In this episode, I’ll discuss iatrogenic hyperchloremia.
Iatrogenic hyperchloremia occurs when excessive chloride levels occur during the treatment of another condition. While loss of hypotonic fluids via excessive carbonic anhydrase inhibitor use is probably the first thing a pharmacist thinks of for iatrogenic causes of hyperchloremia, this is a rare occurrence compared to the number of patients who develop hyperchloremia from crystalloid IV fluid administration, especially normal saline. While small amounts of excess chloride will not result in a significant change to serum levels, large volume administration of normal saline may, and the negative consequences on kidney function and acid/base balance may ensue.
While iatrogenic hyperchloremia has always been a concern, the promotion of aggressive fluid resuscitation with normal saline in sepsis treatment guidelines over the past two decades has contributed to a larger number of patients experiencing iatrogenic hyperchloremia. This has led to more studies of the condition to examine potential adverse effects on patient outcomes. Most of these studies have occurred in the past decade.
Decreased renal perfusion, acute kidney injury, and metabolic acidosis are known consequences of hyperchloremia. The mechanism by which hyperchloremia decreases renal perfusion is likely via feedback in the Loop of Henle. Increased sodium and chloride is detected as an increase in GFR, and vasoconstriction of the afferent arteriole results to bring GFR back into a normal state. When the increase in chloride is due to excessive exogenous administration, the vasoconstriction still occurs, even though GFR was never elevated, leading to sub-normal renal blood flow and the development of acute kidney injury.
The mechanism by which hyperchloremia causes metabolic acidosis is by altering the strong ion difference in the blood. The strong ion difference is the difference between the cations potassium, sodium, magnesium, and calcium compared to the anions chloride, lactate, and bicarbonate. When chloride increases, the strong ion difference decreases. Compensatory mechanisms then try to restore the normal strong ion difference by a decrease in base excess, and the result of lower base excess is metabolic acidosis. Essentially, the bicarbonate gets crowded out by the chloride. Since bicarbonate is primarily what keeps blood from being acidic, losing it results in metabolic acidosis.
The topic in this episode is inspired by an in-depth training available to members of my Hospital Pharmacy Academy on the prevention of iatrogenic hyperchloremia. The Hospital Pharmacy Academy is my online membership site that will teach you practical critical care and hospital pharmacy skills you can apply at the bedside so that you can become confident in your ability to save lives and improve patient outcomes. To get immediate access to this and many other resources to help in your practice, go to pharmacyjoe.com/academy.
If you like this post, check out my book – A Pharmacist’s Guide to Inpatient Medical Emergencies: How to respond to code blue, rapid response calls, and other medical emergencies.
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