1. Critical Care in Cerebro-Vascular
Disease.

2. 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.

3. Stroke?
“STROKE IS A BRAIN ATTACK”
First 180 mins are very important
Don’t lose time!
Every SINGLE SECOND Counts

4. 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.

5. 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.

6. 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.

7. More than 30% die.
Disability after Stroke

8. 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.

9. 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.

10. 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.

11. ICA Stenosis Angio & Doppler

13. 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.

14. D. D. of Acute Ischemic Stroke
(Stroke mimics)
Cerebral Neoplasm
Subdural hemotoma
Epileptic seizure
Traumatic brain injury
Migraine
Neuromuscular & Spinal cord lesions.

15. 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

16. 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.

17. 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.

18. 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

19. DWI-PWI …. Mismatch

20. Salvaging the Ischemic
Penumbra
Minutes
Hours
Time
Days and weeks
Dirnagl U. Trends Neursci. 1999;22:391-97

21. 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.
-

22. 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.

23. 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

24. 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.

25. 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.

26. 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.

27. 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%

28. 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.

33. Trans-Cranial-Doppler(TCD)

34. 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

35. 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

37. 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.

38. 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.

39. 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.

40. 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

41. Sites of Intracerebral
Hemorrhage
Quereshi et al. N Engl J Med. 2001;344:1450-60

42. 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

43. Early Growth of ICH

44. Hematoma Growth
3-Hours
9-Hours

45. 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

46. 28 mL
43 mL
Image courtesy T. Brott, MD.

47. Intra Cerebral Hemorrhage [Classification]
1. Primary – Chronic Hypertension
Amyloid Angiopathy
2. Secondary – AVM
Aneurysm
Coagulopathy
Hemorrhagic infarct
Cerebral Venous Thrombosis
Cavernous Angioma
Cocain

48. Intra Cerebral Hemorrhage
Diagnosis
CT confirms diagnosis.
MRI as sensitive as CT.
Catheter Angiography – Vascular Causes of secondary ICH.

49. 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.

50. Scope of Surgery in ICH
1) Superficial hematomas
2) EVD in IVH & fibrinolysis with TPA
3) Decompressive craniectomy
4) Strokectomy

51. Neuro ICU: Monitoring

52. • 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.

53. 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.

54. 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.

55. 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].

56. ULTRA EARLY HEMOSTATIC THERAPY FOR ICH

57. NOVOSEVEN
Recombinant FVIIa Accelerates & Strengthens Local Hemostasis

58. MORTALITY RATE

59. CONCLUSIONS(NovoSeven)

60. MEAN ICH VOLUME

61. BARTHEL INDEX AT DAY 90

62. 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

63. Frequency of Cerebral Venous Thrombosis

64. 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.

65. 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.

66. Cerebral Venous Thrombosis [CVT]
NEUROPATHOLOGY

67. 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] .

68. Cerebral Venous Thrombosis [CVT]
TREATMENT
* Antibiotics in septic CVT.
* Reduction of ICT - mannitol, acetazolamide,
steroids are not useful.
* Anticonvulsants.
* Thrombolytic therapy.

69. 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.

70. 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.

71. Decompressive craniectomy done after 6 hrs of GCS deterioration.CThead shows significant
reduction in midline shift and decompression of lateral ventricle.

79. •
•
•
•
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

81. DAY 1
• On admission to our unit • Hemodynamically stable
• Neurological examinationDrowsy
Flexing to pain
GCS-8
Pupils - 3 mm equal RL

82. INVESTIGATIONS
• MRI/MR Venogram
Brain scan

83. DIFFUSION WEIGHTED IMAGES

84. MR VENOGRAM

85. INVESTIGATIONS
• Thrombophilia profile
• Routine blood investigations
including the PBS and MCV
• Serum B12 and folic acid
• Serum homocystine levels
• APLA and lupus anticoagulant

86. 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

87. • What will you do ?

88. 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

89. • 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

90. 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

91. SINOGRAM

92. • Inj UROKINASE 5 lakh units over next 12
hours

94. Day-3
• Patient improved, weaned off the ventilator
• Further anticoagulation cont with IV
Heparin

95. DAY 4
• Patient fully conscious no neurodeficit
• Anticoagulation with IV Heparin and oral
warfarine

96. CT VENOGRAM

97. DAY 1
• 53 year old man came with focal convulsion
two episodes
• O/E
Hemodynamically stable
Conscious but confused
Brocas aphasia
No limb weakness

98. CT BRAIN

99. DIAGNOSIS
• We made a diagnosis of venous infarct
• MRI /MR Venogram was done

103. TREATMENT
• Anticoagulation with Heparin
• Anticonvulsant
• Anti-oedema measures – 3% NS

104. DAY- 2
• Patients neurological condition
deteriorated
• Became drowsy
• Developed right side weakness
• GCS dropped to 9

105. 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

106. Day-3
• Post operatively
• Anticoagulation with heparin started
immediately
• Sedated and ventilated
• Patient improved gradually over next 3 days

107. • Right hemiparesis improved
• Further anticoagulation cont with warfarin
• Patient walked home in next few days

108. Thank-you.

109. 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

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

111. 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%]

112. Typical Case of NovoSeven - I
CT after 200 min.
CT after 24 hrs.

113. 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.

114. 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

115. • *
Anticoagulants (medium).
U. Of Michigan Stroke Program

116. 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%]

117. Cascade of Events in Ischemia

118. Stroke diagnosis - CT
Ischemic Stroke
Intracerebral Hemorrhage
Cerebral Venous Thrombosis
Subarachnoid Hemorrhage

119. 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

120. 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

121. 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.

122. 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

123. Typical Case of IV TPA -II

125. Typical Case of IV TPA - I
CT at 90 min.
DWI – 24 hrs.

126. 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.

127. 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%.

128. 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.

129. Typical Case of IV TPA - II
C.T.after 1 hour.
C.T.after 24 hrs.

130. 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.

131. CVT Presenting as TIA