We can broadly divide cerebral haemorrhages into 2 categories:
- Intra-axial haemorrhages - within the substance of the brain. For example, intracerebral haemorrhages.
- Extra-axial haemorrhages - outside the substance of the brain. For example, epidural, subdural and subarachnoid haemorrhages.
Let’s discuss all of these specific types individually…
Pathophysiology
This is when there is bleeding between the dura and the skull which then clots to form a haematoma.
It is mostly due to trauma due to acceleration-deceleration trauma or a blow to the side of the head. It usually has a concomitant skull fracture.
They mostly occur in the temporoparietal region (the pterion) as this is the thinnest region and easily fractured. The artery most often involved is the middle meningeal artery (which is a branch of the maxillary artery). However, it occasionally occurs due to venous extradural haemorrhage (venous blood).
😷 Presentation
- Lucid interval - patients lose consciousness after the injury and then regain their consciousness (the lucid interval) and then they gradually lose their consciousness again.
- Severe headache
- Nausea and vomiting
- Confusion
- Increased ICP
🔍 Investigations
🏆 Non-contrast CT head - shows a distinct biconvex shape.
Examination:
On examination, we may see Cushing’s triad due to raised ICP.
🚨 Complications
A rising ICP with a growing EDH will lead to herniation of the brain which can eventually cause coning of the brain as it is forced through the foramen magnum which then causes brainstem death.
🧰 Management
- Conservative management:
- Surgical management:
If it is solely a small EDH, it may simply be monitored regularly with CT.
Burr hole craniotomy or trauma craniotomy for haematoma evacuation. The prognosis is usually good if it is removed promptly (if it is large enough to warrant surgery).
This is a bleed into the subdural space. Within the subdural space we find bridging veins which rupture and cause a subdural haematoma.
They can be divided into:
- Acute
- Subacute
- Chronic
It too causes a rise in ICP and compresses the parenchyma of the brain. This then can cause a herniation of the brain as well.
Unlike the epidural haematomas, these are not limited by cranial sutures and can spread over a larger area. In infants, 80% are bilateral (however, in adults 80% are unilateral).
Acute subdural haematoma
Caused by high-impact trauma and is often accompanied by brain contusions and EDH.
😷 Presentation
The presentation is totally dependant on the area of injury and the size of the injury/haematoma. It can range from asymptomatic → severe coma.
🔍 Investigations
🏆 Non-contrast CT head - will show a crescent-shaped hyperdense collection. It may also lead to a midline shift if the haematoma is big enough (mass-effect). The more coagulated the blood is, the higher the density on a CT (acute SDH has fresh coagulated blood and is hyperdense as a result).
Chronic subdural haemorrhage
This is an SDH that has been present for weeks-months. It occurs due to atrophy of bridging veins over an extended period of time → slow bleeding.
Presents in alcoholics or elderly.
😷 Presentation
- Confusion
- Vague neurological changes - causing pseudodementia.
⚠️ Risk factors
- Elderly age
- Alcoholism
- DOAC/warfarin use
🔍 Investigations
🏆 Non-contrast CT head - will show a crescent-shaped isodense/dark collection. This is because the clot has had time to age and fibrinolysis has occurred.
🧰 Management
- A-E assessment & stabilisation of the patient.
- Clotting correction if needed.
- Anticonvulsants if the patient has a history/risk of seizures.
- Phenytoin
- Conservative management
- Surgical management
If asymptomatic → regular CT monitoring.
Chronic SDH → surgical decompression with burr holes.
Acute SDH → trauma craniotomy for haematoma evacuation.
The subarachnoid space contains CSF. If a bleed occurs in this region, it is a medical emergency. Half of the patients die immediately or shortly after the haemorrhage. 90% of patients die within the 1st month.
It can be divided into traumatic SAH and spontaneous SAH.
Pathophysiology
The most common cause for a spontaneous SAH is a ruptured intracranial aneurysm (a berry aneurysm). This makes up 80% of spontaneous cases. However, the overall leading cause of SAH is still trauma.
⚠️ Risk factors
- Hypertension
- Smoking
- Family history
- Connective tissue disorders - autosomal dominant polcystic kidney disease, Ehler Danlos, Marfans, neurofibromatosis type 1.
- Female gender
- Alcohol/cocaine abuse
😷 Presentation
Patients to be in the older middle age group (<60 years old).
- Sudden thunderclap headache - peaking within 1-5 minutes and lasting more than an hour.
- Depressed/loss of consciousness
- Nausea and vomiting
- Meningism - photophobia, neck stiffness etc.
- Focal neurological deficits - can be used to identify the location of the aneurysm.
- Ocular changes
Investigations
🏆 Non-contrast CT head - will show hyper-dense filling of the sulci and SAS. It is especially seen in the Circle of Willis. A star shaped sign may be seen at the level of the medulla.
Once a diagnosis is confirmed we need to identify the pathology requiring urgent treatment. This may be done with:
- CT intracranial angiogram - to identify the vascular lesion.
- ± digital subtraction angiogram - to detect blood floe impairments within the blood.
🏆 If CT is negative, a lumbar puncture must be done. A positive diagnosis would be through the detection of bloody CSF. This is called xanthochromia and occurs due to the breakdown of RBCs into bilirubin within the CSF.
- FBC
- Glucose
- U&Es - hyponatraemia is the most common finding.
- Clotting profile
- Troponin I - patients with elevated cardiac troponin I levels have worse neurological status at admission in-hospital mortality.
- ECG - widespread deeply inverted T waves.
🧰 Management
Traumatic and spontaneous SAHs are medical emergencies and require urgent referral to neurosurgery.
- Monitor CNS frequently
- If GCS is <8 - A-E assessment and stabilisation immediately.
- PEARLA
- BP - keep BP <160mmHg but maintain hydration of the patient.
- Nimodipine - a calcium channel blocker that prevents arterial vasospasm and prevents delayed cerebral ischaemia. To be given for 21 days.
- Paracetamol/analgesia for the headache
- Obliteration of ruptured aneurysm
- Endovascular coiling - to prevent blood flow into an aneurysm.
- Ballon angioplasty - if the patient develops subsequent cerebral vasospasm.
- Ventricular drainage - if there is a secondary hydrocephalus.
🚨 Complications
- Obstructive hydrocephalus - due to blockage of the arachnoid granulations → impaired drainage of CSF. Requires shunting.
- Re-bleeding - most common cause of death.
- Arterial vasospasm - leading to cerebral ischaemia.
- Neurological deficits
- Hyponatraemia - should not be managed with fluid resuscitation.
This is a haemorrhage within the parenchyma of the brain.
🔢 Classification
- Primary intracerebral haemorrhage (spontaneous) - initial damage to the parenchyma with no underlying lesion.
- Can be a hypertensive haemorrhage or lobar haemorrhage (due to cerebral amyloid angiopathy)
- Secondary intracerebral haemorrhage - another lesion present which becomes complicated by the haemorrhage.
- Can be due to vascular malformation, venous thrombosis, tumour.
⚠️ Risk factors
- Hypertension
- Vascular lesion - such as aneurysm or arteriovenous malformation.
- Cerebral amyloid angiopathy
- Trauma
- Tumour
- Infarction - particularly in stroke patients who are undergoing thrombolysis.
😷 Presentation
Patients will present similar to an ischaemic stroke with decreased consciousness.
🔍 Investigations
🏆 CT head - showing hyperdensity within the substance of the brain.
🧰 Management
Stroke physicians need to carefully watch. Large clots in patients with impaired consciousness may warrant surgical evacuation.
SAH Grading 1-5