Case-based learning: acute right frontal lobar intracerebral haemorrhage

One-line problem representation

1. Definitions

Intracerebral haemorrhage

• The bleed is lobar because it is in the frontal lobe cortex/subcortex.
• The small SAH is likely blood tracking into adjacent cortical sulci.
• There is mild mass effect and sulcal effacement, but no midline shift, obstructive hydrocephalus, or compressed basal cisterns.

Cerebral amyloid angiopathy

Haematoma mass effect

• Haematoma expansion
• Worsening oedema
• Seizure or non-convulsive status epilepticus
• Hydrocephalus
• Raised intracranial pressure
• Aspiration, hypoxia, infection, or metabolic disturbance

2. Interpretation of this CT report

• No midline shift
• Patent basal cisterns
• No hydrocephalus
• No intraventricular haemorrhage
• No skull fracture
• No large territorial infarction

• Large lobar haemorrhage
• Early local mass effect
• Cortical involvement, which increases seizure risk
• Associated convexity SAH
• Possible CAA, which implies recurrent lobar ICH risk
• Seizure with choking/aspiration risk

3. Key differential diagnosis and cause investigation

Important causes of lobar ICH

1. CAA
2. Haemorrhagic tumour or metastasis
3. Arteriovenous malformation, dural AV fistula, aneurysm, cavernoma
4. Cerebral venous sinus thrombosis
5. Anticoagulant or antiplatelet-associated haemorrhage
6. Coagulopathy or thrombocytopenia
7. Hypertension, although it more often causes deep ganglionic, thalamic, pontine or cerebellar haemorrhage
8. Haemorrhagic transformation of ischaemic infarction
9. Drug-associated haemorrhage, such as sympathomimetics

Recommended investigations

Immediate bedside and laboratory investigations

• Serial neurological observations: GCS, pupils, focal deficit, NIHSS where appropriate
• Continuous or frequent observations: BP, oxygen saturation, respiratory rate, temperature, ECG
• Capillary blood glucose
• FBC including platelet count
• PT/INR, APTT, fibrinogen
• Urea, creatinine, electrolytes, LFTs
• Group and save/crossmatch if clinically indicated
• Medication reconciliation, specifically:
  • DOACs
  • warfarin
  • antiplatelets
  • heparin/LMWH
  • NSAIDs
  • serotonergic drugs and recreational sympathomimetics where relevant
• ECG and assessment for atrial fibrillation or other cardiac indication for antithrombotics

Brain and vascular imaging

• Repeat non-contrast CT head urgently if neurological deterioration occurs, and often planned repeat CT according to local ICH protocol to assess for expansion.
• CTA or MRA, usually early, should be considered where a macrovascular cause is possible. The UK stroke guideline highlights consideration of early non-invasive cerebral angiography, within 48 hours, when a macrovascular cause may be found.
• CT venography or MR venography if there are imaging or clinical features suggesting cerebral venous thrombosis.
• MRI brain with susceptibility-weighted imaging or T2 gradient echo* when stable:
  • Lobar microbleeds
  • Cortical superficial siderosis
  • Underlying cavernoma
  • Haemorrhagic tumour/metastasis
  • CAA diagnostic markers

4. Acute management according to UK stroke practice

A. Location of care and monitoring

• Falling GCS
• New pupillary asymmetry
• New or worsening focal deficit
• Recurrent or prolonged seizures
• Persistent hypoxia or inability to protect airway
• Evidence of hydrocephalus, worsening mass effect, or herniation
• Rapidly rising BP despite treatment

B. Blood pressure

• Use a titratable IV antihypertensive per local protocol, commonly labetalol, nicardipine, or another locally approved agent.
• Aim for smooth BP control, not large fluctuations.
• Document timing of onset, initial BP, target, agent, and response.

C. Antithrombotic medication and haemostatic management

• Warfarin-associated ICH: urgent reversal with four-factor prothrombin complex concentrate plus IV vitamin K, as recommended in the UK guideline.
• DOAC-associated ICH: urgent reversal according to local protocol and drug type, for example andexanet alfa for factor Xa inhibitor-associated ICH where indicated/available, or PCC where appropriate.
• Heparin-associated bleeding: consider protamine where relevant.
• Correct clinically significant thrombocytopenia or coagulopathy with haematology/stroke advice.

