Describe and interpret this arterial blood gas:

History: 43-year-old man found unresponsive after absconding from the psychiatric ward.  He is intubated and ventilated.

pH 7.03 Na 131 mmol/L
pCO2 44.3 mmHg K 5.8 mmol/L
pO2 89.4 mmHg (FiO2 0.8) Cl 108 mmol/L
HCO3 11 mmol/L Glucose 21.3 mmol/L
Lactate 12.6 mmol/L Urea 11.5 mmol/L
Osmolality 372 mOsm/L Albumin 18 g/L

Interpretation

 

What is the pH?

7.03 = severe acidaemia

What is the primary process?

HCO3   11 = Primary metabolic acidosis

Is there compensation?

Expected pCO2 = 1.5 x HCO3 + 8

= 1.5 x 11 + 8

= 24.5 mmHg

Actual pCO2 is higher therefore there is inadequate compensation (ventilation) or respiratory acidosis.

 Are there other clues to diagnosis?

Anion gap = Na – (Cl + HCO3)

= 131 – (108 + 11)

= 12

AG corrected for hypoalbuminaemia = AG + 2.5 x {(40-Albumin)/10}

= 12 + 2.5 x {(40 – 18)/10}

= 17.5

Therefore there is an elevated anion gap acidosis.

Corrected sodium = Na + (glucose – 5)/3

= 131 + (21.3 – 5)/3

= 136.4

Delta gap = (AG – 12) ÷ (24 – HCO3)

= (17.5 – 12) ÷ (24 – 11)

= 0.42

Suggests a coexisting non-anion gap acidosis.

Calculated osmolality = (2 x Na) + urea + glucose

= (2 x 131) + 11.5 + 21.3

= 294.8 mOsm/L

 Osmolar gap = Measured osmolality – calculated osmolality

= 372 – 294.8

= 77.2

Therefore there is an elevated osmolar gap.

Electrolyte Clues

Lactate is markedly elevated.  Urea, potassium and glucose are elevated.  Chloride is at upper limit of normal.  Corrected sodium is normal.  Albumin is markedly low.

Expected PAO2 = (713 x FiO2) – (pCO2 x 1.25)

= (713 x 0.8) – (44.3 x 1.25)

= 515 mmHg

A-a gradient = PAO2 – PaO2

= 515 – 89.4

= 425.6

Normal A-a gradient = Age/4 + 4

= 43/4 + 4

= 14.75

Therefore there is a markedly elevated A-a gradient.


Formulation:

Description:  This ABG of an intubated patient shows a severe metabolic acidaemia with inadequate respiratory compensation, with mixed anion gap and non-anion gap acidoses and elevated osmolar gap.  There is a markedly elevated lactate with elevated urea, potassium and glucose and hypoalbuminaemia.  Corrected sodium is normal and chloride is at the upper limit of normal.  There is a markedly elevated A-a gradient with high oxygen requirement.

Interpretation:  In this clinical context the differential diagnosis is broad, however toxic alcohol ingestion should be considered high on the differential in view of the severe acidosis and elevated osmolar gap.  Elevated lactate may contribute to the elevated anion gap and the osmolar gap, and ketoacidosis is possible.  A serum ethanol should be measured to further assess the elevated osmolar gap – low albumin may suggest chronic liver toxicity from alcohol abuse.  If the osmolar gap persists after correction for ethanol, a serum methanol level and urinary microscopy for crystals may give further information about the underlying cause – if doubt persists, blockade with EtOH and dialysis should be instituted (CVVHD could be justified in view of acid-base status anyway, especially if there is an element of renal failure).  Elevated A-a gradient with high oxygen requirement and inadequate ventilation may suggest underlying aspiration with respiratory failure.

Additional information: History of chronic alcohol abuse.  Serum ethanol was 0.25% accounting for almost all the calculated osmolar gap.  CXR showed whiteout of right lung secondary to aspiration.  Methanol level was negative and there were no urinary crystals.  Final diagnosis was aspiration pneumonia, sepsis and multiorgan failure.  He made a full recovery.

Blood Gas #1
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