated parts of his iliac vein appeared congested, the lumen was smooth and contained no clot. The damaged vein was repaired with continuous 4-0 Prolene sutures (Ethicon, Inc, Somerville, NJ, USA) after the patient was systemically heparinized with 5000 units heparin. Before the sutures were finally ligated, the clamp at the cranial aspect was removed and the caudal clamp was left in place. After the backflow was clear of thrombotic debris, the clamp on his caudal iliac vein was removed and the clamp at the cranial aspect left in place. The left leg was gently massaged from calf to thigh; as a result, some thrombi in the caudal part of the vein were flushed out with the venous blood flow, and the sutures were finally ligated until the venous blood was free of thrombus. His iliac vein, although narrower after repair, was patent (Figure \n).\nAfter the operation, the patient was sent to the surgical intensive care unit with mechanical ventilation. Despite the fact that his left leg showed some signs of compartment syndrome with blisters in his calf, fasciotomy was not performed. He received systemic anticoagulation, initially with low-molecular-weight heparin, then with warfarin, titrating to an international normalized ratio (INR) between 2.0 and 2.5.Three days postoperatively, mechanical ventilation was discontinued and his signs and symptoms improved dramatically. Pulses in his left lower extremity became palpable on postoperative day 5, and the swelling and discoloration decreased. On postoperative day 30, he was taken off the OptEase® filter and the venogram showed a small amount of residual thrombus in his left external iliac vein (Figure \n). The inferior vena cava was patent, with no residual defects around the filter and no thrombus in the filter. He was discharged from the hospital in a stable condition, with full resolution of symptoms, on postoperative day 35 (Figure \nb). He was mostly asymptomatic at a recent 3-month follow-up visit except for slight edema in his left leg after walking. He continues on warfarin, maintaining an INR between 2.0 and 2.5, and wears elastic compression stockings.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 21-year-old female college student presented to the emergency department (ED) with severe pain in her left hip, thigh, and calf. The pain started suddenly when she was playing basketball a few hours earlier. She twisted her torso to shoot the ball and heard a “pop” in her left hip with immediate onset of pain, and she subsequently fell to her knees. She was initially able to ambulate but had worsening pain and rapid progression of swelling and mottling in the left leg from her hip to her ankle. She denied any pain or swelling in that extremity prior to the injury during the basketball game. With the exception of oral contraceptive use, she had no significant medical or family history.\nOn examination her left extremity was mottled, dusky, and cool to the touch from the hip to the toes and she had decreased dorsalis pedis and posterior tibial pulses when compared with the right extremity. The leg was markedly tender to palpation and sensation to light touch was diminished. Passive range of motion of the hip, knee, and ankle elicited severe pain.\nPOCUS was performed at the bedside to evaluate for arterial blood flow and deep venous thrombosis. This demonstrated normal color flow in the femoral and popliteal arteries (), but echogenic material was noted within the left common femoral vein extending distally to the popliteal vein and the veins were non-compressible (). Vascular surgery was immediately consulted, and while awaiting their arrival to the ED the patient was sent for an emergent computed tomography (CT) angiogram, which confirmed arterial patency and extensive deep venous thrombosis in the left popliteal, femoral, and iliac veins (). A heparin bolus was given and the patient was then taken to interventional radiology where she underwent partial thrombectomy, catheter-directed tissue plasminogen activator (tPA) treatment, and placement of an inferior vena cava (IVC) filter. By the next morning her leg was noted to be well-perfused, non-tender, and without swelling, and her pain had resolved. A workup for hypercoagulable states revealed heterozygosity for the Factor V Leiden mutation. She was discharged one week later on warfarin after bridging from enoxaparin.

The patient is a 78-year-old woman who presented to emergency department with 2 days of gradually worsening right lower extremity (RLE) swelling, pain, and paresthesia that was limiting mobility. She was independent with a clinical frailty score of 2. Her past medical history was significant for diabetes mellitus with Hgb a1c 10.5 and a provoked left lower extremity DVT 30 years earlier treated with a course of warfarin and permanent IVC filter placement. She denied prior hypercoagulability workup and reported that her first episode of thrombosis followed a prolonged airplane ride. She was not anticoagulated at the time of presentation. She denied a history of dysrhythmias, prior embolic events, recent travel, injury, surgery, illness, or known exposure to COVID-19. She denied a family history of blood clots or hypercoagulability.\nPhysical examination revealed an RLE that was severely taut with cyanosis with nonpalpable peripheral pulses and multiphasic signaling on Doppler and tenderness to the mid-thigh. The contralateral limb was soft, nontender with color appropriate of ethnicity and palpable peripheral pulses. An RLE venous duplex ultrasound scan was performed with noncompressible veins and loss of spontaneous flow from the right popliteal vein extending to the right common femoral vein consistent with DVT. On presentation, she did not display hemodynamic instability nor complained of cardiopulmonary symptoms.\nBecause of progressive symptoms concerning for PCD and imminent development of venous gangrene in a patient with good functional status, she was admitted directly to the angiography suite for CDT and pharmacomechanical thrombectomy with tissue plasminogen activator (tPA) and heparin. Angiogram revealed thrombus extending proximal to the IVC filter in the mid-IVC (). She was transferred to the intensive care unit for continued CDT with tPA (1 mg/h) and heparin (500 u/h) through a Uni∗Fuse catheter. tPA was discontinued overnight for a fibrinogen of 82 mg/dL. The next morning, she reported subjective improvement of symptoms and return of palpable peripheral pulses with resolution of pain. She returned to the angiography suite for catheter removal and completion venogram that revealed persistent thrombus burden, and the decision to remove the remainder of the clot was made to decrease the risk of recurrence. Using the Penumbra Indigo CAT8 system (Penumbra, Alameda, Calif), mechanical suction thrombectomy, and balloon venoplasty were performed with successful recanalization (). She was transferred to the floor, heparin was discontinued, and rivaroxaban initiated.\nOn postoperative day 2, she was noted to have expressive aphasia and left-sided hemiplegia. A noncontrast computed tomography and computed tomography angiogram of the head and neck were performed without evidence of a hemorrhage or significant carotid or aortic arch atherosclerotic disease. International normalized ratio was therapeutic at 2.0. Given the concern for stroke, a diffusion-weighted magnetic resonance imaging of the brain was obtained () and was notable for the focal area of restricted diffusion within the right thalamus. Because of recent anticoagulation and thrombolysis, she was not a candidate for systemic tPA. Heparin was not reinitiated because of therapeutic international normalized ratio on rivaroxaban. She was transferred to a tertiary center with neurological and neurosurgical capabilities where she underwent a transesophageal echocardiogram with bubble study that revealed a PFO with an atrial septal aneurysm and left-to-right flow noted with color Doppler and a moderate right-to-left shunt during bubble study but no left atrial mass or thrombus. Rivaroxaban was continued and her neurological status improved. She was discharged to a rehabilitation facility with improved left-sided weakness on postoperative day 3. After 2 weeks of rehabilitation, the patient was discharged with a modified Rankin score of 1. Patency of the RLE veins was unknown at the time of discharge, but a repeat duplex ultrasound scan at 8 months after initial presentation showed chronic thrombus in the right common femoral vein, but the RLE venous system remained patent.\nBecause of multiple episodes of thrombosis, she was placed on lifelong anticoagulation with apixaban. Hypercoagulable disorder was suspected but was deferred by her hematologist as diagnosis would not change plan for management.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 66-year-old female presented to the emergency department with three days of acute LLE swelling, pain, cyanosis, inability to bear weight, dyspnea, and hypoxemia (Figure ). She denied recent travel, hormone replacement, or a history of DVT/pulmonary embolism (PE). Her medical history was notable for systemic lupus erythematosus, CREST (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome, Sjogren’s syndrome, and local invasive anal squamous cell carcinoma. Doppler ultrasound revealed LLE thrombus extending from the greater saphenous vein to the popliteal vein. She was admitted to the intensive care unit (ICU) and started on an unfractionated heparin drip.\nThe vascular surgery team was consulted for surgical intervention. After further review of her case, the vascular surgery team elected for an endovascular approach with CDT of LLE. Initial venogram demonstrated extensive clotting of the tibial, popliteal, and femoral venous systems extending into the iliac system (Figures , ). From a tibial approach, a guidewire was advanced up to the common iliac, but a chronic occlusion of the left common iliac vein was found, which could not be crossed. A venous collateral circulation system in communication with the right iliac venous system was identified. In order to decrease the overall clot burden, two 50-cm EKOS endovascular catheters were placed in the left external iliac vein and collateral system. Repeat venogram at 24 hours post-CDT showed significant improvement of the overall clot burden with almost complete resolution of the clot in the LLE; however, the chronic occlusion remained (Figure ). A 20 x 80 mm Boston Scientific Wallstent™ (endoprosthesis stent) was advanced across the total chronic total occlusion and deployed. Post-operative venogram demonstrated significant improvement in flow in the system, with all flow going through the iliac system, and no flow further through the previously seen collaterals. Intravascular ultrasound was advanced through the area, which showed severe compression of the stent. A 12x 40 mm Atlas® dilatation catheter (Bard Peripheral Vascular Inc., Tempe, AZ, USA) was used for angioplasty. Repeat intravascular ultrasound showed persistent compression of the area. A 8 x 40 mm Boston Scientific Mustang™ dilatation catheter (high-pressure balloon) was used to re-attempt angioplasty; however, compression was still noted (Figure ). Regardless, outflow improved throughout the left common iliac system, and no further interventions were performed. The patient returned to the ICU and transitioned to direct oral anticoagulation without any further complications. She was subsequently transferred to a medicine ward for further care.

