an updated account on management of TIA, Ischemic and hemorrhagic stroke in Sri Lanka. This is based on American Stroke Association and NICE guidelines.
2. OUTLINE
• General management
• Transient ischemic attacks
• Ischemic stroke
• Hemorrhagic stroke
• Intracranial hypertension and herniation
3. DEFINITION
The World Health Organization defines stroke as rapidly developing
clinical signs of focal (or global) disturbance of cerebral function,
lasting more than 24 hours or leading to death, with no apparent cause
other than that of vascular origin (40 yrs ago)
ICD 11 Updated definition- the acute focal neurological signs, of
presumed vascular origin, lasting longer than 24 hours or causing
death, but subtypes (ischemic or hemorrhagic) has not been determined
by neuroimaging or other techniques.
• 11% of all deaths
• Significant cause of morbidity
4. CLASSIFICATION
• Ischemic (85%)- due to an interruption of blood supply, or
• Hemorrhagic- due to rupture of a cerebral artery.
• Unable to distinguish between a hemorrhagic and ischemic stroke until imaging
obtained
6. INITIAL PREHOSPITAL
EVALUATION
• History and physical examination
• Determine LKW
• ABCs
• Glucose check
• Stroke severity screen exam
• Obtain IV access and blood for IX
• Contact stroke center and pre hospital notification
7.
8. • Stroke patients are dispatched at the highest level of care
available in the shortest time possible.
• Time between the receipt of the call and dispatch of the
EMSS team is <90 s.
• EMSS response time is <8 min (time elapsed from the call
receipt to arrival on the scene by the equipped and staffed
ambulance).
• The on-scene time is <15 min (barring extenuating
circumstances such as extrication difficulties).
9. EMERGENCY DEPARTMENT
EVALUATION
• Activate stroke code system
• Vital signs
• Maintain oxygen saturation >94%
• Determine time of onset/ LKW
• Determine NIHSS score
• CT/CTA
• Medication list (Anticoagulants)
• IV access (18G)
• IX- CBS, FBC with platelets, PT/INR, PTT and beta HCG, ECG
10. NIHSS SCORE
• reproducibly and quantifiably assess a patient’s
stroke symptoms.
• Scores range from 0 (no deficit) to 42
11. NIHSS - LIMITATIONS
• Limited use in
• in scoring brainstem strokes
• estimating the severity of a right hemispheric stroke.
• In the 2007 AHA/ASA guidelines, an NIHSS of 4 was a threshold
to treat AIS with thrombolytics, but in the 2018 guidelines, a
low score is not an absolute contraindication and potential risks
should be weighed against anticipated benefits.
12. IV FLUID
• Hypovolemia may exacerbate ischemic brain edema and
increase stress on the myocardium.
• Stroke patients should receive maintenance isotonic intravenous
fluids in the form of normal saline.
• The utilization of plasma volume expanders has not
demonstrated benefit.
14. DIAGNOSIS
• The diagnosis of TIA is based on the
• new onset of focal neurological symptoms and signs
• that are explainable by a vascular disease (e.g., arterial occlusion of a
single or group of arteries adequately explain the patient’s signs and
symptoms), and
• the resolution of these signs and symptoms within 24 h (most TIAs
resolve in a much shorter period of time).
• However, up to one-third of TIAs have demonstrable injury on
DW- MRI.
• Condition should be treated with a similar sense of urgency as
unstable angina
16. ABCD2 SCORE
Risk greater with
• frequent TIAs
• cerebral vs ocular events
• Severe carotid stenosis
• Age over 60
• Diabetes
• Symptoms longer than 10 min
• Weakness
• Impairment of speech
• Carotid are more liable than vertebral
basilar to be followed by stroke
19. • Encourage smoking cessation
• Outpatient workup in 1–2 days
• Imaging (USS Carotid , CTA, MRA)
• Consider transthoracic echocardiogram
• If electrocardiogram (ECG) or rhythm strip shows atrial
fibrillation, consider starting anticoagulation (oral anticoagulant
or low molecular weight heparin) or ASA
• Consider 30 day ambulatory cardiac monitor- to detect
intermittent atrial fibrillation
20. HIGH-RISK TIA (ABCD2 SCORES
>3)
• Hospital admission (crescendo attacks, symptomatic carotid
stenosis, cardiac source of emboli, hypercoagulable state)
• Permissive hypertension is encouraged (not to exceed
220/120 mmHg), and BP should be gradually lowered over 24–
48 h
• In a high-risk TIA (ABCD2 score ≥4), the CHANCE trial
demonstrated that dual antiplatelet therapy using a combination
of Clopidogrel (initial dose of 300 mg followed by 75 mg/day)
and Aspirin 81 mg/day for 21 days followed by Clopidogrel 75
mg/day for 90 days was superior to aspirin alone in reducing
21. • the POINT trial from USA showed that combined use of
Clopidogrel at a loading dose of 600 mg once followed by 75
mg/day for 90 days plus Aspirin 50–325 mg/ day for first 21
days was superior to aspirin 50–325 mg/ day for 90 days.
