4.2 Core Workflows and Decision Points

4.2 Head and Spinal Trauma

Traumatic brain injury (TBI) is divided into the primary injury (the impact itself — done before EMS arrives) and the secondary injury (ongoing damage from hypoxia, hypotension, hypoglycemia, and rising intracranial pressure (ICP)). The paramedic cannot reverse the primary injury, so the entire workflow is built around preventing secondary injury. The evidence-based EPIC/Brain Trauma Foundation 'three H bombs' to avoid are hypoxia, hypotension, and hyperventilation.

• Hypoxia: keep SpO2 >= 90% (ideally >= 94%). Even a brief desaturation increases mortality.
• Hypotension: a single episode of systolic < 90 mmHg roughly doubles mortality in severe TBI. The target systolic is >= 110 mmHg — this is exactly why permissive hypotension is contraindicated in TBI.
• Hyperventilation: blowing off CO2 causes cerebral vasoconstriction that reduces brain perfusion; routine hyperventilation worsens outcomes.

Ventilation and ETCO2

Intubated or assisted-ventilation TBI patients are ventilated to normocapnia, ETCO2 35-40 mmHg, at roughly 10 breaths/min in an adult (12 for a child, 20 for an infant). Use waveform capnography to hold that target — guessing the rate by hand is the classic cause of inadvertent hyperventilation.

The only time to deliberately hyperventilate is active herniation: blown/unequal pupil, sudden GCS drop, or posturing. Then mild hyperventilation to ETCO2 30-35 mmHg (about 20 breaths/min adult) is a temporizing measure en route, because transient vasoconstriction can briefly lower ICP. It is a bridge to definitive care, never a maintenance strategy.

Other ICP measures: elevate the head of the bed ~30 degrees if not contraindicated by spinal precautions/hypotension, keep the cervical collar from obstructing venous return, treat hypoglycemia, and manage agitation/pain so straining and coughing do not spike ICP.

Cerebral perfusion pressure (CPP) = MAP − ICP. As ICP rises, CPP falls, so the body raises systemic blood pressure to keep perfusing the brain — which is exactly why hypertension appears in herniation. The paramedic cannot measure ICP in the field, but the logic explains why hypotension is so dangerous (it directly drops CPP) and why you maintain a higher systolic. Also avoid hypocapnia and hypercapnia: low CO2 over-constricts and starves the brain, while high CO2 (from hypoventilation) vasodilates and raises ICP — both extremes are harmful, which is why capnography-guided normocapnia is the goal.

Glasgow Coma Scale and herniation

The Glasgow Coma Scale (GCS) sums three components:

Total 3-15. Severity bands: mild 13-15, moderate 9-12, severe <= 8. The most-tested decision rule: GCS <= 8 = intubate ('less than eight, intubate') — the patient cannot protect the airway. Score the best response, and report the breakdown (e.g., E2V3M4) because the motor score is the most prognostic.

Cushing's triad — hypertension (widening pulse pressure), bradycardia, and irregular/abnormal respirations — signals impending brainstem herniation from dangerously high ICP. It is a late, ominous finding, not early ICP. Other herniation signs: a unilateral fixed, dilated ('blown') pupil, decorticate or decerebrate posturing, and a rapidly falling GCS. These trigger the temporizing mild-hyperventilation strategy and rapid transport to a trauma/neurosurgical center.

Spinal trauma and motion restriction

Spinal cord injury management has shifted from reflexive long-backboard immobilization to spinal motion restriction (SMR). Apply a properly sized cervical collar, keep the spine in line, and move the patient as a unit (the long board is now mainly an extrication/transfer device, with padding and early removal to prevent pressure injury). Manual in-line stabilization is held during any airway maneuver.

Use a validated rule to decide who needs SMR. By NEXUS, no imaging/immobilization criteria require all of: no midline cervical tenderness, no focal neurologic deficit, normal alertness, no intoxication, and no distracting injury. A high cervical (C3-C5) cord injury threatens the diaphragm ('C3, 4, 5 keep the diaphragm alive') and can cause respiratory failure — watch for diaphragmatic breathing and hypoventilation.

Neurogenic shock (a distributive shock from loss of sympathetic tone below the injury) classically presents with hypotension and bradycardia with warm, dry skin — the opposite of the tachycardia seen in hemorrhagic shock, an important distinguishing trap.

Worked scenario and exam traps

A helmeted cyclist struck by a car opens eyes to pain (E2), makes incomprehensible sounds (V2), and withdraws from pain (M4) — GCS 8. The right pupil is 6 mm and sluggish; BP is 178/92, HR 50, with irregular breathing. This is Cushing's triad with a blown pupil = impending herniation. Actions: secure the airway (GCS <= 8), ventilate to mild hyperventilation ETCO2 30-35 / ~20 breaths/min as a temporizing herniation measure, keep SpO2 >= 94% and systolic >= 110 mmHg, elevate the head ~30 degrees if spine allows, and transport emergently to a neurosurgical center.

High-yield traps:

• Routine hyperventilation in TBI is harmful — it vasoconstricts cerebral vessels and worsens ischemia. Only herniation justifies mild hyperventilation, briefly.
• Permissive hypotension is contraindicated in TBI — a single systolic < 90 mmHg episode roughly doubles mortality; target >= 110.
• GCS <= 8 = intubate, and report the motor subscore (most prognostic), not just the total.
• Cushing's triad is a late sign — by the time you see hypertension/bradycardia/irregular respirations, herniation is imminent.
• Hypotension + bradycardia with warm skin = neurogenic shock, not hemorrhage; but always rule out and treat occult hemorrhage first, because trauma patients can have both.