A 49-year-old Chinese man sustained severe knife trauma and was referred to a local hospital. An exploratory laparotomy showed traumatic rupture of his left external iliac vein with massive intraperitoneal bleeding, but his iliac artery was intact. To rescue him, the proximal and distal parts of his injured external iliac vein were ligated (there was no vascular surgeon in the local hospital); however, his left leg quickly became severely swollen, cyanotic and pulseless. Two hours after the first operation, he was transferred to the emergency department of our university hospital with endotracheal tube intubation. On physical examination, he was tachycardic (142 beats per minute), hypotensive (86/50mmHg). His left lower extremity was markedly edematous, cyanotic, mottled (Figure \na) and had no palpable pulse, but his right lower extremity was normal. He was diagnosed with posttraumatic PCD. Considering the high risk of pulmonary embolism during the next surgical procedure, an OptEase® retrievable vena cava filter (Cordis Corp., New Brunswick, NJ, USA) was placed in his inferior vena cava via his right femoral vein under digital subtraction angiography (Figure \n). His abdomen was immediately reopened while his left leg was also prepared for treatment.During the second emergent laparotomy, there was less blood in his pelvic cavity. No active bleeding was identified. His left iliac vein and artery were exposed and his entire iliac artery appeared normal and without rupture. His external iliac vein was ligated but not transected, connected only by the posterior wall, and the caudal part of his iliac vein was significantly dilated. By replacing the vascular clamp in the proximal and distal parts of the rupture, the ligations on both sides of the venous rupture were resolved. A wedge-shaped rupture was revealed, approximately 4cm in length, on the anterolateral side of his left external iliac vein. The edges of the venous rupture were smooth as a result of the knife trauma. Although the ligated parts of his iliac vein appeared congested, the lumen was smooth and contained no clot. The damaged vein was repaired with continuous 4-0 Prolene sutures (Ethicon, Inc, Somerville, NJ, USA) after the patient was systemically heparinized with 5000 units heparin. Before the sutures were finally ligated, the clamp at the cranial aspect was removed and the caudal clamp was left in place. After the backflow was clear of thrombotic debris, the clamp on his caudal iliac vein was removed and the clamp at the cranial aspect left in place. The left leg was gently massaged from calf to thigh; as a result, some thrombi in the caudal part of the vein were flushed out with the venous blood flow, and the sutures were finally ligated until the venous blood was free of thrombus. His iliac vein, although narrower after repair, was patent (Figure \n).\nAfter the operation, the patient was sent to the surgical intensive care unit with mechanical ventilation. Despite the fact that his left leg showed some signs of compartment syndrome with blisters in his calf, fasciotomy was not performed. He received systemic anticoagulation, initially with low-molecular-weight heparin, then with warfarin, titrating to an international normalized ratio (INR) between 2.0 and 2.5.Three days postoperatively, mechanical ventilation was discontinued and his signs and symptoms improved dramatically. Pulses in his left lower extremity became palpable on postoperative day 5, and the swelling and discoloration decreased. On postoperative day 30, he was taken off the OptEase® filter and the venogram showed a small amount of residual thrombus in his left external iliac vein (Figure \n). The inferior vena cava was patent, with no residual defects around the filter and no thrombus in the filter. He was discharged from the hospital in a stable condition, with full resolution of symptoms, on postoperative day 35 (Figure \nb). He was mostly asymptomatic at a recent 3-month follow-up visit except for slight edema in his left leg after walking. He continues on warfarin, maintaining an INR between 2.0 and 2.5, and wears elastic compression stockings.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 66-year-old female presented to the emergency department with three days of acute LLE swelling, pain, cyanosis, inability to bear weight, dyspnea, and hypoxemia (Figure ). She denied recent travel, hormone replacement, or a history of DVT/pulmonary embolism (PE). Her medical history was notable for systemic lupus erythematosus, CREST (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome, Sjogren’s syndrome, and local invasive anal squamous cell carcinoma. Doppler ultrasound revealed LLE thrombus extending from the greater saphenous vein to the popliteal vein. She was admitted to the intensive care unit (ICU) and started on an unfractionated heparin drip.\nThe vascular surgery team was consulted for surgical intervention. After further review of her case, the vascular surgery team elected for an endovascular approach with CDT of LLE. Initial venogram demonstrated extensive clotting of the tibial, popliteal, and femoral venous systems extending into the iliac system (Figures , ). From a tibial approach, a guidewire was advanced up to the common iliac, but a chronic occlusion of the left common iliac vein was found, which could not be crossed. A venous collateral circulation system in communication with the right iliac venous system was identified. In order to decrease the overall clot burden, two 50-cm EKOS endovascular catheters were placed in the left external iliac vein and collateral system. Repeat venogram at 24 hours post-CDT showed significant improvement of the overall clot burden with almost complete resolution of the clot in the LLE; however, the chronic occlusion remained (Figure ). A 20 x 80 mm Boston Scientific Wallstent™ (endoprosthesis stent) was advanced across the total chronic total occlusion and deployed. Post-operative venogram demonstrated significant improvement in flow in the system, with all flow going through the iliac system, and no flow further through the previously seen collaterals. Intravascular ultrasound was advanced through the area, which showed severe compression of the stent. A 12x 40 mm Atlas® dilatation catheter (Bard Peripheral Vascular Inc., Tempe, AZ, USA) was used for angioplasty. Repeat intravascular ultrasound showed persistent compression of the area. A 8 x 40 mm Boston Scientific Mustang™ dilatation catheter (high-pressure balloon) was used to re-attempt angioplasty; however, compression was still noted (Figure ). Regardless, outflow improved throughout the left common iliac system, and no further interventions were performed. The patient returned to the ICU and transitioned to direct oral anticoagulation without any further complications. She was subsequently transferred to a medicine ward for further care.

