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  • KEY POINT: The penumbra surrounding damaged brain tissue may be salvaged with immediate treatment. <br /> The ischemic core (structural lesion) is the immediate area of brain tissue that is irreversibly damaged during stroke when deprived of circulating blood. <br /> The penumbra is an area of reduced blood flow that surrounds the ischemic core and is at great risk of suffering irreversible damage during ischemia. <br /> Tissue within the penumbra is still viable in early hours after stroke onset. <br /> Preclinical studies have shown that the core of irreversibly damaged tissue will expand to include the penumbra unless treatment to protect the brain is instituted within a few hours. <br /> Because the neural tissue within the penumbra remains viable for a short period of time after ischemic stroke, it serves as the target for neuroprotective agents. The key therapeutic strategy is to restore or improve perfusion to ischemic area. Thus, the neural tissue within the penumbra can be saved, if treatment begins quickly. <br /> Dirnagl U. Pathobiology of ischaemic stroke. An integrated view. Trends Neursci. 1999;22:391-97. <br />
  • ICH accounts for 10% to 15% of all strokes and is associated with the highest mortality and morbidity.1 The worldwide incidence of ICH ranges from 10 to 20 cases per 100,000 population.2 Between 35% and 52% of patients with ICH die within 1 month of symptom onset,3-5 and only 20% are functionally independent at 6 months.5 <br /> American Heart Association. Heart Disease and Stroke Statistics–2005 Update. <br /> Qureshi AI et al. N Engl J Med. 2001;344:1450-1460. <br /> Broderick JP et al. J Neurosurg. 1993;78:188-191. <br /> Anderson CS et al. J Neurol Neurosurg Psychiatry. 1994;57:936-940. <br /> Counsell C et al. Cerebrovasc Dis. 1995;5:26-34. <br />
  • As an example, a 15-mL change in the ICH (the difference in size between a ping pong ball and a golf ball) has a major impact on patient outcome. <br /> A patient with a hematoma the size of a ping pong ball has a greater chance of a better outcome than a patient with a hematoma the size of a golf ball. <br /> Hence, active intervention to stop the hematoma from growing in size could be very beneficial. <br />

STROKE STROKE Presentation Transcript

  • Critical Care in Cerebro-Vascular Disease.
  • What is Ischemic Stroke ? DEFn: - (WHO) Rapidly developing clinical signs of focal disturbance of cerebral function with symptoms lasting 24 hrs or longer or leading to death with no apparent cause other than vascular origin.
  • Stroke? “STROKE IS A BRAIN ATTACK” First 180 mins are very important Don’t lose time! Every SINGLE SECOND Counts
  • Acute Ischemic Stroke Destroys Millions of Neurons per Second  For every hour an acute ischemic stroke is untreated,the brain loses 120 million neurons,830 billion synapses,and 447 miles of myelinated fiber- the equivalent of 3 years of normal aging.  During normal aging,the brain loses about 31 million neurons per year.  Untreated,a typical large vessel ischemic stroke can age the brain 36 years,destroying 1.2 billion neurons,8 trillion synapses,and 4,470 miles of myelinated fibers.
  • Stroke Worldwide 15 million strokes occur, 5.5 million die.  In India 4 new cases/minute, 5500 cases/day, 2 million cases/year.  Therapy more effective in acute phase.  Stroke is “TIME” and “BRAIN ATTACK is like Heart Attack.
  • Stroke Care Unit (SCU)  Stroke care unit is the key to stroke treatment.  Lower morbidity & mortality of stroke.  Integrated nursing, physiotherapy and trained staff make best care  Create awareness regarding stroke in medical community & Public.
  • More than 30% die. Disability after Stroke
  • Stroke Awareness • How to diagnose “BRAIN ATTACK”. • Do Not make Home visit. • Quickly Transport Patient to a center which treats stroke—NOT nearby Hospital. • Crush or dissolve Aspirin & give it.Keep flat. • Give O2, control fever, check BSL & Rx. • Do not fool yourself & the pt-steroids, Glucose, Ca….. • Do not give sublingual Nifedipine.
