Stroke

Sudden onset of a constellation of neurological deficits secondary to a vascular event. Stroke:

Haemorrhagic stroke is covered under Intracerebral Haemorrhage.

Stroke is distinguished from TIA by resolution and radiological findings. A TIA is a clinical syndrome with:

  • Abrupt onset of focal neurological symptoms consistent with ischaemia
  • No radiological abnormality
  • Resolution over 24 hours

Epidemiology and Risk

Epidemiology:

Stroke death in Australia in >55’s, stratified by sex.

  • Second most common global cause of death
    Greatly reduced, due to control of hypertension in the community.
  • Third most common cause of disability

Risk factors:

  • Age
    Risk doubles every decade after 55.
  • Smoking
  • Cardiovascular disease
    • AF
    • HTN
    • Dyslipidaemia
    • DM
    • Previous stroke or TIA
    • IE
  • Hypercoagulable state
    • Pregnancy
    • Factor V Leiden
    • Protein C/S deficiency
    • Antithrombin III deficiency
  • Hyperviscosity syndromes
    • Myeloma
    • HHS

Hyperviscosity syndrome describes impaired blood flow and organ perfusion due to ↑ blood viscosity, which occurs due to ↑ concentration of cells or macromolecules, and is characterised by:

  • Hypervolaemia
  • Visual disturbances
  • Neurological dysfunction
    Coma, seizures.

Pathophysiology

All strokes result in interruption of cerebral blood flow, leading to cellular failure:

  • Disruption to receptor and channel function
  • Free radial release
  • Mitochondrial dysfunction
  • Membrane disruption
  • Cell death

An ischaemic stroke has a:

  • Core infarct
    Irretrievably damaged centre of brain, seen as cytotoxic oedema on CT. A large (>50mL) core suggests less recoverable tissue by endovascular therapy.
  • Ischaemic penumbra
    Potentially viable region of brain around the ischaemic core, that is malperfused and dysfunctional but may be recoverable with restoration of blood flow.
    • A large pnenumbra may show better response to endovascular therapy
    • Slow progression of ischaemic penumbra (to core infarction) may indicate better late response to endovascular therapy

Aetiology

Ischaemic:

Large vessel thrombus/embolism is more amenable to endovascular retrieval than small vessel occlusion.

  • Embolic
    • Paradoxical embolism
      PFO, ASD, VSD.
    • Cardiac embolism
      • AF
      • Valves
        • Degenerative
        • Prosthetic
        • Endocarditic
      • LV thrombus
        • Ischaemic
          • Aneurysm
          • Apical thrombus
        • Cardiomyopathy
          Stasis.
    • Carotid embolism
    • Air
      • Surgery
      • Diving
  • Large vessel
    • Atherosclerosis
    • AVM
    • Dissection
    • Vasospasm
    • Large vessel arteritis
      • GCA
      • Takayasu arteritis
  • Small vessel
    • Vasculitis
    • Vasospasm
      Cocaine, other sympathomimetics.
  • Hypoperfusion
    Prolonged hypotension.

Haemorrhagic:

  • Systemic HTN
  • Vascular abnormality
    • Amyloid angiopathy
    • AVM
    • Intracranial aneurysm
    • Vasculitis
  • Tumour
    With haemorrhage into it.
  • Ischaemic stroke
    With haemorrhagic transformation.

Clinical Manifestations

Stroke severity is semi-objectively described using the NIHSS. However, endovascularly correctable stroke may have a low NIHSS score. NIHSS is not a guide for identifying patients for reperfusion therapies.

Stroke symptoms include:

  • Negative
  • Usually focal
    • Motor
      • Limb weakness
      • Dysphagia
      • Ataxia
    • Sensation
    • Speech and language
      • Comprehension
      • Expression
      • Calculation
    • Non-focal include:
      • Syncope
      • Altered conscious state
        Including loss of consciousness or locked-in syndrome.
      • Emotional lability
      • Incontinence
      • Cerebellar signs
        Vertigo, tinnitus, dysphagia, dysarthria, diplopia, ataxia.
  • Maximal at onset

