ED - Head Injuries Flashcards
Assessment of Head Injuries
Definition
History Taking
Examinations
1.) Definition - any head trauma other than superficial facial injuries
- traumatic brain injury occurs when a head injury results in a disturbance of normal brain function
- traumatic brain injury can be categorized as mild (concussion), moderate, or severe
2.) History Taking
- mechanism of injury, high energy mechanisms: fall >1m/5 stairs, high-speed RTC, ejection from a motor vehicle, diving accident
- sx: LOC, confusion, amnesia, N+V, headache, neck pain, visual disturbance
- other hx: anticoagulant medication, recent alcohol or drug intake, PMH inc pre-injury level of functioning, bleeding disorders, surgery, and previous head trauma
3.) Examinations
- GCS, vital signs, visible signs of trauma, cranial nerve exam
- signs of focal neurological deficit: visual or speech disturbance,
problems with balance or walking, reduced muscle power, paraesthesia, abnormal reflexes
- signs of basal skull fracture: CSF rhinorrhoea or otorrhoea, Battle’s sign (bruising of the mastoid process), periorbital haematoma (w/ no eye damage), bleeding from ears or haemotympanum, new deafness
- signs of C-spine injury: neck tenderness, inability to rotate the neck 45 degrees to the left and right (avoid if neck tenderness present)
Brain Injuries
Pathophysiology
Concussion
Types of Severe Traumatic Brain Injury
Complications
1.) Pathophysiology
- primary brain: focal (contusion/haematoma) or diffuse (axonal injury)
- contusions may occur adjacent to (coup) or contralateral (contrecoup) to the side of impact
- diffuse axonal injury (DAI) occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons
- cerebral autoregulatory processes are disrupted following trauma so the brain more susceptible to blood flow changes and hypoxia
- Cushing’s reflex (↑BP, ↓HR) occurs late and is usually pre-terminal
2.) Concussion - transient disturbance in the function of the brain caused by head injury
- sx: headache, dizziness, difficulty concentrating, and confusion
- continuing to play a contact sport increases the risk of further head or non-head injury, worsened severity, and delayed recovery
- most people with persistent symptoms of mild traumatic brain injury recover within 2–3 months of the injury
- intracranial complications usually occur within 24hrs of the injury
3.) Types of Severe Traumatic Brain Injury - intracranial haematomas
- extradural, subdural and subarachnoid haematoma/haemorrhage
- intracerebral haemorrhage: haemorrhagic stroke
4.) Complications
- secondary brain injury: cerebral oedema pushes out CSF and venous blood, prevents arterial blood flow leading to ischaemia
- raised ICP: can lead to tonsillar or tentorial herniation
- SIADH causing hyponatraemia due to pituitary dysfunction
Diffuse Axonal Injury
- can be seen on a CT as a loss of grey-white differentiation
General Management of Head Injuries
CT Head Criteria
Other Investigations
Management of Raised ICP
1.) CT Head Criteria (within 1 hour)
- GCS <13 on initial assessment in ED OR <15 at 2 hours after the injury
- suspected open or depressed skull fracture.
- any sign of basal skull fracture: haemotympanum, ‘panda’ eyes, CSF rhinorrhoea or otorrhoea, Battle’s sign
- focal neurological deficit, post-traumatic seizure.
- more than 1 episode of vomiting
- Within 8 hours: LOC and/or amnesia with the following risk factors: >65s, bleeding or clotting disorders, anticoagulant use, dangerous mechanism of injury^^, >30mins of retrograde amnesia from the onset of the event
2.) Other Investigations
- X-ray C-spine: suspicion of a C-spine injury
- CT-C-spine: abnormal X-ray
- ICP monitoring: GCS 3-8 w/ abnormal CT (consider if normal CT), GCS starts to fall as oedema starts becoming too high
- arterial line should be inserted to monitor the MAP
- ECG: may see global T wave inversion or QT prolongation (in raised ICP)
3.) Management of Raised ICP: CPP = MAP - ICP
- minimum CPP: 70mmHg in adults, 40-70mmHg in children
- hyperventilation to reduce CO2 (↑ICP –>↓CPP –> ischaemia –> ↑CO2)
- therapeutic hypothermia to 32-25°C to prevent secondary injury
- other: elevate bed (↑venous drainage), analgesia/sedation to prevent pain, antipyretic to control fevers (avoid ICP spikes)
- IV mannitol or furosemide: may be used to reduce cerebral oedema to buy time for a few hours to transfer patients to a trauma centre
- decompressive craniotomy: for diffuse cerebral oedema
Depressed skull fractures that are open require formal surgical reduction and debridement, closed injuries may be managed nonoperatively if there is minimal displacement.
