To restate:
41 year old man with left hemipareis s/p right brain aneurysm surgery in the past. Now presents with increasing obtundation, increased urination and abdominal discomfort. Labs follow:
On 2l nasal oxygen:
| ABG | |
|---|---|
| pH | 7.41 |
| pCO2 | 47 |
| pO2 | 95 |
| Electrolyte panel | |||||
|---|---|---|---|---|---|
| Na | 128 | Cl | 83 | BUN | 8 |
| K | 4.2 | HCO3 | 24 | creat | 0.7 |
| Blood Sugar | 742 |
The patient is a large man (110 kg) who now admits to 4 weeks of increased urination and recent constant thirst with a marked increase in water intake.
Now for the hard part, figure out the acid-base problem. Next I will give you his labs 2 days later, then my interpretation.
At this point I see:
- anion gap of 21 – therefore anion gap acidosis
- pCO2 = 47 – hypoventilation thus respiratory acidosis
- Delta gap supports bicarbonate of 33 (add 9 to 24 – the 9 being the difference between the observed anion gap and the expected anion gap)
- Thus when first presented I assumed a mild ketoacidosis (or possible mild lactic acidosis), a respiratory acidosis and a metabolic alkalosis
- I wondered if his obtunded state was causing hypoventilation
- I assumed significant volume contraction (and probably total body potassium depletion) from his glucose induced osmotic diuresis
The next day we have these numbers:
| ABG | |
|---|---|
| pH | 7.35 |
| pCO2 | 48 |
| pO2 | 68 |
| Electrolyte panel | |||||
|---|---|---|---|---|---|
| Na | 139 | Cl | 106 | BUN | 5 |
| K | 4.4 | HCO3 | 26 | creat | 0.6 |
| Blood Sugar | 321 |
After some thought the solution became more clear. I believe that I can explain what happened now. Your turn to try.
{ 3 comments… read them below or add one }
I’m going to say we have a patient with a chronic compensated respiratory acidosis, more likely than not an obstructive sleep apnea or moderate obstructive airway obstruction.
This is the primary problem (r/o hypothyroidism), He now develops glucose intolerance, probably as a result of type II DM with elevated glucose. He is volume depleted, probably mild to moderate hypokalemia with glucosuria and kaliuresis. he compensates by drinking water to give him a low serum sodium and chloride that is actually normal when corrected for the elevated blood glucose (total body free water normal). His osmolarity is not markedly abnormal. There is no or minimal ketoacidosis (? serum/urine ketones – I’m guessing trace to negative) so his pH is a result of the compensation for respiratory acidosis and some metabolic alkalosis due to mild hypokalemia. With volume replacement, potassium replacement and insulin he reverts to his primary problem.
so my guess is primary respiratory acidosis, secondary metabolic alkalosis (compensation), tertiary metabolic alkalosis secondary to volume depletion and total body hypokalemia. Little or no free water deficit.
Nice one, SIR
First ABG and SMA-7 disagree with regard to bicarb – calculated bicarb with given pH and pCO2 from ABG would be 29, yielding total CO2 of about 31. If we assume that the bicarb from the SMA-7 was erroneous (usually the case when there’s significant discrepancy with the ABG) and true total CO2 was about 31, there’s not much of an anion gap. All of the electrolytes have been diluted by the osmotic effect of the severe hyperglycemia – but the chloride is proportionally lower than the sodium. The primary disturbance at presentation then appears to have been chloride depletion metabolic alkalosis, and I don’t think one has to invoke a ketoacidosis or lactic acidosis or come up with a fancy triple disturbance at that point.
Two days later the chloride deficit has been repaired, and the impact of hyperglycemia on sodium is much less – but the pCO2 is still high. Evidently the patient has baseline respiratory acidosis – presumably due to his CNS problem. At least now the calculated and measured bicarbonate agree. In retrospect, his original metabolic alkalosis may have been more completely “compensated” than expected…