Acute secondary adrenal insufficiency after traumatic brain injury

A prospective study

Pejman Cohan, Christina Wang, David L. McArthur, Shon W. Cook, Joshua R. Dusick, Bob Armin, Ronald Swerdloff, Paul Vespa, Jan Paul Muizelaar, Henry Gill Cryer, Peter D. Christenson, Daniel F. Kelly

Research output: Contribution to journalArticle

185 Citations (Scopus)

Abstract

Objective: To determine the prevalence, time course, clinical characteristics, and effect of adrenal insufficiency (AI) after traumatic brain injury (TBI). Design: Prospective intensive care unit-based cohort study. Setting: Three level 1 trauma centers. Patients: A total of EO patients with moderate or severe TBI (Glasgow Coma Scale score, 3-13) and 41 trauma patients without TBI (Injury Severity Score, >15) enrolled between June 2002 and November 2003. Measurements: Serum cortisol and adrenocorticotropic hormone levels were drawn twice daily for up to 9 days postinjury; AI was defined as two consecutive cortisols of ≥15 μg/dL (25th percentile for extracranial trauma patients) or one cortisol of <5 μg/dL. Principal outcome measures included: injury characteristics, hemodynamic data, usage of vasopressors, metabolic suppressive agents (high-dose pentobarbital and propofol), etomidate, and AI status. Main Results: AI occurred in 42 TBI patients (53%). Adrenocorticotropic hormone levels were lower at the time of AI (median, 18.9 vs. 36.1 μg/mL; p = .0001). Compared with patients without AI, those with AI were younger (p = .01), had higher injury severity (p = .02), had a higher frequency of early ischemic insults (hypotension, hypoxia, severe anemia) (p = .02), and were more likely to have received etomidate (p = .049). Over the acute postinjury period, patients with AI had lower trough mean arterial pressure (p = .001) and greater vasopressor use (p = .047). Mean arterial pressure was lower in the 8 hrs preceding a low (≤15 μg/dl) cortisol level (p = .003). There was an inverse relationship between cortisol levels and vasopressor use (p = .0005) and between cortisol levels within 24 hrs of injury and etomidate use (p = .002). Use of high-dose propofol and pentobarbital was strongly associated with lower cortisol levels (p < .0001). Conclusions: Approximately 50% of patients with moderate or severe TBI have at least transient AI. Younger age, greater injury severity, early ischemic insults, and the use of etomidate and metabolic suppressive agents are associated with AI. Because lower cortisol levels were associated with lower blood pressure and higher vasopressor use, consideration should be given to monitoring cortisol levels in intubated TBI patients, particularly those receiving high-dose pentobarbital or propofol. A randomised trial of stress-dose hydrocortisone in TBI patients with AI is underway.

Original languageEnglish (US)
Pages (from-to)2358-2366
Number of pages9
JournalCritical Care Medicine
Volume33
Issue number10
DOIs
StatePublished - Oct 2005

Fingerprint

Adrenal Insufficiency
Hydrocortisone
Prospective Studies
Etomidate
Wounds and Injuries
Propofol
Pentobarbital
Adrenocorticotropic Hormone
Arterial Pressure
Traumatic Brain Injury
Glasgow Coma Scale
Injury Severity Score
Trauma Centers
Hypotension
Intensive Care Units
Anemia
Cohort Studies
Hemodynamics
Outcome Assessment (Health Care)

Keywords

  • Adrenal insufficiency
  • Cortisol
  • Etomidate
  • Hypopituitarism
  • Pentobarbital
  • Pituitary
  • Propofol
  • Stress response
  • Traumatic brain injury
  • Vasopressor

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Cohan, P., Wang, C., McArthur, D. L., Cook, S. W., Dusick, J. R., Armin, B., ... Kelly, D. F. (2005). Acute secondary adrenal insufficiency after traumatic brain injury: A prospective study. Critical Care Medicine, 33(10), 2358-2366. https://doi.org/10.1097/01.CCM.0000181735.51183.A7

Acute secondary adrenal insufficiency after traumatic brain injury : A prospective study. / Cohan, Pejman; Wang, Christina; McArthur, David L.; Cook, Shon W.; Dusick, Joshua R.; Armin, Bob; Swerdloff, Ronald; Vespa, Paul; Muizelaar, Jan Paul; Cryer, Henry Gill; Christenson, Peter D.; Kelly, Daniel F.

