Today we discussed an complicated case of acid base disturbances that our house staff breezed through. Simi presented a young man with acute epigastric pain and emesis after copious alcohol ingestion. It looked like a case of alcohol-induced pancreatitis or gastritis, but his metabolic panel threw everyone for a loop.
Go through the labs on your own and try to find an explain all the acid-base disturbances.
Here is our suggested method for acid-base learning:
- Is the patient acidemic or alkalemic ? A.k.a. is their pH above or below 7.4
- What is the primary disorder? Is the bicarb or the pCO2 driving the acidemia /alkalemia?
- What is the anion gap? Anion Gap = (Na+) – (Cl- + HCO3-). If there is an anion gap present, there is a concurrent anion gap metabolic acidosis.
- Is there another metabolic disorder? In this case, do the delta gap and use it to correct the bicarb. If the corrected
In this case, the patient is alkalemic and the primary disorder is a respiratory alkalosis because the pCO2 is low and the bicarb is normal. Physiologically, the pCO2 is not the main driver of the process, but we pick it as the primary disorder for the sake of our problem solving shchema. The anion gap is 30 in this patient so there is a concurrent anion gap metabolic acidosis. The delta gap is 18 so the corrected bicarb is 43, which is over 30 so there is a concurrent metabolic alkalosis.
The patient’s disorders were likely multifactorial. Lactate was 10 and urinalysis showed trace ketones so AGMA was likely a result of alcohol-induced lactic acidosis with starvation/alcoholic ketoacidosis. The metabolic alkalosis was likely due to both contraction and excessive vomiting. The respiratory alkalosis was likely due to severe epigastric pain and anxiety from alcohol withdrawal.