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DISCLAIMER: These guidelines were prepared by the Department of Surgical Education, Orlando Regional Medical Center. They are intended to serve as a general statement regarding appropriate patient care practices based upon the available medical literature and clinical expertise at the time of development. They should not be considered to be accepted protocol or policy, nor are intended to replace clinical judgment or dictate care of individual patients.
EVIDENCE DEFINITIONS
- Class I: Prospective randomized controlled trial.
- Class II: Prospective clinical study or retrospective analysis of reliable data. Includes observational, cohort, prevalence, or case control studies.
- Class III: Retrospective study. Includes database or registry reviews, large series of case reports, expert opinion.
- Technology assessment: A technology study which does not lend itself to classification in the above-mentioned format. Devices are evaluated in terms of their accuracy, reliability, therapeutic potential, or cost effectiveness.
LEVEL OF RECOMMENDATION DEFINITIONS
- Level 1: Convincingly justifiable based on available scientific information alone. Usually based on Class I data or strong Class II evidence if randomized testing is inappropriate. Conversely, low quality or contradictory Class I data may be insufficient to support a Level I recommendation.
- Level 2: Reasonably justifiable based on available scientific evidence and strongly supported by expert opinion. Usually supported by Class II data or a preponderance of Class III evidence.
- Level 3: Supported by available data, but scientific evidence is lacking. Generally supported by Class III data. Useful for educational purposes and in guiding future clinical research. 1 Approved 05/08/
BRAIN INJURY RESUSCITATION
SUMMARY
Traumatic brain injury (TBI) is the leading cause of death for all age groups in the United States, contributing to over 60% of trauma-related deaths. The primary goals of management in TBI are to minimize cerebral edema, intracranial pressure (ICP), and to optimize cerebral perfusion pressure (CPP) thereby decreasing the incidence of secondary injury.
RECOMMENDATIONS
- Level I ¾ Maintain normal body temperature. Prevent and treat hyperthermia. ¾ Institute isovolemic dehydration with hypertonic saline solution (HSS, i.e.1.5% or 3% NaCl) and mannitol. ¾ Consider resuscitating hypotensive (SBP < 90 mmHg) patients with 4 ml/kg 7.5% HSS (round to nearest 50mL size) ¾ In the absence of seizure activity, prophylactic fosphenytoin administration should be limited to the first seven days post-injury to reduce the incidence of post-traumatic seizures ¾ Steroids should not be used in brain injury resuscitation ¾ Avoid systemic hypotension
- Level II ¾ The patient’s head of bed should be elevated to 30° at all times. ¾ Maintain normocarbia (PaCO 2 35-45 torr) ¾ Intracranial pressure (ICP) monitoring is indicated (unless the patient is deemed non- survivable or operative intervention is planned within 4 hours of injury) in patients with: o Glasgow Coma Score (GCS) ≤ 8 (after resuscitation) AND an abnormal admission computed tomography (CT) scan of the head o GCS ≤ 8 (after resuscitation) with a normal CT scan of the head AND one of the following: age > 40 years, unilateral or bilateral motor posturing, or systemic hypotension ¾ Maintain cerebral perfusion pressure (CPP) within a range of 50-70 mmHg. ¾ Institute mild hypothermia (body temperature 33-35°C) for persistent intracranial hypertension with ICP > 20 mmHg despite maximum medical management including barbiturate therapy
- Level III ¾ Adequate sedation using short-acting agents such as propofol may be instituted ¾ When ICP exceeds 20 mmHg, maintain PaCO 2 between 30 and 35 torr ¾ Consider pentobarbital coma for intractable intracranial hypertension (ICP > 20 mmHg) ¾ In patients < 18 years old, decompressive craniectomy should be considered for intractable intracranial hypertension unresponsive to medical management
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INTRODUCTION
Based on the Monroe-Kellie Doctrine, the intracranial volume [brain (80%), cerebral spinal fluid (CSF) (10%), and cerebral blood volume (10%)] is fixed by the confines of the cranial vault. Cerebral edema, tumor, hematoma, or abscess may impinge upon normal compartment volumes, raising intracranial pressure (ICP). Since brain tissue is capable of minimal compensation in response to abnormal intracranial lesions, the CSF and cerebral blood volume compartments must decrease accordingly to minimize ICP elevations. CSF compensates by draining through the lumbar plexus and decreasing its intracranial volume. Cerebral blood volume and cerebral blood flow (CBF) are directly related to ICP and are normally closely controlled by autoregulation through a wide range of systolic blood pressures, PaCO 2 and PaO 2.
