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Open Access

Incidence of adrenal insufficiency within 10 days of traumatic brain injury

  • F Bernard1,
  • J Outtrim1,
  • D Menon1 and
  • B Matta1
Critical Care20059(Suppl 1):P402

Published: 7 March 2005


Traumatic Brain InjuryCortisol LevelHead InjuryAdrenal InsufficiencyGlasgow Outcome Score

Adrenal insufficiency (AI) is common in septic shock, and the physiologic replacement of hydrocortisone improves outcome [1]. Head injury (HI) has been shown to cause AI in the subacute phase (>10 days) with a reported incidence of approximately 15% [2, 3], but there are no data on early AI, at times when it is most likely to influence ICU management. Furthermore, analysis of available data is confounded by variations in the definition of AI [4, 5]. We aim to describe adrenal function in the first 10 days after injury using various suggested definitions of AI in critical care [4, 5]. We retrospectively analysed patients who had a stimulation test performed within 10 days of admission to our neurointensive care unit. Tetracosactide (Synacthen) was administered as a 250 μg bolus and cortisol levels measured at 0, 30 and 60 min. AI was defined as a baseline cortisol level below 414 mmol/l and failure to rise by 250 mmol/l after Synacthen administration. All patients who showed AI or responded clinically to a trial of steroid therapy received 200–400 mg hydrocortisone per day while on vasopressor therapy.

One hundred and thirteen patients were analysed. Mean age was 35 ± 15 and 79% were male. Four percent, 25% and 70% had mild, moderate and severe HI defined by the GCS on admission. Mean APACHE II and ISS scores were 15 ± 6 and 24 ± 10. The incidence of AI according to baseline cortisol level was 78%. The cortisol level failed to rise in 48% and 27% of patients at time 30 and 60 min, respectively. Primary adrenal insufficiency defined by both low baseline cortisol and failure to react to synacthen was present in 28% and 13% of patients at time 30 and 60 min. All patients had baseline cortisol levels below 690 mmol/l. Cortisol remained below 500 mmol/l after stimulation in 49% and 22% of patients at 30 and 60 min. The incidence of AI, using any of the definitions in the literature, was unrelated to APACHE II or ISS score or GCS on admission, or to ICU length of stay or outcome (defined using the Glasgow Outcome Score).

A 60-min sampling time point may be more appropriate to evaluate the response to Synacthen stimulation. During the first 10 days after HI, secondary AI was present in 78% of patients and primary AI in at least 15%. These incidences might be higher if less stringent definitions are used. Injury and/or illness severity indices do not predict AI. While AI was not predictive of outcome in this study, all subjects with AI received steroid replacement. Such a high incidence of AI may have major therapeutic implications.

Authors’ Affiliations

Addenbrooke's NHS Trust, Cambridge, UK


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© BioMed Central Ltd 2005