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 05/08/2001
Revised 05/16/2006, 04/29/2008, 10/21/2009

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
Maintain normal body temperature. Prevent and treat hyperthermia.
Institute isovolemic dehydration with hypertonic saline solution (HSS, i.e.1.5% or 3% NaCl)
and mannitol.
Consider resuscitating hypotensive (SBP < 90 mmHg) patients with 4 ml/kg 7.5% HSS (round
to nearest 50mL size)
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
Steroids should not be used in brain injury resuscitation
Avoid systemic hypotension

Level II
The patients head of bed should be elevated to 30 at all times.
Maintain normocarbia (PaCO
2
35-45 torr)
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
Maintain cerebral perfusion pressure (CPP) within a range of 50-70 mmHg.
Institute mild hypothermia (body temperature 33-35C) for persistent intracranial hypertension
with ICP > 20 mmHg despite maximum medical management including barbiturate therapy

Level III
Adequate sedation using short-acting agents such as propofol may be instituted
When ICP exceeds 20 mmHg, maintain PaCO
2
between 30 and 35 torr
Consider pentobarbital coma for intractable intracranial hypertension (ICP > 20 mmHg)
In patients < 18 years old, decompressive craniectomy should be considered for intractable
intracranial hypertension unresponsive to medical management
2 Approved 05/08/2001
Revised 05/16/2006, 04/29/2008, 10/21/2009
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
patients 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 (33C) 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 33C 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:
1) the use of HSS was safe; there were no cases of intracranial bleeding or central pontine myelinolysis in
3 Approved 05/08/2001
Revised 05/16/2006, 04/29/2008, 10/21/2009
106 patients tested; 2) hypotensive trauma patients with a GCS 8 had significant improvement in
survival to discharge with HSS as compared with NS or LR; and 3) dextran had no additional benefit of
HSS alone (6-9).

Animal studies that initially evaluated the efficacy of HSS used a fixed dose of 4-6 mL/kg (10). Anderson
et al. found that 4 mL/kg reduced requirements for subsequent fluid resuscitation when used as an initial
treatment for sheep in hemorrhagic shock (11). In clinical human trials, a 250 mL bolus is a standardized
dose for 4 mL/kg based on an estimated body weight. However, a 2008 retrospective review of 30
patients at ORMC with TBI who received hypertonic saline revealed that 250 mL of 7.5% HSS yielded a
mean dose of 3 mL/kg, due to a mean patient weight of 86 kg. Based on this information, doses should
be calculated based 4 mL/kg actual body weight and rounded to the nearest 50 mL dose (Example: 85kg
patient = 350 mL dose).

Mannitol
Mannitol at a dose of 0.25-1 g/kg body weight has been shown to be effective for control of raised
intracranial pressure in TBI patients. The BTF guidelines recommend that mannitol not be used without
ICP monitoring unless the patient demonstrates signs of transtentorial herniation or progressive
neurologic deterioration. In a 1985 retrospective analysis by Mendelow et al. mannitol improved MAP,
CPP, and cerebral blood flow, and lowered ICP (12). In 2007 Sakowitz et al. studied the effects of a 0.5
g/kg bolus of mannitol on ICP in six male TBI patients (GCS <9) with an ICP exceeding 20 mm Hg.
Mannitol was administered in 14 instances of elevated ICP, and it successfully reduced ICP in all cases.
Maximal effect was seen 40 minutes after the start of the 20 minute infusion, and effects lasted up to 100
minutes (13).

Francony et al. reported in 2008 a comparison of equimolar doses of mannitol and 7.45% HSS in
increased ICP in 20 patients, 17 of which had TBI. Patients were stable (including a MAP > 80 mmHg)
with a sustained ICP of > 20 mmHg for 10 minutes or greater. Both groups had a significant reduction of
ICP. Only the mannitol group had a significant increase in CPP. Changes in serum sodium, chloride and
osmolality were not different between the two groups. The authors concluded that both mannitol and HSS
exhibit comparable effectiveness in reducing ICP in stable patients. Factors such as serum sodium and
systemic and brain hemodynamics should be considered in the choice between the two. HSS can be
recommended in patients who are hypotensive (MAP <80 mmHg), hypovolemic or hyponatremic (14).

