A 48–year–old woman presented with six weeks of worsening right upper quadrant pain and lower extremity edema. Associated symptoms included nonbloody diarrhea. She also noted one week of dyspnea while lying flat. Her medical history consisted of osteogenesis imperfecta, hepatitis C, and hypertension. Additionally, she had a recent admission three weeks prior for anemia treated with blood transfusion. Her edema at that time was diagnosed as hepatitis C cirrhosis. Tachycardia of 105 bpm was her only abnormal vital sign. She had severe abdominal tenderness worse in the right upper quadrant, 2+ pitting edema of bilateral lower extremities, and dullness to percussion of the right lower lung. CMP revealed a total protein of 4, albumin 0.8, T.bili 0.4, AST 30, ALT 43, and Alk phos 166. She also had WBC 7, Hb 10, INR 1, and prealbumin of 8. There was no proteinuria on urinalysis. Chest X–ray revealed a moderate right pleural effusion. Right upper quadrant ultrasound lacked findings for cirrhosis. CT of the abdomen with contrast revealed mural thickening and mucosal edema from distal ileum to proximal transverse colon. GI consult lead to colonoscopy, which demonstrated moderate to severe colitis of transverse colon, ascending colon, and cecum with friable and edematous mucosa. Biopsy of the ascending colon diagnosed Crohn’s disease.
Hypoproteinemia and lower extremity edema are common complaints encountered by the hospitalist. Cirrhosis could be suspected in a patient with a history of hepatitis C. However, in the setting of severely low albumin with less impressive liver enzymes, bilirubin and INR, other differentials should be considered. With albumin less than one in the absence of proteinuria or hepatic dysfunction, protein–losing enteropathy moves up on the differential. Protein–losing enteropathy is not a specific disease but a group of disorders with hypoproteinemia and edema that do not involve renal or hepatic systems. Protein loss in the gastrointestinal tract can be due to mucosal ulceration seen with inflammatory bowel disease, altered mucosal permeability as in celiac disease, and lymphatic dysfunction from obstruction or cardiac disease. The work–up is extremely important since only treatment of the underlying disease process will correct the hypoproteinemia.
Patients who are well established in the medical system may ironically fall through the cracks because of a heavy reliance on past diagnoses. It is important for the hospitalist to approach each admission with a critical eye to guide current work–up.