ISCHEMIC STROKE / COMPLICATIONS

Malignant Cerebral Infarction

Created 25/03/2021, last revision 23/09/2023

Definition

malignant cerebral infarction = extensive infarction with large space-occupying edema
- occurs in up to 10% of patients with supratentorial infarcts
- it is traditionally associated with a high mortality rate (up to 80%) [Hacke, 1996]
occurs mainly in cases of ICA and MCA occlusions or with posterior circulation strokes (mainly cerebellar infarctions)
it is characterized by a development of edema within 24 h, clinical deterioration usually in < 72h, sometimes later (e.g., in case of collateral circulation failure and development of infarction in the penumbra
early surgical decompression reduces mortality and increases the number of younger patients with a favorable outcome according to randomized controlled trials (RCTs)

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the initial severe neurological deficit with hemiplegia, deviation of eyes and head, high NIHSS, nausea, vomitus
posterior circulation infarction is associated with altered consciousness, oculomotor dysfunction, altered brainstem reflexes, ataxia, and dysmetria
progressive impairment of consciousness and conus symptoms due to craniocaudal deterioration
Cushing’s triad is present in advanced stages of intracranial hypertension
- hypertension
- bradycardia
- respiratory disorders
  - hypo-, hyperventilation
  - Cheyne-Stokes breathing
  - apneic pauses
cardiovascular lability
cerebellar infarctions are associated with an increased risk of brainstem compression and hydrocephalus development

look for expansive behavior of ischemia and a midline shift on CT
repeat brain CT within the first 48h in high-risk patients [AHA/ASA 2014 I/C]
use MRI for early detection of large DWI lesions
- prediction of fulminant course within 6 h: DWI lesion > 80-89 mL
- prediction of fulminant course beyond 14 h: DWI lesion > 145 mL

tests should exclude extracerebral causes of clinical deterioration
a basic metabolic panel including hepatic enzymes
minerals, including phosphate
coagulation and blood count
toxicology and ASTRUP should be considered in the presence of impaired consciousness not fully explained by structural changes on CT

EEG excludes nonconvulsive status epilepticus (unless NCCT correlates with the severe clinical condition)
TCD / TCCD can be used to monitor blood flow
- occlusion detection (→ TIBI classification)
- signs of intracranial hypertension
ICP monitoring

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routine intensive care for acute stroke patients → see here
consider transport to a hospital capable of performing acute decompressive craniectomy
antiedema therapy
- osmotic therapy Mannitol / NaCl 10% (AHA/ASA 2019 IIa/C-LD)
- there are no data on the benefit of hypothermia, barbiturates, and corticosteroids in stroke patients and they are therefore not recommended
- therapy should be initiated only in patients with developing edema; prophylactic administration of osmotherapy is not recommended
the effect of conservative treatment in malignant ischemia is usually insufficient and not clearly demonstrated

preferred in younger patients
don’t wait for the effect of drug therapy with developing malignant ischemia (as it has only minimal impact)

ventriculostomy in case of obstructive hydrocephalus due to expansive cerebellar infarction (with or without craniectomy) (AHA/ASA 2019 I/C-LD)
suboccipital craniectomy and resection of the infarcted tissue for expansive cerebral ischemia may be a life-saving procedure (AHA/ASA 2019 I/B-NR)
- ischemia leads to brainstem and aqueducts compression, so craniectomy can also relieve obstructive hydrocephalus
- it can be combined with the ventricular drainage
imaging criteria
- compression of the 4th ventricle
- hydrocephalus
- basal cisterns/brainstem compression
- medial cerebellar infarction

decompression releases pressure from the edematous tissue on adjacent tissue ⇒ ↓ ICP and ↑ CPP
potentially life-saving procedure (see below for additional indication criteria)
- age < 60 years – a meta-analysis of the DESTINY, HAMLET a DECIMAL trials demonstrated that decompressive craniectomy within 48 hours in patients aged <60 years results in reduced mortality and improved outcome (AHA/ASA 2019 IIa/A)
- age > 60 years – reduced mortality alone was demonstrated in smaller studies [Won Yu, 2012] and randomized DESTINY II trial
  - n = 112 (surgery 49 vs. control 63), age> 61 years
  - mRS 0-4 39% (surgery) vs. 17% (control), ARR 22, NNT = 5 !!
  - significant reduction of mortality (50%); compared to trials with patients < 60 years of age, there is a significant increase of survivors with very severe deficits and only a minimum of patients with mRS 3 (none 0-2) – questionable cost-effectiveness

craniectomy diameter of at least 12 cm
- 14-15 cm anteroposteriorly
- 0-12 cm from the base to the vertex
concomitant resection of infarcted tissue is rather not recommended

Indication criteria (used in the randomized trials)

age 18 – 60 years (younger patients have a better prognosis, in the age of > 60y, mainly a reduction in mortality can be expected)
NIHSS> 15
somnolence-sopor
ischemia > ½ of the MCA territory according to CT (with or without concurrent infarction in ACA or PCA on the same side)
infarct volume > 145 cm³ according to DWI
< 45 h (surgery completed < 48 h) from symptom onset

Exclusion criteria

Early decompressive craniectomy – a meta-analysis of the three European randomized trials

(DECIMAL 38, DESTINY 32, HAMLET 23, total number of patients = 93) [Vahedi, 2007]

Primary and secondary outcome	craniectomy	control
mRS 0-4 / 1 year	75%	25%
mRS 0-3 / 1 year	43%	21%
survival	78%	29%

total n= 112
- decompressive craniectomy, n = 49
- control group, n = 63
> 61 years of age
mRS 0-4 39% (craniectomy) vs 17% (control), ARR 22, NNT = 5
significant reduction in mortality, but only a small number of patients with mRS ≤ 3 !!!!