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DOI 10.1007/s11894-014-0382-4
Introduction
The definition of hyponatremia has been established as a level
of 130 mEq/L in patients with cirrhosis and/or ascites/edema
and it is believed that approximately 30 % of individuals with
cirrhosis have a serum sodium level less than 130 mEq/ml
[2]. The vast majority of patients with cirrhosis develop
hyponatremia due to expanded volume status, which is an
increase in the extracellular volume as well as plasma, and
typically these patients clinically will present with ascites and
edema. This hypervolemic hyponatremia is a dilutional
hyponatremia and is due to an excess of water retention due
to the distal tubule being unable to excrete free water [4]. A
second less common type of hyponatremia occurs in those
with cirrhosis, and this is typically a hypovolemic
hyponatremia that occurs due to aggressive use of diuretic
therapy to treat edema and/or ascites, or from excess GI losses
that can be seen, for instance, in those receiving lactulose for
encephalopathy. Unlike hypervolemic hyponatremia, these
individuals have a low plasma volume, low extracellular fluid,
and typically have little or no ascites and edema, and present
with signs of azotemia. The vast majority of individuals with
cirrhosis have hypervolemic hyponatremia.
Pathophysiology
Keywords Hyponatremia . Cirrhosis . Liver disease .
Vaptans . Tolvaptan . Satavaptan
This article is part of the Topical Collection on Liver
P. Y. Kwo (*)
Gastroenterology/Hepatology Division, Indiana University School of
Medicine, 975 W. Walnut, IB 327, Indianapolis, IN 46202-5121,
USA
e-mail: pkwo@iu.edu
382, Page 2 of 5
Page 3 of 5, 382
Fig. 1 Management of
hyponatremia
Management of hyponatremia
Hypervolemic hyponatremia
Hypovolemic hyponatremia
Awaiting OLT
clinical symptoms
Fluid restrict to
less than urine
output
382, Page 4 of 5
Conclusion
Clinicians who treat patients with cirrhosis should be alert to
the development of hyponatremia, which remains an additional important marker of advanced liver disease, and may herald
additional complications. Management remains problematic
(Fig. 1). For now, dietary fluid restriction remains the standard
of care, though it can be difficult to adhere to in the clinical
setting. The decision to initiate this should be dependent on
the patients clinical status, and neurologic status should be
assessed carefully. Some have advocated for intervention with
a serum sodium of <120 mEq/l though data to demonstrate
that correcting at this level improves survival is lacking. One
population in which careful management and potential correction of hyponatremia should be considered is in the pretransplant setting where careful management is required to
prevent post-transplant CPM. While V2-receptor antagonists
(vaptans) have been demonstrated to provide short-term correction of sodium levels, safety concerns are limiting their use
and 2 vaptans (tolvaptan and satavaptan) are not approved for
use in those with cirrhosis or are not available in Europe due to
safety concerns. Another vaptan, conivaptan, is approved in
the US, but there are safety concerns regarding hypotension
and bleeding which limits its use. Moreover, thus far, vaptans
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highlighted as:
Of importance
Of major importance
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