1. Epidemiology and Pathophysiology of Intracerebral Hemorrhage
Edward C. Jauch, MD MS FACEP 1

2. Edward C. Jauch, MD MS FACEP Assistant Professor Associate Director of Research Department of Emergency Medicine University of Cincinnati College of Medicine Faculty, Greater Cincinnati / Northern Kentucky Stroke Team 2 54 1 54

3. Global Objectives Review epidemiology of ICH
Understand pathophysiology of ICH
Discuss lessons from acute ischemic stroke
Improve Emergency Medicine practice 54 2 54

4. A Clinical Case

5. Patient Initial Clinical History
57 yo male with sudden onset headache and left sided weakness
Family calls 911
EMS transport to OLFH Hospital
Enroute patients symptoms progress to full hemiplegia
Initial VS: 210 / 120 mmHg, HR 110, R 24 54 3 54

6. Patient ED Presentation
PMHX: HTN for 10 years, hyperlipidemia
SHX: Smoking 30 years
Meds: ACE inhibitor, ASA
ROS: No recent illness or injuries, no new medications 54 3 54

7. Patient ED Presentation
Physical examination:
VS / 140 mmHg, HR 110, RR 22, T 98.6oC
Uncomfortable WM, arouses to voice
HEENT/CV/Lungs/Abd - WNL
Neuro –
LOC mildly depressed
CN with L facial droop and partial gaze palsy, VFI
Motor with dense L hemiplegia
Sensory with mild L sensory loss
Speech slurred but no significant aphasia
NIHSS = 12 54 3 54

8. Key Questions What is your differential diagnosis?
What are the most common ICH etiologies?
What is the pathophysiology of ICH?
What guidelines exist that govern the acute care of ICH patients?
What can be learned regarding ICH management from acute ischemic stroke?
How can the emergent care of ICH patients be enhanced?
ABC’s. Patients with ICH can deteriorate quickly. Constantly reassess
Imaging modality of choice

9. Patient ED Presentation
Initial noncontrast CT scan
Labs:
CBC, chem 7 – WNL
PT, PTT – WNL
ECG – LVH with strain

10. Stroke Subtypes Hemorrhagic 26% Ischemic 71% Other 3%
ICH
13%
SAH
Lacunar
19%
Thromboembolic 6%
Cardioembolic
14%
Other 3%
Unknown
32%
Ischemic 71%
Hemorrhagic 26%
Up to 65,000 ICH per year in U.S.
(NINCDS Stroke Data Bank: Foulkes, Stroke, 1988)

11. ICH Classifications Primary Secondary Hypertensive arteriopathies
Cerebral amyloid angiopathies
Secondary
Neoplasms
Structural lesions
Anticoagulants or thrombolytic agents
Drugs (cocaine, ephedra, etc)
Traumatic brain injury

12. Location Lobar Nonlobar Cerebellar Intraventricular
Associated with amyloid angiopathy
Nonlobar
Associated with hypertension
Cerebellar
Intraventricular

13. Lobar Hemorrhage Secondary to cerebral amyloid angiopathy
Beta-amyloid deposition in vessels of cortex and leptomeninges
Associated with aging
Lobar hemorrhage in young due to AVM, cavernous hemangioma
Amyloid in vessel wall
Lobar hemorrhage is normotensive patient 44

14. Non-lobar Hemorrhage Non-lobar or hypertensive hemorrhage Location
Associated with hypertensive arteriolosclerosis
Location
putamen, pons, thalamus, cerebellum
Mortality
50% 30 day mortality
Exam:
sudden HA with focal findings on exam
The second form of arteriolosclerosis is shown here. The arteriole here has an "onion skin" appearance typical of hyperplastic arteriolosclerosis. This lesion is most often associated with malignant hypertension

15. 19 yo with ephedra induced ICH
Risk Factors
Age
Gender (men > women)
Race (blacks > whites)
Prior stroke
Hypertension
Anticoagulant / thrombolytics
Alcohol / cocaine
19 yo with ephedra induced ICH

16. Less Common Risk Factors
Vascular malformations
Arteriovenous malformations (AVM)
Cavernous angiomas
Intracranial aneurysms
Infections
Cerebral vasculitis
Mycotic aneurysms
Cerebral venous thrombosis

