• every patient with rapidly developing neurological deficits should be evaluated as a potential candidate for recanalization treatment and should be transported ASAP to the nearest stroke center or comprehensive stroke center for emergent diagnostic evaluation and therapy

Definition and clinical presentation of an acute stroke

  • sudden-onset neurological deficit
    • not all stroke subtypes meet this criterion (mild SAH, early phase of sinus thrombosis, etc.)
    • conversely, not all acute-onset focal symptoms are stroke-related → stroke mimics (tumor, trauma, epileptic seizures, hypoglycemia, etc.)
      • other cause at age < 50 years ~ 21%
      • other cause at age > 50 years ~ 3%
  • several pre-hospital tests have been developed to facilitate the stroke detection (FAST, 3-ISS, C-STAT, LAMS, PASS, RACE, FAST+)
Typical clinical course
  • sudden onset
  • usually, the deficit is maximal at the beginning; the undulating and progressive course is possible (thrombus dynamics, quality of collateral circulation)
  • focal, negative symptoms (hemiparesis, hemihypesthesia, dysarthria, aphasia, hemianopsia, etc.-)
    • commonly present in ischemic stroke or intracerebral hemorrhage
    • usually absent in SAH and the early phase of sinus thrombosis
  • associated symptoms – headache, vertigo, and nausea
Common signs and symptoms
  • hemiparesis
  • hemihypesthesia
  • hemianopsia, monocular visual disturbances
  • hemiparesthesias
  • aphasia
  • dysarthria, dysphonia, dysphagia
  • vestibular and cerebellar syndrome
  • oculomotor disorders

→ see topical stroke diagnosis

Less likely stroke symptoms
  • isolated diplopia
  • isolated dysphagia
  • isolated tinnitus/hearing loss
  • vertigo
  • isolated balance disorders and falls
  • isolated confusion (don´t miss aphasia!)
  • the original concept of TIA and RIND is obsolete
  • according to the old definition, a TIA was defined as a sudden focal neurological deficit of presumed vascular origin lasting < 24 hours; however, ~30-50% of such TIAs had an infarction on MR-DWI
  • a new definition of TIA: short-term impairment of neurological function caused by cerebral, spinal cord, or retinal ischemia (with clinical symptoms usually lasting < 1h) unless there is evidence of cerebral infarction [Albers, 2002] [Furie, 2011]
  • cerebral infarction – persistent clinical symptoms or positive imaging studies (i.e., even if neurological findings are normal)

From a practical point of view, both cerebral infarction and TIA are prognostically serious conditions that require urgent diagnosis and therapy → TIA see here

  • triage positive patient = at least 1 major or 2 minor symptoms (see table)
Major stroke symptoms
Minor stroke symptoms
  • hemiparesis or monoparesis
  • central paresis of the facial nerve
  • speech disorder (aphasia, dysarthria)
  • altered level of consciousness (LOC)
    • quantitative (somnolence, sopor, coma)
    • qualitative (delirium)
  • visual disturbance (defect of the visual field, sudden loss of vision in one eye, diplopia)
  • balance disorders with gait disturbance
  • unilateral sensory impairment (hypesthesia, anesthesia, paresthesias)
  • symptoms of potential SAH
    • sudden onset of a severe headache, atypical for the patient (“worst headache ever”)
    • the gradual development of neck stiffness (meningeal syndrome)
  • scale reflects acute stroke severity and predicts proximal MCA occlusion with reasonable accuracy (Singer, 2005)
  • it evaluates 3 parameters:
    • level of consciousness (LOC)
    • gaze
    • motor function
  • each item is graded 0 to 2, where 0 indicated normal findings and 2 severe abnormalities (ie, profound drowsiness or worse, forced gaze deviation, and severe hemiparesis, respectively).
  • the worst score is 6, a score of ≥4 predicts proximal vessel occlusion (T-segment or M1-segment occlusion) almost as accurately as an NIHSS score of ≥14