  • TIA(Mini-Stroke) • A brief episode of neurological dysfunction caused by focal brain or retinal ischemia lasting (less than 1 hr.) without e/o brain infarction.
  • ABCD Score of TIA • A ( age; 1 point for age > 60 years) • B (blood pressure; 1 point for hypertension) • C (clinical features; 2 points for focal weakness, 1 for speech disturbance) • D ( symptom duration; 1 point for 1-10 min, 2 points for 11- 60 min.). Total scores ranged from 0 (lower risks) to 6 ( higher risks). 7 day risk of stroke 0% in those with score < 4, 35% in score of 6, and intermediate with scores of 4 or 5.
  • ICA Stenosis Angio & Doppler
  • Physiology of Brain ♣ 2 % of Body Wt. ♣ 15% Cardiac output ♣ 20% O2 Consumed ♣ 50-60mL/100g/ min ♣ 700 mL/min ♣ 150-169 μmol/100g/min-CMRO2 ♣ 25-30 μmol/100g/min- CMRG1u.
  • D. D. of Acute Ischemic Stroke (Stroke mimics) Cerebral Neoplasm Subdural hemotoma Epileptic seizure Traumatic brain injury Migraine Neuromuscular & Spinal cord lesions.
  • Diagnosis of Stroke for TPA patient Fastest Diagnosis and Evaluation. 1. 2. 3. 4. History : Time of onset, anticoagulation, trauma, recent surgery. Examination : ABC, Cardiac, NIHSS Scale C.T.Scan : Gold std. test MRI / MRA : Sensitive than CT for infarct. If 1 min. is lost, 4 million neurons are lost ! 120 min. after onset 16 hrs. after onset 16 hrs. after onset
  • Diagnosis Tests for Acute Stroke CT – Identification ischemic or hemorrhagic stroke. MRI – Locate & quantify area of infarction and penumbra ECG – Check MI, cardiac ischemia or arrythmia. Bl. Glucose – Check for hypoglycemia or hyperglycemia. Renal functions – Identify baseline renal function. CBC – Identify anemia, polycythemia. Platelet count – Identify thrombocytopenia. PT, aPTT – Baseline coagulation studies.
  • NIHS SCALE. Tested item Title Responses & Scores. 1[A] Level of consciousness 0-alert 1-drowsy 2-obtunded 3-coma/unresponsive 1[B] Orientation questions [ two] 0-answers both correctly. 1-answers one correctly. 2.answers neither correctly. 1[C] Response to commands [ two] 0-performs both tasks correctly 1-performs one task correctly. 2-performs neither. 2. Gaze 0-normal horizontal movements. 1-partial gaze palsy. 2-complete gaze palsy. 3. Visual fields 0-no visual field defect. 1-partial hemianopia. 2-complete hemianopia. 3-bilateral hemianopia. 4. Facial movement 0-normal. 1-minor facial weakness. 2-partial facial weakness. 3-complete unilateral palsy. 5. Motor function [arm] a] Left b] Right 0-no drift 1-drift before 5 seconds. 2-fall before 10 seconds. 3-no effort against gravity. 4-no movement.
  • NIHS SCALE Tested Item Title Responses & Scores. 6 Motor Function [ leg ] a.left b.right 0-no drift 1-drift before 5 seconds. 2-fall before 5 seconds. 3-no effort again gravity 4-no movement 7. Limb ataxia 0-no ataxia. 1-ataxia in one limb 2-ataxia in two limbs. 8. Sensory 0-no sensory loss 1-mild sensory loss. 2-severe sensory loss 9. Language 0-normal. 1-mild aphasia 2-severe aphasia 3-mute global aphasia. 10. Articulation 0-normal. 1-mild dysarthria. 2-severe dysarthria. 11. Extinction or inattention 0-absent 1-mild [ loss 1 sensory modality] 2-severe [ loss 2 modalities ] N
  • DWI-PWI …. Mismatch
  • Salvaging the Ischemic Penumbra Minutes Hours Time Days and weeks Dirnagl U. Trends Neursci. 1999;22:391-97
  • Treatment of Acute Ishaemic Stroke Most strokes are thromboembolic occlusions. Improvement of perfusion is the key. - In Ischemic penumbra, core of infarct is not salvageable. - Adjacent tissue can be saved with TPA. - - FDA [USA] approved IV TPA in 1996 in first 3 hrs. -
  • Actilyse [Alteplase] - TPA Thrombolytic Therapy and Dissolution of Clot Activates tPA Plasminogen (+) Glycoprotein  Activates plasminogen  (-) PAI-1 Plasmin α2 – antiplasmin ( - ) degrades thrombus Fibrin by Clot breaking fibrin. D- Polymers and D-dimers products Fibrin degradation to plasmin.  Dissolution of the fibrin clot after binding it  Metabolized by liver.  Half life is 4-5 min.  Package 50mg.