TBI resuscitation protocols have been demonstrated to lead to less variation in ICP and a decrease in the duration of acute episodes of intracranial hypertension (1). The Brain Trauma Foundation (BTF) (www.braintrauma.org) maintains an extensive evidence-based medicine guideline that is regularly updated as new developments are published. An evidence-based medicine algorithm for resuscitation of the brain injured patient that is based upon the BTF guidelines is attached. The treatment of severe TBI is based on two principles: 1) minimizing the development of cerebral edema and elevated ICP, and 2) optimizing cerebral perfusion pressure (CPP) (CPP = MAP – ICP) in order to ensure adequate cerebral oxygen delivery.
LITERATURE REVIEW
Head of bed elevation The treatment of any patient with TBI should begin with elevation of the head 30 degrees in an attempt to reduce cerebral edema and augment venous drainage. Elevating the head from 0 to 30 degrees has been shown to significantly lower mean ICP from 20 to 14 mmHg with no significant change in the CPP or CBF (2). In patients with suspected or documented spine injury, this is best achieved by placing the patient’s bed in the Reverse Trendelenburg position.
Normo- vs. hypothermia Normal body temperature should be maintained. In 2001, Clifton et al. reported the results of a large, prospective, randomized trial evaluating the use of hypothermia in TBI patients (3). 392 patients were randomized within 6 hours of injury to hypothermia (33°C) vs. normothermia and then rewarmed after 48 hours. Mortality was 28% in the hypothermia group and 27% in the normothermia group (p=0.79). The patients in the hypothermia group demonstrated a great incidence of pneumonia as well as longer hospital length of stay than patients in the normothermia group. The authors concluded that treatment with hypothermia, with a body temperature reaching 33°C is not effective in improving outcomes in patients with severe TBI. A follow-up meta-analysis performed in 2002 by Alderson et al. included 14 prospective, randomized trials with 1094 patients comparing hypothermia with normothermia in TBI (4). These authors concluded that there is no evidence that hypothermia is beneficial in the treatment of head injury, and that earlier, encouraging trial results have not been repeated in larger trials. Based on these randomized trials, routine hypothermia is not recommended as a treatment option for patients with TBI. Hyperthermia, however, should clearly be avoided.
Hypertonic vs. isotonic resuscitation Resuscitation using hypertonic saline solutions (HSS) results in a restoration of intravascular volume, improving tissue perfusion, while producing extravascular dehydration, decreasing tissue edema and vasospasm in critical areas such as the brain. This allows restoration of MAP and resultant improvement in CPP without worsening in cerebral edema (a problem associated with hypotonic and isotonic solutions). The exact mechanism by which HSS acts on the injured brain has yet to be fully elucidated. In a meta-analysis of 6 prospective, randomized trials evaluating HSS for the resuscitation of hypotensive TBI patient, patients who received HSS were twice as likely to survive as those who received saline (p<0.05) (5). From 1990-1995, Vassar et al. performed three prospective, randomized trials that compared a 250mL bolus of 7.5% HSS to a series of alternative solutions (NS, LR, 7.5% HSS with 6% dextran) in the resuscitation of hypotensive (SBP< 90 mmHg) TBI patients. The authors concluded that:
- the use of HSS was safe; there were no cases of intracranial bleeding or central pontine myelinolysis in
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with a 6.3% infection rate and 1.4% hemorrhage rate (21). In a follow-up study in 1990, Eisenberg et al. evaluated 753 TBI patients and correlated with head CT scan findings with ICP measurements. They concluded that TBI patients whose initial CT scans were normal had only a 10-15% chance of developing elevated ICP (22). Although these studies indicated that ICP monitors could be omitted in TBI patients with normal initial CT scan of the head, Lobato et al. went on to show that follow-up CT scans of the head are very important if no ICP monitor is placed. In their study, 1 out of 3 patients with a normal admission CT scan of the head after TBI went on to develop new pathology on the follow-up CT scans performed over the next few days (23). From 1991-1993, three large, prospective studies evaluated the effect of ICP monitors on outcome in TBI patients (24-26). All three concluded that adverse outcome and mortality rates were significantly higher in patients with ICP > 20-25 mmHg. In the study by Marshall et al., ICP > 20 mmHg was found to be highly significant in predicting adverse outcome and death (p < 0.001). In 1993, Ghajar et al. prospectively followed 49 patients with TBI. In the first group of 34 patients, ICP monitors and CSF drainage was undertaken for ICP > 15 mmHg, while no ICP monitors or intracranial hypertension treatment was undertaken for the second group of 15 patients. Mortality for the first group was 12% while that for the second group was 53% (27).
