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Stroke emergency treatment
Emergency treatment of stroke involves several steps: 1. Rapid diagnosis through imaging such as CT or MRI to determine if the stroke is ischemic or hemorrhagic. 2. For ischemic strokes within 3 hours, treatment with rTPA (recombinant tissue plasminogen activator) can dissolve clots and reduce long-term disability if eligibility criteria are met. 3. Intensive monitoring is required after rTPA to control blood pressure and watch for bleeding complications. 4. Surgery may be considered for large hemorrhagic strokes or subarachnoid hemorrhage from aneurysms to relieve pressure on the brain.
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Stroke emergency treatment
- 1. Emergency Treatment ofStroke
- 2. Normal Brain Physiology2-3% of body weight 15% of cardiac output 20% of all O2 25% of all glucose
- 3. Cerebral Ischaemia -Threshold Normal flow, normal function Synaptic transmission failure Membrane pump failure 20 50 10 0 Time in hours CBF (ml/100g brain) Low flow, raised O2 extraction, normal function 1 2 3 4 5
- 4. Cerebral infarct <3hrsOnset Infarct Ischaemic penumbra
- 5. Cerebral infarct 6hrsInfarct Ischaemic penumbra
- 6. Cerebral infarct 24hrsInfarct Ischaemic penumbra
- 7. NA, Dopamine Ca2+i Ischaemic Brain Injury Ischaemia - 02 glucose Anoxic depolarisation lactate Glutamate Hi Free Fe2+ Free radicals Lipolysis NO synthase Proteolysis
- 8. Cerebral Arterial territoryAnterior cerebral Middle cerebral Posterior cerebral Anterior choroidal
- 9. ANY ONE OFTHESE:- Two out of three as TACI Higher Dysfunction Dysphasia Visuospatial Homonymous Hemianopia Motor / Sensory Deficit >2/3 Face / Arm / Leg Higher Dysfunction Alone Limited Motor / Sensory Deficit Partial Ant. Cir. Syndrome (PACS)
- 10. ALL OF THESE:- Higher Dysfunction Dysphasia Visuospatial Homonymous Hemianopia Motor / Sensory Deficit >2/3 Face / Arm / Leg Total Ant. Cir. Syndrome
- 11. Lacunar syndromes (LACS)ANY ONE OF THESE:- Pure Motor Stroke (>2/3 Face/Arm/Leg) Pure Sensory Stroke (>2/3 Face/Arm/Leg) Sensorimotor Stroke (>2/3 Face/Arm/Leg) Ataxic Hemiparesis
- 12. Lacunar Infarct TypesMUST HAVE NONE OF THESE:- New Dysphasia New Visuospatial Problem Proprioceptive Sensory Loss only No Vertebrobasilar features
- 13. Posterior Cir. syndrome(POC) ANY OF THESE FEATURES Cranial Nerve Palsy AND Contralateral Motor/Sensory Deficit Bilateral Motor OR Sensory Deficit Conjugate Eye Movement problems Cerebellar Dysfunction WITHOUT Ipsilateral Long Tract Signs Isolated Homonymous Hemianopia
- 14. Stroke types Al 35-44 yr Infarct 80% 42% Athero-thrombo-embolism 50% Intracranial small vessel 25% Cardioembolic 20% Rare 5% PICH 10% 10% SAH 5% 38% Unknown 5% 10% 75%
- 15. Pre Hospital Care1. Early recognition of Stroke warning signal by patient 2. Call ED if a person has symptoms of acute stroke. 3. Emergency transport and care
- 16. ED immediate careof Stroke 1. Check Vitals, general assessment 2. Stabilize: Respiration, circulation 3. Control Seizure 4. Reduce intracranial tension 5. Maintain blood sugar 6. Maintain temperature
- 17. Emergency tests Completeblood count, PCV, TRBC, platelet, smear for MP, Blood sugar, blood urea, serum creatinine, serum electrolyte, Blood gas, SGOT, SGPT, PT, PTT HIV, Hepatitis profile ECG / X-ray / CBC /
- 18. Stroke Emergency ImagingCT / CTA MRI / MRA/ / PI/ DI Echocardiography Carotid doppler, Transcranial doppler Cerebral Angiography SPECT
- 19. MRA & MRIin Stroke
- 20. When TIA isan emergency? High risk TIA,S 1. A high grade vascular stenosis 2. An antiplatelet failure 3. A cardioembolic 4. Crescendo TIA. Heparin-> warfarin if a long term anticoagulation is required Aspirin if anticoagulant contraindicated
- 21. Carotid endarterectomy inTIA’s High grade ipsilateral carotid stenosis with TIA has high risk (30%) of stroke within first week CE reduces mortality in such cases
