Traumatic Brain Injury (TBI)

• Traumatic Brain Injury (TBI) and Spinal Cord Injury (SCI) are critical, time-sensitive conditions necessitating prompt evaluation, intervention, and medication.
• Prehospital providers should prioritize the reduction of secondary injuries by ensuring adequate perfusion and oxygenation, and by managing intracranial pressure (ICP).

Definition and Mechanisms of Injury

• TBI occurs when an external force disrupts normal brain function, and is classified as primary or secondary.
• Primary Injury results from direct impact, acceleration/deceleration, penetrating trauma, or blast injuries, potentially causing skull fractures, cerebral contusions, diffuse axonal injury (DAI), and penetrating brain injuries.
• Secondary Injury is caused by systemic factors such as hypoxia, hypotension, hypoglycemia, or intracranial factors like edema, ischemia, and increased ICP.
• The goal of treatment is to prevent or limit secondary brain injury.

Types of TBI

• Concussion (Mild TBI) involves temporary functional impairment, possibly with loss of consciousness, and no structural damage visible on imaging, presenting with symptoms like confusion, headache, dizziness, nausea, photophobia, and amnesia.
• Cerebral Contusion (Moderate TBI) includes brain tissue bruising, localized edema, and hemorrhage and may cause focal neurological deficits.
• Diffuse Axonal Injury (DAI) is caused by shearing forces resulting in widespread axonal damage, often leading to coma without intracranial bleeding.

Intracranial Hemorrhages

• Epidural Hematoma involves arterial bleeding with rapid onset, often with a lucid interval.
• Subdural Hematoma involves venous bleeding with slower progression, commonly seen in elderly and alcoholic patients.
• Subarachnoid Hemorrhage involves a "thunderclap" headache and meningeal irritation.
• Intracerebral Hemorrhage is deep brain bleeding, common in hypertensive patients.

Signs and Symptoms of Worsening TBI

• Altered Mental Status (AMS) is a sign of worsening TBI.
• Cushing’s Triad (Late Sign of Brain Herniation) presents as hypertension (widened pulse pressure), bradycardia, and irregular respirations (Cheyne-Stokes, Biot’s).
• Other signs include unequal pupils (anisocoria), seizures, and posturing (decorticate vs. decerebrate).

Goals of Pharmacologic Therapy in TBI

• Maintain Cerebral Perfusion Pressure (CPP), where CPP = MAP - ICP.
• Prevent Hypoxia and Hypotension, maintaining SBP >90 mmHg and SpO₂ >95%.
• Reduce Elevated ICP if suspected.
• Manage seizures, pain, and agitation.

Key Medications Used in TBI

• Oxygen (Gas): Titrate to 94-99% SpO₂; indicated for hypoxia and AMS; ensures adequate cerebral oxygenation, but avoid hyperoxia (>99%).
• Normal Saline (0.9%) or Lactated Ringer’s (LR) (Crystalloid): Administer 250-500mL boluses PRN for hypotension; expands intravascular volume, but avoid hypotonic solutions (D5W).
• Hypertonic Saline (3%) (Hyperosmolar agent): Administer 250mL IV bolus for elevated ICP; draws fluid from brain tissue, but use with caution in CHF and renal disease.
• Mannitol (Osmitrol) (Osmotic diuretic): Administer 1g/kg IV for suspected cerebral edema; reduces ICP by drawing water out of brain tissue; requires intact blood-brain barrier.
• Fentanyl (Sublimaze) (Opioid analgesic): Administer 1mcg/kg IV for pain management; short-acting with minimal hemodynamic impact, but avoid in hypotensive patients.
• Midazolam (Versed), Lorazepam (Ativan), or Diazepam (Valium) (Benzodiazepine): Administer Midazolam 2-5mg IV for seizure control; depresses CNS hyperactivity and can cause hypotension and respiratory depression.
• Ketamine (Dissociative anesthetic): Administer 1-2mg/kg IV for RSI and sedation; maintains BP but may increase ICP, and is controversial in severe TBI.
• Etomidate (Amidate) (Non-barbiturate sedative): Administer 0.3mg/kg IV for RSI induction; has minimal BP effect, but avoid in sepsis.
• Rocuronium (Zemuron) / Succinylcholine (Anectine) (Neuromuscular blocker): Administer 1mg/kg IV for RSI; causes paralysis for intubation. Succinylcholine is contraindicated in crush/burns >48h.

Pathophysiology of SCI

• SCI results from blunt or penetrating trauma to the spine.
• Primary injury involves immediate disruption of the spinal cord.
• Secondary injury includes ischemia, swelling, hemorrhage, and neurogenic shock.

Spinal Shock vs. Neurogenic Shock

• Spinal Shock is a temporary loss of reflexes and motor function below the injury, with flaccid paralysis and absent reflexes, treated with supportive care.
• Neurogenic Shock consists of a loss of sympathetic tone causing hypotension, with bradycardia, warm dry skin, and hypotension, treated with IV fluids and vasopressors (Dopamine, Norepinephrine).

Prehospital Pharmacologic Management of SCI

• Oxygen: Maintain SpO₂ >94% by titrating PRN which then supports tissue oxygenation.
• IV Fluids (NS, LR): Administer 250-500mL bolus PRN for hypotension (MAP >85mmHg); expands volume.
• Atropine: Administer 0.5mg IV, max 3mg for bradycardia; increases HR.
• Dopamine, Norepinephrine: Administer 2-20mcg/kg/min for persistent hypotension and to cause vasoconstriction.

Special Considerations for Medication Calculations

• Always convert pounds to kilograms (1kg = 2.2lb) for weight-based dosing.
• Start low and monitor response, especially for vasopressors, when titrating medications.
• Monitor for pulmonary edema when giving IV fluids and avoid fluid overload.

Summary

• For TBI, prevent hypoxia, hypotension, and increased ICP.
• For SCI, manage neurogenic shock with fluids and vasopressors.
• Medications such as oxygen, hypertonic saline, sedatives, analgesics, and vasopressors play key roles.
• Avoid worsening TBI with inappropriate induction agents during RSI.