aka Metabolic Muddle 003
An 87 year old female presented with a subarachnoid haemorrhage. GCS 8/15. A nasogastric tube was unable to be placed due to patient agitation. As a consequence, the patient was fasted for five days due to concern about swallowing.
Aan arterial blood gas was subsequently obtained:
Q1. Describe the arterial blood gas
- There is a metabolic acidosis with a high anion gap (HAGMA).
- The bicarbonate has decreased by more than the anion gap has increased which is due to a coexistent normal anion gap acidosis (NAGMA).
- There is a respiratory alkalosis. The pCO2 of 12mmHg is much lower than the respiratory compensation you would expect with this degree of metabolic acidosis (expected pCO2 = 1.5 * HCO3 +8 = 25 ).
The combination of these three abnormalities has led to relatively normal pH despite severe acid-base disturbance.
Q2. What are the causes of metabolic acidosis with raised anion gap and what is the likely cause here?
There are two ways of remembering this.
The easy way is to remember ‘left total knee replacement’:
The more complicated way is CAT-MUDPILES:
Cyanide, Carbon monoxide
Phenformin, pyroglutamic acidosis, propylene glycol, paracetamol
Lactic acidosis (many causes)
Ethanol, Ethylene glycol
The history suggests starvation ketoacidosis. There were ketones in the urine confirming this diagnosis.
Q3. What are the causes of normal anion gap acidosis and what is the likely cause here?
Others (eg chloride)
GI loss of bicarb
Renal loss of bicarb
The more difficult way is to remember is USED CARP (the A and the R can be reversed – this is optional):
Small bowel fistula
Carbonic anhydase inhibitors
Renal tubular acidosis
Neurosurgeons like to give everyone lots of normal saline. The chloride is high.
The likely diagnosis is hyperchloraemic metabolic acidosis secondary to normal saline.