- 22. “ Patients whohave improved neurologically but have a persistent neurologic deficit when seen, should be managed as a recent stroke ”
- 23. Aspirin in AcuteStroke “ In acute stroke aspirin is the only proven antiplatelet agent. It should be commenced as soon as the diagnosis of cerebral infarction has been made, using a starting dose of 150-300mg a day and continuing until decisions have been made about secondary prevention”
- 24. Anticoagulant in AcuteStroke Not shown to prevent progression LMH long term improved Hemorrhagic transformation is high Cardioembolic infarct Immediate for small infarct Delayed for large infarct Heparin - 1000 units/hr. PTT 1.5 Heparinoid - 2500 to 3200 units SC BD
- 25. rTPA Inclusion criteriaClinical evidence for an ischemic stroke Age >18 years Signed consent, if possible Onset of stroke within 3 hours of initiation of therapy* Normal PT and PTT If a patient has stroke on awakening from sleep or if the onset of symptoms is not known, then stroke onset is determined from time patient was last seen as "normal" (eg, when he or she went to bed).
- 26. rTPA exclusion criteriaHistorical Stroke or serious head trauma in past 3 months Major surgery or invasive procedure within past 14 days GI or urinary bleeding within past 21 days Puncture of noncompressible artery or biopsy of internal organ within past 7 days Ongoing alcohol or drug abuse Seizure preceding or during stroke
- 27. rTPA exclusion criteriaHistory of intracranial hemorrhage (including subarachnoid bleeds) or known history of cerebral vascular malformations (including aneurysms or arteriovenous malformations) Pericarditis, endocarditis, septic emboli, recent pregnancy, or active inflammatory bowel disease
- 28. rTPA exclusion criteriaClinical, radiologic, or laboratory SBP >185 mm Hg or DBP >110 mm Hg after repeated measurements Rapidly improving or minor symptoms Coma or stupor CT of brain indicative of tumor, blood, or early signs of cerebral edema Elevated PT and/or PTT Serum glucose <50 mg/dl or >400 mg/dL Platelet count <100,000/mm 3
- 29. rTPA Protocol Obtainand review stat CT scan of the brain. Establish peripheral IV access (two separate sites). Obtain CBC, chemistry panel, PT & PTT, type and screen, and urinalysis. Review inclusion and exclusion criteria Determine patient's weight.
- 30. IV rTPAfor Acute Ischaemic Stroke Administer TPA, 0.9 mg/kg (maximum, 90 mg) as a 10% bolus over 1 to 2 minutes, followed by the remaining 90% as a 1-hour infusion Monitor for bleeding and neurologic deterioration. Admit to ICU for 24 hours. Monitor BP Do not give antiplatelet or anticoagulant therapies for 24 hours. Do not perform arterial punctures, invasive procedures, or IM injections for 24 hours. Obtain CT scan of brain 24 hours postinfusion or sooner if neurologic deterioration occurs .
- 31. BP Control duringthrombolysis Monitor BP every 15 minutes for 2 hours after start of infusion Then every 30 minutes for 6 hours Then every hour, from the 8th hour until 24 hours after the start of TPA Then per routine If after two readings 5-10 minutes apart: SBP = 180-230 mm Hg or DBP = 105-120 mm Hg Give labetalol 10 mg IV over 1-2 minutes. May repeat or double the dose every 10 minutes, up to maximum of 150 mg or iv infusion.
- 32. BP Control duringthrombolysis SBP >230 mm Hg or DBP = 121-140 mm Hg Give labetalol 10-20 mg IV over 1-2 minutes. May repeat or double the dose every 10 minutes, up to maximum of 150 mg or infusion. . If response is inadequate, start sodium nitroprusside DBP >140 mm Hg Give sodium nitroprusside 0.5-10 µg/kg/minute
- 33. Emergency CE inacute Stroke 1. Stroke in evolution with a minimal fixed neurologic deficit, 2. A moderately severe neurologic deficit of abrupt onset when the surgery can be completed within the first 3 hours after the onset of deficit, and 3. CT scan without evidence of hemorrhagic transformation of an infarct or edema.