Extradural Haematoma
Pathophysiology
Clinical Features
Investigations
Management
1.) Pathophysiology - collection of arterial blood between the dura and the skull/periosteum
- mostly due to ‘low-impact’ trauma (e.g. a blow to the head or a fall)
- most commonly occurs in the temporal region as the pterion (thin skull) overlies the MMA is more vulnerable to injury
2.) Clinical Features
- initial LOC after a low-impact head injury followed by a ‘lucid interval’ (not always present) where the patient regains consciousness then eventually loses it again
- sx of raised ICP during the lucid interval until LOC occurs again
- lucid interval is lost due to expanding haematoma and brain herniation
- fixed and dilated pupil (terminal): due to compression of CN III as the uncus of the temporal lobe herniates (transtentorial) as the haematoma expands
3.) Investigations
- CT-Head: biconvex (lens/lemon), hyperdense collection around the surface of the brain, limited by the suture lines of the skull
4.) Management - referral would be to NEUROSURGERY
- cautious clinical and radiological observation in patients w/ no neurological deficit
- definitive treatment: craniotomy and evacuation of the haematoma
Subdural Haemorrhage
Pathophysiology
Clinical Features
Investigations
Management
1.) Pathophysiology - venous bleed between dura and arachnoid mater
- chronic: collection of blood that has been present for weeks to months, often due to the rupture of small bridging veins within the subdural space
- risk factors: elderly (esp w/ dementia), alcoholism, infants, on anticoagulation
- acute: collection of fresh blood within the subdural space most commonly caused by high-impact trauma, it is often associated with other underlying brain injuries
2.) Clinical Features
- chronic: several weeks to month progressive history of either fluctuating confusion or consciousness or neurological deficit with a previous hx of a mild head injury
3.) Investigations
- CT-Head: crescentic (banana-shaped) collection, not limited by suture lines of the skull so can compress the brain causing mass effects (e.g. midline shift)
- chronic subdurals are hypodense (darker than the brain) whilst acute subdurals are hyperdense (brighter than the brain)
4.) Management
- conservative: small or incidental finding w/ no associated neurological deficit
- surgical decompression w/ burr holes: large/severe or associated neurological deficit
Subarachnoid Haemorrhage (SAH)
Pathophysiology
Risk Factors
Clinical Features
Imaging/Investigations
1.) Pathophysiology - arterial bleed between the arachnoid and pia mater
- spontaneous SAH: often due to a ruptured ‘berry’ aneurysm (85%), other causes include: infective (mycotic) aneurysm, arteriovenous malformation, arterial dissection, pituitary apoplexy, perimesencephalic SAH (venous)
- traumatic SAH: occurs due to head injury
2.) Risk Factors
- conditions associated with berry aneurysms: ADPKD, CT disorders (Marfan’s or Ehlers-Danlos), coarctation of the aorta
- smoking, alcohol, hypertension, family history
- cocaine use, sickle cell anaemia, neuro-fibromatosis
- peak incidence is 40-50, more common in women and Afro-Caribbean
3.) Clinical Features
- thunderclap headache: sudden onset occipital headache that occurs during strenuous activity, the pain is maximal at onset of the headache
- visual sx: diplopia, orbital pain
- neuro sx: speech, weakness, seizures, LOC
- meningism sx (blood leaks into CSF): photophobia and neck stiffness (not meningitis as it is sudden onset and there is no fever present)
- dizziness, N+V, high blood pressure, coma, seizures, sudden death
- ECG changes (including ST elevation)
4.) Imaging/Investigations
- 1°non-contrast CT Head: ‘star sign’ acute (hyperdense/bright) blood accumulates in basal cistern –> hyper attenuation in subarachnoid
- 2°LP (if CT is negative): done >12hrs from sx onset to allow xanthochromia (bilirubin in RBCs) to be seen, RBCs also increased
- 3°CT/MR Angiography (once SAH is confirmed): to locate the source of the bleeding and identify a causative pathology that needs urgent treatment
Management of a Subarachnoid Haemorrhage
Acute Management
Surgical Intervention
Complications
1.) Acute Management - referral to neurosurgery when confirmed
- intubation and ventilation if reduced consciousness
- vasospasm: nimodipine (CCB) used for prevention
- hydrocephalus: LP or insertion of a shunt
- seizures: antiepileptic medications
2.) Surgical Intervention - repair the vessel and prevent re-bleeding
- most intracranial aneurysms are treated with a endovascular coil (IR): insert a catheter into aneurysm sac to seal it off from the artery
- a minority require a craniotomy and clipping by a neurosurgeon: cranial surgery to clamp neck of aneurysm
3.) Complications - re-bleeding (occurs in 30% of cases)
- vasospasm: vasoconstriction due to CSF irritant, vasospasm can lead to global cerebral ischaemia
- cerebral oedema: hypoxia and extravasated blood
- acute hydrocephalus: blood blocks CSF drainage
- embolus: thrombi occlude smaller distal arteries
- hyponatraemia (SIADH), seizures
