8.4 Traumatic Brain Injury, Burns & Wound Management

Traumatic Brain Injury: Primary vs. Secondary Insult

Traumatic Brain Injury (TBI) is a major contributor to trauma morbidity and mortality across the Caribbean region. Neurotrauma care centers on a fundamental physiological concept: preventing secondary brain injury.

• Primary Brain Injury: Occurs at the precise moment of mechanical impact. Includes direct mechanical contusions, cortical lacerations, skull fractures, intracranial hematomas, and diffuse axonal shearing. It is irreversible by medical interventions; clinical efforts focus on prevention (e.g., helmet and seatbelt legislation).
• Secondary Brain Injury: Evolves over minutes, hours, and days following the primary insult. Driven by systemic insults (hypotension, hypoxemia, hypercapnia, hypoglycemia, hyperthermia) and intracranial cascades (cerebral edema, raised intracranial pressure, impaired autoregulation, cerebral ischemia, excitotoxicity, and free-radical generation).
• Systemic Resuscitation Goals in TBI:
  • Avoid Hypotension: A single episode of hypotension (systolic BP < 90 mmHg) doubles TBI mortality. Brain Trauma Foundation guidelines mandate maintaining systolic BP >= 100 mmHg (for patients 50-69 years) or >= 110 mmHg (for patients 15-49 or >= 70 years).
  • Avoid Hypoxemia: Maintain PaO2 >= 60 mmHg and SpO2 >= 93%. Concurrent hypotension and hypoxemia increase mortality fourfold.
  • Maintain Strict Normocapnia: Target arterial PaCO2 between 35 and 40 mmHg (4.7 to 5.3 kPa). Routine hyperventilation causes severe cerebral vasoconstriction, precipitating secondary cerebral ischemia.

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The Monro-Kellie Doctrine & Cerebral Perfusion Pressure (CPP)

The Monro-Kellie Doctrine

• The cranium is a rigid, non-distensible vault with a fixed internal volume ($V_{\text{total}} = V_{\text{brain}} + V_{\text{blood}} + V_{\text{CSF}}$).
• Because intracranial contents are non-compressible, the expansion of a new space-occupying mass (e.g., hematoma, contusional edema) must be compensated by an equal reduction in the volume of other intracranial compartments.
• Compensatory Reserve: The brain initially compensates by shunting cerebrospinal fluid (CSF) into the compliant spinal subarachnoid space and displacing low-pressure cerebral venous blood into the jugular system.
• Once compensatory reserves are exhausted, the intracranial compliance curve steepens exponentially: tiny increases in hematoma or edema volume trigger precipitous, catastrophic spikes in Intracranial Pressure (ICP).

Cerebral Perfusion Pressure (CPP) Equation

$\text{CPP} = \text{MAP} - \text{ICP}$

• Normal Values: Normal adult ICP is 5 to 15 mmHg. Pathological intracranial hypertension is defined as sustained ICP >= 20 to 22 mmHg, which demands active therapeutic intervention.
• Target CPP: Maintain CPP between 60 and 70 mmHg. If CPP drops below 50-60 mmHg, severe cerebral hypoperfusion and ischemic infarction ensue. Conversely, driving CPP > 70 mmHg with excessive vasopressors increases the risk of acute respiratory distress syndrome (ARDS) and cerebral hyperperfusion edema.

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Glasgow Coma Scale (GCS) & TBI Stratification

The Glasgow Coma Scale (GCS) Scoring System

• TBI Severity Stratification:
  • Mild TBI (GCS 13 - 15): Concussion; requires clinical decision rule assessment (Canadian CT Head Rule or New Orleans Criteria) to direct non-contrast CT imaging.
  • Moderate TBI (GCS 9 - 12): High risk of deterioration; mandates immediate non-contrast head CT and admission to a high-dependency unit.
  • Severe TBI (GCS 3 - 8): Absolute indication for immediate endotracheal intubation (RSI) with cervical spine precautions to protect the airway against aspiration and optimize ventilation.

