Presented at morning report:
56 yo man with known osteoarthritis and hyperlipidemia presents complaining of weakness and confusion
| Na | 140 | Cl | 105 | BUN | 18 | glu | 128 |
| K | 3.3 | CO2 | 16 | creat | 0.9 |
| pH | 7.47 |
| pCO2 | 24 |
| pO2 | 74 |
| HCO3 | 18 |
1. What is the acid-base disorder – be complete?
2. What additional tests do you want?
3. Provide at least 2 possible causes for these numbers.
{ 11 comments… read them below or add one }
You have an interesting set of data here. And complicated. So let’s try and break it down.
1) Is there an anion gap? Yes. The gap is 19. So the delta gap is 7
2) What is the primary status? Acidosis or alkalosis? The pH is 7.47 so the primary process is an alkalosis
3) Is the CO2 high or low? It’s low, so this is a primary respiratory alkalosis.
4) What should the bicarb be on the BMP to compensate this primary respiratory alkalosis? It should be around 15. Yours is 16 so it’s close enough. It’s compensating just as it should.
In any other problem we would be done. You have a primary respiratory alkalosis with an incomplete compensating nongap metabolic acidosis. But there’s a problem. We have an anion delta gap of 7. Therefor not only should there be a compensating nongap acidosis, there should also be a gap metabolic acidosis that pushes your expected bicarb down another 7 from 15 to 8. But it’s not 8, it’s 16. Therefore you also have a primary metabolic alkalosis.
So here is my guess.
1) Primary respiratory alkalosis
2) Primary gap metabolic acidosis
3) Primary metabolic alkalosis
4) Compensating metabolic acidosis
Additional tests?
1) Lactate level
2) EtOh level
3) CPK level
4) Salicylate level
Without additional history, I don’t think any other tests are necessary to manage him safely.
I’ll give you four possible causes
1) Salicylate poisoning. This causes a combined primary respiratory alkalosis with gap metabolic acidosis. He could get his metabolic alkalosis from being confused and not drinking, giving him a volume contracted state
2) Advanced liver disease. This can cause a primary respiratory alkalosis. If he’s a drunk, you could also have a primary gap metabolic acidosis and be volume contracted if he fell, hit his head and got confused or if he has hepatic encephalopathy
3) Rhabdo. That could cause his gap acidosis, but I’m not aware how a primary respiratory alkalosis occurs, unless he’s just anxious from being weak and he’s hyperventilating and also not drinking well because of the confusion.
4) Sepsis. This can cause a primary respiratory alkalosis (or perhaps a secondary response to gap acidosis). And if he isn’t drinking well, he gets a volume contraction as well.
But my bet is on aspirin overdose.
As a rheumatologist I can’t say I’ve looked at ABG’s in over twenty years. (except on your blog), but you do mention osteoarthritis, so how about; Salicylate toxicity with primary resp alkalosis and either compensating metabolic acidosis or primary met acidosis from the ASA. Hypoxia from salicylate induced pulmonary edema.
1. What is the acid-base disorder – be complete?
Mixed respiratory alkalosis and high-anion gap metabolic acidosis with a normal delta gap. As PO2 is 74, knowing the FiO2 would be useful.
2. What additional tests do you want?
salicylate level (got a feeling this the important one), Hb, lactate, albumin (may affect anion gap)
Other may may be useful depending on H&P – ketones (starvation), ethanol level, serum osmolality, CXR, lipid levels
3. Provide at least 2 possible causes for these numbers.
My top 2 to think of are:
salycylate poisoning and sepsis
Other contributors to respiratory alkalosis and/or HAGMA might include: tox (xanthines, nicotine), mechanical ventilation, APO, PE, pneumonia, anemia.
I agree this chap most likely has salycilate toxicity given that he has a respiratory alkalosis and HAGMA and has reason to OD on salicylates (osteoarthritis). Sepsis (e.g. pneumonia) would be 2nd on my list, but there are losts of possible combinations of resp alkalosis and HAGMA (e.g. GI bleed, anemia and hypovolemic shock). Would be nice to know the FiO2 as the PO2 is low at 74.