  • Randomized rTPA study of NINDS [1995] OTT 3h Dose & pts NINDS rt-PA Stroke No.of treatment group 291 0.9mg/kg rt-PA Study(part 1) placebo NINDS rt-PA Stroke 3h 333 Study (part 2 ) 0.9mg/kg rt-PA placebo NINDS rt-PA Stroke 3h 624 Study ( parts I & II 0.9mg/kg rt-PA placebo 3-mo death(%) NA 6 NA 0 NA 7 NA 17 21 Combined ) For 1000 pts treated within 3hrs, 140 are less dead or dependent 27%recovered >10 points at 24 Hrs. ICH% Minimal or no disability in 30% at 90 days. 1 6.4 0.6
  • Randomized trial rTPA Study OTT No.of Dose & 3-mo ICH% pts 6h 0.9mg/kg rt-PA 10.9 6.7 6.9 1.3 0.9mg/kg rt-PA 17.9 19.8 12.7 6.5 0.9mg/kg rt-PA 10.3 11.8 placebo ECASS II - 1998 6h 613 placebo ECASS I - 1995 death(%) placebo ATLANTIS part B - 1999 3-5h treatment group 10.5 3.1 620 800 TPA safe within 3 hours of OTT gives excellent results.
  • Thrombolytic Therapy - IV -t-PA I. Inclusion Criteria 1. Within 3 hours of the stroke and patient not needing ventilator. 2. CT Scan head Normal or < 1/3 MCA hypo density. II. Exclusion Criteria 1. 2. 3. 4. 5. 6. BP > 185/110 mm on admission. Use of Oral Anticoagulants. Major surgery preceding FOURTEEN days. Head injury - LAST THREE MONTHS. Prior Intracranial hemorrhage/Recent GI bleed. Prolonged PT / aPTT / INR / low Platelet count.
  • IV-TPA-WONDERFUL THERAPY.  FDA-USA approved Rx of Ischemic Stroke.  Improved outcome within 3 hours in properly selected patients.  Results are best within 90 minutes.  Results are better within 90 -180 minutes. TPA reverses ischemic changes saving brain.
  • Patient Outcome after IV-TPA TPA Within 3 hrs After Acute Ischemic Stroke Percent with Hematoma 4% Percent with major Hemorrhagic Complications 3% Percent with major neurological improvement in 2 hours Percent with major neurological improvement in 24 hours 40% 53%
  • Intraarterial TPA. IA-TPA in selected pts. In < 6 hours due to MCA & BA occlusion In BA occlusion it can be given even after > 12 hours. In future IA-TPA will be rewarding.
  • Trans-Cranial-Doppler(TCD)
  • Management of Blood Pressure. • • • • • Agitation, Pain,Respiratory distress,Drugs. Cushing response.-P-M Jn. Cerebellar Strokes. Usually normalization occurs within 24 hrs. Rx of Hi BP is controversial & ?detrimental. Rx if impending CCF,Extreme surges of BP,use of TPA,worsening of brain oedema . • Rx if MAP>130,CPP>85. • DoC –Labetelol-bolus or infusion. Enalapril-1mg
  • Neurogenic Pulmonary Oedema • In SAH, usually soon after the ictus.DD is massive aspiration,Contusion or pulmonary embolism. • Traditionally thought to be of neurogenic origin due to massive sympathetic discharge sec to ant.hypothalamic injury. • Cardiogenic origin-focal myocardial necrosis, subendocardial ischemia producing LV dysfunction
  • Clinical features & Management. • Sweating,Hypertension,tachypnea,frothy sputum.Typical xray - diffuse infiltrates & hypoxemic respiratory failure. • Recruitment of the collapsed alveoli with PEEP & definite improvement occurs within hrs. • Dobutamine can be considered if the response is poor & to improve forward flow.
