hemorrhagic stroke

1. 60 year old male hypertensive patient on irregular
treatment brought to emergency department with
 c/o 1 hour h/o
-sudden onset of DOAOM towards right,
-slurring of speech,
-weakness of left upper limb & left lower limb
simultaneously.
a/w severe headache & projectile vomiting

2. O/e BP – 200/100mmHg, PR – 52/minute,
RR – 24/minute, TEMP - normal
Neuro – L side UMN facial palsy,
non fluent aphasia,
power grade 0/5 UL & LL left side,
plantar extensor with brisk DTR left side.
no neck rigidity
Other systems - WNL

3. What will do next?
ASSESS Airway, breathing, circulation
Check RBS = NORMAL
URGENT NCCT BRAIN

5. DIAGNOSIS ???

6. HEMORRHAGIC STROKE
-DR VIPIN VENGAYIL
DNB RESIDENT

7. Etiology of ICH (overall)
Hypertension (m/c)
Vascular malformations
Cerebral amyloid angiopathy
Intracranial tumors
Bleeding diathesis, anticoagulation,
fibrinolysis
Granulomatous angiitis & vasculitides
Sympathomimetic agents (amphetamine,
cocaine)
Hemorrhage into cerebral infarct
Trauma

8. Clinical features
Features of RAISED ICT
 Headache, vomiting, decreased LOC
 Correlated with hematoma size and prognosis
 Progressive over time
 Seizures in lobar ICH
Focal neurological deficits depending on the location
of ICH

9. Hypertension and ICH
Most important risk factor (>70% of 1ry ICH)
Bifurcation of small penetrating arteries (50–700
μm diameter)
Atherosclerosis
 Lipid deposition, layering of platelet and fibrin aggregates,
breakage of elastic lamina, atrophy and fragmentation of
smooth muscle, dissections, and granular or vesicular
cellular degeneration
Charcot and Bouchard aneurysm
 Fibrinoid necrosis of the subendothelium  focal dilatations
 rupture of microaneurysm

11. N Engl J Med 2001;344(19):1450–1460

12. N Engl J Med 2001;344(19):1450–1460
Lobar hemorrhage 25%
• Penetrating cortical
branches of ACA,
MCA, & PCA
• Peripheral location ∴
lower frequency of
coma
• Lower mortality
• Better functional
outcome

13. N Engl J Med 2001;344(19):1450–1460
Basal ganglia 35-40%
• Ascending
lenticulostriate
branches of MCA
• Wide spectrum of
severity extending to
coma and
decerebrate rigidity
• Ventricular extension
carries very poor
prognosis

15. N Engl J Med 2001;344(19):1450–1460
Thalamus 10-15%
• Ascending
thalamogeniculate
branches of PCA
• Abrupt
hydrocephalus from
aqueductal
obstruction from
intraventricular clot
• Responds to
ventriculostomy

18. N Engl J Med 2001;344(19):1450–1460
Pons 5%
• Paramedian branches
of the basilar artery
• Bilateral carries very
poor prognosis
(coma, quadriplegia,
decerebrate
posturing, horizontal
ophthalmoplegia,
pinpoint reactive
pupils)

20. N Engl J Med 2001;344(19):1450–1460
Cerebellum 5-10%
• Penetrating branches
of the PICA, AICA,
SCA
• Abrupt onset vertigo,
h/a, n/v, inability to
walk in absence of
weakness
• Ipsilateral ataxia,
horizontal gaze palsy,
peripheral facial palsy
• Unpredictable
deterioration to coma

23. Lobar hemorrhage

25. Vascular malformations
Aneurysms, AVM, cavernous angiomas
Younger, female patients, familial history
Imaging may show concurrent SAH
Dx by MRI and cerebral angiography
Usually supratentorial, lobar ICH
Cavernous angioma: on MRI (T2) central
nidus of irregular bright signal mixed
with mottled hypointensity, surrounded
by peripheral hypointense ring

26. Vascular malformations

36. Management principles
A-B-C: Airway support
 Decreased level of consciousness
 Bulbar muscle dysfunction
Blood pressure control
Anticoagulation reversal
Intracranial pressure control
Monitoring
“Neurological and cardiovascular deterioration greatest in
the 24hours following symptom onset”

45. Elevated icp
Hypertonic saline & mannitol
Elevate head end of bed
Intubation & acute hyperventilation
Csf drainage if necessary