The patient is a 78-year-old woman who presented to emergency department with 2 days of gradually worsening right lower extremity (RLE) swelling, pain, and paresthesia that was limiting mobility. She was independent with a clinical frailty score of 2. Her past medical history was significant for diabetes mellitus with Hgb a1c 10.5 and a provoked left lower extremity DVT 30 years earlier treated with a course of warfarin and permanent IVC filter placement. She denied prior hypercoagulability workup and reported that her first episode of thrombosis followed a prolonged airplane ride. She was not anticoagulated at the time of presentation. She denied a history of dysrhythmias, prior embolic events, recent travel, injury, surgery, illness, or known exposure to COVID-19. She denied a family history of blood clots or hypercoagulability.\nPhysical examination revealed an RLE that was severely taut with cyanosis with nonpalpable peripheral pulses and multiphasic signaling on Doppler and tenderness to the mid-thigh. The contralateral limb was soft, nontender with color appropriate of ethnicity and palpable peripheral pulses. An RLE venous duplex ultrasound scan was performed with noncompressible veins and loss of spontaneous flow from the right popliteal vein extending to the right common femoral vein consistent with DVT. On presentation, she did not display hemodynamic instability nor complained of cardiopulmonary symptoms.\nBecause of progressive symptoms concerning for PCD and imminent development of venous gangrene in a patient with good functional status, she was admitted directly to the angiography suite for CDT and pharmacomechanical thrombectomy with tissue plasminogen activator (tPA) and heparin. Angiogram revealed thrombus extending proximal to the IVC filter in the mid-IVC (). She was transferred to the intensive care unit for continued CDT with tPA (1 mg/h) and heparin (500 u/h) through a Uni∗Fuse catheter. tPA was discontinued overnight for a fibrinogen of 82 mg/dL. The next morning, she reported subjective improvement of symptoms and return of palpable peripheral pulses with resolution of pain. She returned to the angiography suite for catheter removal and completion venogram that revealed persistent thrombus burden, and the decision to remove the remainder of the clot was made to decrease the risk of recurrence. Using the Penumbra Indigo CAT8 system (Penumbra, Alameda, Calif), mechanical suction thrombectomy, and balloon venoplasty were performed with successful recanalization (). She was transferred to the floor, heparin was discontinued, and rivaroxaban initiated.\nOn postoperative day 2, she was noted to have expressive aphasia and left-sided hemiplegia. A noncontrast computed tomography and computed tomography angiogram of the head and neck were performed without evidence of a hemorrhage or significant carotid or aortic arch atherosclerotic disease. International normalized ratio was therapeutic at 2.0. Given the concern for stroke, a diffusion-weighted magnetic resonance imaging of the brain was obtained () and was notable for the focal area of restricted diffusion within the right thalamus. Because of recent anticoagulation and thrombolysis, she was not a candidate for systemic tPA. Heparin was not reinitiated because of therapeutic international normalized ratio on rivaroxaban. She was transferred to a tertiary center with neurological and neurosurgical capabilities where she underwent a transesophageal echocardiogram with bubble study that revealed a PFO with an atrial septal aneurysm and left-to-right flow noted with color Doppler and a moderate right-to-left shunt during bubble study but no left atrial mass or thrombus. Rivaroxaban was continued and her neurological status improved. She was discharged to a rehabilitation facility with improved left-sided weakness on postoperative day 3. After 2 weeks of rehabilitation, the patient was discharged with a modified Rankin score of 1. Patency of the RLE veins was unknown at the time of discharge, but a repeat duplex ultrasound scan at 8 months after initial presentation showed chronic thrombus in the right common femoral vein, but the RLE venous system remained patent.\nBecause of multiple episodes of thrombosis, she was placed on lifelong anticoagulation with apixaban. Hypercoagulable disorder was suspected but was deferred by her hematologist as diagnosis would not change plan for management.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 49-year-old Chinese man sustained severe knife trauma and was referred to a local hospital. An exploratory laparotomy showed traumatic rupture of his left external iliac vein with massive intraperitoneal bleeding, but his iliac artery was intact. To rescue him, the proximal and distal parts of his injured external iliac vein were ligated (there was no vascular surgeon in the local hospital); however, his left leg quickly became severely swollen, cyanotic and pulseless. Two hours after the first operation, he was transferred to the emergency department of our university hospital with endotracheal tube intubation. On physical examination, he was tachycardic (142 beats per minute), hypotensive (86/50mmHg). His left lower extremity was markedly edematous, cyanotic, mottled (Figure \na) and had no palpable pulse, but his right lower extremity was normal. He was diagnosed with posttraumatic PCD. Considering the high risk of pulmonary embolism during the next surgical procedure, an OptEase® retrievable vena cava filter (Cordis Corp., New Brunswick, NJ, USA) was placed in his inferior vena cava via his right femoral vein under digital subtraction angiography (Figure \n). His abdomen was immediately reopened while his left leg was also prepared for treatment.During the second emergent laparotomy, there was less blood in his pelvic cavity. No active bleeding was identified. His left iliac vein and artery were exposed and his entire iliac artery appeared normal and without rupture. His external iliac vein was ligated but not transected, connected only by the posterior wall, and the caudal part of his iliac vein was significantly dilated. By replacing the vascular clamp in the proximal and distal parts of the rupture, the ligations on both sides of the venous rupture were resolved. A wedge-shaped rupture was revealed, approximately 4cm in length, on the anterolateral side of his left external iliac vein. The edges of the venous rupture were smooth as a result of the knife trauma. Although the ligated parts of his iliac vein appeared congested, the lumen was smooth and contained no clot. The damaged vein was repaired with continuous 4-0 Prolene sutures (Ethicon, Inc, Somerville, NJ, USA) after the patient was systemically heparinized with 5000 units heparin. Before the sutures were finally ligated, the clamp at the cranial aspect was removed and the caudal clamp was left in place. After the backflow was clear of thrombotic debris, the clamp on his caudal iliac vein was removed and the clamp at the cranial aspect left in place. The left leg was gently massaged from calf to thigh; as a result, some thrombi in the caudal part of the vein were flushed out with the venous blood flow, and the sutures were finally ligated until the venous blood was free of thrombus. His iliac vein, although narrower after repair, was patent (Figure \n).\nAfter the operation, the patient was sent to the surgical intensive care unit with mechanical ventilation. Despite the fact that his left leg showed some signs of compartment syndrome with blisters in his calf, fasciotomy was not performed. He received systemic anticoagulation, initially with low-molecular-weight heparin, then with warfarin, titrating to an international normalized ratio (INR) between 2.0 and 2.5.Three days postoperatively, mechanical ventilation was discontinued and his signs and symptoms improved dramatically. Pulses in his left lower extremity became palpable on postoperative day 5, and the swelling and discoloration decreased. On postoperative day 30, he was taken off the OptEase® filter and the venogram showed a small amount of residual thrombus in his left external iliac vein (Figure \n). The inferior vena cava was patent, with no residual defects around the filter and no thrombus in the filter. He was discharged from the hospital in a stable condition, with full resolution of symptoms, on postoperative day 35 (Figure \nb). He was mostly asymptomatic at a recent 3-month follow-up visit except for slight edema in his left leg after walking. He continues on warfarin, maintaining an INR between 2.0 and 2.5, and wears elastic compression stockings.

