Aaron Lindsay

G Decaux

JG Verbalis

M Martín-Llahí

P Angeli

P Ginès

R Moreau

RH Sterns

RJ Groszmann

S Sherlock

SJ Ellis

SW Biggins

T Hilden

WR Kim

English

PubMed

Crossref

CASE REPORT Open Access
Profound hyponatremia in cirrhosis: a case report
Aaron Lindsay
Abstract
Introduction
Cirrhosis of the liver commonly leads to a state of chronic hypervolemic hyponatremia. Profound exacerbation of
the hyponatremic state may occur in patients with decompensated cirrhosis in conjunction with acute stressors
such as infection or binge alcohol ingestion.
Case presentation
A 47 year old man with a history of alcoholic cirrhosis presented to the hospital with symptomatic profound hypo-
natremia (serum sodium concentration of 105 meq/L) due to a recent infection and binge drinking. The patient
was treated with antibiotics, diuretics and hypertonic saline and was placed on a fluid restricted diet. The serum
sodium level corrected slowly over four days with symptomatic improvement occurring after two days. A brief dis-
cussion of the symptoms and treatment of acute and chronic hyponatremia in the setting of cirrhosis is included.
Conclusion
In patients with cirrhosis, it is important to recognize the symptoms of hyponatremia, identify and treat any exacer-
bating conditions early in their course, and correct the serum sodium concentration slowly with frequent
monitoring.
Introduction
Cirrhosis of the liver frequently leads to a state of
chronic hypervolemic hyponatremia. The cause of the
hyponatremia is related to a decrease in systemic vascu-
lar resistance [1], which is more prominent in the
splanchnic circulation, and compensatory neurohormo-
nal mechanisms that are activated due to the hemody-
namic changes. The hyponatremia may be worsened in
the setting of binge alcohol drinking which leads to the
ingestion of large amounts of fluid containing little
sodium [2]. Hyponatremia in cirrhosis can be a severe
problem and has been shown to be an independent pre-
dictor of mortality in patients waiting for liver trans-
plantation [3,4]. Here is presented a case of a patient
with alcoholic cirrhosis who presents to the hospital
with a serum sodium concentration of 105 meq/L.
Case presentation
A 47-year-old Caucasian male was admitted with a three
day history of shortness of breath, weakness, anorexia,
and unsteady gait, including a recent fall. The patient
had a medical history significant for peptic ulcer disease,
hypertension, and alcoholic cirrhosis. His family history
was not significant. He reported smoking 2 packs per
day and drinking 8-12 beers per day for the past 20
years. Over the previous 6 months, the patient had been
unemployed and reported increased alcohol consump-
tion. On physical exam, the patient was noted to have
marked ascites with a prominent fluid wave and bulging
flanks, bilateral pitting edema above the knees, and
crackles as well as dullness to percussion in the left
lower lobes. In addition, chest radiographs revealed a
left lower lobe pneumonia. Significant laboratory studies
included a WBC of 19.4 × 109/L, AST of 107 U/L, ALT
of 66 U/L, and serum sodium concentration of 105
meq/L. The patient was treated with IV furosemide (40
mg × 1 dose) and 3% NaCl in addition to fluid restric-
tion because of his symptomatic and profound hypona-
tremia. His serum sodium concentration increased to
120 meq/L over 48 hours and 130 meq/L over 96 hours
with the use of 3% NaCl and fluid restriction, and his
weakness, anorexia, and unsteady gate improved. His
pneumonia was treated with Vancomycin (1 g IV every
12 hrs) and Piperacillin/Tazobactam (3.375 mg IV every
6 hrs) which resulted in symptomatic and radiographic
Correspondence: ajl39@case.edu
Case Western Reserve University, School of Medicine, 10900 Euclid Ave,
Cleveland, OH 44106, USA
Lindsay Cases Journal 2010, 3:77
http://www.casesjournal.com/content/3/1/77
© 2010 Lindsay; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properly cited.
improvement. He was discharged from the hospital on
oral spironolactone (200 mg/day) and furosemide (40
mg/day) with recommendations for abstinence from
alcohol, a low sodium diet, and fluid restriction.
Discussion
Chronic hyponatremia (defined as a serum sodium con-
centration below 130 meq/L) occurs in up to 22 percent
of people with cirrhosis [5], and is often asymptomatic
if the serum sodium concentration is above 120 meq/L
[6,7]. The percent of people with cirrhosis affected by
chronic hyponatremia increases to 50 percent if a cutoff
for serum sodium concentration of 135 meq/L, the
lower limit of normal, is used [5]. The frequency of
such profound hyponatremia as seen at presentation in
the patient in this case (serum sodium concentration of
105 meq/L) is unclear; a population survey reported that
the prevalence of patients with cirrhosis and serum
sodium concentrations less than or equal to 120 meq/L
is 1.2 percent [6].
The most common reason for chronic hyponatremia
in cirrhosis is impairment in renal solute-free water
secretion due to increased antidiuretic hormone secre-
tion and decreased effective arterial volume [5,8]. The
brain is able to compensate for the increased osmolar
pressure (which leads to cerebral edema) in chronic
hyponatremia by extruding intracellular osmolytes, such
as potassium, glutamine and myoinositol, which can
take 48 hours for full effect [5,7,9]. This adaptive
mechanism explains why patients with chronic hypona-
tremia and serum sodium concentrations above 120
meq/L are often asymptomatic.
If there is an acute exacerbating condition however,
such as infection or binge drinking as in this patient,
the serum sodium concentration can rapidly drop to
dangerously low levels for which the brain is unable to
compensate acutely. Acute worsening of chronic hypo-
natremia may have various etiologic factors, including:
generalized haemodynamic derangement with low per-
ipheral resistance, reduced effective arterial volume,
hypothalamic overproduction of antidiuretic hormone,
elevated renin and angiotensin, hypotonic fluid ingestion
and reduced glomerular filtration, all of which may lead
to marked water retention [5,7,8]. The ingestion of large
amounts of alcohol, a hypotonic fluid containing little
sodium, may worsen the underlying chronic hyponatre-
mia present in cirrhosis [2] and is believed to be a factor
for the acute decompensation seen in this patient.
Common symptoms of chronic hyponatremia include
fatigue, nausea, dizziness, lethargy, confusion, and gait
disturbances [10,11]. In the setting of acute hyponatre-
mia, or acute on chronic hyponatremia, seizures, coma,
and respiratory arrest may occur [10]. It should be
noted that the symptoms experienced by the patient
presented in this report are likely multifactorial and due
to both the profound hyponatremia and comorbid lobar
pneumonia. Treatment of hyponatremia in patients with
cirrhosis includes sodium and fluid restriction and con-
tinued treatments with spironolactone and loop diure-
tics. However, care must be taken when administering
diuretics as they can exacerbate the reduction in tissue
perfusion that occurs in cirrhosis, further impairing the
ability to excrete free water [12]. Bolus infusions of 3%
NaCl are reserved for patients with profound hyponatre-
mia and severe symptoms [13]. Vasopressin receptor
antagonists are newer therapies and their precise role in
treating hypervolemic hyponatremia in patients with cir-
rhosis is not well-defined [5,7]. The serum sodium con-
centration in symptomatic hyponatremia should be
corrected at a rate no more than 10 meq/L in the first
24 hours, 18 meq/L in the first 48 hours, and 20 meq/L
in the first 72 hours to prevent iatrogenic brain injury
and central pontine myelinolysis [13,14]. In patients
with cirrhosis, it is important to recognize the symp-
toms of hyponatremia, identify and treat any exacerbat-
ing conditions early in their course, and correct the
serum sodium concentration slowly with frequent
monitoring.
Consent
Written informed consent was obtained from the patient
for publication of this case report. A copy of the written
consent is available for review by the Editor-in-Chief of
this journal.
Abbreviations
ALT: alanine transaminase; AST: aspartate transaminase; IV: intravenous; NaCl:
Sodium Chloride; WBC: white blood cell count.
Competing interests
The author declares that he has no competing interests.
Received: 18 March 2010 Accepted: 23 March 2010
Published: 23 March 2010
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doi:10.1186/1757-1626-3-77
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Profound hyponatremia in cirrhosis: a case report