OK, DB, now tell me that he has a PE
BTW, Happy, I think the delta gap is normal:
AG = Na – (Cl – HCO3) = 14 – (105 + 18) = 17 (normal is 2-10 in my book, some say up to 12 or 16) (need to correct for albumin)
delta HCO3 = = = 7
delta gap = delta AG – delta HCO3 = (AG – normal AG) – (25 – HCO3) = (17-10) – (25 – 18) = 7- 7 = 0
this suggests there is a 1:1 relationship between AG and decrease in HCO3.
Hospitalist Baby:
You and I are on the same page on this one.
I’ll go with the simple approach- chronic respiratory alkalosis. PH is not as high as someone who has hyperventilated to pCO2 of 24 acutely. Metabolic compensation.
With this history, I agree chronic salicylate intoxication is a primary concern, level is important. With confusion, sepsis and chronic liver disease are also in the DD (by the way if he were pregnant I’d put that in there, that’s what a pregnant woman’s ABGs often look like – a pregnancy test is pending I hope).
On a more serious note, if he happens to come back with an elevated salicylate level, this is an extremely underrated emergency. In many ways it is more serious than acute salicylate intoxication (which would have a more profound acidosis). I believe Anderson reported this in Scandinavia in the 1970′s in the Annals (but don’t take my word for that – Google it) and it had a 10-20% mortality. These people often have coagulation problems – which confuses them with chronic liver disease. I have seen a couple die- of intracranial events and one who herniated after being intubated. Just a theory – the chronic hyperventilation causes decreased cerebral blood flow and a cerebral event or further restriction of cerebral blood flow with intubation causes a massive brain insult.
On the other hand if this is something different, as Gilda used to say, “Never mind”. Just riffing on the case.
Wasn’t Scandinavia but it was Annals -
Unrecognized Adult Salicylate Intoxication
ROBERT J. ANDERSON, DANIEL E. POTTS, PATRICIA A. GABOW, BARRY H. RUMACK, and ROBERT W. SCHRIER
Ann Intern Med December 1, 1976 85:745-748;
Hospitalist Baby:
I’m with you on this one.
Chronic respiratory alkalosis. PH is not as high as if the patient hyperventilated to a pCO2 of 24 acutely. Metabolic compensation.
Given this history, chronic salycilate toxicity would be at the top of my list, too. ASA level crucial. With history of abnormal mental status, agree with sepsis, chronic liver disease as other possibilities -lactate,cultures and LFTs. Throw in a pregnancy test, pregnant women also have ABGs that often look like this.
On a more serious note, Chronic salicylate toxicity if that’s what this is, is an extremely serious condition, more so than acute salicylate toxicity. It has a mortality of 10-20% in severe cases- good review by Anderson in Annals 1976. PAtients often have coagulopathy, which causes confusion with chronic liver disease.
I have seen several die – from intracranial bleeds and one who herniated after intubation.
Just a theory – these people probably have decreased cerebral blood flow form chronic low pCO2 – an increase in intracranial pressure or a further decrease in blood flow after intubation must be particularly dangerous -again, just a theory.
Where I trained
1) We ignore K+ when calculating AG
2) A normal AG is 12, unless you are a VA patient, then it’s 12-20
Hospitalist:I’m with you on this one, baby.
Chronic respiratory alkalosis, pH is not as high as it should be if the patient is hyperventilating to a pCO2 of 24 – metabolic compensation.
Given this history, have to think of chronic salicylate intoxication, needs a level. With the abnormal mental status, I’d consider liver disease and sepsis- LFTs, lactate and cultures. Might get a pregnancy test also, that’s what a lot of pregnant women’s ABGS look like.
Seriously though, if this is chronic salicylate intoxication it is extremely serious, more serious than acute intoxication – mortality 10-15%. Anderson wrote a good article in the Annals in 1976.