The patient is a 78-year-old woman who presented to emergency department with 2 days of gradually worsening right lower extremity (RLE) swelling, pain, and paresthesia that was limiting mobility. She was independent with a clinical frailty score of 2. Her past medical history was significant for diabetes mellitus with Hgb a1c 10.5 and a provoked left lower extremity DVT 30 years earlier treated with a course of warfarin and permanent IVC filter placement. She denied prior hypercoagulability workup and reported that her first episode of thrombosis followed a prolonged airplane ride. She was not anticoagulated at the time of presentation. She denied a history of dysrhythmias, prior embolic events, recent travel, injury, surgery, illness, or known exposure to COVID-19. She denied a family history of blood clots or hypercoagulability.\nPhysical examination revealed an RLE that was severely taut with cyanosis with nonpalpable peripheral pulses and multiphasic signaling on Doppler and tenderness to the mid-thigh. The contralateral limb was soft, nontender with color appropriate of ethnicity and palpable peripheral pulses. An RLE venous duplex ultrasound scan was performed with noncompressible veins and loss of spontaneous flow from the right popliteal vein extending to the right common femoral vein consistent with DVT. On presentation, she did not display hemodynamic instability nor complained of cardiopulmonary symptoms.\nBecause of progressive symptoms concerning for PCD and imminent development of venous gangrene in a patient with good functional status, she was admitted directly to the angiography suite for CDT and pharmacomechanical thrombectomy with tissue plasminogen activator (tPA) and heparin. Angiogram revealed thrombus extending proximal to the IVC filter in the mid-IVC (). She was transferred to the intensive care unit for continued CDT with tPA (1 mg/h) and heparin (500 u/h) through a Uni∗Fuse catheter. tPA was discontinued overnight for a fibrinogen of 82 mg/dL. The next morning, she reported subjective improvement of symptoms and return of palpable peripheral pulses with resolution of pain. She returned to the angiography suite for catheter removal and completion venogram that revealed persistent thrombus burden, and the decision to remove the remainder of the clot was made to decrease the risk of recurrence. Using the Penumbra Indigo CAT8 system (Penumbra, Alameda, Calif), mechanical suction thrombectomy, and balloon venoplasty were performed with successful recanalization (). She was transferred to the floor, heparin was discontinued, and rivaroxaban initiated.\nOn postoperative day 2, she was noted to have expressive aphasia and left-sided hemiplegia. A noncontrast computed tomography and computed tomography angiogram of the head and neck were performed without evidence of a hemorrhage or significant carotid or aortic arch atherosclerotic disease. International normalized ratio was therapeutic at 2.0. Given the concern for stroke, a diffusion-weighted magnetic resonance imaging of the brain was obtained () and was notable for the focal area of restricted diffusion within the right thalamus. Because of recent anticoagulation and thrombolysis, she was not a candidate for systemic tPA. Heparin was not reinitiated because of therapeutic international normalized ratio on rivaroxaban. She was transferred to a tertiary center with neurological and neurosurgical capabilities where she underwent a transesophageal echocardiogram with bubble study that revealed a PFO with an atrial septal aneurysm and left-to-right flow noted with color Doppler and a moderate right-to-left shunt during bubble study but no left atrial mass or thrombus. Rivaroxaban was continued and her neurological status improved. She was discharged to a rehabilitation facility with improved left-sided weakness on postoperative day 3. After 2 weeks of rehabilitation, the patient was discharged with a modified Rankin score of 1. Patency of the RLE veins was unknown at the time of discharge, but a repeat duplex ultrasound scan at 8 months after initial presentation showed chronic thrombus in the right common femoral vein, but the RLE venous system remained patent.\nBecause of multiple episodes of thrombosis, she was placed on lifelong anticoagulation with apixaban. Hypercoagulable disorder was suspected but was deferred by her hematologist as diagnosis would not change plan for management.

Write a detailed clinical case vignette based on the following key phrases: Deep Vein Thrombosis, Peripheral Arterial Disease, Thrombolysis

A 17-year-old female patient reported to the department two years back with the chief complaint of swelling in the right lower jaw region for the last four months. On extraoral examination a nontender swelling approximately of the size 4 cm × 2.5 cm was appreciated in the left mandibular region extending from lateral incisor to lower third molar region. There was expansion of buccal and lingual cortical plates. Incisional biopsy revealed unicystic mural ameloblastoma.\nThe patient was operated on under GA. Lesion was completely enucleated. Impacted teeth (33, 34, 35, and 36) were extracted. Peripheral osteotomy was done. Primary closure was achieved. A regular follow-up is being done. There is no sign of recurrence.

A 28-year-old female patient reported to the department with the chief complaint of swelling in the lower left back tooth region for the last three months. On extraoral examination, there was a swelling approximately of the size 4 cm × 4 cm extending from left commissure of lip to the posterior border of ramus of mandible and from ala-tragus line to 1 cm below the lower border of mandible. On intraoral examination there was bony expansion in buccal and lingual cortical plate and perforation of lingual cortical plate. Incisional biopsy was done. It revealed follicular type of ameloblastoma. Segmental resection with disarticulation of the left mandible was done followed by reconstruction with rib graft using reconstruction plate. A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 12-year-old boy reported to our institute with a chief complaint of swelling on the left side of the face for the past six months (). The patient was apparently normal 6 months back after which he noticed the swelling. The patient's general, family, and medical history was not contributory.\nExtraorally, there was a presence of diffuse swelling involving the left side of the face, extending superiorly to the left zygomatic arch, inferiorly to the lower border of the mandible, anteriorly to the corner of the mouth, and posteriorly to the retromolar portion of the mandible. There was no obliteration of nasolabial folds seen. On palpation, the swelling was hard, noncompressible, and nonreducible along with diffuse expansion of the middle and lower 3rd of the facial region.\nIntraoral examination revealed a swelling involving the retromolar trigone and molar regions with obliteration of the mucobuccal fold. On palpation, the lesion was firm to hard in consistency and nontender with expansion of left buccolingual cortical plates.\nRadiological examination of orthopantomogram showed the presence of unilocular radiolucencies extending from the last erupted molar to retromolar region ().\nBased on the above clinical and radiological findings, provisional diagnosis of unicystic ameloblastoma was given. Incisional biopsy was carried out, and the specimen was sent to the Department of Oral Pathology and Microbiology. The gross specimen measured around 1 × 0.6 × 0.4 cm to 0.2 × 0.2 × 0.1 cm in dimension, which was firm in consistency, creamish brown in colour, and irregular in shape. The histopathological examination showed sheets of odontogenic islands lined by tall columnar cells enclosing stellate reticulum-like cells along with squamous metaplasia in the connective tissue stroma extending into the peripheral epithelium. (Figures and ). These features suggested the diagnosis of acanthomatous ameloblastoma. IHC Ki-67 also showed mild positivity in fewer areas ().\nFurther radiological investigations proceeded with CT scan neck (plain and contrast) and CT Brain (). Serial axial sections of the neck were studied from the nasopharynx up to the thoracic inlet before and after intravenous contrast. The findings revealed that an expansile lytic lesion of size 5.2 × 3.4 × 6.5 cm (AP × Trans × CC) with a largely preserved peripheral cortical rim (with few areas of dehiscence), and no matrix calcification was seen arising from the left mandibular ramus involving the coronoid process but sparing the condyle (superior limit approximately 5 mm from the condyle). On contrast administration, heterogeneous enhancement with multiple nonenhancing foci (likely necrotic areas) was noted. Also, an area of few air pockets was seen within. Serial axial sections of the brain were studied. The findings revealed an expansile lytic lesion arising from the left mandibular ramus, with relative preservation of the surrounding cortical rim (with few areas of dehiscence) and no focal space occupying the lesion. There were no metastatic disseminations evident on these imaging findings which conclude the conventional type of ameloblastoma.\nSurgical treatment was planned under general anaesthesia. Extraction of 74, 34 and hemimandibulectomy of the left mandible was carried out. The resected mandible was reconstructed by free fibular graft. The weight and measurement of the resected specimen was 87 gms and 9 × 6 × 4 cm, respectively. Histopathological examination of the resected specimen revealed anastomosing follicular islands of the odontogenic epithelium lined by tall columnar cells enclosing stellate reticulum-like cells. Squamous metaplasia of the stellate reticulum-like cells was observed. Areas of cystic degeneration of the stellate reticulum-like cells were also seen. A reactive change of lymphoid tissue was seen. Based on the clinical, radiological, and histopathological examination, a final diagnosis of acanthomatous ameloblastoma was made (Figures –). A three-month postoperative follow-up of the patient showed good prognosis with no recurrence.

A 28-year-old female patient reported to the department with the chief complaint of swelling in the lower left back tooth region for the last three months. On extraoral examination, there was a swelling approximately of the size 4 cm × 4 cm extending from left commissure of lip to the posterior border of ramus of mandible and from ala-tragus line to 1 cm below the lower border of mandible. On intraoral examination there was bony expansion in buccal and lingual cortical plate and perforation of lingual cortical plate. Incisional biopsy was done. It revealed follicular type of ameloblastoma. Segmental resection with disarticulation of the left mandible was done followed by reconstruction with rib graft using reconstruction plate. A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 60-year-old male patient reported to the department of OMFS, Raja Rajeswari Dental college, Bangalore, with the chief complaint of swelling on left middle third of face for the past four months. On extraoral examination a diffuse swelling measuring approximately 5 × 4 cm was felt which extended from ala of nose to the tragus of ear and infraorbital margin to below the commissure of lip. On intraoral examination a bony hard swelling was present extending from midline to 1st premolar region and cervical margin to the nasal floor. Incisional biopsy was done. It revealed follicular type of ameloblastoma. Partial maxillectomy was done under general anaesthesia (). A regular follow-up is being done. There is no sign of recurrence.