• INR, APTT, fibrinogen, platelet count
• Last dose of all anticoagulants/antiplatelets
• Renal function, especially for DOAC clearance
• Indication for anticoagulation, for example AF, VTE or mechanical valve

D. Venous thromboembolism prophylaxis

• Use intermittent pneumatic compression unless contraindicated.
• The neurosurgical team specifically states that prophylactic-dose LMWH may continue. This is a patient-specific specialist recommendation and should be reconciled with the stroke consultant/local ICH protocol and timing of stable imaging.
• Do not confuse prophylactic LMWH with therapeutic anticoagulation.
• Document the rationale and review daily, especially if the haematoma enlarges or coagulation results become abnormal.

E. Neurosurgical management

• No significant midline shift
• No hydrocephalus
• No ventricular obstruction
• No reported herniation physiology
• No posterior fossa haematoma

F. General acute stroke care

• Maintain oxygenation. Treat hypoxia and identify aspiration-related respiratory compromise.
• Avoid hypotonic fluids and avoid unnecessary fluid overload.
• Treat fever and investigate its cause.
• Avoid hypo- and hyperglycaemia.
• Provide pressure-area care, early rehabilitation assessment and delirium prevention.
• Assess capacity and establish escalation/ceiling-of-care decisions based on the patient’s wishes, prognosis and multidisciplinary discussion. Avoid premature limitation of active treatment solely because an ICH is present.

5. Seizure management

Immediate seizure approach

1. ABCDE
   • Protect airway.
   • Give oxygen and suction if needed.
   • Check glucose immediately.
   • Obtain IV access and monitoring.
2. If seizure persists for 5 minutes or recurs without recovery:
   • Follow local convulsive status epilepticus protocol, usually an IV or buccal benzodiazepine first-line.
3. Start an antiseizure medicine after a confirmed clinical seizure, commonly levetiracetam where suitable, using local formulary and neurology/stroke advice.
4. Correct seizure-provoking abnormalities:
   • Sodium, calcium, magnesium
   • Glucose
   • Hypoxia
   • Infection/fever
   • Alcohol or sedative withdrawal if relevant
5. Consider EEG if:
   • Persistent reduced consciousness is unexplained
   • Recurrent subtle motor phenomena occur
   • Concern exists for non-convulsive status epilepticus

• Semiology, duration, focal onset, loss of awareness, recovery phase
• Oxygen saturation during event
• Tongue bite, incontinence, injury
• Rescue medication and response
• Whether aspiration or choking occurred during/post seizure

6. Aspiration/choking after seizure

Immediate management

• ABCDE assessment
• Sit upright if safe and if airway is protected
• Suction oral secretions/vomit
• Oxygen to target saturations, with ABG/VBG if hypoxic or unwell
• Escalate early to anaesthetics/critical care if ongoing airway compromise, low GCS, recurrent vomiting, inability to clear secretions, persistent hypoxia or respiratory fatigue
• Keep the patient nil by mouth, including oral medication, until swallow screening and where indicated specialist swallow assessment
• Refer to Speech and Language Therapy
• Ensure mouth care and safe positioning
• Consider NG feeding only after multidisciplinary assessment, with attention to aspiration risk and local stroke protocol

Aspiration pneumonitis versus aspiration pneumonia

Respiratory investigations after aspiration

• Clinical examination and observations
• Chest X-ray if respiratory symptoms, hypoxia, fever or suspected pneumonia
• ABG/VBG if unwell or hypoxic
• FBC, CRP and cultures where infection is suspected
• Consider viral testing according to local policy
• Repeat assessment because chest radiographic changes can lag behind clinical aspiration

7. Secondary prevention and longer-term plan

Blood pressure

CAA and future antithrombotics

• Reassess any indication for antiplatelet or anticoagulant treatment carefully.
• Involve stroke, neurology and, where relevant, cardiology/haematology.
• Consider MRI markers of CAA burden before deciding on long-term antithrombotics.
• Do not restart therapy automatically after “two weeks”. The local neurosurgical advice gives an immediate holding period, but the eventual restart decision needs an individual risk-benefit assessment.

Rehabilitation

• Physiotherapy, occupational therapy, speech and language therapy
• Cognitive, behavioural and executive-function assessment, particularly because frontal-lobe injury may affect judgement, initiation, personality, continence and attention
• Falls assessment and seizure safety advice
• Driving advice: do not drive and notify the DVLA as applicable. Seek stroke/neurology-specific advice on duration of restriction because it depends on the seizure, haemorrhage, residual deficit and licence class.
• Smoking cessation, alcohol moderation, medication review and vascular risk-factor optimisation

8. Suggested documentation wording

Acute right frontal lobar intracerebral haemorrhage with small adjacent convexity subarachnoid haemorrhage, mild local mass effect but no midline shift, hydrocephalus or intraventricular extension. Pattern is suspicious for cerebral amyloid angiopathy, though further vascular and MRI assessment is required to exclude alternative structural causes, including haemorrhagic lesion/metastasis and macrovascular pathology.

