INTRODUCTION: Pancreatic duct disruption is a known complication of pancreatitis which leads to the formation of pancreatic pseudocysts, pancreatic ascites, and high amylase pleural effusions. Pancreatic pseudocysts migrate along with the pancreatic tissue and rupture either into surrounding organs or into the free peritoneal cavity. Splenic complications of pancreatitis are rare and include splenic vein thrombosis, splenic artery rupture, splenic rupture or infarction, and splenic hematoma. CASE DESCRIPTION/METHODS: 39 y/o alcoholic male admitted for acute pancreatitis. Imaging revealed pseudocysts and ascites. Initially, he improved with supportive care but abdominal pain recurred owing to splenic rupture with resultant splenic hematoma. Splenic artery coiling was employed to stop bleeding. He returned for recurrent abdominal pain and new chest pain with interval increase in size of pseudocyst and interval development of pleural effusion. EUS revealed a multiloculated pancreatic pseudocyst, as well as pancreatic duct disruption. Transgastric drainage of the pseudocyst was performed with an Axios stent. Repeat endoscopy at interval showed complete resolution of the cyst. DISCUSSION: Studies estimate the incidence of pancreatic pseudocyst rupture into the spleen at a rate of up to 1.1% of patients with acute pancreatitis. Another study of patients with chronic pancreatitis reports splenic pseudocyst as the most common lesion, followed by splenic rupture and hematoma. A more recent study of 500 men with chronic alcoholic pancreatitis found that only 2.2% develop splenic complications with intrasplenic pseudocyst being the most common lesion, followed by splenic rupture and subcapsular hematoma. Findings associated with the highest risk of developing splenic complications included pancreatic tail necrosis, distal pseudocyst, or splenic vein occlusion. Previously, the mainstay of treatment for splenic hematoma was splenectomy with distal pancreatectomy. However, with the advent of advanced endoscopic procedures, patients are safely managed with splenic artery embolizationand EUS guided pancreaticogastrostomy or percutaneous drainage. Endoscopic drainage and percutaneous drainage of symptomatic pseudocysts are preferred to surgical management. Furthermore, recent reviews show that endoscopic drainage is superior to percutaneous drainage with lower rates of reintervention, shorter hospital stays, and need for less follow-up imaging.
BACKGROUND Acute gastric remnant bleeding is a rare complication of bariatric surgery. Furthermore, acute bleeding from the gastric remnant resulting in gastric remnant outlet obstruction has not been described previously. Endoscopic management of gastric remnant bleed has been challenging due to difficulty accessing the excluded stomach. Traditionally, this necessitates surgical intervention. Recently, however, the adoption of endoscopic ultrasound-directed transgastric intervention provides an alternative approach to management. CASE SUMMARY A 65-year-old male with a prior gastric bypass presented with the sudden onset of progressive abdominal distension, nausea, and melena of two days duration. His imaging illustrated a massively distended stomach. A nasogastric tube did not result in drainage of fluid or decompression of his abdomen. His endoscopy revealed a normal-appearing gastro-jejunal anastomosis and confirmed the distended "fluid"-filled gastric remnant. An endoscopic ultrasound-directed gastrogastrostomy was created to decompress the gastric remnant. Two liters of blood was suctioned before a large adherent clot was visualized in the gastric antrum. The patient underwent emergent angiography with embolization of the gastroduodenal artery. He was discharged with a stable hemoglobin level and resolution of symptoms. Healing superficial gastric ulcers were visualized on a follow-up endoscopy. Gastric biopsies were consistent with Helicobacter pylori infection for which the patient was treated, and successful eradication was achieved. CONCLUSION This patient benefited from a timely diagnosis and effective therapy of an acute gastric remnant obstruction from a bleeding ulcer with endoscopic ultrasound-directed transgastric intervention.
Figure 1. a: Lesion development prior to EMR. b: Cap-assisted underwater technique piecemeal EMR performed using hot 20 mm and 10 mm snares. c: Lesion was completely removed, retrieved, and APC ablation was performed on residual tissue adjacent to the resection site, as well as resection bed.
INTRODUCTION: Extra-hepatic portal vein obstruction (EHPVO) presents with manifestations of portal hypertension, including variceal bleed. Cirrhosis is the leading cause of portal hypertension (90%), and EHPVO can mask as cirrhosis, especially in a patient with risk factors such as alcohol abuse and incarceration. CASE DESCRIPTION/METHODS: 37 y/o male with h/o DVT and alcohol abuse presented to our ER for abdominal pain and hematemesis. He was a chronic alcoholic but quit drinking 6 months prior. On admission, he was afebrile, mildly tachycardic but not hypotensive. Examination showed non-specific diffuse abdominal tenderness and jaundice. Labs showed Hb 5.8 g/dL, platelets 66/mcL, INR 2.13. Liver enzymes were normal, except T Bili of 5.1 mg/dL, and albumin 3.8 g/dL. Entire cirrhotic work-up was negative. CT abdomen showed nodular liver, splenomegaly, mild ascites, and gastroesophageal varices. Doppler US showed hepatopedal flow within the main portal vein. Triple-phase CT showed portal vein thrombosis (PVT) with cavernous transformation. EGD revealed large esophageal varices with red wale sign, which were banded. No gastric or duodenal varices. Colonoscopy revealed diffuse melena up to the terminal ileum, but no varices. Liver biopsy was negative for cirrhosis. The patient was found to have a heterozygous Factor V Leiden (FVL) gene mutation. Anticoagulation was not initiated due to recent bleed. He was re-admitted, unconscious after massive GI bleeding at home. Repeat banding was performed. SMA angiography and portography showed complete occlusion of the main SMA, splenic vein, and PV. DISCUSSION: For patients with portal hypertension secondary to portal vein thrombosis, the Bevano VI guidelines on portal hypertension recommend primary prophylaxis with non-selective beta-blockers and endoscopic variceal ligation. Failure of primary prophylaxis requires secondary prophylaxis with TIPS. However, surgical devascularization, such as the modified Sugiura procedure, is a great option with lower rates of re-bleeding and higher rates of survival compared to surgical shunts. Decompressive portal therapy is an important treatment aspect for our patient due to his need for lifelong anticoagulation in the setting of inherited thrombophilia.
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