Learning objectives

  • Causes of Haemorrhagic Stroke
  • Investigations
  • Management


Haemorrhagic strokes can often be sudden and devastating and Intracerebral haemorrhage makes up 15% approximately of all strokes with an additional 5% due to Subarachnoid haemorrhage. Mortality is high with 30-50% of patients dying within 30 days. In comparison with Ischaemic strokes they are much less common and comprise only a quarter of the number of ischaemic strokes. They tend to be more likely to present with severe headache, seizures and coma. Immediate CT scanning is diagnostic and highly sensitive and specific.


Haemorrhage can result from vessel rupture at any point in the vascular tree from the main artery coming of the circle of Willis to small penetrating arteries and arterioles, capillary beds and to draining venous system. The largest will be the rupture of Berry/Saccular aneurysms but these tend to cause high-pressure bleeding as seen in the classical subarachnoid haemorrhage. Rupture of smaller intraparenchymal vessels arterioles and smaller vessel can cause primary intracerebral haemorrhage. Various aetiologies exists from amyloid angiopathy to lipohyalinosis and microaneurysm formation and hypertension. Vascular anomalies such as arteriovenous malformations and cavernous angiomas (Cavernomas) can also bleed as well as disorders such as hereditary haemorrhagic telangiectasis. Other causes include tumours. Coagulopathies cause bleeds and these may be related to clotting defects which may be due to the use of antiplatelet drugs or Warfarin or DOACs or heparins or simply liver failure or haemophilias or thrombocytopenia. Often times risk factors such as a hypertensive bleed on an anticoagulant can appear to exacerbate what may have been a limited haemorrhage as haemostasis is difficult to achieve. Haemorrhage is locally destructive causing tissue damage and haematoma formation and pressure necrosis and even infarction in surrounding brain. Secondary effects include bleeding into and obstruction of the ventricular system. Venous sinus thrombosis obstruction and resulting back pressure can result in intraparenchymal haemorrhage but this appears to be due to pressure rather than vessel rupture so paradoxically patients are anticoagulated.

Bleeds are most often at or close to arterial pressure and spread out from a tear in the vessel usually splitting surrounding white fibre bundles or lie between and disrupt brainstem nuclei. Low-pressure bleeds may occur such as with cavernomas and venous infarction. With venous infraction it is the high venous pressure that pushes red cells out of the post-capillary vessels rather than a tear in a vessel and perhaps explains that anticoagulation is not disastrous in these patients as paradoxically it allows reperfusion, lowers venous pressure and reduces bleeding. Secondary oedema often exacerbates increased intracranial pressure and coma/coning. Blood can also extend into the ventricular system and can lead to obstructive hydrocephalus. Intraventricular haemorrhage in particular haemorrhage is a poor sign and often associated with clinical deterioration and worsening coma. Older atrophied brain may allow more room for expansion and less severe rises in ICP.


Haemorrhagic strokes make up a slightly higher proportion of all stroke cases in those of Afro-Caribbean origins and in those in Japan. Hypertension is likely the factor in the former and alcohol intake may be a factor in the latter.

Left Thalamic "Deep" bleed with haemorrhage into the ventricular system. This patient needed close monitoring for the development of obstructive hydrocephalus

Left Thalamic "Deep" bleed with Intraventricular haemorrhage


The main causes of haemorrhagic stroke are listed below. They depend very much on the age of the patient. For example cerebral amyloid angiopathy is largely a disease of the older generation (over the age of 70) and along with hypertension is the commonest cause of bleeds in the elderly. In younger patients structural lesions are all the more common such as AVM and even berry aneurysms. Other causes of stroke include the ever-increasing use of anticoagulation particularly with Warfarin but also the newer agents such as Dabigatran, Apixaban and Rivaroxaban. So, begin to think of why immediately. The patient on anticoagulants will need immediate reversal of the coagulopathy as quickly as possible. One of the main differentials when seeing a patient with an unclear history found on the floor with retrograde amnesia and intracerebral haemorrhage is which came first the bleed or the fall. A deep bleed is likely to be hypertensive but a lobar bleed especially with overlying soft tissue swelling on the CT skull or a fracture may suggest the fall came first and the blood is due to a head injury.

