Anjum Shahid ( PMRC Research Centre, Jinnah Postgraduate Medical Centre, Karachi. )
Hurna Quresbi ( PMRC Research Centre, Jinnah Postgraduate Medical Centre, Karachi. )
Fatima Nizami ( PMRC Research Centre, Jinnah Postgraduate Medical Centre, Karachi. )
Sarwar J. Zuberi ( PMRC Research Centre, Jinnah Postgraduate Medical Centre, Karachi. )
Serum and urinary electrolytes were estimated in 33 patients with hepatitis and 35 with cirrhosis. Forty two percent patients with hepatitis and 46% with cirrhosis bad hyponatraemia while 30% with hepatitis and 37% with cirrhosis had low serum potassium levels. Low urinary sodium was found in 27.3% cases of hepatitis and 40% cirrhotics and low urinary potassium in 21.2% and 45.7% cases of hepatitis and cirrhosis respectively. Hypokalaemia and low urinary sodium appear to be bad progaostic findings in cirrhosis (JPMA 33: 289, 1983).
Impairment in electrolyte metabolism was associated with the severity of liver disease (Baldus et al., 1964). Prominent amongst the renal complications of cirrhosis was progressive impairment of renal sodium handling leading to the formation of ascites and peripheral edema (Epstein, 1979). Hyponatraemia is common in cirrhosis (Shear et al., 1965) and hyperaldosteronism is probably the most important factor which results from an increased release of renin by the kidney (Wilkinson et aL, 1975).
Patients with severely impaired hepatic function had greater degrees of potassium depletion and failed to replenish body potassium stores when potassium supplements were given (Casey et al., 1965).
Electrolyte abnormalities occur at all stages of liver disease. Serum and urinary electrolytes were therefore determined in patients withhepatitis and cirrhosis.
Material and Methods
Sodium, potassium, chloride and bicarbonate were estimated in 33 patients with hepatitis, 35 with cirrhosis and 100 control subjects.
Sodium and potassium were determined by flame photometry in blood and twenty four hour urine samples. Serum chloride was estimated by the method of Schales and Schales (1941). Serum bicarbonate was estimated by micro carbon dioxide system, a simplified version of classical Van Slyke method (Harleco Kit).
Abnormalities in fluid and electrolyte metabolism have not been found in patients with hepatitis (Laragh and Ames, 1963). In the present study hyponatraemia was observed in 42% cases. However, the low value was transient and of the hyponatraemics only 14% died and the remaining recovered. Hypokalaemia was evident in 30% patients and all of them recovered. Serum chloride and bicarbonate showed no abnormalities in patients with hepatitis.
Cirrhosis showed a pattern of physiological disturbances in water and electrolyte metabolism together with the changes in renal and adrenal cortical function (Laragh and Ames, 1963). Abnormal renal retention of sodium is a characteristic finding (Wilkinson et aL, 1975). In the present series low serum sodium was found in 45.7% cases. Follow up of these patients revealed an overall mortality rate of 62.5%. Dilutional type of hyponatraemia is frequent in patients with cirrhosis of the liver (Ring Larsen, 1975). Corrective measures using salt therapy should, therefore, be av s it will further decrease the level due uid retention. Restriction of fluid intake t half or even less than the output will serve the purpose and the false hyponatraemia will be corrected.
The severity of the hepatic disease appeared important in the diminuition of body stores of potassium (Casey et al., 1965). Various factors including diet, gastrointestinal losses and diuretic treatment influence the potassium status of cirrhotics. Studies using exchangeable potassium (42k) have shown that cirrhotics even without edema or ascites may be depleted of total body potassium in the presence of normal serum potassium (Aikawa et al., 1953; Burrows et al., 1953). As reported earlier serum potassium determinations are poor indicators of body potassium stores in patients with cirrhosis (Heinemann and Emirgil, 1960; Casey et al., 1965). Hypokalaemia in the present series was found in 37% cirrhotics. In this case the mortality rate was 46%. Regarding hypokalaemia, effective measures should be taken into consideration and potassium should be given orally or intravenously. Oral administration is preferred. It is presumed that timely correction of potassium could have altered the fate of those patients who went into coma and died.
In the present series, serum chloride and bicarbonate had normal mean values in cirrhosis.
Liver is involved in the regulation of renal sodium excretion. Failure of excretion in liver disease could be related to the metabolic and functional impairment of this organ (Kramer, 1975). Urinary sodium excretion was low in patients with cirrhosis (Baldus et al., 1964). Hepatitis in the present study showed abnormalities in urinary sodium. Wide variation in the level (14-360 meq/24 hrs) was observed. However the abnormality was transient and all the patients recovered. Low urinary sodium was found in 40% cirrhotics and the mortality rate was high (66.6%) in cases of extremely low values. The overall mortality was 43%. Level also showed wide variation (2.0-492 meq/24 has) and a value as low as 2.0 meq/ 24 hrs was found.
Low urinary potassium was found in 21% cases of hepatitis and 46% cirrhotics. All cases of hepatitis with low urinary potassium recovered, whereas in cirrhosis the mortality rate was 31.25%.
Hence electrolytes should be repeatedly done in patients with decompensated liver disease and hypokalaemia should be corrected immediately which may improve the prognosis.
1. Aikawa, J.K., Felts, J.H.Jr. and Harrell, G.T. (1953) Alterations in the body potassium content in cirrhosis of the liver. Gastroenterology, 24 :437.
2. Baldus, W.P., Feichter, R.N., Summerskill, W.HJ., Hunt, J.C. and Wakim, K.G.(1964) The kidney in cirrhosis. II. Disorders of renal function. Ann. Intern. Med., 60:366.
3. Burrows, B., Denton, J., Fergusons, B. and Ross, 3. (1953) Changes in boay potassium in hepatic decompensation. Clin. Res. Proc., 1:111.
4. Casey, T.H., Summerskilj, W.HJ. and Orvis, Al. (1965) Body and serum potassium in liver disease. I. Relationship to hepatic function and associated factors. Gastroenterology, 48:198.
5. Casey, T.H., Summerskill, W.H.J., Bickford, RJ. And Rosevear, J.W. (1965) Body and serum potassium in liver disease. II. Relationship to arterial ammonia, blood pH and hepatic coma. Gastroenterology, 48:208.
6. Epstein, M. (1979) Deranged sodium homeostasis in cirrhosis. Gastroenterology, 76 : 622.
7. Heinemann, H.O., and Emirgil, C. (1960) Hypokalaemia in liver disease. Metabolism, 9:869.
8. Kramer, HJ. (1975) Natriuretic hormone - its possil)le role in fluid and electrolyte disturbances in chronic liver disease. Postgrad. Med. 3., 51:532.
9. Laragh, J.H. and Ames, R.P. (1963) Physiology of body water and electrolytes in hepatic disease. Med. Clin. N. Am., 47 : 587.
10. Ring Larsen, H. (1975) The significance of hyponatraemia in liver failure. Postgrad. Med. 3., 51 : 542.
11. Schales, 0. and Schales, S.S. (1941) cited by Varley, H. Practical clinical biochemistry. 4th ed. Heinemann, London, 1967.
12. Shear, L., lUeinerman, J. and Gabuzda, GJ. (1965) Renal failure in patients with cirrhosis of the liver. I. Clinical and pathologic characteristics. Am. J. Med., 39 : 184.
13. Wilkinson, S.F., Moodie, H., Alam, A. and Williams, R. (1975) Renal retention of sodium in cirrhosis and fulminant hepatic failure. Postgrad. Med. J., 51 :527.