Head Injury & Neurosurgical Emergencies

Head injury is the single most exam-loaded topic in trauma surgery for NEET PG, blending physiology (ICP, CPP, Monro–Kellie), radiology (lens vs crescent), and crisp management algorithms. Master GCS, the two classic haematomas, herniation syndromes, and Cushing's triad and you will reliably bag 2–4 questions.

Core definitions & classification

Traumatic brain injury (TBI) is structural injury and/or physiological disruption of brain function from an external force. Damage is split into two temporally distinct processes:

• Primary injury — occurs at the moment of impact (contusion, laceration, diffuse axonal injury, vascular tear). It is irreversible; prevention (helmets, seatbelts) is the only remedy.
• Secondary injury — evolves over hours–days from hypoxia, hypotension, raised ICP, oedema, seizures, hyper/hypocapnia, hyperthermia, and infection. It is preventable/treatable, and the entire thrust of neurotrauma management is to limit it.

High-yield: The two greatest enemies of the injured brain are hypoxia (SpO₂ < 90%) and hypotension (SBP < 90 mmHg) — each independently doubles mortality. The single biggest avoidable cause of death is secondary injury.

Severity grading by GCS

Severity	GCS score	Notes
Mild	13–15	Concussion; most common; brief or no LOC
Moderate	9–12	Admit, serial CT, observe
Severe	3–8	GCS ≤ 8 = intubate (cannot protect airway)

Glasgow Coma Scale (GCS)

Devised by Teasdale and Jennett (1974, Glasgow). Score range 3 (worst) to 15 (best). Always document the best response and break down the components (E + V + M).

Eye opening (E /4)	Verbal (V /5)	Motor (M /6)
4 Spontaneous	5 Oriented	6 Obeys commands
3 To speech	4 Confused	5 Localises to pain
2 To pain	3 Inappropriate words	4 Withdraws (flexion)
1 None	2 Incomprehensible sounds	3 Abnormal flexion (decorticate)
	1 None	2 Extension (decerebrate)
		1 None

High-yield: Lowest possible GCS = 3, not 0. The motor component is the best single predictor of outcome. Intubated patients: verbal scored as 1T (e.g. E4VtM6).

Memory cues: Decorticate = abnormal flexion, arms flexed toward the core/cord (lesion above red nucleus). Decerebrate = extension (lesion in brainstem, worse prognosis). Decerebrate > decorticate in severity.

Paediatric GCS uses a modified verbal scale (coos/babbles = best). For children, use the children's coma scale.

Pathophysiology — ICP, CPP & Monro–Kellie

The skull is a rigid box containing brain (~80%), blood (~10%), CSF (~10%).

Monro–Kellie doctrine: Total intracranial volume is fixed. An increase in any one compartment (e.g. haematoma) must be compensated by displacement of CSF and venous blood; once compensation is exhausted, ICP rises steeply.

Normal ICP = 7–15 mmHg (adult, supine). Treatment threshold = ICP > 20–22 mmHg.

Cerebral perfusion pressure (CPP) = MAP − ICP.

• Target CPP 60–70 mmHg.
• CPP < 50 → ischaemia; CPP < 60 raises mortality.

Therefore you can improve perfusion by raising MAP or lowering ICP. Cerebral autoregulation (maintains constant flow over MAP 50–150 mmHg) is often lost after TBI, making the brain pressure-passive and vulnerable.

CO₂ effect: CO₂ is a potent cerebral vasodilator. Hypercapnia → vasodilation → ↑ICP. Brief, controlled hyperventilation (PaCO₂ 30–35 mmHg) transiently lowers ICP — a temporising measure only, as aggressive hyperventilation (< 30) causes ischaemia.

Cushing's triad & herniation

When ICP rises critically, brainstem ischaemia triggers a sympathetic surge.

