Incidence of cortisol deficiency in patients with traumatic brain injury

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Cortisol deficiency due to hypothalamic or pituitary injury has been uncommonly reported after traumatic brain injury (TBI), and the incidence is unknown. Diabetes insipidus after TBI, which usually reflects posterior pituitary injury, is however frequently recognized.

Blood cortisol concentrations are usually high in ICU patients - often 2-3 times greater than the normal morning peak values of 500 nmol/l. Cortisol has a relatively short half-life and a permissive action on catecholamine efficacy, so cortisol deficiency could manifest rapidly, and cause hypotension.

In 80 patients with severe TBI (GCS <9), and in 12 controls (severe multi-trauma without TBI), we measured blood cortisol and ACTH concentrations on days 1,3 and 7 of ICU admission. Fifteen of 80 patients (19%) had absolute cortisol deficiency with morning blood cortisol concentrations <140 nmol/l (normal 140-500) and ACTH <10 ng/l (normal <65) on days 3 or 7 of ICU admission. These patients had a mortality of 21% compared to 4% in the others. Twenty-four of the 80 patients (30%) had blood cortisol concentrations <250 nmol/l. None of the controls had a blood cortisol concentration <140 nmol/l. TBI patents with blood cortisol concentrations <250 nmol/l had greater elevation of intracranial pressure 32± 45 vs 9± 23 h >20 mmHg (P<0.05), and greater peak vasopressor doses 18± 14 vs 9± 16 μg/min (P<0.05) than the others.

Absolute cortisol deficiency occurs during the first 7 days of ICU admission in 19% of patients with severe TBI, and is likely to be of hypothalamic or pituitary origin. These patients had greater vasopressor doses suggesting that cortisol deficiency may contribute to vasopressor-resistant hypotension in patients with severe TBI.