I’ve seen a couple of these guys die, they develop a coagulopathy (which gets them confused with liver patients) and a couple have bled into their heads.
Saw one die when he was overventilated on the ventilator and herniated.
Just a theory- these guys may run cerebral hypoperfusion due to the chronically low pCO2. A space occupying lesion that increases ICP or further diminution of cerebral blood flow after intubation may aggravate cerebral hypoperfusion.
Just a theory.
A pH of 7.47 is mild alkalosis.
The bicarbonate level of 18 mmol/L indicates metabolic acidosis.
The pCO2 of 24 mm Hg indicates respiratory alkalosis.
The acid-base classification is compensated respiratory alkalosis or mixed respiratory alkalosis and metabolic acidosis.
Despite increased respiration and decreased pCO2, the pO2 is only 74 mm Hg. This rules out primary hyperventilation. Renal function appears to be normal, so renal acidoses are unlikely. The mild hypokalemia is probably secondary to the alkalosis. The high anion gap could be lactic acidosis or some form of toxic acidosis. Therefore, the differential diagnoses include:
1. pulmonary edema (or some other form of alveolar wall thickening)
2. decreased usable alveolar surface area (pneumonia, atelectasis, airway obstruction, etc.)
3. reduced pulmonary perfusion
4. an increase in the hemoglobin-oxygen binding strength resulting in poor oxygenation of tissues (This is unlikely because the pO2 of arterial blood should remain normal while the pO2 of venous blood should be greatly reduced.)
5. carbon monoxide poisoning
Additional Tests or Procedures:
1. A thorough chest examination.
2. Examination for cyanosis.
3. Carboxyhemoglobin percentage.
4. Chest films probably will not be useful for the diagnosis, but they will be helpful for subsequent comparisons.
5. A B-natriuretic peptide level to rule out congestive heart failure.
6. Troponin level to rule out silent myocardial infarction.
7. A ventilation-perfusion study if no other cause has been found.
8. Hemoglobin and hematocrit (with a CBC and manual blood smear review if anemia is present).
9. Calcium, ionized calcium, phosphate, magnesium, total protein, albumin
10. Urinalysis with microscopy.
Possible causes:
Two commenters suggest salicylate poisoning. That is unlikely because the initial hyperventilation of salicylism should be accompanied by a high-normal arterial blood pO2. In the later stages of severe salicylism, the patient develops the deadly combined respiratory acidosis and metabolic acidosis (which this patient does not have). Hyperventilation with low pCO2 AND low pO2 usually indicates pulmonary problems (with items 4 & 5 above being exceptions).
Congestive heart failure is possible, but there is no history of heart disease. He could have had a silent myocardial infarction with subsequent heart failure, but the probability is low.
Many different pneumonias (microbiological, chemical, or immune-mediated) could produce these abnormalities.
Drugs or toxins that alter hemoglobin-oxygen binding can cause this.
Moderately severe carbon monoxide poisoning can present like this if enough time has elapsed for a compensatory response by the kidneys.
Happy Hospitalist listed rhabdomyolysis as a possible cause, but there is no evidence for this. Urinalysis will rule this out.
Dr. T, a clinical pathologist
Took me three tries to get my response in – sorry about that.
Dr. T focuses in on the widened A-a gradient. There is clearly some oxygenation problem here, it is mild (assuming the patient is on room air- where is that FIO2?) and doesn’t lend itself to any specific diagnosis. It does not rule out salicylism because as one commentator mentioned this can be associated with noncardiogenic pulmonary edema.
Of course the patient’s previous pulmonary status comes into play -smoker, lung disease, etc.
The widened A-a gradient need not even be a primary pulmonary problem since you can see this in liver disease as a result of peripheral shunting.
I’m assuming the hook in the problem is in the acid-base situation instead of the widened A-a gradient since you can’t really diagnose anything without a lot more info.