A 53-year-old man, with a history of DM II, hypertension, and history of stroke, presents with 3 days of fatigue. He has an elevated K on routine labs. He recently started taking Aleve twice daily for knee pain.
| Electrolyte panel | |||||
|---|---|---|---|---|---|
| Na | 138 | Cl | 115 | BUN | 35 |
| K | 7.3 | HCO3 | 14 | creat | 1.8 |
| Blood Sugar | 154 |
| ABG | |
|---|---|
| pH | 7.18 |
| pCO2 | 38 |
| pO2 | 76 |
Define his acid-base abnormality and speculate on the etiology.
{ 6 comments… read them below or add one }
Only a 1st (almost 2nd) year here but it would seem that the patient has an acute metabolic acidosis caused by his use of Naproxen. My hypothesis is that he has chronic renal impairment (that was possibly subclincal prior to this?) secondary to his HTTN and DMII. The addition of naproxen, a renally excreted drug, was enough to disturb kidney function enough to cause the metabolic disturbances seen here.
A few questions
-His co2, o2, bicarb levels all look about normal. Wouldn’t there be an automatic respiratory attempt at correcting the pH by increasing respiration that would cause decreased bicarb and co2?
-Was there a arrhythmia when he presented?
-Was he on any diuretics for his HTTN? If so, assuming they were not K sparing and he was compliant, would that have somewhat alleviated his hyperkalemia? Or did it, and it just kept him from getting a legendarily high K?
Love these cases, please keep them coming.
He has the following disorders:
1. nongap metabolic acidosis.
2. acute respiratory acidosis. The calculated HC03 from the Henderson- Hasselbach is 14 which agrees with the chem 7 HC03 of 14. The expected pc02 is 14x 1.5 +8 =29. Actual is 38 therefore there is a superimposed primary respiratory acidosis.
He likely has an underlying Type 4 RTA with a superimposed ARF from the aleve. He also has an acute gastritis and a slow GI bleed causing a K load. The aleve itself can also cause hyperkalemia.
Therefore the hyperkalemia is from (1) underlying type 4 RTA from his DM (2) ARF from the aleve (3) K load from a mild UGIB from gastritis from the aleve.
The nongap acidosis is from ARF and type 4 RTA
The respiratory acidosis is from the percocet he was taking due to uncontrolled knee pain which lead to hypoventilation in the setting of his old stroke.
I am a practicing nephrologist and have always enjoyed your many acid-base and electrolyte posts, but have only recently decided to stop lurking and start commenting. I agree with several of the points made by the above commenters, but would like to highlight some differences and additions.
So-called “Type 4 RTA” is a common feature of various disorders that impair collecting duct function; it is virtually never seen in the absence of structural renal disease. I would be willing to bet that the patient had pre-existing renal impairment, not just “ARF from Aleve”. Some patients with Type 4 RTA have impaired renin secretion, and that renin secretion depends in part on renal prostaglandins, the synthesis of which may have been impaired by the naproxen. I should also point out that hyperkalemia impairs ammoniagenesis in the kidney, as well as the entry of ammonium ions into the tubule – even so, the metabolic acidosis seems quite severe here for hyperkalemic distal RTA alone. Was there any other history to suggest another source of bicarbonate loss? Don’t forget that DKA can actually produce a non-gap acidosis, although you said that this was Type II DM. Finally, the poor respiratory compensation for the acidosis suggests underlying pulmonary disease, respiratory muscle paralysis from hyperkalemia, or both. This is clearly an ICU case…
Metabolic acidosis with superimposed respiratory acidosis.
The hyperkalemia is explained by the connection of acidosis and hyperkalemia. They are always connected, if you have one you’ll likely have the other. I cannot find any information about aleve causing increases in potassium, but I’ll keep looking.
Respiratory acidosis is caused either by the hyperkalemia and/or pulmonary edema secondary to hypertension. Either way, it’s preventing proper respiration.
Metabolic acidosis is likely caused by renal failure.
Of note: since this patient has diabetes type 2, which puts him at a greater risk of heart attack, he should not take aleve or similar NSAIDs for his knee pain. Tylenol or aspirin is recommended.
On another note, would it be possible for you to not use so many medical abbreviations, or better yet explain your abbreviations?
In an earlier post about antibiotics, you used ARF for what I believe meant Acute Rheumatic Fever. Here though a commenter used ARF to mean either Acute Respiratory Failure, or Acute Renal Failure. I believe he meant the former. Either way, this is very confusing especially for students outside the United States. It’s not something I’m looking forward to dealing with when I get back, and believe I’ll have to print out a cheat sheet.
I agree with many of the excellent comments above.. as a practicing nephrologist, like Pro Nephros above.. I thought I would stop lurking and at least stick my 2 cents in… I have nothing to add to the description of the A-B d/o.. and NSAIDs are surely ‘good for business’ as a nephrologist. The one thing I would add and always be careful about is spurious hyperkalemia. HyperK can get one excited.. but, it needs to be real and I would like an ECG as well. Next, what is the TTKG?