Cushing's triad = (1) Hypertension (widened pulse pressure) + (2) Bradycardia + (3) Irregular respiration (Cheyne–Stokes). Signals impending herniation — a terminal/late sign demanding immediate decompression. (Note: this differs from Cushing's reflex hypertension-bradycardia pair.)

Uncal (transtentorial) herniation is the classic exam scenario: an expanding temporal mass pushes the uncus over the tentorium →

1. Compression of CN III (parasympathetic fibres on its surface) → ipsilateral fixed, dilated pupil ("blown pupil").
2. Compression of the ipsilateral corticospinal tract / contralateral crus (Kernohan's notch) → contralateral hemiparesis (or false-localising ipsilateral).
3. Progressive ↓ consciousness, Cushing's triad, death.

High-yield: A unilateral fixed dilated pupil + ipsilateral haematoma = uncal herniation → emergency surgical evacuation. The blown pupil is ipsilateral to the lesion; weakness is usually contralateral.

Other herniations: subfalcine (cingulate, under falx → ACA infarct), central (downward, bilateral), tonsillar (cerebellar tonsils through foramen magnum → respiratory arrest), transcalvarial (through skull defect).

The traumatic intracranial haematomas

Extradural (epidural) haematoma — EDH

• Source: Arterial — classically the middle meningeal artery, torn by a fracture of the pterion (temporoparietal squamous temporal bone). The pterion is the thinnest part of the skull where frontal, parietal, temporal and sphenoid meet.
• Classic story: Young patient, blow to temple → brief LOC → lucid interval (talks-and-dies) → rapid deterioration as arterial blood accumulates.
• CT: Biconvex / lens-shaped (lentiform) hyperdensity that does NOT cross suture lines (dura is tightly adherent at sutures). May cross the midline/dural folds.
• Prognosis: Good if evacuated early — bleed is extradural, brain often undamaged.

Subdural haematoma — SDH

• Source: Venous — torn bridging (cortical) veins between cortex and dural sinuses.
• Risk groups: Elderly and alcoholics (brain atrophy stretches bridging veins); shaken babies.
• CT: Crescent-shaped (concavo-convex) collection that DOES cross suture lines but NOT the midline (limited by falx).
• Density evolves with age — a favourite MCQ:

Age of SDH	CT density vs cortex
Acute (< 3 days)	Hyperdense (white)
Subacute (3 days–3 weeks)	Iso-dense (hardest to spot; look for mass effect)
Chronic (> 3 weeks)	Hypodense (dark)

High-yield, exam-favourite contrast: EDH = arterial (middle meningeal), biconvex LENS, does NOT cross sutures, lucid interval, young. SDH = venous (bridging veins), CRESCENT, crosses sutures, elderly/alcoholic.

Chronic SDH presents weeks after trivial trauma in the elderly with fluctuating confusion, headache, or focal deficit ("great imitator" of dementia/stroke) → treated by burr-hole drainage.

Other lesions

• Cerebral contusion / intracerebral haematoma — coup (impact site) and contrecoup (opposite pole, classically inferior frontal/temporal). "Salt-and-pepper" haemorrhagic CT; may "blossom" on repeat scan.
• Traumatic subarachnoid haemorrhage (tSAH) — blood in sulci; most common CT finding after TBI; prognostic marker.

Diffuse axonal injury (DAI)

• Mechanism: Rotational / shear–acceleration–deceleration forces (high-speed RTA) tear axons at grey–white junction, corpus callosum and dorsolateral midbrain.
• Clinical hallmark: Deep, immediate, prolonged coma with GCS profoundly low yet a near-normal or only subtly abnormal CT — the classic "GCS–CT mismatch."
• Investigation of choice: MRI (especially GRE/SWI sequences) shows microhaemorrhages; CT often misses it.
• Prognosis: Poor; a leading cause of persistent vegetative state.

High-yield: Comatose trauma patient with a normal CT → think DAI → confirm with MRI.

