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Management of Intracerebral Haemorrhage

Management of Intracerebral Haemorrhage

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Page 1: Management of Intracerebral Haemorrhage

Management of Intracerebral Haemorrhage

Page 2: Management of Intracerebral Haemorrhage

It’s the worst type of stroke….

• Least treatable form of stroke

• Evidence-base limited – most

• Overall mortality 35-50%

• Half of these would die within first 24 hours

• <20% independent at 6 months

Page 3: Management of Intracerebral Haemorrhage

It’s nasty Proportion of all strokes Disability-associated life

years lost (USA-2010) Deaths - USA IN 2013

Ischaemic stroke 85% 39.4 million 3.3 million

Haemorrhage 15% 62.8 million 3.2 million

Page 4: Management of Intracerebral Haemorrhage

Why should we rush to diagnose?

• Make sure it’s not ischaemic stroke - ?tPA

• Most small ICH survivable with good med. care

• Large ICH: comprehensive MDT care can reduce morbidity and mortality

• Early deterioration in the first few hours is common

Page 5: Management of Intracerebral Haemorrhage

Causes Primary ICH Secondary ICH

Hypertensive – deep with ventricular extension - lipohyalinosis : putamen, thalamus, pons, cerebellum

AVM/aneurysm

Tumours

Vasculitic

Amyloid angiopathy – asymptomatic micro-bleeds or symptomatic lobar

Drugs like cocaine

Venous sinus thrombosis

Coagulation disorders/anticoagulants

Page 6: Management of Intracerebral Haemorrhage

Classification Primary ICH Secondary

Hypertensive - lipohyalinosis

Coagulation disorder/Anticoagulants

Amyloid angiopathy AVM/aneurysm

Vasculitis

Drugs like cocaine

Venous sinus thrombosis

Tumours

Page 7: Management of Intracerebral Haemorrhage

Common causes

• Hypertension

• Cerebral amyloid angiopathy

• Coagulation disturbance: A/C; tPA; blood diseases

• Aneurysm, AVM

• Vasculitis

• Cocaine

• Venous sinus thrombosis

Page 8: Management of Intracerebral Haemorrhage

Hypertensive ICH

• Predilection for deep GM of basal ganglia and brainstem

• Rupture of microaneurysms on deep perforating arteries

• 50% extend into ventricles: worse prognosis

• BP may be normal at the time of haemorrhage

• Haematomas may expand during the first 24 hours

Page 9: Management of Intracerebral Haemorrhage

Hypertensive bleed

Page 10: Management of Intracerebral Haemorrhage

Amyloid angiopathy

• Deposition of β-pleated proteins within the media and adventitia of small & medium sized vessels : superficial layers of cortex & lepto-meninges

• Increases with age – loss of elasticity, micro aneurysms, fibrinoid degeneration

• Lobar haemorrhages – mostly frontal and parietal

• Usually spares BG, brainstem, cerebellum

• Multiple, recurrent

• May be small or very large

Page 11: Management of Intracerebral Haemorrhage

Amyloid bleeds

Page 12: Management of Intracerebral Haemorrhage

Cerebral microbleeds

• T2*-weighted GRE sequences allow identification of small foci of haemosiderin

• Important biomarker of underlying vasculopathies: • Deep perforating vascular disease in BG, thalamus, brainstem, cerebellum

• Cerebral amyloid angiopathy: strictly peripheral cortical or sub-cortical

Uncertain why some bleeds remain small, others become large. Even small bleeds may produce some symptoms, not usually recognised as TIAs.

Amyloid attacks are usually stereotypical, chiro-oral pareasthesia

Page 13: Management of Intracerebral Haemorrhage
Page 14: Management of Intracerebral Haemorrhage

Cerebral haemorrhage in haematological malignancies

• A patient with myelodysplasia transformed into AML

• Hyperleucocytosis, low or abnormal platelets, prolonged PT, DIC, sepsis

• Hypertension

• Often multiple sites, prognosis poor

Page 15: Management of Intracerebral Haemorrhage

Haematological disorders

Transfusion dependent myelodysplasia, presented

with slurred speech

Page 16: Management of Intracerebral Haemorrhage

European Cooperative Acute Stroke Study (ECASS) classification of intracerebral haemorrhage (ICH) following thrombolysis (from Berger and colleagues38).

Derex L , Nighoghossian N J Neurol Neurosurg Psychiatry 2008;79:1093-1099

©2008 by BMJ Publishing Group Ltd

Page 17: Management of Intracerebral Haemorrhage

Haemorrhagic transformation

• Occurs in some infarcts, up to 15% in acute phase

• On CT/MRI: lack of homogeneity of the haemorrhagic lesion which lies within an infarct (arterial territory location)

• Cardio-embolic infarcts more likely

• Larger doses of antithrombotic doses

• Better to do MRI scan, look for DWI +ve lesion around the bloodor other areas

Page 18: Management of Intracerebral Haemorrhage
Page 19: Management of Intracerebral Haemorrhage

Plain CT head is the best

What to look for in a CT scan?