There is one study against ICP monitoring for TBI. In 1986, Smith et al. reported a prospective, randomized study of 80 patients with severe head injury (GCS ≤8) (28). All patients were intubated and moderately hyperventilated, ICP was monitored and CT of the head was obtained every 2-3 days. Group I received mannitol for ICP > 25 mmHg and pentobarbital for ICP > 35 mmHg. Group II empirically received mannitol 0.25g/kg every 2 hours. The mortality in the specifically treated group was 35% while in the empirically treated group it was 42%. Although suggesting a better outcome in Group I, the difference was not statistically significant. This study was limited by its sample size; as it would have taken 349 patients in each group (rather than about 40) to demonstrate a 10% improvement in mortality.
ICP monitoring will provide no benefit to the patient whose TBI is deemed to be non-survivable or in the patient who will undergo neurosurgical intervention within four (4) hours of injury. ICP monitoring should not, therefore, be implemented in such patients. ICP monitoring should be performed for patients who, after resuscitation, have a GCS ≤ 8 in the following scenarios:
- Abnormal admission computed tomography (CT) scan of the head
- Normal admission CT scan of the head AND one of the following: o Age > 40 years o Unilateral or bilateral motor posturing o Systemic hypotension (systolic blood pressure < 90 mmHg)
Cerebral perfusion pressure (CPP) Prospective studies have identified a CPP > 60 mmHg as a resuscitation endpoint associated with improved outcome following TBI. In comparative studies, artificial attempts to maintain to CPP above 70 mmHg have been associated with an increased incidence of adult respiratory distress syndrome (ARDS) without any improvement in outcome as compared to CPP > 60 mmHg (29-31). The current BTF guidelines recommend a target CPP of 50-70 mmHg to avoid cerebral hypoperfusion as well as avoid the detrimental effects of over-resuscitation.
Hyperventilation Modest levels of hyperventilation (PaCO 2 30-35 torr) are now advocated over the more aggressive hyperventilation of years past. Prospective, randomized data comparing a PaCO 2 of 25 versus 35 torr demonstrated improved outcome at both 3 and 6 months in the latter group, although no difference was apparent at 1 year (31). Hyperventilation has also been shown to be the second most common cause of decreased jugular venous bulb oximetry (SjvO 2 ), a measurement analogous to mixed venous oximetry (SvO 2 ) (32).
Sedation The goal of sedative therapy in patients with TBI is to prevent secondary neuronal damage due to increases in ICP or inadequate CPP. Additionally, sedatives must not interfere with performance of a clinical neurological examination (33). Selection of drug therapy in this population is challenging as there is no one agent that is considered ideal. Propofol is a sedative-hypnotic agent that has a favorable
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pharmacokinetic profile and beneficial effects on cerebral metabolic rate, making it an effective drug for routine sedation as well as controlling intracranial hypertension following brain injury. Its short half-life not only allows for ease of titration, but also for rapid awakening when neurological evaluation is necessary. Propofol is eliminated by hepatic conjugation to inactive metabolites and its pharmacokinetics are not altered in the presence of renal or hepatic disease. Its beneficial effects on the cerebrovasculature are mediated via dose-dependant decreases in cerebral blood flow and metabolic rate (34).
Although propofol is an effective sedative in the neurotrauma population, consideration must be given to several adverse effects. First, due to potent respiratory depressant effects, patients must be mechanically ventilated prior to administration. Second, cardiovascular depressant effects occur due to reductions in preload, contractility, and systemic vascular resistance, which result in a decreased mean arterial pressure. This, in turn, can lead to a decreased CPP. Finally, reports have documented the development of a fatal syndrome associated with high-dose propofol infusion that is characterized by metabolic acidosis, rhabdomyolysis, and refractory arrhythmias. This syndrome appears to be both dose and duration dependant. Although the etiology remains unclear, consideration must be given to the lipid vehicle as well as the calcium-channel and beta-blocking properties of propofol as contributors to these adverse effects. The largest series describing propofol infusion syndrome reports that it occurs at doses greater than 83 mcg/kg/minute for greater than 24 hours (35). This is well above the usual clinical dose, even for TBI. High-dose propofol should, therefore, be utilized with caution. Due to limited information on this syndrome in adults, a heightened awareness and consistent approach to monitoring is necessary.
CT Scan CT scan abnormalities are infrequently found in patients with minor head injuries (GCS = 15) and a loss of consciousness (6-9%). However, in patients with TBI (GCS ≤ 8) they are much more common (68- 94%) (23,26). The absence of abnormalities on CT scan at admission does not preclude the occurrence of raised ICP and significant new lesions may develop in 40% of patients (23). The presence on CT scan of one or more of the following has been associated with an 84-100% chance of having an unfavorable outcome: compressed cisterns, midline shift > 5mm, multiple unilateral or bilateral contusions, and extracerebral hematoma with swelling (23,26).
