Postgraduate Medicine
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Preventing portal systemic encephalopathy Frederick Steigmann To cite this article: Frederick Steigmann (1979) Preventing portal systemic encephalopathy, Postgraduate Medicine, 65:2, 118-126, DOI: 10.1080/00325481.1979.11715055 To link to this article: http://dx.doi.org/10.1080/00325481.1979.11715055
Published online: 07 Jul 2016.
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Citing articles: 1 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ipgm20 Download by: [Australian Catholic University]
Date: 24 August 2017, At: 15:44
Preventing portal systemic encephalopathy in the patient with cirrhosis
Frederick Steigmann, MD
Downloaded by [Australian Catholic University] at 15:44 24 August 2017
Consider What factors are involved in the development ofportal systemic encephalopathy? Wh y is ammonia thought to play a toxic role in the condition? How does endogenous ammonia formation relate to diet?
Portal systemic encephalopathy is a serious complication of cirrhosis. It can be prevented if the patient avoids the contributing factors-ingestion of alcohol, inappropriate diet, infection, stress, hepatotoxic agents-and if other complications are treated promptly. Once the liver has become scarred by mature fi brous septa and shows marked regenerative nodule formation, the cirrhotic process may be irreversible. Liver biopsy specimens from patients with cirrhosis often show a scarcity of parenchymal tissue, although the patient may evidence little functional abnormality. Life expectancy of patients with cirrhosis varies according to observer and geographie area; morbidity and mortality are higher in the poor than in the more affluent. Death usually occurs from hepatic failure or from upper gastrointestinal bleeding due to esophageal varices, gastritis, or peptic ulcer. Persistent hypoalburninemia, hypoprothrombinemia,' jaundice, 2 and ascitesJ signify decreased survival time. Pregnancy may be a risk for both mother and fetus, particularly when ascites develops in the mother.4 Portal systemic encephalopathy (PSE) is a serious complication of cirrhosis associated with reduced time of survival. Prevention of PSE requires removal of ali of the factors which singly or in combination lead to its occurrence. Factors involved in development ofPSE Malfunction of almost any organ system in a patient with cirrhosis may lead to PSE. The toxic sub-
118
stance mainly involved is ammonia. s Ammonia-The production of ammonia in the intestine is due largely to bacterial action on protein from food, enzymes, desquamated intestinal cells, and blood (100 ml of blood equals severa! grams of protein). The colon is a major site of ammonia formation in both normal and cirrhotic patients6; in persons with cirrhosis, ammonia-forming bacteria are found not only in the colon but also as high as the duodenum. Constipation, with its associated stasis, increases intestinal production and absorption of ammonia and other nitrogenous products. 7 Ammonia is formed in the stomach by the action of urease on urea from blood plasma, in the liver by necrosis, and in muscle by deamination of adenosine monophosphate. ln the kidney, glutaminase acts on glutarnine to produce ammonia. Conditions that affect kidney function, such as hypokalemia and renal tubular acidosis, may lead to increased activity of glutaminase and increased formation ofammonia.s Hyperdiuresis, with its associated hypokalemia and hypovolemia, results in decreased hepatic and renal function and hyperammonemia. Progressive azotemia from kidney disease may result in increased production of ammonia through action of urease on the large amount of
VOL 65/NO 2/FEBRUARY 1979/POSTGRADUATE MEDICINE
Downloaded by [Australian Catholic University] at 15:44 24 August 2017
)
urea in the intestinal tract. Hyperammonemia ammonernia may occur in acute tubular necrosis following episodes of bleeding, shock, shock, dehydration, and electrolyte imbalance and in instances of reduced renal plasma flow and glomerular filtration as a result of increased vascular resistance. resistance. Abdominal paracentesis may impair electrolyte balance and reduce plasma flow. Infection in any organ results in tissue catabolism with dehydration, hypoxia, hypotension, hyperthermia, impaired hepatic and renal function, and hyperammonemia. Surgery enhances tissue catabolism and is poorly tolerated by patients atients with cirrhosis. Hyperammonemia may result from om transfusion ofblood, since ammania ia concentration increases increasd al9 lt may mostt daily in stored blood. blood.9 It also result from ingestion of drugs that contain ammonium salts or of foodss that con tain preformed amcontain mania es and • 1o 10 and amines; win wines cheeses have considerable quantities ""'"'"''"have oftyramine. ............... Foods that contain short-chain fatty acids increase the short-
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Preventing portal systemic encephalopathy Frederick Steigmann To cite this article: Frederick Steigmann (1979) Preventing portal systemic encephalopathy, Postgraduate Medicine, 65:2, 118-126, DOI: 10.1080/00325481.1979.11715055 To link to this article: http://dx.doi.org/10.1080/00325481.1979.11715055
Published online: 07 Jul 2016.
