Hepatorenal syndrome (patient information): Difference between revisions
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{{Hepatorenal syndrome (patient information)}} | {{Hepatorenal syndrome (patient information)}} | ||
{{CMG}}; '''Assistant Editor-in-Chief:''' Meagan E. Doherty | {{CMG}}; '''Assistant Editor-in-Chief:''' Meagan E. Doherty; {{SKA}} | ||
==Overview== | ==Overview== | ||
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* [[Abdominal swelling]] | * [[Abdominal swelling]] | ||
* Change in mental status | * Change in mental status | ||
** Confusion | ** [[Confusion]] | ||
** [[Delirium]] | ** [[Delirium]] | ||
** [[Dementia]] | ** [[Dementia]] | ||
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* Decreased urine production | * Decreased urine production | ||
* [[Nausea]] and [[vomiting]] | * [[Nausea]] and [[vomiting]] | ||
* Weight gain | * [[Weight gain]] | ||
* Yellow skin | * Yellow skin | ||
Many other diseases of the kidney are associated with liver disease and must be excluded before making a diagnosis of hepatorenal syndrome. They include the following: | Many other diseases of the kidney are associated with liver disease and must be excluded before making a diagnosis of [[hepatorenal syndrome]]. They include the following: | ||
*[[Renal failure|Pre-renal failure]]: Pre-renal failure usually responds to treatment with intravenous fluids, resulting in reduction in serum [[creatinine]] and the excretion of sodium.<ref>Arroyo V, Gines P, Gerbes AL, Dudley FJ, Gentilini P, Laffi G, Reynolds TB, Ring-Larsen H, Scholmerich J. Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis. International Ascites Club. Hepatology. 1996 Jan;23(1):164-76. PMID 8550036</ref> | *[[Renal failure|Pre-renal failure]]: Pre-renal failure usually responds to treatment with intravenous fluids, resulting in reduction in serum [[creatinine]] and the excretion of sodium.<ref>Arroyo V, Gines P, Gerbes AL, Dudley FJ, Gentilini P, Laffi G, Reynolds TB, Ring-Larsen H, Scholmerich J. Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis. International Ascites Club. Hepatology. 1996 Jan;23(1):164-76. PMID 8550036</ref> | ||
*[[Acute tubular necrosis]] (ATN): This can be difficult to confidently diagnose. It may be an inability to concentrate the urine, if any is being produced. The urine sediment should be bland, microscopy may show [[hyaline cast]]s. ATN may recover with supportive treatment only or progress to [[end-stage renal failure]]. In cirrhosis, urinary sodium is not a reliable guide to the development of ATN, as [[fractional sodium excretion]] may stay below 1 percent, due to the gradual worsening of renal [[ischaemia]]. | *[[Acute tubular necrosis]] ([[ATN]]): This can be difficult to confidently diagnose. It may be an inability to concentrate the urine, if any is being produced. The urine sediment should be bland, microscopy may show [[hyaline cast]]s. ATN may recover with supportive treatment only or progress to [[end-stage renal failure]]. In cirrhosis, urinary sodium is not a reliable guide to the development of ATN, as [[fractional sodium excretion]] may stay below 1 percent, due to the gradual worsening of renal [[ischaemia]]. | ||
*Other causes may include [[glomerulonephritis|glomerular disease]] secondary to [[Hepatitis B]] or [[Hepatitis C]],<ref>Han SH. Extrahepatic manifestations of chronic hepatitis B. ''Clin Liver Dis.'' 2004 May;8(2):403-18. PMID 15481347</ref> drug toxicity (notably [[gentamicin]]) or [[Radiocontrast|contrast nephropathy]]. | *Other causes may include [[glomerulonephritis|glomerular disease]] secondary to [[Hepatitis B]] or [[Hepatitis C]],<ref>Han SH. Extrahepatic manifestations of chronic hepatitis B. ''Clin Liver Dis.'' 2004 May;8(2):403-18. PMID 15481347</ref> drug toxicity (notably [[gentamicin]]) or [[Radiocontrast|contrast nephropathy]]. | ||
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==Sources== | ==Sources== | ||
*http://www.nlm.nih.gov/medlineplus/ency/article/000489.htm | *http://www.nlm.nih.gov/medlineplus/ency/article/000489.htm | ||
{{reflist}} | {{reflist|2}} | ||
[[Category:Patient information]] | [[Category:Patient information]] | ||
[[Category:Gastroenterology]] | [[Category:Gastroenterology]] | ||
[[Category:Nephrology]] | [[Category:Nephrology]] | ||
[[Category:Intensive care medicine]] | [[Category:Intensive care medicine]] | ||
{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} |
Latest revision as of 19:20, 21 December 2017
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Hepatorenal syndrome |
Hepatorenal syndrome On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor-in-Chief: Meagan E. Doherty; Sunny Kumar MD [2]
Overview
Hepatorenal syndrome is a condition in which the kidneys fail suddenly in a person with cirrhosis of the liver. It is a serious complication of cirrhosis.
