Haemorrhagic Stroke: Intracerebral Haemorrhage

Original Editor -Lucinda hampton

Top Contributors - Ahmed M Diab, Lucinda hampton, Janine van Dyk, Kim Jackson, Vidya Acharya, Alexandra Stead, Tony Lowe, Khloud Shreif and Dinu Dixon

Introduction

Intracerebral haemorrhage (ICH) is the most disabling and deadly form of stroke. 15% of acute strokes are haemorrhagic strokes which are caused by an acute haemorrhage. There are two main types of haemorrhagic strokes - intracerebral haemorrhage (ICH) and subarachnoid haemorrhage which accounts for about 5% of all strokes. This page relates to ICH i.e. bleeding within the brain tissue itself, a life-threatening type of stroke that deprives the brain of oxygen and blood supply. It has the highest morbidity and mortality rates that have not changed over the last 30 years. The incidence of haemorrhage increases exponentially with age and is higher in men than in women.

The below video gives a great overview.

Clinically Relevant Anatomy

The most common sites of involvement are:

1. The region of the putamen-external capsule in the distribution of the lenticulostriate branches of the middle cerebral artery (50%). The putamen (a common site for hypertensive bleed) is involved in learning and motor control, including speech articulation, and language functions, reward, cognitive functioning, and addiction. Image is of putamen's position in skull.
2. The thalamus in the distribution of the small penetrating vessels from the posterior cerebral and posterior communicating arteries (10%)
3. The cerebellum in the distribution of the deep penetrating branches of the superior cerebellar artery (10%); and
4. The pons in the distribution of the paramedian branches of the basilar artery (10%)

The remaining 20% occur into the white matter of various lobes of the cerebral hemispheres. For more see Brain Anatomy

Mechanism of Injury / Pathological Process

ICH is almost invariably associated with hypertension and is presumed to result from weakening of arterial walls under chronic excessive pulse pressure, with ruptured vessels showing prominent degeneration of the media and smooth muscles and, less frequently, fibrinoid necrosis of the sub-endothelium with micro-aneurysms and focal dilatations.A second major mechanism is cerebral amyloid angiopathy (CAA), characterised by deposition of amyloid-β peptide at capillaries, arterioles and small-and medium-sized arteries in the cerebral cortex, leptomeninges and cerebellum; CAA in the cerebral small vessels leads to sporadic ICH in elderly, commonly associated with variations in the gene encoding apolipprotein E epsilon 2 and 4 on chromosome 19, while duplication of the amyloid-β precursor protein (APP) locus on chromosome 21 is found in families with familial early-onset Alzheimer's disease and CAA. CAA-related ICH occurs mainly in elderly patients, and in aging individuals, especially those with Alzheimer's disease, amyloid deposition in the penetrating cortical vessels makes them more friable and prone to haemorrhage; the resulting bleed is typically labor (immediately subcortical), and CAA becomes more likely as the aetiology when there is no prior history of hypertension. Once bleeding begins, the mass effect of the primary haemorrhage may cause it to migrate and dissect through less-dense white matter and into the ventricles, raising intracranial pressure. The resulting haematoma incites local oedema and neuronal damage in the adjacent brain parenchyma, typically lasting from 5 days to 2 weeks, with the largest increase in oedema occurring in the first 72 hours; thrombin within the haematoma plays a central role in promoting this perihaematomal oedema, while haemoglobin and its breakdown products, heme and iron, are potent mitochondrial toxins that lead to cell death.

Risk Factors

Risk factors of intracerebral haemorrhage can be divided into two categories: modifiable and non-modifiable risk factors.

Modifiable risk factors

Modifiable risk factors include:

1. Hypertension
2. Smoking
3. Excessive alcohol consumption
4. Decrease low-density lipoprotein cholesterol, low triglycerides
5. Anticoagulation
6. Use of the antiplatelet agent
7. Sympathomimetic drugs for example Cocaine, Heroin, Amphetamine, PPA and Ephedrine

Non-Modifiable Risk factors

Non-Modifiable Risk factors include:

1. Old age
2. Males
3. People from Asian ethnicity
4. Cerebral amyloid angiopathy
5. Cerebral microbleeds
6. Chronic kidney disease

Other factors

Other factors suggested to be related to the risk include:

1. Multi-parity
2. Poor working conditions ( blue- collar occupation, longer working times)
3. Long sleep duration

   

Clinical Presentation

Sudden onset of focal neurological deficit which progresses over minutes to hours is the major presenting feature of ICH. The nature of the deficits reflects the location of the initial bleeding and subsequent oedema. The presentation of clinical features depends on the extent of lesion, location of lesion, structures involved along with ventricular involvement. Common associated features include:

• seizures,
• vomiting,
• headache, and
• diminished level of consciousness

Both headache and diminished level of conscious are uncommon in acute ischaemic strokes.

