Head injury, imaging and haemorrhage

Traumatic Brain Injury, Intracranial Haemorrhage & Spinal Cord Clearance

Traumatic brain injury (TBI) and spinal column trauma represent major emergencies where timely neuroresuscitation and adherence to validated diagnostic decision rules directly determine neurological outcomes. In Australian clinical practice, management focuses on preventing secondary brain injury (induced by systemic hypotension, hypoxia, hypercapnia, and intracranial hypertension) following the irreversible primary mechanical insult.

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Traumatic Brain Injury: Classification & The Glasgow Coma Scale

The Glasgow Coma Scale (GCS) remains the gold standard tool for assessing depth of consciousness and stratifying injury severity. Scoring must be documented before administering sedative or neuromuscular blocking agents.

Glasgow Coma Scale (GCS 3–15)

• Eye Opening (1–4):
  • 4: Spontaneous
  • 3: To verbal command / sound
  • 2: To pressure / painful stimulus
  • 1: None
• Verbal Response (1–5):
  • 5: Oriented (knows name, place, month)
  • 4: Confused conversation
  • 3: Inappropriate words (random, exclamatory speech)
  • 2: Incomprehensible sounds (moaning, groaning)
  • 1: None
• Motor Response (1–6):
  • 6: Obeys commands
  • 5: Localizes to central painful stimulus (crosses midline/moves hand above clavicle)
  • 4: Normal flexion / withdrawal to peripheral pain
  • 3: Abnormal flexion (decorticate posturing: adduction, arm flexion, leg extension)
  • 2: Extension (decerebrate posturing: adduction, internal rotation, forearm pronation)
  • 1: None

Severity Stratification & Clinical Rule

• Mild TBI: GCS $13\text{ to }15$. High percentage of emergency visits; risk of insidious intracranial haematoma.
• Moderate TBI: GCS $9\text{ to }12$. Requires admission, neurosurgical consultation, and repeat non-contrast CT brain.
• Severe TBI: GCS $\le 8$. Clinical Rule: "A GCS of 8 or less mandates immediate definitive endotracheal intubation" with manual in-line stabilization to protect against aspiration and maintain strict neuroprotective ventilation.

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Indications for Urgent Neuroimaging: Canadian CT Head Rule

In adult patients presenting with mild TBI (loss of consciousness, amnesia, or confusion), the Canadian CT Head Rule (CCHR) guides the necessity of an immediate non-contrast CT brain. The rule applies to patients with an initial GCS of 13 to 15 after witnessed trauma.

High Risk (Mandates CT to Rule Out Neurosurgical Lesion)

1. GCS score $< 15$ at 2 hours post-injury.
2. Suspected open or depressed skull fracture.
3. Any clinical sign of basal skull fracture:
   • Haemotympanum (blood behind the tympanic membrane).
   • "Raccoon eyes" (periorbital ecchymosis without direct orbital trauma).
   • Battle's sign (mastoid ecchymosis behind the ear).
   • Cerebrospinal fluid (CSF) rhinorrhoea or otorrhoea (halo or ring sign on filter paper).
4. Two or more discrete episodes of vomiting.
5. Age $\ge 65$ years.

Medium Risk (Mandates CT to Rule Out Significant Brain Injury)

1. Retrograde amnesia for events preceding impact $> 30$ minutes.
2. "Dangerous" mechanism of injury:
   • Pedestrian struck by motor vehicle.
   • Occupant ejected from a motor vehicle.
   • Fall from an elevation $> 1\text{ metre}$ or five stairs.