• Site: deep (HT) or lobar (CAA, drugs, coagulation, vascular anomaly)

• Size (ABC/2 = volume)

• Ventricular extension

• Mass effect

• Hydrocephalus

• Signs of early herniation

Page 20: Management of Intracerebral Haemorrhage

Is any other imaging required acutely?

• CT-angiography: contrast extravasation (spot sign) carries poorer prognosis, but doesn’t change management

• MRI: stigmata of amyloid angiopathy

• Better make sure you have clotting profile and know drug history (recreational, DOACs) or bleeding disorder

• Low threshold for repeat CT

Page 21: Management of Intracerebral Haemorrhage

How to identify the cause of ICH?

• Previous ICH in same location suggests AVM

• Recurrent ICH in distant area to previous bleed likely to be CAA

• Family history: cavernomas, HHT

• Previous seizures: AVM, tumour

• History of cognitive decline: CAA

• H/O cancer suggests haemorrhagic metastases (melanoma, kidney)

• Valvular heart disease: septic emboli from endocarditis

• Screen for recreational drugs: cocaine, amphetamines

• Antecedent history: venous sinus thrombosis

Page 22: Management of Intracerebral Haemorrhage

Limitations to management

• Evidence-base from trials missing or inconclusive

• Therapies based on expert opinions

• Traditional therapeutic nihilism

• Early DNR

• Admission to neuro-ICU vs general ICU - decreased mortality

Page 23: Management of Intracerebral Haemorrhage

First 24-48 hours

Maintaining adequate oxygenation + avoid hypercapnia + MAP:

• GCS≤8

• Decreased airway reflexes

• Aspiration

• Impaired central respiratory drive

• Planned EVD or haematoma evacuation

Page 24: Management of Intracerebral Haemorrhage

Immediate management

• ABC: intubate if GCS≤8, or significant respiratory distress

• Correct clotting defect

• Correct hypoxaemia

• In hydrocephalus or early herniation, urgent neuro-surgery consult

Page 25: Management of Intracerebral Haemorrhage

Managing Blood Pressure -1

High BP

• Haematoma expansion

• Neurological deterioration

• Poor outcome

Lowering high BP

• Exacerbation of peri-haematomal ischaemia

• Adverse effect on perfusion of other vital organs, especially if chronically elevated BP

Page 26: Management of Intracerebral Haemorrhage

BP Guidelines for Lobar ICH

• For all Patients where ICP elevation likely consider ITU/HDU monitoring and discuss with neurosurgery.

• All other stroke patients with SBP >180mmHg for 3 consecutive readings 5 mins apart monitor on HASU and treat :- sBP>200 and/or currently on BP meds-Give IV bolus 20mg Labetolol, sBP<200 but >180 then IV Bolus 10mg Labetalol

• Monitor BP every 5 mins and if >180/110 after 10 mins give further IV labetalol bolus 20-40mg.

• Monitor BP every 15 mins and if remains >180/110 then transfer to HDU for labetolol infusion aim for sBP just below 180.

• Stop Labetalol if sBP <150 or dBP <90 • If Labetalol infusion contra-indicated GTN infusion second line agent.

Page 27: Management of Intracerebral Haemorrhage

Managing Blood Pressure -2

INTERACT-2

• Lower sBP within 6 hours of onset to <140mm vs <180mm

• Achieved sBP 150 vs 164

• No adverse effect; no reduction in death or severe disability at 90 days; ordinal shift for disability with lower BP

ATACH-2

• Lower sBP within 3 hours of onset to <140mm vs <180mm

• Achieved sBP 129 vs 141

• More renal adverse effect (9% vs 4%) with lower BP; trial stopped after 1000 patients

If presenting BP 150-200mm, lower rapidly to 140mm (AHA/ASA 2015 recommendation. For >220mm, unclear… Is there another reason for raised BP?

Page 28: Management of Intracerebral Haemorrhage

Blood pressure management

• Haematoma expansion <=> ischaemia in peri-haematomal brain

• INTERACT-2 and ATACH-2 trials of acute lowering of BP

• Reduced haematoma expansion

• No reduction in mortality

• Ordinal shift in disability

Page 29: Management of Intracerebral Haemorrhage

Blood pressure management -2

• Acute lowering of BP after ICH is probably safe

• Check BP 5 minutes apart x3

• RCP guidance 2016: If sBP>150 mm within 6 hours of onset, lower it to 140 mm; maintain for at least 7 days

• Don’t lower BP if GCS ≤5; very large haematoma; death expected; known structural cause; surgery planned

Page 30: Management of Intracerebral Haemorrhage

Reversal of anticoagulation

• Always do coagulation tests: platelets, PT/APTT

• Seek h/o bleeding or systemic disorders; drugs

• Warfarin: Prothrombin complex concentrate – better than FFP due to smaller volume, higher amount of factors and rapid infusion

