Approach to a Child with Traumatic Brain Injury (TBI)

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Alogrithm

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classDef start fill:#1b5e20,color:#ffffff,stroke:#66bb6a;
classDef step fill:#0d47a1,color:#ffffff,stroke:#42a5f5;
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A(Pediatric TBI Protocol
Initial Assessment):::start
B1[Airway Management
Check GCS and reflexes]:::step
B2[Breathing and Circulation
Normoventilation Isotonic Fluids]:::step
B3[Neuro Assessment
NCCT Head and ICP Monitor]:::step
B4[AVOID
Steroids Hypotonics]:::alert

A --> B1
A --> B2
A --> B3
A --> B4

C1{GCS 8 or less}:::decision
B1 --> C1
C1 -->|Yes| D1[Intubate
Cerebroprotective meds]:::step
C1 -->|No| D2[Maintain Airway
Strict C-Spine Control]:::step

C2{Raised ICP Status}:::decision
B3 --> C2

T0[General Measures
Head 30 deg Sedation AEDs]:::step
T1[Tier 1 Osmotherapy
Hypertonic Saline or Mannitol]:::step
T2[Tier 2 Therapies
Barbiturate Coma]:::step
T3[Tier 3 Surgical
Decompressive Craniectomy]:::step

C2 -->|Baseline| T0
C2 -->|Tier 1| T1
C2 -->|Tier 2| T2
C2 -->|Tier 3| T3

Initial Assessment And Stabilization

Immediate priority demands rapid assessment and stabilization of airway, breathing, and circulation.
Primary goal involves preventing secondary brain injury from hypoxia and ischemia.

Airway Management

Secure airway while strictly maintaining cervical spine stabilization.
Implement cerebroprotective drug-assisted intubation to prevent reflex spike in intracranial pressure.
Administer premedications including intravenous lidocaine, thiopental, and short-acting non-depolarizing neuromuscular blocking agents.

Indications For Endotracheal Intubation

Glasgow coma scale score of 8 or less.
Rapidly declining Glasgow coma scale with drop of 3 or more.
Absent protective airway reflexes.
Apnea.
Signs of impending brain herniation.

Breathing And Ventilation

Administer supplemental oxygen immediately to treat or prevent hypoxia.
Target oxygen saturation greater than 92% and PaO2 between 80-120 mmHg.
Maintain strict normoventilation targeting PaCO2 between 35-40 mmHg.
Avoid prophylactic hyperventilation.
Reserve hyperventilation strictly as temporary rescue measure for acute signs of impending herniation.

Circulation And Hemodynamics

Maintain euvolemia and normal mean arterial pressure to ensure adequate cerebral perfusion pressure.
Utilize isotonic crystalloids such as 0.9% normal saline as fluid of choice.
Administer fluid boluses of 20 ml/kg normal saline for circulatory failure or hypotension.
Initiate vasopressors if required to target mean arterial pressure greater than 50th percentile for age.

Neurological Evaluation And Monitoring

Clinical Examination

Perform thorough neurological examination to establish baseline and detect focal deficits.
Quantify coma depth objectively utilizing modified Glasgow coma scale.
Assess pupillary size, symmetry, and reactivity to light as critical surrogate markers for brainstem function.
Identify unilateral fixed and dilated pupil as sign of impending uncal herniation.

Hemodynamic Targets And Monitoring

Calculate cerebral perfusion pressure as mean arterial pressure minus intracranial pressure.
Target minimal acceptable cerebral perfusion pressure greater than 40-50 mmHg for infants and toddlers.
Target minimal acceptable cerebral perfusion pressure greater than 50-60 mmHg for older children.

Invasive Intracranial Pressure Monitoring Indications

Severe traumatic brain injury with Glasgow coma scale 3-8 after resuscitation plus abnormal admission head CT.
Severe traumatic brain injury with normal CT accompanied by motor posturing or hypotension.

Neuroimaging

Perform non-contrast computed tomography of head as primary rapid imaging modality.
Identify surgically correctable lesions in emergency setting.
Evaluate for epidural or subdural hematomas and intraparenchymal hemorrhage.
Assess for midline shift, effacement of basilar cisterns, and loss of grey-white matter differentiation indicative of diffuse cerebral edema.

Stepwise Management Of Raised Intracranial Pressure

Escalate medical management through specific therapeutic tiers based on clinical response and intracranial pressure monitoring.

Therapeutic Tier	Interventions And Clinical Targets
General Measures	Maintain head in midline position with 30° elevation to facilitate venous drainage. Ensure cervical collar avoids obstructing venous return.
Metabolic Control	Maintain normothermia below 38°C. Treat fever aggressively with antipyretics. Maintain strict blood glucose between 80-120 mg/dL to prevent hyper- and hypoglycemic brain injury.
Sedation And Analgesia	Administer adequate sedation and analgesia to blunt noxious stimuli. Utilize endotracheal lidocaine prior to suctioning.
Seizure Prophylaxis	Administer prophylactic phenytoin or levetiracetam for 7 days. Indicated in severe traumatic brain injury, parenchymal injury, or depressed skull fractures.
Tier 1 Osmotherapy	Hypertonic Saline (3% NaCl): Preferred agent, particularly in hypovolemia. Administer 5 ml/kg bolus over 30 mins, followed by 0.5-1.5 ml/kg/hr infusion. Target serum sodium 155-160 mEq/L. Mannitol (20%): Administer 0.5-1 g/kg bolus every 4-6 hours. Avoid continuous infusions. Contraindicated in hypotension or serum osmolality greater than 320 mOsm/kg.
Tier 2 Therapies	Moderate Hyperventilation: Target PaCO2 28-34 mmHg. Reserve strictly for acute impending herniation or acute neurological deterioration. Barbiturate Coma: Initiate thiopentone or pentobarbital infusion titrated to achieve burst suppression on EEG. Requires invasive hemodynamic monitoring due to profound myocardial depression.
Tier 3 Surgical	Decompressive Craniectomy: Indicated for medically refractory intracranial hypertension with diffuse swelling on CT, or for evacuation of mass lesions.

Therapies Strictly Contraindicated

Avoid corticosteroids completely.
Corticosteroids proven to worsen outcomes with no benefit for traumatic cytotoxic edema.
Avoid hypotonic fluids strictly.
Fluids such as 5% dextrose or 0.45% saline increase free water clearance into brain, exacerbating cerebral edema.
Avoid routine prophylactic hyperventilation.
Decreasing PaCO2 routinely without signs of herniation induces severe cerebral vasoconstriction, causing secondary ischemic infarction.