Types by Anatomy

  • Lobar (Cortex + subcortical white matter) haemorrhages
  • Deep haemorrhages - putaminal, thalamic, caudate, basal ganglia
  • Brainstem haemorrhage - pontine
  • Cerebellar Haemorrhage
  • Subarachnoid haemorrhage

List of differing causes

Causes of Haemorrhagic strokeMore Information
Hypertension Usually deep bleeds but may also be lobar. Found in the basal ganglia, thalamus, cerebellum, pons
Amyloid angiopathy Usually lobar bleeds
Aneurysmal Usually interlobar bleeds MCA in sylvian fissure, Midline with Anterior communicating
Arteriovenous Malformation Typically lobar bleeds but can also be deep
Anticoagulants/Bleeding disorders Usually lobar bleeds
Drugs Cocaine, Amphetamine
Venous Infarction Headache, seizures
Sickle Cell Disease Can cause both ischaemic and haemorrhagic stroke
Vasculitis Inflammation and disruption of vessel wall. Can be PAN, SLE, WG, Takayasu's disease, Temporal arteritis, Sarcoid, Behcet's disease
Infective endocarditis with septic emboli Causes mycotic aneurysms which can bleed. Careful with anticoagulating patients with active endocarditis
Tumours Can be primary brain tumours or metastases

Bleeding is a dynamic process and may well continue after the initial scan

Bleeding Factors that are important

There is quite a lot of evidence with serial scans that bleeding continues over hours and that haematomas can continue to expand. Any coagulopathy should be corrected. Once a hemispheric bleed reaches a volume of about 60 mls the local compensatory mechanisms fail and there is pressure on the brainstem which leads to coning and death. There is probably more space for haematoma expansion with a less marked rise in ICP in older patients with generalised atrophy. Acute Intracerebral Haemorrhage often causes acute hypertension which can worsen bleeding - careful reduction from very high levels (sustained over 180 mmHg) but not too much or this may lead to cerebral hypoperfusion and further insults. Sometimes small bleeds precede larger bleeds and this is particularly important with subarachnoid haemorrhage where the patient presents with a bleed and sustains a fatal rebleed several days later. The emphasis here is to get the patient to neurosurgery to stabilise the aneurysm with coiling or clipping. Vasospasm which can mimic an ischaemic stroke can also be seen post-SAH. Cerebral AVM can also rebleed. Complications with intracerebral bleeds include raised ICP and hydrocephalus, coning as well as seizures.


Out of all strokes only 15% of are due to intracerebral haemorrhage. Only 5% are due to subarachnoid haemorrhage. Prognosis of all haemorrhages is worse than ischaemic stroke with a 30-50% death expectation within 30 days

Clinical findings
Deep bleeds (42%)
  • Putaminal bleed (40% of bleeds occur here. Supply from lateral striate arteries): Contralateral hemiparesis and hemisensory loss. Conjugate horizontal eye deviation, homonymous hemianopia and aphasia (dominant), neglect (non dominant)
  • Thalamic bleed (4%): Similar to putaminal. May have vertical gaze palsy, miosis and poorly reactive pupils, convergence paraparesis
  • Caudate bleed: Confusion, disorientation, contralateral hemiparesis
  • Basal ganglia/Internal Capsule: Coma due to raised ICP, Contralateral hemiparesis and hemisensory loss and homonymous hemianopia and aphasia (dominant)

Lobar Bleeds(40%)

  • Frontal Lobe (19% of bleeds): headache, abulia, C/L hemiparesis (arm more than leg)
  • Parietal Lobe(5%): C/L hemisensory loss, aphasia (dom), homonymous quad/hemianopia
  • Temporal Lobe(13%): local headache, receptive aphasia (dom), confusion, homonymous quad/hemianopia
  • Occipital Lobe(5%): C/L hemianopia

Cerebellar (8%) - usually unilateral. Life threatening if over 3 cms and needs surgical evacuation

  • Nausea, vomiting, Ataxia, vertigo, diplopia
  • Headache, ataxia, past pointing, nystagmus to affected side
  • Midline lesions present with truncal ataxia

Brainstem (6%)

  • Pontine - coma, quadriplegia, decerebration, bilateral miosis, horizontal gaze palsy, locked in
  • Nausea, vomiting, vertigo, diplopia
  • Headache, ataxia, past pointing, nystagmus to affected side

Complications of ICH

  • Intraventricular extension associated with headache and sudden deterioration and coma.
  • Obstructive Hydrocephalus
  • Cerebral Oedema
  • Partial and Generalised Seizures
  • Rising Intracranial pressure
  • Systemic Hypertension - can worsen bleeding and cerebral autoregulation

