Describe Head Injury in detail.

The Concept — Prevent the Second Injury

The brain is enclosed in a rigid skull, which is the key to understanding head injury. Damage occurs in two phases. The primary injury happens at the instant of impact (contusion, laceration, diffuse axonal injury) and cannot be undone. The secondary injury develops over the following minutes to days — from hypoxia, hypotension, an expanding haematoma, raised intracranial pressure, and seizures — and, critically, much of it is preventable and treatable. The entire management of head injury is therefore aimed at preventing secondary brain injury.

WHY Pressure Is the Enemy — the Monro-kellie Doctrine

Because the skull is a fixed box containing brain, blood and CSF, any new volume — a haematoma or swelling — must be offset by squeezing out CSF and venous blood. This buys time (the patient may look deceptively well), but once this compensation is exhausted the intracranial pressure (ICP) rises steeply. Since cerebral perfusion pressure = mean arterial pressure − ICP, a rising ICP (or a falling blood pressure) chokes off the brain's blood supply, causing ischaemia; unchecked, the brain is forced through the tentorium or foramen magnum (herniation), which is fatal. This is why hypoxia and hypotension are so dangerous — they compound an already threatened blood supply.

Types of Head Injury

• Skull fractures — linear, depressed, or base-of-skull (signs: 'raccoon eyes', Battle's sign, and CSF leak from the nose or ear).
• Intracranial haematomas — extradural (arterial, lucid interval), subdural (venous), subarachnoid, and intracerebral.
• Diffuse injuries — concussion, cerebral contusion, and diffuse axonal injury (from rotational shearing).

Assessment

The core tools are the Glasgow Coma Scale (which grades severity — mild 13–15, moderate 9–12, severe ≤ 8), the pupils (a fixed, dilated pupil suggests uncal herniation compressing the third nerve), lateralising limb signs, and the mechanism of injury. Deterioration is judged by a falling GCS, which is why serial observation is essential.

Signs of Raised Icp

Warning signs include a falling conscious level, headache and vomiting, pupillary changes, and the ominous, late Cushing's response — hypertension with bradycardia and irregular breathing, a reflex attempt to maintain cerebral perfusion that signals critically high ICP and impending herniation.

Investigation & Management

A CT head is the investigation of choice, showing haematoma, fracture, midline shift and effacement of the basal cisterns. Management is directed squarely at preventing secondary injury: maintain oxygenation and blood pressure (avoid hypoxia and hypotension at all costs), nurse head-up, secure the airway (intubate if GCS ≤ 8), and treat raised ICP with mannitol or hypertonic saline, controlled ventilation, sedation and seizure control. A significant haematoma requires urgent neurosurgical evacuation, and ICP may be monitored directly in severe cases.

The Intracranial Haematomas in Detail

Understanding the haematomas by their source clarifies their behaviour. An extradural haematoma is arterial (middle meningeal artery, temporal fracture), collects fast, and gives the classic lucid interval — appearing biconvex on CT. A subdural haematoma is venous (bridging veins), commoner in the elderly and anticoagulated, may be acute or chronic, and appears crescent-shaped. A subarachnoid haemorrhage layers blood in the CSF spaces, and an intracerebral haematoma/contusion lies within the brain itself. Each raises ICP and may need evacuation.

WHO Needs a CT Scan?

Not every head injury needs imaging, and structured criteria (such as NICE or the Canadian CT Head rules) select those at risk of a significant lesion. High-risk features prompting an urgent CT head include a GCS below 13 at any point (or below 15 at 2 hours), a suspected skull fracture, any focal neurological deficit, more than one episode of vomiting, a post-traumatic seizure, and dangerous mechanisms — with a lower threshold in patients on anticoagulants.

Concussion & Complications

Concussion is a transient disturbance of brain function after injury (headache, confusion, amnesia) with a normal CT; it is managed with rest and graded return to activity, with caution about repeated injury. Longer-term complications of significant head injury include post-traumatic epilepsy, chronic subdural haematoma, CSF leak with meningitis risk, cognitive and behavioural change, and post-concussion syndrome — which is why follow-up matters even after apparent recovery.

• Mannitol 0.25–1 g/kg IV, or hypertonic saline, for acutely raised ICP.
• GCS severity: mild 13–15, moderate 9–12, severe ≤ 8 (intubate).
• Target: avoid hypoxia (SpO₂ > 94%) and hypotension (maintain cerebral perfusion).

Secondary injury is preventable — that is where treatment acts.

• Primary injury (at impact, irreversible) vs secondary injury (hypoxia, hypotension, haematoma, raised ICP — preventable); management targets the secondary injury.
• Monro-Kellie: fixed skull; a mass is compensated by displacing CSF/blood until ICP rises steeply → falling cerebral perfusion (CPP = map − ICP) → ischaemia → herniation.
• Assess with GCS (severe ≤8), pupils (fixed dilated = herniation), lateralising signs; lucid interval suggests extradural haematoma.
• Raised ICP: falling GCS, vomiting, pupillary change, Cushing's response (hypertension + bradycardia — late).
• CT head is investigation of choice; maintain O2 and BP, head-up, intubate if GCS ≤8, mannitol/hypertonic saline, evacuate significant haematoma.