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Emergency Neurotrauma

Head Injuries in Emergency Medicine

Dr Brett Gerrard Emergency Medicine Specialist Middlemore Hospital

Overview

What is neurotrauma?

How do we classify injuries

What goes wrong?

Pathogenesis of brain injury

How bad is it?

Assessment of Head Injuries

How do we fix it?

Resuscitation in neurotrauma

Definition

 Approx 700 per 100 000 NZ population  Responsible for the majority of trauma deaths  Occurs on a continuum  Classification can guide approach to investigation and therapy    Minimal Mild Moderate-Severe

Minimal Head Injuries

 No loss of consciousness  Normal alertness and memory  No neurological deficit  GCS 15  No signs of skull fracture

Mild Head Injuries

 Brief (<5min) loss of consciousness  Amnesia (retrograde vs anterograde)  GCS 14-15  Impaired alertness  No signs of skull fracture

Moderate or severe Head injury

 Prolonged (>5min) loss of consciousness  Persistant GCS <14  Focal neurological deficit  Seizure  Signs of skull fracture

Pathogenesis of Brain Injury

 Primary (Immediate)  Forces and disruptive mechanisms of original incident  Secondary (2-24 hours post injury)  Multiple factors  Cerebral hypoxia due to impaired blood flow complicated by     Vasospasm Oedema Cellular dysfunction This is the injury that we can potentially prevent!

Classification of Neurotrauma Injuries

1 Skull fractures 2 Concussion 3 Contusion 4 Diffuse axonal injury 5 Intracranial haematoma 6 Penetrating injury

Skull Fracture

 Increased risk of associated neurotrauma.

 Location of fracture important    Base of skull Cribiform plate Depressed fractures

Concussion

 “Transient alteration in cerebral function, usually associated with LOC and often followed by rapid or complete resolution”  Disturbance in RAS  Symptoms include    Headache Altered cognition Nausea  Second Impact Syndrome

Contusion

 Bruising of the brain substance  Usually due to blunt trauma  Fractures are uncommon  May lead to haematoma and oedema formation  Most common in frontal and temporal lobes

Diffuse Axonal Injury

 Predominant mechanism of injury in neurotrauma  Physical forces (shearing and rotational) disturb the axonal network at a miscroscopic level  Minimal changes may be evident on CT  Clinical sequelae can range    subtle neuropsychiatric changes Severe cognitive impairment Psychomotor retardation

Intracranial Haemorrhage

 Defined anatomically     Subdural Extradural Intracerebral Subarachnoid

Extradural

 Uncommon  Usually associated with temporal bone fracture  Expanding haematoma strips dural away from bone  Increasing intracranial pressure and uncal herniation  Lenticular shape on CT

 May be acute, subacute or chronic  Much higher risk in elderly  Seen in non accidental shaking in children  Acute subdural high mortality rate approx 50%

Subdural

Intracerebral

 Most commonly frontal and parietal lobes  Clinical sequelae dependent on site  May be primary or secondary due to underlying contusion  Symptoms and complicationsmay be delayed

Subarachnoid

 Relatively common in severe head trauma.

 May co-exist with other bleeding sources  Extention into the interventricular spaces may lead to raised ICP.

 Subarachnoid blood can lead to cerebral vasospasm and secondary ischaemic brain injury

Penetrating Trauma

 Very high levels of morbidity and mortality  High velocity   Gunshot Impalement  Low velocity   Knife Crush  Generally very dismal outlook although…

Assessment of Neurotrauma

History

Examination

Investigations

History

 Detailed history can help attribute degree of risk  High Risk mechanisms are utilised by several clinical rules      Pedestrian/cyclist struck by car Fall from height of >1m or 5 stairs Ejected from vehicle Penetrating injury/blow to head with weapon Suspicion of NAI

 Patient factors  Risk factors for bleeding     Co-morbidities Drugs Extremes of age Difficulties in patient evaluation

 Was there loss of consciousness?

  How long?

Any seizures?

 Can you remember what happened?

 Before? (Retrograde)  After? (Anterograde)  Any vomiting?

 How many times?

 Do you have a headache?

 Does it improve with medication?

Examination

 Integral part of primary and secondary survery     ABC evaluation still remains priority Remember risk of cervical spine injuries Facial injuries Assessment of neurological disturbance     AVPU (Paediatric scoring system) GCS (Glasgow Coma Score) Focal neurological signs Early signs of raised intracranial pressure

 GCS slide

Signs of Skull Fracture

 Rhinorrhoea  Haemotympanum  Battles Sign  Racoon Eyes

Investigations “To CT or not to CT?”

 Minimal Head Injuries  No imaging required  Moderate-Severe Head Injuries      Prolonged (>5min) loss of consciousness Persistant GCS <14 Focal neurological deficit Seizure Signs of skull fracture CT =Investigation of choice

 Mild Head Injuries……?

 Several clinically derived decision rules have been developed     New Orleans CHIP Canadian CT Head Rule CATCH  Why not just scan EVERYBODY??

Risks of CT

 Sedation/compliance  Time  Costs  Ionizing radiation

Indications for Head CT in Trauma

 A CT scan is indicated for an adult patient with a head injury if they have one of the following:

1. A Dangerous Mechanism

    Pedestrian hit by a car Fall from >1 metre (or 5 stairs) Blow to head with weapon Ejected from vehicle Based on Canadian CT Head Rules Stiel et al. Lancet. 2001 May 5;357(9266):1391-6 Initial Data approx 3100 patients GCS 13-15.

Indications for Head CT in Trauma

2. Patient History factors

     Age >65 On warfarin or dabigatran Vomited 2 or more times Knocked out for >5 min Persistant retrograde amnesia >30min or persistant anterograde amnesia Based on Canadian CT Head Rules Stiel et al. Lancet. 2001 May 5;357(9266):1391-6 Initial Data approx 3100 patients GCS 13-15.

Indications for Head CT in Trauma

3. Patient Exam findings

   GCS 13 or less on arrival Persistant GCS <15 after 2 hours Signs of a skull fracture Based on Canadian CT Head Rules Stiel et al. Lancet. 2001 May 5;357(9266):1391-6 Initial Data approx 3100 patients GCS 13-15.

Paediatric Head Injury Issues

 Differences in mechanism  Differences in anatomy  Signs may be subtle  More prone to cerebral oedema  Difficult in assessing GCS  Potential for non accidental injury  Radiation exposure