Skull fractures & their signs

• Base of skull fracture clinical signs:
  • Raccoon eyes (bilateral periorbital ecchymosis) — anterior fossa.
  • Battle's sign (mastoid bruising) — middle fossa, appears after ~24–48 h.
  • CSF rhinorrhoea / otorrhoea, haemotympanum.
  • "Halo/double-ring" sign on filter paper; fluid tests positive for β₂-transferrin (tau protein) — the confirmatory test for CSF leak.
• Depressed fracture — operate if depressed greater than the skull thickness, open/contaminated, or causing deficit.
• Avoid nasogastric tube via the nose in suspected base-of-skull fracture (risk of intracranial passage) — use the oral route.

Diagnosis & investigation of choice

Investigation of choice for acute head injury = Non-contrast CT (NCCT) head — fast, detects fresh blood (hyperdense), fractures, mass effect, midline shift.

Whom to scan? Indian/ATLS practice scans any moderate–severe injury; for mild TBI use validated rules:

Canadian CT Head Rule (GCS 13–15) — CT if any high-risk: GCS < 15 at 2 h, suspected open/depressed/basal fracture, ≥ 2 episodes vomiting, age ≥ 65, or any sign of skull-base fracture; medium-risk: amnesia > 30 min, dangerous mechanism.

MRI — superior for DAI, brainstem, posterior fossa, and subacute/isodense SDH; not first-line in the unstable acute patient.

ICP monitoring (Brain Trauma Foundation): indicated in severe TBI (GCS 3–8) with an abnormal CT, or normal CT with ≥ 2 of (age > 40, motor posturing, SBP < 90). External ventricular drain (EVD/ventriculostomy) is the gold standard — it both measures ICP and allows therapeutic CSF drainage.

Management — stepwise approach

ABCDE / ATLS comes first — the brain cannot be saved without oxygen and perfusion.

Resuscitation flow: Secure airway (intubate if GCS ≤ 8) → ventilate to PaCO₂ 35–45, SpO₂ > 94% → restore circulation, keep SBP ≥ 110 (avoid hypotension) → rapid GCS + pupils → NCCT head → neurosurgical referral.

Medical control of raised ICP (tiered)

1. Head-end elevation 30°, head midline (improves venous drainage), avoid tight ties.
2. Sedation & analgesia; treat pain/agitation that spike ICP.
3. Osmotherapy:
   • Mannitol 0.25–1 g/kg IV bolus (osmotic diuretic; caution if hypotensive/renal failure), OR
   • Hypertonic (3%) saline — preferred when hypotensive/hypovolaemic.
4. Brief hyperventilation to PaCO₂ 30–35 — temporary bridge to surgery only.
5. Maintain CPP 60–70, normothermia, normoglycaemia, seizure control.
6. Refractory ICP: barbiturate coma (thiopentone) or decompressive craniectomy.

High-yield: Steroids are CONTRAINDICATED in TBI — the CRASH trial showed increased mortality. (Steroids are for vasogenic oedema of tumours, not trauma.)

Seizure prophylaxis

Phenytoin (or levetiracetam) for early (< 7 day) post-traumatic seizures in high-risk injuries — reduces early but not late seizures; do not continue long-term routinely.

Surgical management

• Burr hole — emergency life-saving evacuation/exploration; classic site for temporal EDH is over the pterion/temporal region. Definitive evacuation of EDH/acute SDH is via craniotomy.
• Chronic SDH → burr-hole drainage ± subdural drain.
• Decompressive craniectomy — remove a large bone flap + open dura to give swollen brain room.

Decompressive craniectomy indications: Refractory raised ICP despite maximal medical therapy; large haematoma with midline shift and deteriorating GCS; malignant cerebral oedema. DECRA & RESCUEicp trials: craniectomy lowers ICP and mortality but at the cost of more survivors in severe-disability/vegetative states.

Operate emergently for: EDH with mass effect, acute SDH > 10 mm or midline shift > 5 mm, depressed/open fractures, and any haematoma with a deteriorating exam or blown pupil.

