STROKE

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? “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.

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

Stroke Care Unit (SCU)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)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

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.

Physiology of Brain

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 patientDiagnosis of Stroke for TPA patient

Fastest Diagnosis and Evaluation.1. History : Time of onset, anticoagulation, trauma, recent surgery. 2. Examination : ABC, Cardiac, NIHSS Scale 3. C.T.Scan : Gold std. test 4. 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-alert1-drowsy2-obtunded3-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 correctly1-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] 0-no drift a] Left 1-drift before 5 seconds. b] Right 2-fall before 10 seconds.

3-no effort against gravity.4-no movement.

NIHS SCALETested Item Title Responses & Scores.

6 Motor Function [ leg ] 0-no drift a.left 1-drift before 5 seconds. b.right 2-fall before 5 seconds.

3-no effort again gravity4-no movement

7. Limb ataxia 0-no ataxia.1-ataxia in one limb2-ataxia in two limbs.

8. Sensory 0-no sensory loss1-mild sensory loss.2-severe sensory loss

9. Language 0-normal.1-mild aphasia2-severe aphasia

3-mute global aphasia.

10. Articulation 0-normal.1-mild dysarthria.2-severe dysarthria.

11. Extinction or inattention 0-absent1-mild [ loss 1 sensory modality]2-severe [ loss 2 modalities ] N

DWI-PWI …. Mismatch

Salvaging the Ischemic Penumbra

Dirnagl U. Trends Neursci. 1999;22:391-97

Minutes

Days and weeksTime

Hours

Treatment of Acute Ishaemic Treatment of Acute Ishaemic StrokeStroke

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.FDA [USA] approved IV TPA in 1996 in first 3 hrs.

Glycoprotein Activates plasminogen to plasmin. Dissolution of the fibrin clot after binding it Metabolized by liver. Half life is 4-5 min. Package 50mg.

Actilyse [Alteplase] - Actilyse [Alteplase] - TPATPA

Thrombolytic Therapy and Dissolution of Clot

Plasminogen

tPA ( + )

( - )

PAI-1 Plasmin

2 – antiplasmin ( - )

Fibrin

Clot

D- Polymers and D-dimers

Fibrin degradation products

Activates

degrades thrombus by breaking fibrin.

Randomized rTPA study of NINDS [1995]

OTT No.of Dose & 3-mo ICH%

pts treatment group death(%)

NINDS rt-PA Stroke 3h 291 0.9mg/kg rt-PA NA 6

Study(part 1) placebo NA 0

NINDS rt-PA Stroke 3h 333 0.9mg/kg rt-PA NA 7

Study (part 2 ) placebo NA 1

NINDS rt-PA Stroke 3h 624 0.9mg/kg rt-PA 17 6.4

Study ( parts I & II placebo 21 0.6

Combined )

For 1000 pts treated within 3hrs, 140 are less dead or dependent

27%recovered >10 points at 24 Hrs. Minimal or no disability in 30% at 90 days.

Randomized trial rTPA

Study OTT No.of Dose & 3-mo ICH%

pts treatment group death(%)

ATLANTIS part B - 1999 3-5h 613 0.9mg/kg rt-PA 10.9 6.7

placebo 6.9 1.3

ECASS I - 1995 6h 620 0.9mg/kg rt-PA 17.9 19.8

placebo 12.7 6.5

ECASS II - 1998 6h 800 0.9mg/kg rt-PA 10.3 11.8

placebo 10.5 3.1

TPA safe within 3 hours of OTT gives excellent results.

Thrombolytic Therapy - IV -t-PAThrombolytic Therapy - IV -t-PAI. Inclusion Criteria

1. Within 3 hours3 hours of the stroke and patient not needing ventilator. 2. CT Scan head Normal or < 1/3 MCA hypo density. II. Exclusion Criteria

1. BP > 185/110 mm on admission. 2. Use of Oral Anticoagulants. 3. Major surgery preceding FOURTEEN days. 4. Head injury - LAST THREE MONTHS. 5. Prior Intracranial hemorrhage/Recent GI bleed. 6. 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-Patient Outcome after IV-TPATPA

TPA Within 3 hrs After Acute Ischemic Stroke

4%

3%

40%

53%

Percent with Hematoma

Percent with major Hemorrhagic Complications

Percent with major neurological improvement in 2 hours

Percent with major neurological improvement in 24 hours

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. IV &IA(IMS Trial) showed 56% of recanalisation.