Supratentorial Stroke Syndromes

Supratentorial Stroke Syndromes
Vessel Both Hemispheres Dominant Hemisphere Non-Dominant Hemisphere
ACA
  • Contralateral hemiparesis weakness/numbness
    Leg >> arm.
  • “Alien hand” syndrome
    Independent, involuntary, and sometimes complex upper limb movements.
  • Executive dysfunction
    • Apathy
    • Personality change
  • Urinary incontinence

Transcortical Motor Aphasia:

  • Word finding difficulties
  • Halting speech
  • Preserved repetition
  • Preserved comprehension
  • Confusion
  • Contralateral hemineglect
Proximal MCA
  • Contralateral face and arm weakness
    May have numbness.
  • Conjugate ipsilateral eye deviation
  • Aphasia
  • Bilateral apraxia
    Loss of skilled movements.
  • Contralateral hemineglect
  • Loss of insight into deficit
  • Drowsiness
PCA
  • Hemianopia/superior quadrantanopia
  • Contralateral arm and leg ataxia with tremor
  • Contralateral sensory loss
  • Contralateral pain
    Neuropathic character, with hyperalgesia and allodynia.
  • Contralateral hemiplegia
    Uncommon.
  • ↓ Arousal
  • Cortical blindness with bilateral infarction
    May be unrecognised by the patient, leading to confabulation (Anton Syndrome).
  • Limbic disruption
    Disorientation, euphoria, apathy, other mood changes.
  • Preservation of writing but not reading
  • Difficulty naming objects
  • Difficulty giving uses for objects
  • Inability to recognise faces

The left hemisphere is almost always dominant.

The anterior cerebral circulation refers to blood supply derived primarily from the internal carotid arteries and generally supplies the supratentorial brain excluding the occipital lobes.

The posterior circulation arises from the vertebrobasilar system, and supplies the occipital lobes, cerebellum, and brainstem.

A degree of overlap may occur through the posterior communicating artery in the circle of Willis.

Circle of Willis

Brainstem Stroke Syndromes

Identification of brainstem stroke syndromes can be (somewhat) simplified with application of three broad principles:

  1. Neural pathways run vertically, either medially or laterally, through the entire length of the brainstem
  2. Cranial nerves arise from different structures within the brainstem
  3. The branches of the posterior circulation that supply the brainstem are divided into:
    • Paramedian branches, which supply medial structures:
      • Basilar artery perforators
    • Circumferential branches, which supply lateral structures:
      • Anterior inferior cerebellar artery
      • Posterior inferior cerebellar artery
      • Superior cerebellar artery

The relevant principles are summarised as the Brainstem Rule of Four, which states that there are:

  1. Four cranial nerves:
    • Above the pons
      CN III-IV. As CN I and II arise above the midbrain, they will be unaffected by a brainstem lesion.
    • In the pons
      CN V-VIII.
    • In the medulla
      CN IX-XII.

Brainstem vascular syndromes can be geographically localised to the medial or lateral aspect of a specific structure by identifying both the affected pathway and cranial nerves.

  1. Four midline motor nuclei, and they are all* factors of 12

*This refers to nerves 3, 4, 6, and 12; 1 and 2 are also factors of 12 but are not motor nerves. Motor nuclei (e.g. CN VII) that are not listed are not midline.

  1. Four structures in the midline
    These begin with “m”:
    • Motor pathway (Corticospinal tract)
      Contralateral arm and leg.
    • Motor nuclei
      Nuclei of the midline motor cranial nerves, listed in rule 2.
    • Medial lemniscus
      Contralateral vibration and proprioception.
    • Medial longitudinal fasciculus
      Ipsilateral internuclear ophthalmoplegia.

Ipsilateral internuclear ophthalmoplegia is a failure of adduction of the ipsilateral eye towards the nose, with nystagmus on lateral gaze of the contralateral eye.

  1. Four structures to the side (lateral)
    These begin with “s”:
    • Spinothalamic pathway
      Contralateral pain and temperature.
    • Spinocerebellar pathway
      Ipsilateral ataxia.
    • Sympathetic pathway
      Ipsilateral Horner’s syndrome.
    • Sensory nucleus of CN V
      Ipsilateral facial pain and temperature.

