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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 2  |  Issue : 1  |  Page : 30-32

Acute liver failure due to hypoxic hepatitis successfully treated with plasma exchange


Department of Surgery and Gastroenterology, Meenakshi Mission Hospital and Research Centre, Madurai, Tamil Nadu, India

Date of Submission07-Jun-2021
Date of Decision07-Aug-2021
Date of Acceptance12-Oct-2021
Date of Web Publication01-Jan-2022

Correspondence Address:
Allwin James
Department of Surgery and Gastroenterology, Meenakshi Mission Hospital and Research Centre, Melur Main Road, Madurai - 625 107, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ghep.ghep_30_21

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  Abstract 


Hypoxic hepatitis (HH) is an uncommon cause for acute liver failure (ALF). It is also called as shock liver, ischemic, or congestive hepatopathy. HH is usually associated with premorbid cardiac illnesses such as acute myocardial infarction, rheumatic cardiac disease, cardiomyopathies, or shock due to any etiology. It occurs when hepatocytes suffer hypoxic or ischemic injury. If the primary disease is treated, the natural history of HH is usually self-limiting. However, in up to half of the patients, it can lead to multiple organ ischemic insults such as worsening liver injury or acute renal failure, where the treatment is based on the major organ of involvement. Here, we present a patient with ALF due to hypoxic liver injury with a primary cardiac disease and a favorable outcome following plasma exchange therapy in our tertiary care center.

Keywords: Acute liver failure, hypoxic hepatitis, plasma exchange


How to cite this article:
James A, Palaniappan A, Ardhanari R, Janardhanan S. Acute liver failure due to hypoxic hepatitis successfully treated with plasma exchange. Gastroenterol Hepatol Endosc Pract 2022;2:30-2

How to cite this URL:
James A, Palaniappan A, Ardhanari R, Janardhanan S. Acute liver failure due to hypoxic hepatitis successfully treated with plasma exchange. Gastroenterol Hepatol Endosc Pract [serial online] 2022 [cited 2022 Jan 29];2:30-2. Available from: http://www.ghepjournal.com/text.asp?2022/2/1/30/334697




  Introduction Top


Acute liver failure (ALF) is defined as severe liver injury, characterized by encephalopathy and coagulopathy (international normalized ratio [INR] ≥1.5) of acute onset without preexisting liver disease, with an insult fewer than 26 weeks' duration.[1] ALF can be triggered by multiple causes, of which the incidence of hypoxic hepatitis (HH) varies between 2% and 2.5%.[2] To the best of our knowledge, very few such cases are treated with plasma exchange (PE) as salvage therapy.


  Case Report Top


A 21 year old male, known case of rheumatic heart disease (RHD), severe mitral and tricuspid regurgitation, moderate aortic regurgitation, and pulmonary arterial hypertension with normal ejection fraction (60%) was advised for valve replacement surgery 5 years ago, but was unwilling for the same. He was not on regular follow-up or treatment. He now presented with sudden onset of palpitations and giddiness to emergency department. On arrival, he was hypotensive (90/70 mm Hg) and tachycardic (156 bpm) with irregular pulse. His saturation and sensorium were normal. Electrocardiogram revealed atrial fibrillation with fast ventricular rate (AF with FVR). He was diagnosed with cardiogenic shock due to new onset AF and admitted under the cardiology department. He was resuscitated with noradrenaline, rate control measures, and colloids.

Baseline investigations revealed leukocytosis (total counts-16,500), prerenal failure (blood urea-85 mg/dl, serum creatinine-2.1 mg/dl) and liver function tests (total bilirubin [TB]-9.8/conjugated bilirubin-4.4/aspartate transaminase (AST)-3902/alanine transaminase (ALT)-3599/gamma-glutamyl transferase-44/alkaline phosphatase-138/total protein-5.3/albumin (ALB)-2.4) consistent with HH. INR was 5.4. Hypotension improved over 24 h of admission and inotropes were stopped; however, AF with FVR persisted. He was referred to medical gastroenterology department for altered liver functions. Diagnosis of cardiorenal syndrome and ALF due to ischemic hepatopathy was made. He was started on anti-encephalopathic measures (Oral Lactulose 15 g thrice daily), oral N-acetylcysteine and IV antibiotics, despite which he developed altered sensorium due to hepatic encephalopathy (HE) on day 2. Plasma ammonia was 234 mmol/dl and worsened to Grade IV HE. Etiological workup such as acute viral hepatitis, auto-immune hepatitis, and Wilson disease were negative.