• The SAMMPRIS trial showed that in patients with TIA from
stenosis of a major intracranial artery (70–99%), medical
management with aspirin 325 mg/day and Clopidogrel
75 mg/day with aggressive medical management of primary
risk factors was superior to combined medical therapy and
intracranial stenting group.
22. • Progress trial 2001(Perindopril pROtection aGainst REcurrent
Stroke Study) showed Rx with ACEI & thiazide → larger ↓BP and
↓CVA than with perindopril alone. Consider these two agents
routinely if history of prevention CVA or TIA, whether HT or
normotensive.
23. SURGICAL OR ENDOVASCULAR MEASURES
• Carotid revascularization-
• 70-99% - surgery when perioperative morbidity and mortality risk <6%
• 50-69%- moderate benefit
• <50%- no surgery
• Closure of PFO and right to left shunt
• 18-60 yrs, cryptogenic stroke or TIA, NO uncontrolled DM, HT, or
specific indication for long term anticoagulation
24. CLINICAL PEARLS IN TIA MX
• a brief episode of neurological dysfunction caused by focal
brain or retinal ischemia.
• A substantial risk of stroke exists in the early period after TIA.
ABCD2 score is the recommended risk stratification tool for TIA.
• Early specialist assessment and modification of risk factors
(diabetes, AF, hypertension, hypercholesterolemia, and
smoking) reduces the risk of subsequent stroke.
• Aspirin should be started immediately unless there are
contraindications.
25. • Patients who have a TIA affecting the anterior circulation, and
who are potentially fit for surgery, should have carotid imaging
• Patients with crescendo TIA (two or more TIAs in a week) should
have specialist assessment within 24 hours of symptom onset.
• Patients who are discharged from the ED should be advised that
they cannot drive for at least one month. They may resume
driving after this period if clinical recovery is satisfactory.
29. • In a young patient, consider:
• Vasculitis
• Thrombophilia
• SAH
• Venous-sinus thrombosis or
• Carotid artery dissection (e.g. via near-
strangling or fibromuscular dysplasia).
30. 1ST HOUR
• Activate stroke code system
• Vital signs
• Supplemental oxygen to maintain spO2 >94%
• Determine LKW & NIHSS
• CT
• Medication list
• IV access and blood for IX- CBS, CBC with platelets, PT/INR,
APTT, ECG
31. LKW<3 H: IV THROMBOLYSIS
• If a patient is deemed a candidate for thrombolysis and there is
no reason to suspect abnormal laboratory test results,
thrombolytics should be administered without waiting for these
laboratory test values to prevent further delay.
• If the patient’s coagulation and platelet count results are
abnormal (INR>1.7 or PT is abnormally elevated, platelet count
<100,000 mm3 ), then thrombolytics should be discontinued.
32.
33. • One relative contraindication is “clearing neurological deficit.” If
a patient has plateaued or still has significant stroke symptoms
without contraindication, treatment with thrombolysis should
proceed as it would otherwise.
• Also, some patients will present with stuttering symptoms. If
symptoms completely resolve, clinicians should reset the clock
to start a new thrombolysis candidacy window; if there are still
symptoms—however mild—the time of onset remains
unchanged. Patients with stuttering symptoms tend to be at
high risk for extending their vascular occlusions.
34. IV ALTEPLASE
• 2 peripheral IV lines
• Calculate actual body weight
• 0.9 mg/kg (max 90mg)
• 10% given in bolus over 1st minute
• Rest given over 1 hour infusion
• Stop immediately if neurological deterioration
• Improves chance of recovery without significant disability at 90 days
from 26% to 39% if given with in 3 hrs
35. BP CONTROL
• If the patient is a potential thrombolysis candidate,
interventions to control BP should be initiated immediately.
• Target BP goal for patients eligible for IV tPA is
<185/110 mmHg, and once IV tPA is initiated, BP must be
maintained below 180/105 mmHg for 24 h after
administration of IV tPA to limit the risk of intracranial
hemorrhage.
36.
37. DURING THROMBOLYSIS
• BP and neurological assessment
• every 15 min for the first 2 h after starting alteplase,
• every 30 min for the next 6 h,
• hourly for the next 16 h .
