A few people had a go. Well done!
This is a tough one. This is my roundabout way of working it out. Probably not as slick as it should be but….it does the job. It IS a triple acid base abnormality and the diagnosis is probably salicylate toxicity.
Sure the patient has a fever and is vomiting and may be septic, but lets look at the solution.
pH is 7.8- so it is an alkalosis
CO2 is 15- so it is a RESPIRATORY ALKALOSIS
Lets look for compensation–
If I use the numbers we use in the Fellowship Course:
Met Acid pCO2 = 1.5 x Bic + 8 or pCO2 = last 2 digits of pH (if pH>7.1)
Met Alk pCO2 = 1 x Bic + 8 or pCO2 = last 2 digits of pH (if pH<7.6)
Resp Aci ∆10mm pCO2 = ∆1mmol Bic acutely (or 0.05 pH)
∆4mmol Bic chronically
Resp Alk ∆10mm pCO2 = ∆2mmol Bic acutely (or 0.05 pH)
∆5mmol Bic chronically
Given that the pCO2 is decreased by a min of 25mmHg, we would expect in a pure respiratory alkalosis, HCO3 to change by 4-5mmol acutely or 10 mmol chronically, ie go to 20 or lower. As the HCO3 is higher, it indicates a METABOLIC ALKALOSIS
We can confirm this by calculating as below, but don’t really need to:
∆Bic = 25-Bic (25 = Normal Bic)
∆AG = AG-10 (2-10 = Normal AG)
∆Bic >> ∆AG then Mixed High and Normal Anion gap Acid
if ∆Bic << ∆AG then Additional Metabolic Alkylosis
In this case :
∆Bic = 25-Bic = 25-23 =2 ∆AG = AG-10 = 21 as ∆Bic << ∆AG there is also a METABOLIC ALKALOSIS
If we measure the ANION GAP, it is: (119) – (65+23) = 31, so there is a raised anion gap.
METABOLIC ACIDOSIS is really the only thing that can give such a raised AG
Anion Gap: (119) – (65+23) = 31
The A-a gradient is:
= (FiO2(Patm-PH2O)- PaCO2/0.8) -PaO2
= 74.4- so a much increased A-a gradient
The calculated osmolarity is 2(Na) +U + Glc = 238+10.3+4.5 = 252.8mmol/L
We cannot calculate the GAP but a usual osmolarity is 270-290 mmol/L. There it is not a raised aosmolarity that we would ascribe to alcohols.
There is also hyponatraemia, hypokalaemia and hypocloraemia and there is renal renal impairment.
SO LETS PUT IT ALL TOGETHER:
Causes of high anion gap metabolic acidosis are:
M- methanol X– as low osmolarity
U-Uraemia X– Urea is not that high
D-DKA – X– Not likely as BSL is not high
P – Paraldehyde – X -Unlikely
I- Iron, isoniazid – X -Could be but no real reason
L -Lactate – Could be because of the vomiting
E – Ethylene Glycol X– unlikely as has low osmolarity.
S -Salicylate OD – could be- remember the patient is giving no history, which is strange.
So from this group we have Lactate and Salicylates
What are some of the causes of Respiratory Alkalosis?
The 2 big ones are infection and salicylates
The metabolic alkalosis is probably secondary to the vomiting.
Certainly sepsis and dehydration must be considered. Can salicylates cause this?
Lets look at the phases of salicylate overdose:
Phase 1 (12 hours)
There is hyperventilation from respiratory center stimulation. This leads to respiratory alkalosis. Potassium and sodium bicarbonate are excreted in the urine. This phase may last as long as 12 hours.
Phase 2 (12-24 hours)
There is paradoxic aciduria.
The patient can become dehydrated and hypokalaemic. There is a metabolic acidosis.
Nausea and vomiting can be the earliest signs of salicylate toxicity. Hyperthermia may indicate severe toxicity.
So in conclusion, certainly we need to exclude sepsis and other causes, however on this ABG and electrolytes, salicylate toxicity seems the most likely cause!