17. ICH Rate by Age
Rate per 100,000 / year
Age (years)

18. Systolic Blood Pressure & Incidence
Incidence Rate/100,000
Systolic Blood Pressure (mmHg)

19. Ethnicity of ICH Risk Age and sex adjusted rate
U.S. 15 per 100,000
World wide per 100,000
Higher in African American and Japanese
Rates 13.5 per 100,000 Caucasian per 100,000 AA per 100,000 Japanese

20. Anticoagulation and Thrombolytic Related Hemorrhage
Warfarin anticoagulation
6-11 fold increased risk of ICH
Higher levels with increased risk
Most occur in therapeutic range
Thrombolysis and Symptomatic ICH
6.4% in thrombolysis treatment group
tPA related hemorrhages typically lobar
20% occur outside area of infarct
0.6% in placebo group

21. Mortality and Morbidity
Estimated lifetime cost $123,565
Of the 37,000-65,000 ICH per year
35-52% were dead at 1 month
50% of deaths occurred within 48 hours
10% independent at 30 days
20% independent at 6 months

22. 30 Day Outcome of ICH
No. cases
Modified Oxford Handicap Scale

23. Clinical Presentation
Symptoms and signs
82% change in mental status
>75% hemiparesis/plegia
63% headache
22% vomiting
2/3 progression of symptoms, 1/3 maximal at onset

24. Clinical Presentation by Location
Lobar
Headache (headache location related to ICH site)
Motor, sensory deficit, or VF deficits (not all)
Deep
Unilateral motor, sensory, VF loss
Aphasia (D) or neglect (ND)
Cerebellum
Nausea, vomiting, ataxia, coma
Pontine
Coma, quadriplegia, pinpoint pupils

25. ICH Progression Symptoms often progress, associated with ICH growth
26% with 33% or greater growth in 1 hour
12% with 33% or greater growth 1-20 hours
This gives us a window of therapeutic opportunity

26. Prognostic Information
Volume of hemorrhage
Clinical presentation
Intraventricular extension
(Kothari, Stroke)

27. Hematoma Volume Calculation
Formula for volume of an ellipsoid
4/3Л (A/2)(B/2)(C/2)
Simplified ABC/2

28. Prognosis Worse Better Volume > 60 cm3 and GCS < 9
91% dead at 30 days
Patients with volume over 30 cm3 only 1 / 71 independent at 30 days
Intraventricular extension
Better
Volume < 30 cm3 and GCS 9 or higher
19% dead at 30 days
(Broderick, Stroke)

29. Pathophysiology Initial hemorrhage into surrounding tissues causes:
Cytotoxic and vasogenic edema formation in the perihematomal parenchyma
Neurotoxicity from released serum proteins
Elevated intracranial pressure due to
Hematoma mass effect
Perihematomal edema
Intraventricular extension and hydrocephalus
Results in decreased perfusion

30. Current Recommendations for Management of Intracerebral Hemorrhage
Emergency Medicine representation
New guidelines due 2005
(Broderick, Stroke 1999)
Edward C. Jauch, MD MS FACEP 30

31. Emergent Evaluation Baseline labs Neuroimaging
CBC, coags, electrolytes
Neuroimaging
CT remains gold standard
Identify ICH
Identify complications (hydrocephalus, herniation)
MRI / MRA
Useful to evaluate for structural abnormalities
AVM, aneurysms
Angiography
Rarely emergently indicated
Identify vascular issues preoperatively in occult ICH

32. Medical Management ABC’s Blood pressure control ICP management Other
Hyperventilation
Osmotherapy
No role for glycerol, corticosteroids, hemodilution
Other
Prevention of hyperthermia
Fluid management (CVP at 5-12 mm Hg)
Modifications for age, comorbidities, size, severity, location
Seizure control
Find somebody to take the patient

33. Blood Pressure Management
No definitive data (yet)
Hypertension very common
MAP > 140 in 34%, > 120 in 78%
Many return to baseline over first 24 hours
Prospective
Retrospective
Case Series
Results
Meyer et al. 1962
Lower BP good
Dandapani et al. 1995
Qureshi et al. 1999
Lower BP bad
Brott T et al 1995
Hematoma enlargement not associated with degree of HTN
(Dr. Aninda Acharya, St.Louis University, Internet Stroke Center)

