Describe and interpret this arterial blood gas:
History: 24-year-old man with a severe intellectual disability, believed to be lethargic and drowsy by his family. He has had a cough for 1 week.
| pH 7.31 | Na 174 mmol/L |
| pCO2 52 mmHg | K 3.1 mmol/L |
| pO2 120 mmHg (FiO2 0.4) | Cl 137 mmol/L |
| HCO3 25 mmol/L | Glucose 33 mmol/L |
| Osmolality 402 mmol/kg | Urea 25.7 mmol/L |
[expand title=”Interpretation”]
What is the pH?
7.31 = acidaemia
What is the primary process?
pCO2 52 = primary respiratory acidosis
Is there compensation?
Expected HCO3 = 24 + {(Measured pCO2 – 40)/10}
= 24 + {(52 – 40)/10}
= 25.2
Therefore there is full metabolic compensation for an acute respiratory acidosis.
Are there other clues to diagnosis?
Expected PAO2 = (713 x FiO2) – (pCO2 x 1.25)
= (713 x 0.4) – (52 x 1.25)
= 220.2
A-a gradient = PAO2 – PaO2
= 220.2 – 120
= 100.2
Therefore there is a significantly elevated A-a gradient.
Corrected sodium = Na + (glucose – 5)/3
= 174 + (33 – 5)/3
= 183.3
There is severe hypernatraemia.
Calc osmolality = (2 x Na) + urea + glucose
= (2x 174) + 25.7 + 33
= 406.7
Osmolar gap = Measured osmolality – Calculated osmolality
= 402 – 406
= -4
Therefore there is no osmolar gap
Electrolyte clues:
Serum osmolality is markedly elevated. There is hyperglycaemia, severe hypernatraemia and severe hyperchloraemia. Urea is markedly elevated. Potassium is slightly low.
Formulation:
Description: This ABG shows a fully compensated primary acute respiratory acidosis with an elevated A-a gradient. There is severe hyperglycaemia and evidence of significant dehydration with severe hypernatraemia, hyperchloraemia and elevated urea. There is significant hyperosmolality but no osmolar gap. Potassium is slightly low.
Interpretation: In this clinical context, this gas would be consistent with severe hypernatraemic dehydration, and type 2 diabetes complicated by the hyperglycaemic hyperosmolar syndrome (ADA diagnostic criteria: glucose >33 mmol/L, pH >7.3, serum HCO3 >15 mmol/L). It is likely there is some alteration of conscious state leading to failed ventilation and acute respiratory acidosis. With the history of cough and elevated A-a gradient, a LRTI could be suspected as the precipitating factor. Treatment will include gradual rehydration, correction of potassium, insulin, and management of sepsis.
Additional information: Strong ion difference Na – Cl = 37, suggesting a normal anion gap. Urine osmolality 609 mmol/kg.
Patient has a rare congenital abnormality, limited mobility and severe intellectual delay (2y old), eats a mostly soft diet and has a “well-established preference for sugary foods and drinks, particularly strawberry [milk].” First presentation of type 2 diabetes with hyperglycaemic hyperosmolar syndrome secondary to sepsis, HbA1C 11%.
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