Age
- >55 yrs doubles risk per decade until 80 yrs
- >80 yrs incidence is 25x of >70 yrs
- Relative risk for age >70 is 7
- Rate of spontaneous intracerebral hemorrhage in a 70-year-old is approximately 0.15% per year
Arteriopathies
- Cerebral Amyloid angiopathy:
- Deposition of beta amyloid protein (bifringent “apple-green” under polarised light when stained with Congo red) without systemic amyloidosis
- Can lead to fibrinoid necrosis
- Present in 50% of those >70 yrs old
- Most do not haemorrhage
- Associated with Alzheimer diseases as amyloid in CAA is similar to smile plaques in Alzheimer’s
- Lobar > deep
- Lobar ICH is commonly the result of cerebral amyloid angiopathy (CAA).
- Amyloid deposition in small-sized to medium-sized cortical perforators may lead to the rupture of these vessels, resulting in asymptomatic microhaemorrhages or symptomatic lobar haemorrhages.
- Mechanism
- Deposition of amyloid in vessel wall —> potentiate plasminogen —> inc. clot breakdown (? Issue with patients who need tPA for MI or CVA)
- apoE 4 allele typically have their first haemorrhage > 5 yrs earlier than noncarriers
- Aβ-induced cellular toxicity,
- Stimulates inflammatory reaction
- Oxidative stress to cells
- Common esp. old patients who are normotensive
- Repeated lobar haemorrhages
- Criteria for the diagnosis of CAA
Definite CAA | Full post-mortem exam showing all 3 of the following: A. lobar, cortical, or corticosubcortical haemorrhage B. severe CAA C. absence of another diagnostic lesion |
Probable CAA with supporting pathological evidence | Clinical data & pathological tissue showing all 3 of the following: A. lobar, cortical, or corticosubcortical haemorrhage B. some degree of vascular amyloid deposition in specimen C. absence of another diagnostic lesion |
Probable CAA | Clinical data and MRI findings showing all 3 of the following: A. age > 60 yrs B. multiple haemorrhages restricted to the lobar, cortical, or corticosubcortical region C. absence of another cause of haemorrhage |
Possible CAA | Clinical data and MRI findings: A. age 60 yrs B. single lobar, cortical, or corticosubcortical haemorrhage without another cause* , or multiple haemorrhages with a possible but not a definite cause* or with some haemorrhages in an atypical location (e.g. brain stem) |
* | e.g. excessive anticoagulation (INR > 3.0), head trauma, ischemic CVA, CNS tumor, cerebrovascular malformation, vasculitis or blood dyscrasia |
- Fibrinoid necrosis
- Lipohyalinosis: subintimal lipid rich hyaline material
- Cerebral arteritis: necrotising angiitis
- Men>women
Race
- Black > white: more HTN in blacks
- Oriental more
Previous CVA: 23x more risk
- 43% of CVA (ischaemic stroke) can undergo haemorrhagic transformation within 1 month
- Due to:
- Dislodgement
- Recanalization of arterial occlusion
- May occur as early as less than 24hrs after CVA
- 2 types
Type 1 | Type 2 | |
Location | Multifocal | Unifocal |
CT | Heterogenous within boundaries of CVA Less hyper dense than primary ICH | Extend outside original CVA boundaries Hyperdense (hard to distinguish from primary ICH fq misdiagnosed) |
Amount of blood | Diffuse | Extensive |
Due to | Can say a more natural bleed due to recanalization/dislodgement | Anticoagulation therapy enlarging haematoma |
HTN
- RR for ICH in HTN is 4
- Hard to make argument as a causation as chicken and egg paradox.