Normal functions of the cranial nerves:

  • CN I: Olfactory
    Smell.
  • CN II: Optic
    Vision; including brightness, colour, and contrast.
  • CN III: Oculomotor
    Ipsilateral eye adduction, supraduction, and infraduction.
  • CN IV: Trocholear
    Ipsilateral downward and inward eye movement.
  • CN V: Trigeminal
    Ipsilateral facial pain, temperature, and light touch.
  • CN VI: Abducent
    Ipsilateral eye abduction.
  • CN IX: Glossopharyngeal
    Ipsilateral pharyngeal sensation.
  • CN X: Vagus
    Ipsilateral palate.
  • CN XI: Accessory
    Ipsilateral trapezius and SCM.
  • CN XII: Hypoglossal
    Ipsilateral tongue.
Application of the Rule of 4
Syndrome Vessel Rules Features
Medial medullary syndrome (Dejerine Syndrome)
  • Vertebral artery
  • Anterior spinal artery
Medial
  • Contralateral weakness
  • Contralateral vibration and proprioception
Medulla
(CN IX-XII)
  • Ipsilateral tongue weakness
Lateral medullary syndrome (Wallenberg Syndrome) Anterior Inferior Cerebellar Artery Lateral
  • Contralateral pain and temperatures
  • Ipsilateral ataxia
  • Ipsilateral Horner’s syndrome
  • Ipsilateral facial sensory loss
Medulla
(CN IX-XII)
  • Loss of gag reflex
  • Dysarthria
  • Dysphagia
Lateral pontine syndrome (Marie-Foix Syndrome) Posterior Inferior Cerebellar Artery Lateral
  • Contralateral pian and temperature
  • Ipsilateral ataxia
Pons
(CN IV-VIII)
  • Ipsilateral facial weakness
  • Ipsilateral hearing loss, vertigo, nystagmus
Locked-in Syndrome Basilar Artery Medial
  • Whole body weakness
  • Lateral gaze weakness
  • Dysarthria
Lateral
  • Whole body sensory loss
Pons
(CN IV-VIII)
  • Bilateral facial weakness

Presence of both lateral and medial features suggests a basilar artery problem.

Investigations

Bedside:

  • BSL
  • ECG
    Screen for AF.

Laboratory:

  • Blood
    • FBE
      Anaemia, polycythaemia.
    • Blood cultures
      If considering endocarditis.
    • Lipids
    • ESR/CRP
      ↑ Suggests vasculitis.
    • Thrombophilia screen
    • Pregnancy

Thrombophilia screen is covered under Thrombophilia.

Imaging:

CT non-con should be repeated 24 hours after perfusion therapy to evaluate for complications.

  • CT non-contrast
    • Grey-white differentiation (<1 hour)
      Occurs early and suggests irreversibly infarcted brain tissue.
    • Vasogenic oedema (3-6 hours)
      Hypodensity developing due to irreversible infarction.
    • ICH
      Rapidly changes management plan.
    • Hyperdense vessel
      Thrombus may be visible in an intracranial vessel (particularly MCA, indicating large vessel occlusion.
  • CT angiography
    • Occlusion
      Identification of large vessel occlusion to guide endovascular therapy.
    • Dissection
    • Athersclerosis
  • CT perfusion
    • Penumbra identification
      Identifies volume of ischaemic penumbra for supratentorial stroke.
  • MRI
    • Identification of stroke
      Particularly for the posterior fossa, which is more poorly imaged on CT.
    • Identification of ICH
    • DWI and FLAIR mismatch
      Identifies penumbra.
  • Echocardiography
    PFO, endocarditis.

Echocardiography is more useful in younger patients, who are less likely to have “classical” embolic causes.

Diagnostic Approach and DDx

Diagnosis relies on identifying both:

  • A stroke syndrome
  • The corresponding radiological deficit

Differential diagnoses include:

  • Migraine
    Positive migraine symptoms (visual symptoms, paraesthesias) are less consistent with ischaemic stroke.
  • Post-ictal deficit
    Should improve over minutes-hours.
  • Mass lesion (e.g. Tumour, abscess)
    More gradual onset.
  • PRES
  • Intoxication

Management

  • Activate a Stroke Code
    Rapid activation of neurology, radiology, and interventional radiology dramatically streamlines care for these patients. Establish:
    • Weight
      To allow TPA to be dispensed.
    • Time Last Seen Well
      To establish onset, and eligibility for reperfusion.
    • Anticoagulation status
  • Expedite reperfusion
  • Optimise physiology

Resuscitation:

