Mednotes

L13 Nervous System Traumatic head injury

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tagsnervoussystem, lecture
aliasesL13 Nervous System Traumatic head injury

13 min read

Overview

Traumatic brain injury covered from epidemiology and definition through to outcome. The organising idea is the split between primary injury (what the impact itself does: skull fracture, penetrating injury, focal and diffuse damage) and secondary injury (what happens afterwards, intracranial and systemic, and is potentially preventable). Severity is graded by Glasgow Coma Scale on admission and post-traumatic amnesia during admission. The specific lesions (extradural, acute subdural, subarachnoid, intracerebral haematoma, contusions, diffuse axonal injury, traumatic brain swelling) are each defined by aetiology, location and frequency, and are illustrated by three worked cases. The last part is assessment (ATLS, neurological examination, imaging criteria), management (surgical and medical), the complications of post-traumatic epilepsy and brain death, and outcome scoring with prognosis by GCS.

Epidemiology

  • Incidence 800/100,000.
  • Leading cause of death in males aged 15 to 24 years.
  • Two thirds are dead on arrival at hospital.
  • Mode of injury depends on sex and age: male road traffic accident, female horseriding.
  • Leading cause of long-term disability.

Definition and classification

Definition (Jennett, 1977): a definite history of a blow to the head, presence of a cut or bruise, or altered level of consciousness no matter how brief.

Severity is graded two ways:

  • On admission: GCS.
  • During admission: post-traumatic amnesia (PTA).
SeverityGCSPTA
Mild13-150-24 hrs
Moderate9-121-7 days
Severe5-81-4 weeks
Critical3-4>4 weeks

Glasgow Coma Scale

Three components, scored and summed. Eye opening 1-4, vocal response 1-5, best motor response 1-6.

Eye opening:

  • 4 opens eyes spontaneously
  • 3 opens eyes in response to speech
  • 2 opens eyes in response to painful stimulation (eg endotracheal suctioning)
  • 1 does not open eyes in response to any stimulation

Motor response:

  • 6 follows commands
  • 5 makes localized movement in response to painful stimulation
  • 4 makes nonpurposeful movement in response to noxious stimulation
  • 3 flexes upper extremities / extends lower extremities in response to pain
  • 2 extends all extremities in response to pain
  • 1 makes no response to noxious stimuli

Verbal response:

  • 5 is oriented to person, place and time
  • 4 converses, may be confused
  • 3 replies with inappropriate words
  • 2 makes incomprehensible sounds
  • 1 makes no response

How and why it is used: observe, speak, inflict pain judiciously. It measures the severity of the initial injury and is a prognostic indicator.

Primary versus secondary injury

Primary head injury:

  • Skull fracture, calvarial or basilar.
  • Penetrating injury.
  • Focal TBI: contusion, haematoma.
  • Diffuse TBI: concussion, diffuse axonal injury.

Secondary brain injury, intracranial: haematoma, swelling, raised ICP, vasospasm, infection, epilepsy, hydrocephalus.

Secondary brain injury, systemic: hypoxia, hypercarbia, hypotension, severe hypocarbia, fever, anaemia, hyponatraemia.

The list of TBI problems that structures the rest of the lecture: skull fracture, penetrating injury, extradural haematoma, acute subdural haematoma, subarachnoid haemorrhage, intracerebral haematoma, cerebral contusions, diffuse axonal injury, traumatic brain swelling.

Skull fracture and penetrating injury

Skull fracture classification, three axes:

  • Pattern, eg linear, depressed.
  • Anatomical, eg vault, base.
  • Type, eg closed, open.

Factors determining fracture: force of impact and the ratio of force to area, rate of loading, location of impact.

Penetrating head injury causes: local trauma to the structures damaged, haemorrhage, infection, and focal or associated injuries. Illustrated by skull X-rays showing a knife blade embedded through the skull into the cranial cavity.

Extradural haematoma

  • 2% of all head injuries, 15% fatalities.
  • Aetiology: arterial 50%, venous 40%.
  • Location: temporoparietal 75%, frontal 10%, posterior fossa 5%.
  • CT appearance: lens-shaped (biconvex) hyperdense collection along the inner skull margin with mass effect.

Acute subdural haematoma

  • 5-22% of severe TBI.
  • Aetiology: ruptured bridging veins, burst lobe, brain laceration.
  • Severe diffuse injury in more than 50%.
  • Mortality 60-70%.

