# Question 8.3

b) A 75-year-old woman with a reduced level of consciousness is intubated and ventilated following a single grand mal convulsion.

List the pathophysiological disturbances revealed by the following arterial blood gas and electrolyte profile taken 10 mins after intubation and give the likely explanation.

 Parameter Measured value Normal range FiO2 1.0 pH 7.05* 7.35-7.45 PaCO2 43 (5.6) 35-45 mmHg (4.6-6.0 kPa) PaO2 280 (36.8) 80-100 mmHg (10.5-13.0 kPa) HCO3 11.5* 22-27 mmol/l Base Excess -16.8* -2 to +2 mmol/L Sodium 128* 135-145 mmol/l Potassium 3.1* 3.2-4.5 mmol/l Chloride 82* 100-110 mmol/l Glucose 79* 3.0-6.0 mmol/l Lactate 9.2* < 2.0 mmol/l Urea 22.0* 3.5-7.2 mmol/l Creatinine 120* 50-100 μmol/l

Uncompensated metabolic acidosis (or metabolic + respiratory acidosis) with raised anion gap not solely due to elevated lactate.
Marked hyperglycaemia (candidates will say this but does not deserve a mark)

Hyperosmolar hyperglycaemic syndrome with component of ketoacidosis and post-ictal lactic acidosis.

## Discussion

This ABG interpretation question is testing the candidate's knowledge of the sodium correction equation.

There is a widened A-a gradient, around 370mmHg. The expected PaO2 is around 650mmHg.

There is marked acidaemia; this is due to a metabolic acidosis.

The metabolic acidosis is poorly compensated - the expected CO2 is 24. Thus, there is also a respiratory acidosis.

This is because the patient is ventilated, and has no voluntary compensation mechanisms.

The anion gap is (128) - (82 + 11) = 35, or 38.1 when calculated with potassium. Some, but not all of this is accounted for by the raised lactate.
The delta ratio, assuming a normal anion gap is 12 and a normal bicarbonate is 24, would therefore be (35 - 12) / (24 - 11) = 1.76
This suggests a pure high anion gap metabolic acidosis. The glucose of 79 would suggest that ketones may be contributing to the high anion gap.

There is also some renal impairment.

There is hypernatremia- when adjusted for glucose, the sodium level is ~ 150 mmol/L.

(for every 5.6mmol/L of glucose, sodium drops by 1.6mmol/L)

Thus this is a hyperosmolar state with respiratory acidosis following intubation, metabolic acidosis likely due to ketones, and lactic acidosis likely due to seizures.

Specific summaries dealing with these topics are available:

## References

Hyperglycemic Comas by P. VERNON VAN HEERDEN from Vincent, Jean-Louis, et al. Textbook of Critical Care: Expert Consult Premium. Elsevier Health Sciences, 2011.

Oh's Intensive Care manual: Chapter 58  (pp. 629) Diabetic  emergencies  by Richard  Keays

Umpierrez, Guillermo E., Mary Beth Murphy, and Abbas E. Kitabchi. "Diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome." Diabetes Spectrum15.1 (2002): 28-36.

ARIEFF, ALLEN I., and HUGH J. CARROLL. "Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of theraphy in 37 cases." Medicine 51.2 (1972): 73-94.

Gerich, John E., Malcolm M. Martin, and Lillian Recant. "Clinical and metabolic characteristics of hyperosmolar nonketotic coma." Diabetes 20.4 (1971): 228-238.

Kitabchi, Abbas E., et al. "Hyperglycemic crises in adult patients with diabetes." Diabetes care 32.7 (2009): 1335-1343.

Kitabchi, Abbas E., et al. "Hyperglycemic crises in adult patients with diabetes a consensus statement from the American Diabetes Association." Diabetes care 29.12 (2006): 2739-2748.