Pre-hospital management and triage

Monitoring and securing of vital signs, symptomatic therapy

  • rapid assessment of vital signs (ABC) – A – airway, B – breathing, C – circulation
    • maintain arterial blood oxygen saturation >94%, and do not administer oxygen to non-hypoxic patients  (AHA/ASA 2018 I/C-LD)
    • secure airways if needed
    • monitor blood pressure – correct hypotension, do not treat hypertension with few exceptions (→ hypertension in the acute stage of stroke see here)
  • secure venous access
    • a green cannula (18G, inner diameter 1.3 mm) – if CTP is a standard part of the imaging protocol
    • a pink cannula  (20G, inner diameter 1.1 mm) – if CTA alone is planned
  • check glycemia, do not administer glucose (except in hypoglycemia), and administer nothing per os
  • ECG
  • symptomatic therapy (antiemetic and anticonvulsant drugs, etc.)

Triage of patients with suspected stroke

  • the emergency service should recognize the clinical signs of stroke (FAST, FAST PLUS, 3I-SS, etc.),  determine the relevant medical history and the exact time of onset, and look for thrombolysis contraindications (see below)
  • the candidate for recanalization treatment should be transported urgently to the Stroke Center or the Comprehensive Stroke Center) (AHA/ASA 2019 I/B-NR)
    • for patients with suspected LVO, direct transport to the nearest CSC may be preferred (AHA/ASA 2019 IIb/B-NR)
    • data analysis of the DAWN trial did not show a different outcome of a transfer to a stroke center with secondary transport to CSC vs. direct transport to CSC [Aghaebrahim,2019]
    • patients with suspected LVO, who are found to have a contraindication to IVT, should be transferred directly to CSC after prior consultation (AHA/ASA 2019 IIb/C-EO)
    • if a symptomatic LVO is detected in the stroke center, then the nearest CSC should be consulted immediately
When the patient should be transferred primarily to a center providing endovascular treatment
presumed LVO < 4.5h from the onset of symptoms, if the time of initiating IVT in the stroke center and CSC would not differ significantly
an acute stroke patient with known absolute  IVT contraindication (anticoagulant therapy, endocarditis, aorta dissection, recent birth, etc.)
signs and symptoms of SAH
When the patient should be transferred from the stroke center to the CSC
selected patients with LVO < 24h after onset of symptoms see mechanical recanalization
patients at risk of malignant ischemia where a decompressive craniectomy is considered
patients with artery dissection indicated for interventional procedure
patients with ICH, SAH, or IVH suggested for surgical intervention
patients with cerebral sinus thrombosis who are probable candidates for endovascular intervention or surgery

Relevant informations to obtain

  • try to find out:
    • the exact time of stroke onset, or
    • the time when the patient was last seen well, or
    • at least the time when the patient was found by a witness
  • in the wake-up stroke (WUS), try to narrow down the onset time (find out when the patient went to sleep, if he went to the toilet during the night, etc. )
  • ensure the phone contact of a person able to specify the circumstances of stroke onset and provide the patient’s anamnestic data
  • get a personal and medical history, focus on known contraindications to thrombolysis
    • use of the anticoagulant drugs (warfarin, DOACs) and the time of the last dose
    • recent surgery or bleeding
    • predisposition to bleeding
    • allergies and adverse reactions (to iodine contrast agent, medical and food allergies, etc.)
    • history of renal insufficiency
  • paramedics should optimally get a list of diagnoses and patient’s medications from the relatives and/or bring available medical records
  • assess the patient’s pre-stroke biological status and life-expectancy

Initial hospital management

An overview of basic procedures is presented – perform them as quickly as possible, many of them can be done simultaneously, before or during thrombolysis

  • recanalization therapy should be started as soon as possible after arrival at the hospital
  • it is recommended to follow the approved internal stroke protocol
    • the patient is brought to the emergency department, stroke unit, or directly to the CT department
    • the imaging of the brain and cerebral vessels (± perfusion) is performed
  • none of the following procedures (except for stabilization of vital signs, BP correction, and non-contrast CT scan) should delay recanalization therapy
  • monitor baseline vital signs during transport and diagnostic evaluation (at least oximetry and pulse rate during the CT exam)