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Intracranial Hematomas & Brain Herniation Syndromes

Extradural (Epidural) Hematoma (EDH)

• Mechanism & Anatomy: Caused by direct blunt impact to the temporal or pterion region, fracturing the thin squamous temporal bone and tearing the middle meningeal artery (or middle meningeal vein) traversing the bony groove.
• Clinical Presentation: Classically presents with a transient initial loss of consciousness, followed by a 'lucid interval' (lasting minutes to several hours) where the patient appears neurologically intact, followed by rapid neurological deterioration (unilateral dilated pupil, contralateral hemiparesis, coma).
• Non-Contrast CT Brain: Biconvex (lentiform), hyperdense extra-axial mass. Does not cross cranial suture lines because the periosteal dura is firmly attached to cranial sutures.
• Management: Obtain urgent neurosurgical assessment. Evacuate EDH > 30 cm3 and urgently treat deterioration or coma with anisocoria. Selected EDH < 30 cm3, thickness < 15 mm, midline shift < 5 mm, GCS > 8 and no focal deficit can be observed with serial CT in a neurosurgical centre.

Subdural Hematoma (SDH)

• Mechanism & Anatomy: Acceleration-deceleration shearing forces tear the cortical bridging veins traversing the subdural space to drain into the superior sagittal sinus. Highly prevalent in elderly patients and chronic alcoholics due to cerebral atrophy, which places bridging veins under continuous mechanical tension.
• Clinical Classification:
  • Acute SDH (< 72 hours): Manifests rapidly with severe coma and focal deficits; carries high mortality (50-60%).
  • Chronic SDH (> 14 days): Liquefied 'motor oil' hematoma; presents insidiously with headaches, cognitive decline, gait ataxia, or personality changes.
• Non-Contrast CT Brain: Acute SDH is usually a crescentic hyperdense collection crossing sutures, bounded by dural reflections such as the falx and tentorium. Chronic SDH is usually hypodense; rebleeding can produce mixed density.

Brain Herniation Syndromes

• Uncal (Lateral Transtentorial) Herniation: The medial temporal lobe (uncus) herniates medially and downward through the tentorial notch.
  • Compresses cranial nerve III (oculomotor): causes an ipsilateral fixed and dilated ('blown') pupil due to loss of parasympathetic pupilloconstrictor fibers.
  • Compresses the ipsilateral cerebral peduncle: produces contralateral hemiparesis / hemiplegia.
  • Kernohan's Notch Phenomenon: Occasionally, the contralateral cerebral peduncle is forced against the opposite tentorial edge, causing paradoxical ipsilateral hemiparesis.
• Cushing's Triad: Late, terminal sign of severe intracranial hypertension and imminent medullary herniation: (1) Severe hypertension with widened pulse pressure, (2) Profound bradycardia, and (3) Irregular, Cheyne-Stokes respirations.

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Medical & Surgical Management of Elevated ICP

1. First-Line Positioning & Sedation:
   • Elevate head of bed to 30 degrees with head maintained in a neutral midline position (avoids internal jugular vein compression, maximizing venous outflow).
   • Provide adequate analgesia (fentanyl) and sedation (propofol) to prevent coughing, straining, and ventilator dyssynchrony.
   • Avoid hypotonic fluids (e.g., 0.45% saline, 5% dextrose) which exacerbate cerebral edema; use 0.9% normal saline.
2. Hyperosmolar Pharmacotherapy:
   • Mannitol 20%: 0.25 to 1.0 g/kg IV bolus over 15-20 minutes. Reduces ICP via rapid plasma expansion, reduced blood viscosity, and osmotic fluid extraction from brain parenchyma into the intravascular space. Monitor serum osmolarity (hold if > 320 mOsm/L) and avoid hypovolemic hypotension.
   • Hypertonic Saline (3% NaCl): 250 mL IV bolus. Particularly advantageous in hypotensive trauma patients because it expands intravascular volume, increases MAP, and reduces ICP without inducing osmotic diuresis. Target serum sodium 145-155 mEq/L.
3. Controlled Ventilation: Target normocapnia (PaCO2 35-40 mmHg). Mild hyperventilation (PaCO2 30-35 mmHg) is reserved strictly as a brief emergency bridge for active uncal herniation while transferring to the operating room.
4. Surgical Decompression: Placement of an External Ventricular Drain (EVD) for therapeutic CSF drainage and ICP monitoring, or emergency decompressive craniectomy for medically refractory intracranial hypertension.