Case, 28-year-old male, car versus power pole, unconscious when found, time unknown. Ambulance: ventilated, GCS 4, vitals OK. Fixed and dilated left pupil. CT showed subdural haematoma with shift. Craniotomy and evacuation of the haematoma. In ICU there were ongoing bleeds with ICP increasing above 30 and unmanageable. Induced coma, mannitol and hypothermia were used, with ongoing deterioration, and treatment was withdrawn at 1 week.

Subarachnoid haemorrhage

  • Trauma is the commonest cause of SAH, and the injury can be trivial.
  • Aetiology: injury to vessels in the subarachnoid space, leak from contusions.
  • Significance: hydrocephalus and vasospasm.
  • Intraventricular haemorrhage is rare.

Intracerebral haematoma

  • Defined as greater than 2 cm with no surface contact.
  • 20% of severe TBI.
  • Aetiology: shearing of small vessels, coalescence of petechiae, delayed secondary bleed.
  • Location: frontal or temporal 80-90%, multiple in 20%.

Cerebral contusions

  • Common.
  • Definition: surface haemorrhage, necrosis and infarction.
  • Aetiology: extravasation from injured vessels, bleeding into an infarct.
  • Location: gyral injury related to skull corrugation and to barriers.
  • Contra-coup pattern: injury at the site opposite the impact, shown on CT as bilateral petechial haemorrhages near the frontal horns and a contralateral hypodense region.

Case, 69-year-old male, fell off a ladder. In A&E GCS 13 with two seizures, admitted. CT showed frontal and sub-frontal petechiae. Deteriorated over 24 hours with decreased level of consciousness and respiratory difficulty. Second CT showed progression of the contusions and a right frontal subdural bleed. Right frontal lobectomy to relieve ICP. Did well.

Diffuse axonal injury

  • Aetiology: rotational acceleration.
  • Location: subcortical white matter and deep white matter.
  • Poor prognosis.
  • Pathology shows multiple small haemorrhagic (petechial) foci scattered through white matter; CT may show little.

Case, 32-year-old male, road traffic accident, GCS 3 at the scene. Ventilated; in hospital E1V1M4 = GCS 6. CT appeared normal with some petechiae. Neurological testing showed extensor responses, indicating upper brainstem injury. At 9 days E4V1M2 = GCS 7, breathing unassisted, left ICU, still with extensor responses. No anatomical abnormality on CT, so the injury was likely diffuse axonal injury.

Traumatic brain swelling and raised ICP

  • Cerebral oedema types: vasogenic or cytotoxic, osmotic or hydrostatic.
  • Distribution: focal, regional or generalised, with brain shift.
  • Monro-Kellie doctrine: the cranium is a fixed volume, .
  • The consequence is raised intracranial pressure.
  • Cerebral perfusion pressure: .
  • Effects: reduction in cerebral blood flow, and cerebral herniation.

Cerebral herniation

Classification:

  • Supratentorial: subfalcine; lateral (uncal); central (down).
  • Infratentorial: central (up); tonsillar.

Effects: compression of brain or cranial nerve, and vascular occlusion.

Warning

The slide diagram shows arrows a-e at five brain locations keyed to the five herniation types, but the slide does not state which letter corresponds to which type, so the mapping is not given.

Secondary post-traumatic brain lesions

  • Medial temporal necrosis caused by the tentorium.
  • Focal infarction due to arterial compression against structures, eg PCA against the tentorium.
  • Border zone infarcts due to ischaemia.
  • Diffuse ischaemic necrosis due to high ICP.
  • Duret haemorrhages in the brainstem, caused by transtentorial herniation.

Clinical assessment

Advanced Trauma Life Support protocol, in order:

  1. Primary survey: AVPU.
  2. Resuscitation: ABC.
  3. Secondary survey: head to toe.
  4. Definitive care.

Also take a history and look for evidence of alcohol or drug use.

Neurological examination:

  • External signs of head and spine injury.
  • Neurological examination: level of consciousness, cranial nerve examination, limb/torso examination, brainstem reflexes.
  • Cardiorespiratory patterns.
  • Urinary retention or incontinence.

Imaging

Radiological options: plain X-ray of skull and cervical spine, CT scan of head and C0 to C2, MRI scan, cerebral angiography.

Skull X-ray in TBI:

  • No value in screening where a CT scan is available.
  • If no CT scan is available and the patient does not fulfil criteria for transfer for CT, skull X-ray should be done to stratify risk.
  • In mild TBI (GCS 15), the presence of a skull fracture raises the risk of intracranial haematoma from 1/6000 to 1/30.

