GENERAL THERAPY

Early management of patients with suspected stroke

Created 07/06/2022, last revision 13/11/2023

  • any patient with rapidly evolving neurological deficits should be evaluated as a potential candidate for recanalization therapy and transported ASAP to the nearest Stroke Center (SC) or Comprehensive Stroke Center (CSC) for urgent diagnostic evaluation and treatment

Definition and clinical presentation of acute stroke

→ An Updated Definition of Stroke for the 21st Century – AHA/ASA 2013

  • stroke is a cerebrovascular emergency typically characterized by sudden loss of neurologic functions
  • stroke can be classified into 2 main categories:
    • ischemic
      • arterial occlusion (synonym for ischemic stroke)    Cerebellar infarct caused the PICA occlusion
      • venous thrombosis (cerebral sinus or vein thrombosis)  Hyperdense sign in the right sigmoid and straight sinus thrombosis (80 HU)
    • hemorrhagic
      • intracerebral hemorrhage Density of an acute hematoma on non-contrast CT (NCCT)
      • subarachnoid hemorrhage  SAH caused by the rupture of a posterior communicating artery (PComA) aneurysm
  • sudden onset of neurological deficit
    • not all stroke subtypes meet this criterion (mild SAH, the early phase of cerebral sinus thrombosis, etc.)
    • conversely, not all acute-onset focal symptoms are stroke-related → stroke mimics (tumor, migraines, trauma, epileptic seizures, hypoglycemia, etc.)
      • other cause at age < 50 years ~ 21%
      • other cause at age > 50 years ~ 3%
  • several prehospital tests have been developed to facilitate stroke detection (FAST, 3-ISS, C-STAT, LAMS, PASS, RACE, FAST+)
Typical clinical course
  • sudden onset, with the deficit usually being maximal initially; the undulating and progressive course is possible (due to thrombus dynamics, quality of collateral circulation, etc.)
  • focal, negative symptoms (hemiparesis, hemihypesthesia, dysarthria, aphasia, hemianopsia, etc.-)
    • common in ischemic stroke or ICH
    • 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

→ Topical diagnosis of stroke

Less likely stroke symptoms
  • isolated diplopia
  • isolated dysphagia
  • isolated tinnitus/hearing loss
  • vertigo
  • isolated imbalance and falls
  • isolated confusion (don’t miss aphasia!)

Notes regarding stroke classification based on time parameters

  • the original concepts of transient Ischemic Attack (TIA) and Reversible Ischemic Neurological Deficit (RIND) are now 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 the 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 and/or positive imaging studies (i.e., even if neurological findings are normal)

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

FAST test

  • 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 (visual field defects, sudden loss of vision in one eye, diplopia)
  • balance and gait disturbance
  • unilateral sensory impairment (hypesthesia, anesthesia, paresthesias)
  • symptoms of potential SAH
    • sudden onset of a severe, atypical headache (“worst headache ever”)
    • the gradual development of neck stiffness (meningeal syndrome)

3I-SS test

  • the 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 functions
  • each item is graded from 0 to 2, with 0 representing normal findings and 2 severe abnormalities
  • the worst score is 6 (i.e., profound drowsiness or worse, forced gaze deviation, and severe hemiparesis, respectively)
  • a score of ≥4 predicts proximal vessel occlusion (T-segment of ICA or M1 segment) almost as accurately as an NIHSS score ≥14

Pre-hospital management and triage

Monitoring vital signs, symptomatic therapy

  • perform a rapid assessment of vital signs (ABC) – A – airway, B – breathing, C – circulation
    • maintain arterial blood oxygen saturation >94%, and do not administer oxygen to nonhypoxic patients  (AHA/ASA 2018 I/C-LD)
    • secure airway if necessary
    • monitor blood pressure – correct hypotension; hypertension should be treated cautiously (→ 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 for hypoglycemia), and avoid oral administration
  • perform ECG
  • initiate symptomatic therapy as needed (antiemetics, anticonvulsants, etc.)

