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TEXTBOOK PRESENTATION
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See Chapter 17-6: Cirrhosis, Edema for a full discussion. Patients with cirrhosis may have ascites, variceal hemorrhage, encephalopathy, jaundice, hypoalbuminemia, coagulopathy, and elevated transaminases.
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Hyponatremia is a marker of advanced cirrhosis found in 3% of patients with Child-Pugh class A, 16% in those with class B, and 31% of those with class C.
Hyponatremia is associated with a higher frequency of adverse outcomes (including hepatorenal syndrome, hepatic encephalopathy, spontaneous bacterial peritonitis, and death), especially if there is no clear precipitant of the hyponatremia.
One study of hospitalized patients reported a 25% mortality among cirrhotic patients without hyponatremia compared with 93% among those with hyponatremia. A study of outpatient cirrhotic patients reported a 23% 3-year mortality rate in patients without hyponatremia vs. 53% in those with hyponatremia.
Furthermore, greater degrees of hyponatremia are associated with an increasing risk of the hepatorenal syndrome and hepatic encephalopathy (Table 24-5).
Among patients with cirrhosis and ascites, 22% have sodium ≤ 130 mEq/L.
Pathogenesis of hyponatremia in cirrhosis
Decreased effective circulating volume (caused by hypoalbuminemia, splanchnic and systemic dilatation) decreases mean arterial pressure, triggering the release of ADH which in turn causes water retention and hyponatremia. Other intrarenal changes also contribute to the hyponatremia.
NSAIDs may decrease the GFR aggravating both edema and hyponatremia. NSAIDs also lower renal PGE2, which normally antagonizes ADH.
Hyponatremia may act synergistically with hyperammonemia to increase cerebral edema and encephalopathy.
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EVIDENCE-BASED DIAGNOSIS
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While several physical findings are specific for cirrhosis, none are sufficiently sensitive to rule out cirrhosis in a patient (see Table 17-2).
However, because hyponatremia develops in advanced cirrhosis, certain physical exam findings are common in cirrhotic patients with hyponatremia.
Ascites present in 100%
Ascites is a very sensitive sign of cirrhosis in hyponatremic patients. Its absence effectively rules out cirrhosis in these patients.
Peripheral edema seen in 59%
Laboratory studies:
Mean urine sodium 4 mEq/L (measurements made after diuretics have been stopped for 5 days). (Decreased effective circulating volume causes increased renal reabsorption of sodium.)
NT-proBNP. Patients with HF also occasionally have ascites, which can erroneously suggest cirrhosis. One study in patients with ascites found that a serum NT-proBNP distinguished HF from cirrhosis. 98% ...