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Home , Acute pancreatitis, Hepatic encephalopathy, Pancreatitis

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Deepak Gunjan, Vishal Sharma 10.5005/jp-journals-10068-0020 CASE REPORT

Acute as a Precipitant of Acute-on-chronic Failure in a Patient with Underlying C-related 1Deepak Gunjan, 2Vishal Sharma

by and/or in a patient with previ- ABSTRACT ously diagnosed or undiagnosed chronic .1 A 66-year-old male, had coronary artery disease and dia- Also, it has been purported to include any precipitating betes mellitus, presented with acute onset epigastric pain event resulting in deterioration of hepatic function and with radiation to back. He had non-bilious of 4 days often associated with failure.2 The causes of acute duration. Initial blood investigation showed elevated serum in ACLF are variable, and it can be infectious and . Abdominal imaging revealed , edematous 1 pancreatitis with per-pancreatic fat stranding, and evidence of noninfectious. Interestingly, one report ascribes up to 3 chronic liver disease. Further etiological work-up for chronic 60% of cases of acute insults in ACLF to be nonhepatic. liver disease showed anti- (HCV) reactiv- We describe here the case of ACLF where acute biliary ity. Small varices were detected on upper gastrointestinal pancreatitis was the acute insult resulting in presentation endoscopy. During hospitalization, he developed ascites, with and ascites in a patient with the previously non-cholestatic jaundice, and . Ascitic fluid analysis showed evidence of spontaneous bacterial undiagnosed liver disease because of HCV. and serum-ascites gradient of 1.8 g/dL. He was treated with intravenous and syrup CASE REPORT and discharged with the advice for maintaining salt restricted diet and was initiated on . Biliary A 66-year-old male, a retired government employee was acting as a precipitant for acute-on-chronic (ACLF) a known diabetic and had coronary artery disease. He is an uncommon event. This case highlights acute pancreatitis presented with acute onset epigastric pain abdomen with as a noninfectious and nonhepatic insult to precipitate ACLF radiation to the back of 4 days duration. The pain was in previously unknown chronic liver disease related to HCV. associated with recurrent bouts of non-bilious vomiting. Keywords: Acute-on-chronic liver failure, Ascites, Cirrhosis, After 2 days of onset of pain, he developed non-cholestatic , , Pancreatitis. jaundice and progressive diffuse abdominal distention. How to cite this article: Gunjan D, Sharma V. Acute Pan- On , he had pallor, icterus, hepato- creatitis as a Precipitant of Acute-on-chronic Liver Failure splenomegaly, and ascites. On investigations, his hemo- in a Patient with Underlying Hepatitis C-related Cirrhosis. globin was 12.8 g/dL, total leukocyte count–8000/µL, and J Gastrointest Infect 2018;8(1):46-47. platelet count–68,000/µL. revealed Source of support: Nil elevated (total bilirubin–9.41 mg/dL, conjugated Conflict of interest: None bilirubin–6.13 mg/dL) and transaminases (aspartate aminotransferase–101 U/L, alanine aminotransferase–135 INTRODUCTION U/L), alkaline phosphatase–62 U/L, Acute-on-chronic liver failure (ACLF) is a distinct clini- 30 seconds (control–14 seconds) and amylase- 392 U/L cal entity. Various definitions are ni vogue for ACLF. It (normal <100 U/L). Ascites was high as indicated by has been defined as acute hepatic insult manifesting as serum-ascites albumin gradient (SAAG) of 1.8 g/dL) and jaundice and coagulopathy, complicated within 4 weeks amylase of 29 U/L. There was evidence of spontaneous bacterial peritonitis with 600 cells per mm3 with neu- trophilic predominance. The ascitic fluid cultures were 1,2 Assistant Professor sterile. On etiological workup for chronic liver disease, 1 Department of , All India Institute of Medical anti-HCV was reactive. HCV RNA levels were >106 IU/mL Sciences, New Delhi, India and the genotype was 3. Ultrasonography of abdomen 2Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, India showed small liver with an irregular outline, spleno- Corresponding Author: Vishal Sharma, Assistant Professor, megaly, ascites, and cholelithiasis. Contrast-enhanced Department of Gastroenterology, Postgraduate Institute of computed tomography was performed on the abdomen, Medical Education and Research, Chandigarh, India, e-mail: and it showed evidence of edematous pancreatitis with fat [email protected] stranding, ascites and nodular liver. Upper gastrointestinal 46 JGI