Due to worsening liver failure, he was initiated on low-volume PE. Three sessions were done on consecutive days from day 2 to 4 of admission. PE was performed by centrifugation using Fresenius Kabi Com. tec-Aphaeresis equipment. Citrate was used as anticoagulant. The volume of plasma to be exchanged for each session was calculated with respect to body weight (35 ml/kg), i.e., 2100 ml per session as his weight was 60 kg. Each session of PE was done with 10 units of fresh frozen plasma (1500 mL), 20% albumin (100 mL) daily and 500 ml of 0.9% saline for volume replacement at the flow rate of 50 ml/min over 4 h span. Following each session of PE he was given hydrocortisone IV 100 mg to avoid any transfusion related reactions. There was no hypotension during all sessions. Electrolytes and calcium were monitored and corrected as needed. Serial LFTs showed declining liver enzymes and improving INR [Graph 1] and [Graph 2]. On day 3 of PE, he recovered dramatically from HE. The decision to stop with three sessions was made due to his clinical improvement. He was given a short course of oral steroids (Tablet Wysolone 20 mg) for 2 weeks following PE and stopped. Acute kidney injury was attributed to cardiorenal syndrome, which improved with normalization of blood pressure. The rate control of AF was achieved with beta blockers.



Hence, PE was helpful in treating hypoxic ALF in this patient, and the need for liver transplant was obviated. On day 21 since admission, he was discharged in a stable condition with TB of 7.1 mg/dl and INR of 1.6. On day 50, liver functions and INR normalized. He became fit for valve replacement surgery. PE in ALF of any etiology can be life-saving in a patient who is not a candidate for emergent liver transplant due to underlying comorbidities.


  Discussion Top


HH (shock liver/ischemic hepatitis) is a clinical syndrome seen as a rapid increase in liver enzymes due to hypoxia or ischemia of the liver.[3] Diagnosis is based on the presence of the following criteria namely (1) presence of a condition precipitating hypoxia to the liver, (2). acute (10–300 times upper limit of normal) and transient increase (5–25 days) in liver enzymes, and (3) exclusion of other causes mimicking HH.[4] Etiologies include primary heart pathologies (RHD, ischemic heart disease, cardiomyopathies– 78%), chronic respiratory failure, circulatory shock and/or sepsis. The pathogenesis of HH is largely unknown. It has been suggested that after systemic hypotension, decreased blood flow to the liver results in anoxic/hypoxic hepatocellular injury. Our patient had a background RHD and developed new onset AF, precipitating cardiogenic shock, hypoxic liver injury, and ALF.

In HH, there is rapid increase in aminotransferases and lactate dehydrogenase levels, reaching maximum values at around 24 h after shock. Aspartate transaminase is higher than alanine transaminase levels in 75% of the cases. The rise in lactate dehydrogenase is characteristic of HH, differentiating it from viral hepatitis.[5] Our patient had high serum aminotransferase levels (AST [3902 IU] >ALT [3599 IU]) consistent with HH. The patient developed worsening of sensorium due to HE, with raised plasma ammonia (234 mmol/dl) and worsening coagulopathy (INR 5.4) consistent with ALF.

