Academic Editor: Carmen Bernal Bellido
Affilation: University Hospital Virgen del RocÃo
A 69 year old female with a history of pancreatic mucinous cystadenoma (treated with Whipple procedure) and recently presumed liver cirrhosis presented to the hospital with melanotic stools. The source of the bleeding was initially thought to be secondary to upper gastrointestinal (GI) varices due to portal hypertension from the liver disease. Upper endoscopy found no active bleeding and confirmed grade 2 gastric varices with gastric wall edema. Due to persistent symptoms and inability to locate the exact source, she went to the operating room for possible transjugular intrahepatic portosystemic shunt (TIPS) but was not found to have any porto-systemic gradient. Instead, she was found to have an isolated stenosis of the left gastric vein, which was treated with balloon angioplasty and eventual splenectomy. Upper GI varices usually occur due to portal hypertension from liver disease. Extra hepatic causes are much rarer. We report a case of upper GI bleed from gastric varices secondary to left gastric vein stenosis rather than portal hypertension. The stenosis was due to a rare complication of a Whipple procedure. The case is unique as there are no reported cases of gastric varices secondary to left gastric vein stenosis.
Upper GI varices are a common complication of portal hypertension
A 69 year old female with a history of pancreatic mucinous cystadenoma (treated with Whipple procedure) and recently presumed liver cirrhosis presented to the hospital with dizziness and melanotic stools. On presentation, she was hypotensive with a blood pressure of 85/50 mmHg and tachycardic with a heart rate of 115 beats per minute. Her physical exam was pertinent for pale skin, dry oral mucosa, and delayed capillary refill. Her complete blood count showed a hemoglobin level of 5.7 g/dL which was a significant drop from her baseline of 10 g/dL. Her liver functions tests and coagulation parameters were within normal limits. Computed tomography (CT) of the abdomen with contrast showed a mildly nodular liver and no signs of bleeding. She was resuscitated with blood transfusions and intravenous fluids. Her GI bleed was treated with octreotide and pantoprazole infusions. Gastroenterology specialists were consulted immediately. Patient was taken for an esophagogastroduodenoscopy (EGD) next morning which failed to find an active bleeding source but showed grade 2 gastric varices with significant gastric wall edema. Despite medical management, patient continued to have persistent symptoms. CT enterography also revealed prominent gastric varices and gastric body wall edema (
RBC scan showed a possible bleeding source in the stomach. Patient was then taken to the operating room by interventional radiology for possible embolization or TIPS. Surprisingly, there was no porto-systemic pressure gradient. Instead, patient was found to have an isolated left gastric vein stenosis (
|Test (Ab = Antibody, Ag = Antigen)||Result|
|Liver kidney microsomal Ab||Negative|
|Anti- Smooth Ab||Negative|
|Alpha Feto Protein||1 ng/mL|
|HIV Ag Ab Combo Screen||Negative|
|Vitamin B12||403 pg/mL|
|Anti-Neutrophilic cytoplasmic Ab||Negative|
When a patient with liver disease presents with upper GI bleeding, the culprit is usually considered to be bleeding varices. Even though upper GI varices are most commonly associated with liver cirrhosis, they can sometimes occur due to extra hepatic causes
Our patient was presumed to have a diagnosis of liver cirrhosis due to previously diagnosed low grade esophageal and gastric varices (on EGD) and mild nodularity of the liver contours on abdominal imaging. When she presented to the hospital with melanotic stools, it was reasonably assumed that she was having a variceal bleed. As mentioned, patient did not have a porto-systemic pressure gradient which was inconsistent with liver cirrhosis and in turn, portal hypertension as the driving force of the variceal bleeding. Patient was in fact misdiagnosed with liver cirrhosis. Instead, she was found to have a left gastric vein stenosis causing increase in pressure in her gastric venous circulation resulting in the gastric varices and gastric body wall edema. Due to the slow flow of the bleeding, it was not detectable on EGD or angiography but the tagged RBC scan was able to show stomach as the likely source of bleeding. Due to the fragility of the involved blood vessel, balloon angioplasty was chosen as a treatment modality instead of stenting. To further aid the situation, splenic artery was embolized to reduce venous flow to the stenosed blood vessel. Despite these interventions, patient required repeat angioplasty and eventual splenectomy to finally resolve her bleeding. While there are reports of isolated gastric varices due to splenic vein compromise, left gastric vein stenosis is a very rare phenomenon with no reported cases in the literature
In conclusion, though, portal hypertension from liver disease is a common cause of upper GI varices, rare causes such as extra hepatic vein stenosis should also be considered in the differential. Clinicians must be aware of the vascular anatomy in understanding such causes as any distal hindrance in venous flow can cause back pressure resulting in proximal variceal formation and subsequent bleeding.