Luminary Learning Gastrointestinal Disorder- Issue 1

Latest Concepts in Inpatient Hepatic Encephalopathy Management •  5 of the pathway. An increase in the number of organ failure is associated with increase in the mor- tality rate [8]. The pathophysiology of HE in ACLF is multifactorial and hyperammonemia and systemic inflammation are important factors [2]. Studies in animal models have shown that induction of hyperammonemia leads to brain edema and the reduction of ammonia level could reduce brain swelling [19]. In addition, reduction in ammonia level prevented brain edema and delayed the development of coma in response to LPS challenge in an animal model [20]. Clinically, HE associ- ated with ACLF may lead to cerebral edema and increased intracranial pressure whereas isolated hepatic encephalopathy typically will not [21]. Cerebral edema has been observed in imaging studies [22] and confirmed by electron microscopic studies in animal models showing astrocyte swelling and collapsed microvessels [23]. Management of Hepatic Encephalopathy in the Hospitalized Patient General Approach Early risk stratification to differentiate isolated HE from HE associated with ACLF is necessary (Fig. 2). This is due to the significant difference in short-term mortality between these two groups [14]. Prognostic scores including the chronic liver failure-sequential organ failure assessment (CLIF-SOFA) score may be utilized to determine the severity of ACLF [8]. If HE associated with ACLF is detected, intensive care unit admission should be considered. Airway protection should be considered in all patients with grades 3–4 HE, particularly those with ACLF, or if there is evolving respiratory failure. Inotropes or vasopressors should be considered to maintain adequate cerebral perfusion. Fig. 1: Pathophysiology of ACLF. Asrani et al. [7]. PAMP pathogen-associated molecular pattern, SBP  spontaneous bacterial peritonitis, TNF  tumor necrosis factor, UTI urinary tract infection ACLF using a four-part model of predisposing event, injury resulting from precipitating event, response to injury, and organ failure (Fig. 6.1 ) [ 7 , 16 ]. Predisposition is the underlyin 1. PREDISPOSITION Cirrhosis Alcohol Viruses / drugs Ischemic / reperfusion Bacterial translocation Infection (SBP, UTI, etc) PAMPs Lymphocyte Neutrophil DAMPs Hepatocyte Kupffer cell Proinflammatory cytokines TNF α , IL1 β , IL6 2. INJURY 3. RESPONSE 4. ORGAN FAILURE Fig. 6.1 Pathophysiology of ACLF. Asrani et al. 7 . PAMP pathogen-asso- ciated molecular pattern, SBP spontaneous bacterial peritonitis, TNF tumor necrosis factor, UTI urinary tract infection