A 28-year-old female patient reported to the department with the chief complaint of swelling in the lower left back tooth region for the last three months. On extraoral examination, there was a swelling approximately of the size 4 cm × 4 cm extending from left commissure of lip to the posterior border of ramus of mandible and from ala-tragus line to 1 cm below the lower border of mandible. On intraoral examination there was bony expansion in buccal and lingual cortical plate and perforation of lingual cortical plate. Incisional biopsy was done. It revealed follicular type of ameloblastoma. Segmental resection with disarticulation of the left mandible was done followed by reconstruction with rib graft using reconstruction plate. A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 28-year-old female patient reported to the department with the chief complaint of swelling in the lower left back tooth region for the last three months. On extraoral examination, there was a swelling approximately of the size 4 cm × 4 cm extending from left commissure of lip to the posterior border of ramus of mandible and from ala-tragus line to 1 cm below the lower border of mandible. On intraoral examination there was bony expansion in buccal and lingual cortical plate and perforation of lingual cortical plate. Incisional biopsy was done. It revealed follicular type of ameloblastoma. Segmental resection with disarticulation of the left mandible was done followed by reconstruction with rib graft using reconstruction plate. A regular follow-up is being done. There is no sign of recurrence.

A 28-year-old male patient reported to the department with the chief complaint of pain in the left lower jaw region for the last three months. Extraoral examination revealed a diffuse hard swelling measuring approximately 3 cm × 2 cm. On intraoral palpation there was expansion of buccal and lingual cortical plates. Decompression and packing with BIPP paste were done to prevent pathological fracture. After 6 months enucleation with curettage was done. Incisional biopsy revealed unicystic mural ameloblastoma. The patient was operated on under LA. A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 25-year-old male patient reported to the department with the chief complaint of swelling in the lower left back tooth region for the last year. On extraoral examination we could palpate a swelling approximately of the size 6 cm × 3 cm extending from the commissure of lip to the posterior border of the mandible. On intraoral palpation there was expansion of buccal and lingual cortical plates and perforation of lingual cortical plates. Incisional biopsy was done. It revealed plexiform ameloblastoma. The patient was operated on under GA. Segmental resection with disarticulation of the left mandible was done followed by reconstruction with microvascular fibula free flap using reconstruction plate. A regular follow-up is being done. There is no sign of recurrence.

A 28-year-old female patient reported to the department with the chief complaint of swelling in the lower left back tooth region for the last three months. On extraoral examination, there was a swelling approximately of the size 4 cm × 4 cm extending from left commissure of lip to the posterior border of ramus of mandible and from ala-tragus line to 1 cm below the lower border of mandible. On intraoral examination there was bony expansion in buccal and lingual cortical plate and perforation of lingual cortical plate. Incisional biopsy was done. It revealed follicular type of ameloblastoma. Segmental resection with disarticulation of the left mandible was done followed by reconstruction with rib graft using reconstruction plate. A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 12-year-old boy reported to our institute with a chief complaint of swelling on the left side of the face for the past six months (). The patient was apparently normal 6 months back after which he noticed the swelling. The patient's general, family, and medical history was not contributory.\nExtraorally, there was a presence of diffuse swelling involving the left side of the face, extending superiorly to the left zygomatic arch, inferiorly to the lower border of the mandible, anteriorly to the corner of the mouth, and posteriorly to the retromolar portion of the mandible. There was no obliteration of nasolabial folds seen. On palpation, the swelling was hard, noncompressible, and nonreducible along with diffuse expansion of the middle and lower 3rd of the facial region.\nIntraoral examination revealed a swelling involving the retromolar trigone and molar regions with obliteration of the mucobuccal fold. On palpation, the lesion was firm to hard in consistency and nontender with expansion of left buccolingual cortical plates.\nRadiological examination of orthopantomogram showed the presence of unilocular radiolucencies extending from the last erupted molar to retromolar region ().\nBased on the above clinical and radiological findings, provisional diagnosis of unicystic ameloblastoma was given. Incisional biopsy was carried out, and the specimen was sent to the Department of Oral Pathology and Microbiology. The gross specimen measured around 1 × 0.6 × 0.4 cm to 0.2 × 0.2 × 0.1 cm in dimension, which was firm in consistency, creamish brown in colour, and irregular in shape. The histopathological examination showed sheets of odontogenic islands lined by tall columnar cells enclosing stellate reticulum-like cells along with squamous metaplasia in the connective tissue stroma extending into the peripheral epithelium. (Figures and ). These features suggested the diagnosis of acanthomatous ameloblastoma. IHC Ki-67 also showed mild positivity in fewer areas ().\nFurther radiological investigations proceeded with CT scan neck (plain and contrast) and CT Brain (). Serial axial sections of the neck were studied from the nasopharynx up to the thoracic inlet before and after intravenous contrast. The findings revealed that an expansile lytic lesion of size 5.2 × 3.4 × 6.5 cm (AP × Trans × CC) with a largely preserved peripheral cortical rim (with few areas of dehiscence), and no matrix calcification was seen arising from the left mandibular ramus involving the coronoid process but sparing the condyle (superior limit approximately 5 mm from the condyle). On contrast administration, heterogeneous enhancement with multiple nonenhancing foci (likely necrotic areas) was noted. Also, an area of few air pockets was seen within. Serial axial sections of the brain were studied. The findings revealed an expansile lytic lesion arising from the left mandibular ramus, with relative preservation of the surrounding cortical rim (with few areas of dehiscence) and no focal space occupying the lesion. There were no metastatic disseminations evident on these imaging findings which conclude the conventional type of ameloblastoma.\nSurgical treatment was planned under general anaesthesia. Extraction of 74, 34 and hemimandibulectomy of the left mandible was carried out. The resected mandible was reconstructed by free fibular graft. The weight and measurement of the resected specimen was 87 gms and 9 × 6 × 4 cm, respectively. Histopathological examination of the resected specimen revealed anastomosing follicular islands of the odontogenic epithelium lined by tall columnar cells enclosing stellate reticulum-like cells. Squamous metaplasia of the stellate reticulum-like cells was observed. Areas of cystic degeneration of the stellate reticulum-like cells were also seen. A reactive change of lymphoid tissue was seen. Based on the clinical, radiological, and histopathological examination, a final diagnosis of acanthomatous ameloblastoma was made (Figures –). A three-month postoperative follow-up of the patient showed good prognosis with no recurrence.

A 17-year-old female patient reported to the department two years back with the chief complaint of swelling in the right lower jaw region for the last four months. On extraoral examination a nontender swelling approximately of the size 4 cm × 2.5 cm was appreciated in the left mandibular region extending from lateral incisor to lower third molar region. There was expansion of buccal and lingual cortical plates. Incisional biopsy revealed unicystic mural ameloblastoma.\nThe patient was operated on under GA. Lesion was completely enucleated. Impacted teeth (33, 34, 35, and 36) were extracted. Peripheral osteotomy was done. Primary closure was achieved. A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 60-year-old male patient reported to the department of OMFS, Raja Rajeswari Dental college, Bangalore, with the chief complaint of swelling on left middle third of face for the past four months. On extraoral examination a diffuse swelling measuring approximately 5 × 4 cm was felt which extended from ala of nose to the tragus of ear and infraorbital margin to below the commissure of lip. On intraoral examination a bony hard swelling was present extending from midline to 1st premolar region and cervical margin to the nasal floor. Incisional biopsy was done. It revealed follicular type of ameloblastoma. Partial maxillectomy was done under general anaesthesia (). A regular follow-up is being done. There is no sign of recurrence.

A 17-year-old female patient reported to the department two years back with the chief complaint of swelling in the right lower jaw region for the last four months. On extraoral examination a nontender swelling approximately of the size 4 cm × 2.5 cm was appreciated in the left mandibular region extending from lateral incisor to lower third molar region. There was expansion of buccal and lingual cortical plates. Incisional biopsy revealed unicystic mural ameloblastoma.\nThe patient was operated on under GA. Lesion was completely enucleated. Impacted teeth (33, 34, 35, and 36) were extracted. Peripheral osteotomy was done. Primary closure was achieved. A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 17-year-old female patient reported to the department two years back with the chief complaint of swelling in the right lower jaw region for the last four months. On extraoral examination a nontender swelling approximately of the size 4 cm × 2.5 cm was appreciated in the left mandibular region extending from lateral incisor to lower third molar region. There was expansion of buccal and lingual cortical plates. Incisional biopsy revealed unicystic mural ameloblastoma.\nThe patient was operated on under GA. Lesion was completely enucleated. Impacted teeth (33, 34, 35, and 36) were extracted. Peripheral osteotomy was done. Primary closure was achieved. A regular follow-up is being done. There is no sign of recurrence.