Triage of patients with suspected stroke

  • emergency services should recognize the clinical signs of stroke (FAST, FAST PLUS, 3I-SS, etc.), obtain relevant medical history and the exact time of onset, and look for contraindications to thrombolysis (see below)
  • patients eligible for recanalization treatment should be urgently transported to a Stroke Center or Comprehensive Stroke Center) (AHA/ASA 2019 I/B-NR)
    • for patients with suspected Large Vessel Occlusion (LVO), direct transport to the nearest CSC may be preferable  (AHA/ASA 2019 IIb/B-NR)
    • data analysis from the DAWN trial showed no significant difference in outcome between patients transferred to a Stroke Center with secondary transport to a CSC and those with direct transport to a CSC [Aghaebrahim,2019]
    • patients with suspected LVO for whom IVT is contraindicated should be directly transferred to a CSC after prior consultation (AHA/ASA 2019 IIb/C-EO)
    • if a symptomatic LVO is detected in the SC, the nearest CSC should be consulted immediately

When the patient should be transported to a Comprehensive Stroke Center?

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 IVT initiation would not differ significantly between SC and CSC
an acute stroke patient with a known absolute contraindication to  IVT (anticoagulant therapy, endocarditis, aortic dissection, recent delivery, etc.)
signs and symptoms of SAH
When to transfer the patient from the SC to the CSC
selected patients with LVO < 24h after symptoms onset → mechanical recanalization
patients at risk of malignant ischemia for whom decompressive craniectomy is considered
patients with arterial dissection indicated for interventional procedure
patients with ICH, SAH, or IVH who are candidates for surgical intervention
patients with cerebral sinus thrombosis who are likely candidates for endovascular or surgical intervention

Relevant information to obtain

  • try to find ascertain:
    • the exact time of stroke onset or
    • the time the patient was last seen well or
    • at least the time when a witness found the patient
  • in wake-up stroke (WUS), try to narrow down the onset time (determine when the patient went to sleep, whether they woke up during the night, etc.)
  • obtain phone contact with someone who can specify the circumstances of stroke onset and provide the patient’s personal and medical history
  • collect a detailed personal and medical history, focusing on known contraindications to thrombolysis
    • use of anticoagulants (warfarin, DOACs) and the time of the last dose
    • recent surgery or bleeding
    • predisposition to bleeding
    • allergies and adverse reactions (to iodinated contrast media, drugs, food, etc.)
    • history of renal insufficiency
  • paramedics should obtain a list of the patient’s diagnoses and  medications from family members and bring any 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 begin ASAP after arrival at the hospital
  • it is recommended to follow the approved in-house stroke protocol
    • the patient is taken to the emergency department, stroke unit, or directly to the CT department
    • brain and vascular imaging (± perfusion) are performed
  • none of the following procedures (except for stabilization of vital signs, blood pressure correction, and non-contrast CT scan) should delay the initiation recanalization therapy
  • monitor baseline vital signs during transport and diagnostic evaluation (at least oximetry and pulse rate during the CT scan)

Initial assessment and stabilization of vital functions

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Intravenous access and laboratory testing

  • collect blood samples for the following tests:
    • blood glucose – the only test required before starting the IVT (AHA/ASA 2019 I/B-NR)
    • bilirubin, osmolality, liver panel (AST, ALT, GMT)
    • urea, creatinine, estimated Glomerular Filtration Rate (eGFR)
    • ionogram (Na, K, Cl)
    • inflammatory markers
    • cardiac enzymes (CK, CKMB, LD) + high-sensitivity troponin T (hs-troponin T) (AHA/ASA 2019 I/C-LD)
      • elevation observed in 5-34% of patients
      • MI can cause stroke, and conversely, stroke can provoke MI
      • approximately 10% of mild troponin T elevations are not due to MI (potential causes include 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 or cardiac MRI should be performed)
    • complete blood count (CBC)
    • coagulation test
      • APTT, prothrombin time, AT III, fibrinogen
      • specific tests to detect DOAC activity
      • INR (if the patient is using warfarin) can be quickly determined with a bedside coagulometer (CoaguChek)
    • other tests
      • ASTRUP
      • toxicology screen (alcohol, drugs)
      • pregnancy test
      • D-dimer
  • insert IV cannula (2 cannulas are required if thrombolysis is planned)
    • if a peripheral vein cannot be secured, cannulate the femoral or jugular vein
  • consider placing a urinary catheter
    • palpate the bladder for fullness; urinary retention may cause agitation