• Always recheck INR 15 minutes after PCC

• Always give vitamin K 5-10 mg iv

• For heparin: Protamine sulphate

• LMWH: Protamine will partially antagonise, so also give PCC

• NOAC’s: specific inhibitor or PCC

Page 31: Management of Intracerebral Haemorrhage

Reversing coagulopathy - Warfarin

• 10 mg vitamin K iv stat

• PCC if INR ≥ 1.4

• Repeat INR after 60 min., if INR still ≥1.4, consider 2-4 units of FFP

• Jehovah’s witness: can use recombinant factor VIIa, but there is increased risk of thrombosis

Page 32: Management of Intracerebral Haemorrhage

Reversing coagulopathy - Dabigatran

• Check the timing of last dose

• Within 3-5 half-lives (or beyond if renal impairment), use Idarucizumad 5 g in 2 divided doses

• If not available, use PCC 50 units/kg (also for factor Xa inhibitors)

• If continued haemorrhage, consider haemodialysis

Page 33: Management of Intracerebral Haemorrhage

Reversing coagulopathy - Heparins

• UFH: stop infusion, calculate the dose given over the previous 2-3 hours; Protamine 1mg/100 units (max 50 mg); repeat ½ dose if APTT still prolonged

• LMWH: for Dalteparine, use Protamine 1mg/100 anti-Xa units (max 50 mg); may repeat ½ dose if renal insufficiency

Page 34: Management of Intracerebral Haemorrhage

Reversing coagulopathy - Alteplase

• Immediate Cryoprecipitate 10 units

• Check fibrinogen level, if <150 mg/dl, may repeat Cryo.

• If Cryo unavailable, use Tranexemic acid 10-15 mg/kg iv

Page 35: Management of Intracerebral Haemorrhage

Reversing coagulopathy - Platelets

• Platelet transfusion to treat antiplatelet drugs (any agent) related ICH may be harmful, do not use

• Consider if ICH in context of severe thrombocypopaenia

Page 36: Management of Intracerebral Haemorrhage

Haemostatic therapy

• FAST-trial: rFVIIa reduced haematoma expansion, but not mortality or disability; more thrombosis

• TICH-2: Tranexemic acid 1000mg stat, followed by 1000mg infusion over 8 hours

Page 37: Management of Intracerebral Haemorrhage

Body temperature management

• Fever is common after ICH, especially with ventricular haemorrhage

• Hyperthermia is associated with poor outcome, as is longer duration

• Search for infection

• Keep temperature <37.5°C

• Paracetamol; external cooling

Page 38: Management of Intracerebral Haemorrhage

Seizure control

• 8% develop clinical seizures within 30 days

• Sub-clinical seizures on EEG may occur in 30%

• Treat seizures aggressively

• Prophylactic AED not recommended

• In otherwise unexplained unconsciousness after ICH, consider non-convulsive seizures

Page 39: Management of Intracerebral Haemorrhage

VTE prevention

• Hydration and early mobilisation

• IPC

• What about patients with very high risk of DVT (previous DVT/PE, CCF, obesity)? • In neurologically stable patients, LMWH from day 2, or day 3,4 found to be

safe in a small RCT

Page 40: Management of Intracerebral Haemorrhage

Osmotherapy

• Hypertonic solutions of LMW agents like Mannitol increase serum osmolarity, thus create gradient between Blood:brain and reduce cerebral oedema

• In stroke, BBB is broken, so it may worsen cerebral oedema

• Mannitol 100 ml of 20% rarely used as bridging measure in acute ICP crisis pending EVD

Page 41: Management of Intracerebral Haemorrhage

Surgery

• STICH: overall no benefit from haematoma evacuation in supratentorial ICH over conservative management

• Initial GCS ≤8 : universally unfavourable outcome

• Any groups who might benefit: • Superficial lobar haematoma (≤1 cm from cortical surface)

• GCS score of 9-12

• volume 20-50 ml

• age 50-69 years

Page 42: Management of Intracerebral Haemorrhage

Surgical vs conservative approach

ICH localisation Clinical or CT features Treatment

BG/thalamus GCS >12; ICH volume <30 ml Conservative

GCS <9: ICH volume >60 ml Conservative

GCS 9-12; ICH volume 30-60 ml and/or deteriorating

Consider evacuation

BG/thalamus + IVH 3rd, 4th ventricle Additional EVD

Lobar GCS 9-12; ICH volume 20-60 ml, and/or deteriorating

Consider evacuation

Cerebellum ICH >3cm and/or expansive behaviour or hydrocephalus

Evacuation and /or EVD

Pons, midbrain, medulla - Conservative

Page 43: Management of Intracerebral Haemorrhage

Hemicraniectomy

• No large trials

• Sometimes done with supratentorial haematoma evacuation when progression of brain swelling is anticipated

• In venous sinus thrombosis with large haemorrhagic venous infarcts, midline shift and impending tentorial herniation, excellent outcome in small series

Page 44: Management of Intracerebral Haemorrhage

Resumption of anticoagulation

• High thrombo-embolic risk: resume after 7-10 days (US) or 10-14 days (European)