- Non-lobar ICH is most often the result of long-standing high blood pressure resulting in lipohyalinosis of small perforating arteries of the basal ganglia, thalamus, pons and cerebellum, leading to deep haemorrhages, often with extension into the ventricles
- The most common locations of hypertensive ICH are the
- Recent child birth:
- Eclampsia And Preeclampsia
- Mortality of eclampsia is 6% (mainly due to ICH)
- Postpartum cerebral angiopathy
- Hormonal changes —> initially thickening of vascular intima and/or vasospasm due to acute HTN
- Physical factors:
- Strenuous exe
- Exposure to cold
- Post traumatic haemorrhagic transformation of contusion
Alcohol
- Acute use
- Relative risk of ICH with EtOH consumption
- *1 standard drink = 12 g EtOH
Period prior to ICH | Amount* (g EtOH) | Relative risk |
24 hours | 41-120 | 4.6 |
ㅤ | > 120 | 11.3 |
1 week | 1-150 | 2.0 |
ㅤ | 151-300 | 4.3 |
ㅤ | > 300 | 6.5 |
- Chronic use
- >3 drinks/day inc risk of ICH by 7x
- ETOH associated ICH were more lobar haemorrhage
- Smoking: NOT ASSOCIATED WITH ICH
Vascular abnormalities
- AVM Rupture
- Venous Angioma rupture
- ?? Rare migraine: during or following an attack
- Aneurysmal rupture
- Saccular (berry)
- Proximal at Circle of Willis (COW)
- Long standing aneurysm pulsation —> inflammation—> fibrosis —> Aneurysm adherent to brain -> rupture causing ICH rather than SAH
- Distal to COW: MCA
- Microaneurysm (Charcot Bouchard)
- Due to HTN
CNS infection
- ESP: Fungal which can attack blood vessels
- Granulomas
- Herpes simplex encephalitis: form small lesions that can progress to haemorrhagic ones
- Venous or dural sinus thrombosis
Tumour
- Metastatic to brain
- Melanoma: 40% can cause haemorrhage
- Choriocarcinoma: 60%
- Renal cell carcinoma
- Bronchogenic carcinoma 9%
- Primary brain tumours
- Glioblastoma
- Medulloblastoma
- Lymphoma
- Benign brain tumours
- Meningioma: especially angioblastic variant
- Pituitary adenoma
- Oligodendroglioma
- Hemangioblastoma
- Vestibular schwannoma
- Cerebellar astrocytoma
Recent surgery
- Carotid endarterectomy: sudden inc. CBF —> cerebral haemorrhage
- Procedures require heparin: Endovascular procedures, cardiac surgery
- Post AVM surgery:
- Incomplete AVM excision
- Normal pressure breakthrough
- AVM steal blood —> removal of AVM —> same volume of blood now going through a region of higher vascular resistance (despite the arterioles have been chronically dilated) —> increased local BP —> haemorrhage
- Post craniotomy: partial resection of glioma —> bleeding from tumour
Drugs
- Sympathomimetics:
- Cocaine, amphetamine, phencyclidine
- Appetite suppressants or nasal decongestant
- Phenylpropanolamine
- Pseudoephedrine
- Dietary supplements weight loss: ephedra alkaloids (ma huang)
- Anticoagulants:
- Warfarin:
- 10% patient develop a significant bleeding complication per year (this 10% includes other bleeding)
- 0.3%/year: risk of ICH in patients on warfarin, this increases to 1.8%/year for patients around 80yrs
- Inc. risk of bleed
- Inc. length of time used
- Variability of INR
- Cerebral amyloid angiopathy
- Antiplatelets:
- Aspirin:
- 1 ASA QDS, inc. risk of ICH by 0.5%/yr. Nowadays we don’t use such high doses of aspirin
- Low dose (100mg/d) did not increase risk of ICH in >60 with moderate HI (GCS > 9)
- Clopidogrel
- NSAIDS
- Thrombolytic therapy
- RR is 6% vs placebo for ischaemic CVA
- RR is 1% For MI and other thrombosis. Risk even higher if patient has other vascular abnormality
- Birth control pills: questionable association
Coagulopathies
- Leukaemia
- Thrombocytopenia
- Thrombotic Thrombocytopenic purpura: Deficiency of ADAMTS13 —> cannot breakdown large vWF multimers
- Aplastic anaemia
- Liver dysf(x): Reduce clotting factors —> hypocoag
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