October 2009
Swagata Tripathy
Abstract
Metabolic alkalosis is a commonly seen imbalance in the intensive care unit (ICU). Extreme metabolic alkalemia, however, is less common. A pH greater than 7.65 may carry a high risk of mortality (up to 80%). We discuss the entity of life threatening metabolic alkalemia by means of two illustrative cases - both with a pH greater than 7.65 on presentation.
The cause, modalities of managing and complications of this condition is discussed from the point of view of both the traditional method of Henderson and Hasselbalch and the mathematical model based on physiochemical model described by Stewart. Special mention to the pitfalls in managing patients of metabolic alkalosis with concomitant renal compromise is made.
Introduction
Extreme metabolic alkalemia has been associated with a high risk of mortality of up to 45% with a pH of 7.55 and 80% when pH is greater than 7.65. Appropriate intervention and correction is warranted when arterial blood pH exceeds 7.55.
We discuss two cases who presented to our intensive care unit with extreme metabolic alkalemia (pH 7.65). One was managed with simple replacement measures. The other defied even better known interventions for management of alkalemia. We discuss the manifestations, causes and management of ‘extreme’ life threatening alkalemia.
Case reports
A 60-year-old man presented to the emergency department with the complaints of weakness, difficulty in breathing, decreased appetite and absolute constipation for ten days. He was restless and disoriented. Hemodynamic parameters were normal.
Investigations and systemic examination revealed severe metabolic alkalosis (pH 7.66) with dyselectrolytemia and volume depletion. His respiratory and neurologic systems were unremarkable. The abdomen was distended and multiple fluid and air levels seen on an abdominal radiogram, confirmed sub acute intestinal obstruction.
Despite denials of use of any diuretics or laxatives, when his regular medicines were checked, loop diuretics and combinations with potassium sparing diuretics were recovered-confirming long term diuretic abuse. All diuretics were removed from patient's bedside and patient was hydrated to achieve a central venous pressure (CVP) of at least 10 cm water (opening CVP 1 cm water) and a urine output of more than 1 ml/kg/hour. Obstipation was relieved by manual evacuation of hard dried up faeces - the cause of sub acute intestinal obstruction.
Supplementation of potassium, chloride, sodium and magnesium led to improvement of serum electrolytes and resolution of alkalemia over 36 hours. The patient's respiratory distress, weakness and lassitude resolved. Patient was discharged after four days without any complains.