34. Blood Pressure Management34
(Broderick, Stroke 1999)
Edward C. Jauch, MD MS FACEP

35. Management of Increased ICP
Definition
ICP > 20 mm Hg for > 5 mins
Treatment goal
ICP < 20 mm Hg
CPP > 70 mm Hg
Recommendations
ICP monitoring with GCS < 9
Management
Osmotherapy
Hyperventilation
Ventricular drainage

36. Management of ICP (Broderick, Stroke 1999)36
(Broderick, Stroke 1999)
Edward C. Jauch, MD MS FACEP

37. Seizure Therapy 25% will have seizure Much more common if lobar
Most in first 72 hours
Phenytoin is drug of choice
Does not convey life long epilepsy

38. What can be Fixed? Stop the bleeding Remove the blood Reduce the edema
Until now no option
Remove the blood
Multiple trials without clear impact
Reduce the edema
No treatment yet

39. Surgical Treatment
Direct evacuation, endoscopic, stereotactic

40. Surgical Treatment Recommendations
7000 procedures a year in U.S. despite lack of data
Largest surgical trial negative (in press)
MISTIE trial of stereotactic evacuation with tPA
(3/05) Surgery in 24 hrs, stable clot for 6 hrs 40
(Broderick, Stroke 1999)

41. The Potential Future With Novo 7 What Can We Learn From Acute Ischemic Stroke?41

42. Time Will Always Mean Brain!
(Lancet 2004; 363: 768–74)

43. Same Chain: No Weak Links
Development: Protocol and pathway development
Detection: Early recognition
Dispatch: Early EMS activation
Delivery: Transport & management
Door: ED triage
Data: ED evaluation & management
Decision: Neurology input, therapy selection
Drug: Thrombolytic & future agents
Disposition: Admission or transfer
How to introduce this section?
What are the elements of stroke management involving the Emergency Department
Also add “D” for Diagnosis 43

44. Emergent Triage and ED Evaluation Must be a Priority
Challenges in trauma centers
Sharing resources
ED demands
The diagnosis of stroke remains based on three important and integral elements:
The history and physical
Biochemical testing
Neuroimaging

45. NINDS Recs: Same for ICH
Door-to-MD: minutes
Door-to-Stroke minutes
Team notification:
Door-to-CT scan: 25 minutes
Door-to-Drug: minutes
(80% compliance)
Door-to-Admission 3 hours
I.) AT this National Symposium, experts developed in-hospital Time
Intervals to allow the stroke patient to be treated and evaluated in a
expedient manner. These recommendations Include:
A.) Emergency department arrival to initial physician evaluation:
10 minutes
B.) Emergency department arrival to Stroke Team Notification:
15 minutes
C.) Emergency department arrival to CT Scan initiation:
25 minutes
D.) And they recommended that 80% of eligible stroke patients
presenting to the emergency department should be treated
with tPA within 60 minutes.
NEXT SLIDE
(NINDS Stroke Symposium 2003)

46. There Will Be Major Barriers
EM education of disease and treatment
Timely radiology involvement
Access to neurologic expertise
Neurology does not admit ICH
Neurosurgeons won’t rush in
EM will be point person like tPA
Post treatment management
ICU beds
Complications likely to occur early
Cost
Whose cost center
“Drip and ship” model

47. Who Cares for Patients with ICH?
Shortage of neurosurgeons
Shortage of neurocritical care
Neurologists not experienced with ICH
Emergency Medicine primarily focused on stabilization
Example – Cincinnati
30% neurosurgical shortage
Nonoperative ICH to neurology
Only 4 of 15 hospitals with neurosurgery coverage
Only 1 level 1 trauma largely due to neurosurgery

48. Potential Solution: Utilize Primary Stroke Centers
Patient care areas
Acute stroke teams
Written care protocols
EMS participation
Emergency Department participation
Stroke unit*
Neurosurgical services**
Support services
Organizational support
Stroke center director
Neuroimaging
Laboratory
Outcome & quality measures
CME
Secondary stroke center likely required for most ICH
(Brain Attack Coalition, JAMA 2000)

49. ED Treatment and Patient Outcome

50. Questions. www. ferne. org ferne@ferne
Questions?? Edward Jauch, MD, MS (513)
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