Post-traumatic seizure prophylaxis
Several studies have shown that TBI patients with no history of seizure disorder or witnessed post-
traumatic seizure activity are still at increased risk of developing post-traumatic seizures if they have one
or more of the following risk factors: GCS <10, cortical contusion, depressed skull fracture, EDH, SDH,
intracerebral hematoma, penetrating head wound, or seizure within 24 hours of injury (15). In these
patients, seizure prophylaxis reduces the risk of seizures in the early period (up to 7 days after injury), but
does not alter late seizure occurrence (beyond 7 days). Thus, seizure prophylaxis should be discontinued
after 7 days in the absence of seizure activity (16).

Steroids
Multiple prospective, randomized studies have demonstrated no benefit to ICP lowering or improvement
in outcome with the use of steroids in TBI patients (17-19). The Brain Trauma Foundation (BTF)
recommends against the use of steroids as the standard of care for all TBI patients.

ICP Monitors
The BTF recommends the use of ICP monitors as a guideline and not a standard of care (20). No
prospective, randomized study exists comparing ICP monitoring with intervention for intracranial
hypertension vs. no ICP monitoring in TBI patients with GCS 8. Studies supporting ICP monitoring for
TBI patients are as follows. In 1982, Narayan et al. published a sentinel study evaluating 207 TBI patients
with ICP monitors with the following conclusions: 1) elevation of IP at any stage was associated with
poorer outcome; 2) patients with persistently elevated ICP refractory to therapy almost always died; 3)
comatose patients with an abnormal CT scan had a 53%-63% incidence of ICH, while patients with a
normal CT scan at admission had a 13% incidence of ICP elevation; and 4) ICP monitors are associated
4 Approved 05/08/2001
Revised 05/16/2006, 04/29/2008, 10/21/2009
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
5 Approved 05/08/2001
Revised 05/16/2006, 04/29/2008, 10/21/2009
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 (34C to 35C) 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.


