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Emergency Treatment of Stroke
Normal Brain Physiology 2-3% of body weight 15% of cardiac output 20% of all O2 25% of all glucose
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
Cerebral infarct <3hrs Onset Infarct Ischaemic penumbra
Cerebral infarct 6hrs Infarct Ischaemic penumbra
Cerebral infarct 24hrs Infarct Ischaemic penumbra
NA, Dopamine Ca2+ i   Ischaemic Brain Injury Ischaemia - 02     glucose   Anoxic depolarisation    lactate Glutamate Hi   Free Fe2+  Free radicals Lipolysis   NO synthase  Proteolysis
Cerebral Arterial territory Anterior cerebral Middle cerebral Posterior cerebral Anterior choroidal
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Partial Ant. Cir. Syndrome (PACS)
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Total Ant. Cir. Syndrome
Lacunar syndromes (LACS) ,[object Object],[object Object],[object Object],[object Object],[object Object]
Lacunar Infarct Types ,[object Object],[object Object],[object Object],[object Object],[object Object]
Posterior Cir. syndrome (POC)   ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
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%
Pre Hospital Care ,[object Object],[object Object],[object Object]
ED immediate care of Stroke ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Emergency tests ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Stroke Emergency Imaging ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
MRA & MRI in Stroke
When TIA is an emergency? ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Carotid endarterectomy in TIA’s ,[object Object],[object Object]
“ Patients who have improved neurologically but have a persistent neurologic deficit when seen, should be managed as a recent stroke ”
Aspirin in Acute Stroke ,[object Object]
Anticoagulant in Acute Stroke ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
rTPA Inclusion criteria ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
rTPA exclusion criteria ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
rTPA exclusion criteria ,[object Object],[object Object],[object Object]
rTPA exclusion criteria ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
rTPA Protocol ,[object Object],[object Object],[object Object],[object Object],[object Object]
IV  rTPA for Acute Ischaemic Stroke ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
BP Control during thrombolysis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
BP Control during thrombolysis ,[object Object],[object Object],[object Object],[object Object],[object Object]
Emergency CE in acute Stroke ,[object Object],[object Object],[object Object]
“ Role of Neuro-protection in Stroke is not clear and not recommended routinely”
Subarachnoid hemorrhage ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Primary Intracerebral hemorrhage ,[object Object],[object Object],[object Object],[object Object],[object Object]
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Stroke emergency treatment

  • 2. Normal Brain Physiology 2-3% 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 <3hrs Onset Infarct Ischaemic penumbra
  • 5. Cerebral infarct 6hrs Infarct Ischaemic penumbra
  • 6. Cerebral infarct 24hrs Infarct 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 territory Anterior cerebral Middle cerebral Posterior cerebral Anterior choroidal
  • 9.
  • 10.
  • 11.
  • 12.
  • 13.
  • 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.
  • 16.
  • 17.
  • 18.
  • 19. MRA & MRI in Stroke
  • 20.
  • 21.
  • 22. “ Patients who have improved neurologically but have a persistent neurologic deficit when seen, should be managed as a recent stroke ”
  • 23.
  • 24.
  • 25.
  • 26.
  • 27.
  • 28.
  • 29.
  • 30.
  • 31.
  • 32.
  • 33.
  • 34. “ Role of Neuro-protection in Stroke is not clear and not recommended routinely”
  • 35.
  • 36.

Notas del editor

  1. 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
  2. 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.
  3. 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 (&gt;130 mm Hg mean blood pressure or &gt;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).
  4. 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.
  5. CT Brain Fast ICH &gt;1cm can be detected SAH in 95% can be detected Early CT changes of infarction &lt;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.
  6. 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
  7. 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.
  8. 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.
  9. 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.
  10. 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
  11. 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 (&lt;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.