Head Trauma Imaging

Initial Imaging & Skull Fractures - Scan Smart, Spot Breaks

• Primary Scan: NCCT head is crucial for acute trauma.
  • X-ray skull: Very limited role; mainly if CT unavailable.
• Key CT Indications:
  • GCS < 15 (2h post-injury)
  • Suspected open/depressed fracture
  • Basal skull fracture signs (Battle's, raccoon eyes)
  • Vomiting > 1 episode
  • Age ≥ 65 years
  • Retrograde amnesia > 30 min
  • Dangerous mechanism
  • Focal deficit, seizure
• Skull Fracture Types:
  • Linear: Most common.
  • Depressed: Fragment inward; surgery if > bone thickness.
  • Basal: Clinical signs vital; CSF leak risk.
  • Comminuted: Multiple fragments.
  • Diastatic: Sutural separation (children).
  • Growing: Leptomeningeal cyst (infants/young children).

⭐ NCCT head is the investigation of choice in acute head trauma, rapidly identifying life-threatening injuries.

EDH & SDH - Bleeds Between Layers

⭐ The "lucid interval," a temporary improvement in neurological status after head trauma followed by rapid deterioration, is a classic presentation of EDH.

SAH & ICH/Contusions - Blood In Spaces & Substance

• Subarachnoid Hemorrhage (SAH): Blood in CSF spaces (sulci, cisterns).
  • NCCT: Hyperdense CSF. Key sites: Sylvian fissure, basal cisterns.
  • Causes: Trauma (overall #1), ruptured aneurysm (spontaneous #1).
  • Complications: Vasospasm (Day 4-14), hydrocephalus.
• Intracerebral Hemorrhage (ICH) & Contusions: Blood in brain parenchyma.
  • ICH: Frank bleed. Common: frontal, temporal lobes.
  • Contusions: Cortical "bruises"; mixed density (hemorrhage + edema).
    • Locations: Inferior frontal, anterior temporal (coup-contrecoup).
    • May "blossom" (evolve) over 24-48h.

⭐ Overall most common cause of SAH is trauma; for spontaneous SAH, it's a ruptured berry aneurysm.

DAI, Herniation & Peds Pearls - Axons, Squeezes & Small Skulls

• Diffuse Axonal Injury (DAI)
  • Mechanism: High-velocity rotational shear forces; axons stretch & tear.
  • Key sites: Grey-white matter junction, corpus callosum (esp. splenium), brainstem (dorsolateral midbrain/pons).
  • CT: Often normal or subtle petechial hemorrhages.
  • MRI: Modality of choice. SWI/GRE for microhemorrhages; FLAIR/DWI for non-hemorrhagic lesions.
  • 📌 Adams Staging: Grade 1 (lobar WM), Grade 2 (+corpus callosum), Grade 3 (+brainstem).
• Herniation Syndromes
  • Subfalcine: Cingulate gyrus under falx → ACA compression.
  • Uncal (Transtentorial): Medial temporal lobe (uncus) → CN III palsy (ipsilateral dilated pupil), contralateral hemiparesis (Kernohan's notch phenomenon). PCA often compressed.
  • Central: Diencephalon/midbrain downward → Duret hemorrhages (secondary brainstem bleeds).
  • Tonsillar: Cerebellar tonsils through foramen magnum → cardiorespiratory arrest.
• Pediatric Pearls
  • Non-Accidental Injury (NAI): Suspect with interhemispheric SDH, unexplained skull fractures (esp. complex/diastatic), retinal hemorrhages.
  • Growing skull fracture (Leptomeningeal cyst): Post-traumatic dural tear with CSF/brain herniation through fracture line.
  • Brain: ↑water content, incomplete myelination → greater susceptibility to diffuse injury.

⭐ DAI lesions are classically found at the grey-white matter interface, corpus callosum, and dorsolateral brainstem; MRI is crucial as CT can be normal in up to 50% of cases.

High‑Yield Points - ⚡ Biggest Takeaways

• NCCT Head: Initial modality for acute trauma; identifies fractures, hematomas.
• EDH: Lentiform, arterial (MMA), doesn't cross sutures, lucid interval common.
• SDH: Crescentic, venous (bridging veins), crosses sutures, can be acute or chronic.
• Traumatic SAH: Blood in sulci/cisterns; common, may indicate severe injury.
• DAI: MRI superior for punctate hemorrhages (grey-white junction, corpus callosum, brainstem).
• Signs of raised ICP: Effacement of sulci/cisterns, midline shift, herniation.