scholarly journals Correlation of Serum Sodium with Severity of Hepatic Encephalopathy

2016 ◽  
Vol 3 (01) ◽  
pp. 3-10
Author(s):  
Muhammad Arshad ◽  
Shah Zeb ◽  
Muhammad Atif Tauseef ◽  
Najeeb Ullah

INTRODUCTIONHepatic encephalopathy (HE) is neuropsychiatric syndrome for which symptoms, manifested on a continuum, is deterioration in mental status, with psychomotor dysfunction, impaired memory, increase reaction time, poor concentration, disorientation, and in severe form coma and may develop at an annual rate of 8% in cirrhotic patients in Far Eastern studies. Fluctuation in serum sodium level is a frequent complication of advanced cirrhosis related to impairment in the renal capacity to eliminate solute-free water that causes retention of water that is disproportionate to the retention of sodium, thus causing a reduction in serum sodium concentration and hypo-osmolality. Hyponatremia is a common finding in patients with decompensated cirrhosis due to an abnormal regulation of body fluid homeostasis.OBJECTIVETo determine the correlation of serum sodium with severity of hepatic encephalopathyMATERIAL AND METHODSThis study was conducted at Naseer Teaching Hospital Peshawar. Duration of the study was 01 year and the study design was cross sectional (Correlation) study in which a total of 408 patients were observed by using – 0.1411 of correlation coefficient between serum sodium and hepatic encephalopathy 95% confidence level and 80% power of test. More over non probability consecutive sampling was used for sample collection.RESULTSIn this study mean age was 65 years with SD ± 0.315. Sixty two percent patients were male and 38% patients were female. Mean serum sodium level was 123 meq/L with SD ± 0.21. Five percent patients had severity of grade I, 39% patients had severity of grade II, 48% patients had severity of grade III and 8% patients had severity of grade IV. Correlation of severity of hepatic encephalopathy with serum sodium level was analyzed as all the 20 patients with severity of grade I had serum sodium level ranged 131-133 meq/L. All the 159 patients with severity of grade II had serum sodium level ranged 126-130 meq/L. In 196 patients with severity of grade III, 45 patients had serum sodium level ranged 126-130 meq/L while 151 patients had serum sodium level ranged 120-125 meq/L where as all the 33 patients with severity of grade IV had serum sodium level ranged 120-125 meq/L.CONCLUSIONHyponatremia was a common feature in patients with cirrhosis and its severity increased with the severity of liver disease. The existence of serum sodium concentration < 135 mmol/L was associated with greater frequency of hepatic encephalopathy. It was also noticed that more severe the hyponatremia, greater will be the grade of hepatic encephalopathy. Close monitoring of serum sodium concentration should be performed in patients with cirrhosis in order to prevent the rapid development of cirrhosis related complications.

Author(s):  
Yatendra Singh ◽  
Subhash Chandra Joshi ◽  
Mohammad Khalil ◽  
Ramlal Ola

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. Hyponatremia in cirrhosis is associated with increased morbidity and mortality. we report a case of52 year old man with a history of alcoholic cirrhosis presented to the hospital with symptomatic profound hyponatremia (serum sodium concentration of 102 meq/L). 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 five days. In patients with cirrhosis, it is important to recognize the symptoms of hyponatremia, identify and treat any exacerbating conditions early in their course, and correct the serum sodium concentration slowly with frequent monitoring. Key words: hyponatremia, cirrhosis, liver


2010 ◽  
Vol 30 (8) ◽  
pp. 1137-1142 ◽  
Author(s):  
Mónica Guevara ◽  
María E. Baccaro ◽  
Jose Ríos ◽  
Marta Martín-Llahí ◽  
Juan Uriz ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-4
Author(s):  
Guo Shen ◽  
Hainv Gao

Dilutional hyponatremia is common in decompensated cirrhosis and can be successfully treated by tolvaptan, a vasopressin V2-receptor antagonist. Data were lacking regarding the effects of tolvaptan on cirrhotic patients with a Child-Pugh score of >10 and a serum sodium concentration of <120 mmol/L. We report a case of forties man with a 20-year history of chronic hepatitis B presenting with yellow urine and skin. Laboratory tests demonstrated prolonged prothrombin time, markedly elevated total bilirubin, severe hyponatremia, and a Child-Pugh score of >10. The patient was diagnosed with dilutional hyponatremia and was treated with recommended dosage tolvaptan at first. The serum concentration of sodium recover but the patient felt obviously thirsty. As the dosage of tolvaptan was decreased accordingly from 15 mg to 5 mg, the patient still maintained the ideal concentration of serum sodium. This case emphasizes that cirrhotic patient with higher Child-Pugh scores and serum sodium concentration of <120 mmol/L can be treated with lower dose of tolvaptan.


SpringerPlus ◽  
2013 ◽  
Vol 2 (1) ◽  
pp. 519 ◽  
Author(s):  
Yeo-Jin Kang ◽  
Eun Bae ◽  
Kyungo Hwang ◽  
Dae-Hong Jeon ◽  
Ha Jang ◽  
...  

2010 ◽  
Vol 42 (9) ◽  
pp. 1669-1674 ◽  
Author(s):  
MATTHEW D. PAHNKE ◽  
JOEL D. TRINITY ◽  
JEFFREY J. ZACHWIEJA ◽  
JOHN R. STOFAN ◽  
W. DOUGLAS HILLER ◽  
...  

2017 ◽  
Author(s):  
Richard H Sterns ◽  
Stephen M. Silver ◽  
John K. Hix ◽  
Jonathan W. Bress

Guided by the hypothalamic antidiuretic hormone vasopressin, the kidney’s ability to conserve electrolyte–free water when it is needed and to excrete large volumes of water when there is too much of it normally prevents the serum sodium concentration from straying outside its normal range. The serum sodium concentration determines plasma tonicity and affects cell volume: a low concentration makes cells swell, and a high concentration makes them shrink. An extremely large water intake, impaired water excretion, or both can cause hyponatremia. A combination of too little water intake with too much salt, impaired water conservation, or excess extrarenal water losses will result in hypernatremia. Because sodium does not readily cross the blood-brain barrier, an abnormal serum sodium concentration alters brain water content and composition and can cause serious neurologic complications. Because bone is a reservoir for much of the body’s sodium, prolonged hyponatremia can also result in severe osteoporosis and fractures. An understanding of the physiologic mechanisms that control water balance will help the clinician determine the cause of impaired water conservation or excretion; it will also guide appropriate therapy that can avoid the life-threatening consequences of hyponatremia and hypernatremia.


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