Neurosurgery notes/Trauma/Primary head Injury/Contusion

Contusion

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Primary head Injury

General

  • AKA
    • Haemorrhagic contusions
    • Traumatic intraparenchymal haemorrhages

Definition

  • Focal or multifocal and located in cortical or subcortical regions from direct impact or an acceleration/ deceleration injury.

Numbers

  • 20% of moderate TBI

Location

  • Frontal and temporal lobes most common

Pathology

  • Acceleration/deceleration and or direct impact → damaged small arteries/veins/capillaries → bruise (contusion) on the surface of brain → ICH form (consist of a semi-liquid mass of blood with surrounding oedema) → brain swelling → herniation
    • These mass lesions evolve over days and change consistency while oedema begins to recede.
  • Intermediary contusions
    • Subcortical lesions affecting the corpus callosum, basal ganglia, hypothalamus, and brainstem.
  • Cortical impact murine models
    • Demonstrate that cerebral oedema peaks at 24 hours coincident with a marked reduction of cerebral blood flow (CBF) to contused cortex.
    • CBF normalizes after day seven post- trauma, during which focal areas of hyperaemia appear adjacent to regions of low flow
  • Studies of the human brain after nonpenetrating head injury show contusions being more severe in
    • Frontal and temporal lobes
    • Patients who do not experience lucid intervals
  • Cellular analyses
    • Necrosis as the predominant finding
    • Apoptosis as part of the secondary injury cascade.
    • Tumour necrosis factor increases immediately and rapidly in CSF during acute neuronal degeneration and gradually decreases within a few hours.
    • Neutrophils and macrophages accumulate with elevated chemokines to sustain the cerebral inflammatory cascade.
  • Raised ICP due to
    • Cerebral swelling
    • Delayed haematoma formation in the pericontusional area
  • Contrecoup injury
    • In addition to the injury to the brain directly under the point of impact, the brain may rebound after the impact and be thrust against the skull at a point diagonally opposite the blow, the so-called contrecoup (French: “counter blow”) injury.
    • This may produce contusions typically located subjacent to bony prominences
      • Frontal and Occipital bones
      • Sphenoid wing
      • Petrous bone
  • Posttraumatic brain swelling: This term encompasses two distinct processes:
    • Increased cerebral blood volume (hyperaemia):
      • May result from loss of cerebral vascular autoregulation.
        • Aka: diffuse or “malignant cerebral oedema,”
          • This hyperaemia may sometimes occur with extreme rapidity
        • Carries close tka o 100% mortality
        • More common in children.
        • Management consists of aggressive measures to maintain
          • ICP < 20mm Hg
          • CPP> 60mm Hg.
            • CPP≥ 70mm Hg is generally recommended.
    • True cerebral oedema:
      • Classically at autopsy these brains “weep fluid.”
      • Both vasogenic and cytotoxic cerebral oedema can occur within hours of head injury and occasionally may be treated with decompressive craniectomy.

CT findings

  • High attenuation areas: usually produce less mass effect than their apparent size.
    • Most common in areas where sudden deceleration of the head causes the brain to impact on bony prominences
    • Contused areas may progress (“blossom”) to frank parenchymal hematomas.
    • Surgical decompression may be considered if herniation threatens.
  • Low attenuation areas: representing associated oedema
      Features
      Spontaneous ICH
      Traumatic ICH
      Size of ICH
      Larger
      Small/medium
      Location
      Deeper
      Superficial
      Age
      Older
      Younger
    • Hence sICH cannot be generalized to tICH

Management

ICP monitoring

  • Regardless of the need for surgical intervention.
  • ?? BEST ICP trial

Conservative management

  • Indication
    • No focal neurologic deficits AND
    • Non- significant mass effect on imaging
  • As all head injury management

Surgical intervention

  • Aimed at
    • Preventing secondary damage,
    • Brainstem compression,
    • Herniation of the brain.
  • Indication (expert opinion) BTF
    • Supratentorial
      • Focal lesion +
        • Progressive neurological deterioration
        • Medically refractory raised ICP
        • A hematoma volume more than 50 cm3 (>50 ml)
        • GCS score of 6 to 8 in a patient + Frontal or temporal haemorrhage more than 20 cm3 (>20 ml) + either midline shift of more than 5 mm / cisternal compression on CT scan
      • Refractory intracranial hypertension+ Diffuse injuries + radiographic evidence for transtentorial herniation
      • Trauma STICH
        • ICH volume of attenuation significantly raised above that of the background white and gray matter great than 10mL
    • Posterior fossa
      • Evidence of neurologic dysfunction/deterioration + significant mass effect on the basal cisterns, fourth ventricle, or signs of obstructive hydrocephalus
  • STICTH trial (trauma)
    • Early surgery vs conservative +/- late surgery (>12 hrs)
    • Poorer outcome in late surgery
    • For cerebral tICH not post fossa
      • Kaplan-Meier’s survival analysis. Log-rank test, p=0.0081.
      Kaplan-Meier’s survival analysis. Log-rank test, p=0.0081.
      notion image
    • Trial were mostly recruited in resource- limited settings where ICP monitoring was not usually available
    • More than 2/3 were recruited from sites without completing logs so we do not know how many were screened and was eligible
    • Unilateral lesions portray better prognosis while bilateral lesions can be delayed in clinical presentation.

Complications

  • Secondary deterioration
    • Can be delayed as long as 10 days
  • Hyponatraemia
    • Can exacerbate this risk
    • Daily serum Na
  • Hypernatremia
    • SIADH syndrome of inappropriate antidiuretic hormone can coexist in the context of TBI.

Outcome

  • Depends on
    • Location of ICH
    • Size of ICH