In: Critical Care Medicine, Vol. 33, No. 10, 10.2005, p. 2358-2366.

Research output: Contribution to journalArticle

Cohan, P, Wang, C, McArthur, DL, Cook, SW, Dusick, JR, Armin, B, Swerdloff, R, Vespa, P, Muizelaar, JP, Cryer, HG, Christenson, PD & Kelly, DF 2005, 'Acute secondary adrenal insufficiency after traumatic brain injury: A prospective study', Critical Care Medicine, vol. 33, no. 10, pp. 2358-2366. https://doi.org/10.1097/01.CCM.0000181735.51183.A7
Cohan, Pejman ; Wang, Christina ; McArthur, David L. ; Cook, Shon W. ; Dusick, Joshua R. ; Armin, Bob ; Swerdloff, Ronald ; Vespa, Paul ; Muizelaar, Jan Paul ; Cryer, Henry Gill ; Christenson, Peter D. ; Kelly, Daniel F. / Acute secondary adrenal insufficiency after traumatic brain injury : A prospective study. In: Critical Care Medicine. 2005 ; Vol. 33, No. 10. pp. 2358-2366.
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abstract = "Objective: To determine the prevalence, time course, clinical characteristics, and effect of adrenal insufficiency (AI) after traumatic brain injury (TBI). Design: Prospective intensive care unit-based cohort study. Setting: Three level 1 trauma centers. Patients: A total of EO patients with moderate or severe TBI (Glasgow Coma Scale score, 3-13) and 41 trauma patients without TBI (Injury Severity Score, >15) enrolled between June 2002 and November 2003. Measurements: Serum cortisol and adrenocorticotropic hormone levels were drawn twice daily for up to 9 days postinjury; AI was defined as two consecutive cortisols of ≥15 μg/dL (25th percentile for extracranial trauma patients) or one cortisol of <5 μg/dL. Principal outcome measures included: injury characteristics, hemodynamic data, usage of vasopressors, metabolic suppressive agents (high-dose pentobarbital and propofol), etomidate, and AI status. Main Results: AI occurred in 42 TBI patients (53{\%}). Adrenocorticotropic hormone levels were lower at the time of AI (median, 18.9 vs. 36.1 μg/mL; p = .0001). Compared with patients without AI, those with AI were younger (p = .01), had higher injury severity (p = .02), had a higher frequency of early ischemic insults (hypotension, hypoxia, severe anemia) (p = .02), and were more likely to have received etomidate (p = .049). Over the acute postinjury period, patients with AI had lower trough mean arterial pressure (p = .001) and greater vasopressor use (p = .047). Mean arterial pressure was lower in the 8 hrs preceding a low (≤15 μg/dl) cortisol level (p = .003). There was an inverse relationship between cortisol levels and vasopressor use (p = .0005) and between cortisol levels within 24 hrs of injury and etomidate use (p = .002). Use of high-dose propofol and pentobarbital was strongly associated with lower cortisol levels (p < .0001). Conclusions: Approximately 50{\%} of patients with moderate or severe TBI have at least transient AI. Younger age, greater injury severity, early ischemic insults, and the use of etomidate and metabolic suppressive agents are associated with AI. Because lower cortisol levels were associated with lower blood pressure and higher vasopressor use, consideration should be given to monitoring cortisol levels in intubated TBI patients, particularly those receiving high-dose pentobarbital or propofol. A randomised trial of stress-dose hydrocortisone in TBI patients with AI is underway.",
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T2 - A prospective study

AU - Cohan, Pejman

AU - Wang, Christina

AU - McArthur, David L.

AU - Cook, Shon W.

AU - Dusick, Joshua R.

AU - Armin, Bob

AU - Swerdloff, Ronald

AU - Vespa, Paul

AU - Muizelaar, Jan Paul

AU - Cryer, Henry Gill

AU - Christenson, Peter D.

AU - Kelly, Daniel F.

