Traumatic Brain Injury nursing care: what to assess and what to do first

Recognising it at the bedside

A single Glasgow Coma Scale score tells you less than the trend. A patient sitting at 14 who drops to 12 over an hour has deteriorated meaningfully even though 12 still sounds stable on paper, and that trajectory is what prompts escalation, not the absolute number. Pupil checks matter just as much: a newly sluggish or unequal pupil, or one that becomes fixed and dilated, signals rising pressure on the third cranial nerve and needs immediate reporting.

Cushing's triad, widening pulse pressure, bradycardia and irregular respirations, is a late and ominous sign of rising intracranial pressure, not an early one. Waiting for it means missing the window where intervention still helps. Watch instead for restlessness, increasing confusion, a new headache that will not settle, vomiting without nausea, and any change in motor response, since these precede the classic triad by hours in many patients.

Why the classic presentation misleads

Textbook head injury descriptions often centre on loss of consciousness at the scene, but many significant traumatic brain injuries involve no loss of consciousness at all, particularly in older adults on anticoagulants who can develop a slow subdural bleed over days. A patient who walked in talking can still be harbouring an expanding haematoma.

The other misleading assumption is about drainage. Clear fluid leaking from the nose or an ear after head trauma looks unremarkable, even reassuring compared with blood, but it is treated as cerebrospinal fluid until proven otherwise because a basilar skull fracture has torn the dura. It is never packed with gauze, since packing blocks the natural drainage route, raises intracranial pressure, and gives bacteria a direct route into the CSF and meninges. Testing for the halo sign or sending fluid for beta-2 transferrin confirms it, but the nursing response comes before the lab result.

Priority nursing actions

Elevate the head of the bed to 30 degrees and keep the neck in neutral alignment, since flexion, rotation or a tight cervical collar can obstruct venous drainage and raise intracranial pressure further. Maintain a patent airway and adequate oxygenation, because hypoxia and hypercapnia both dilate cerebral vessels and worsen pressure.

If clear fluid drains from the nose or ear, place a loose sterile gauze underneath to collect it and let it drain freely; do not pack it, and do not suction the nose. Avoid nasogastric tubes in suspected basilar skull fracture, since a tube can pass through the fracture into the cranial vault; use an orogastric route instead if gastric access is needed.

Space nursing activities and minimise stimulation, since clustered care and noxious stimuli both spike intracranial pressure. Monitor for seizure activity and keep the environment quiet and dimly lit where the patient's condition allows.

Labs and diagnostics to expect

A non-contrast CT head is the first-line study and shows haemorrhage, midline shift and skull fracture rapidly, which is why it precedes most other diagnostics after significant trauma. Serum sodium is checked repeatedly, since traumatic brain injury predisposes to both syndrome of inappropriate antidiuretic hormone, causing hyponatraemia, and diabetes insipidus, causing hypernatraemia with high urine output, and the two require opposite management.

Coagulation studies matter early, particularly in patients on anticoagulants or antiplatelets, since correcting coagulopathy can be the single most time-critical intervention in a bleed. Arterial blood gases guide oxygenation and carbon dioxide targets, and if an intracranial pressure monitor or external ventricular drain is placed, continuous ICP and cerebral perfusion pressure readings become part of routine charting, with a target ICP generally kept below 20 to 22 mmHg and cerebral perfusion pressure kept above 60 mmHg.

Complications and their early signs

Cerebral herniation is the complication that kills quickly, and its earliest sign is often a change in level of consciousness rather than the fixed, dilated pupil that appears later. A widening pulse pressure with bradycardia is Cushing's response and means herniation risk is already advanced, so it demands an immediate call, not a repeat set of observations.

Post-traumatic seizures can occur within the first week and sometimes present subtly as twitching or a brief stare rather than a full convulsion. Diabetes insipidus shows as high-volume dilute urine output with rising serum sodium and thirst in a patient who is often too impaired to report thirst, so intake and output charting has to substitute for the history the patient cannot give. Infection from an undetected CSF leak can present days later as a new fever and headache with no obvious source, which is another reason the leak is taken seriously from the first assessment.

Teaching that changes outcomes

Patients and families need to understand that mild traumatic brain injury symptoms, headache, poor concentration, irritability, sleep disturbance, can persist for weeks and are not a sign that something new has gone wrong. Return-to-activity guidance should be gradual, particularly return to contact sport or heavy exertion, since a second impact before the first has healed carries disproportionate risk.

Teach the family the specific warning signs that mean returning immediately: worsening headache, repeated vomiting, increasing confusion, unequal pupils, seizure, or any new weakness, and give them a clear, written threshold rather than a vague instruction to call if things seem wrong. For patients discharged with a history of clear nasal or ear drainage, reinforce that they should never blow their nose forcefully or use a straw, since either can force air backward through a healing dural tear.