TCRN – Trauma Certified Registered Nurse

Traumatic brain injury (TBI) is an alteration in brain function caused by an external mechanical force: direct impact, rapid acceleration-deceleration, a penetrating object, or a blast wave. Severity is classified by the Glasgow Coma Scale (GCS) score after resuscitation, supported by the duration of loss of consciousness (LOC) and post-traumatic amnesia (PTA).

Primary brain injury occurs at the moment of impact and includes contusions, lacerations, diffuse axonal injury, and intracranial hemorrhage. Secondary brain injury develops over hours to days from hypoxia, hypotension, cerebral edema, raised intracranial pressure, seizures, fever, infection, and metabolic derangements such as hypo- or hyperglycemia and hyponatremia. Primary injury cannot be reversed, so trauma nursing care centers on preventing secondary injury.

Contact injuries occur when a moving object strikes the stationary head or the moving head strikes a stationary object. Acceleration-deceleration injuries result from rapid velocity changes that move the brain within the skull, and rotational (angular) forces produce shearing throughout brain tissue. Motor vehicle collisions and falls are the leading blunt mechanisms; falls dominate in older adults and young children.

The coup-contrecoup pattern describes injury at the impact site and on the opposite side of the brain. When the moving head strikes a stationary object, the contrecoup injury is often the larger lesion; when a moving object strikes the stationary head, the coup injury predominates. The brain slides across the irregular bony floor of the anterior and middle fossae, so the frontal and temporal lobes are the most frequently contused.

At the cellular level, membrane disruption causes massive calcium and sodium influx, excess glutamate release produces excitotoxicity, and mitochondrial failure impairs energy production and generates reactive oxygen species. Inflammatory mediators amplify the damage. Cerebral autoregulation is often impaired, so cerebral blood flow passively follows systemic blood pressure: hypotension causes ischemia and hypertension worsens edema.

Cerebral edema develops by two mechanisms. Vasogenic edema follows blood-brain barrier disruption, with protein-rich fluid leaking into the extracellular space around contusions. Cytotoxic edema follows ion-pump failure, with water moving into cells after ischemia. Both add volume within a fixed skull and drive intracranial pressure upward, typically peaking 24–72 hours after injury.

The GCS scores the best eye, verbal, and motor responses. The motor score is the strongest single predictor of outcome. Apply a graded stimulus: peripheral fingertip (nail-bed) pressure is appropriate for eye opening and withdrawal, whereas a central stimulus (trapezius pinch or supraorbital notch pressure) is required to test localization, because peripheral stimuli may produce only spinal reflex flexion. Record the best response, note right-left asymmetry, and document factors that limit scoring, such as periorbital swelling, sedation, or intubation (verbal score recorded with a T modifier).

Assess pupil size in millimeters, shape, equality, and direct and consensual reactivity. Normal pupils are about 2–5 mm and brisk. A unilateral dilated, sluggish or fixed pupil indicates ipsilateral oculomotor (CN III) compression from uncal herniation until proven otherwise. Bilateral midposition fixed pupils (4–5 mm) suggest midbrain injury; bilateral pinpoint pupils suggest a pontine lesion or opioid effect; bilateral fixed dilated pupils indicate severe brainstem injury or herniation and carry a poor prognosis.

The Cushing response, the combination of hypertension with a widening pulse pressure, bradycardia, and irregular respirations, is a late sign of critically raised intracranial pressure with brainstem compression. It demands immediate herniation management rather than treatment of the individual vital signs.

The scalp has five layers: skin, dense connective tissue, galea aponeurosis, loose areolar tissue, and periosteum. The loose areolar layer permits avulsions and large subgaleal hematomas, and the rich blood supply means scalp lacerations can cause hemorrhagic shock, especially in children. Control bleeding with direct pressure, pressure dressings, or rapid wound approximation (staples or sutures).

Clear drainage from the nose or ear is tested for beta-2 transferrin, the most specific marker for CSF; glucose testing and the halo (ring) sign on gauze are supportive but less reliable. Do not pack the nose or ear; place a loose drip pad, elevate the head of bed if permitted, and teach the patient not to blow the nose, sneeze with the mouth closed, or strain.

Concussion is a mild TBI with transient neurologic dysfunction and no structural lesion on standard imaging, produced by rotational forces that cause ionic flux and an energy crisis in neurons. Symptoms fall into four domains: physical (headache, nausea, dizziness, balance and visual problems, light and noise sensitivity), cognitive (fogginess, poor concentration and memory), emotional (irritability, anxiety, sadness), and sleep (drowsiness or insomnia).

Validated decision rules such as the Canadian CT Head Rule (adults) and PECARN (children) guide imaging in minor head injury; anticoagulation and older age lower the threshold. Discharge teaching lists red flags that require immediate return: worsening headache, repeated vomiting, seizure, focal weakness or numbness, increasing confusion or drowsiness, slurred speech, and unequal pupils. Recovery uses brief relative rest followed by graduated return to activity and learning; symptoms that persist beyond about 3 months define persistent post-concussive symptoms.

A single episode of hypoxia (SpO2 < 90% or PaO2 < 60 mmHg) or hypotension markedly increases mortality after severe TBI. Brain Trauma Foundation (BTF) guidelines (4th edition) recommend maintaining SBP ≥ 100 mmHg for ages 50–69 and ≥ 110 mmHg for ages 15–49 and over 70. Additional targets include normocarbia (PaCO2 about 35–45 mmHg, usually 35–40), normothermia, euglycemia, normonatremia, and correction of coagulopathy.