46. ICP monitoring consider if
 Reduced LOC (GCS <8)
 Clinical evidence of cerebral herniation
 Significant IVH
 Hydrocephalus
waves
 A (plateau)- pathologic
 B (respiratory)
 C (Cardiac) waveforms

47. Blood pressure & ICH
BP is elevated on admission even in patients who
have no history of hypertension
 MAP > 120mmHg in over 2/3 of patients
Precipitant of the hemorrhage?
Reflection of chronic hypertension?
Attempt to maintain CPP?
Sympathetic activation 2ry to pain & anxiety?
Tends to return to baseline 7-10 days post ICH

48. Acute management of BP
How fast should BP be lowered?
 Rapidly lowering MAP by ≈ 15% does not lower CBF
 Reductions of 20% can affect CBF
 Current guidelines suggest a reduction of ≤ 20% in the
first 24 hrs
Which agents should be used?
 Short and rapidly acting IV antihypertensive
 Labetalol, hydralazine, esmolol, nicardipine
 Sodium nitroprusside and nitroglycerin should avoid
d/t vasodilation and increase ICP

49. ACC/AHA Guideline 2015

51. General Monitoring and Nursing Care
 In a Canadian study of 49 hospitals that included ICH patients, a higher
proportion of registered nurses at the hospital and better nurse-
physician communication were independently associated with lower
30-day mortality even after adjustment for disease severity,
comorbidities & hospital characteristics

54. Other principles
Glucose should be monitored. Both hyperglycemia and
hypoglycemia should be avoided (150 - 200mg%)
Clinical seizures or electrographic seizures should be
treated with anti seizure drugs
Prophylactic antiseizure medication is not recommended

55. Ivh 45% pt, a/w poor outcomes
Although the insertion of a VC should theoretically aid in
drainage of blood and CSF from the ventricles, VC use alone may
be ineffective because of difficulty maintaining catheter patency
& slow removal of intraventricular blood.
 Thus, there has been recent interest in the use of thrombolytic
agents as adjuncts to VC use in the setting of IVH
 IVH: Recommendations
1. Although intraventricular administration of rtPA in IVH
appears to have a fairly low complication rate, the efficacy and
safety of this treatment are uncertain (Class IIb; Level of
Evidence B). (Revised from the previous recommendation)
 2. The efficacy of endoscopic treatment of IVH is uncertain

56. Hematoma expansion
Hematoma enlargement
 >70% have hematoma enlargement w/in 3 hrs of symptom
onset; 1/3 clinically significant
 Most occur within 3 hrs, can be up to 12 hrs
 Independent predictor of worse outcome & ↑ mortality

57. Hematoma expansion
Journal of the
Neurological
Sciences 261
(2007) 99–107

60. Recombinant Factor VIIa
Factor VIIa has locally action at sites of tissue
injury and vascular-wall disruption by binding
tissue factor & generating thrombin and
activating platelets
Recombinant FVIIa directly activates fX on the
surface of activated plts resulting in acceleration
of coagulation
Factor Seven for Acute Hemorrhagic Stroke
(FAST) trial, N Engl J Med 2008;358:2127-37
 841 patients, within 4 hours of onset of stroke
 Placebo vs. 20 μg/kg vs. 80 μg/kg of rFVIIa
 1ry end point: 90-day functional outcome or death

61. Recombinant Factor VIIa
Significant reduction in growth of hematoma
volume in the 80 μg/kg group
No significant difference in functional outcome
and mortality
Venous thromboembolic events were similar in all
three groups (limits its usage)
Arterial thromboembolic events were significantly
more frequent in the 80 μg/kg group

62. ABC of hematoma size
Broderick, JP et al. Stroke 1993;24:987-993
 1.26 million subjects from Greater Cincinnati

63. CT-A “Spot Sign”
Focal area of
enhancement within the
hematoma on CTA have
been shown to be:
 Independent predictor of
hematoma expansion
 Associated with longer
median hospital stay
 Independent of time to
presentation
 Sensitivity 91%, specificity
89%, NPV 96%

65. CT-A “Spot Sign”
Recent proposal of a “Spot Sign” definition
(Can J Neurol Sci 2009;36:456-461)
 Serpiginous and/or spot-like appearance
 Within the margin of the parenchymal hematoma without
connection to an outside vessel
 >1.5mm diameter in maximal axial dimention
 >Double the HU density compared to background
hematoma (>150 HU)
 Multiple or single in number
Comparison to unenhanced CT for mimickers
 Calcifications (tumour, choroid, infectious, etc)