PY - 2005/10

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N2 - Objective: To determine the prevalence, time course, clinical characteristics, and effect of adrenal insufficiency (AI) after traumatic brain injury (TBI). Design: Prospective intensive care unit-based cohort study. Setting: Three level 1 trauma centers. Patients: A total of EO patients with moderate or severe TBI (Glasgow Coma Scale score, 3-13) and 41 trauma patients without TBI (Injury Severity Score, >15) enrolled between June 2002 and November 2003. Measurements: Serum cortisol and adrenocorticotropic hormone levels were drawn twice daily for up to 9 days postinjury; AI was defined as two consecutive cortisols of ≥15 μg/dL (25th percentile for extracranial trauma patients) or one cortisol of <5 μg/dL. Principal outcome measures included: injury characteristics, hemodynamic data, usage of vasopressors, metabolic suppressive agents (high-dose pentobarbital and propofol), etomidate, and AI status. Main Results: AI occurred in 42 TBI patients (53%). Adrenocorticotropic hormone levels were lower at the time of AI (median, 18.9 vs. 36.1 μg/mL; p = .0001). Compared with patients without AI, those with AI were younger (p = .01), had higher injury severity (p = .02), had a higher frequency of early ischemic insults (hypotension, hypoxia, severe anemia) (p = .02), and were more likely to have received etomidate (p = .049). Over the acute postinjury period, patients with AI had lower trough mean arterial pressure (p = .001) and greater vasopressor use (p = .047). Mean arterial pressure was lower in the 8 hrs preceding a low (≤15 μg/dl) cortisol level (p = .003). There was an inverse relationship between cortisol levels and vasopressor use (p = .0005) and between cortisol levels within 24 hrs of injury and etomidate use (p = .002). Use of high-dose propofol and pentobarbital was strongly associated with lower cortisol levels (p < .0001). Conclusions: Approximately 50% of patients with moderate or severe TBI have at least transient AI. Younger age, greater injury severity, early ischemic insults, and the use of etomidate and metabolic suppressive agents are associated with AI. Because lower cortisol levels were associated with lower blood pressure and higher vasopressor use, consideration should be given to monitoring cortisol levels in intubated TBI patients, particularly those receiving high-dose pentobarbital or propofol. A randomised trial of stress-dose hydrocortisone in TBI patients with AI is underway.

AB - Objective: To determine the prevalence, time course, clinical characteristics, and effect of adrenal insufficiency (AI) after traumatic brain injury (TBI). Design: Prospective intensive care unit-based cohort study. Setting: Three level 1 trauma centers. Patients: A total of EO patients with moderate or severe TBI (Glasgow Coma Scale score, 3-13) and 41 trauma patients without TBI (Injury Severity Score, >15) enrolled between June 2002 and November 2003. Measurements: Serum cortisol and adrenocorticotropic hormone levels were drawn twice daily for up to 9 days postinjury; AI was defined as two consecutive cortisols of ≥15 μg/dL (25th percentile for extracranial trauma patients) or one cortisol of <5 μg/dL. Principal outcome measures included: injury characteristics, hemodynamic data, usage of vasopressors, metabolic suppressive agents (high-dose pentobarbital and propofol), etomidate, and AI status. Main Results: AI occurred in 42 TBI patients (53%). Adrenocorticotropic hormone levels were lower at the time of AI (median, 18.9 vs. 36.1 μg/mL; p = .0001). Compared with patients without AI, those with AI were younger (p = .01), had higher injury severity (p = .02), had a higher frequency of early ischemic insults (hypotension, hypoxia, severe anemia) (p = .02), and were more likely to have received etomidate (p = .049). Over the acute postinjury period, patients with AI had lower trough mean arterial pressure (p = .001) and greater vasopressor use (p = .047). Mean arterial pressure was lower in the 8 hrs preceding a low (≤15 μg/dl) cortisol level (p = .003). There was an inverse relationship between cortisol levels and vasopressor use (p = .0005) and between cortisol levels within 24 hrs of injury and etomidate use (p = .002). Use of high-dose propofol and pentobarbital was strongly associated with lower cortisol levels (p < .0001). Conclusions: Approximately 50% of patients with moderate or severe TBI have at least transient AI. Younger age, greater injury severity, early ischemic insults, and the use of etomidate and metabolic suppressive agents are associated with AI. Because lower cortisol levels were associated with lower blood pressure and higher vasopressor use, consideration should be given to monitoring cortisol levels in intubated TBI patients, particularly those receiving high-dose pentobarbital or propofol. A randomised trial of stress-dose hydrocortisone in TBI patients with AI is underway.

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KW - Cortisol

KW - Etomidate

KW - Hypopituitarism

KW - Pentobarbital

KW - Pituitary

KW - Propofol

KW - Stress response

KW - Traumatic brain injury

KW - Vasopressor

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