  • Nosocomial Respiratory Infections • Commonest cause of death, morbidity, economic & mental stress , prolongation of ICU & hospital stay. • Poor ICU practices. • Overuse of antibiotics. • Poor airway management.Intubation v/s Tracheostomy. • RT v/s PEG.
  • Deteriorating Stroke • Worsening of the clinical status after initial stabilization. • Usually occurs in the 2nd week after the ictus. • Causes are extra cerebral & not intracranial. • Infection- Respiratory or UTI or Pressure sore. • Renal failure & Electrolyte changes due to poor intake, Mannitol,Excessive losses. • Poor nutritional support.
  • Cerebral Hemorrhage • 10-15% stroke • 20-30% in Asia • Up to 50%, 30 day mortality • Little effective therapy • New therapies will be based on pathophysiology
  • Sites of Intracerebral Hemorrhage Quereshi et al. N Engl J Med. 2001;344:1450-60
  • ICH – Worse Outcomes Than Ischemic Stroke 100% 90% 80% Independent 70% 60% Dependent 50% 40% 30% Dead 20% 10% 0% ICH Ischemic 1. American Heart Association. Heart Disease and Stroke Statistics-2005 Update; 2. Qureshi AI. et al. N Engl J Med. 2001;344:1450-1460; 3. Broderick JP. et al. Stroke. 1999;30:905-915; 4. Broderick JP. et al. N Engl J Med. 1992;326:733-736
  • Early Growth of ICH
  • Hematoma Growth 3-Hours 9-Hours
  • Hemorrhage and Volume • Expect good recovery for small volume <10 mL* – e.g. (2x3x3) • Mortality 90% for comatose patients with large volume >60 mL* – e.g. (4x5x6) Volume = (x)(y)(z) / 2
  • 28 mL 43 mL Image courtesy T. Brott, MD.
  • Intra Cerebral Hemorrhage [Classification] 1. Primary – Chronic Hypertension Amyloid Angiopathy 2. Secondary – AVM Aneurysm Coagulopathy Hemorrhagic infarct Cerebral Venous Thrombosis Cavernous Angioma Cocain
  • Intra Cerebral Hemorrhage Diagnosis CT confirms diagnosis. MRI as sensitive as CT. Catheter Angiography – Vascular Causes of secondary ICH.
  • STICH – Trial ( Lancet-2005)  Conservative treatment – 500 pts.  Surgical drainage within 4 days – 500 pts.  No benefit of one mode of treatment over other.  6 mon : Favorable outcome in 24% of conservative & 26% in surgical group.  Subgroup analysis : Advantage of surgical treatment superficial ( < 1 cm from cortical surface) lobar hematomas(only). which cannot be improved by surgery.
  • Scope of Surgery in ICH 1) Superficial hematomas 2) EVD in IVH & fibrinolysis with TPA 3) Decompressive craniectomy 4) Strokectomy
  • Neuro ICU: Monitoring
  • • 50 (M) / Sudden onset unconsciousness / GCS = 7. • CT brain showing large IV bleed. • CT Brain (7 days after IV Urokinase instillation) • Patient fully conscious and no neurological deficit.
  • Discussion • • • The role of ICP monitoring is well established in treatment of traumatic brain injury [3] but no yet fully explored in patients with CVD. We studied the use of ICP monitoring in 10 patients with CVD, GCS<8 and who showed evidence of raised ICP on CT Brain. We observed 100% mortality in patients with persistently elevated ICP (>30mmHg)--consistent with other studies [5]. • The incidence of CSF infection was found to be directly related to the duration of ICP monitoring [Table 4]. This is consistent with other studies [2] reporting dramatic increase in ventriculostomy related infections after day-5 of IV catheter insertion.
