Review the:› Epidemiology of head injury› Various intracranial lesions› Pathophysiology of increased ICP› Management of head injury

2 cases per 1000 children per year Mild TBI: 82% Moderate to severe TBI: 14% Fatal TBI: 5% (7000 deaths per year)

Motor vehicle accidents Falls Non-accidental trauma Sports injuries

Coup contusion › Adjacent to the site of injury › Brain accelerates against the fixed skull› Injury to parenchyma and blood vessels

Contrecoup contusion› Deceleration and recoil of the brain› Contralateral lesions

Classic: arterial origin, blood collects between skull and dura

Due to tearing of bridging veins, blood collects between dura and cortex

Disruption of small vessels on the cortex, occur along the falx, tentorium, or outer cortical surface

Axonal injury: › Etiology: deceleration and shearing forces› Axonal swelling and degeneration› CT findings:

Normal initially Delayed edema and petechial hemorrhages

› Areas affected: Basal ganglia Thalamus Deep hemispheric nuclei Corpus callosum

Cytotoxic Edema› Intracellular swelling› Due to cellular injury (DAI, hypoxia-ichemia)› Irreversible

Vasogenic Edema› Increased endothelial permeability› Therapy may prevent secondary injury› Seen with tumors, hematomas, infarcts, CNS infections

Interstitial Edema› Increased fluid in periventricular white matter› Etiology - hydrostatic CSF pressure

Intracranial Volume = Brain + CSF + Blood

Normal:› Brain 80%› CSF 10%› Blood 10%

Bleed/edema increases intracranial volume →

Compress intracranial vessels → Impairs blood flow → Ischemia

CPP = MAP – ICP› > 70 in adults› Children ????

1. Hypertension, tachycardia, and dilated pupils2. Hypotension, bradycardia, and posturing3. Hypertension, bradycardia, and dilated pupils4. Hypertension, bradycardia, and irregular

respirations5. Hypotension, tachycardia, and posturing

1. Hypertension2. Bradycardia3. Irregular respirations

Etiology:› When MAP < ICP, the hypothalamus

stimulates sympathetic output› Increase in BP stimulates carotid

baroreceptors and leads to a vagal response and bradycardia

1. 22. 33. 44. 55. 6

Eyes: Motor:› 4 opens spontaneously - 6 follows

commands› 3 opens to verbal command - 5 localizes pain› 2 opens to pain - 4 withdraws to

pain› 1 no response - 3 decorticate

Verbal: - 2 decerebrate› 5 oriented - 1 no response› 4 confused conversation› 3 inappropriate words› 2 incomprehensible sounds› 1 no response

Mild: GCS ≥ 13 Moderate: 9-12 Severe: ≤8

Battle’s sign

1. Etomidate2. Lidocaine3. Fentanyl4. Succinylcholine5. Rocuronium

Indications for intubation:› GCS ≤ 8› Hypoxia› Loss of airway

protective reflexes› Hypoventilation

Rapid sequence intubation:› C-spine stabilization› Preoxygenation› Cricoid pressure› Induction Meds:

Thiopental – ICP ( cerebral metabolic rate) (may lower BP) or

Etomidate – ICP or Benzodiazepine (may lower BP) + Opiate for analgesia for injuries/ laryngoscopy +/- Lidocaine (may blunt ICP assoc. with laryngoscopy)

› Neuromuscular blockade

1. Insertion of an ICP monitor2. 3% normal saline bolus3. Mannitol4. Hyperventilation to CO2 of 25-30

5. Therapeutic hypothermia

Try to keep CO2 normal (35-40) in patients with ICP

Risk of ischemia with hyperventilation

Hyperventilation used only for acute herniation

Maintain CPP to avoid secondary injury Hypoxemia and hypotension each occur

in 1/3 of patients 1 episode of hypotension mortality 2x Eval source of shock:

› Internal bleeding?› Spinal cord injury?

Indications:› GCS ≤ 8› Neuro exam impossible

(sedated, needs to go to OR for other injuries

Types:› Ventriculostomy most

reliable, also therapeutic› Intraparenchymal –

measurement drift› Subarachnoid, subdural,

epidural – less reliable

Head midline Head of bed to 30 degrees Promote venous drainage

Benefits:› Decrease cerebral metabolic demands

associated with pain and stress› Prevent spikes in ICP that may occur with

suctioning, etc.› Facilitate mechanical ventilation› Anticonvulsant and antiemetic actions› Prevent shivering

Benefits:› airway and intrathoracic pressure –

facilitate cerebral venous outflow› Prevent shivering and posturing› Facilitate mechanical ventilation

1. Can only be given through a central venous line

2. Does not cause hypotension3. Can only be used if serum osmolarity <

3204. Dose is 10 mL/kg5. Can only be used if serum sodium is <

160

3% normal saline› Creates osmotic gradient› Decreases ICP and increases CPP› Used as boluses and/or continuous infusion› Goal: serum sodium > 150› Max serum osm: 360 ??

Mannitol› Mechanisms:

blood viscosity creates osmotic gradient between plasma and

brain

› 0.25-1 g/kg doses› May repeat every 6-8 hours› Max serum osm: 320› Adverse effects:

ATN Hypovolemia

Ventriculostomy catheter

1. Continuous EEG monitoring should be present when a pentobarbital coma is induced

2. The hallmark of pentobarbital coma is burst suppression

3. Pentobarbital causes profound myocardial depression

4. Pentobarbital use requires the approval of a neurologist

5. Pentobarbital reduces cerebral blood flow

Consider in:› Patients with refractory intracranial

hypertension Mechanisms:

› Lowers resting cerebral metabolic rate by 50%› Decreases cerebral blood flow and cerebral

blood volume› Neuroprotective: inhibits free radical-mediated

lipid peroxidation, stabilizes membranes

Monitoring:› Burst suppression

on EEG Adverse effects:

› Myocardial depression

Avoid hyperthermia› Increase cerebral metabolism› Inflammation› Lipid peroxidation› Excitotoxicity› Seizures

Decompressive craniectomy Favorable surgical outcomes:

› Within 48hrs of injury› Secondary GCS› Herniation

Unfavorable:› Unimproved GCS of 3› Extensive secondary

brain insults

Begin by 72 hours Full replacement by 7 days Patients with injury have increased

resting metabolism expenditure Increased mortality when head injured

patients not fed within 1 week

1. Antiepileptic medications decrease the incidence of late seizures

2. Children < 2yo have a lower risk of seizures3. Most early seizures occur in the first 24 hours4. Seizures do not affect the outcome of

traumatic brain injury5. All children with traumatic brain injury should

be treated with antiepileptic medications until 1 week post-injury

Posttraumatic seizures› Early: within 7 days› Late: after 7 days

Adverse effects:› Increase brain metabolic demands› Increase ICP› Lead to secondary brain injury

Risk of seizures:› Early:

20-39% incidence in severe TBI risk if low GCS < 2 yrs have 3x greater risk Majority occur within first 24 hours

Risk of seizures› Late:

7-12% incidence in severe TBI Increased incidence in depressed skull

fracture Relation to early seizures? Prophylactic anticonvulsants do not affect

incidence