Metabolic mayhem post-subacrachnoid hemorrhage

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

  1. There is a metabolic acidosis with a high anion gap (HAGMA).
  2. The bicarbonate has decreased by more than the anion gap has increased which is due to a coexistent normal anion gap acidosis (NAGMA).
  3. 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’:

Renal Failure

The more complicated way is CAT-MUDPILES:

Cyanide, Carbon monoxide
Alcoholic ketoacidosis
Methanol, metformin
Diabetic Ketoacidosis
Phenformin, pyroglutamic acidosis, propylene glycol, paracetamol
Isoniazid, Iron
Lactic acidosis (many causes)
Ethanol, Ethylene glycol
Starvation, salicylates

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?

The easy way to remember is OGRe:

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
Extra Chloride
Carbonic anhydase inhibitors
Addisons disease
Renal tubular acidosis
Pancreatic fistula

Neurosurgeons like to give everyone lots of normal saline. The chloride is high.

The likely diagnosis is hyperchloraemic metabolic acidosis secondary to normal saline.

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  1. says


    Calculation of the AG (141 -- 117 -- 11) gives a value of 13. 12 +/-5 seems to be considered normal & not suggesting HAGMA. This leaves NAGMA & resp alkalosis secondary to excess iv saline & CNS pathology respectively. I’d be interested on your thoughts!

    I use Huffed & PUFT for resp alkalosis:

    H hypoxia & [psych] hyperventilation
    P pregnancy
    U ‘uncus’ [tenuous] CNS pathology
    F failures (LVF, liver)
    T toxins (salicylates & sympathomimetics)


      • says

        Hi Ellen

        Corrected Na should not be used for calculation of the anion gap.

        The anion gap reflects the balance between positively and negatively charged electrolytes in the extracellular fluid. Glucose is electrically neutral and does not directly alter the anion gap. However, glucose is osmotically active so water is pulled into the extracellular fluid. This has a dilutional effect on all extracellular electrolyte concentrations, both positive or negative, and so the anion gap is minimally altered.

        This paper has a more detailed explanation:

        Beck, LH. Should the actual or the corrected serum sodium be used to calculate the anion gap in diabetic ketoacidosis? CLEVELAND CLINIC JOURNAL OF MEDICINE 2001; 68 (8) 673-674.


  2. drdeannechiu says

    I’m using GREED instead of USED CARP. I think of NAGMA as a nagging ma, who only married for the money..

    GI bicarb loss -- small bowel losses (fistulae/-ostomy), diarrhoea
    Renal bicarb loss -- RTA, ureteric
    Excess Chloride
    Drugs -- Carbonic Anhydrase Inhibitors,