Vascular
General
- Haemorrhage within brain parenchyma
- Aka hypertensive haemorrhage
Numbers
- Second most common form of stroke (20% of all strokes)
- Twice the incidence of SAH
- Most deadly stroke
- Onset during activity, rare during sleep: raised BP or inc. CBF
- 30 day mortality: 44% (SAH is 46%)
Location of haemorrhage
50% | Lenticulostriates: the source of putaminal haemorrhages (possibly secondary to micro-aneurysms of Charcot-Bouchard) |
15% | Thalamoperforators: Pons and thalamus |
15% | Cerebellum |
15% | Cerebral white matter |
5% | Brainstem (Paramedian branches of BA) |
- Lobar vs deep
- Early Deterioration, Hematoma Expansion, and Outcomes in Deep versus Lobar Intracerebral Hemorrhage with 841 patients enrolled in FAST and 728 with supratentorial ICH
- Numerically LOWER rate of early neurological deterioration
- Smaller baseline hematoma volumes
- ↓ risk for hematoma expansion
- BETTER overall functional outcome
- WORSE functional outcome when adjusting for variables known to correlate with outcome
- Numerically HIGHER rate of early neurological deterioration
- Larger baseline hematoma volumes
- ↑ risk for hematoma expansion
- WORSE overall functional outcome
- BETTER functional outcome when adjusting for variables known to correlate with outcome
- Extension of deep haemorrhage
- Cerebral amyloid angiopathy
- Most common cause of lobar ICH in elderly with normal BP
- Trauma
- Haemorrhage transformation of ischaemic infarction
- Tumour
- AVM
- Rupture of aneurysm
- Idiopathic
- 50% patients with lobar
- Vs classical TIAs
- Lobar haemorrhage —> numbness, tingling or weakness in that region —> an acute minimal volumetric ischaemic focus of the brain initiates a cascade of spreading depolarisation (the same SD for migraine) —> an electrical depression over the cortex spreads like the manner reminiscent of a Jacksonian-march —> to causes regions around the Ischaemic focus to have neurological deficit
- Frontal lobe
- Frontal H/A
- Contralateral hemiparesis (arms mainly with mild leg and face weakness)
- Parietal lobe
- Contralateral hemisensory loss
- Mild hemiparesis
- Occipital lobe
- Ipsilateral eye pain ????
- Contralateral homonymous hemianopsia
- Some may have sparing of superior quadrant ????
- Temporal lobe:
- Dominant side
- Fluent dysphasia
- Poor auditory comprehension
- Good repetition
- Most common site for ICH
- Smooth gradual deterioration in 62%
- H/A only 14%, 72% no H/A
- Contralateral hemiparesis —> hemiplegia —> comma/death
- Rare for papilledema or tearson syndrome (subhyaloid pre-retinal haemorrhage or vitreous haemorrhage)
- Presentation
- H/A 30%
- Contralateral hemi sensory loss commonly
- Obstructive hydrocephalus
- If involves other region
- Internal capsule: hemiparesis
- Upper brainstem (posterior commissure): vertical gaze palsy, retraction nystagmus, skew deviation, loss of convergence, ptosis, miosis, anisocoria, unreactive pupils,
- Haemorrhage >3.3cm on CT all patients died
- Aetiology
- HTN is a factor in 2/3 of cerebellar bleed
- AVM more common to cause as aneurysm rare here
- May be related to recent spinal or Supratentorial surgery
- Presentation
- Compression of 4th ventricle/extension of haemorrhage into ventricular system —> Hydrocephalus —> Inc. ICP —> lethargy, N/V, Cushing response
- Direct compression of brainstem
- Pressure on facial colliculus—> facial palsy
- Patient can become comatose without having hemiparesis
Lobar | Deep | |
Location | Supratentorial lobes | Basal ganglia, thalamus, infratentorial structures |
Vessel S(x) abnormality | More likely | Less likely |
Frequency | Less common (15%) | More common (85%) |
Outcomes | More benign | More malignant |
Pathology | Arteriosclerosis or amyloid angiopathy | Arteriosclerosis |
Deep
Lobar
Lobar
Aetiology
TIA like symptoms may precede lobar haemorrhage
Presentation:
Deep
Putaminal haemorrhage:
Thalamus haemorrhage
Cerebellar haemorrhage aetiology (The ones described above + special ones below)
Clinical progression:
- Development of neurological deficit is more progressive on onset, over minutes to hours
- Embolic/ischaemic CVA: where deficit is maximal at onset
- Severe headache (most common), vomiting, altered consciousness
Delayed deterioration due to
- Rebleed
- More common in deep (basal ganglia) than lobar
- Haematoma enlargement decreases with time
- Spot sign on CTA (small enhancing foci within acute ICH) correlates with inc. risk of rebleeding
- 4% of ICH
- Risk factors
- Diastolic BP:
- 10%/ year risk >90mmHg vs 1.5% for DBP <90mmHg
- DM
- Tobacco: smoking is not a risk factor for ICH but is risk factor for rebleed
- ETOH
- Recurrent haemorrhages
- AVM
- Amyloid angiopathies (lobar rebleed)
Early rebleed:
35% | <3hrs |
15% | 3-6hrs |
14% | 6-24 hrs |
Late rebleed
- Oedema
- Due to
- Oedemogenic toxin release from clot (mainly)
- Thrombin can inc. BBB permeability and causes vasoconstriction.