IV thrombolysis related note on blood samples

  • in patients who are not receiving anticoagulant therapy or do not have known thrombocytopenia or a bleeding abnormality, IVT can be initiated without waiting for INR, aPTT, and platelet count, if their evaluation and determination would postpone the initiation of thrombolysis
  • if tests subsequently reveal an INR > 1.7 or aPTT above the upper laboratory limit, or a platelet count < 100 000/μL, IVT must be immediately stopped
  • the risk of unexpected thrombocytopenia or coagulopathy 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)
    • time of stroke symptom onset or when the patient was last seen well
    • duration of transient symptoms, as longer durations increase the likelihood of detecting a DWI lesion.
    • circumstances of stroke onset, including signs of potential epileptic seizure
    • history of previous stroke, myocardial infarction (MI), hypertension (HT), dyslipidemia (DLP), diabetes
    • 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
  • start symptomatic therapy (e.g., analgesics, antiemetics)

Brain and vascular imaging

  • perform all tests as quickly as possible (AHA/ASA 2019 I/B-NR)
  • do not administer antiplatelets/anticoagulants before brain imaging; only provide necessary symptomatic therapy
    • administer IV midazolam bolus if the patient is agitated or IV antiemetics
  • start with non-contrast brain CT (NCCT) or MRI (FLAIR, DWI, GRE) – sufficient for IVT indication
    • distinguish ischemia from hemorrhage and other etiology (tumor, inflammatory involvement, trauma)
    • MRI is as effective as NCCT in differentiating hemorrhage (AHA/ASA 2019 I/B-NR)
    • assess location and extent of the infarct
  • vascular imaging – perform CT angiography/MR angiography in all candidates for mechanical recanalization therapy (usually after tPA bolus) (AHA/ASA 2019 I/A)
    • examine extra- and intracranial circulation and assess the aortic arch (exclude dissection!) Aortic dissection on CTA
    • consider extending the emergent CTA to the heart level to detect left atrial appendage (LAA) thrombus or pulmonary embolism Pulmonary embolism on CTA LAA thrombus on CTA CTA showing thrombus in LAA  (Popkirov, 2019)
    • assess vascular pathology (occlusion, extra-/intracranial stenosis) and access route to the occlusion site and collateral circulation
    • vascular imaging is also useful in TIA patients to exclude occlusion or high-risk stenosis
    • do not wait for creatinine level in patients with no history of renal impairment; the risk of CIN is low (AHA/ASA 2019 IIa/B-NR)
    • management of patients with a history of renal insufficiency is not specified in the recent guidelines
  • detection of tissue viability (via multimodal imaging techniques such as CT perfusion, MR DWI/PWI mismatch)
    • testing should not delay IVT administration and is not necessary for patients within the 4.5h window (AHA/ASA 2018 III/B-NR)
    • in patients < 6h after stroke onset and with ASPECTS ≥ 6, CTP is unnecessary to indicate mechanical recanalization (THRACE and MR CLEAN trials showed positive results without CTP). Further RCTs will decide whether stratification by CTP is helpful in this time window
    • expanded indications for recanalization therapy are discussed here
    • multimodal imaging may also be considered after secondary transport to CSC to avoid futile endovascular procedure  see the discussion here

Clinical-radiologic correlation

  • a vascular neurologist (strokologist, stroke specialist) should be able to correctly indicate and interpret various imaging modalities and ultimately make clinical-imaging correlations
  • after considering all this knowledge together with a careful risk-benefit assessment, they can decide on the appropriate therapy
  • the decision tree is most complex in acute ischemic stroke, where the diagnostic evaluation should help to answer the following questions:
  • is it a stroke/TIA?
  • what type of stroke is it (ischemic, hemorrhagic)?
  • what part of the brain/arterial territory is affected?
  • is a relevant artery occluded?
  • can the affected part of the brain be saved (e.g., with IVT or thrombectomy)?
  • what is the most likely cause of the stroke, and what should be done to prevent recurrence?

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Early management of patients with suspected stroke
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