  • Discussion • • • Majority of patients with raised ICP responded to CSF drainage. Mannitol was required in 4 patients only. ICP monitoring also helps in early identification of raised intracranial pressure before pupillary signs develop. In all but 1 patients, the IV catheter was inserted in the ICU itself.
  • Discussion • Studies have shown high mortality in patients with IVH. External ventricular drainage and surgery have shown to offer no significant improvement [4]. • Use of the IV Urokinase has shown improvement in 30 day mortality rate from 60-80% to 30-35% [4]. • In our study, 5 patients with IVH received IV Urokinase; of which 4 patients survived and 1 expired [Table 2].
  • ULTRA EARLY HEMOSTATIC THERAPY FOR ICH
  • NOVOSEVEN Recombinant FVIIa Accelerates & Strengthens Local Hemostasis
  • MORTALITY RATE
  • CONCLUSIONS(NovoSeven)
  • MEAN ICH VOLUME
  • BARTHEL INDEX AT DAY 90
  • 100 Determining the ICH Score Component 80 ICH Score Points GCS Score 60 3-4 5-12 1 13-15 30-Days 40 Mortality – (%) 20 2 0 ICH Vol. [mL] >30 <30 Overall 0 1 2 3 4 5 The ICH Score and 30-days mortality. Risk of 30-day mortality increases progressively with each increase in the ICH score. All patients with an ICH score of 5 died. 0 Yes 1 No 0 1 0 IVH Infratentorial ICH Yes 1 No 0 >80 1 <80 0 Age Total (ICH Score-Hemphill-2001) ICH Score 0-6
  • Frequency of Cerebral Venous Thrombosis
  • Cerebral Venous Thrombosis [CVT] • • • • • Purperial CVT is frequent in India. CVT can occur in both male and female at any age. CVT in cancer patients on chemotherapy. Ladies on oral contraceptives and Anaemia. CVT is more common in India than in the West.
  • Cerebral Venous Thrombosis [CVT] CT, MRI and M.R.V. make early diagnosis. CVT is more common than previously assumed. Outcome is favourable with Heparin, if diagnosis made early.
  • Cerebral Venous Thrombosis [CVT] NEUROPATHOLOGY
  • Cerebral Venous Thrombosis [CVT] CLINICAL FEATURES * Onset is Acute,Subacute and Chronic. * Headache, diplopia, vomiting, seizure, hemiplegia, monoplegia, aphasia * Status epilepticus and coma. * Mental changes, confusion & drowsiness in deep CVT & may mimic Psychiatric illness. * Chronic Daily Headache [ CDH] .
  • Cerebral Venous Thrombosis [CVT] TREATMENT * Antibiotics in septic CVT. * Reduction of ICT - mannitol, acetazolamide, steroids are not useful. * Anticonvulsants. * Thrombolytic therapy.
  • Decompressive Craniectomy • Decompressive craniectomy was previously considered a last resort in the management of raised ICP in TBI (Traumatic Brain Injury ) and CVA (Cerebrovascular Accident) refractory to conventional medical therapy. • Early decompressive craniectomy reduces raised ICP and improves survival and functional outcome.
  • 47yrs old male admitted with left hemiplegia,GCS -11,unequal pupils.MRI Brain shows right temporoparietal hemorrhagic infarct with compression of Rt lateral ventricle,midline shift and transfalcine herniation.
  • Decompressive craniectomy done after 6 hrs of GCS deterioration.CThead shows significant reduction in midline shift and decompression of lateral ventricle.
  • • • • • HISTORY Young, 21 year old male patient H/o Headache for 15 days on and off Severe headache and vomiting for 3 days Repeated left focal seizures becoming generalized • Become drowsy after seizure • CT Scan brain- Reported as normal • Patient shifted to Jehangir Hospital
  • DAY 1 • On admission to our unit • Hemodynamically stable • Neurological examinationDrowsy Flexing to pain GCS-8 Pupils - 3 mm equal RL
  • INVESTIGATIONS • MRI/MR Venogram Brain scan
  • DIFFUSION WEIGHTED IMAGES
  • MR VENOGRAM
  • INVESTIGATIONS • Thrombophilia profile • Routine blood investigations including the PBS and MCV • Serum B12 and folic acid • Serum homocystine levels • APLA and lupus anticoagulant
  • Management • Heparin to maintain PTTK between 22 ½ times • Anti edema measures- 3%NS • Antiepileptics • No improvement in 12 hours • GCS dropped by 1 point • Decerebrate right side to pain
  • • What will you do ?