Haemorrhagic stroke mimics

  • Head Trauma: - look for soft tissue injury. Can be difficult sometimes to work out did patient fall and hit head and have bleed or did the bleed come first. The pattern of bleeding tends to be different and does not fit the typical pattern of amyloid or hypertension. There may well be subarachnoid extension or subdural bleeding. There may be superficial cutaneous haematomas suggesting direct skull trauma. One may see classical contre-coup injuries and bleeding. Any bleeding is made worse by co-existing antithrombotic medications.
  • Tumours with Haemorrhage: - primary or metastatic. If there is suspicion then arrange MRI or CT with contrast once the haematoma has resolved. See the table below for a list of metastatic tumours that are more often associated with bleeding.

Metastatic Tumours that Bleed
Bronchogenic carcinoma
Thyroid carcinoma
Renal cell carcinoma

Ischaemic strokes can have secondary haemorrhage: These can be easily mistaken as primary ICH rather than infarction and haemorrhage. See below

Causes of Ischaemic Strokes that can cause Haemorrhage
Haemorrhagic Transformation - seen with embolic strokes that reperfuse and may be exacerbated if thrombolysis or anticoagulated
Endocarditis with mycotic aneurysms from cardioembolism and worse if anticoagulated
Cerebral Venous thrombosis with seondary back pressure bleeding
Sickle Cell disease
Cerebral Vasculitis
Moyamoya disease

As with ischaemic stroke it is not enough to simply diagnose haemorrhage without considering the likely pathology behind it, particularly so in the younger patient. The underlying aetiology may be anything from bleeding within a small tumour mimicking stroke to a vascular anomaly or even a venous infarction with haemorrhage requiring anticoagulation. In most cases of those over the age of 70 the diagnosis will be that of longstanding hypertensive disease or amyloid angiopathy or a mixture of both. Hospital post mortems are becoming much less common and so preciseness in the diagnosis in these cases is difficult and various criteria have been set to give a degree of precision about the diagnosis. In recent years advances particularly in imaging have led us to the discovery of 'microhaemorrhages/microbleeds'. Their exact importance and risk to patients is a subject of much research. One of the difficulties is that often the same patients are at risk of both thrombosis and haemorrhage and a weighing up of maximising therapeutic benefit and reducing harm is proving challenging. The last decade has also seen advances in the understanding of those with haemorrhagic stroke who may benefit from surgery. The evidence base continues to grow and clinicians continue to try to use this evidence most effectively for patients. Here we shall discuss the various causes and effects of haemorrhagic stroke.


Tests tend to be much fewer and the differential easier than ischaemic strokes. In the older patient with a lobar bleed due to suspected amyloid angiopathy there may be no reason to do any further imaging. In a younger patient it would be vital to get MRI/MRA or CTA or CT angiography if is there was any concern about an underlying vascular anomaly at risk of bleeding again in the future. The usual range of testing is shown below.

Investigations after a Haemorrhagic Stroke
  • Bloods: FBC, CRP, ESR, Glucose, U&E (Hyponatraemia with SAH). LFTs.
  • Coagulation screen and platelets: are vital to exclude coagulopathy or severe thrombocytopenia
  • CT Imaging : very high sensitivity to picking up blood and is the initial investigation of choice. CT shows haematoma in brain substance with possible extension into ventricles. Maybe hydrocephalus and signs of raised ICP. Presence of intraventricular blood is a poor prognostic indicator
  • MRI: Imaging : Almost as good as CT initially but most helpful after the first week when the haematoma has resolved. Old bleeds show a slit like appearance with signs of haemosiderin. Repeat interval scan at 6 weeks can help exclude an underlying lesion. It is useful now to do the so called 'black blood' sequences where blood breakdown products appear black. Gradient echo or T2 * (T2 star) sequences are useful.
  • MRA: Shows the circle of Willis and can identify aneurysms and AVM.
  • MRV: Consider if the bleed could possibly be a cerebral venous thrombosis with haemorrhage.
  • CTA: Allows imaging of aneurysms and dissections and vascular malformations.
  • Cerebral angiography (DSA): Reserved for selected cases in tertiary centres for those with SAH or AVM. There is a small probably less than 1% stroke risk associated with the procedure.
  • Echocardiography: CRP and general work up if endocarditis suspected as septic emboli can bleed.
  • Lumbar puncture for red cells and xanthochromia as indicated if SAH suspected

