INTRODUCTION: Hyponatremia is defined as serum sodium concentration [Na+] of less than 135 mEq/L; Current treatment recommendations for asymptomatic hyponatremia patients include the correction of 0.5 mmol/L per hour to avoid osmotic demyelination. In this report we present a case of extreme hyponatremia associated with cirrhosis and its successful correction with the use of combination of a vasopressin receptor antagonist and normal saline infusion.
CASE PRESENTATION: A 41 year old man presented with progressively increasing bilateral lower extremity swelling. He also had watery diarrhea. His past medical history was significant for cirrhosis secondary to alcohol abuse. On physical examination, he was afebrile His abdomen was distended, non-tender with normal bowel sounds. On laboratory studies, his sodium was 94 mmol/L, potassium 3.2 mmol/L, chloride 59 mmol/L. Fractional excretion of sodium was 0.08%. The patient was placed on IV normal saline and conivaptan infusion. The serum sodium was measured every 4 hours initially and increased by 12meq/hr in the first 24 hours and to 122 meq/L by completion of 3 days of conivaptan infusion. By day 6, his sodium improved to 134. His level of alertness improved as the serum sodium increased.
DISCUSSIONS: The severe hyponatremia of serum [Na+] of 94 mEq/L in this patient was likely multifactorial caused mainly by cirrhosis, beer potomania and diarrhea. Patients with cirrhosis can have hypovolemic hyponatremia secondary to diuretic use and more commonly hypervolemic hyponatremia due to marked impairment of renal solute -free water excretion. Both can be differentiated on the basis of history and physical examination by the presence or absence of edema or ascites. The treatment of hyponatremia is determined by the severity, duration and volume status. Severe symptomatic hyponatremia is a medical emergency and use of hypertonic saline for rapid correction is recommended. Rapid correction in asymptomatic patients can lead to central pontine myelinolysis.(1)Until recently, treatment options for euvolemic and hypervolemic hyponatremia consisted mainly of water restriction, diuresis or hypertonic solutions. These treatment modalities are limited by variable efficacy, slow onset of action, non-compliance and serious toxicities. AVP receptor antagonist is a new class of drugs being used in treatment of hyponatremia like Conivaptan. (2) This case is interesting as this patient had very low serum sodium and was treated with a combination of conivaptan and normal saline infusion together. The result was a gradual and progressive reversal of hyponatremia without any neurological deficits or signs of dehydration. Our principle of conivaptan and normal saline infusion was based on the basic step of blockage of V2 receptors. This would enhance the free water excretion from the body and saline leading to retention of salt. Also giving volume to the patient enabled us to use conivaptan infusion for longer without any signs or symptoms of dehydration.
CONCLUSION: We suggest a novel mechanism of using conivaptan and isotonic fluid infusion together as treatment for severe hypervolemic hypernatremia with intravascular volume depletion, contrary to fluid restriction.
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