  • Treatment • • • • • • Patient taken up for the surgery Small craniotomy done to expose SSS SSS opened No bleeding from SSS due to thrombosis Purse string sutures taken on dura over SSS Fogarty catheter no 4 introduced and pushed posteriorly and bulb inflated , large quantity of the clots evacuated • Infant feeding tube placed in SSS
  • • During the operation Inj UROKINASE 1 lack unit was injected slowly into the SSS • Post operative patient was sedated and ventilated • Inj UROKINASE total 5 lakh units over 24 hours infused thro catheter placed into the SSS
  • Day - 2 • To check the effect of thrombectomy and thrombolysis with urokinase,we did imaging • Dye injected into the SSS thro same infant feeding tube ,subtracted images were taken
  • SINOGRAM
  • • Inj UROKINASE 5 lakh units over next 12 hours
  • Day-3 • Patient improved, weaned off the ventilator • Further anticoagulation cont with IV Heparin
  • DAY 4 • Patient fully conscious no neurodeficit • Anticoagulation with IV Heparin and oral warfarine
  • CT VENOGRAM
  • DAY 1 • 53 year old man came with focal convulsion two episodes • O/E Hemodynamically stable Conscious but confused Brocas aphasia No limb weakness
  • CT BRAIN
  • DIAGNOSIS • We made a diagnosis of venous infarct • MRI /MR Venogram was done
  • TREATMENT • Anticoagulation with Heparin • Anticonvulsant • Anti-oedema measures – 3% NS
  • DAY- 2 • Patients neurological condition deteriorated • Became drowsy • Developed right side weakness • GCS dropped to 9
  • SURGERY • • • • • • • • Decompression craniotomy was done Left frontal craniotomy Evacuation of intacerebral hematoma Thrombosed SSS in its anterior part is seen Small opening made in SSS Fogarty catheter inserted into SSS Long sheaths of thrombi were pulled out Catheter removed
  • Day-3 • Post operatively • Anticoagulation with heparin started immediately • Sedated and ventilated • Patient improved gradually over next 3 days
  • • Right hemiparesis improved • Further anticoagulation cont with warfarin • Patient walked home in next few days
  • Thank-you.
  • D.D.OF Family Physician Non-Neurological Neurological - Rheumatism, Sprain. General debility Vitamin deficiency Radial N.Palsy Carpal Tunnel Syndrome Cervical Spondylosis STROKE? TIA may cause confusion. Stroke Diagnosis is not a Simple Task! NO WAIT AND WATCH POLICY
  • Every human being is the author of his own health or disease. “ The Buddha”
  • STROKE STUDY-JAN.1999 to DEC.2000 500 consecutive stroke patients – Arterial Ischaemic Strokes - 370 [74%] Venous Stroke - 50 [10%] 84% Intracerebral Hemorrhage - 55 [11%] Subarachnoid Hemorrhage - 25 [ 5%]
  • Typical Case of NovoSeven - I CT after 200 min. CT after 24 hrs.
  • Case Study of NovoSeven 90 Min. 24 Hrs. 67 yrs/M, Hypertension –12 yrs., Right Hemiplegia, BP – 170/110. NIHSS-Adm-8, NovoSeven given at 180 min. NIHSS-24 hrs.-3. NIHSS – 72 hrs-0.