- 34. “ Role ofNeuro-protection in Stroke is not clear and not recommended routinely”
- 35. Subarachnoid hemorrhage Bedrest Analgesic Blood pressure control Oral nimodipine 60mg q6hx21 days Angiography for localization of bleeding If aneurysm Immediate surgical clipping for Grade 1-3 patient without contraindication Grade 4-5 with intracerebral clot and deterioration
- 36. Primary Intracerebral hemorrhageSmall (<3cm) hematoma has good prognosis Large hematoma (>6cm) in comatose patient have poor prognosis. Surgical evacuation for 3-6cm superficial lobar hematoma in a conscious patient Cerebellar hematoma with deteriorating level of consciousness Control of BP
- 37.
Editor's Notes
- #2 With control of Hypertension, diabetes, Cardiac disease, lipid control Stopping smoking and alcohol, use of anti-platelet agents and endarterectomy over last 25 year there is fall of stroke incidence to reach a plateau Further fall in the incidence is only possible through acute stroke treatment
- #16 Warning signal of stroke Sudden weakness or numbness of the face, arm, or leg on one side of the body. Sudden dimness or loss of vision, particularly in one eye. Sudden difficulty speaking or trouble understanding speech Sudden severe headache with no known cause. Unexplained dizziness, unsteadiness or sudden falls, especially with any of the other signs. Double vision, drowsiness, and nausea or vomiting. Presentation of acute stroke Alteration in consciousness Stupor or coma Confusion or agitation Seizures Aphasia or other higher cognitive disturbances Dysarthria Facial weakness or asymmetry (ipsilateral or contralateral to limb weakness) Incoordination, weakness, paralysis, or Sensory loss of one or more limbs (usually one half of the body) Ataxia, poor balance, or clumsiness or difficulty walking Visual loss Monocular or binocular May be partial loss of the field Vertigo, double vision, unilateral hearing loss, Nausea, vomiting, headache, photophobia, or phonophobia Recommendations There is general agreement that separate educational programs tailored to the public, EMS personnel, and physicians should be developed. There is general agreement that an observer should dial 911 if a person has symptoms of acute stroke. There is general agreement that EMS personnel should be trained in the early recognition and emergent care of stroke. There is general agreement that EMS transport of patients with acute stroke to a medical center should be expedited and should be the highest priority. Early admission of most patients to a unit that has a specialized interest in the treatment of stroke is strongly recommended (Level of Evidence I, Grade A Recommendation). A team of physicians, nurses, and technicians that is devoted to the early care of patients with stroke should be assembled. Rapid transfer of a patient to a hospital that has a specialized stroke care unit is strongly recommended.
- #17 Recommendations There is general agreement to recommend airway support and ventilatory assistance in the care of patients with acute stroke who have depressed levels of consciousness (Levels of Evidence III through V, Grade C). There is general agreement to recommend supplemental oxygen to hypoxic patients (Levels of Evidence III through V, Grade C). There are insufficient data about the efficacy of hyperbaric oxygen to recommend this therapy for most patients with stroke. There is general agreement that most patients with acute ischemic stroke do not need treatment with parenteral antihypertensive drugs (Level of Evidence II, Grade B). Oral antihypertensive drugs are preferred. Cautious use of antihypertensive agents is recommended for patients with markedly elevated blood pressure (>130 mm Hg mean blood pressure or >220 mm Hg systolic blood pressure) (Levels of Evidence III through V, Grade C). There is general agreement to recommend treatment of the sources of fever and use of antipyretics to control an elevated body temperature (Levels of Evidence III through V, Grade C). There are insufficient clinical data about the use of hypothermia to recommend this therapy. There is general agreement to recommend control of hypoglycemia or hyperglycemia after stroke (Levels of Evidence III through V, Grade C).
