An extradural (or epidural) haemorrhage is bleeding which forms between the dura mater and the skull, usually after trauma.
Pathophysiology
- The most common cause of extradural haemorrhages are head traumas that result in skull fractures.
- The most common culprit of bleeding is the middle meningeal artery, a vessel underlying the pterion. The pterion is a weak point in the skull due to it being the point at which all 4 bones of the skull join at.
- In case of an extradural bleed, blood will start to rapidly collect between the dura and the skull due to the higher pressures associated in the arterial system. This forms a collection of blood i.e. a haematoma.
- The haematoma becomes restricted due to the bony skull and cannot expand outwards and starts to push inwards onto the brain instead.
- This will lead to rising pressures in the cranium, known as a raised intracranial pressure which is what produces symptoms such as vomiting, loss of consciousness or drowsiness.
- Cushing reflex is something that is seen in cases of acutely raised intracranial pressure.
- If intracranial pressure rises above the mean arterial pressure, it starts to result in cerebral ischaemia due to compression of the vasculature of the brain.
- At first, this activates the sympathetic nervous system to cause vasoconstriction and thus raise blood pressure in attempts to increase perfusion to the brain.
- This then results in baroreceptors detecting raised blood pressure, thus activating the parasympathetic nervous system in response to a high blood pressure. This causes a bradycardia.
- Finally, as ICP continues to rise, it can put pressure on the brainstem which results in irregular breathing patterns.
- The headache associated with these types of bleeds is thought to arise due to tearing of the dura mater away from the skull.
Clinical Features
A typical history usually involves the following:
- Trauma to the head
- Brief loss of consciousness
- A lucid interval: patient regains consciousness – this can be falsely reassuring but blood will continue to accumulate in this time. This period can last a few hours and sometimes even days.
- Deterioration: As intracranial pressure starts to rise, you begin to get symptoms which could be;
- Severe headache
- Vomiting
- Seizures
- GCS: Eventually with a rising intracranial pressure, patients will begin to get drowsy and their GCS will start to drop
- Cushing’s reflex: This is a physiological response to raised intracranial pressure. It is a triad of hypertension, bradycardia, and irregular breathing.
Investigations
Bloods
- FBC, U&E, CRP: Baseline
- Clotting: Checking for coagulopathy
- Blood Glucose: Rule out hypoglycaemia in case the patient is presenting with seizures/low GCS
- Group & Save: In case the patient goes to theatre
Imaging
- CT Scan: A positive finding will show a hyperdense biconvex or lens shaped opacity (basically a white collection on CT). It will be quite localised i.e. it won’t span the whole skull. This is because it is limited by the dura which is very firmly attached at suture sites of the skull.
Management
- Patients should initially be stabilised using an A-E approach (Airway, Breathing, Circulation, Disability and Exposure).
- Patients require urgent neurosurgical input in order to assess if the patient will be managed conservatively or surgically.
- The Brain Trauma Foundation recommends patients who have a haematoma which is greater than 30cm3should have surgical treatment although other factors such as co-morbidities would need to be considered prior to taking a patient to theatre.
- Conservative management usually involves neurological observations (regularly monitoring GCS and pupil response) alongside serial CT head scans whilst surgical management usually involves craniotomy/Burr hole procedures.
References
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4611902/
https://www.ncbi.nlm.nih.gov/pubmed?term=3354356
https://emedicine.medscape.com/article/1137065-medication
https://braintrauma.org/guidelines/guidelines-for-the-surgical-management-of-tbi#/:guideline/surgical-management-of-acute-epidural-hematomas