A Mysterious Cause of Gastrointestinal Bleeding Disguising Itself as Diverticulosis and Peptic Ulcer Disease: A Review of Diagnostic Modalities for Aortoenteric Fistula

An 81-year-old male with a history of hypertension, hyperlipidemia, smoking, and peptic ulcer disease (PUD) presented with 2 episodes of maroon stools for 3 days and was found to be orthostatic. His PUD was thought to have accounted for a previous upper gastrointestinal (GI) bleed. A colonoscopy revealed 3 polyps and a few diverticuli throughout the colon that were considered to be the source of the bleeding. Two months later, the patient had massive lower GI bleeding and developed hypovolemic shock with a positive bleeding scan in the splenic flexure; however, angiography was negative. A repeat colonoscopy revealed transverse/descending colon diverticular disease and the patient was scheduled for a left hemicolectomy for presumed diverticular bleeding. Intraoperatively, an aortoenteric (AE) fistula secondary to an aorto-bi-iliac bypass graft placed during an abdominal aortic aneurysm (AAA) repair 14 years prior was discovered and was found to be the source of the bleeding. The patient had an AE fistula repair and did well postoperatively without further bleeding. AE fistulas can present with either upper GI or lower GI bleeding, and are universally deadly if left untreated. AE fistulas often present with a herald bleed before life-threatening bleeding. A careful history should always be elicited in patients with risk factors of AAAs such as hypertension, hyperlipidemia and a history of smoking. Strong clinical suspicion in the setting of a scrupulous patient history is the most important factor that allows for the diagnosis of an AE fistula. There are numerous diagnostic modalities for AE fistula, but there is not one specific test that universally diagnoses AE fistulas. Nuclear medicine scans and angiography should not be completely relied on for the diagnosis of AE fistulas or other lower GI bleeds for that manner. Although the conventional paradigm for evaluating lower GI bleeds incorporates nuclear medicine scans and angiography, there is evidence that early endoscopy with enteroscopy may have a better role in severe lower GI bleeding

A rare cause of chronic mesenteric ischemia from fibromuscular dysplasia: a case report

<p>Abstract</p> <p>Introduction</p> <p>Chronic mesenteric ischemia is a condition that is classically associated with significant atherosclerosis of the abdominal arteries, causing postprandial abdominal pain out of proportion to physical examination. The abdominal pain is exacerbated after meals due to the shunting of blood away from the intestines to the stomach, causing relative ischemia. More than 95% of chronic mesenteric ischemia cases are due to atherosclerosis. We report the first known case of chronic mesenteric ischemia from fibromuscular dysplasia. To the best of our knowledge, this is also the first known case in the literature where postprandial abdominal pain was the presenting symptom of fibromuscular dysplasia.</p> <p>Case presentation</p> <p>A 44-year-old Caucasian woman with a history of hypertension and preeclampsia, who had taken oral contraceptive pills for 15 years, presented with an intractable, colicky abdominal pain of two weeks duration. This abdominal pain worsened with oral intake. It was also associated with diarrhea and vomiting. Physical examination revealed stage III hypertension out of proportion to her risk factors and diffuse abdominal pain without peritoneal signs. An abdominal computed tomography scan, completed in the emergency room, revealed nonspecific colitis. Laboratory work revealed leukocytosis with a left shift, an erythrocyte sedimentation rate of 79 and a C-reactive protein level of 100. She was started on intravenous flagyl and intravenous ciprofloxacin. However, all microbial cultures were negative including three cultures for clostridium difficile. Urine analysis revealed nephritic range proteinuria. The laboratory profile was within normal limits for perinuclear-anti-neutrophil cytoplasmic antibody, cytoplasmic-anti-neutrophil cytoplasmic antibody, anti-saccharomyces cerevisiae antibody, antinuclear antibody test, celiac profile, lactate, carbohydrate antigen-125 and thyroid stimulating hormone. A colonoscopy was completed, which revealed diffuse colonic lymphoid reactive hyperplasia. A small bowel series was negative for any inflammation. An indium scan, pan-computed tomography scan and transvaginal ultrasound were also negative. Magnetic resonance angiography of her abdomen revealed proximal superior mesenteric artery stenosis, which was confirmed by computed tomography angiogram findings of severe proximal and distal superior mesenteric artery stenosis, consistent with the appearance of fibromuscular dysplasia on angiography in the absence of vasculitis or atherosclerotic disease. The patient's superior mesenteric artery stenosis was subsequently angioplastied suboptimally and had to be stented with an Angioplus stent. One month after she was admitted, her abdominal pain and tolerance to oral feeds improved tremendously.</p> <p>Conclusion</p> <p>Fibromuscular dysplasia most commonly presents with renal artery stenosis, which rarely causes abdominal pain. This case illustrates how fibromuscular dysplasia can present as a rare cause of chronic mesenteric ischemia, similar to chronic mesenteric ischemia from atherosclerosis.</p

