Title: Clinical Implications of Hyponatremia in Cirrhosis
Abstract: Hyponatremia in cirrhosis is caused by a generalized circulatory disorder, features of which include vasodilation, portal hypertension, reduced systemic vascular resistance, increased cardiac output and systemic hypotension. Hypotension activates baroreceptor neurons in the heart and great vessels, causing the hypothalamus to override its normal osmotic controls and release antidiuretic hormone. The resulting renal water retention, mediated via vasopressin V2 receptors in the collecting ducts, leads to systemic hypo-osmolality and hyponatremia. Low serum sodium is a predictor of mortality in cirrhosis, as well as in other disorders associated with circulatory failure such as congestive heart failure or pneumonia. Low serum sodium often accompanies other manifestations of advanced cirrhosis, including refractory ascites, hepatorenal syndrome and hepatic encephalopathy. Hyponatremia worsens with diuretic therapy in cirrhosis and may render patients diuretic-intolerant. Low sodium predicts cirrhotic mortality independently of MELD score, and inclusion of sodium in MELD-based survival models improves their predictive accuracy. Hyponatremia, even when severe, is well tolerated if it develops slowly, though there is some evidence that hyponatremia per se may aggravate cognitive impairment and hepatic encephalopathy. Patients with hypona-tremia at the time of liver transplantation have higher post-transplant morbidity and mortality, andare particularly at risk to develop osmotic demyelination. Cirrhotic hyponatremia may improve with water restriction, diuretic withdrawal, albumin infusion, pressor therapy or administration of aquaretic vaptan agents, but it is not known whether these treatments improve outcomes. Pretransplant correction of serum sodium may be indicated to prevent post-transplant osmotic demyelination.
Publication Year: 2011
Publication Date: 2011-01-01
Language: en
Type: book-chapter
Indexed In: ['crossref']
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Cited By Count: 1
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