Persistent intracranial hypertension (ICP > 20 mmHg) Shiozaki et al. in a prospective, randomized trial, identified a select group of patients (severe TBI with GCS ≤ 8 and persistent ICP > 20 mmHg) that had a statistically significant improvement in mortality with mild hypothermia (34°C to 35°C) when compared to normothermia. The mortality rate for the hypothermic group compared to the normothermic group was 31% and 71% respectively (p<0.05) (36). As a result, mild hypothermia may be considered in patients with ICP > 20 mmHg refractory to other interventions. Pentobarbital is similarly not recommended except for refractory elevations in ICP > 20 mmHg.
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- Gharjar JB, Hariri RJ, Patterson RH. Improved outcome from traumatic coma using only ventricular CSF drainage for ICP control. Advances in Neurosurg. 1993; 21:173-7.
- Smith HP, Kelly DL, McWhorter JM, et.al. Comparison of mannitol regimens in patients with severe head injury undergoing intracranial pressure monitoring. J Neurosurg. 1986; 65:820-4.
- Juul N, Morris GF, Marshall SB, et.al. Intracranial hypertension and cerebral perfusion pressure: influence on neurological deterioration and outcome in severe head injury. The Executive Committee of the International Selfotel Trial. J Neurosurg. 2000; 92(1):106.
- Robertson CS, Valadka AB, Hannay HJ, et.al. Prevention of secondary ischemic insults after severe head injury. Crit Care Med. 1999; 27:2086-95.
- Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris, OA, et al. IX. Cerebral perfusion thresholds. J Neurotrauma 2007; 24:S59-S64.
- Muizelaar JP, Marmarou A, Ward JD, et.al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg. 1991; 75:731-9.
- Rhoney DH. Neurotrauma. Pharmacotherapy Self-Assessment Program, Book 6, Critical Care/Urgent Care. 4 th^ Ed. American College of Clinical Pharmacy. 2002; pp 181-224.
- Propofol monograph. Micromedex. [Accessed 17-Apr-2008].
- Cremer OL, Moons KGM, Bouman EAC, et.al. Long-term propofol infusion and cardiac failure in adult head-injured patients. Lancet. 2001; 357:117-8.
- Shiozaki T, Hayakata T, Taneda M, et.al. A multicenter prospective randomized controlled trial of the efficacy of mild hypothermia for severely head injured patients with low intracranial pressure. Mild Hypothermia Study Group in Japan. J Neurosurg. 2001; 94(1):50-4.
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BRAIN INJURY RESUSCITATION ALGORITHM
Significant seizure risk?
Initiate fosphenytoin IV 15-20 mg/kg, followed by fosphenytoin IV 5 mg/kg/day divided q 8 hrs (round doses to nearest 25 mg)
Yes
No
No
Moderate-Severe Brain Injury (GCS <12)
Discontinue antionvulsant therapy after 7 days if no seizure activity or pre-existing seizure history
Elevate head of bed 30 degrees at all times
Na < 150, Osm < 320? Yes
Utilize normal saline / normal saline with sodium acetate for maintenance IV fluid
Until cleared, place bed in 30 degrees Reverse Trendelenberg
Cervical, thoracic, lumbar spine cleared?
Yes
Yes
Ensure adequate airway. Avoid hypoxia and maintain normocarbia. Maintain normothermia. Maintain MAP 70-80 mmHg. Avoid systemic hypoperfusion. Consider central venous access. Initiate “Stress Ulcer Prophylaxis”, “Deep Venous Thrombosis Prophylaxis” guidelines Initiate appropriate sedation using propofol (if intubated) & analgesia using fentanyl
Administer 7.5% hypertonic saline 250 mL IV bolus x 1 (alternative: 4 mL/kg)
Is patient hypotensive?
No No
ICP > 20? Yes
CPP < 60?
Initiate Pentobarbital. Titrate to suppress bursts to 3-5/min. Support cardiac function.
Transfer to EEG-capable room. Place EEG monitor. Place right heart catheter.
Start norepinephrine infusion. Titrate to maintain CPP 50-70 mmHg
Sustained ICP > 20? Yes
Mannitol 0.25 gm/kg IV q 6 hrs (round doses to nearest 12.5 gms) Check serum Na, Osm q 6 hrs.
No
Consider high-dose propofol (>50 mcg/kg/min) (See High-Dose Propofol Infusion Guideline)
Yes
GCS < 8? Yes
No
No
Consider decompressive craniectomy
Acute neuro changes present?
Notify ICU Attending. Notify Neurosurgery. Consider Head CT if patient stable
Yes
Consider placing ICP monitor if clinically appropriate
Administer 3% normal saline at 20 mL/hr, consider mannitol for isovolemic dehydration
No
No
