Management of Traumatic Brain Injury (TBI)

For the purposes of this syllabus, the neurosurgical management of TBI will be addressed only as it applies to the PICU team’s ability to monitor ICP and drain CSF; the decision whether to evacuate intracranial blood or remove brain tissue is made solely by the neurosurgeon



1.      To understand the role of the ABC’s in TBI and to be able to assess the severity of head injury with GCS scoring.

2.      To understand the Monro-Kellie model (physiology of the cranial vault) and the regulation of cerebral blood flow

3.      To understand the uses and pitfalls of intracranial monitors

4.      To understand and be able to apply the correct medical therapies in TBI



Role of the Cardiopulmonary Systems in TBI

Respiratory Support – like in all other critical illnesses and traumas, the first tenant in the resuscitation of TBI involves making sure the patient has a patent airway and has effective oxygenation and ventilation.  If this is not the case, or if the patient is at risk for respiratory compromise (i.e. has a Glascow Coma Scale number of 8 or less) then he or she should be intubated and mechanically ventilated. 

It is vital that in the course of intubation, the appropriate drugs be used (for example, no ketamine should be used because it increases ICP and succinylcholine should be avoided if possible), and the patient should be well oxygenated via BMV while preparing for intubation.

Unless the patient is acutely herniating, there should be little to no hyperventilation (keep a goal CO2 ~35) as this will provide adequate blood flow to the brain (see next section)


Cardiovascular Support – it is of vital importance that the patient have an adequate vascular volume (i.e. the patient should be euvolemic) and blood pressure.   If either of these conditions are not met, the patient should be adequately fluid resuscitated and/or pressors started.  It should also be noted that shock is almost never due to head injury alone, so other sources should be sought.


Hypoxia, hypercarbia, and hypotension are associated with increased mortality rates and thus must be avoided



Physiology of TBI

            Monro-Kellie Model – this model describes the relationship of the contents in the cranial vault. The total volume of the intracranial space is made up of brain, blood, and CSF, and this volume is fixed. Each component is fairly noncompliant, so if one of them expands (i.e. cerebral swelling, bleeding, hydrocephalus, etc) the intracranial pressure (ICP) rises and can cause herniation and/or impaired perfusion.


            Cerebral Blood Flow – CBF is autoregulated locally over a broad range of perfusion pressures and is responsive to a variety of metabolic factors in addition to endogenous mediators of vascular tone (i.e. NO, endothelin, etc).  Clinically, this is most important when dealing with the effects of pCO2 and mean arterial pressure (MAP) on the injured brain.

1.      pCO2 – hypercarbia (and subsequent decreased pH) will increase CBF and hypocarbia and increased pH (via hyperventilation) will decrease CBF.  As mentioned earlier this will lower ICP by reducing the blood component in the above model.  However, because you are reducing CBF, you are also reducing the delivery of oxygen and removal of waste from the brain.

2.      MAP – this is the driving force of blood going to the brain.  This is useful when calculating cerebral perfusion pressure (CPP) which = MAP-ICP.  This number should be >70 in adults, >50-60 in children depending on age.  Low CPP (<40) has been associated with bad outcome and higher CPP has been associated with better outcome, but it is unclear whether manipulation of the MAP to get a better CPP is beneficial.


Pathophysiology of brain injury (where is the increased pressure coming from?)

1.      Primary injury (hematoma)

2.      Secondary injury (cerebral hypoxia-ischemia)

a.       Occurs at a local level; decreased perfusion and O2 delivery leads to depletion of glycogen and ATP within 10 minutes; lose ATP-dependent membrane pumps which results in cytotoxic edema

b.      If cells don’t die, they may release excitatory neurotransmitters (esp. glutamate) which may lead to increased intracellular Ca++ which can then activate enzymes involved in inflammation (phospholipases), breakdown of cell structure (proteases), generation of free radicals (kinases), and breakdown of DNA (endonucleases)



Intracranial Monitoring Devices

Intraparenchymal Device: fiberoptic catheter inserted into the parenchyma of the brain that can monitor ICP

            Advantages – accurate, reliable, low risk of infection

            Disadvantages – provide no therapeutic value  

Intraventricular Device: fluid-filled catheter inserted into a ventricle that can monitor ICP and drain CSF

Advantages – has therapeutic and diagnostic value; CSF easily obtained for appropriate studies

Disadvantages – increased risk of infection, risk of hemorrhage, technical difficulties, risk of ventricular collapse (which then makes the device ineffective)  


Therapies for Traumatic Brain Injury


The main goals of management of TBI involve lowering ICP and maintaining CPP by improving perfusion to the brain and decreasing the cellular energy requirement.  The following is an increasingly invasive and risky list of therapies for TBI.  This list only provides potential therapies and each patient should be considered individually.


1.      Must ensure adequate oxygenation, ventilation, and perfusion (ABC’s).  Intubation using rapid sequence

2.      Neck stabilization/head in neutral position elevated at 30°

3.      NPO on IVF = .9NS at maintenance with a goal of normal glucose and eletrolytes

4.      Must watch the patient’s glucose, electrolytes, urine output, urine specific gravity (as DI and SIADH can occur with TBI), serum osmoles, etc.