- Mass effect of clot causes local ischaemia (small effect)
- Hydrocephalus
- Intraventricular extension
- Post fossa ICH
- Seizure
Dutch ICH surgery trial
- Age ≥ 18 years
- NIH Stroke Scale score ≥ 2
- Supratentorial ICH confirmed by non-contrast CT, without a CT angiography confirmed causative vascular lesion (e.g. aneurysm, arteriovenous malformation, dural arteriovenous fistula, cerebral venous sinus thrombosis) or other known underlying lesion (e.g. tumor, cavernoma)
- Minimal ICH volume of 10 mL
- Intervention can be started within 8 hours of symptom onset
- Written informed consent (deferred)
- Pre-stroke mRS ≥ 3
- ICH-GS score ≥ 11
- Hemorrhage due to hemorrhagic transformation of an infarct
- Untreated coagulation abnormalities, including INR > 1.3 (point of care measurement allowed) and treatment with thrombin or oral factor Xa antagonists
- Moribund (e.g. coning, bilateral dilated non-responsive pupils) or progressively deteriorating clinical course with imminent death
- Pregnancy
- DIST-IMPLANT sub-study: patients that use immunosuppressive or immune modulating medication
Inclusion checklist
Exclusion checklist
Management: Pharmacological coagulopathy
- WHAT THIS STUDY ADDS
- Accuracy of CT angiography for the detection of macrovascular causes of ICH is modest, less than previously assumed, and warrants digital subtraction angiography when the result of CT angiography is negative
- The additional value of MRI/MRA after negative CT angiography consists mainly of diagnosis of non-macrovascular
- Both posterior fossa location in the absence of hypertension and the absence of signs of small vessel disease on non-contrast CT seem to be independent predictors of an underlying macrovascular cause of ICH
- N= 298
69/298 (23%) had a macrovascular cause
ㅤ | PPT |
CT angiography- | 72% (60-92%) |
CTA+ MR- | 35% (14-62%) |
CTA+DSA | 100% |
Morbidity of DSA | 0.6% |
Investigation - UK RCP guidelines
- F- Patients with intracerebral haemorrhage in whom the haemorrhage location or other imaging features suggest cerebral venous thrombosis should be investigated urgently with a CT or MR venogram. [2023]
- G- The DIAGRAM score (or its components: age; intracerebral haemorrhage location; CTA result where available; and the presence of white matter low attenuation [leukoaraiosis]) on the admission non-contrast CT) should be considered to determine the likelihood of an underlying macrovascular cause and the potential benefit of intra-arterial cerebral angiography. [2023]
- H- Early non-invasive cerebral angiography (CTA/MRA within 48 hours of onset) should be considered for all patients with acute spontaneous intracerebral haemorrhage aged 18-70 years who were independent, without a history of cancer, and not taking an anticoagulant, except if they are aged more than 45 years with hypertension and the haemorrhage is in the basal ganglia, thalamus, or posterior fossa.
