![[NCCT]
{NCCT}
C](https://image.slidesharecdn.com/stroketreatmentprotocol-230117191606-5d10ddee/85/Stroke-Treatment-Protocol-pptx-12-320.jpg)
![Management- ICH
1. Blood Pressure- <140 [sbp]
IV medications
• Labetalol
• Nicardipine
• Esmolol
• Enalapril
• Hydralazine
• Nitroglycerine](https://image.slidesharecdn.com/stroketreatmentprotocol-230117191606-5d10ddee/85/Stroke-Treatment-Protocol-pptx-29-320.jpg)
Stroke Treatment Protocol.pptx
- 1. Stroke Treatment Protocol Dr Magan Solanki Medicine unit H Unit head Dr Prabhat kanvaria sir
- 3. WHO DEFINITION OF STROKE A NEUROLOGICAL DEFICIT OF • Sudden onset • With focal rather than global dysfunction • In which, after adequate investigations, symptoms are presumed to be of non-traumatic vascular origin, and • lasts for >24 hours
- 4. Transient Ischemic Attack (TIA) An acute focal neurological deficit resulting from cerebrovascular disease • With resolution of signs and symptoms within 24 hours • No evidence of ischemia / infarction on imaging studies
- 6. Stroke Risk Factors: Non modifiable 1. AGE 2. Gender - male 3. Race – Blacks > Asians or Hispanics> Whites 4. Family History. 5. Coagulation Disorders 6. Cardiac Disease
- 7. Stroke Risk Factors: Modifiable 1. Hypertension 2. Diabetes mellitus 3. Hypercholesterolemia 4. Elevated LDL or Low HDL 5. Elevated homocystein 6. Smoking 7. Alcohol Abuse 8. Oral Contraceptive 9. Pregnancy 10. Obesity 11. Sleep apnea 12. Carotid stenosis
- 8. Common Types andIncidence: • Infarction: Incidence 80% - mortality 20% • 50% - Thrombotic – atherosclerosis • Large-vessel 30% (carotid, middle cerebral) • Small vessel 20% (lacunar stroke) • 30% Embolic (heart dis / atherosclerosis) • Young, rapid, extensive. • Hemorrhage: Incidence 20% - mortality 80% • Berry aneurysm, Microaneurysm, Atheroma • Intracerebral or subarachnoid.
- 10. Harrison 21th
- 11. EMERGENCY EVALUATION OF ACUTE ISCHEMIC STROKE Assess ABCs, vital signs Provide oxygen by nasal cannula wherever necessary Obtain IV access; obtain blood samples(CBC, ’lytes, coagulation studies) Obtain 12-lead ECG, check rhythm, place on monitor Check blood sugar; treat if indicated
- 12. [NCCT] {NCCT} C
- 14. MEDICAL MANAGEMENT Supportive treatment I.V. thrombolysis- alteplase , tenecteplase Anti thrombotic tretment Neuroprotection Stroke centers and Rehabilitation
- 16. Endovascular options Endovascular intervention a. I.A. thrombolysis b. Angioplasty and stenting c. Mechanical clot disruption d. Clot extraction (Mechanical thrombectomy) • Carotid end artrectomy
- 17. INTRAVENOUS THROMBOLYSIS IN AIS
- 19. Perform neurological examination Every 15 min during the infusion thereafter for the next 6 hrs then hourly until 24 hour aftr treatment If pt develop severe headache, acute HTN, nausea , vomiting, discontinue the process and obtain an emergency CT scan
- 20. INTRA ARTERIALTHROMBOLYSIS Major stroke >6hrs due to occlusion of MCA CEREBRAL angiography
- 21. Mechanical thrombectomy CRITERIA FOR MECHANICAL THROMBECTOMY 1. mRS (modified Rankin score) of 0-1 2. Large vessel Occlusion (LVO): Internal carotid artery or MCA segment 1 3. Age >18yr 4. NIHSS score > 6 5. ASPECT (Alberta Stroke Program Early CT) Score of >6 6. Treatment can be initiated (groin puncture) within 6 hours of symptom onset
- 24. Hemorrhagic stroke Types 1. Intracerebral Hemorrhage(15%) • Caused by bleeding within the brain tissue itself 2. Sub Arachnoid Hemorrhage(5%) • Caused by extravasation of blood into the subarachnoid space
