management of intracerebral haemorrhage
TRANSCRIPT
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
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
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
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
Classification Primary ICH Secondary
Hypertensive - lipohyalinosis
Coagulation disorder/Anticoagulants
Amyloid angiopathy AVM/aneurysm
Vasculitis
Drugs like cocaine
Venous sinus thrombosis
Tumours
Common causes
• Hypertension
• Cerebral amyloid angiopathy
• Coagulation disturbance: A/C; tPA; blood diseases
• Aneurysm, AVM
• Vasculitis
• Cocaine
• Venous sinus thrombosis
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
Hypertensive bleed
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
Amyloid bleeds
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
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
Haematological disorders
Transfusion dependent myelodysplasia, presented
with slurred speech
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
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
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
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
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
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
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
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
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
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.
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?
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
Resumption of anticoagulation
• High thrombo-embolic risk: resume after 7-10 days (US) or 10-14 days (European)