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Intracranial Haematomas: Extradural, Subdural, Subarachnoid & DAI

1. Extradural (Epidural) Haematoma (EDH)

• Anatomy & Mechanism: Traumatic impact over the lateral skull at the pterion (where the frontal, parietal, temporal, and sphenoid bones articulate). Fractures tear the underlying middle meningeal artery (or occasionally dural venous sinuses).
• Clinical Presentation: Classically, a transient post-traumatic loss of consciousness followed by a "lucid interval" lasting hours, during which the patient is neurologically intact. As the arterial collection expands under systemic arterial pressure, intracranial pressure rises acutely, precipitating rapid deterioration: severe headache, vomiting, progressive stupor, ipsilateral uncal herniation (fixed dilated pupil), and contralateral hemiparesis.
• CT Findings: A hyperdense, biconvex (lentiform) extra-axial mass. Because the dura mater is tightly anchored to the inner calvarium at cranial sutures, extradural haematomas do not cross suture lines, but they can cross dural venous reflections (falx and tentorium).
• Management: Emergent neurosurgical craniotomy and evacuation. If transfer to a neurosurgical centre is delayed and signs of transtentorial herniation are active, emergency bedside burr hole trephination may be life-saving.

2. Subdural Haematoma (SDH)

• Anatomy & Mechanism: Acceleration-deceleration or rotational shearing forces cause tearing of the delicate bridging cortical veins that traverse the subdural space between the cerebral cortex and the superior sagittal sinus.
• Acute SDH: High-energy blunt trauma in younger individuals. Frequently associated with severe underlying parenchymal contusions. Patients present in severe coma with midline shift. Mortality is high ($40\%\text{ to }60\%$). CT shows a hyperdense, crescentic (concavoconvex) collection that crosses cranial suture lines, but is bounded by the falx and tentorium. Surgical evacuation via formal craniotomy is indicated if thickness $> 10\text{ mm}$ or midline shift $> 5\text{ mm}$.
• Chronic SDH: Common in elderly patients and individuals with chronic alcohol use disorder. Cerebral atrophy stretches the bridging veins across a widened subdural space, rendering them vulnerable to rupture from trivial or forgotten head trauma weeks prior. Presents insidiously with progressive headache, confusion, personality changes, unsteady gait, or fluctuating focal neurological deficits (frequently misdiagnosed as dementia or stroke). CT shows a hypodense or isodense crescentic collection. Managed with burr hole evacuation or twist-drill drainage.

3. Traumatic Subarachnoid Haemorrhage (tSAH) & Diffuse Axonal Injury (DAI)

• tSAH: Traumatic disruption of small pial vessels leads to blood within the sulci, fissures, and basal cisterns. Symptoms include severe headache, photophobia, and meningism. Managed conservatively unless accompanied by hydrocephalus.
• Diffuse Axonal Injury (DAI): Severe rotational acceleration-deceleration forces generate tissue shear stresses, severing axons at the interface between tissues of differing density—most notably the grey-white matter junction, corpus callosum, and upper brainstem. Patients present in profound, prolonged coma out of proportion to initial imaging. Non-contrast CT is frequently normal or shows only punctate petechial microhaemorrhages. MRI brain (susceptibility-weighted imaging [SWI] or gradient-echo [GRE]) is the diagnostic gold standard.

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Raised Intracranial Pressure & Herniation Syndromes

The Monro-Kellie hypothesis dictates that the rigid adult cranial vault has a fixed total volume containing brain parenchyma ($80\%$), blood ($10\%$), and CSF ($10\%$). Once compensatory displacement of CSF and venous blood is exhausted, small volume increases cause exponential rises in intracranial pressure (ICP).

• Severe TBI: Specialist protocols commonly treat sustained ICP above 22 mmHg, while integrating examination, imaging and cerebral perfusion. Avoid hypoxia and hypotension. Hyperventilation is a short rescue measure for impending herniation, not routine prophylaxis.
• Cerebral Perfusion Pressure (CPP): Defined by the equation:

$$\text{CPP} = \text{MAP} - \text{ICP}$$

Target CPP in severe TBI is $60\text{ to }70\text{ mmHg}$. Systemic hypotension ($MAP < 80\text{ mmHg}$) severely compromises cerebral blood flow, causing secondary ischaemic infarction.

Primary references (checked 7 October 2026): Acute spinal cord haemodynamic guidance.