A 28-year-old male patient reported to the department with the chief complaint of pain in the left lower jaw region for the last three months. Extraoral examination revealed a diffuse hard swelling measuring approximately 3 cm × 2 cm. On intraoral palpation there was expansion of buccal and lingual cortical plates. Decompression and packing with BIPP paste were done to prevent pathological fracture. After 6 months enucleation with curettage was done. Incisional biopsy revealed unicystic mural ameloblastoma. The patient was operated on under LA. A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 25-year-old male patient reported to the department with the chief complaint of swelling in the lower left back tooth region for the last year. On extraoral examination we could palpate a swelling approximately of the size 6 cm × 3 cm extending from the commissure of lip to the posterior border of the mandible. On intraoral palpation there was expansion of buccal and lingual cortical plates and perforation of lingual cortical plates. Incisional biopsy was done. It revealed plexiform ameloblastoma. The patient was operated on under GA. Segmental resection with disarticulation of the left mandible was done followed by reconstruction with microvascular fibula free flap using reconstruction plate. A regular follow-up is being done. There is no sign of recurrence.

A 17-year-old female patient reported to the department two years back with the chief complaint of swelling in the right lower jaw region for the last four months. On extraoral examination a nontender swelling approximately of the size 4 cm × 2.5 cm was appreciated in the left mandibular region extending from lateral incisor to lower third molar region. There was expansion of buccal and lingual cortical plates. Incisional biopsy revealed unicystic mural ameloblastoma.\nThe patient was operated on under GA. Lesion was completely enucleated. Impacted teeth (33, 34, 35, and 36) were extracted. Peripheral osteotomy was done. Primary closure was achieved. A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 12-year-old boy reported to our institute with a chief complaint of swelling on the left side of the face for the past six months (). The patient was apparently normal 6 months back after which he noticed the swelling. The patient's general, family, and medical history was not contributory.\nExtraorally, there was a presence of diffuse swelling involving the left side of the face, extending superiorly to the left zygomatic arch, inferiorly to the lower border of the mandible, anteriorly to the corner of the mouth, and posteriorly to the retromolar portion of the mandible. There was no obliteration of nasolabial folds seen. On palpation, the swelling was hard, noncompressible, and nonreducible along with diffuse expansion of the middle and lower 3rd of the facial region.\nIntraoral examination revealed a swelling involving the retromolar trigone and molar regions with obliteration of the mucobuccal fold. On palpation, the lesion was firm to hard in consistency and nontender with expansion of left buccolingual cortical plates.\nRadiological examination of orthopantomogram showed the presence of unilocular radiolucencies extending from the last erupted molar to retromolar region ().\nBased on the above clinical and radiological findings, provisional diagnosis of unicystic ameloblastoma was given. Incisional biopsy was carried out, and the specimen was sent to the Department of Oral Pathology and Microbiology. The gross specimen measured around 1 × 0.6 × 0.4 cm to 0.2 × 0.2 × 0.1 cm in dimension, which was firm in consistency, creamish brown in colour, and irregular in shape. The histopathological examination showed sheets of odontogenic islands lined by tall columnar cells enclosing stellate reticulum-like cells along with squamous metaplasia in the connective tissue stroma extending into the peripheral epithelium. (Figures and ). These features suggested the diagnosis of acanthomatous ameloblastoma. IHC Ki-67 also showed mild positivity in fewer areas ().\nFurther radiological investigations proceeded with CT scan neck (plain and contrast) and CT Brain (). Serial axial sections of the neck were studied from the nasopharynx up to the thoracic inlet before and after intravenous contrast. The findings revealed that an expansile lytic lesion of size 5.2 × 3.4 × 6.5 cm (AP × Trans × CC) with a largely preserved peripheral cortical rim (with few areas of dehiscence), and no matrix calcification was seen arising from the left mandibular ramus involving the coronoid process but sparing the condyle (superior limit approximately 5 mm from the condyle). On contrast administration, heterogeneous enhancement with multiple nonenhancing foci (likely necrotic areas) was noted. Also, an area of few air pockets was seen within. Serial axial sections of the brain were studied. The findings revealed an expansile lytic lesion arising from the left mandibular ramus, with relative preservation of the surrounding cortical rim (with few areas of dehiscence) and no focal space occupying the lesion. There were no metastatic disseminations evident on these imaging findings which conclude the conventional type of ameloblastoma.\nSurgical treatment was planned under general anaesthesia. Extraction of 74, 34 and hemimandibulectomy of the left mandible was carried out. The resected mandible was reconstructed by free fibular graft. The weight and measurement of the resected specimen was 87 gms and 9 × 6 × 4 cm, respectively. Histopathological examination of the resected specimen revealed anastomosing follicular islands of the odontogenic epithelium lined by tall columnar cells enclosing stellate reticulum-like cells. Squamous metaplasia of the stellate reticulum-like cells was observed. Areas of cystic degeneration of the stellate reticulum-like cells were also seen. A reactive change of lymphoid tissue was seen. Based on the clinical, radiological, and histopathological examination, a final diagnosis of acanthomatous ameloblastoma was made (Figures –). A three-month postoperative follow-up of the patient showed good prognosis with no recurrence.

A 60-year-old male patient reported to the department of OMFS, Raja Rajeswari Dental college, Bangalore, with the chief complaint of swelling on left middle third of face for the past four months. On extraoral examination a diffuse swelling measuring approximately 5 × 4 cm was felt which extended from ala of nose to the tragus of ear and infraorbital margin to below the commissure of lip. On intraoral examination a bony hard swelling was present extending from midline to 1st premolar region and cervical margin to the nasal floor. Incisional biopsy was done. It revealed follicular type of ameloblastoma. Partial maxillectomy was done under general anaesthesia (). A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 12-year-old boy reported to our institute with a chief complaint of swelling on the left side of the face for the past six months (). The patient was apparently normal 6 months back after which he noticed the swelling. The patient's general, family, and medical history was not contributory.\nExtraorally, there was a presence of diffuse swelling involving the left side of the face, extending superiorly to the left zygomatic arch, inferiorly to the lower border of the mandible, anteriorly to the corner of the mouth, and posteriorly to the retromolar portion of the mandible. There was no obliteration of nasolabial folds seen. On palpation, the swelling was hard, noncompressible, and nonreducible along with diffuse expansion of the middle and lower 3rd of the facial region.\nIntraoral examination revealed a swelling involving the retromolar trigone and molar regions with obliteration of the mucobuccal fold. On palpation, the lesion was firm to hard in consistency and nontender with expansion of left buccolingual cortical plates.\nRadiological examination of orthopantomogram showed the presence of unilocular radiolucencies extending from the last erupted molar to retromolar region ().\nBased on the above clinical and radiological findings, provisional diagnosis of unicystic ameloblastoma was given. Incisional biopsy was carried out, and the specimen was sent to the Department of Oral Pathology and Microbiology. The gross specimen measured around 1 × 0.6 × 0.4 cm to 0.2 × 0.2 × 0.1 cm in dimension, which was firm in consistency, creamish brown in colour, and irregular in shape. The histopathological examination showed sheets of odontogenic islands lined by tall columnar cells enclosing stellate reticulum-like cells along with squamous metaplasia in the connective tissue stroma extending into the peripheral epithelium. (Figures and ). These features suggested the diagnosis of acanthomatous ameloblastoma. IHC Ki-67 also showed mild positivity in fewer areas ().\nFurther radiological investigations proceeded with CT scan neck (plain and contrast) and CT Brain (). Serial axial sections of the neck were studied from the nasopharynx up to the thoracic inlet before and after intravenous contrast. The findings revealed that an expansile lytic lesion of size 5.2 × 3.4 × 6.5 cm (AP × Trans × CC) with a largely preserved peripheral cortical rim (with few areas of dehiscence), and no matrix calcification was seen arising from the left mandibular ramus involving the coronoid process but sparing the condyle (superior limit approximately 5 mm from the condyle). On contrast administration, heterogeneous enhancement with multiple nonenhancing foci (likely necrotic areas) was noted. Also, an area of few air pockets was seen within. Serial axial sections of the brain were studied. The findings revealed an expansile lytic lesion arising from the left mandibular ramus, with relative preservation of the surrounding cortical rim (with few areas of dehiscence) and no focal space occupying the lesion. There were no metastatic disseminations evident on these imaging findings which conclude the conventional type of ameloblastoma.\nSurgical treatment was planned under general anaesthesia. Extraction of 74, 34 and hemimandibulectomy of the left mandible was carried out. The resected mandible was reconstructed by free fibular graft. The weight and measurement of the resected specimen was 87 gms and 9 × 6 × 4 cm, respectively. Histopathological examination of the resected specimen revealed anastomosing follicular islands of the odontogenic epithelium lined by tall columnar cells enclosing stellate reticulum-like cells. Squamous metaplasia of the stellate reticulum-like cells was observed. Areas of cystic degeneration of the stellate reticulum-like cells were also seen. A reactive change of lymphoid tissue was seen. Based on the clinical, radiological, and histopathological examination, a final diagnosis of acanthomatous ameloblastoma was made (Figures –). A three-month postoperative follow-up of the patient showed good prognosis with no recurrence.