- #18 CT of the brain without contrast Electrocardiogram Chest x-ray Lateral cervical spine x-ray (if the patient is comatose or has cervical spine pain or tenderness) Hematologic studies Complete blood count Platelet count Prothrombin time Partial thromboplastin time Serum electrolytes Blood glucose Arterial blood gas levels (if hypoxia is suspected) Renal and hepatic chemical analyses Lumbar puncture (if subarachnoid hemorrhage is suspected and CT is negative) Electroencephalogram (if seizures are suspected) There is general agreement to strongly recommend that emergent CT be the initial brain imaging study. There is general agreement to strongly recommend that electrocardiography, chest x-ray, and cardiac monitoring be components of the emergent evaluation of patients with suspected ischemic stroke. There is general agreement to recommend the other diagnostic studies listed in Table 5 on an emergency basis. Diagnostic studies aimed at establishing a likely etiology of acute ischemic stroke, including ultrasound or other imaging of intracranial or extracranial vessels, can, in some circumstances, be helpful in making decisions about treatment. However, there is general agreement that these tests should not delay treatment, and their use should be tailored to specific clinical situations.
- #19 CT Brain Fast ICH >1cm can be detected SAH in 95% can be detected Early CT changes of infarction <3hrs Increased density in an intracranial artery suggestive of sluggish CBF as a result of an acute occlusion Hypodensity in the region of the suspected ischemia, Blurring of cortical gray and white matter differentiation, Loss of definition of gray and white matter in the basal ganglia. A large infarction produces edema more quickly, causing a localized mass effect ventricular distortion with midline shift and compression, Decreased size of adjacent cortical sulci and subarachnoid cisterns.
- #24 19,345 acute ischaemic stroke 300 mg aspirin, 5,000 or 10,000 heparin bd. High heparin more dead/stroke day 14 160 - 300 mg aspirin within 48 hr. :- avoid 10 deaths/non fatal stroke per 1,000 Rx 2 wks 13 fewer dead/dependent per 1,000 Rx first 6 months 7 fewer recurrent ischaemic or unknown CVA 2 wks
- #31 Guidelines for the Use of Intravenous TPA in Acute Ischemic Stroke Results from randomised controlled trials and statistical reviews support, under specified conditions, the therapeutic use of intravenous TPA (0.9 mg/kg, max 90 mg) with 10% of the dose given as a bolus followed by an infusion lasting 60 minutes within 3 hours of onset of an ischaemic stroke . Treatment within a time limit of 6 hours may be beneficial for long term outcome after ischaemic stroke. The available documentation in support for use within the six hour interval is less than for treatment of patients within a three hour time limit (grade B evidence). Treatment is not recommended if early changes of a recent cerebral infarction involve more than one third of the vascular territory. This treatment is not recommended unless given within a strict quality control protocol demonstrating a low complication rate in centers with expertise in neurological and neuroradiological evaluation and general management of stroke patients. The organisational implications of this need clarification before general treatment recommendations are given. Intravenous tPA is not recommended when the time of onset of stroke cannot be ascertained reliably, including stroke recognised upon awakening. Patients should be excluded from treatment according to the criteria used in the large randomised trials of tPA in acute stroke. Further trials of the use of tPA in acute ischaemic stroke are warranted, in particular for documentation of treatment effect beyond three hours after onset of stroke and for new compounds. Patients should give informed consent, but may require that treatment with active tPA will be considered with regard to inclusion- and exclusion criteria.
- #34 Urgent carotid endarterectomy for recent ischemic stroke is generally limited to conscious patients with: 1) stroke in evolution with a minimal fixed neurologic deficit, 2) a moderately severe neurologic deficit of abrupt onset when the surgery can be completed within the first 3 hours after the onset of deficit, and 3) CCT without evidence of hemorrhagic transformation of an infarct or edema. This usually means patients are only considered for surgery when the deficit occurs while the patient is in a hospital where expert facilities are available for rapid diagnosis and treatment. However, there is no firm data to mandate this approach.