• While the half-life of alteplase is approximately 5 min, and only
20% of the medication is still present and active at 10 min after
completion of the infusion, PT and activated partial
thromboplastin time (APTT) are prolonged and fibrinogen levels
are decreased for 24 h or more.
38. RISK OF ICH AFTER IV TPA
• 50% or greater mortality rate.
• This is often accompanied by a marked rise in blood pressure
(BP); however, a marked rise or fall in BP alone may signal an
ICH.
39. DETERIORATION DURING OR AFTER IV TPA
(24H)
• Stop alteplase infusion
• Obtain a non-contrast head CT scan STAT
• Obtain CBC, PT, PTT, INR, fibrinogen level, type and cross-match
• Vital signs every 15 min (neurological assessment for signs of increased
intracranial pressure).
• Assess GCS/pupil response.
• Treat BP and use noninvasive interventions to lower intracranial pressure (ICP) (raise the head
of bed, neck midline)
• Supportive therapy, including management of BP, ICP, cerebral perfusion pressure
(CPP), temperature, and glucose should be performed.
40. • Cryoprecipitate (contains fibrinogen): 10 units infused over 10–
30 min; administer additional dose for fibrinogen level <150 mg/dl.
• fibrinogen concentrate has been used to replenish the fibrinogen levels. The
initial dose is 2 gm of IV fibrinogen followed by further dosing based on
fibrinogen levels.
• prothrombin complex concentrate (25– 50 U/kg) and fresh frozen plasma (12
ml/kg) may be as an adjunctive therapy to normalize the INR.
• Antifibrinolytics
• Tranexamic acid 1000 mg (10–15 mg/kg) IV or ε-aminocaproic acid 4–5 g IV
over 1 h, followed by 1 g IV until bleeding is controlled.
• One bag of single donor platelets or 6–8 bags of random donor
platelets may also be transfused.
• Consult neurosurgery.
• For small, asymptomatic, hemorrhagic conversion, conservative
medical management may be considered after weighing the risks and
benefits of reversal agents.
41. INTRA ARTERIAL
THROMBECTOMY
• If the patient has an LVO—e.g., proximal (M1)
MCA, intracranial internal carotid artery (ICA),
basilar or vertebral artery—or suspected LVO
and the patient is within 6 h of LKW time,
mechanical thrombectomy treatment should
be considered. If the patient is a candidate
for IV thrombolytics, it should be
administered expeditiously, regardless of
endovascular procedure candidacy.
42.
43. ENDOVASCULAR TREATMENT (LKW 6-
24 HRS)
• Based on the results of the DAWN and DEFUSE 3 trials, it is
recommended that in patients presenting with an AIS within 6–
24 h of LKW time who have an LVO in the anterior circulation,
obtaining a CTP, DWI— MRI+MRI perfusion is recommended to
aid in selection of patients for mechanical thrombectomy who
meet the eligibility criteria.
44. ADMISSION/ TRANSFER
• Keep glucose 140–180 mg/dL; Hyperglycemia is associated
with worsen outcomes and increased risk of ICH following AIS.
• Administer IV fluids, preferably isotonic saline, at 1.5 ml/kg/h
initially, with a goal of euvolemic.
• Continue bedside cardiac monitoring principally to detect
paroxysmal atrial fibrillation and should continue for at least 72
h after admission.
45. • Treat fever sources with appropriate antibiotics or therapies
while preventing fever with antipyretics.
• If thrombolytic was administered, avoid indwelling urinary
catheter, nasogastric tubes, and IA catheters for 4 h, and do
not give anticoagulant/antiplatelet therapy for 24 h. Urinary
catheters should in general be avoided unless absolutely
needed.
• While elevation of the head of bed is recommended for
decreasing the risk of aspiration pneumonia, it was not found to
make any difference in disability outcome of the stroke injury.
• Patients should be nil per oral (NPO) until evaluated for
swallowing difficulties by a speech therapist
• Early mobilization and active rehabilitation
46. CLINICAL PEARLS IN AIS MX
• LKW in wake-up stroke is time patient went to bed.
• In cases of stuttering symptoms, the clock is reset only if patient is 100%
back to baseline.
• With patients on direct oral anticoagulation, determine the last time the
patient took their medication.
• Low NIHSS is not a contraindication to thrombolysis.
• Observing patients after thrombolysis for response is not required prior
to mechanical thrombectomy.
• Consider short-term dual antiplatelet therapy in patients with TIA and
ischemic stroke.
49. ETIOLOGY
• Hemorrhagic stroke generally occurs in small arteries or
arterioles
• Chronic hypertension (~60% of cases)- basal ganglia, pons, thalamus,
cerebellum
• Cerebral amyloid angiopathy (CAA)- lobar distribution
• Coagulopathy (warfarin, antiplatelet meds)
• Vascular anomalies (AVM, cavernous malformation) Sympathomimetic drugs
(cocaine, methamphetamine)
• infarcts into which secondary hemorrhage has occurred
• Central nervous system bleeds (hypertension, head injury,
aneurysm rupture).