Submit your article to this journal
View related articles
Citing articles: 1 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ipgm20 Download by: [Australian Catholic University]
Date: 24 August 2017, At: 15:44
Preventing portal systemic encephalopathy in the patient with cirrhosis
Frederick Steigmann, MD
Downloaded by [Australian Catholic University] at 15:44 24 August 2017
Consider What factors are involved in the development ofportal systemic encephalopathy? Wh y is ammonia thought to play a toxic role in the condition? How does endogenous ammonia formation relate to diet?
Portal systemic encephalopathy is a serious complication of cirrhosis. It can be prevented if the patient avoids the contributing factors-ingestion of alcohol, inappropriate diet, infection, stress, hepatotoxic agents-and if other complications are treated promptly. Once the liver has become scarred by mature fi brous septa and shows marked regenerative nodule formation, the cirrhotic process may be irreversible. Liver biopsy specimens from patients with cirrhosis often show a scarcity of parenchymal tissue, although the patient may evidence little functional abnormality. Life expectancy of patients with cirrhosis varies according to observer and geographie area; morbidity and mortality are higher in the poor than in the more affluent. Death usually occurs from hepatic failure or from upper gastrointestinal bleeding due to esophageal varices, gastritis, or peptic ulcer. Persistent hypoalburninemia, hypoprothrombinemia,' jaundice, 2 and ascitesJ signify decreased survival time. Pregnancy may be a risk for both mother and fetus, particularly when ascites develops in the mother.4 Portal systemic encephalopathy (PSE) is a serious complication of cirrhosis associated with reduced time of survival. Prevention of PSE requires removal of ali of the factors which singly or in combination lead to its occurrence. Factors involved in development ofPSE Malfunction of almost any organ system in a patient with cirrhosis may lead to PSE. The toxic sub-
118
stance mainly involved is ammonia. s Ammonia-The production of ammonia in the intestine is due largely to bacterial action on protein from food, enzymes, desquamated intestinal cells, and blood (100 ml of blood equals severa! grams of protein). The colon is a major site of ammonia formation in both normal and cirrhotic patients6; in persons with cirrhosis, ammonia-forming bacteria are found not only in the colon but also as high as the duodenum. Constipation, with its associated stasis, increases intestinal production and absorption of ammonia and other nitrogenous products. 7 Ammonia is formed in the stomach by the action of urease on urea from blood plasma, in the liver by necrosis, and in muscle by deamination of adenosine monophosphate. ln the kidney, glutaminase acts on glutarnine to produce ammonia. Conditions that affect kidney function, such as hypokalemia and renal tubular acidosis, may lead to increased activity of glutaminase and increased formation ofammonia.s Hyperdiuresis, with its associated hypokalemia and hypovolemia, results in decreased hepatic and renal function and hyperammonemia. Progressive azotemia from kidney disease may result in increased production of ammonia through action of urease on the large amount of
VOL 65/NO 2/FEBRUARY 1979/POSTGRADUATE MEDICINE
Downloaded by [Australian Catholic University] at 15:44 24 August 2017
)
urea in the intestinal tract. Hyperammonemia ammonernia may occur in acute tubular necrosis following episodes of bleeding, shock, shock, dehydration, and electrolyte imbalance and in instances of reduced renal plasma flow and glomerular filtration as a result of increased vascular resistance. resistance. Abdominal paracentesis may impair electrolyte balance and reduce plasma flow. Infection in any organ results in tissue catabolism with dehydration, hypoxia, hypotension, hyperthermia, impaired hepatic and renal function, and hyperammonemia. Surgery enhances tissue catabolism and is poorly tolerated by patients atients with cirrhosis. Hyperammonemia may result from om transfusion ofblood, since ammania ia concentration increases increasd al9 lt may mostt daily in stored blood. blood.9 It also result from ingestion of drugs that contain ammonium salts or of foodss that con tain preformed amcontain mania es and • 1o 10 and amines; win wines cheeses have considerable quantities ""'"'"''"have oftyramine. ............... Foods that contain short-chain fatty acids increase the short-
