Hepatic encephalopathy risk factors: Difference between revisions

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Revision as of 18:52, 19 December 2017

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:

Overview

There are no established risk factors for [disease name].

OR

The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.

Risk Factors

There are no established risk factors for [disease name].

OR

The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].

Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].

Common Risk Factors

Common risk factors in the development of [disease name] include:^[1]^[2]^[3]^[4]

Less Common Risk Factors

Less common risk factors in the development of hepatic encephalopathy include:^[5]^[6]^[7]

References

↑ Djiambou-Nganjeu H (2017). "Hepatic Encephalopathy in Liver Cirrhosis". J Transl Int Med. 5 (1): 64–67. doi:10.1515/jtim-2017-0013. PMC 5490964. PMID 28680841.
↑ Acharya SK (2015). "Management in acute liver failure". J Clin Exp Hepatol. 5 (Suppl 1): S104–15. doi:10.1016/j.jceh.2014.11.005. PMC 4442864. PMID 26041950.
↑ Ferenci P (2017). "Hepatic encephalopathy". Gastroenterol Rep (Oxf). 5 (2): 138–147. doi:10.1093/gastro/gox013. PMC 5421503. PMID 28533911.
↑ Bleibel W, Al-Osaimi AM (2012). "Hepatic encephalopathy". Saudi J Gastroenterol. 18 (5): 301–9. doi:10.4103/1319-3767.101123. PMC 3500018. PMID 23006457.
↑ Jepsen P, Christensen J, Weissenborn K, Watson H, Vilstrup H (2016). "Epilepsy as a risk factor for hepatic encephalopathy in patients with cirrhosis: a cohort study". BMC Gastroenterol. 16 (1): 77. doi:10.1186/s12876-016-0487-3. PMC 4960784. PMID 27457247.
↑ Guevara M, Baccaro ME, Ríos J, Martín-Llahí M, Uriz J, Ruiz del Arbol L; et al. (2010). "Risk factors for hepatic encephalopathy in patients with cirrhosis and refractory ascites: relevance of serum sodium concentration". Liver Int. 30 (8): 1137–42. doi:10.1111/j.1478-3231.2010.02293.x. PMID 20602681.
↑ Jepsen P, Watson H, Andersen PK, Vilstrup H (2015). "Diabetes as a risk factor for hepatic encephalopathy in cirrhosis patients". J Hepatol. 63 (5): 1133–8. doi:10.1016/j.jhep.2015.07.007. PMID 26206073.

Template:WH Template:WS

[pmid28680841-1] Djiambou-Nganjeu H (2017). "Hepatic Encephalopathy in Liver Cirrhosis". J Transl Int Med. 5 (1): 64–67. doi:10.1515/jtim-2017-0013. PMC 5490964. PMID 28680841.

[pmid26041950-2] Acharya SK (2015). "Management in acute liver failure". J Clin Exp Hepatol. 5 (Suppl 1): S104–15. doi:10.1016/j.jceh.2014.11.005. PMC 4442864. PMID 26041950.

[pmid28533911-3] Ferenci P (2017). "Hepatic encephalopathy". Gastroenterol Rep (Oxf). 5 (2): 138–147. doi:10.1093/gastro/gox013. PMC 5421503. PMID 28533911.

[pmid23006457-4] Bleibel W, Al-Osaimi AM (2012). "Hepatic encephalopathy". Saudi J Gastroenterol. 18 (5): 301–9. doi:10.4103/1319-3767.101123. PMC 3500018. PMID 23006457.

[pmid27457247-5] Jepsen P, Christensen J, Weissenborn K, Watson H, Vilstrup H (2016). "Epilepsy as a risk factor for hepatic encephalopathy in patients with cirrhosis: a cohort study". BMC Gastroenterol. 16 (1): 77. doi:10.1186/s12876-016-0487-3. PMC 4960784. PMID 27457247.

[pmid20602681-6] Guevara M, Baccaro ME, Ríos J, Martín-Llahí M, Uriz J, Ruiz del Arbol L; et al. (2010). "Risk factors for hepatic encephalopathy in patients with cirrhosis and refractory ascites: relevance of serum sodium concentration". Liver Int. 30 (8): 1137–42. doi:10.1111/j.1478-3231.2010.02293.x. PMID 20602681.

[pmid26206073-7] Jepsen P, Watson H, Andersen PK, Vilstrup H (2015). "Diabetes as a risk factor for hepatic encephalopathy in cirrhosis patients". J Hepatol. 63 (5): 1133–8. doi:10.1016/j.jhep.2015.07.007. PMID 26206073.

