Hepatic encephalopathy: current management strategies and treatment, including management and monitoring of cerebral edema and intracranial hypertension in fulminant hepatic failure

Zafirova, Zdravka; O'Connor, M.G.

doi:10.1097/aco.0b013e32833724c3

Cited by 27 publications

(12 citation statements)

References 29 publications

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“…The severity of hepatic encephalopathy is graded from 0 (minimal hepatic encephalopathy) to 4 (coma) using the West Haven classification [ 27 ]. Gastrointestinal bleeding, sepsis, hyponatraemia and uraemia can aggravate the symptoms and predispose the patient to respiratory failure and aspiration [ 28 ]. The control of ammonia production and uptake in the gastrointestinal tract, as well as the increase of its elimination, are the corner stones in the management of hepatic encephalopathy.…”

Section: Pathophysiology Of Chronic Liver Diseasementioning

confidence: 99%

Perioperative management of liver surgery—review on pathophysiology of liver disease and liver failure

2018

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Section: Pathophysiology Of Chronic Liver Diseasementioning

confidence: 99%

Perioperative management of liver surgery—review on pathophysiology of liver disease and liver failure

2018

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“…Early airway protection prevents pulmonary complications like aspiration pneumonia and facilitates treatment of cerebral edema by hyperventilation. 26 There is still disagreement about the benefits and risks of invasive intracranial pressure monitoring. Cerebral edema and raised intracranial pressure are less severe in comparison with those patients with acute liver failure.…”

Section: General Supportive Carementioning

confidence: 99%

Small-for-Size Syndrome: Bridging the Gap Between Liver Transplantation and Graft Recovery

Rajakumar¹,

Kaliamoorthy²,

Rela³

et al. 2017

Semin Cardiothorac Vasc Anesth

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In living donor liver transplantation, optimal graft size is estimated from values like graft volume/standard liver volume and graft/recipient body weight ratio but the final functional hepatic mass is influenced by other donor and recipient factors. Grafts with insufficient functional hepatic mass can produce a life-threatening condition with rapidly progressive liver failure called small-for-size syndrome (SFSS). Diagnosis of SFSS requires careful surveillance for signs of inadequate hepatocellular function, residual portal hypertension, and systemic inflammation that suggest rapidly progressive liver failure. Early diagnosis, symptom control, and addressing the cause of SFSS may prevent the need for retransplantation. With increased attention to avoiding donor risk, intensivists will be confronted with more SFSS recipients. In this review, we aim to outline a systematic approach to the medical management of patients with SFSS by providing a concise synopsis of general supportive care-neurological, cardiovascular, and renal support, mechanical ventilation, nutritional support, infection control, and tailored immunosuppression-with an aim to avoid end-organ damage or death and a review of current interventions including liver support devices, portal flow modulating drugs, and other experimental interventions that aim to preserve existing hepatic mass and improve conditions for hepatic regeneration. We examine evidence for SFSS interventions to provide the reader with information that may assist in clinical decision making. Points of controversy in care are purposefully highlighted to identify areas where additional experimental work is still needed. A full understanding of the pathophysiology of SFSS and measures to support liver regeneration will guide effective management.

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“…Commonly used methods to counteract HE may be divided into several types according to treatment access: Administration via the oral, rectal or intravenous routes; artificial liver transplantation; and full liver transplantation (9)(10)(11)(12)(13). Oral drugs mainly act by reducing the production and absorption of ammonia.…”

Section: Introductionmentioning

confidence: 99%

pH-sensitive microemulsion-based gels for removal of colonic ammonia: A novel preventative oral preparation for hepatic encephalopathy in rats

Zhang

Duan

Tian

et al. 2015

Molecular Medicine Reports

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Abstract.Microemulsions with limited stability in mimetic gastrointestinal environments have previously demonstrated potential for the effective removal of ammonia from artificial colonic fluid. Specialized pH-sensitive microemulsion-based gels for the removal of colonic ammonia (MBG-RCA), however, possess relative stability in the gastrointestinal (GI) tract of normal rats, indicating potential use in in vivo applications. An investigation of the effects of oral MBG-RCA was conducted in order to evaluate the reduction of intestinal ammonia and the prevention of hepatic encephalopathy (HE) in rat models. Eighty rats were allocated into eight 4-day treatment groups: The HE model (intraperitoneal injection of thioacetamide) group; the high-, medium-and low-dose MBG-RCA therapeutic groups (15, 10 and 5 ml/kg MBG-RCA, respectively); and the normal, blank, lactulose and acetic acid control groups, each of which received daily treatment administration. Oral MBG-RCA effects were identified using behavioral monitoring observed by an infrared night vision supervisory control system, electroencephalograms, blood ammonia levels, intestinal ammonia levels, liver functionality and pathological observation. High-and medium-dose oral administrations of MBG-RCA significantly decreased the blood and intestinal ammonia levels (P<0.05), improved liver functionality and reduced the clinical manifestations of HE in rats. MBG-RCA demonstrated high clearance of rat colonic ammonia while maintaining sufficient stability in the GI tract, indicating the potential for the development of new clinically relevant oral preparations for the prevention of HE. Additionally, such preparations are advantageous in that ammonia is eliminated without the production of potentially harmful metabolic byproducts. IntroductionElimination of excess ammonia is the primary method of prevention and treatment of hepatic encephalopathy (HE), a progressive condition in which neurological function is impaired as the liver fails to remove toxic metabolites, particularly ammonia, from the bloodstream. The majority of intestinal ammonia is produced in the colon; however, no clinically viable oral treatment exists for the elimination of this excess ammonia, resulting in continuous low clearance levels due to poor ammonia elimination in the body.HE is a syndrome caused by serious hepatic diseases as a result of metabolic disturbance and dysfunction of the central nervous system. Its clinical manifestation includes deposition changes, ethological abnormalities and mental retardation. In severe cases, it may develop into a coma or even be life-threatening. A number of researchers have divided HE into three categories: Type A is associated with acute liver failure; type B is caused by severe portosystemic shunting without liver disease; and type C is associated with chronic liver disease and hepatic cirrhosis (1). Acute liver failure models are well recognized as a representative model of type A HE. These models may be used to examine the pathological response of HE to v...

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Hepatic encephalopathy: current management strategies and treatment, including management and monitoring of cerebral edema and intracranial hypertension in fulminant hepatic failure

Abstract: Current diagnostic tests are imperfect, and modern therapy is nonspecific. No cost-efficient or more effective alternatives to either are likely to enter into clinical practice in the short-term future.

Cited by 27 publications

References 29 publications

Perioperative management of liver surgery—review on pathophysiology of liver disease and liver failure

Perioperative management of liver surgery—review on pathophysiology of liver disease and liver failure

Small-for-Size Syndrome: Bridging the Gap Between Liver Transplantation and Graft Recovery

pH-sensitive microemulsion-based gels for removal of colonic ammonia: A novel preventative oral preparation for hepatic encephalopathy in rats

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