- #35 Neuroprotective treatment of acute stroke There is a growing body of evidence about early neuroprotective drug treatment in experimental focal brain ischaemia. Accordingly, many different principles of treatment might be expected to work in a clinical situation. In animal models, different pathophysiological components in the complicated cascade of changes in the brain after the ictus can be pharmacologically counteracted, separately and under carefully controlled conditions. This have given rise to an optimism in acute neuroprotective treatment in stroke patients. However, a series of large randomised studies have failed to show any significant effects of the drugs tested so far. Heterogeneity in stroke populations, combined illnesses in elderly individuals, narrow time windows and blunt methods of treatment effects could be possible reasons for discrepancies between experimental situations n animals and in stroke patients. The three studies discussed at this meeting concerning lubeluzole, clomethiazole and piracetam did not show significantly favourable treatment effects with respect to the chosen primary outcome variables. For clomethiazole, post hoc analysis showed that there may be an effect on large supratentorial infarctions and for piracetam post hoc subgroup analysis indicated a possible effect for treatment within 7 hours, particularly for large infarctions. This has motivated further studies targeted to elucidate the role for these drugs in future acute stroke treatment. Early inflammatory mechanisms including cytokine effects on blood-brain barrier, on cellular functions and on apoptosis comprise a field of intense scientific interest. However, for the moment no recommendation can be given except for competent early care in a stroke unit. In conclusion, no neuroprotective drug can be recommended at present for use in routine acute stroke care.
- #36 Surgical Treatment. The CCT scan is used to diagnose SAH since it confirms approximately 95% of all such hemorrhages.12 and is useful in detecting increased intracerebral density in large arteriovenous malformations. When the diagnosis of SAH is highly suspected and the CT scan is normal a lumbar puncture to detect blood in the cerebrospinal fluid is necessary. Patients with SAH should be transferred to a hospital where skilled neurosurgical care is immediately available, preferably admitted to a neuro-intensive care unit. There are no data to indicate that such a transfer is dangerous for patients with a recent SAH. Management also requires angiographic localization of the aneurysm or aneurysms causing the bleed and the clinical grading of the patient (Table 6).45 It is current practice to consider early (preferably within 24 hours of admission) surgery in all patients in good neurologic condition (Hunt and Hess grades 1, 2, and 3) if the aneurysm is surgically accessible and there are no medical complications that would prevent safe surgical treatment. No definitive data at the present time mandates this approach although much anecdotal evidence indicating its value has accumulated.6 At the present time there are no clear guidelines as to the timing of surgery for patients with Hunt and Hess grades 4 and 5. Patients in these grades who have acute hydrocephalus should have emergency ventriculostomy. In grades 4 and 5 patients with an intracerebral hematoma, surgical evacuation of the clot and emergency clipping of the aneurysm may be life-saving. These patients are at greater risk of having a poor outcome following any surgical procedure to treat the bleeding source. Surgery should be delayed for patients who have severe vasospasm with infarction
- #37 Surgical Treatment. Primary intracerebral hemorrhage carries extremely high morbidity and mortality rates, especially when the hemorrhage occurs in the basal ganglia or thalamus or there is a large lobar hemorrhage.49 Discussions about the efficacy of emergency surgical treatment have continued for several decades. Earlier studies showed there was no value in surgical clot removal over standard medical management).50 More recent studies of hematoma removal have shown promise for open surgical decompression but only if it is accomplished early after the onset of symptoms.51 Selection of patients is critical and reliable criteria need to be determined by further study.52 The hematoma size and level of consciousness are critical. Awake patients with small hematomas (<3 cm diameter) will usually recover without surgery while comatose patients with large hemorrhages (6 cm diameter) will usually do very poorly, regardless of management. The best candidates for surgery may be patients with moderate to large hematomas who are still awake. At the present time there is no definitive proof of the value of early evacuation of deep intracranial hematomas. Patients with ICH need careful blood pressure control to prevent rehemorrhage. Elevations in systemic arterial blood pressure should not be treated urgently unless 1) the systolic pressure exceeds 200 mm Hg or the diastolic pressure exceeds 110 mm Hg on repeated measurements over 30 to 60 minutes or 2) unless cardiac failure/ischemia or arterial dissection have been identified. Blood pressures 200/110 mm Hg are reduced to near normotensive levels if the patient is known not to be hypertensive. For patients known to be hypertensive, blood pressure levels are reduced cautiously to lower levels near to the prehemorrhage levels, so as not to interfere with cerebral perfusion. In stuporous or comatose patients it is important to maintain normal cerebral perfusion pressure, which could be compromised by aggressively lowering systemic arterial pressure. In these patients monitoring the intracranial pressure is an important tool to maintain good cerebral perfusion pressure.