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[2]

[3]

[4]

[5]

[6]

[7]

@@ Line 25: / Line 25: @@
 ===Common Risk Factors===
 *Common risk factors in the development of [disease name] include:<ref name="pmid28680841">{{cite journal| author=Djiambou-Nganjeu H| title=Hepatic Encephalopathy in Liver Cirrhosis. | journal=J Transl Int Med | year= 2017 | volume= 5 | issue= 1 | pages= 64-67 | pmid=28680841 | doi=10.1515/jtim-2017-0013 | pmc=5490964 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28680841  }} </ref><ref name="pmid26041950">{{cite journal| author=Acharya SK| title=Management in acute liver failure. | journal=J Clin Exp Hepatol | year= 2015 | volume= 5 | issue= Suppl 1 | pages= S104-15 | pmid=26041950 | doi=10.1016/j.jceh.2014.11.005 | pmc=4442864 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26041950  }} </ref><ref name="pmid28533911">{{cite journal| author=Ferenci P| title=Hepatic encephalopathy. | journal=Gastroenterol Rep (Oxf) | year= 2017 | volume= 5 | issue= 2 | pages= 138-147 | pmid=28533911 | doi=10.1093/gastro/gox013 | pmc=5421503 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28533911  }} </ref><ref name="pmid23006457">{{cite journal| author=Bleibel W, Al-Osaimi AM| title=Hepatic encephalopathy. | journal=Saudi J Gastroenterol | year= 2012 | volume= 18 | issue= 5 | pages= 301-9 | pmid=23006457 | doi=10.4103/1319-3767.101123 | pmc=3500018 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23006457  }} </ref>
-**[null Cirrhosis]
+**[[Cirrhosis]]
-**[null Acute hepatic failure]
+**[[Acute liver failure|Acute hepatic failure]]
-**[null GI bleeding]
+**[[Gastrointestinal bleeding|GI bleeding]]
-**[null Portacaval shunt]
+**[[Portacaval shunt]]
 ===Less Common Risk Factors===
@@ Line 37: / Line 37: @@
 **[[Renal failure]]
 **[[Bilirubinemia|Hyperblilirubinemia]]
-**[null Hypokalemia]
+**[[Hypokalemia]]
-**[null Metabolic alkalosis]
+**[[Metabolic alkalosis]]
-**[null Sepsis]
+**[[Sepsis]]
-**[null Hypovolemia]
+**[[Hypovolemia|Hypovolomia]]
-==Overview==
-==Risk Factors==
-Virtually any [[metabolism|metabolic]] disturbance may precipitate hepatic encephalopathy. Common culprits are:
-* [[Hyponatremia]] (often arising as a result of [[diuretic]] treatment or simply as a complication of the [[edema]] typically found in advanced [[cirrhosis]])
-* [[Hypokalemia]] (again, often as a result of diuretic use)
-* [[Alkalosis]]
-* Dehydration
-* [[Hypoglycemia]] (a condition to which people with cirrhosis are susceptible)
-* [[Renal failure]] of even mild degree.
-Likewise, there are a number of medications the use of which may bring on hepatic encephalopathy. These include:
-* [[Benzodiazepines]], (e.g. [[diazepam]], [[lorazepam]]) [[narcotics]]
-* [[Diuretics]]
-Alcohol ingestion, whether or not it is the cause of the patient's liver disease, may also precipitate hepatic encephalopathy.
-Infection is an important precipitant of hepatic encephalopathy. In some cases, the only clinical manifestation of the infection is the development of the encephalopathy. In fact, this is a frequent phenomenon in patients in whom [[ascites]] becomes infected (i.e. [[spontaneous bacterial peritonitis]]).
-Sometimes, hepatic encephalopathy arises as a result of patient non compliance with dietary protein restriction. Indeed, given the general lack of palatability of low protein diets, non-compliance is common and, hence, so is its effect to precipitate encephalopathy.
-Bleeding into the [[stomach]] or [[small intestine]] (both of which occur with increased frequency in people with liver disease and/or [[portal hypertension]]) may also lead to hepatic encephalopathy. Blood contains large quantities of protein in the form of plasma proteins and hemoglobin. Hence, the presence of blood in the stomach or small intestine represents a protein load which, as a result of bacterial metabolism in the lumen of the gut, is converted to potentially toxic products such as ammonia.
-Certain surgical procedures employed to treat [[portal hypertension]] commonly lead to the development of hepatic encephalopathy. For example, operations to relieve pressure in the portal vein by connecting it to the [[splenic vein]] or other systemic venous vessels, have the effect of diverting incoming intestinal venous blood away from the liver. This means that such ammonia-carrying blood will not be able to be "purified" by the liver. Encephalopathy can result. Similarly, the more recently developed TIPS procedure ([[transjugular intrahepatic portosystemic shunt]]) often precipitates hepatic encephalopathy (~30 percent of patients undergoing it).
 ==References==