1. Intracerebral Hemorrhage & high ICP management
Emergency Lecture Series
July 10, 2013
Abdulla Alkuwaiti R2

2. Content Pathophysiology Epidemiology Clinical features
Causes/Risk factors
Types of ICH
Radiological Findings
Management/ including increase ICP
Prognosis

3. Pathophysiology
Thrombin and iron, released upon red blood cell (RBC) lysis, are 2 major factors causing brain injury after ICH.
Thrombin at high concentrations kills neurons and astrocytes in vitro.
Hemoglobin degradation can result in iron release. The iron causes marked brain edema, even in small concentration.
Ya Hua, “Intracerebral hemorrhage: introduction brain injury afteriIntracerebral hemorrhage, ther role of Thrombin and Iron” Stroke.2007; 38: 

4. Secondary Damage Hematoma expansion ≥ 80 ml fatal Cerebral edema
Secondary injury

5. Epidemiology
Accounts for 15% of strokes in the West and 30% in the East
12-15 cases per 100,000 per year
More common in Hispanics, Blacks, Asian than in whites
Canada: 2008/2009
Total 11%: AGE 20-29: 17%, 30-39: 16%, 40-49: 11%, 50-59: 12%, 60-69: 12%, 70-79: 10%, 80-89: 10%, 90+: 7%
Male 53%, female 47%
The quality of stroke care in Canada, Canadian stroke network 2011

6. Clinical Features Sudden headache +/- N & V
Smooth progressive onset over minutes to hours
Usually during activity
Confusion
Neurodeficit: hemiplegia
Depressed level of consciousness
Seizures

7. Case: 26F

8. Post op

9. Post Angio

10. ICH Score Component ICH score points GCS 3 - 4 2 5 - 12 1 13 - 15
ICH volume
≥ 30 ml
≤ 30 ml
IVH
yes no
Infratentorial
Age > 80

11. Mortality and ICH Score

12. Classification of ICH PRIMARY (78-88%) SECONDARY
Hypertensive angiopathy (fibrohyalinosis)
Amyloid angiopathy
Anticoagulant Associated
SECONDARY
AVM
Aneurysm
Cavernoma
Neoplasm
Coagulopathy
Alcoholic liver disease
Hemophilia
Hemorrhagic infarct
Toxic-cocaine

13. Risk factors
AGE: Incidence significantly doubles with each decade after age 55. Above 80 years of age risk increases 25 times
Gender: more common in men
Race: more common in blacks, hispanics, asians, less in whites
Previous CVA
Alcohol consumption: >3 drinks per day increases the risk of ICH by 7 folds
Drugs: cocaine, amphetamine
Cigarette smoking does not increase the risk of ICH

14. Risk Factors
Oral Anticoagulant: warfarin risk of bleed in afib patient is 2.2% per year
Antiplatelets: ASA alone (1.3% per year risk) no significant increase in risk but ASA and plavix together increase risk to 2.4% per year.
rTPA: risk of ICH is 6.4% in the next 36hrs

15. Genetic predisposition
The E2 and E4 alleles of the apolipoprotein E gene play an important role in the occurrence of certain forms of ICH as labor hemorrhages
O’Donnel et al, 2000

16. Types of Intracerebral Hemorrhage
Putaminal hemorrhage (35%)
Caudate Hemorrhage (5%)
Thalamic Hemorrhage (10-15%)
Mesencephalic Hemorrhages (rare)
Pontine Hemorrhage (5%)
Medullary Hemorrhages (rare)
Cerebellar Hemorrhage (5-10%)
Lobar Hemorrhage (25%)

17. IVH
Extension of ICH to IVH is a common feature of caudate and thalamic hemorrhages, and of large putaminal and lobar hemorrhages

18. Lobar Hemorrhages 2nd most common (25%) Nonhypertensive mechanisms:
Young (AVM sympathomimetic agents)
Elderly: cerebral amyloid angiopathy
Usually subcortical frontal vs parietal vs temporal vs occipital
Seizures in up to 28% of patients
Mortality rate is lower than other bleeds, and long term functional outcome maybe better.

19. Radiological Findings
Spot
Sign
shape: spot-like, serpiginous, or linear
location: within the margin of a parenchymal hematoma without connection to an outside vessel
size: >1.5 mm diameter in at least one dimension
density: at least double the density (HU) of the hematoma
number: single or multiple
not caused by hyperdensity in same location on NCCT

20. Radiological Findings
Spot sign: predictor of expansion (PREDICT 2012)
PPV 61%
NPV 78%
Sensitivity 51%
Specificity 85%
Mortality at 3 months was 43·4% (23 of 53) in CTA spot-sign positive versus 19·6% (31 of 158) in CTA spot-sign-negative patients (p=0·002).
Demchuk AM, Prediction of haematoma growth and outcome in patients with intracerebral haemorrhage using the CT-angiography spot sign (PREDICT): a prospective observational study. Lancet Neurol. 2012 Apr;11(4):

21. MRI Brain

22. Management of ICH ABC  ICU admission Early control of elevated BP
Correction of coagulopathy and platelet abnormalities
Identification and control of urgent surgical issues, such as threatening mass effect, intracranial HTN and hydrocephalus
Definitive diagnosis of the cause of the hemorrhage and definitive treatment of the underling cause