According to the American Society for Apheresis guidelines (2019), high-volume PE is Category I indication with Grade 1A recommendation and PE is Category III indication with Grade 2B recommendation for the treatment of ALF.[6] In a study by Zachariah et al. from south India, low-volume PE with low-dose steroids were found to improve outcome of ALF of varied etiology.[7] Our patient was given short course of steroids which also helped to improve liver functions, hence steroids may have a role in decreasing liver injury following such cardiac insult. In an Indian randomized control study, standard volume PE was shown as safe and effective treatment strategy in improving survival of patients with ALF. It decreases cytokine storm and ammonia levels.[8] To the best of our knowledge, there are very few cases of hypoxic liver injury treated with PE with complete recovery.[9],[10] Following three sessions of PE, our patient showed a significant improvement in HE and a normalizing trend in liver and renal parameters. Hence, PE can be used as a life-saving procedure in patients with ALF of any etiology, who are not candidates of liver transplant due to comorbidities, especially in resource-constrained settings.


  Conclusion Top


HH is an uncommon cause for ALF, which can be successfully treated with therapeutic low volume PE. Early diagnosis, PE and maintaining hemodynamic stability remain the cornerstones in the management of HH.

Acknowledgment

We would like to thank the Department of Surgery and Gastroenterology, Meenakshi Mission Hospital and Research Centre, Madurai.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given his consent for images and other clinical information to be reported in the journal. The guardian understands that names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Sundaram V, Jalan R, Wu T, Volk ML, Asrani SK, Klein AS, et al. Factors associated with survival of patients with severe acute-on-chronic liver failure before and after liver transplantation. Gastroenterology 2019;156:1381-91.e3.  Back to cited text no. 1
    
2.
Tapper EB, Sengupta N, Bonder A. The incidence and outcomes of ischemic hepatitis: A systematic review with meta-analysis. Am J Med 2015;128:1314-21.  Back to cited text no. 2
    
3.
Birrer R, Takuda Y, Takara T. Hypoxic hepatopathy: Pathophysiology and prognosis. Intern Med 2007;46:1063-70.  Back to cited text no. 3
    
4.
Waseem N, Chen PH. Hypoxic hepatitis: A review and clinical update. J Clin Transl Hepatol 2016;4:263-8.  Back to cited text no. 4
    
5.
Henrion J, Schapira M, Luwaert R, Colin L, Delannoy A, Heller FR. Hypoxic hepatitis: Clinical and hemodynamic study in 142 consecutive cases. Medicine (Baltimore) 2003;82:392-406.  Back to cited text no. 5
    
6.
Padmanabhan A, Connelly-Smith L, Aqui N, Balogun RA, Klingel R, Meyer E, et al. Guidelines on the use of therapeutic apheresis in clinical practice-evidence-based approach from the writing committee of the American Society for Apheresis: The eighth special issue. J Clin Apher 2019;34:171-354.  Back to cited text no. 6
    
7.
Zachariah U, Kumar SE, Alexander V, Patel L, Goel A, Eapen CE. Low-volume plasma exchange and low-dose steroid to treat severe liver injury. Gastroenterol Hepatol Endosc Pract 2021;1:47-54.  Back to cited text no. 7
  [Full text]  
8.
Maiwal R, Bajpai M, Singh A, Agarwal T, Kumar G, Bharadwaj A, et al. Standard-volume plasma exchange improves outcomes in patients with acute liver failure: A randomised controlled trial. Clin Gastroenterol Hepatol. Published online January 28, 2021. Epub ahead of print. Available from: https://doi.org/10.1016/j.cgh.2021.01.036. [Last accessed on 2021 Oct 30].  Back to cited text no. 8
    
9.
Cheng YL, Chang CH, Chen WT, Tsai MH, Lee WC, Tu KH, et al. Prognostic factors and treatment effect of standard-volume plasma exchange for acute and acute-on-chronic liver failure: A single-center retrospective study. Transfus Apher Sci 2018;57:537-43.  Back to cited text no. 9
    
10.
Li M, Sun J, Li J, Shi Z, Xu J, Lu B, et al. Clinical observation on the treatment of acute liver failure by combined non-biological artificial liver. Exp Ther Med 2016;12:3873-6.  Back to cited text no. 10
    




 

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