Drug-related acid-base disturbance – a review article

Each issue of the journal Emergency Clinics of North America is devoted to the review of a single topic of relevance to emergency medical care. The topic for the February 2014 issue was clinical toxicology and one of the 11 review articles in this issue, written by an emergency care doctor with specialist interest in clinical toxicology, focuses on the acid-base disturbances that can occur in the poisoned patient. 

In general terms the article serves to remind that abnormal blood gas results can be caused by a huge range of drugs/toxins, and that it is often appropriate to order arterial blood gas analysis for assessment of patients suspected of having, accidentally or deliberately, taken a drug overdose.

The article begins with a very brief overview of acid-base physiology and a general discussion of how blood gas results are used to classify acid-base disturbance to one of four classes: respiratory acidosis, metabolic acidosis, respiratory alkalosis and metabolic alkalosis. The concept of anion gap is explained. 

This first introductory part of the article is followed by a focus on each of the four acid-base disturbances in turn, highlighting the toxicological causes of each. So for example, we learn that a major toxicological cause of respiratory alkalosis is salicylate due to its ability to directly stimulate the medullary respiratory center, and thereby increase respiratory rate and tidal volume. 

A range of drugs listed by the author can cause lung pathology (pulmonary fibrosis, pulmonary edema) that results in impaired gas exchange and compensatory increased respiratory rate with consequent respiratory alkalosis. Under the heading of respiratory acidosis there is discussion of the hypoventilatory effect of opioid drugs and other drugs (e.g. barbiturates) that depress respiration and cause respiratory acidosis. 

The toxicological causes of metabolic alkalosis discussed include bicarbonate present in antacid preparations; excessive use of such drugs can cause the milk-alkali syndrome, which is characterized by the triad: metabolic alkalosis, hypercalcemia and renal failure. 

Of all acid-base disturbances metabolic acidosis is the most common, so that much the largest section of the article is devoted to discussion of the mechanisms that give rise to metabolic acidosis and how specific drugs impact on these mechanisms. 

There is discussion of drugs that can cause or potentiate hyperchloremic (non-anion gap) metabolic acidosis as well as those that can cause or potentiate the more common type of metabolic acidosis, anion gap metabolic acidosis. The mnemonic “CAT-MUDPILES” devised to aid memory of the many causes of anion gap metabolic acidosis (including drug-/toxin-related causes) is critically discussed. 

Finally there is extensive discussion of the drug-/toxin-related causes of lactic acidosis (the L of the CAT-MUDPILES mnemonic), alcoholic ketoacidosis (the A of the CAT-MUDPILES mnemonic) and the way toxic alcohols (e.g. ethylene glycol, the E of the CAT-MUDPILES mnemonic) cause anion gap metabolic acidosis. 

Supported by 33 references this is a valuable overview of an important blood gas topic that generally gets scarce attention in the medical literature, beyond individual case reports highlighting a single drug.