Haematoma expansion manifests in up to 40% of cases, significantly worsening clinical trajectories in this critical stroke subtype.

Diagnostic Procedures

The early risk of neurological deterioration and cardiopulmonary instability in ICH is high, making urgent diagnosis and management critical:

• History is critical as it is important to know whether there is any history of trauma, hypertension, excessive use of alcohol, any use of drugs either by prescription or recreation that could play a role eg cocaine, warfarin, aspirin, clopidogrel, or any hematologic disorder.
• Physical examination - priority is to assess vital signs and determine if intubation is required for safety during imaging.
• It is important to determine if acute myocardial injury is a risk in patients with severely elevated blood pressure (BP)

Investigation

CT scan: CT head is the major test in use to differentiate between acute ICH, SAH (subarachnoid haemorrhage), and ischaemic stroke. It is an extremely sensitive test to detect both ICH and SAH and to identify the size and location of the haemorrhage. haematoma expansion, highly associated with clinical deterioration and poor outcomes, is evident in nearly 40% of cases within the first 3 hours after onset of symptoms is also well-documented with CT scanning CT with contrast and CT angiography (CTA) may identify associated aneurysms, tumours and underlying AVMs

MRI: MRI scanning is more sensitive for AVMs

Digital subtraction angiography (DSA): DSA is the gold standard for the identification of aneurysms and AVMs.

Prognosis

Several clinical and radiological factors are associated with poor outcome after ICH; the table below summarises these poor prognostic factors alongside their associated impact on mortality.

Poor prognostic factor	Associated mortality impact
Low Glasgow Coma Scale (GCS) score	Most powerful predictor of 30-day mortality, along with ICH volume
ICH volume ≥ 30 cm³	Hemispheric lesions > 30cc carry high mortality; GCS <9 with haematoma >60cc with nearly 90% mortality
Intraventricular extension of haemorrhage	With associated hydrocephalus, 43% mortality at 30 days
Infra-tentorial origin	Brainstem haemorrhages carry poor prognosis even when small
Old age (≥80)	Higher risk of mortality
Advanced white matter lesions	Poor prognostic factor
Underweight at admission	Poor prognostic factor
Hyperglycaemia at admission	Poor prognostic factor
Chronic kidney disease (estimated glomerular filtrarion rate ≤ 60 mL/minute/m²)	Poor prognostic factor

Management

Acute management of ICH centres on limiting haematoma expansion and preventing secondary injury:

• Anticoagulation reversal: Anticoagulants should be discontinued immediately. Reversal agents include prothrombin complex concentrate for vitamin K antagonists such as warfarin.
• Blood pressure management: By intensive blood pressure control.
• Surgical evacuation: a procedure to remove a blood clot from the brain tissue, which helps lower intracranial pressure and limit secondary injury.

Physiotherapy Assessment and Treatment Approaches

While general stroke physiotherapy assessment and treatment principles apply, ICH carries specific considerations that differ from ischemic stroke in terms of the timing of mobilisation.

Timing of mobilisation

Unlike ischemic stroke, ICH carries a risk of hematoma expansion, which is the strongest predictor of morbidity and mortality after ICH and most commonly occurs within the first 24 hours. Evidence is mixed on timing: rehabilitation activities such as stretching and functional task training may be considered 24 to 48 hours after moderate ICH, whereas early aggressive mobilisation within the first 24 hours appears to worsen 14-day outcomes. Conversely, early mobilisation within 48 hours, or 24–72 hours from onset, has been shown to improve functional prognosis in mild-to-moderate ICH.

Factors that may delay safe mobilisation

Low consciousness level at admission, an infratentorial (below-the-tentorium) lesion, recent surgery, elevated inflammatory markers, and ongoing haematoma growth are all associated with delayed mobilisation and warrant closer monitoring before progressing activity.

Once these ICH-specific mobilisations risks and timing, considerations have been addressed, general stroke physiotherapy assessment tools and treatment techniques apply as in any stroke presentation, see Stroke: Assessment and Stroke: Physiotherapy Treatment Approaches.

Recovery

Early mobilisation and involvement of the neuro-rehabilitation team is essential to maximizing recovery. People with severe ICH have the potential to do better than those with severe ischaemic stroke.

Summary

Intracerebral haemorrhage (ICH) is bleeding directly into the brain parenchyma, most commonly caused by chronic hypertensive vascular change or cerebral amyloid angiopathy. It typically presents with sudden focal neurological deficit, often with headache, vomiting, seizures or diminished consciousness, and is diagnosed principally by CT. Outcome is strongly influenced by factors such as GCS score, haematoma volume and intraventricular extension. For physiotherapists, the key distinction from ischaemic stroke is the need for individualised timing of mobilisation given the early risk for haematoma expansion, after which standard stroke rehabilitation principles apply.