Complications

• Herniation and brainstem death (most feared, early).
• Post-traumatic epilepsy (early vs late).
• CSF leak → meningitis (base-of-skull fracture).
• Hydrocephalus (communicating, post-tSAH).
• Diabetes insipidus / SIADH / cerebral salt wasting (sodium disturbances — distinguish by volume status).
• Post-concussion syndrome (headache, dizziness, poor concentration after mild TBI).
• Carotid-cavernous fistula (pulsatile proptosis, bruit, chemosis).
• Chronic traumatic encephalopathy (repetitive injury, e.g. boxers — "punch-drunk").
• Persistent vegetative state (especially DAI).

Key differentials & quick discriminators

Feature	EDH	Acute SDH	DAI
Vessel	Middle meningeal artery	Bridging veins	Axonal shear
CT shape	Biconvex lens	Crescent	Often near-normal
Crosses sutures?	No	Yes	—
Lucid interval	Classic	Uncommon	Absent (deep coma)
Typical patient	Young, temporal blow	Elderly/alcoholic	High-speed RTA
Best imaging	CT	CT (MRI if isodense)	MRI/GRE
Prognosis	Good if early	Variable/poor	Poor

Non-traumatic mimics of altered sensorium to exclude: spontaneous SAH (thunderclap headache, "worst headache of life," berry aneurysm), hypoglycaemia, intoxication, hypoxia, post-ictal state, and stroke. Always check glucose in any unconscious patient.

Recently asked / exam angle

• Lens vs crescent on CT — direct "name the haematoma" picture questions (EDH = biconvex, SDH = crescent). Extremely frequent.
• "Does not cross suture line" = EDH; "crosses suture but not midline" = SDH.
• Lucid interval → EDH; middle meningeal artery vessel match.
• GCS calculation vignettes (compute E+V+M; "lowest = 3"; "GCS ≤ 8 → intubate"; motor = best predictor).
• Cushing's triad components and that it is a late sign of raised ICP.
• Uncal herniation → ipsilateral fixed dilated pupil + CN III.
• Steroids contraindicated in head injury (CRASH trial) — repeated negative-answer MCQ.
• DAI: low GCS with normal CT → MRI.
• β₂-transferrin = confirmatory test for CSF leak; halo sign.
• CPP = MAP − ICP; target values; mannitol dose 0.25–1 g/kg.
• Decompressive craniectomy indications (refractory raised ICP) — DECRA/RESCUEicp.
• Battle's sign / raccoon eyes localisation (middle vs anterior fossa).

Rapid revision

1. GCS range 3–15; ≤ 8 = severe = intubate; motor score is the best outcome predictor.
2. CPP = MAP − ICP; target CPP 60–70, normal ICP 7–15, treat if > 20–22 mmHg.
3. Hypoxia + hypotension = the two killers; avoid SBP < 90 and SpO₂ < 90.
4. EDH = middle meningeal artery, lens-shaped, no suture crossing, lucid interval, young.
5. SDH = bridging veins, crescent, crosses sutures, elderly/alcoholic; isodense at ~2 weeks.
6. Cushing's triad = HTN (wide pulse pressure) + bradycardia + irregular breathing = impending herniation.
7. Uncal herniation → ipsilateral blown pupil (CN III) + contralateral weakness.
8. DAI = shear injury, deep coma with normal CT; diagnose by MRI/GRE.
9. Steroids are contraindicated in TBI (CRASH trial); mannitol 0.25–1 g/kg or 3% saline for ICP.
10. Investigation of choice = NCCT head; β₂-transferrin confirms CSF leak; avoid nasal NG tube in basal fracture.
11. EVD = gold standard ICP monitor + therapeutic CSF drainage; ICP monitoring if severe TBI + abnormal CT.
12. Decompressive craniectomy for refractory raised ICP / malignant oedema (DECRA, RESCUEicp).