A 28-year-old male patient reported to the department with the chief complaint of pain in the left lower jaw region for the last three months. Extraoral examination revealed a diffuse hard swelling measuring approximately 3 cm × 2 cm. On intraoral palpation there was expansion of buccal and lingual cortical plates. Decompression and packing with BIPP paste were done to prevent pathological fracture. After 6 months enucleation with curettage was done. Incisional biopsy revealed unicystic mural ameloblastoma. The patient was operated on under LA. A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 12-year-old boy reported to our institute with a chief complaint of swelling on the left side of the face for the past six months (). The patient was apparently normal 6 months back after which he noticed the swelling. The patient's general, family, and medical history was not contributory.\nExtraorally, there was a presence of diffuse swelling involving the left side of the face, extending superiorly to the left zygomatic arch, inferiorly to the lower border of the mandible, anteriorly to the corner of the mouth, and posteriorly to the retromolar portion of the mandible. There was no obliteration of nasolabial folds seen. On palpation, the swelling was hard, noncompressible, and nonreducible along with diffuse expansion of the middle and lower 3rd of the facial region.\nIntraoral examination revealed a swelling involving the retromolar trigone and molar regions with obliteration of the mucobuccal fold. On palpation, the lesion was firm to hard in consistency and nontender with expansion of left buccolingual cortical plates.\nRadiological examination of orthopantomogram showed the presence of unilocular radiolucencies extending from the last erupted molar to retromolar region ().\nBased on the above clinical and radiological findings, provisional diagnosis of unicystic ameloblastoma was given. Incisional biopsy was carried out, and the specimen was sent to the Department of Oral Pathology and Microbiology. The gross specimen measured around 1 × 0.6 × 0.4 cm to 0.2 × 0.2 × 0.1 cm in dimension, which was firm in consistency, creamish brown in colour, and irregular in shape. The histopathological examination showed sheets of odontogenic islands lined by tall columnar cells enclosing stellate reticulum-like cells along with squamous metaplasia in the connective tissue stroma extending into the peripheral epithelium. (Figures and ). These features suggested the diagnosis of acanthomatous ameloblastoma. IHC Ki-67 also showed mild positivity in fewer areas ().\nFurther radiological investigations proceeded with CT scan neck (plain and contrast) and CT Brain (). Serial axial sections of the neck were studied from the nasopharynx up to the thoracic inlet before and after intravenous contrast. The findings revealed that an expansile lytic lesion of size 5.2 × 3.4 × 6.5 cm (AP × Trans × CC) with a largely preserved peripheral cortical rim (with few areas of dehiscence), and no matrix calcification was seen arising from the left mandibular ramus involving the coronoid process but sparing the condyle (superior limit approximately 5 mm from the condyle). On contrast administration, heterogeneous enhancement with multiple nonenhancing foci (likely necrotic areas) was noted. Also, an area of few air pockets was seen within. Serial axial sections of the brain were studied. The findings revealed an expansile lytic lesion arising from the left mandibular ramus, with relative preservation of the surrounding cortical rim (with few areas of dehiscence) and no focal space occupying the lesion. There were no metastatic disseminations evident on these imaging findings which conclude the conventional type of ameloblastoma.\nSurgical treatment was planned under general anaesthesia. Extraction of 74, 34 and hemimandibulectomy of the left mandible was carried out. The resected mandible was reconstructed by free fibular graft. The weight and measurement of the resected specimen was 87 gms and 9 × 6 × 4 cm, respectively. Histopathological examination of the resected specimen revealed anastomosing follicular islands of the odontogenic epithelium lined by tall columnar cells enclosing stellate reticulum-like cells. Squamous metaplasia of the stellate reticulum-like cells was observed. Areas of cystic degeneration of the stellate reticulum-like cells were also seen. A reactive change of lymphoid tissue was seen. Based on the clinical, radiological, and histopathological examination, a final diagnosis of acanthomatous ameloblastoma was made (Figures –). A three-month postoperative follow-up of the patient showed good prognosis with no recurrence.

A 25-year-old male patient reported to the department with the chief complaint of swelling in the lower left back tooth region for the last year. On extraoral examination we could palpate a swelling approximately of the size 6 cm × 3 cm extending from the commissure of lip to the posterior border of the mandible. On intraoral palpation there was expansion of buccal and lingual cortical plates and perforation of lingual cortical plates. Incisional biopsy was done. It revealed plexiform ameloblastoma. The patient was operated on under GA. Segmental resection with disarticulation of the left mandible was done followed by reconstruction with microvascular fibula free flap using reconstruction plate. A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 28-year-old male patient reported to the department with the chief complaint of pain in the left lower jaw region for the last three months. Extraoral examination revealed a diffuse hard swelling measuring approximately 3 cm × 2 cm. On intraoral palpation there was expansion of buccal and lingual cortical plates. Decompression and packing with BIPP paste were done to prevent pathological fracture. After 6 months enucleation with curettage was done. Incisional biopsy revealed unicystic mural ameloblastoma. The patient was operated on under LA. A regular follow-up is being done. There is no sign of recurrence.

A 60-year-old male patient reported to the department of OMFS, Raja Rajeswari Dental college, Bangalore, with the chief complaint of swelling on left middle third of face for the past four months. On extraoral examination a diffuse swelling measuring approximately 5 × 4 cm was felt which extended from ala of nose to the tragus of ear and infraorbital margin to below the commissure of lip. On intraoral examination a bony hard swelling was present extending from midline to 1st premolar region and cervical margin to the nasal floor. Incisional biopsy was done. It revealed follicular type of ameloblastoma. Partial maxillectomy was done under general anaesthesia (). A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 25-year-old male patient reported to the department with the chief complaint of swelling in the lower left back tooth region for the last year. On extraoral examination we could palpate a swelling approximately of the size 6 cm × 3 cm extending from the commissure of lip to the posterior border of the mandible. On intraoral palpation there was expansion of buccal and lingual cortical plates and perforation of lingual cortical plates. Incisional biopsy was done. It revealed plexiform ameloblastoma. The patient was operated on under GA. Segmental resection with disarticulation of the left mandible was done followed by reconstruction with microvascular fibula free flap using reconstruction plate. A regular follow-up is being done. There is no sign of recurrence.

