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Management of hyponatraemia in cirrhotic ascites

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V.N. Mahesh MRCP
Department of Gastroenterology and Hepatology
Freeman hospital, Newcastle Upon Tyne hospitals NHS trust

Citation: V. Mahesh : Management of hyponatraemia in cirrhotic ascites . The Internet Journal of Gastroenterology. 2008 Volume 7 Number 1

Introduction
Pathophysiology
Management
Corresponding address

Abstract

Hyponatremia is a commonly encountered problem in patients with ascites and its incidence increase with the use of diuretics. Management of such patients often poses problems and since symptomatic hyponatremia is unusual in cirrhosis, and hence close electrolyte monitoring is essential. Here ways of managing this condition with evidence supporting these methods is analysed.

Introduction

Hyponatraemia is a common clinical problem faced during treatment of cirrhotic patients.

The prevalence of this condition has increased due to diuretic usage, which has become a standard part of the treatment. Management of these patients is often complex due to problems with salt restriction and worsening ascites and the need for recurrent paracentesis and more complex procedures in patients with resistant ascites.

Pathophysiology

The primary mechanism of development of hyponatremia is different to development of ascites in itself. Patients with cirrhosis and ascites usually have a marked reduction in systemic vascular resistance (SVR)- mostly in the splanchnic circulation and in mean arterial pressure (MAP) plus an increase in cardiac output.(¹).Ability to excrete water is reduced with the advancement of cirrhosis(²) combined with increased ADH-antidiuretic hormone release as shown in studies by Arroyo et al.(³). Hyponaatremia acts as a prognostic marker of worsening liver disease, especially with values below 130meq/L, as shown by Papadakis et al. Degree of hyponatraemia parallels severity of liver disease and hyponatraemia <120mmols is seen in <1-2% patients.(⁴).

Management

Diagnosis is simple with testing of serum biochemistry. There is no firm evidence regarding the frequency of estimation of serum electrolytes but common clinical practice is to test every week after a dose change and once stable clinical status is achieved, frequency of testing can be reduced to once in two weeks, should suffice.

Management of such patients often poses problems and since symptomatic hyponatremia is unusual in cirrhosis, only modest water restriction that is tolerated by the patient is followed in our clinical setting as first step.

Withholding diuretic doses, especially furosemide when plasma sodium drops below 126meq/L along with fluid restriction should be the next step, with monitoring of urine output as a measure of fluid restriction. This can be followed by cessation of spironolactone if sodium levels do not respond to the initial measures.

Overly rapid drop in sodium levels should be avoided since it can precipitate hepatic encephalopathy. No studies or controlled trials have done in this specific condition, and use of normotonic or hypertonic saline to raise plasma sodium has been attempted, but being cautious not to increase it by more than 12meq/l per day is necessary to avoid central pontine myelinolysis. Alcoholic patients are more prone to neurological complications on rapid correction in plasma sodium levels (⁵).

Other treatments including vasopressin receptor analogues, demeclocycline etc have been tried, but no definite benefit (⁶). Paracentesis is an option independent of the fluid restriction, since indications are only tense ascites with respiratory splinting, peripheral pedal edema or failed diet and diuretics. But if fluid has to be lost urgently, paracentesis is preferred over persistence with diuretics. Monitoring renal functions very closely during this period helps to prevent/treat hepatorenal syndrome early and improve outcomes.

Corresponding address

68, Chirton Dene Quays
North Shields
Tyne & Wear, United Kingdom
NE29 6YW
07886749899

References

1. Groszmann, RJ. Hyperdynamic circulation of liver disease 40 years later: Pathophysiology and clinical consequences. Hepatology 1994; 20:1359. (s)

2. Arroyo, V, Bosch, J, Gaya, J, et al. Plasma renin activity and urinary sodium excretion as prognostic indicators in nonazotemic cirrhosis with ascites. Ann Intern Med 1981; 94:198. (s)

3. Arroyo, V, Claria, J, Gaya, J, et al. Antidiuretic hormone and the pathogenesis of water retention in cirrhosis with ascites. Semin Liver Dis 1994; 14:44. (s)

4. Papadakis, MA, Fraser, CL, Arieff, AI. Hyponatraemia in patients with cirrhosis. Q J Med 1990; 76:675. (s)

5. Tanneau, RS, Henry, A, Rouhart, F, et al. High incidence of neurologic complications following rapid correction of severe hyponatremia in polydipsic patients. J Clin Psychiatry 1994; 55:349. (s)

6. Miller, PD, Linas, SL, Schrier, RW. Plasma demeclocycline levels and nephrotoxicity: Correlation in hyponatremic cirrhotic patients. JAMA 1980; 243:2513 (s)

7. Bichet D, Szatalowicz V, Chaimovitz C, et al. Role of vasopressin in abnormal water excretion in cirrhotic patients. Ann Int Med 1982;96:413-17. (s)

8. Gatta A, Caregaro L, Angeli P, et al. Impaired renal water excretion in liver cirrhosis. The role of reduced distal delivery of sodium. Scand J Gastroenterol 1988;23:523-8. (s)

9. Gerbes AL, Gulberg V, Gines P, et al. Therapy of hyponatremia in cirrhosis with a vasopressin receptor antagonist: a randomized double-blind multicenter trial. Gastroenterology 2003;124:933-9. (s)

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