Investigation
COR | LOE | Recommendations | ㅤ | ㅤ |
1 | B-NR | In patients with lobar spontaneous ICH and age <70 years, deep/posterior fossa spontaneous ICH and age <45 years, or deep/ posterior fossa and age 45 to 70 years without history of hypertension, acute CTA plus consideration of venography is recommended to exclude a macrovascular causes or cerebral venous thrombosis. | - Lobar < 70 years - Deep/post. fossa < 45 years - Deep/post. fossa, no hypertension | Acute CT angiogram +/- venography |
1 | B-NR | In patients with spontaneous IVH and no detectable parenchymal hemorrhage, catheter intra-arterial digital subtraction angiography (DSA) is recommended to exclude a macro- vascular cause. | - Spontaneous IVH - No parenchymal haemorrhage | Catheter angiography |
1 | C-LD | In patients with spontaneous ICH and a CTA or magnetic resonance angiography (MRA) suggestive of a macrovascular cause, catheter intra-arterial DSA should be performed as soon as possible to confirm and manage underlying intracranial vascular malformations. | - If CTA suggests a cause… | Catheter angiography |
2a | B-NR | In patients with (a) lobar spontaneous ICH and age <70 years, (b) deep/posterior fossa ICH and age <45 years, or (c) deep/posterior fossa and age 45 to 70 years without history of hypertension and negative noninvasive imaging (CTA+-venography and MRI/MRA), catheter intra-arterial DSA is reasonable to exclude a macrovascular cause. | - Lobar < 70 years - Deep/post. fossa < 45 years - Deep/post. fossa 45-70 years, no hypertension, negative cross-sectional imaging | Catheter angiography |
2a | B-NR | In patients with spontaneous ICH with a negative CTA/venography, it is reasonable to perform MRI and MRA to establish a nonmacrovascular cause of ICH (such as CAA, deep perforating vasculopathy, cavernous malformation, or malignancy). | ㅤ | ㅤ |
2a | C-LD | In patients with spontaneous ICH who undergo CT or MRI at admission, CTA plus consideration of venography or MRA plus consideration of venography performed acutely can be useful to exclude macrovascular causes or cerebral venous thrombosis. | ㅤ | ㅤ |
2b | C-LD | In patients with spontaneous ICH and a negative catheter intra-arterial DSA and no clear macrovascular diagnosis or other defined structural lesion, it may be reasonable to perform a repeat catheter intra-arterial DSA 3-6 months after ICH onset to identify a previously obscured vascular lesion. | - No microvascular diagnosis - Negative DSA | Catheter angiography repeated at 3-6 months |
ICH and IVH treatment
- CLEAR III TRIAL
- Small ICH with IVH obstructing 3rd/4th ventricle
- Low dose Intraventricular r-tPA vs placebo
- n=500, 73 sites, 2009-2014
- Summary
- 1/3 patients achieved clot removal with r-tPA
- No significant difference in functional outcome, may increase survival rates with severe disability
Posterior fossa ICH - treatment
Indications for Surgery
- Neurological deterioration
- Brainstem compression
- Obstructive hydrocephalus
- ICH volume >15ml
- EVD alone???
Decompressive craniectomy
- SWITCH TRIAL
- NIHSS >10, >30ml, GCS <14, Basal ganglia/thalamus, including IVH/SAH
- 42 centres, n=201
- Decompressive craniectomy and medical management vs medical management
- Summary
- Weak evidence that decompressive craniectomy might be superior to best medical management alone in patients with severe, deep ICH (ARR 13%)
- Arterial carbon dioxide tension (PaCO2): 2.7-10.5kPA
- Arterial oxygen tension (PaO2): <6.7kPA
- Rebleeding risk after 1st bleed around 4%
- Cerebral blood flow is maintained at a constant rate between mean arterial pressures of 50 - 150 mmHg BUT IT IS 10mmg Higher for cerebral prefusion pressure 60-160mmHg
Algorithm for determining revascularization procedures in cases in which parent artery occlusion is required
Intervention | Selection Criteria |
PAO w/out bypass | BTO†: no evidence of failure to tolerate occlusion; SPECT: no perfusion abnormality |
PAO w/ low-flow bypass (EC-IC) | BTO: no evidence of failure to tolerate occlusion on angiography or clinically during normotensive condition; failure to tolerate occlusion on clinical testing in hypotensive state, w/ or w/out abnormal EEG changes; SPECT: no perfusion abnormality |
PAO w/ high-flow bypass (vein or radial artery) | BTO: failure to tolerate occlusion in all tests; SPECT: asymmetrical perfusion |
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