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Perioperative management of
traumatic brain injury
Parichat Curry1, Darwin Viernes1, Deepak Sharma1,2
ABSTRACT
Traumatic brain injury (TBI) is a major public health problem and the leading cause of death
and disability worldwide. Despite the modern diagnosis and treatment, the prognosis
for patients with TBI remains poor. While severity of primary injury is the major factor
determining the outcomes, the secondary injury caused by physiological insults such as
hypotension, hypoxemia, hypercarbia, hypocarbia, hyperglycemia and hypoglycemia, etc.
that develop over time after the onset of the initial injury, causes further damage to brain
tissue, worsening the outcome in TBI. Perioperative period may be particularly important
in the course of TBI management. While surgery and anesthesia may predispose the
patients to new onset secondary injuries which may contribute adversely to outcomes,
the perioperative period is also an opportunity to detect and correct the undiagnosed
pre-existing secondary insults, to prevent against new secondary insults and is a potential
window to initiate interventions that may improve outcome of TBI. For this review,
extensive Pubmed and Medline search on various aspects of perioperative management
of TBI was performed, followed by review of research focusing on intraoperative and
perioperative period. While the research focusing specifically on the intraoperative and
immediate perioperative TBI management is limited, clinical management continues to
be based largely on physiological optimization and recommendations of Brain Trauma
Foundation guidelines. This review is focused on the perioperative management of TBI,
with particular emphasis on recent developments.
INTRODUCTION
Traumatic brain injury (TBI) is a major public health
problem and the leading cause of death and disability
worldwide.[1] Approximately 1.7 million people sustain
TBI every year in the United States, leading to 275,000
hospitalizations and 52,000 deaths.[1] TBI is a contributing
factor in about 30.5% of all injury-related deaths in the
United States.[1] TBI occurs most often in children aged 04
years, adolescents aged 1519 years and elderly aged 65
years and more.[1] In all age groups, males have a higher
rate of TBI than females. [1] Falls and motor vehicletrac injury are the leading causes of TBI in the United
States.[1] In the recent years, prehospital and intensive
care of patients with TBI has improved substantially and
evidence-based guidelines for management have been
developed.[2-13] However, despite the modern diagnosis
and treatment, the prognosis for patients with TBI
remains poor, emphasizing the need for further research
and improvement in care. This review will focus on
PATHOPHYSIOLOGY OF TRAUMATIC
BRAIN INJURY
Pathophysiology of TBI involves primary and secondary
injuries to the brain. Primary injury is the damage
caused by the initial trauma involving mechanical
impact to the brain tissue and skull due to acceleration
deceleration or rotational forces, resulting in skull fracture,
brain contusion, expanding intracranial hematoma
or diffuse axonal injury. [14] The primary injury then
initiates inflammatory process, edema formation and
excitotoxicity, resulting in further increase in intracranial
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Curry, et al.: Management of traumatic brain injury
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Curry, et al.: Management of traumatic brain injury
maintain CPP;
treat increased ICP;
provide optimal surgical conditions;
avoid secondary insults such as hypoxemia, hyper
and hypocarbia, hypo and hyperglycemia; and
provide adequate analgesia and amnesia.
Anesthetic technique
Important pharmacodynamic and pharmacokinetic
differences exist between intravenous and volatile
anesthetic agents. Intravenous agents including
thiopental, propofol and etomidate cause cerebral
vasoconstriction and reduce CBF, CBV, CMRO2 and ICP.[39]
Opioids have no direct eects on cerebral hemodynamics
in the presence of controlled ventilation.[40] All volatile
anesthetic agents (isoflurane, sevoflurane, desflurane)
decrease CMRO2 and may cause cerebral vasodilation,
resulting in increasing CBF and ICP. But at concentration
less than 1 minimum alveolar concentration (MAC), the
cerebral vasodilatory e ects are minimal and hence
they may be used in low concentrations in patients
with TBI.[41] Nitrous oxide can increase CMRO2 and cause
cerebral vasodialation and increased ICP and should be
avoided.[42] Importantly, the eects of anesthetic agents
(inhalation vs. total intravenous anesthesia) on outcome
of TBI have not been demonstrated. In the absence of
conclusive evidence, either anesthetic technique may
be employed judiciously. However, more importantly,
the principles of anesthetic management should adhere
to the current guidelines for the management of severe
TBI [Table 1].[2-13]
Ventilation
Ventilation should be adjusted to ensure adequate
oxygenation and gas exchange. Inspired oxygen
concentration is adjusted to maintain PaO 2 >60
mmHg. 2 Monitoring arterial PCO 2 is recommended
since end-tidal CO2 may not be reliable. Hypercarbia
should be avoided but hypocarbia must not be used
indiscriminately.[12] Excessive hyperventilation may cause
cerebral vasoconstriction leading to ischemia.[12] Hence,
hyperventilation should be used judiciously for shortterm control of ICP and to facilitate surgical exposure
during craniotomy. Normocarbia should be restored
before dural closure to avoid development of tension
pneumocephalus. Monitoring cerebral oxygenation
is recommended when utilizing hyperventilation for
prolonged periods. In the intraoperative period, this may
be accomplished by jugular venous oximetry[9,43] and in
the postoperative period by brain tissue oxygenation
(PbtO 2) or CBF monitoring (e.g. using Transcranial
Doppler ultrasonography).[9]
Monitoring
In additional to standard American Society of
Anesthesiology (ASA) monitors, arterial catheterization is
recommended for beat-to-beat blood pressure monitoring
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Curry, et al.: Management of traumatic brain injury
Recommendations
Blood pressure
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Curry, et al.: Management of traumatic brain injury
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Curry, et al.: Management of traumatic brain injury
SUMMARY
Perioperative period may be important in TBI
management. While it may predispose the patient to new
onset secondary injuries which may contribute adversely
to outcomes, it is also an opportunity to detect and correct
the undiagnosed pre-existing secondary insults. It may
also be a potential window to initiate interventions that
may improve the outcome of TBI. While research focused
specifically on the intraoperative and perioperative
International Journal of Critical Illness and Injury Science | Vol. 1 | Issue 1 | Jan-Jun 2011
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Curry, et al.: Management of traumatic brain injury
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