Question 1:

PH = 7.19, that is moderate acidaemia

PCO2 = 28 (low/ < 40), HCO3 is 19 (low/ <24) so we have metabolic acidosis.

Once we get metabolic acidosis, we need to calculate the compensation using Winter’s formula and we need to calculate the anion gap.

Winter’s formula (expected PCO2 = 1.5x HCO3 + 8   +/- 2 accordingly, expected PCO2 should be (1.5 x 19 +8) = 36.5 (range between 34.5 to 38.5). Since PCO2 is less than 34.5 so we have additional respiratory alkalosis.

AG = Na – (Cl + HCO3) = 141 – (104 + 19) = 18 high. So, we have high anion gap metabolic acidosis. (HAGMA).

Next step is to calculate the delta ratio, that is AG – 12/ 24 – HCO3 = 1.2 ( between 0.8 and 2) So, we have a pure HAGMA.

Other findings: Lactate = 17.4, that is very high. (Lactataemia).

So, The final interpretation is High anion metabolc acidosis with respiratory Alkalosis.

Question 2:

Looking at the mnemonic of CAT MUDPILES ( for potential causes of high anion gap metabolic acidosis:

C: Cyanide poisoning is a possibility, Unlikely to be due to CO poisoning or a Congenital heart disease.

A: Aminoglycosides, Unlikely

T: Toluene (Glue sniffing) is a possibility,

M: Methanol : unlikely – usually is associated with high osmolar gap.

U: Uremia – unlikely, Cr is within normal range

D: DKA – Unlikely, BSL is within normal range.

P: Paracetamol, Phenformin and Paraldehyde – Paracetamol toxicity, usually lactic acidosis is a late finding. Phenformin, is not available as medication anymore- withdrawn due to high risk of HAGMA, Paraldehyde, unlikely.

I:  INH and Iron both are possibilities

**** The acidosis in Iron poisoning is multifactorial. Some textbooks  suggest that the acidosis is mainly due to the physicochemical effects of the iron ion itself. Other sources suggests that acidosis is due to raised lactate, of which not all is generated by direct effects of the iron, but rather due to the fluid loss (from an ulcerated gut), cardiogenic shock (due to the myocardial mitochondrial toxicity) and fulminant hepatic failure. (Iron has a direct toxic effect on the mitochondria).

L: Lactate, high lactate is the cause in this situation but what caused the lactate to be high is the dilemma.

E: Ethanol intoxication has been widely linked to high lactate. However, the level is rarely exceed 5 mmol/L and is very unlikely to be the only cause for lactic acidosis. So, in this case ethanol intoxication is unlikely to be the only cause of HAGMA in this patient.

S: Salicylates, this is usually associated with HAGMA and respiratory alkalosis.

 

Causes of Respiratory Alkalosis:

Use the mnemonic CHAMPS:

C: Central Nervous system mediated causes (Pain, tumor, trauma)

H: Hypoxia or Hyperventilation

A: Anxiety

M: Mechanical ventilation

P: Progesterone/ pregnancy

S: Sepsis or Salicylate.

 

So in this patient we have a lot of possibilities

 

Question 3: management

We follow the usual approach of RRSIDEAD.

Patient was moved to resuscitation bay, he calmed down after midaz and he maintained stable vitals.

Among the above causes of lactic acidosis (We excluded cyanide toxicity based on history and normal COBb). Paracetamol toxicity was the only condition that required immediate antidote administration as (Time to NAC) is crucial to protect the liver from significant toxicity. NAC was started.

However, repeated blood gas after 30 minutes was completely normal. What Happened???

This Patient was very aggressive, needed 4 large security guards to restrain him. He was using his skeletal muscles to maximum strenuous activity. When skeletal muscles are deprived of oxygen, pyruvate converts to lactate. Lactate produced during strenuous muscle activity is taken up from blood plasma by the liver, where it is converted to pyruvate and thence to glucose or glycogen.

Accordingly NAC was stopped, Patient had normal paracetamol level and it turned out that he didn’t take any medication. Just alcohol.