What are the symptoms of Hepatorenal syndrome?
- Abdominal swelling
- Change in mental status
- Coarse muscle movements, jerking
- Dark-colored urine
- Decreased urine production
- Nausea and vomiting
- Weight gain
- Yellow skin
Many other diseases of the kidney are associated with liver disease and must be excluded before making a diagnosis of hepatorenal syndrome. They include the following:
- Pre-renal failure: Pre-renal failure usually responds to treatment with intravenous fluids, resulting in reduction in serum creatinine and the excretion of sodium.[1]
- Acute tubular necrosis (ATN): This can be difficult to confidently diagnose. It may be an inability to concentrate the urine, if any is being produced. The urine sediment should be bland, microscopy may show hyaline casts. ATN may recover with supportive treatment only or progress to end-stage renal failure. In cirrhosis, urinary sodium is not a reliable guide to the development of ATN, as fractional sodium excretion may stay below 1 percent, due to the gradual worsening of renal ischaemia.
- Other causes may include glomerular disease secondary to Hepatitis B or Hepatitis C,[2] drug toxicity (notably gentamicin) or contrast nephropathy.
What causes Hepatorenal syndrome?
Hepatorenal syndrome occurs when there is a decrease in kidney function in a person with a liver disorder. Because less urine is removed from the body, nitrogen-containing waste products build up in the bloodstream (azotemia).
Who is at highest risk?
The disorder occurs in up to 10% of patients hospitalized with liver failure. It is caused by the built-up effects of liver damage and kidney failure in people with:
Other risk factors include:
- Blood pressure that falls when a person rises or suddenly changes position (orthostatic hypotension)
- Diuretic use
- Gastrointestinal bleeding
- Infection
- Recent abdominal paracentesis
When to seek urgent medical care?
This disorder most often is diagnosed in the hospital during treatment for a liver disorder.
Diagnosis
This condition is diagnosed when other causes of kidney failure are ruled out.
A physical examination will not directly reveal kidney failure. However, the exam will usually show signs of chronic liver disease:
- Excess fluid in the abdomen (ascites)
- Hepatic encephalopathy
- Jaundice
- Other signs of liver failure
Other signs include:
- Abnormal reflexes
- Decreased testicle size
- Dull sound in the abdomen when tapped with the tips of the fingers, and visible fluid wave when examined by feel
- Increased breast tissue
- Sores (lesions) on the skin
The following may be signs of kidney failure:
- Absent or low urine production, less than 400 cc/day
- Fluid retention in the abdomen or extremities
- Increased BUN and creatinine levels
- Increased urine specific gravity and osmolality
- Low serum sodium
- Very low urine sodium concentration
The following may be signs of liver failure:
- Abnormal PT
- Increased ammonia levels
- Low serum albumin
- Paracentesis with ascites
- Signs of hepatic encephalopathy (an EEG may be performed if such signs are present)
Treatment options
Treatment aims to improve liver function and ensure that there is enough blood in the body and the heart is pumping adequately.
The disorder is generally treated in the same way as kidney failure from any other cause.
- All unnecessary medicines are stopped, especially the antibiotic neomycin, ibuprofen and other NSAIDs, and diuretics ("water pills").
- Dialysis may improve symptoms.
- Medications such as octreotide, albumin, and dopamine may be used temporarily to improve kidney function.
- Surgery to place a shunt (called a Levine shunt) from the abdominal space (peritoneum) to the jugular vein may relieve some of the symptoms of kidney failure. However, surgical shunts are rarely placed, because severe liver disease makes surgery very risky. A nonsurgical shunt (known as TIPS) may be tried in some patients.
Prevention of Hepatorenal syndrome
Intravenous albumin: A randomized controlled trial found that intravenous albumin on the day of admission and on hospital day 3 can reduce renal impairment.[3]
Where to find medical care for Hepatorenal syndrome?
Directions to Hospitals Treating Hepatorenal syndrome
What to expect (Outlook/Prognosis)?
The predicted outcome is poor. Death usually occurs as a result of secondary infections or hemorrhage.
Possible complications
- Bleeding
- Damage to, and failure of, many organ systems
- End-stage kidney disease
- Fluid overload with congestive heart failure or pulmonary edema
- Hepatic coma
- Secondary infections
Sources
- ↑ Arroyo V, Gines P, Gerbes AL, Dudley FJ, Gentilini P, Laffi G, Reynolds TB, Ring-Larsen H, Scholmerich J. Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis. International Ascites Club. Hepatology. 1996 Jan;23(1):164-76. PMID 8550036
- ↑ Han SH. Extrahepatic manifestations of chronic hepatitis B. Clin Liver Dis. 2004 May;8(2):403-18. PMID 15481347
- ↑ Sort P, Navasa M, Arroyo V, et al (1999). "Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis". N. Engl. J. Med. 341 (6): 403-9. PMID 10432325