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

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

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

ICH Ischemic

Dead

Dependent

Independent

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

Recombinant FVIIa Accelerates & Strengthens Local Hemostasis

NOVOSEVEN

MORTALITY RATE

CONCLUSIONS(NovoSeven)

MEAN ICH VOLUME

BARTHEL INDEX AT DAY 90

Determining the ICH Score

Component ICH

Score Points

GCS Score

3-4 2

5-12 1

13-15 0

ICH Vol. [mL]

>30 1

<30 0

IVH

Yes 1

No 0

Infratentorial ICH

Yes 1

No 0

Age

>80 1

<80 0

Total ICH Score 0-6

100

80

60

40

20

0

Overall 0 1 2 3 4 5

30-Days Mortality – (%)

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.

(ICH Score-Hemphill-2001)

Frequency of Cerebral Venous Thrombosis

Cerebral Venous Thrombosis [CVT]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 Cerebral Venous Thrombosis [CVT][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.


NEUROPATHOLOGY


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] .

* Antibiotics in septic CVT.* Reduction of ICT - mannitol, acetazolamide,

steroids are not useful.* Anticonvulsants.* Thrombolytic therapy.


TREATMENT

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 examination-

Drowsy

Flexing to pain

GCS-8

Pupils - 3 mm equal RL

INVESTIGATIONS

• MRI/MR Venogram Brain scan

DIFFUSION WEIGHTED IMAGESDIFFUSION WEIGHTED IMAGES

MR VENOGRAMMR 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 2-2 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

SINOGRAMSINOGRAM

• 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 BRAINCT 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 PhysicianD.D.OF Family Physician

Non-Neurological - Rheumatism, Sprain.- General debility - Vitamin deficiency

Neurological - 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 Every human being is the author of his own health or disease. “ The Buddha”health or disease. “ The Buddha”

STROKE STUDYSTROKE STUDY--JAN.1999 to JAN.1999 to DEC.2000DEC.2000

500 consecutive stroke patients –

Arterial Ischaemic Strokes - 370 [74%]

Venous Stroke - 50 [10%]

Intracerebral Hemorrhage - 55 [11%]

Subarachnoid Hemorrhage - 25 [ 5%]

84%

CT after 200 min. CT after 24 hrs.

Typical Case of NovoSeven - I

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

U. Of Michigan Stroke Program

• * Anticoagulants (medium).

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 Cerebral Venous Thrombosis

Intracerebral Hemorrhage 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 IschemiaCauses 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

Re&&&cognize Symptoms Quickly

ANT A

Ant. Circulation

Unilat weakness

Unilat sensory loss or inattention

Isolated dysarthria

Dysphasia

Vision :-

H.H.

Monocular blindness

HEADACHE

Post. Circulation

Isolated H.H.

Diplopia & disconjugate eyes

Vomiting, Vertigo

Inco-ordination & unsteadiness

Unilateral or bilateral weakness and/or sensory loss

Nonspecific :-

Dysphagia.

Loss of consciousness

Typical Case of IV TPA -II

Typical Case of IV TPA - I

CT at 90 min. DWI – 24 hrs.

Typical case of IV Typical case of IV TPA-ITPA-I

{ 82/M.}

R.Hemiplegia with aphasia : 10.30 p.m.

Admission : 11.30 p.m.

C.T.Scan : 12 midnight : Normal.

NIHSS : 21 on Adm.

IV TPA (OTT) : 12.30 A.M.(120 min)

NIHSS : 1 hour : 8

NIHSS : 24 hours : 4

C.T.Scan after 24 hours. DWI after 24 hours.

• 59 Yrs, Dr smoking 30 years, diabetes 10 years.

• 15-3-03 5.30 a.m. - Left hemiplegia on waking up.• 6.30 a.m. - C.T.Head - Right PT. Infarct.• 7.45 a.m. - NIHSS - 17.• 8.00 a.m. -150 min. IV TPA(OTT)• 9.00 a.m. - NIHSS - 11• 16-3-03 - NIHSS - 8

•

Carotid Endartectomy [CEA] [CEA]

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%.

Carotid Angioplasty & Carotid Angioplasty & Stenting(CAS)Stenting(CAS)

Typical Case of NovoSeven – I

{63/F}

Hypertension – 2 yrs, drugs omitted – 15 days.

Sudden L hemiplegia and coma.

NIHSS – 200 min - 16.

NovoSeven – 210 min, 2.4 mg given.

NIHSS - 24 hr –14.

NIHSS – 30 days – 0.

CT – 200 min.

CT – 24 hr.

C.T.after 1 hour. C.T.after 24 hrs.

Typical Case of IV TPA - II

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

STROKE

Investor Relations

Transcript of STROKE