- 25. Intracerebral Hemorrhage 1. An acute and spontaneous extravasation of blood in to the brain parenchyma that may extend into ventricles and subarachnoid space. 2. 10-15% of all cases of stroke. 3. Classification: • Primary ICH: Hemorrhage originate from spontaneous rupture of small arteries or arterioles damaged by chronic HTN or amyloid angiopathy. • Secondary ICH: Haemorrhage results from trauma, rupture of Aneurysm, vascular malformation, coagulopathy, haemorrhagic transformation of cerebral infarct, intracranial neoplasm, venous angioma, dural sinus thrombosis
- 26. Clinical features- ICH 1. Onset of a sudden focal neurological deficit while the patient is active, which progresses over minutes to hours, as Weakness or paresis, Facial droop , blindness, Dysarthria ;Seizure 2. Headache is more common in ICH 3. Vomiting 4. Increased systolic BP and impaired level of consciousness
- 27. Diagnosis- ICH
- 28. Prognosis- ICH
- 29. Management- ICH 1. Blood Pressure- <140 [sbp] IV medications • Labetalol • Nicardipine • Esmolol • Enalapril • Hydralazine • Nitroglycerine
- 30. 2. Intracranial Pressure: • Place ICP monitor or EVD drain in patients with GCS < 8. • GOAL: Maintain ICP < 20mmHg • Minimal Cerebral Perfusion Pressure > 60mmHg 3. Haemostatic therapy: Eptacog alpha (Recombinant fac VII) 4. Anticonvulsant therapy: • Lorazepam, Phenytoin, Fosphenytoin, valproic acid, phenobarbital 5. Fever control 6. Management of Hypergylcemia: • Insulin if Blood sugar > 185mg/dl 7. Nutrition 8. DVT prophylaxis
- 31. Surgical Management- ICH 1. Aims: • Decompression to reduce or prevent elevated ICP • Removal of acute haematoma to reduce mass effect • Minimise toxicity from blood breakdown products to surrounding brain 2. Options: • Ventriculostomy • Stereotactic aspiration of haematoma • Endoscopic haematoma evacuation • Craniotomy • Hemicraniectomy
- 32. SUBARACHNOID HAEMORRHAGE • Neurological emergency characterised by haemorrhage into the subarachnoid space. • One of the most important cause of sudden, acute severe headache. • 85 % of non traumatic cases are due to ruptured cerebral aneurysm • Incidence: F > M (3:2) • Risk higher in blacks than in whites • Incidence increases with age and peaks at 50
- 33. Causes of SAH 1. Trauma: Most common cause 2. Vascular: • Ruptured intracranial aneurysm, AVM, Tumors with hemorrhage 3. Vasculopathy • Collagen vascular disease, Amyloid angiopathy, Arterial dissection 4. Haematological • Anticoagulant,leukemia, Hepatic or renal induced coagulopathy 5. Drugs : Cocaine, Amphetamine
- 34. Clinical Presentation of SAH 1. Prodormal events: • Symptoms:Headache, dizziness, orbital pain, diplopia, visual loss • Signs: Sensory or motor disturbance, seizure, ptosis, dysphasia 2. Focal neurological findings 3. CLASSIC presentation: • Sudden onset severe headache(Thunderclap headache) • Nausea/vomiting
- 35. Complications of hemorrhage Hydrocephalus Rebleeding Vasospasm Seizure Cardiac dysfunction
- 36. Management of SAH Medical management of SAH focuses on • Protecting the airway • Managing the BP • Preventing rebleeding prior to treatment • Managing vasospasm(Calcium channel antagonist Nimodipine) • Treating Hydrocephalus(EVD or permanent ventricular shunting) • Preventing Pulmonary embolus • Bed rest in quiet room and stool softner,if needed, to prevent straining. • If headache or neck pain is severe, Mild sedation and analgesia. • Adequate Hydration
- 37. Managing raised ICP For stupurous patient, Emergency Ventriculostomy to measure ICP . Medical therapies: Mild hyperventilation, Mannitol and sedation Maintain adequate cerebral perfusion pressure(60-70mmHg) while avoiding excessive elevation/fall of arterial pressure
- 38. Surgical mx of SAH 1. Clipping of the aneurysm 2. Coiling of the aneurysm