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Head Injury / Traumatic Brain Injury

Category: Trauma Sources: raw/protocols/nm-sop-guidelines-treatment-2022.pdf Last updated: 2026-04-03

Overview

Traumatic brain injury (TBI) results from mechanical forces causing primary injury (direct tissue damage at the time of trauma) and secondary injury (ongoing damage from hypoxia, hypotension, hyperventilation, and elevated intracranial pressure). The EMT-B cannot reverse primary injury, but CAN prevent secondary injury by maintaining oxygenation and blood pressure above critical thresholds.

The two priorities in TBI: prevent hypoxia (SpO2 ≥94%) and prevent hypotension (SBP ≥110 in adults). Every episode of hypoxia or hypotension in TBI patients doubles mortality.

Concept Link

The airway and breathing priorities that drive TBI secondary injury prevention are the same reason primary-assessment puts A before B before C. The time-to-death rationale there applies here: even a brief period of apnea or obstruction during transport causes the hypoxic secondary injury described above.

Why Hypoxia and Hypotension Are the Killers

Primary vs. Secondary Injury

When the skull decelerates against a dashboard or the brain shears against a bony ridge, the damage that happens at that moment is called primary injury — the direct mechanical destruction of neurons, axons, and blood vessels. This is fixed at the instant of impact. No intervention in the field, the ED, or the ICU can undo it.

What kills or permanently disables TBI patients is frequently not the primary injury — it is secondary injury: the cascade of physiological insults that destroy brain tissue that was injured but still viable at the time of impact. The EMT-B cannot reverse primary injury. The EMT-B can absolutely prevent secondary injury. This is the entire basis of TBI prehospital care.

Mechanism of Hypoxia as a Killer

The brain is the highest-oxygen-demand organ in the body. At baseline, the brain consumes approximately 20% of total body oxygen despite being only 2% of body weight. When a TBI disrupts normal cerebral regulation, this demand increases further — injured neurons are metabolically stressed and require even more oxygen to maintain membrane function.

When SpO2 drops, oxygen delivery to the brain falls. In the injured brain, the consequence is cerebral ischemia layered on top of the primary injury. The neurons that survived the initial impact but were functionally impaired begin to die. This is additive damage — the patient's outcome is now determined by both the primary injury AND the hypoxic insult.

Even brief episodes of hypoxia matter. Studies of severe TBI patients consistently show that a single episode of SpO2 <90% is associated with a doubling of mortality and significantly worse neurological outcomes in survivors. The threshold in NM protocol is SpO2 ≥94% — above the danger zone by a margin, because field conditions (transport, movement, airway manipulation) can cause transient drops.

Mechanism of Hypotension as a Killer

The brain depends on continuous blood flow. Cerebral perfusion pressure (CPP) is the driving force of that flow:

CPP = MAP − ICP

Where MAP is mean arterial pressure and ICP is intracranial pressure.

In a healthy brain, ICP is roughly 10–15 mmHg. A moderate MAP of 80 mmHg gives a CPP of ~65–70 mmHg — well above the ~50 mmHg threshold below which cerebral autoregulation begins to fail.

In a significant TBI, ICP rises. Edema, hemorrhage, and vascular reactivity dysregulation all push ICP up. ICP of 30–40 mmHg is not unusual in severe TBI. Now the same MAP of 80 mmHg yields a CPP of only 40–50 mmHg — below the threshold needed for adequate brain perfusion.

Add hypotension: if SBP falls to 90 mmHg, MAP falls to approximately 70 mmHg. With ICP at 35 mmHg, CPP = 70 − 35 = 35 mmHg. The brain is no longer being adequately perfused. Neurons that survived the primary injury begin to die from ischemia.

This is why the NM protocol threshold for TBI fluid resuscitation is SBP ≥110 mmHg — not 90. The extra pressure margin exists to maintain CPP in the face of elevated ICP that the prehospital provider cannot measure or control.

The Numbers Are Not Arbitrary

  • SpO2 ≥94% — the floor below which hypoxic secondary injury accelerates
  • SpO2 <90% — threshold at which studies document doubled TBI mortality; a single episode at this level changes outcomes
  • SBP ≥110 mmHg — sufficient MAP to maintain CPP above ischemic threshold in the presence of elevated ICP
  • SBP <90 mmHg — the point at which CPP almost certainly falls below adequate perfusion in any patient with significant TBI; also associated with doubled mortality in the literature

What it costs the patient: A single episode of SpO2 <90% lasting even a few minutes — caused by a mispositioned airway adjunct, a vomiting event not recognized in time, or oxygen running low in the unit — can permanently worsen a patient's neurological outcome independent of anything that happened at the scene of injury. The same applies to a brief period of hypotension from undertreated hemorrhage or inadequate IV fluid maintenance. These are not hypothetical risks. They are the primary mechanism of preventable death and disability in TBI patients.

The prehospital provider who maintains oxygenation and blood pressure throughout transport is doing more for this patient's brain than anything that will happen in the first hour after hospital arrival.