A 60-year-old male patient reported to the department of OMFS, Raja Rajeswari Dental college, Bangalore, with the chief complaint of swelling on left middle third of face for the past four months. On extraoral examination a diffuse swelling measuring approximately 5 × 4 cm was felt which extended from ala of nose to the tragus of ear and infraorbital margin to below the commissure of lip. On intraoral examination a bony hard swelling was present extending from midline to 1st premolar region and cervical margin to the nasal floor. Incisional biopsy was done. It revealed follicular type of ameloblastoma. Partial maxillectomy was done under general anaesthesia (). A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

A 25-year-old male patient reported to the department with the chief complaint of swelling in the lower left back tooth region for the last year. On extraoral examination we could palpate a swelling approximately of the size 6 cm × 3 cm extending from the commissure of lip to the posterior border of the mandible. On intraoral palpation there was expansion of buccal and lingual cortical plates and perforation of lingual cortical plates. Incisional biopsy was done. It revealed plexiform ameloblastoma. The patient was operated on under GA. Segmental resection with disarticulation of the left mandible was done followed by reconstruction with microvascular fibula free flap using reconstruction plate. A regular follow-up is being done. There is no sign of recurrence.

A 28-year-old male patient reported to the department with the chief complaint of pain in the left lower jaw region for the last three months. Extraoral examination revealed a diffuse hard swelling measuring approximately 3 cm × 2 cm. On intraoral palpation there was expansion of buccal and lingual cortical plates. Decompression and packing with BIPP paste were done to prevent pathological fracture. After 6 months enucleation with curettage was done. Incisional biopsy revealed unicystic mural ameloblastoma. The patient was operated on under LA. A regular follow-up is being done. There is no sign of recurrence.

Write a detailed clinical case vignette based on the following key phrases: Ameloblastoma, Mandible, Surgical Treatment

An 11-year-old girl visited our Emergency Department with fever, cough, abdominal pain and vomiting. Hypocalcemia (serum calcium, 5.0 mg/dL; ionized calcium, 0.74 mM) was noted on laboratory analysis, with normal albumin (4.3 mg/dL), and upper normal limit level of phosphorus (5.6 mg/dL).\nShe was born with 3,040 g of body weight at 37 weeks of pregnancy at our hospital and was the second child of phenotypically normal Korean parents. Imperforate anus with rectovestibular fistula and partial cleft palate were found at birth. Atrial septal defect (ASD, 3.5-mm width) was diagnosed on echocardiography performed on the first day of life. However, the karyotyping revealed normal chromosomal pattern by GTG banding. Descending colostomy was performed on the first day of life and followed by colostomy repair at 9 months of age. Pena operation (posterior sagittal anorectoplasty) was performed at 4 months of age and transposition anoplasty was done at 7 months of age. Palatoplasty for cleft palate was performed at 14 months of age, and again at 9 years of age, velopharyngeal insufficiency was surgically corrected by superiorly based pharyngeal flap with lateral port control. Echocardiography at 20 months of age showed no intracardiac anomaly, suggesting spontaneous closure of previously observed ASD. She had suffered from frequent respiratory tract infections with otitis media and chronic constipation, but there was no history of severe systemic infection. Her developmental milestones were delayed, and she was diagnosed for mild intellectual disability at 8 years of age (Intelligence quotient 57 on Korean Wechsler intelligence scale for children). She was attending a public school without specific behavioral problems, although her academic performance was poor.\nOn the third day of life, her calcium (9.2 mg/dL), phosphorus (4.5 mg/dL), and ionized calcium (1.05 mM/L) levels were normal. Her calcium level was also normal on preoperative screening before surgery at 4, 7, and 9 months of age (10.5, 10.8, and 10.6 mg/dL, respectively). Her calcium level was in low normal range on laboratory studies at 20 months and 7 years of age (9.1 and 8.9 mg/dL, respectively). The parents denied any history of hypocalcemic symptoms during her infancy or childhood.\nHer facial features appeared mildly dysmorphic, with hypertelorism, short philtrum and small down-turned mouth. Hypernasal speech was not observed. At the time of hypocalcemia onset at 11 years of age, her height was 141 cm (25th percentile) with weight 31 kg (10th–25th percentile). Her midparental height was 157 cm (10th–25th percentile). Her wrist X-ray showed bone age of 12 years without any evidence of rickets. Serum magnesium level was normal (1.63 mg/dL). The parathyroid hormone (PTH) level was inappropriately low (10.8 pg/mL; reference rage, 15–65 pg/mL) considering her plasma calcium level, suggesting hypocalcemia due to hypoparathyroidism. Serum 25(OH)D level was also decreased (11.4 ng/mL; reference range, 30–100 mg/mL). Her thyroid function was normal (thyroid-stimulating hormone, 0.28 uIU/mL; free T4, 1.68 pg/mL).\nIntravenous calcium (calcium gluconate, 100 mg/kg) was given during the first 3 days after admission, followed by oral calcium (calcium lactate, 300 mg/kg/day). Vitamin D (calcitriol, 0.75 µg/day) treatment was started on the 2nd hospital day. She was discharged on the 6th hospital day when her calcium level was 6.5 mg/dL. Her calcium level increased to 8.3 mg/dL on follow-up visit at 1 week after discharge, and her PTH level was still low (9.0 pg/mL). Although 25(OH)D level has been normalized (25.5 and 30.5 ng/mL after 2 months and 3 months, respectively) after treatment, daily administration of calcium (calcium carbonate, 62.5 mg/kg/day) and calcitriol (0.5 µg/day) was required to maintain normocalcemia (serum calcium 9.2 and 8.3 mg/dL after 2 and 3 months, respectively).\n22q11DS was suspected based on her history of velopharyngeal insufficiency and mental retardation, and fluorescence in situ hybridization analysis confirmed a deletion of chromosome 22q11.2 ().

A 12-year-old boy presented with a new onset generalized tonic-clonic seizure. He is the first child of a phenotypically normal mother. The patient was born at term after an uneventful pregnancy by an uncomplicated caesarean section with low birth weight of 2,900g (10–25th percentile). At 8 months the child underwent surgical repair of a cleft palate and at age 2 years had two episodes of febrile convulsion. He had a learning disability in his school-aged years. On family history, his father had a prominent forehead, small down-turned mouth, micrognathia, and nasal voice (). He had not undergone any prior specific evaluation, but seemed to have normal intelligence without any neuropsychiatric symptoms including a seizure history.\nPhysical examination revealed prominent forehead, small down-turned mouth, micrognathia (), and repaired cleft palate with not well formed uvula (). His height was 146 cm (25–50th percentile) and weight was 38.5 kg (25–50th percentile). Chvostek’s and Trousseau’s signs were negative. He had mild mental retardation with an intelligence quotient (IQ) of 68 on the Korean version of Wechsler Intelligence Scale for Children (K-WISC).\nThe electrocardiogram (ECG) was abnormal due to a prolonged corrected QT interval and the chest radiograph failed to show a thymus shadowing. Computed tomography (CT) of the heart revealed right aortic arch (), and CT of the brain showed multiple calcifications in the bilateral basal ganglia and both frontal white matters (). The electroencephalogram (EEG) revealed generalized intermittent slow waves without any epileptiform discharges.\nLaboratory tests showed hypocalcemia (calcium 6.5 mg/dL, ionized calcium 2.8 mg/dL), hyperphosphatemia (9.1 mg/dL) and normal level of magnesium (1.8 mg/dL). Parathyroid hormone (PTH) was decreased to 4.76 pg/mL (reference range 15–65 pg/mL) and 25-vitamin D3 was decreased to 13.6 ng/mL (reference range 30–60 ng/mL). Peripheral blood count, hepatic, renal and thyroid function tests were all normal except thrombocytopenia (144,000/μL). Immunological studies showed normal levels of Immunoglobulins but T cell subpopulation analysis was abnormal. T lymphocyte was decreased to 42.8 %/μL (reference range 52–78%/μL), CD4/CD8 T cell ratio was decreased to 0.79 (reference range 0.8–3.0).\nFluorescent in situ hybridization (FISH) analysis was performed using peripheral blood and chromosomal study was carried out using DiGeorge/VCFS TUPLE1 region probe (22q11.2) with an ARSA control probe (22q13) which confirmed a 22q11.2 deletion. His father revealed the same chromosomal abnormality, which suggests paternal inheritance in this case.\nThe patient was treated with calcium citrate and calcitriol. He remained asymptomatic with normalization of his serum calcium level with medications.

Write a detailed clinical case vignette based on the following key phrases: Hypoparathyroidism, 22q11.2 Deletion Syndrome, Developmental Abnormalities