Important

CT scan guidelines: GCS <9 after resuscitation; drowsiness or confusion more than 2 hours post injury (GCS 9-14); deterioration in GCS greater than 2; focal neurological signs or seizures; skull fracture or penetrating injury; age over 50 years.

Management

Overall aims:

  • Diagnosis of the type of brain and/or spinal injury.
  • Treatment of the primary brain or spinal cord injury.
  • Treatment and prevention of systemic causes of secondary injury.
  • Monitoring of clinical progression.

Surgery in acute TBI:

  • Intracranial pressure monitoring, eg fibreoptic monitor, external ventricular drain.
  • Evacuation of intracranial haematoma.
  • Debridement of compound and depressed skull fractures.
  • Salvage procedures in intractable raised ICP, eg craniectomy, lobectomy.

Medical management:

  • Clinical surveillance.
  • Invasive monitoring of BP, CVP, ICP.
  • Treatment of raised ICP, directed at (a) the cause and (b) the effect.
  • Identification of delayed surgical problems.

Post-traumatic epilepsy

  • Occurs in 5% of all TBI.
  • Classified by timing (immediate versus early versus late onset) and by seizure type (simple or complex partial versus generalised).
  • High risk patients are identified.
  • Prophylaxis in severe TBI is with phenytoin.

Brain death

  • There is a legal definition.
  • Brain death criteria: Glasgow Coma Score 3; no brainstem reflexes; no ventilatory effort.
  • Precise physiological requirements apply.
  • Two sets of tests at least 2 hours apart.

Outcome and prognosis

Outcome measures: Glasgow Outcome Scale and Karnofsky Disability Assessment.

Prognostic indicators: age, comorbidity, GCS, brainstem reflexes, CT appearances, ICP, EEG, SSEP.

Glasgow Outcome Scale:

  1. Death: severe injury or death without recovery of consciousness.
  2. Persistent vegetative state: severe damage with a prolonged state of unresponsiveness and a lack of higher mental functions.
  3. Severe disability: severe injury with permanent need for help with daily living.
  4. Moderate disability: no need for assistance in everyday life, employment is possible but may require special equipment.
  5. Low disability: light damage with minor neurological and psychological deficits.

Prognosis by admission GCS:

GCSGOS 4-5GOS 1-2
11-1591%6%
8-1059%27%
5-728%54%
3-413%80%

Self-test

  1. State Jennett’s 1977 definition of traumatic brain injury.
  2. Give the GCS range and the post-traumatic amnesia duration for each of the four severity grades.
  3. List the three components of the Glasgow Coma Scale with the score range of each.
  4. A patient localises to pain, opens eyes to speech and replies with inappropriate words. Calculate the GCS and state the severity grade.
  5. Distinguish primary from secondary brain injury, and list the intracranial and systemic causes of secondary injury.
  6. List the three axes by which a skull fracture is classified, with an example of each.
  7. Describe the epidemiology, aetiology and typical location of extradural haematoma.
  8. Distinguish acute subdural haematoma from extradural haematoma by aetiology and mortality.
  9. Explain why trauma matters as a cause of subarachnoid haemorrhage and what its two main consequences are.
  10. Define intracerebral haematoma and list its three aetiologies.
  11. Define cerebral contusion and explain what determines where contusions occur.
  12. Describe the aetiology, location and prognosis of diffuse axonal injury, and explain why the CT may look normal.
  13. State the Monro-Kellie doctrine and the equation for cerebral perfusion pressure, and predict what happens to CPP as ICP rises.
  14. Classify the types of cerebral herniation and give the two effects of herniation.
  15. List the secondary post-traumatic brain lesions and the mechanism of each.
  16. List the four stages of the ATLS protocol in order and what each involves.
  17. When is a skull X-ray still useful in TBI, and by how much does a skull fracture change the risk of intracranial haematoma in mild TBI?
  18. List the CT scan guidelines for TBI.
  19. List the four categories of surgery in acute TBI.
  20. State the incidence, classification and prophylaxis of post-traumatic epilepsy.
  21. State the three brain death criteria and the testing requirement.
  22. List the five grades of the Glasgow Outcome Scale.
  23. What proportion of patients with an admission GCS of 3-4 reach GOS 4-5, and what proportion reach GOS 1-2?
  24. Integrative: a 28-year-old is brought in ventilated with GCS 4, vitals normal and a fixed dilated left pupil. Explain what lesion and process this suggests, what the CT is likely to show, and how it is managed.

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