66. Anticoagulation associated ICH
Goal of treatment: fully reverse INR to normal range
High dose Vitamin K 10-20 mg IV for 3days
 Effect takes 12-24hrs
 Helps achieving sustained reversal of INR
Fresh frozen plasma 15-20ml/kg
 Volume overload, insufficient factor IX
 ABO compatibility, thawing, infusion time (30hrs)
Prothrombin Complex
Concentrate(PCC,Octaplex)
 Combination of II, VII, IX, X, variable protein C and S
 Dosage dependant on initial INR
 Smaller volume, correct INR as fast as 30 min

67. Anticoagulation associated ICH
ICH associated with IV heparin
Rapidly normalize activated partial
thromboplastin time
Protamine sulfate 1 mg per 100 U heparin,
adjusted for time since last heparin dose
 30-60 min: 0.5 to 0.75 mg per 100U heparin
 60-120 min: 0.375 to 0.5 mg per 100 U heparin
 >120min: 0.25 to 0.375 mg per 100 U heparin
Slow IV injection (<5 mg/min, max dose 50 mg)
Beware of systemic hypotension

68. AAICH – restarting anticoagulation
1% recurrent ICH in initial 3 mths post ICH
Risk estimated to double with anticoagulation
Stroke.
2007;38:200
1-2023

69. Miscellaneous
Venous thromboembolism prophylaxis
 Intermittent pneumatic compression
 Heparin SQ prophylaxis (3-5 d if no bleeding)
 IVC filter (proximal venous thrombosis)
Hyperglycemia
 Associated with poor outcome and ↑ mortality
 Marker of outcome or contributor?
Hyperpyrexia
 Associated with poor outcome and neuro deterioration
 Septic workup, treat with antipyretics or cooling devices
 Often central in origin

71. 4. Supratentorial hematoma evacuation in deteriorating
patients might be considered as a life-saving measure
(New recommendation)
5. DC with or without hematoma evacuation might reduce
mortality for patients with supratentorial ICH who are in a
coma, have large hematomas with significant midline shift,
or have elevated ICP refractory to medical management
(New recommendation)
6. The effectiveness of minimally invasive clot evacuation
with stereotactic or endoscopic aspiration with or without
thrombolytic usage is uncertain
(Revised from the previous guideline)

73. Decompressive craniectomy
Surgical removal of cranial bone flap to relieve
intracranial pressure
Useful in large ischemic CVA with profound edema
Role in traumatic brain injury still needs to be
established

75. Minimally Invasive Neurosurgery
for Hemorrhage (newer)
Evacuation Minimally invasive surgery generally
refers to the concept of creating minimal trauma to
normal appearing tissue during the process of
removing the hematoma
This stands in distinction from the open craniotomy
in which a large bone flap is created; the brain is
exposed, retracted, and manipulated to inspect the
site of bleeding and suction blood from multiple
areas.

76. 1.endoscopic evacuation of the hematoma
In endoscopic evacuation, a small burr hole is
created, and an endoscope measuring from 5 to 8
mm diameter is inserted through normal brain tissue
into the hematoma.
Suction and irrigation are applied to remove the
hematoma.
The brain is then visualized via the endoscope to
determine the site of bleeding and to determine the
amount of ICH evacuated.

77. 2. stereotactic aspiration and thrombolysis
This technique involves using image guidance to
place a catheter into the main body of the hematoma
and aspirate blood.
A catheter is left in the body of the hematoma, and
during the course of several days, repeated small
doses of thrombolytics (recombinant tissue-type
plasminogen activator) are instilled via the catheter
into the brain to clear the blood slowly during the
course of 72 to 96 hours.

79. Conclusions
ICH has an increasing incidence, but continues to
have a very poor prognosis
Hypertension is a major risk factor
Acute BP reduction of 15-20% is safe
Anticoagulation should be reversed ASAP
Intraventricular extension & midline shift a/w poor
prognosis
Early detection/ imaging & treatment DECREASES
morbidity & mortality but for a limited extent
Physiotherapy & rehabilitation play definite role.

80. ICH
TIME = LIFE
DOCTOR

81. THANK YOU..