Management of Intracerebral Haemorrhage

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Gervase George
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1 Management of Intracerebral Haemorrhage

2 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

3 It s nasty Proportion of all strokes Disability-associated life years lost (USA-2010) Ischaemic stroke 85% 39.4 million 3.3 million Haemorrhage 15% 62.8 million 3.2 million Deaths - USA IN 2013

4 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

5 Causes Primary ICH Hypertensive deep with ventricular extension - lipohyalinosis : putamen, thalamus, pons, cerebellum Amyloid angiopathy asymptomatic micro-bleeds or symptomatic lobar Secondary ICH AVM/aneurysm Tumours Vasculitic Drugs like cocaine Venous sinus thrombosis Coagulation disorders/anticoagulants

6 Classification Primary ICH Hypertensive - lipohyalinosis Amyloid angiopathy Secondary Coagulation disorder/anticoagulants AVM/aneurysm Vasculitis Drugs like cocaine Venous sinus thrombosis Tumours

7 Common causes Hypertension Cerebral amyloid angiopathy Coagulation disturbance: A/C; tpa; blood diseases Aneurysm, AVM Vasculitis Cocaine Venous sinus thrombosis

8 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

9 Hypertensive bleed

10 Amyloid angiopathy Deposition of β-pleated proteins within the media and adventitia of small & medium sized vessels : superficial layers of cortex & leptomeninges 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

11 Amyloid bleeds

12 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

14 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

15 Haematological disorders Transfusion dependent myelodysplasia, presented with slurred speech

16 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: by BMJ Publishing Group Ltd

17 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

19 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

20 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

21 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

22 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

23 First hours Maintaining adequate oxygenation + avoid hypercapnia + MAP: GCS 8 Decreased airway reflexes Aspiration Impaired central respiratory drive Planned EVD or haematoma evacuation

24 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

25 Managing Blood Pressure -1 High BP Haematoma expansion Neurological deterioration Poor outcome Lowering high BP Exacerbation of perihaematomal ischaemia Adverse effect on perfusion of other vital organs, especially if chronically elevated BP

26 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.

27 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 mm, lower rapidly to 140mm (AHA/ASA 2015 recommendation. For >220mm, unclear Is there another reason for raised BP?

28 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

29 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

30 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

31 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

32 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

33 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

34 Reversing coagulopathy - Alteplase Immediate Cryoprecipitate 10 units Check fibrinogen level, if <150 mg/dl, may repeat Cryo. If Cryo unavailable, use Tranexemic acid mg/kg iv

35 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

36 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

37 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

38 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 nonconvulsive seizures

39 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

40 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

41 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 ml age years

42 Surgical vs conservative approach ICH localisation Clinical or CT features Treatment BG/thalamus GCS >12; ICH volume <30 ml Conservative BG/thalamus + IVH 3 rd, 4 th ventricle Lobar Cerebellum GCS <9: ICH volume >60 ml GCS 9-12; ICH volume ml and/or deteriorating GCS 9-12; ICH volume ml, and/or deteriorating ICH >3cm and/or expansive behaviour or hydrocephalus Conservative Consider evacuation Additional EVD Consider evacuation Evacuation and /or EVD Pons, midbrain, medulla - Conservative

43 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

44 Resumption of anticoagulation High thrombo-embolic risk: resume after 7-10 days (US) or days (European)

Hypertensive Haemorrhagic Stroke. Dr Philip Lam Thuon Mine

Hypertensive Haemorrhagic Stroke Dr Philip Lam Thuon Mine Intracerebral Haemorrhage Primary ICH Spontaneous rupture of small vessels damaged by HBP Basal ganglia, thalamus, pons and cerebellum Amyloid