Springer - Publisher Connector

Ginès P: Hyponatremia in cirrhosis: clinical features and management. Gastroenterol Clin Biol

Hyperdynamic circulation of liver disease 40 years later: Pathophysiology and clinical consequences. Hepatology

Hyponatremia in cirrhosis: pathogenesis, clinical significance, and management. Hepatology

Hyponatremia in cirrhosis. Pathophysiology, prevalence, prognostic value, treatment. Acta Gastroenterol Belg

Is asymptomatic hyponatremia really asymptomatic?

JG: Complications of diuretic therapy in hepatic cirrhosis. Lancet

JK: The treatment of hyponatremia. Semin Nephrol

P: Hyponatremia in cirrhosis: Results of a patient population survey. Hepatology

RH: Hyponatremia treatment guidelines 2007: Expert panel recommendations. Am J Med 2007, 120:S1. doi:10.1186/1757-1626-3-77 Cite this article as: Lindsay: Profound hyponatremia in cirrhosis: a case report.

Severe hyponatraemia: Complications and treatment.

Svendsen TL: Electrolyte disturbances in beer drinkers. A specific “hypo-osmolality syndrome”. Lancet

Terrault NA: Serum sodium predicts mortality in patients listed for liver transplantation. Hepatology

Therneau TM: Hyponatremia and mortality among patients on the liver-transplant waiting list.

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Profound hyponatremia in cirrhosis: a case report

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