Today we discussed a case of a patient with history of 3 primary malignancies s/p Whipple remotely, presenting with chronic watery diarrhea found to have ascites on exam, severe hypoalbuminemia, and later imaging evidence of SVC occlusion (unclear if due to thrombosis vs. surgical scarring), complicated by mesenteric varices--overall consistent with chronic mesenteric ischemia with malabsorptive diarrhea and ascites with low SAAG due to malnutrition. Some learning points:
1) The serum albumin to ascites gradient (SAAG) can help differentiate the etiology of ascites, as nicely summarized in this diagram by Dr. Mansoor:
2) The rational clinical exam for ascites: check out this oldie but goodie from JAMA about how to "divine fluid in the abdomen." Highlights are: best likelihood ratio from the physical exam is for the fluid wave with a LR of 6! Shifting dullness LR=2.7, flank dullness= 2, bulging flanks=2.
3) Anticoagulation for patients with mesenteric thrombosis is in some cases, controversial. In a clinical update in Circulation from 2015: "Anticoagulation is prescribed in acute, subacute, and chronic MVT. Several small, retrospective investigations have demonstrated the benefit of anticoagulation in acute MVT... In chronic MVT, anticoagulation may promote recanalization and prevents new thrombosis. One study in patients with chronic MVT showed that 93% of patients treated with anticoagulation either partially or completely recanalized the occluded vessel. Few data are available for patients with portal hypertension resulting from chronic MVT, although heightened consideration should be given to the risk of bleed in those with esophageal varices." The standard is warfarin since NOACS have not been extensively studied.
4) Protein-losing gastroenteropathy should be suspected in patients with edema and hypoalbuminemia in whom there is no other apparent cause of protein loss (eg, proteinuria) or inadequate synthesis (eg, liver diseases) or supply (eg, protein malnutrition). The diagnosis of protein-losing gastroenteropathy is established by an increase in alpha-1 antitrypsin clearance (which you can assess with a 24 hour stool collection).