Abstract

This article reviews issues related to traumatic brain injuries.

Epidemiology

• Approximately 1.6 million head injuries occur every year in the U.S.

• Nearly 60,000 deaths from TBI yearly

• Accounts for ~50% of deaths from trauma

• Financial burden: $100 billion annually

• Mortality: 25-35%

• Primary contributing factors: MVA, Falls, Alcohol

Pathophysiology:

Primary brain injury:

Focal: cerebral contusions, hematomas, fractures Diffuse axonal injury:shearing/inertial forces

Secondary brain injury:

Due to neuronal damage from systemic physiologic tesponses to the initial injury Hypotension, hypoxia

Cerebrovascular Regulation:

Monroe-Kellie doctrine:

The cranial vault is a fixed space consisting of 3 compartments: Parenchyma (80%) CSF (10%) Blood (10%)

Therefore, expansion of one compartment results in a compensatory decrease in another in order to maintain ICP

Cerebral Blood Flow is determined by:

CPP PaO2 PaCO2 Cerebral metabolic demand

Normal CBF: 50 ml/min/100g of brain tissue or 60-160 mm Hg)

Autoregulation: CBF is maintained over a wide range of CPP; between 50-150 mm Hg, by autoregulation of cerebral vasculature, but becomes deranged with brain injury (CBF becomes linearly dependent on MAP)

Effects of BP, PaO2, and PaCO2 on CBF:

Decreased paO2/CaO2: ⇑ CBF Cerebral vasodilation ⇑ cerebral blood volume ⇑ICP

Increased paCO2: ⇑ CBF Cerebral vasodilation

CPP = MAP - ICP Normal: 70-100 mm Hg Used to assess the adequacy of cerebral perfusion because CBF is Difficult to measure clinically

Evolution of CBF after TBI: Initial hypoperfusion phase Hyperemia (increased CBF) Second hypoperfusion phase (cerebral vasospasm) Recovery phase (CBF ~ CMRO2) Begins 2-3 weeks after onset Continues for weeks, months

ICP: Reflects the volume of: Brain parenchyma CSF Intravascular blood

Normal: < 15 mm Hg

CBV + CSF + Parenchyma

Ischemia Hydrocephalus Edema Acidosis comm.vs.noncom. Ischemia ⇑ paCO2` (cytotoxic) Hyperthermia Vasogenic ⇑ venous P (impaired BBB)

Clinical signs of elevated ICP:

• Depressed level of consciousness

• Hypertension

• +/- Bradycardia

• Irregular respiratory pattern

• Headache

• Nausea/Vomiting

• Papilledema

• Third or Sixth CN palsies

Initial Management and Resuscitation:

Primary survey (ABCDE's)

Monitor hemodynamic and oxygenation status Avoid or immediately correct: Hypotension (SBP < 90 mm Hg) Hypoxia (paO2 < 60, O2 Saturation < 90%) Maintain MAP > 90 mm Hg to allow CPP > 70 mm Hg

Secondary survey (AMPLE hx)

Neurological reevaluation: GCS (pre- & postresuscitation scores important)

Eye opening

• Spontaneous 4

• Voice 3

• Pain 2

• None 1

Best verbal response

• Oriented 5

• Confused 4

• Inappr. Words 3

• Incompr. Sounds 2

• None 1

Best Motor response

• Obeys commands 6

• Localizes pain 5

• Withdraws to pain 4

• Flexion 3

• Extension 2

• None 1

• GCS Severity of TBI

• 13 -15 Mild

• 9 - 12 Moderate

• 3 -8 Severe

• Pupillary light reaction

• Oculoocephalics (Doll's eyes)

• Oculovestibulars (Caloric)

Management of TBI:

General Principles: CT of head & Neurosurgical evaluation

1. Patient positioning: HOB > 30 degrees Cervical collar Head midline 2. Fluid management: NS, LR 3. Fever management 4. Stress ulcer prophylaxis 5. DVT prophylaxis 6. Monitor electrolytes (Na, Mg)

Management of Intracranial Hypertension:

Airway Management:

Intubation-Indications: Respiratory distress Motor posturing/Absence of response to pain Hypoxia/Hypercapnia GCS < 8 Seizures Increased ICP Need for analgesics/sedatives Significant associated injuries

Rapid sequence intubation recommended: Preparation Preoxygenation Pretreatment (LOAD) Paralysis AFTER induction Protection + Positioning Placement with proof Post Intubation management

Treatment of Elevated ICP:

Reduction of Cerebral Blood Volume:

Avoid hypoxia or hypercarbia Hyperventilation - no longer used in the modern era

In the absence of increased ICP, chronic prolonged Hyperventilation therapy (paCO2 < 25) should be avoided after severe TBI.

