S2757 Not All Ascites Is From Cirrhosis

Abstract

Introduction: New onset ascites commonly occurs in cirrhosis. Although uncommon, myxedema ascites should be considered when other more common causes of ascites are excluded and there is biochemical evidence of hypothyroidism. We present a case of myxedema ascites confounded initially by presence of alcoholic cirrhosis. Case Description/Methods: A 59-year-old African American male with a past medical history of alcohol misuse, CAD, Hashimoto’s disease s/p radioablation therapy with subsequent hypothyroidism, presented with chest pain and abdominal distension. Acute coronary syndrome was ruled out, and pain was attributed to a GI etiology. A contrast CT of abdomen/pelvis was done showing evidence of cirrhosis and large volume ascites, concerning for acute decompensation. A chronic liver disease panel was noncontributory, and etiology was thought to be secondary to alcohol misuse. Paracentesis revealed SAAG < 1.1, total protein 4.2, with negative cultures and cytology. Further evaluation revealed TSH of 86 with T4 < 0.1 and constellation of symptoms (cold intolerance, weight gain, puffiness, esophageal dysmotility causing burning chest pain, hypothyroidism induced myopathy) pointed to severe hypothyroidism. He was treated with IV levothyroxine for 3 days followed by oral therapy with complete resolution of the ascites, and the etiology was thought to be secondary to myxedema. Discussion: Cirrhosis causing portal hypertension is the commonest cause of ascites. Hypothyroidism is a rare cause of ascites wherein the fluid accumulation occurs because of increased capillary permeability. This results in ascitic fluid are high in total protein ( >2.5 g/dl; mean - 3.9 g/dl) and variable SAAG (mean - 1.5 g/dl; range 0.8–2.3 g/dl). Table 1 mentions common causes of ascites classified based on SAAG. WBC counts in ascitic fluid can be low or high, consisting predominantly of lymphocytes. Myxedema ascites responds well to thyroid replacement therapy and is completely reversible, without any role for diuretics. In our case a presumptive diagnosis of decompensated cirrhosis was made based on imaging evidence of ascites and cirrhosis, but ascitic fluid studies refuted portal hypertension. Further negative cytology, low WBCs, negative bacterial and tubercular cultures ruled out malignancies or infectious peritonitis. Based on further constellation of symptoms, biochemical abnormalities, and a good response to intravenous levothyroxine, patient was diagnosed with myxedema ascites.Table 1.: Classification of most frequent causes of ascites. SAAG, serum ascites albumin gradient.Figure 1.: (a) Coronal section showing ascites (red arrows) (b) Axial section showing widened hepatic fissure (green arrows) and ascites (red arrows).