Harbingers of poor outcome the day after severe brain injury: hypothermia, hypoxia, and hypoperfusion.

BACKGROUND Traumatic brain injury (TBI) can be compounded by physiologic derangements that produce secondary brain injury. The purpose of this study is to elucidate the frequency with which physiologic factors that are associated with secondary brain injury occur in patients with severe closed head injuries and to determine the impact of these factors on outcome. METHODS The records of 81 adult blunt trauma patients with Glasgow Coma Scale scores < or = 8 and transport times < 2 hours to a Level I trauma center were retrospectively reviewed searching for the following 11 secondary brain injury factors (SBIFs) in the first 24 hours postinjury: hypotension, hypoxia, hypercapnia, hypocapnia, hypothermia, hyperthermia, metabolic acidosis, seizures, coagulopathy, hyperglycemia, and intracranial hypertension. We recorded the worst SBIF during six time periods: hours 1, 2, 3, 4, 5 to 14, and 16 to 24. Occurrence of each SBIF was then correlated with outcome. RESULTS Hypocapnia, hypotension, and acidosis occurred more frequently than other SBIFs (60-80%). Hypotension, hyperglycemia, and hypothermia were associated with increased mortality rate. Patients with episodes of hypocapnia, acidosis, and hypoxia had significantly longer intensive care unit length of stay (LOS). These three SBIFs and hyperglycemia related to longer hospital LOS as well. Hypotension and acidosis were associated with discharge to a rehabilitation facility rather than home. Finally, multivariate regression analysis revealed that hypotension, hypothermia, and Abbreviated Injury Scale score of the head were independently related to mortality, whereas other SBIFs, age, Injury Severity Score, and Glasgow Coma Scale score were not. Metabolic acidosis and hypoxia were related to longer intensive care unit and hospital LOS. CONCLUSION Our early management of head-injured patients stresses avoidance and correction of SBIFs at all costs. Nonetheless, SBIFs occur frequently in the first 24 hours after traumatic brain injury. Six of the 11 factors studied are associated with significantly worse outcomes. Hypotension and hypothermia are independently related to mortality. Because these SBIFs are potentially preventable, protocols could be developed to decrease their frequency.

[1]  S. Shackford,et al.  The deleterious effects of intraoperative hypotension on outcome in patients with severe head injuries. , 1992, The Journal of trauma.

[2]  D. Marion,et al.  Intercenter variance in clinical trials of head trauma--experience of the National Acute Brain Injury Study: Hypothermia. , 2001, Journal of neurosurgery.

[3]  G. Bouma,et al.  Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia. , 1991, Journal of neurosurgery.

[4]  M. Rosner,et al.  Cerebral perfusion pressure management in head injury. , 1990, The Journal of trauma.

[5]  R. Chesnut,et al.  Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain injury in the Traumatic Coma Data Bank. , 1993, Acta neurochirurgica. Supplementum.

[6]  P. Silverston,et al.  Pulse oximetry at the roadside: a study of pulse oximetry in immediate care. , 1989, BMJ.

[7]  N R Temkin,et al.  A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. , 1990, The New England journal of medicine.

[8]  P. Gildenberg,et al.  The incidence and significance of hemostatic abnormalities in patients with head injuries. , 1989 .

[9]  S. Wisniewski,et al.  Treatment of traumatic brain injury with moderate hypothermia. , 1997, The New England journal of medicine.

[10]  J L Tocher,et al.  Measuring the burden of secondary insults in head-injured patients during intensive care. , 1994, Journal of neurosurgical anesthesiology.

[11]  R. Grossman,et al.  Continuous monitoring of jugular venous oxygen saturation in head-injured patients. , 1992, Journal of neurosurgery.

[12]  C. Weigle,et al.  Continuous measurement of jugular venous oxygen saturation in response to transient elevations of blood pressure in head-injured patients. , 1994, Journal of neurosurgery.

[13]  K. Welch,et al.  The Metabolic Effects of Mild Hypothermia on Global Cerebral Ischemia and Recirculation in the Cat: Comparison to Normothermia and Hyperthermia , 1989, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[14]  S. Shackford,et al.  Epidemiology and pathology of traumatic deaths occurring at a Level I Trauma Center in a regionalized system: the importance of secondary brain injury. , 1989, The Journal of trauma.

[15]  M. Westphal,et al.  Cyclo-Oxygenase Inhibitors and Thromboxane Synthase Inhibitors Differentially Regulate Migration Arrest, Growth Inhibition and Apoptosis in Human Glioma Cells , 2002, Acta Neurochirurgica.

[16]  E. Hall,et al.  Mild pre- and posttraumatic hypothermia attenuates blood-brain barrier damage following controlled cortical impact injury in the rat. , 1996, Journal of neurotrauma.

[17]  A. Unterberg,et al.  Secondary insults in severe head injury—Do multiply injured patients do worse? , 2001, Critical care medicine.

[18]  J. Morris,et al.  Base deficit stratifies mortality and determines therapy. , 1992, The Journal of trauma.

[19]  H Yonas,et al.  Acute regional cerebral blood flow changes caused by severe head injuries. , 1991, Journal of neurosurgery.

[20]  J. Povlishock,et al.  Moderate hypothermia reduces blood-brain barrier disruption following traumatic brain injury in the rat , 2004, Acta Neuropathologica.

[21]  H. Winn,et al.  Hyperglycemia and neurological outcome in patients with head injury. , 1991, Journal of neurosurgery.

[22]  G. Clifton,et al.  A phase II study of moderate hypothermia in severe brain injury. , 1993, Journal of neurotrauma.

[23]  J. Cruz.  Continuous monitoring of cerebral oxygenation in acute brain injury: assessment of cerebral hemometabolic regulation. , 1991, Minerva anestesiologica.

[24]  H. Eisenberg,et al.  High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury. , 1988, Journal of neurosurgery.

[25]  A. Marmarou,et al.  Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. , 1991, Journal of neurosurgery.

[26]  S. Stein,et al.  Delayed brain injury after head trauma: significance of coagulopathy. , 1992, Neurosurgery.

[27]  R. Dempsey,et al.  Relationship between admission hyperglycemia and neurologic outcome of severely brain-injured patients. , 1989 .