Acute Pancreatitis as a Precipitant of ACLF in Hepatitis endoscopy revealed three columns of small varices. Rest pancreatitis; however, in our patient ascitic fluid amylase of the workup for liver disease including was within normal limits but SAAG was high. Kuo surface antigen, autoimmune marker, iron profile, and et al5 studied the association of acute pancreatitis with serum ceruloplasmin were normal. He was treated with fulminant hepatic failure and acutely decompensated intravenous ceftriaxone and syrup lactulose. He was chronic liver disease. These workers found that acute discharged with the advice to maintain a salt-restricted pancreatitis is associated with severe hepatocellular syn- diet and was initiated on diuretics. At 4 weeks of follow- thetic dysfunction, increased risk of organ failure, more up, he was free of ascites, and his bilirubin had reduced rapid decompensation, and significantly greater mortal- to 2.3 mg/dL. ity.5 However, there is no evidence to link the chronic liver disease to the occurrence of biliary pancreatitis. In DISCUSSION this case, the patient presented with acute biliary pan- In ACLF, there is rapid deterioration in a patient with creatitis, which precipitated the ACLF in HCV related known or unknown chronic liver disease. It is associated chronic liver disease and complicated by spontaneous with increased mortality and prolongs hospitalization. bacterial peritonitis, jaundice, and hepatic encephalopathy. Both hepatic (acute ) and non-hepatic In conclusion, acute pancreatitis as a precipitant of insults (drugs, , etc.) can precipitate ACLF like- ACLF is a rare event and is, therefore, being reported. The .1,3 ACLF can be complicated by spontaneous present report also highlights the fact that non-infectious bacterial peritonitis, hepatic encephalopathy, jaundice, non-hepatic etiologies must be considered in the differ- renal failure, respiratory failure, and . It has ential diagnoses in patients with ACLF where the acute been postulated that systemic inflammatory response precipitant is uncertain. (SIRS) leads to a transition from stable cirrhosis to ACLF and pro-inflammatory are responsible for REFERENCES its various manifestations and organ failures that may 1. Sarin SK, Kumar A, Almeida JA, Chawla YK, Fan ST, et al. 2 accompany ACLF. Acute-on-chronic liver failure: consensus recommendations Acute pancreatitis is an acute inflammatory condition of the Asian Pacific Association for the study of the liver of the due to premature activation of proteases (APASL). international. 2009 Mar 1;3(1):269-282. within pancreatic acinar cells. activation leads . 2 Jalan R, Fernandez J, Wiest R, Schnabl B, Moreau R, Angeli P,et al. Bacterial in cirrhosis: a position statement based to and production of proinflammatory 4 on the EASL Special Conference 2013. Journal of hepatology. cytokines resulting in SIRS and organ failures. Thus, 2014 Jun 1;60(6):1310-1324. SIRS is a common denominator in both ACLF and acute 3. Duseja A, Chawla YK, Dhiman RK, Kumar A, Choudhary N, pancreatitis which leads to disease manifestations. Jaun- Taneja S. Non-hepatic insults are common acute precipitants dice can be a feature of acute pancreatitis in cases of in patients with acute on chronic liver failure (ACLF). Dig Dis choledocholithiasis, cholangitis and common duct Sci 2010;55:3188-3192. 4. Banks PA, Freeman ML. Practice guidelines in acute pancre- (CBD) compression due to fluid collections. In index atitis. Am J Gastroenterol 2006;101:2379-2400. case, there was no evidence of choledocholithiasis, chol- 5. Kuo PC, Plotkin JS, Johnson LB. Acute pancreatitis and ful- angitis or CBD compression. Ascites do occur in acute minant hepatic failure. J Am Coll Surg 1998;187:522-528.

Journal of Gastrointestinal Infections, January-December 2018;8(1):46-47 47