  • A
    • Airway protection
      • Indications vary, but in RCTs have included:
        • GCS <8
        • Other aspiration risk
        • Respiratory failure (PCO2 > 48mmHg, PO2 < 60mmHg)
      • Removes the mortality and morbidity benefits of stroke unit admission
      • Is a very bad prognostic sign
  • B
    • Normoxaemia
      Investigate for a secondary cause (e.g., aspiration).
    • Normocapnoea
      Hyperventilation may be required for high ICP.
  • C
    • Blood pressure monitoring and control
      Invasive if haemodynamically unstable or mechanically ventilated.
  • D
    • EVD
      May be required if obstructive hydrocephalus develops.
    • ICP control
      • Hyperventilation
      • Osmotic therapy
  • E
    • Maintain normothermia
      Treat temperature >38°C.

Supportive Care:

  • A
    • Tracheostomy

Disposition:

  • Mortality and morbidity are improved with specialist stroke unit admission
    Avoid ICU admission if possible.

Ischaemic Stroke

These management aims are in addition to the above.

Resuscitation:

  • C
    • Hypertension
      Aims SBP/DBP
      • Before thrombolysis: <185/<110
      • After thrombolysis: <180/105
      • No thrombolysis: <220/<120 or end-organ damage
        ↓ Cautiously (aim <15% reduction/24 hours) if not urgently required - ↑ morbidity with rapid ↓.
      • Agents
        • Labetalol 10-20mg IV
    • Hypotension
      Much less common.
      • Aim SBP >90mmHg
      • Treat cause, and otherwise use noradrenaline

Specific therapy:

  • Reperfusion
    • Intravenous thrombolysis
    • Intraarterial thrombolysis
      ↑ Recanalisation rates but ↑↑ ICH.
    • Thrombectomy
  • Pharmacological
    • Aspirin
      Load (300mg) within 48 hours, but delay:
      • 24 hours following thrombolysis
      • Indefinitely if craniectomy planned
      • Clopidogrel should be used if aspirin is contraindicated
    • Anticoagulation
      If required for another indication (e.g. AF), commence >4-14/7 after the stroke, depending on risk of haemorrhagic transformation. Delay is unlikely to be harmful given the repeat stroke risk (from AF) is probably low over this period.
    • Statin
      High dose (e.g. atorvastatin 80mg).
  • Procedural
    • Craniectomy
      Two scenarios where this may be considered:
      • MMCAS with mass effect
        ↑ Survival with survivors having moderate-severe disability.
      • Cerebellar infarction with posterior fossa syndrome
        Much better outcomes than for MMCAS.
    • EVD
      Indicated for secondary hydrocephalus.

Reperfusion

Thrombolysis (if indicated) should be given as soon as possible after ICH is excluded and hypertension is controlled.

Reperfusion Strategies
Technique Intravenous thrombolysis Thrombectomy
Timing
  • Onset <4.5 hours
    Earlier is better.
  • Early: <6 hours
    Earlier is better.
  • Extended: <24 hours
    With significant volume of salvageable tissue.
Comments
  • Alteplase 0.9mg/kg, up to 90mg
    10% over 1/60, remainder over 60/60.
  • For wake-up strokes with unknown onset, can be beneficial if <4.5 hours of recognition
  • Risks are significant and should be discussed with the patient and family prior to commencing
    The evidence is controversial and different professional societies disagree. In general, thrombolysis:
    • Improves functional outcome
      • NNT ~3 to improve mRS by 1
      • NNT for mRS 0-3: 10
      • NNT for mRS 0-2: 13
    • ↑↑ Risk of ICH
      • NNH symptomatic ICH 42 (13-119)
      • NNH death 122 (30-830)
    • Has no mortality benefit
  • The greater penumbra:core, the better the outcome
    Even a long time from LSW.
  • Few trials for basilar strokes due to lack of equipoise driven by real-world benefit
  • Concern about ↑ haemorrhagic transformation at high infarct volumes, although outcome benefit persists
Indications
  • “Significant” stroke
    Thresholds vary, but NIHSS >~5
  • mRS 0-1 at baseline
  • Large vessel occlusion
    M1, M2, ICA, basilar.
  • “Significant” stroke
  • mRS 0-1 at baseline
Absolute Contraindications

Intracranial:

  • ICH/SAH
  • Completed stroke

Surgical:

  • Intracranial/spinal surgery within 3/12

Bleeding Risk:

  • Bacterial endocarditis
  • Uncontrolled hypertension (>185/110)
  • Aortic dissection
  • UGIB within 21/7
  • Major trauma within 14/7
  • Uncontrolled coagulopathy

Intracranial:

  • Completed stroke

Procedural:

  • Contrast allergy
  • Unable to achieve carotid/vertebral access

Bleeding risk:

  • Uncontrolled coagulopathy
Relative Contraindications

Neurological:

  • Rapidly improving symptoms
  • Seizure at the time of stroke, with residual post-ictal signs

Other:

  • Major surgery within 14/7
  • Major GI/GU bleeding within 21/7
  • MI within 3/12
  • Pregnancy

Marginal and Ineffective Therapies

  • B
    • Hyperventilation
  • D
    • ICP monitoring
    • Seizure prophylaxis
  • H
    • Heparin infusion

Anaesthetic Considerations

GA and sedation have been compared with no clear evidence of superiority

My approach is tailored to the individual patient, with a strong preference towards whatever will allow the proceduralist to expedite reperfusion.

  • A
    • Extubation
      Should be extubated as soon as feasible.
  • C
    • Arrhythmia
      Correct electrolytes.
    • Blood pressure control
      • Prior to revascularisation: SBP <185 and MAP >10-20% of baseline
      • After revascularisat ion: SBP <160
  • D
    • CVA
    • ICP management
  • H
    • Bleeding
      If thrombolysed prior.
  • Other
    • Off the floor

Complications

  • Death
    30% 1-month mortality.
  • A
    • Aspiration
      Dysphagia common both with brainstem and hemispheric stroke.
  • B
    • Pneumonia
      Including VAP, if intubated.
    • PE
      Accounts for 10% of deaths following stroke.
  • C
    • Dysrhythmia (40%)
      Common.
  • D
    • Malignant Infarction of the Middle Cerebral Artery (MMCAS)
    • Haemorrhagic transformation (5%)
      Bleeding into a previously ischaemic stroke.
      • Risks
        • Large infarct
        • Coagulopathy
        • Vascular risk factors
        • Hypertension
      • Management
        • Stop any residual thrombolysis
        • Repeat imaging
        • Correct coagulopathy
          • Cryoprecipitate 10U
          • TXA 1g
        • Neurosurgical evacuation may be indicated if mass effect
    • Cerebral oedema and ↑ ICP
    • Hydrocephalus
      • Obstructive
        May be both more common and more severe following cerebellar than cortical infarction.
      • Ex-vacuo
        Loss of brain tissue resulting in ↑ CSF volume.
    • Seizure (<10%)
      Uncommon. Risk ↑ with stroke severity, and may indicated haemorrhagic transformation.
    • Hyperglycaemia (40%)
      • Common
      • Associated with mortality and morbidity
      • Tight control harmful
  • E
    • Fever (50%)
  • H
    • DVT
      Early mobilisation. Prophylactic heparin should be started >24 hours following reperfusion.
    • Anaemia
      Transfusion threshold not established.

Things to consider if the stroke patient deteriorates:

  • Haemorrhagic transformation
  • Reinfarction/reocclusion
  • ICP
  • Seizure
  • Hypoglycaemia

Malignant Middle Cerebral Artery Infarction Syndrome

A massive swelling of the MCA territory secondary to a proximal occlusion, leading to significant mass effect on the contralateral side. MMCAS:

Outcomes at 12 months for patients randomised to decompressive craniectomy or non-surgical treatment for MMCAS (Vahedi et al, 2007).

  • Defined by >50% of MCA stroke affected on CT
  • Occurs in 1-10% of patients with MCA CVA
  • Has a mortality of 80%
  • Decompressive craniectomy
    Controversial; but appropriate with:
    • Early (<48 hours) intervention
    • Young (<60) patient
    • Multidisciplinary decision
    • Shared decision making with family, noting:
      • Significantly ↑ survival
      • Significantly ↑ survival with disability
        • Majority of new survivors are at least moderately-severely disabled
        • Many new survivors will be slight-moderate disability

Prognosis

Outcome is highly dependent on the particulars of the individual neurology. With this in mind, poor prognostic factors include:

Degree of disability following stroke is commonly quantified using the Modified Rankin Scale (mRS):

  • 0: Asymptomatic.
  • 1: No significant disability. Some symptoms, but IADLs.
  • 2: Slight disability. Unable to to carry out all previous activities, but IADLs.
  • 3: Moderate disability. Requires some help, able to walk unassisted.
  • 4: Moderately severe disability. Assistance with PADLs and walking.
  • 5: Severe disability. Constant nursing care, bedridden, incontinent.
  • 6: Dead
  • Age
    >85 has 35% in-hospital mortality.
  • Requiring mechanical ventilation
    ~50% in-hospital mortality (lowest for ischaemic stroke) and significantly ↑ disability in survivors.

Key Studies

Endovascular therapy:

  • MR CLEAN (2015)
    • 500 patients >18 with occlusion of ACA or MCA
      • <6 hours from onset
      • NIHSS >2
    • Intra-arterial therapy vs usual care
      Majority (83%) mechanical thrombectomy, very few (0.4%) received intra-arterial thrombolysis, 16% received no intervention
    • Significant improvement in 90 day mRS, NIHSS at discharge, and final infarct volume
    • Multiple centres in the Netherlands
    • Slightly unbalanced group sizes
    • Higher ischaemic stroke rate at 90 days in treatment group
      Confounded by concurrent carotid stenting in some of this group.
  • DAWN (2018)
    • 206 patients >18 with occlusion of ICA or M1
      • Mismatch between clinical deficit (by NIHSS) and radiological infarct volume
        Designed to identify patients with viable penumbra.
      • Thrombolysis failed or contraindicated
      • NIHSS >10
      • Known to be normal 6-24 hours prior
    • Mechanical thrombectomy vs. standard medical therapy
    • Significant improvement in mechanical thrombectomy group
      49% functionally independent in thrombectomy group, compared to 13% in medical therapy group. Secondary outcomes also all improved.
    • Closed early
    • Industry sponsored
    • Required particular imaging
  • DEFUSE-3 (2018)
    • 182 patients 18-90 with occlusion of ICA or M1
      • NIHSS >6
      • <70mL infarct volume with >15mL penumbra
    • Thrombectomy plus medical therapy vs. medical therapy alone
    • Significant improvement in functional independence (45% vs 17%) at 90 days with endovascular approach
    • Required particular imaging and software access, may not be generalisable
  • DIRECT-MT (2020)
    • 636 patients >18 with occlusion of ICA or M1/M2
      • <4.5 hours from onset
      • NIHSS >2
      • Eligible for thrombolysis
    • Thrombectomy alone vs. thrombolysis and thrombectomy
    • No difference between groups in mortality or mRS
  • Yoshimura et al. (2022)
    • 203 Japanese adults with:
      • NIHSS >6
      • ASPECTS score 3-6
        Indicating large ischaemic region.
    • Endovascular therapy vs medical care
      98% of endovascular group received thrombectomy.
    • rt-rPA 0.6mg/kg was permitted
    • Significant improvement in mRS 0-3 at 90 days; RR 2.43
    • ICH rate within 48 hours in endovascular therapy group

Decompressive craniectomy:

  • DESTINY (2007)
    • 32 patients 18-60 with large (>2/3rds of territory) unilateral MCA stroke
      • 12-36 hours from diagnosis
      • NIHSS >18 (dominant) or >20 (non-dominant)
    • Decompressive craniectomy vs. non-surgical
    • Improved survival in surgical group, worse disability
    • Stopped early for statistical significance in mortality end-point
  • DECIMAL (2007)
    • 38 French adults <55 within 24 hours of MMCAS
    • Multicentre (13), single-blind RCT
    • Stopped early for slow recruitment
    • Early decrompressive craniectomy vs. medical management
    • Significantly ↓ mortality (22% vs. 75%) in the craniectomy group
    • Signifincantly ↑ neurological morbidity in the craniectomy group

  • HAMLET (2009)
    • 64 Dutch adults with MMCAS within 4 day of stroke onset
    • Decompressive craniectomy vs. medical management
    • ↓ Mortality (22% vs. 59%) with craniectomy
    • Majority of survivors have ↑ functional disability