5.      Seizure control; patients will receive prophylactic antiepileptics

6.       Fevers need to be aggressively treated with antipyretics

7.      Gentle hyperventilation (CO2 ~35) if on mechanical ventilation


9.      Neurosurgical involvement (i.e. ICP monitoring, evacuation of blood, etc.)

10.  Drainage of CSF through an intraventricular device

11.  Mannitol (for serum osmoles < 310-320) for acute episodes of increased ICP

12.  If ICP’s are persistently high, pharmacological paralysis AFTER LEVEL OF SEDATION IS MADE ADEQUATE

13.  Manipulation of MAP to maintain higher CPP via pressors

14.  Hypertonic saline (?)

15.  Barbiturate Coma

16.  Decompressive Craniotomy

17.  Cooling techniques (?)









1.      Upon arrival to the ER, an assessment will be made by the ER staff concerning the patients’ respiratory, hemodynamic, and neurologic status.  Patients with poor gas exchange and/or hemodynamic instability will be first stabilized prior to any radiographic studies or neurosurgical interventions.


2.      If a patient has a GCS < or = to 8, endotracheal intubation using head injury precautions should be performed.  Intubation should also be considered in cases of hemodynamic instability or if a patient needs sedation for transport.  When stable, the patient should then have the appropriate studies performed. Appropriate sedation and analgesia should be used while the patient is intubated and/or transported.




3.      The goals for gas exchange should be normoxia (SaO2 > 90%, PaO2 > 60) and normocarbia (pCO2 ~ 40).  Hyperventilation to a pCO2 ~ 30-35 should only used if there are clinical signs of intracranial hypertension as manifest by signs of herniation (pupillary dilatation, motor posturing, deteriorating mental status, etc) for the first 24 hours after injury.




4.      The goal for blood pressures should be > than 5th % for age, until further physiologic parameters (i.e. CPP) can be determined. Arterial catheters and central venous catheters should be considered in patients with respiratory, hemodynamic, or neurologic instability.  See parameters at the end of this section





5.      Patients with mild (GCS 14-15) and moderate head injuries (GCS 9-13) may have their neurologic status monitored clinically, without ICP monitoring devices (this will be at the discretion of the Attending Neurosurgeon).


6.      In cases of severe head injury an ICP monitor should be placed.  Severe head injury is defined as:                                                                                                        

(a). GCS < or = 8 and an abnormal head CT scan or

(b). GCS < or = 8 and motor posturing and systemic hypotension


 Those patients with moderate TBI that will undergo anesthesia for the management of extracranial injuries should also have ICP monitoring.  Other surgical options and type of monitor used (i.e. parenchymal monitor vs. ventricular drain) will be determined by the Attending Neurosurgeon.




7.      Appropriate sedation and analgesia regimens for patients with secured airways will be determined by the PICU Attending, once the patient arrives in the PICU.  Neuromuscular blockade will only be used in the acute setting of increased ICP or for transport. Intravenous lidocaine may be given prior to noxious stimuli (ex. endotracheal tube suctioning).


8.      While in the PICU, the patient’s head will be elevated to 30o and in midline.  The patient’s temperature will be aggressively controlled with antipyretics and will be held less than 38.5o C.  Seizure prophylaxis will be administered. All patients will be given NS at a maintenance rate for the first 24-48 hours. Glucose levels will be followed and will be maintained between 80-150 when possible.


9.      Acute rises in ICP (>20) or decreased CPP (> 70 in adults, > 50 in children between 8 and 16 years of age, and > 40 in children less than 8 years of age) will be managed with sedation and/or mannitol or 3% saline.  Mannitol may only be used for a serum osmolarity < or = 320.  When using 3% saline, a serum osmolarity of 360 may be used as the cutoff. Mild hyperventilation (Pco2 = 30-35) may be used for acute rises in ICP while the osmotic agent is being obtained. EtCO2 can be used to titrate the degree of hyperventilation.



10.  If the patient’s ICP remains stable but elevated, the PICU attending will then consider the use of vasoactive drugs to improve CPP.




11.  If medical management of ICP is unsuccessful, or if the need for osmotherapy is more frequent than every 4 hours, than a ventricular drain, if not already present, should be placed.  The patient will then be placed on prophylactic antibiotics per the Neurosurgery EVD protocol.




12.   If the ICP continues to be > 20, despite sedation, osmotherapy, and ventricular drainage, and if the time since injury is > 24 hours, the patient can then be hyperventilated to a pCO2 = 30-35. End-tidal CO2 will be used to titrate this therapy


13.  If the ICP continues to be > 20, despite sedation, osmotherapy, mild hyperventilation, and ventricular drainage, the patient will then be placed in a pentobarbital coma with continuous EEG monitoring until burst suppression is achieved. Burst suppression will be defined as the presence of generalized bursts of sharp and slow waves followed by generalized amplitude suppression for 8-12 seconds. Other sedating and analgesic agents should then be discontinued.



14.  If the ICP continues to be elevated, the Attending Neurosurgeon should then consider the use of decompressive craniectomy.


15.  If ICP remains persistently high (>20), the PICU Attending should consider 3% saline infusion.





Cardiopulmonary Resuscitation: See Physiologic Parameters Below*

Intubation using Head Injury Precautions

Appropriate Sedation/Analgesia for Radiographic Studies

ICP monitor/Other Neurosurgical Intervention for Severe Head Injury

Sedation/Analgesia, Osmotherapy, Vasoactive Drugs for High ICP or Low CPP *

Ventricular Drain if Medical Therapy Unsuccessful

Mild Hyperventilation to a pCO2 = 30-35 if > 24 hrs since injury

Pentobarbital Coma for Unrelenting High ICP or Low CPP *

Consideration of Decompressive Craniectomy

Consideration of 3% Saline Infusion




Goal Physiologic Parameters:

            SaO2 > 90%, PaO2 > 60

            PCO2 ~ 40

            Mean BP > 5 % for age

            ICP < 20

            CPP:    >70 in patients 17 years of age or older

                        >50 in patients 8-16 years of age

                        >40 in patients < 8 years of age