Neurosurgical advice: no acute operative intervention. Hold regular antithrombotic medication for two weeks; continue prophylactic-dose LMWH as advised; ensure normal coagulation and platelet profile.

Complicated by clinical seizure and choking/possible aspiration. Managed with ABCDE, oxygen/airway precautions, seizure treatment, NBM pending swallow assessment, SLT referral and monitoring for aspiration pneumonitis/pneumonia. Urgent repeat CT and re-escalation to neurosurgery/stroke team if neurological deterioration occurs.

Practical learning points for the doctor

1. Lobar ICH is not automatically hypertensive. Consider CAA, tumour, vascular malformation and cerebral venous thrombosis.
2. Neurological deterioration is an imaging indication. Repeat CT promptly and re-contact neurosurgery.
3. Treat a witnessed seizure after ICH, but do not routinely give prophylactic antiseizure medication to all patients without seizures.
4. Keep patients NBM after a seizure/aspiration event until swallow safety is established.
5. Do not automatically give antibiotics after aspiration. Distinguish chemical pneumonitis from bacterial aspiration pneumonia.
6. Anticoagulant reversal is time-critical when anticoagulant-associated ICH is present.
7. “Hold blood thinners for two weeks” is not the same as a long-term restart plan. In probable CAA, restart decisions require specialist individualised assessment.
8. Document the rationale for LMWH clearly. This is prophylactic-dose treatment under neurosurgical advice, not therapeutic anticoagulation.

Latest UK guidance relevant to ICH and post-stroke seizures

1. Acute intracerebral haemorrhage

Key ICH recommendations

Applied to this patient

• Right frontal haemorrhage is lobar and cortical, which is consistent with possible CAA but also warrants assessment for a structural lesion, particularly with known malignancy.
• No shift, hydrocephalus, or cisternal effacement supports the neurosurgical decision for no immediate operation.
• The instruction to withhold regular blood thinners for two weeks is an immediate neurosurgical plan, not a final long-term antithrombotic decision.
• A seizure, choking episode and possible aspiration require airway assessment, NBM pending swallow assessment, and close respiratory observation.

2. Post-stroke seizures

1. The UK National Clinical Guideline for Stroke, for acute stroke/ICH care.
2. NICE NG217: Epilepsies in children, young people and adults, updated 30 January 2025 and reviewed in 2026, for seizure, epilepsy and status epilepticus treatment. See NICE seizure emergency guidance.
3. Local stroke, neurology and status epilepticus pathways.

Definitions

• Acute symptomatic seizure: seizure within 7 days of stroke or ICH.
• Post-stroke epilepsy: usually refers to unprovoked seizure(s) occurring more than 7 days after stroke. A late unprovoked seizure carries a high recurrence risk and commonly justifies longer-term antiseizure therapy after specialist review.

Seizure management after ICH

NICE treatment of convulsive status epilepticus

1. Give a benzodiazepine as first-line treatment.
2. If the seizure does not stop within 5-10 minutes, give a second benzodiazepine dose, following the emergency plan where available.
3. If seizures persist after two benzodiazepine doses, give IV:
   • levetiracetam, or
   • phenytoin, or
   • sodium valproate.

Evidence update relevant to ICH

3. Suggested patient-specific plan for the ward round

1. Confirm seizure details: onset, duration, semiology, recovery, rescue medication, glucose, hypoxia, injury.
2. Treat as an acute symptomatic seizure due to cortical/lobar ICH, with stroke/neurology advice on antiseizure medication and duration.
3. Request EEG if reduced consciousness persists, recurrent events occur, or there is concern for non-convulsive seizure activity.
4. Aspiration precautions: NBM, speech and language therapy swallow assessment, oxygenation monitoring, suction/positioning, chest assessment and CXR only if respiratory symptoms or hypoxia suggest aspiration injury/infection.
5. ICH bundle: BP target as per local ICH protocol, neuro-observations, FBC/platelets/coagulation profile, review antithrombotics, urgent repeat CT if deterioration.
6. Investigate cause: CTA/MRA as appropriate, then MRI brain with susceptibility-weighted imaging to support/refute CAA and exclude a haemorrhagic lesion.
7. Driving advice: document that the patient must not drive and needs DVLA/neurology advice before return to driving, particularly following a seizure and haemorrhagic stroke.