Guideline:

The use of prophylactic hyperventilation (PaCO2 <35) therapy during the first 24 hours after severe TBI should be avoided due to concerns of compromising cerebral perfusion at a time when CBF is reduced.

Options:

Hyperventilation therapy may be necessary for brief periods when there is an acute neurological deterioration or for longer periods if there is ICH refractory to sedation, paralysis, CSF drainage, & osmotic diuretics. Jugular venous oxygen saturation, arterial-jugular venous O2 content differences & CBF monitoring may help identify cerebral ischemia if hyperventilation resulting in a PaCO2 < 30 is necessary.

Promote venous drainage (elevate HOB) Treat severe hypertension Medications

Barbiturate Coma:

Guideline: High dose barbiturate therapy may be considered in HD stable salvageable SHI patients with ICH refractory to maximal medical and surgical interventions Pentobarbital: Eisenberg RCT: Loading dose: 10 mg/kg over 30 minutes 5 mg/kg q 1 hour x 3 Maintenance: 1 mg/kg/hr Moniter EEG for 30-60s. burst suppression pattern

Reduction of CSF Volume:

Decrease CSF production (lasix, acetazolamide) Ventricular drainage/ICP monitoring Indications: SHI (GCS <8 after resuscitation) + abnormal CT SHI with a normal CT if >2 present at admission: Age > 40 Unilateral/bilateral motor posturing SBP <90 mm Hg Not routinely indicated in patients with mild or moderate head injury Physicians may choose to monitor ICP in conscious patients with traumatic mass lesions Initiate ICP therapy at an upper threshold of 20-25 mm Hg Published clinical experience indicates that ICP monitoring:

1. Aids in the earlier detection of intracranial mass lesions

2. Can limit the indiscriminate use of therapies to control ICP which themselves can be potentially harmful

3. Can reduce ICP by CSF drainage

4. Helps in determining prognosis

5. May improve outcome

Reduction of Brain Tissue Volume:

Administer Lasix (0.5 - 1 mg/kg IV) Osmotic therapy: Guidelines: Mannitol is effective for control of elevated ICP after SHI Effective doses range from 0.25 - 1 g/kg (Effect begins within 10-20'; peaks @ 20-60'; duration 4-6 h) (Monitor Sna, Sosm; maintain Sosm <320) (Maintain euvolemia by adequate fluid replacement) Options: Indications prior to ICP monitoring: Signs of transtentorial herniation Progressive neurological deterioration not attributable to extracranial pathology Intermittent boluses may be more effective than continuous infusion Surgical Decompression: Decompressive hemicraniectomy

Prophylactic Anticonvulsants:

Standard: The prophylactic use of Phenytoin, Carbamazepime, or Phenobarbital is NOT recommended for prevention of late post-traumatic seizures (> 7 days) Options: Anticonvulsants may be used to prevent early (<7 days) PTS in patients at high risk for seizures following head injury Risk factors include: GCS score <10 Cortical contusion Depressed skull fracture SDH, Epidural hematoma Intracerebral hematoma Penetrating head wound Seizure within 24 hours of injury Phenytoin and Carbamezipime have been shown to be effective. However, available evidence does not indicate that prevention of early PTS improves outcome following head injury.

Medical Management:

Nutritional support Patients with SHI: Hypermetabolic, hypercatabolic, hyperglycemic Altered immune function (cellular immunity) Altered gastric motility ( ICP, Dilantin, NMB) Early (within first 24h) administration of enteral nutrition blunts the hypermetabolic response after injury in critically ill patients Initial goal: 25-30 kcal/kg/day 1.5-2.0 g protein/kg/day Replace 140% of RME in nonparalyzed patients, & 100% of RME in paralyzed patients Provide at least 15% of calories as protein by the 7th post-traumatic day. Algorithm:

Change to intact protein/high nitrogen formula when TF tolerated for 3 days

Medical Complications:

CV: MI Pulmonary: PNA, Aspiration (peaks 5-10d post-trauma) ARDS Endocrine/Metabolic: SIADH, Cerebral salt wasting DI Skin: Pressure ulcers Electrolyte disturbances Hypotension PNA* Independent predictors of increased Sepsis* morbidity/mortality Coagulopathy: Peaks during the first 3 days Due to: Blood transfusion/resuscitation Brain tissue injury/destruction Medications (Sepsis) Associated with the systemic release of parenchymal tissue thromboplastin, etc. DIC ~ degree of brain injury Principles of therapy: Routinely monitor platelets, coags Maintain platelets > 100,000 Treat the underlying pathology

Prognosis and Outcome:

Extent of recovery is dependent on: Patient's age Severity of injury Type of intracranial disorder Recovery is often slow Significant disability is common Rehabilitation