Hypertensive Haemorrhage

The student often sees blood pressure as a cause of acute haemorrhage due to acute rises in blood pressure causing sudden vessel rupture and catastrophic bleeding. In reality hypertensive bleeds are the result of a chronic low-grade damage to usually the deep penetrating vessels over a number of years. These are the same vessels that occlude in the formation of lacunar strokes so it is no wonder that they occupy the same anatomical areas of the brain such as the putamen, basal ganglia, internal capsule, thalamus and pons and cerebellum. Hypertension likely is also a mechanism for the more superficial lobar bleeds though amyloid is also in the differential diagnosis too. The clinical presentation has already been discussed and need not concern us more here. Non-contrast CT head is the imaging of choice and in an older hypertensive patient with a deep bleed no further imaging is needed unless there are other concerns as to the aetiology.


If on warfarin and INR > 1.4 give IV Vitamin K 10 mg stat and Octaplex or FFP. This may require discussion with haematology. Consult with neurosurgeons especially if cerebellar haematoma and/or developing hydrocephalus. IV steroids have no evidence base and may be harmful. Statins and all anticoagulants should be stopped. Always think is this venous infarction with haemorrhage as the patient will then warrant MRV acutely and possible urgent anticoagulation

Intracerebral Hemorrhage (ICH) Score

GCS3-4 +2
Age< 80 0
>=80 +1
ICH volume > 30 mlsYes+1
Intraventricular haemorrhageYes+1
Infratentorial origin of bleedYes+1


Stroke UnitAdmit direct to HASU from ambulance or the Emergency department depending on local protocols. Specialist nursing and therapy skills. Stroke specialist review. Immediate imaging. Multidisciplinary stroke care. Regular Neurological observations - Temperature, Pulse, BP, GCS, Pupillary responses
HypertensionCurrent recommendations is to reduce BP to < 160 mmHg usually with IV antihypertensive agents e.g. Labetalol
Neurosurgery for Haematoma evacuationConsult with neurosurgeons especially if cerebellar haematoma and/or developing hydrocephalus for external ventricular drainage (EVD) or evacuation of the lesion and shunting. Little evidence to suggest neurosurgical benefit in supratentorial bleeds. The exception being young patient with a superficial bleed close to the cortex and easily accessed. Infratentorial bleeds benefit from clot evacuation or shunt insertion for hydrocephalus especially if there are signs of developing coma and haematoma > 3 cm.
CoagulopathyAll anti-platelet agents or anticoagulation must be stopped. Avoid LMWH for VTE prophylaxis in the short term and IPC is the VTE prophylaxis of choice. If on warfarin and INR > 1.4 give IV Vitamin K 10 mg stat and Prothrombin complex concentrates or FFP e.g. OCTAPLEX/BERIPLEX (Vitamin K clotting factor replacement). Discuss with haematologists. Platelet administration is NOT recommended in the setting of antiplatelet-related ICH due to data from PATCH trial
IV steroids have no evidence base and may be harmful raising blood pressure and causing hyperglycaemia. They should be avoided
IV MannitolIntravenous mannitol should not be used routinely for treatment of raised intracranial pressure in patients with primary intracerebral haemorrhage
Anticoagulants/antithrombotic stoppedstop clopidogrel or aspirin or warfarin. Even in those with metal heart valve the current recommendation is to switch to aspirin for a weekend then consider restarting anticoagulant. Much will depend on size of the bleed, is there a recurring pathological process and other such factors.
Statins Statins are often stopped as concerns about increased haemorrhage risk
VTE preventionIPC is the VTE method of choice along with early mobility. Some centres would consider low dose LMWH prophylaxis several weeks after a bleed depending on the risk of recurrence balance with the risk of DVT/PE. Each patient should always have an individualised VTE assessment carried out regularly.
HyperglycaemiaSliding scale if Blood glucose high. Tight control can lead to harmful episodes of subclinical hypoglycaemia.
SeizuresConsider Valproate 300 mg bd or Phenytoin IV/Oral for seizures.
Further scanningIf SAH suspected then make the diagnosis through CT and LP if needed. Patient needs neurosurgical input and transfer to centre for management. For typical ICH then unless elderly and hypertension or amyloid explain the bleed consider repeat MRI/MRA after 4 weeks when haematoma has resolved to look for tumour or any vascular anomaly.

Next: >> Hyperacute stroke

Top of Page