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Unraveling metabolic alkalosis: a complex case history
Summarized from Marston N, Kehl D, Copp J et al. Alkalotics Anonymous: Severe metabolic alkalosis. Am J Med 2014; 127: 25-27
Metabolic alkalosis, a disturbance of acid-base homeostasis, with many possible causes, is characterized by a primary increase in blood pH and bicarbonate (HCO3). Hypoventilation is the compensatory respiratory response to metabolic alkalosis that results in increased pCO2.
The often complex nature of the etiology of metabolic alkalosis is nicely conveyed by a recently published case study report of severe metabolic alkalosis. This concerns a 64-year-old man who was brought to the emergency department of his local hospital by his sister after a 3-week history of worsening confusion, difficulty walking, lack of food intake, and vomiting.
The patient has a long-term history of alcohol abuse, post-traumatic stress disorder, and gastroesophageal reflux disease. His sister reported that he had become more withdrawn over the past few weeks during which time his diet comprised only Pepsi and alcohol.
Initial assessment revealed: acute kidney injury (serum creatinine 9.28 mg/dL (820 mmol/L) but within normal range a few months previously); hypokalemia (potassium 3.0 mmol/L); hypocalcemia (ionized calcium 0.75 mmol/L); severe hypochloremia (chloride 59 mmol/L).
Blood gas results (pH 7.64, HCO3 62 mmol/L, pCO2 58 mmHg (7.7 kPa)) confirmed partially compensated severe metabolic alkalosis. This was complicated by a superimposed high-anion-gap metabolic acidosis secondary to acute renal failure and lactic acidosis.
Much of this case study report is taken over to a helpful general discussion of the mechanisms that give rise to metabolic alkalosis and the diagnoses to be considered in assessing the patient who presents with metabolic alkalosis. The authors explain how this knowledge was applied in the assessment and care of their patient.
In this case, hypovolemia, secondary to vomiting and decreased oral intake, was considered the cause of acute kidney injury. Although vomiting and volume contraction were considered contributory factors in the development of metabolic alkalosis, its severity suggested that additional mechanism(s) were involved; initially these factors remained undefined.
The patient was admitted to intensive care where his treatment included fluid resuscitation and hemodialysis. The precipitating, main cause of metabolic alkalosis was eventually identified when on further questioning the patient’s sister informed intensive care staff that her brother had recently been taking four spoonfuls of baking soda (sodium bicarbonate) every day to alleviate dyspepsia.
The combination of excessive bicarbonate ingestion and accompanying vomiting and volume depletion sufficiently explained the development of severe metabolic alkalosis and associated electrolyte disturbance in this case.
The patient made a full recovery from his immediate life-threatening metabolic state and was scheduled for endoscopy for further investigation of possible gastrointestinal disease. This revealed resolving duodenal ulcers and also the presence of a vitamin bottle cap that the patient recalled accidentally swallowing.
The authors of this report speculate that the time course from swallowing the bottle cap to hospital admission is consistent with the hypothesis that the bottle cap caused gastric irritation, with resulting vomiting and dyspepsia that provoked the patient to take the baking soda, which in turn caused metabolic alkalosis. In this case, it seems, an ingested bottle top might have been the primary cause of metabolic alkalosis!
On a less speculative note, the authors caution that the use of baking soda and other bicarbonate-containing antacid drugs available over the counter is common among alcoholics and should be considered as the cause of metabolic alkalosis in alcoholics who present with symptoms (e.g. dyspepsia, reflux) of gastrointestinal disease.
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