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Burn Management: TBSA, Parkland Formula & Inhalation Injury

Wallace Rule of Nines (Adult TBSA Estimation)

• Head and neck: 9%
• Anterior trunk: 18% (chest 9%, abdomen 9%)
• Posterior trunk: 18% (upper back 9%, lower back/buttocks 9%)
• Each upper extremity: 9% (anterior 4.5%, posterior 4.5% x 2 = 18%)
• Each lower extremity: 18% (anterior 9%, posterior 9% x 2 = 36%)
• Perineum and genitalia: 1%
• The patient's palmar surface (including fingers) represents approximately 1% TBSA (useful for estimating scattered burns).
• Critical Clinical Rule: First-degree burns (superficial erythema only, no blisters, e.g., sunburn) are strictly excluded from total body surface area (TBSA) fluid calculations.

Fluid Resuscitation: The Parkland Formula

Indicated for partial-thickness and full-thickness burns involving >= 20% TBSA in adults.

$\text{Total 24-Hour Fluid (Ringer's Lactate)} = 4\text{ mL} \times \text{Body Weight (kg)} \times \%\text{TBSA}$

• Administration Schedule:
  • Administer 50% of the calculated fluid over the first 8 hours calculated from the EXACT TIME OF THE BURN INJURY (not from the time of hospital arrival).
  • Administer the remaining 50% over the subsequent 16 hours.
• Resuscitation Endpoint: Titrate IV fluid rates hourly to maintain target urine output of 0.5 mL/kg/hour in adults (30-50 mL/h) or 1.0 mL/kg/hour in children < 30 kg. In high-voltage electrical injuries with myoglobinuria, target 1.5 to 2.0 mL/kg/hour to prevent acute tubular necrosis.
• Warning (Fluid Creep): The formula is merely an initial starting point. Over-resuscitation leads to pulmonary edema, orbital compartment syndrome, and abdominal compartment syndrome.

Inhalation Injury

• Caused by thermal burns to the upper supraglottic airway and toxic smoke inhalation (carbon monoxide, hydrogen cyanide) to the lower tracheobronchial tree.
• Clinical Indicators: History of closed-space fire, facial burns, singed nasal vibrissae, carbonaceous soot in sputum, hoarseness, inspiratory stridor, and pharyngeal blistering.
• Management: Intubate early for stridor, progressive oropharyngeal edema, respiratory failure, impaired protective reflexes or other high-risk features. Stable patients with superficial facial burns or singed hair alone can be observed with repeated airway assessment. Anticipated transfer and evolving edema influence the decision.

Escharotomy Indications

• Indicated for circumferential full-thickness (3rd-degree) burns forming a rigid, leathery eschar.
• Thoracic Escharotomy: Indicated when circumferential chest wall burns restrict respiratory expansion, causing high peak airway pressures (> 35-40 cmH2O) and hypoventilation.
• Extremity Escharotomy: Indicated when circumferential limb eschar impairs vascular perfusion, leading to distal pulselessness, cyanosis, and limb compartment syndrome. Incisions are made through the eschar along mid-medial and mid-lateral lines down to subcutaneous tissue without cutting deep fascia.

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Wound Management & Tetanus Prophylaxis

Principles of Emergency Wound Care

• Perform high-pressure irrigation with sterile normal saline (using a 35-mL syringe and 19-gauge needle delivering 7-8 psi) to remove particulate contaminants and lower bacterial loads.
• Debride non-viable, devitalized tissue conservatively.
• Primary closure is indicated for clean wounds presenting < 6-8 hours from injury (up to 12-24 hours for highly vascular facial wounds). Heavily contaminated wounds or crush wounds require delayed primary closure.

Tetanus Prophylaxis Guidelines

• Tetanus-Prone Wounds Include: Puncture wounds, wounds > 6 hours old, crush injuries, avulsions, gunshot wounds, burn wounds, frostbite, and wounds contaminated with dirt, feces, or saliva.
• When administering both Tetanus Toxoid (Td/Tdap) and Human Tetanus Immunoglobulin (TIG), use separate syringes and inject into distinct anatomical sites (e.g., opposite deltoids) to prevent antigen-antibody neutralization.