Initial assessment and vital functions stabilisation

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Intravenous access and laboratory tests

  • collect blood samples
    • blood glucose – the only test required before starting the IVT (AHA/ASA 2019 I/B-NR)
    • bilirubin, osmolality, liver tests (AST, ALT, GMT)
    • urea, creatinine, eGFR
    • ionogram (Na, K, Cl)
    • inflammatory markers
    • cardiac enzymes (CK, CKMB, LD) + hs-troponin T  (AHA/ASA 2019 I/C-LD)
      • elevation in 5-34% of patients
      • IM can cause stroke and conversely, stroke can provoke IM
      • approximately 10% of mild troponin T elevations are not due to MI (hypertensive crisis, tachycardia, cardiac failure, pulmonary embolism, renal failure, aortic dissection)
      • even borderline elevations of hs-troponin T may be associated with MI (in cryptogenic stroke with suspected cardioembolism, TTE and cardiac MRI should be performed)
        complete blood count
    • complete blood count (CBC)
    • coagulation
      • APTT, prothrombin time, AT III, fibrinogen
      • specific tests to detect DOACs´ activity
      • INR (if the patient is on warfarin) can be quickly determined with a coagulometer (CoaguChek)
    • other tests
      • ASTRUP
      • toxicology screen including alcohol
      • pregnancy test
      • D-dimers
  • insert IV cannula  (2 pcs in case of thrombolysis)
    • if the peripheral vein cannot be secured, cannulate the femoral or jugular vein
  • consider urinary catheter insertion
    • palpate the bladder to check its filling, urinary retention may cause restlessness
  • patients who are not on any anticoagulant therapy or who do not have known thrombocytopenia or a known bleeding abnormality, IVT can be initiated without knowing the actual  INR, aPTT and platelet count if their evaluation and determination would postpone initiation of IV thrombolysis
  • if an INR > 1.7 or aPTT above the upper laboratory limit or a platelet count < 100 000/μl are detected, IVT must be stopped immediately
  • the risk of unexpected thrombocytopenia or coagulation disorders is very low – 0.3-0.4% [Rost, 2009], [Cucchiara, 2007]

AHA/ASA guidelines 2019

Medical history, clinical examination, symptomatic therapy

  • medical history (from the patient or witnesses)
    • when the symptoms of stroke started or when the patient was last seen well
    • with transient symptoms estimate their duration (longer duration increases the likelihood of DWI lesion detection)
    • stroke onset circumstances,  look for signs of a potential epileptic seizure
    • history of previous stroke, MI, HT, DLP, DM
    • history of coagulation disorders, recent bleeding or surgery
    • medications (especially anticoagulation), comorbidities, allergies, previous reaction to an iodinated contrast agent
    • history of smoking, drug or alcohol abuse
  • clinical examination
    • internal + neurological examination + NIHSS   → topical clinical diagnostics see here
  • address symptomatic therapy (analgesics, antiemetics, etc.)

Brain and vessels imaging

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Clinical-radiological correlation

  • a vascular neurologist (strokologist) should be able to correctly indicate and analyze different imaging modalities (including neurosonology) and finally perform a clinical-imaging correlation
  • taking all this knowledge into account, together with careful consideration of the risk-benefit, he/she can decide on the appropriate therapy
  • the decision tree is most complex in acute ischemic stroke, where diagnostic evaluation should help to answer the following questions:
  • is it stroke/TIA?
  • what type of stroke is it (ischemic, hemorrhagic)?
  • what part of the brain/arterial territory is affected?
  • is any relevant artery occluded?
  • can the affected part of the brain be saved (e.g., with IVT, thrombectomy)?
  • what is the likely etiology, and how to proceed with stroke prevention?
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