  • DESTINY II (2007)
    • 112 patients >60 with large unilateral MCA stroke
      • <48/24 of diagnosis
      • NIHSS >14 (non-dominant) or >19 (dominant hemisphere)
      • Red
    • Decompressive hemicraniectomy vs. non-surgical
    • Double survival (57% vs 24%) in surgical group, but vast majority of survivors have moderate-severe (or worse) disability

Other:

  • SETPOINT2 (2022)
    • ~380 German and American adults with ischaemic stroke, haemorrhage, or SAH predicted to need:
      • >2 weeks of ventilation
      • Tracheostomy
    • Percutaneous tracheostomy at day 5 vs. day 10
    • No difference in survival without significant disability at 6 months
    • Very morbid cohort
      Poor neurological outcomes in general with high craniectomy rate.

Further Reading

  • The IBCC has a phenomenal in-depth chapter on ischaemic stroke
  • NeuroEMCRit has a two-part (one, two) overview of ischaemic stroke

References

  1. Vahedi, Katayoun, Jeannette Hofmeijer, Eric Juettler, Eric Vicaut, Bernard George, Ale Algra, G. Johan Amelink, et al. Early Decompressive Surgery in Malignant Infarction of the Middle Cerebral Artery: A Pooled Analysis of Three Randomised Controlled Trials. The Lancet Neurology 6, no. 3 (1 March 2007): 215–22.
  2. Jüttler, Eric, Andreas Unterberg, Johannes Woitzik, Julian Bösel, Hemasse Amiri, Oliver W. Sakowitz, Matthias Gondan, et al. Hemicraniectomy in Older Patients with Extensive Middle-Cerebral-Artery Stroke. New England Journal of Medicine 370, no. 12 (20 March 2014): 1091–1100..
  3. Saver, Jeffrey L. Number Needed to Treat Estimates Incorporating Effects over the Entire Range of Clinical Outcomes: Novel Derivation Method and Application to Thrombolytic Therapy for Acute Stroke. Archives of Neurology 61, no. 7 (July 2004): 1066–70.
  4. Farag, Ehab, Maged Argalious, and Gabor Toth. Stroke Thrombectomy Perioperative Anesthetic and Hemodynamic Management. Journal of NeuroInterventional Surgery, 13 June 2022.
  5. Powers, William J., Alejandro A. Rabinstein, Teri Ackerson, Opeolu M. Adeoye, Nicholas C. Bambakidis, Kyra Becker, José Biller, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 50, no. 12 (December 2019): e344–418.
  6. Epstein, Elliot, and Huma Naqvi. Acute Hydrocephalus Following Cerebellar Infarct. BMJ Case Reports 2010 (February 22, 2010): bcr06.2009.1957
  7. Davies, Leo, and Candice Delcourt. Current Approach to Acute Stroke Management. Internal Medicine Journal 51, no. 4 (2021): 481–87.
  8. Bersten, A. D., & Handy, J. M. (2018). Oh’s Intensive Care Manual. Elsevier Gezondheidszorg.
  9. Bösel J, Niesen WD, Salih F, et al. Effect of Early vs Standard Approach to Tracheostomy on Functional Outcome at 6 Months Among Patients With Severe Stroke Receiving Mechanical Ventilation: The SETPOINT2 Randomized Clinical Trial. JAMA. 2022;327(19):1899-1909.
  10. Yoshimura S, Sakai N, Yamagami H, et al. Endovascular Therapy for Acute Stroke with a Large Ischemic Region. New England Journal of Medicine. 2022;386(14):1303-1313.
  11. Vahedi K, Vicaut E, Mateo J, et al. Sequential-Design, Multicenter, Randomized, Controlled Trial of Early Decompressive Craniectomy in Malignant Middle Cerebral Artery Infarction (DECIMAL Trial). Stroke. 2007;38(9):2506-2517. doi:10.1161/STROKEAHA.107.485235
  12. ACEM. Position Statement: IV thrombolysis for ischaemic stroke. 2021 V5.
  13. Gates P. The rule of 4 of the brainstem: a simplified method for understanding brainstem anatomy and brainstem vascular syndromes for the non-neurologist. Internal Medicine Journal. 2005;35(4):263-266. doi:10.1111/j.1445-5994.2004.00732.x
  14. Dünser MW, Dankl D, Petros S, Mer M. Clinical Examination Skills in the Adult Critically Ill Patient. Springer International Publishing; 2018.