Hemobilia caused by a ruptured hepatic cyst: a case report

<p>Abstract</p> <p>Introduction</p> <p>Hemobilia is a rare cause of upper gastrointestinal bleeding. More than 50% of hemobilia cases are related to iatrogenic trauma from hepatobiliary procedures, and needle biopsy of the liver represents the most common cause. A minority of hemobilia cases are due to hepatobiliary disorders such as cholangitis, hepatobiliary cancers, choledocholithiasis, and vascular abnormalities in the liver. The classic presentation of hemobilia is the triad of right upper quadrant (biliary) pain, obstructive jaundice, and upper gastrointestinal bleeding. We report a rare case of hemobilia caused by a spontaneous hepatic cyst rupture, where our patient presented without the classical symptoms, in the absence of therapeutic or pathological coagulopathy, and in the absence of spontaneous or iatrogenic trauma.</p> <p>Case presentation</p> <p>A 91-year-old African-American woman was referred to our out-patient gastroenterology clinic for evaluation of mild epigastric pain and intermittent melena. An abdominal computed tomography scan was remarkable for multiple hepatic cysts. Esophagogastroduodenoscopy revealed multiple blood clots at the ampulla of Vater. Endoscopic retrograde cholangiopancreatography showed a single 18 mm-sized filling defect in the common hepatic duct wall at the junction of the right and left hepatic duct, adjacent to one of the hepatic cysts. The ruptured hepatic cyst communicated to the bile ducts and was the cause of hemobilia with an atypical clinical presentation.</p> <p>Conclusion</p> <p>Hemobilia is an infrequent cause of upper gastrointestinal bleeding and rarely occurs due to hepatic cyst rupture. To the best of our knowledge, this is only the second case report in the literature that describes hemobilia due to hepatic cyst rupture. However, it is the first case in the literature of hemobilia due to hepatic cyst rupture in the absence of iatrogenic or spontaneous trauma, and in the absence of a spontaneous or pathological coagulopathy.</p

Recurrent hypothermia and hypoglycemia as the initial presentation of hepatitis C

Hepatitis C most commonly manifests with asymptomatic elevations in transaminase levels or in advanced stages, may present with hepatic encephalopathy or ascites. We report the first case in the literature, in which the initial manifestation of hepatitis C induced chronic liver disease was recurrent hypoglycemia and hypothermia. In our case, the hypoglycemia was induced by glycogen depletion from hepatitis C induced chronic liver disease. In chronic liver disease, glycogen stores are depleted from extensive fibrosis and it has been shown that glycogen depletion may herald hepatic encephalopathy, which later manifested in our patient

Hypergastrinemia and recurrent type 1 gastric carcinoid in a young Indian male: Necessity for antrectomy?

Carcinoid tumors are the most common neuroendocrine tumors. Gastric carcinoids represent 2% of all carcinoids and 1% of all gastric masses. Due to the widespread use of Esophagogastroduodenoscopy for evaluating a variety of upper gastrointestinal symptoms, the detection of early gastric carcinoids has increased. We highlight an alternative management of a young patient with recurrent type 1 gastric carcinoids with greater than 5 lesions, as well as lesions intermittently greater than 1 cm. Gastric carcinoids have a variable presentation and clinical course that is highly dependent on type. Type 1 gastric carcinoids are usually indolent and have a metastasis rate of less than 2%, even with tumors larger than 2 cm. There are a number of experts as well as organizations that recommend endoscopic resection for all type 1 gastric carcinoid lesions less than 1 cm, with a follow-up every 6-12 mo. They also recommend antrectomy for type 1 gastric carcinoids with greater than 5 lesions, lesions 1 cm or greater, or refractory anemia. However, the American Society of Gastrointestinal Endoscopy guidelines state that type 1 gastric carcinoid surveillance is controversial based on the evidence and could not make an evidence-based position statement on the best treatment modality. Our report illustrates a rare cause of iron deficiency anemia in a young male (without any medical history) due to multiple recurrent gastric carcinoid type 1 lesions in the setting of atrophic gastritis causing hypergastrinemia, and in the absence of a vitamin B12 deficiency. Gastric carcinoid type 1 can present in young males without an autoimmune history, despite the known predilection for women aged 50 to 70 years. Type 1 gastric carcinoids can be managed by endoscopic resection in patients with greater than 5 lesions, even with lesions larger than 1 cm. This course of treatment enabled the avoidance of early antrectomy in our patient, who expressed a preference against more invasive measures at his young age

Metastatic Renal Cell Cancer and a Gastric Mass: An Unusual Finding

Renal cell cancer (RCC) accounts for approximately 3% of all adult malignancies. RCC has a metastasis rate of approximately 25%, which is most commonly to the lungs (>50%). On the contrary, RCC metastasis to the gastrointestinal tract (excluding the liver) is very uncommon and ranges from 0.2 to 0.7%. Thus, a gastric cancer in a patient with known metastatic RCC would most likely be secondary to metastasis. We present the first reported case of a metastatic RCC coexisting with a new-onset primary gastric cancer and a review of management using guidelines from metastatic RCC to the stomach. An 82-year-old African American male with papillary RCC status post left nephrectomy with recurrence of liver metastasis presented with failure to thrive shortly after his third cycle of chemotherapy despite stable disease by imaging studies. He had received 7 chemotherapy cycles of Gemzar, Nexavar, and Avastin prior to admission. He subsequently had a drop in his hemoglobin and was found to have hemoccult positive stool in the setting of recent Avastin. Endoscopic evaluation showed a 3 cm ulcerated mass in the cardia which was biopsied. The biopsy showed invasive and poorly differentiated gastric adenocarcinoma unrelated to his RCC. The patient subsequently underwent partial gastrectomy with loop gastrojejunostomy for resection of his stage 1 primary gastric adenocarcioma. The surgery also facilitated future chemotherapy (Avastin), which could not be given prior to surgery due to its side effect of bleeding. The patient did not receive adjuvant chemoradiation for his gastric cancer due to his comorbidities at the time and was doing well at a one month follow-up. Metastatic RCC and primary gastric cancer can coexist, especially when there is an overlap of risk factors such as smoking or nitrosamines. The management of a gastric cancer in the setting of metastatic RCC is similar to the management of solitary primary gastric carcinoma. Treatment of the primary gastric cancer can facilitate future chemotherapy such as Avastin, which has been recently approved for the treatment of metastatic RCC