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Q1: What additional history would help in making a diagnosis?
History of ingestion of antacids. The patient gave a history of using at least half to one bottle of antacids and several tablets of “Tums” (calcium carbonate) a day for heartburn and indigestion.
Q2: What is the most likely explanation for the electrolyte disturbance?
The triad of hypercalcaemia, alkalosis, and renal failure suggests a diagnosis of milk alkali syndrome with excessive ingestion of milk of magnesia. The alkalosis was aggravated by vomiting and nasogastric suction leading to volume contraction.
An abdominal film was obtained and intestinal obstruction was excluded. The patient was treated with normal saline and other supportive measures. His electrolytes and renal function normalised within the next 24 hours (table 1).
The patient described above presented with a severe metabolic alkalosis (bicarbonate of 65 mmol/l) and hypermagnesaemia. The pathogenesis of metabolic alkalosis in this case is complex and multifactorial. The triad of hypercalcaemia, alkalosis, and renal failure suggests a diagnosis of milk alkali syndrome. However, this syndrome is generally associated with hypokalaemia and hypomagnesaemia. In the patient presented here, excessive ingestion of milk of magnesia (Mg(OH)2) in the presence of renal failure led to reduced excretion of magnesium thus causing hypermagnesaemia. The alkalosis was further aggravated by vomiting, nasogastric aspiration, and volume contraction. Dehydration led to further deterioration in renal function.
Alkalosis of this severity has only been reported sporadically.1 2 Voyce et alreported a case of severe alkalaemia with a pH of 7.81, as a result of combined metabolic and respiratory alkalosis.3 A serum bicarbonate concentration of 96 mmol/l has been reported in a patient due to excessive ingestion of sodium bicarbonate.2Severe alkalaemia may be fatal and a mortality as high as 41% has been reported with severe metabolic alkalosis.4
Metabolic alkalosis is categorised as saline responsive if the urine chloride concentration is less than 15 mmol/l or saline resistant if the urine chloride is greater than 25 mmol/l. Volume depletion, either from gastrointestinal losses, diuretics, or renal compensation for hypercapnia are among the most common causes of chloride responsive metabolic alkalosis. Chloride resistant metabolic alkalosis results from mineralocorticoid excess or potassium depletion. Evaluation of patients with metabolic alkalosis includes assessment of extracellular fluid volume, and urinary electrolytes which helps to determine if the alkalosis is chloride responsive. Fluid repletion is the mainstay of treatment of chloride responsive metabolic alkalosis. In cases of very severe alkalosis infusion of dilute hydrochloric acid (0.01N) may be required. The management of chloride resistant alkalosis requires treatment of the underlying cause.5
Hypermagnesaemia occurs rarely, and is usually iatrogenic.6 Elderly patients with renal failure are at increased risk of developing hypermagnesaemia. Clinical manifestations of hypermagnesaemia include vomiting, altered mental status, and respiratory depression. Discontinuation of magnesium is sufficient to correct the problem in most cases, however, haemodialysis may be required to treat severe cases.6
This case describes a complex and potentially fatal electrolyte and acid-base disorder, resulting from available and commonly used non-prescription medication. History remains an invaluable guide to the diagnosis of such complex problems. Elderly patients should be particularly warned against abuse of laxatives and antacids.
Metabolic acidosis secondary to milk alkali syndrome and nasogastric aspiration with milk of magnesia overdose.
This work was supported by NIH Grant HL-07123.
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