  • 10 leading causes of death in USA 2004 :  Heart disease  Cancer  Stroke  Chronic lower respiratory disease  Accidents  Diabetes  Alzheimer’s disease  Influenza and pneumonia – 61, 472  Kidney disease – 42,762  Septicemia – 33,464
  • • * Anticoagulants (medium). U. Of Michigan Stroke Program
  • STROKE STUDY FROM JAN.1999 TO DEC.2000 500 consecutive stroke patients. Arterial Ischemic Stroke - 370 [75%] Intracerebral Hemorrhage - 55 [11%] Venous Stroke - 50 [10%] Subarachnoid Hemorrhage - 25 [ 4%]
  • Cascade of Events in Ischemia
  • Stroke diagnosis - CT Ischemic Stroke Intracerebral Hemorrhage Cerebral Venous Thrombosis Subarachnoid Hemorrhage
  • Stroke more frequent than Heart Attack ! (OXVASC) Study period 2002-2005 Patients between 45-85 yrs Study of 911, 06 individuals with Vascular events ( Cerebrovascular Coronary and peripheral) 2024 Vascular events in 1657 individuals. - (45%) Cerebrovascular - (42%)Cardiovascular - (9%)Peripheral - (4%) Unclassified Non-fatal Stokes and TIA’s 20% higher than Coronary events. - P. Rothwell Lancet-2005
  • 10 leading causes of death in USA 2004 :  Heart disease  Cancer  Stroke(1st cause of disability)  Chronic lower respiratory disease  Accidents  Diabetes  Alzheimer’s disease  Influenza and pneumonia  Kidney disease  Septicemia
  • Causes of Cerebral Ischemia Vascular Disorder Cardiac Disorders Hematologic Disorders Alcohol & smoking common causes of stroke in young Hypertension accounts for 50% of strokes In 30 % cause unknown.
  • Ishemic Stroke Symptoms & Signs ANT A Re&&&cognize Ant. Circulation Symptoms Quickly Post. Circulation Unilat weakness Isolated H.H. Unilat sensory loss or inattention Diplopia & disconjugate eyes Isolated dysarthria Vomiting, Vertigo Dysphasia Inco-ordination & unsteadiness Vision :- Unilateral or bilateral weakness and/or sensory loss H.H. Monocular blindness Nonspecific :Dysphagia. Loss of consciousness HEADACHE
  • Typical Case of IV TPA -II
  • Typical Case of IV TPA - I CT at 90 min. DWI – 24 hrs.
  • Typical case of IV TPA-I { 82/M.} R.Hemiplegia with aphasia : 10.30 p.m. • 59 Yrs, Dr smoking 30 years, diabetes Admission : 11.30 p.m. 10 years. C.T.Scan : 12 midnight : Normal. NIHSS : 21 on Adm. • 15-3-03 5.30 a.m. - Left hemiplegia on IV TPA : 12.30 A.M.(120 min) waking up. (OTT) • NIHSS 6.30 1 hour -: C.T.Head : a.m. 8 Right PT. Infarct. NIHSS : 24 hours : 4 • 7.45 a.m. - NIHSS - 17. • 8.00 a.m. -150 min. IV C.T.Scan after TPA(OTT) 24 hours. DWI after 24 hours.
  • Carotid Endartectomy [CEA] Carotid Angioplasty & Stenting(CAS)  10-20% of ischemic strokes & TIAs have ICA stenosis.  ECST & NASCET documented benefit of CEA.  CAS avoid surgical incision.  CAS done in those who are unfit for G.A.  Both indicated if ICA stenosis > 70%.
  • Typical Case of NovoSeven – I {63/F} Hypertension – 2 yrs, drugs omitted – 15 days. Sudden L CT – 200 min. hemiplegia and coma. NIHSS – 200 min - 16. NovoSeven – 210 min, 2.4 mg given. NIHSS - 24 hr –14. NIHSS – 30 days – 0. CT – 24 hr.
  • Typical Case of IV TPA - II C.T.after 1 hour. C.T.after 24 hrs.
  • CVT Presenting as TIA. 49 yrs/M,Chronic alcoholic c/o headache for 3 day LUL weakness 3 episodes in 2 days, CT Scan – Hyperdense SSS posteriorly. DWI – Left parietal infarct. MRV – Extensive venous thrombosis of both transverse and SSS thrombosis. Excellent recovery after LMWH.
  • CVT Presenting as TIA