Key Points

  • Herniation syndrome: rising ICP compresses the brainstem — presents as Cushing's triad (bradycardia + hypertension + irregular respirations), unilateral or bilateral fixed dilated pupils, posturing (decerebrate/decorticate), deteriorating LOC
  • Herniation is the true emergency — do NOT hyperventilate routinely; ONLY hyperventilate for herniation signs (GCS ≤8, signs of herniation) to temporarily lower ICP
  • Normal ventilation target: EtCO2 35–40 mmHg
  • Herniation ventilation target: EtCO2 30–35 mmHg — ONLY as a short-term bridge
  • glasgow-coma-scale (GCS): Eyes (1–4) + Verbal (1–5) + Motor (1–6); total 3–15; GCS ≤8 = severe TBI — always document as breakdown (E/V/M), not just total
  • Scalp wounds bleed profusely but skull fractures with brain involvement should NOT have direct pressure applied with deep probing
  • Assume c-spine injury with any significant head injury

Assessment Relevance

History (history-taking): - MOI: MVC, fall, assault, penetrating injury; velocity and force involved - Time of injury and whether LOC occurred; duration of LOC if present - Amnesia (retrograde = before impact; anterograde = after) - Vomiting since injury (post-concussive sign) - Medications: anticoagulants (warfarin, NOACs) increase intracranial hemorrhage risk significantly - Prior head injuries

Physical exam (secondary-assessment): - GCS: Eyes, Verbal, Motor — document and trend - Pupils: size (normal 3–5mm), equality, reactivity — unilateral fixed/dilated = herniation on same side; bilateral = severe brainstem involvement - Cushing's triad: bradycardia + hypertension + irregular respirations = herniation emergency - Focal neurologic deficits - HEENT: Battle's sign (bruising behind ear — delayed, 24–48h), raccoon eyes (periorbital bruising — delayed), CSF from ears/nose (basilar skull fracture) - Scalp wounds: bleeding severity does NOT correlate with brain injury severity - SpO2 continuously: prevent any desaturation <90% - BP: maintain SBP ≥110 in adults with moderate/severe TBI

Procedures

  1. Scene size-up (scene-size-up): MOI (high-speed MVC, fall from height); resource request; c-spine consideration
  2. Primary assessment (primary-assessment): airway (open and patent?), breathing (rate and adequacy), circulation (hemorrhage control, BP)
  3. Maintain c-spine stabilization throughout — spinal-immobilization-supine
  4. Oxygen: maintain SpO2 ≥94% — see oxygen-administration; avoid desaturation <90%
  5. Wound care: control scalp bleeding with direct pressure (without probing); moist sterile dressing over potential open skull wound — do NOT apply pressure over suspected skull fracture with brain involvement
  6. Assess and document GCS on scene
  7. Minimize scene time (<10 minutes); transport to appropriate trauma center
  8. En route: IV/IO access; maintain SBP ≥110 (ALS scope)
  9. If severe TBI with herniation signs: controlled ventilation at EtCO2 30–35 mmHg (ALS scope; EMT-B manually ventilates at slightly increased rate as directed by protocol)
  10. Reassessment every 5 minutes (reassessment): trend GCS, pupils, vital signs
  11. Elevate head of bed 30 degrees for severe TBI (reduces ICP without compromising BP)

NM Protocol Notes

From NM EMS Treatment Guidelines (2022):

EMT-B scope: - Maintain cervical stabilization throughout - Oxygen: prevent desaturation <90%; maintain SpO2 ≥94% with supplemental O2 as needed - If unable to maintain airway: advanced airway (follow Respiratory Arrest/Distress Guidelines); 1 breath every 6 seconds - Nasal airways and nasal intubation should NOT be used in severe facial trauma

Breathing management: - Moderate/severe TBI: Continuous waveform capnography and EtCO2 if available; target EtCO2 35–40 mmHg (normal ventilation) - Severe TBI with herniation signs (GCS ≤8 or Unresponsive on AVPU): Hyperventilate to target EtCO2 30–35 mmHg — short-term option ONLY for herniation signs

Circulation — fluid resuscitation targets: - Moderate/severe closed head injury: - Adults (>10 years): maintain SBP ≥110 mmHg - Pediatric <1 month: SBP >60; 1–12 months: >70; 1–10 years: >70 + (2 × age in years) - IV/IO isotonic solution en route to maintain above targets; consider second IV/IO - Wound care: direct pressure for scalp bleeding (no suspected open skull); moist sterile dressing for potential open skull wound

Disability: - Evaluate blood glucose if indicated - Perform and trend GCS (moderate/severe: GCS ≤13 or P/U on AVPU) - Early signs of deterioration: confusion, agitation, drowsiness, vomiting, severe headache - Monitor for herniation signs - Elevate head of bed 30 degrees for severe head injury

Monitoring: - Continuous pulse oximetry - Frequent BP measurement - Initial and serial neuro assessment (reassess with any change in mentation) - Continuous waveform ETCO2 if available for moderate/severe

Transport: Transport as soon as possible to appropriate facility; consider ALS

See glasgow-coma-scale for full scoring tables, trending guidance, and common mistakes.

NREMT Relevance

High-priority NREMT topic: - GCS components and scoring — know each component - GCS ≤8 = severe TBI; requires airway consideration - Cushing's triad: bradycardia + hypertension + irregular respirations = herniation - Hyperventilation: ONLY for herniation signs; NOT routine; excessive hyperventilation causes worse outcomes - Prevent hypoxia (SpO2 ≥94%) and hypotension (SBP ≥110 adults) — secondary injury prevention - Anticoagulant medications: greatly increase risk of intracranial hemorrhage; document in hand-off - Battle's sign and raccoon eyes: delayed basilar skull fracture signs; not seen acutely

Sources

  • raw/protocols/nm-sop-guidelines-treatment-2022.pdf — Head Injury/TBI protocol (p. 74–75)