Hepatic encephalopathy natural history, complications and prognosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
Hepatic encephalopathy may occur as an acute, potentially reversible disorder or it may occur as a chronic, progressive disorder that is associated with chronic liver disease. If left untreated, patients with hepatic encephalopathy may progress to develop brain edema (may lead to brain herniation, secondary structural damage to the brain, and death. Common complications of hepatic encephalopathy include status epilepticus, aspiration, hypernatremia, severe perianal irritation and eventually death. Prognosis of patients with hepatic encephalopathy is generally poor. Factors known to be associated with a poorer prognosis in cases of hepatic encephalopathy include, male sex, hyperbilirubinemia, increased alkaline phosphatase levels, hyperkalemia, hyperalbuminemia and decreased prothrombin activity.
Natural History, Complications, and Prognosis
Natural history
- Hepatic encephalopathy may occur as an acute, potentially reversible disorder or it may occur as a chronic, progressive disorder that is associated with chronic liver disease.[1]
- If left untreated, patients with hepatic encephalopathy may progress to develop brain edema (may lead to brain herniation, secondary structural damage to the brain, and death)[2]
Complications
- Common complications of hepatic encephalopathy include:[3][4]
- Status epilepticus
- Aspiration(due to overuse of lactulose)
- Hypernatremia(due to overuse of lactulose)
- Severe perianal skin irritation(due to overuse of lactulose)
- death
Prognosis
- Prognosis of patients with hepatic encephalopathy is generally poor:[5][6]
- One year survival rate of patients with hepatic encephalopathy is approximately 42%.
- Three year survival rate of patients with hepatic encephalopathy is approximately 23%.
- The presence of some factors is associated with a particularly poorer prognosis among patients with hepatic encephalopathy. These factors include the following:
- Elevated plasma ammonia (≥79.5 µmol/L)[7]
- Male sex
- Increased serum bilirubin
- Increased alkaline phosphatase
- Increased potassium and blood urea nitrogen
- Decreased serum albumin
- Decreased prothrombin activity
References
- ↑ Toris GT, Bikis CN, Tsourouflis GS, Theocharis SE (2011). "Hepatic encephalopathy: an updated approach from pathogenesis to treatment". Med Sci Monit. 17 (2): RA53–63. PMC 3524698. PMID 21278704.
- ↑ Dara N, Sayyari AA, Imanzadeh F (2014). "Hepatic encephalopathy: early diagnosis in pediatric patients with cirrhosis". Iran J Child Neurol. 8 (1): 1–11. PMC 3943054. PMID 24665321.
- ↑ Eleftheriadis N, Fourla E, Eleftheriadis D, Karlovasitou A (2003). "Status epilepticus as a manifestation of hepatic encephalopathy". Acta Neurol Scand. 107 (2): 142–4. PMID 12580865.
- ↑ Ferenci P (2017). "Hepatic encephalopathy". Gastroenterol Rep (Oxf). 5 (2): 138–147. doi:10.1093/gastro/gox013. PMC 5421503. PMID 28533911.
- ↑ García-Martínez R, Simón-Talero M, Córdoba J (2011). "Prognostic assessment in patients with hepatic encephalopathy". Dis Markers. 31 (3): 171–9. doi:10.3233/DMA-2011-0840. PMC 3826802. PMID 22045403.
- ↑ Bustamante J, Rimola A, Ventura PJ, Navasa M, Cirera I, Reggiardo V; et al. (1999). "Prognostic significance of hepatic encephalopathy in patients with cirrhosis". J Hepatol. 30 (5): 890–5. PMID 10365817.
- ↑ Sheikh MF, Mookerjee RP, Agarwal B, Acharya SK, Jalan R (2019). "Prognostic Role of Ammonia in Cirrhotic Patients". Hepatology. doi:10.1002/hep.30534. PMID 30703853.