6 Approved 05/08/2001
Revised 05/16/2006, 04/29/2008, 10/21/2009
REFERENCES
1. McKinley B, Pramley C, Tonnesin A. Standardized management of intracranial pressure: a
preliminary clinical trial. J Trauma. 1999; 46:271-9.
2. Feldman Z, Kanter M, Robertson c, et.al. Effect of head elevation on intracranial pressure, cerebral
perfusion pressure, and cerebral blood flow in head injured patients. J Neurosurg. 1992; 76(2):207-
11.
3. Clifton GL, Miller ER, Choi SC, et.al. Lack of effect of induction of hypothermia after acute brain
injury. N Engl J Med. 2001; 344:556-63.
4. Alderson P, Gadkary C, Signorini DF. Therapeutic hypothermia of head injury. Cochrane Database
Syst Rev. 2004 Oct 18;(4).
5. Wade C, Grady J, Kramer G, et.al. Individual patient cohort analysis of the efficacy of hypertonic
saline/dextran in patients with traumatic brain injury and hypotension. J Trauma. 1997;42(Suppl):S61-
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6. Vasser MJ, Perry CA, Gannaway WL, et.al. 7.5% sodium chloride/dextran for resuscitation of trauma
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8. Vasser MJ, Fischer RP, OBrien PE, et.al. A multicenter trial for resuscitation of injured patients with
7.5% sodium chloride. The effect of added dextran 70. The Multicenter Group for the Study of
Hypertonic Saline in Trauma Patients. Arch Surg. 1993; 128:1003-13.
9. Doyle JA, Davis DP, Hoyt DB, et.al. The use of hypertonic saline in the treatment of traumatic brain
injury. J Trauma. 2001; 50(2):367-83.
10. Kramer GC. Hypertonic resuscitation: Physiologic mechanisms and recommendations for trauma
care. J Trauma. 2003; 54:S89-S99.
11. Anderson JT, Wisner DH, Sullivan PE, et.al. Initial small-volume hypertonic resuscitation of shock and
brain injury: short- and long-term effects. J Trauma. 1997; 42:592-601.
12. Mendellow AD, Teasdale GM, Russell T, et.al. Effect of mannitol on cerebral blood flow and cerebral
perfusion pressure in human head injury. J Neurosurg. 1985; 63:43-48.
13. Sakowitz OW, Stover JF, Sarrafzadeh AS, et.al. Effects of mannitol bolus administration on
intracranial pressure, cerebral extracellular metabolites, and tissue oxygenation in severely head-
injured patients. J Trauma. 2007; 62:292-298.
14. Francony G, Fauvage B, Falcon D, et.al. Equimolar doses of mannitol and hypertonic saline in the
treatment of increased intracranial pressure. Crit Care Med. 2008; 36:795-800.
15. Yablon SA. Post-traumatic seizures. Arch Phys Med Rehabil. 1993; 74:983-1001.
16. Temkin N, Dikmen S, Wilensky A, et.al. A randomized, double blind study of phenytoin for the
prevention of post-traumatic seizures. N Engl J Med. 1990; 323:499-502.
17. Braakman R, Schouten HA, Blaauw-van DM, et.al. Megadose steroids in severe head injury. J
Neurosurg. 1983; 58:326-30.
18. Dearden NM, Gibson JS, McDowell DG, et.al. Effect of high-dose dexamethasone on outcome from
severe head injury. J Neurosurg. 1986; 64:81-8.
19. Marshall LF, Maas AL, Marshall SB, et.al. A multicenter trial on the efficacy of using tirilazad mesylate
in cases of head injury. J Neurosurg. 1998; 89:519-25.
20. Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris, OA, et al. VI. Indications for
intracranial presure monitoring. J Neurotrauma 2007; 24:S37-S44.
21. Narayan RK, Kishore PR, Becker DP, et.al. Intracranial pressure: to monitor or not to monitor? A
review of our experience with severe head injury. J Neurosurg. 1982; 56:650-9.
22. Eisenberg HM, Frankowski RF, Constant CF, et.al. High-dose barbiturates control elevated
intracranial pressure in patients with severe head injury. J Neurosurg. 1988; 69:15-23.
23. Lobato RD, Sarabia R, Rivas JJ, et.al. Normal CT scans in severe head injury. J Neurosurg. 1986;
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24. Gopinath SP, Contant CF, Robertson CS, et.al. Critical thresholds for physiological parameters
inpatients with severe head injury. Congress of Neurological Surgeons, Vancouver, BC. 1993.
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patients with severe head trauma. J Neurosurg. 1991; 75:S59-S66.
26. Marshall LF, Gautille T, Klauber MR, et.al. The outcome of severe closed head injury. J Neurosurg.
1991; 75:S28-S36.
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27. 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.
28. 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.
29. Juul N, Morris GF, Marshall SB, et.al. Intracranial hypertension and cerebral perfusion pressure:
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30. Robertson CS, Valadka AB, Hannay HJ, et.al. Prevention of secondary ischemic insults after severe
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31. Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris, OA, et al. IX. Cerebral
perfusion thresholds. J Neurotrauma 2007; 24:S59-S64.
32. 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.
33. Rhoney DH. Neurotrauma. Pharmacotherapy Self-Assessment Program, Book 6, Critical Care/Urgent
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34. Propofol monograph. Micromedex. [Accessed 17-Apr-2008].
35. Cremer OL, Moons KGM, Bouman EAC, et.al. Long-term propofol infusion and cardiac failure in adult
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8 Approved 05/08/2001
Revised 05/16/2006, 04/29/2008, 10/21/2009
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