50.
51. ICH- THE GOLDEN HOUR
• Airway compromise
• Herniation and brain(stem) compression
• Hematoma expansion
• Elevated intracranial pressure
• Secondary brain injury
• Seizures
• Fever
• Hyperglycemia
52. 1ST HOUR
• History – medical hx, medications, social HX
• FBC with platelet count, PT, INR, APTT
• NCCT Brain- hematoma size, location, IVH
• GCS
• Calculate ICH Score
53. ICH SCORE
• Each point increase in the ICH
score is associated with an
increased risk of mortality and a
decreased likelihood of good
functional outcome.
• It should not be used for
prognosis; use it as a method for
communicating disease severity
55. COAGULOPATHY REVERSAL
MEDICATION REVERSAL
UFH Protamine
antiplatelets Consider DDAVP (0.4 mcg/kg) single IV dose
• Platelets NOT recommend unless undergoing
neurosurgical procedure
Factor Xa
inhibitors
• Rivaroxaban
• Apixaban
• LMWH
Andexanet alfa
• Consider activated charcoal (50 gm) if last oral dose
was within 2h
• PCC or FEIBA if Andexanet alfa not available
• Protamine for LMWH given < 8 hrs for partial reversal
Direct
Thrombin
Inhibitors
Idarucizumab
Activated charcoal (50 gm) if last oral dose was within 2h
PCC or FEIBA if Idarucizumab not available
56. SURGERY
location Surgery urgently
Cerebellar ICH • Declining neuro exam
• Size > 3cm
• Compressive effects brainstem
• Hydrocephalus
Supratentorial
ICH
• ICH causing mass effects/ herniation in
severely affected but salvageable patient
and as a life saving measure
• Still defining role of minimally invasive
aspiration techniques
58. CLINICAL PEARLS IN ICH MX
• Hematoma expansion occurs within first 6-12 hours in up to 40% of
patients.
• Spot sign on contrast CT and BAT score on noncontract CT can help
identify patients at risk for hematoma expansion.
• Admission to a NCCU is associated with improved ICH outcomes.
• Lower SBP to 140-180 mmHg with the specific target determined by
patient- related factors.
• Urgent coagulopathy reversal is important to minimize hematoma
expansion.
59. • Current recommendations do not endorse routine seizure
prophylaxis.
• Use short course in patients with lobar ICH and those undergoing
surgical hematoma evacuation
• ERICH study- Levetiracetam used as prophylaxis was not associated with
poor outcome at 3 months
• If level of consciousness is out of proportion to imaging,
consider subclinical seizures.
64. CLINICAL SIGNS AND SYMPTOMS
EARLY LATE
Headache Changes in level of consciousness or reduction
in GCS or FOUR score >2 points
Irritability, Seizure Ipsilateral change in pupillary size, shape and
light responsiveness
Vomiting Contralesionally hemiparesis (new or
worsening)
Photophobia,
nystagmus,
diplopia
Contralesionally change in pupillary size and
ipsilesional hemiparesis (Kernohan’s
phenomenon)
Lethargy Cushing's triad
66. ICP WAVEFORM
• ICP waveform
• P1 - (Percussion wave) thought to reflect arterial pulsation
• P2 - (Tidal wave) thought to reflect degree of intracranial compliance
• P3 - (Dichrotic wave) thought to reflect aortic valve closure
• ICP wave form analysis
• When P2 > P1, suggests that brain has poor compliance / at risk for impending
herniation
67.
68.
69. HYPEROSMOLAR THERAPY
• Mannitol IV 0.5-1 g/kg bolus through peripheral IV line over 5-
15 min repeated every 4-6 hrs
• Decide on repeat dosing with osmolar gap
• No therapeutic benefit if osmolar gap >20 mOsm/kg
• HTS 2-23.4%
• >7.5% in central line
• Serum Na every 4-6 hrs
• Na target <160 mEq/L
70. SEDATION AND ANALGESIA
• Propofol reduce CMRO2 and cerebral blood volume
• Bolus 1-2 mg/kg or infusion
• PENTOBARBITAL (bolus 5-15 mg/kg over 30 min- 2h,
maintenance infusion of 1-4 mg/kg/hr)
71. SURGICAL DECOMPRESSION
• For those failing medical management:
• Review decompressive surgical options with neurosurgery
• Evacuation of mass lesion
• decompression craniectomy
• Placing an EVD