23. General Supportive Care
HOB 30°
SO2 ≥ 95%
Glucose control, hypoglycemia should be avoided
T° control ≤ 37.5° C
Pain control, sedation

24. Prognosis and Acute Blood Pressure
↑ Early Neurological Deterioration
↓ Functional Outcome (90 days)
1 month mortality (%)
1 month mortality (%)
MAP (mm Hg)
Fogelhom et al, Stroke, 28: , 1997
Okumura et al, J. Hypertension, 23: , 2005

25. Blood Pressure and Hematoma Evolution
Target max SBP
No Enlargement
Hematoma Enlargement
140 mmHg 16 2 9%
p=0.025
150 mmHg 14 1
160 mmHg 22 8
30%
170 mmHg 5
Ohwaki et al, Stroke, 35: , 2004 25

26. Blood pressure control
Blood pressure on initial arrival to the ER and every 15 minutes until blood pressure has stabilized, showed be corrected within 1 hour of presentation.
Target < 180 mmHg
Close blood pressure monitoring (e.g. every 30 to 60 min) should continue for at least the first 24 to 48 hours.
There is evidence demonstrating it is safe to target systolic blood pressure to less than 160 mmHg.
American and Best practice canadian guidelines for stroke management

27. BP Control Meds
Labetalol: 10-20mg iv over 2 minutes, then 40-80mg iv every 10 min, until BP is controlled. Max dose 300mg per day. Fu heart rate, avoid bradycardia.
Enalopril iv to 1.2 mg every 4-6 hours
Hydralazine iv 10-20mg every 4-6 hours
Nicardipine 5mg/hr titrate by 2.5mg/hr every 5 min to a maximum dose of 15mg/hr
Sodium Nitroprusside: it can increase ICP so to be avoided in neurological emergencies unless everything else fails. Risk of cyanide toxicity can occur with rapid and prolonged infusion. Metabolic acidosis, elevated lactate levels and lactate/pyruvate ratios, and increased mixed venous oxygen content suggest clinical toxicity.

28. Antiepileptics
Clinical seizures should be treated with antiepileptic drugs
Patients with a change in mental status who are found to have electrographic seizures on EEG should be treated with antiepileptic drugs
Prophylactic anticonvulsant medication should not be used
American and Best practice canadian guidelines for stroke management

29. Statins
The SPARCL trial of high-dose atorvastatin in secondary stroke prevention reported an excess of ICH with active treatment compared with placebo (55 versus 33; P
0.02).
2012 meta-analysis of 31 RCT trial on statin and risk of intracerebral hemorrhage, there was no significant increase

30. Reversing coagulopathies
Check Coag and platelets
Correct thrombocytopenia below 100, some references say below 75.
If on ASA or plavix, should be held and transfused platelets
Warfarin should be stopped and treated with prothrombin complex concentrate (PCC) (contains factor 2, 7, 9, 10, protein c and protein s) and Vitamin K 10 mg IV. Fresh-frozen plasma 2-6 units and Vitamin K could be used as alternative if PCC is not available
If on heparin best reversed with protamine sulfate (1.0 to 1.5 mg/1000 U heparin
American and Best practice canadian guidelines for stroke management

32. Reverse anticoagulation
Dabigatran reversal may benefit from PCC but the evidence is weak and efforts should be directed toward improving renal clearance with consideration of hemodialysis in emergency situations.
Rivaroxaban and apixaban are more likely to benefit from PCC administration than dabigatran but are unlikely to benefit from hemodialysis.
F Robert ‘The role of anticoagulats, antiplatelets, and their reversal strategies in the management of intracerebral hemorrhage’ Neurosurg focus 34 (5): 2013

33. Factor V11a Recombinant Factor VIIa
Within 4 hours prevents hematoma growth
Increases the risk of arterial thromboembolic
No clinical benefit for survival or outcome.
It is not recommended for use outside of clinical trials at this time
American and Best practice canadian guidelines for stroke management

34. Hematoma Evolution and rFVIIa
5.8ml
4.5ml
3.3ml
rFVIIa within 4 hours:
Dose dependent attenuation of hematoma expansion
no effect on mRS at 90 days
Mayer et al. NEJM 2005; 352:

35. Treatment of ICHT No Δ in outcome Intubation Hyperventilation Sedation
Steroids: NO role
Osmotic agents
Mannitol
Hypertonic saline
No Δ in outcome

36. Intracranial Pressure control
Elevate the HOB to 30 degrees
Analgesia and sedation, particularly in unstable, intubated patients
ICP monitor should be considered for patients with GCS <8, those with clinical evidence of transtentorial herniation, or those with significant IVH or hydrocephalus.
Osmotic diuretics (eg, mannitol and hypertonic saline solution)
neuromuscular blockade
Goal of maintaining cerebral perfusion pressure (CPP) of 50 to 70 mmHg

37. ICP control
The ICP lowering effect of hyperventilation to a PaCO2 of 25 to 30 mmHg is dramatic and rapid. However, the effect only lasts for minutes to a few hours.

38. ICP control
Glucocorticoids should not generally be used to lower the ICP in patients with ICH. No improvement in outcome
American and Best practice canadian guidelines for stroke management

39. Surgical Indications
Cerebellar bleed: >3cm, and deteriorating, vs brain stem compression, vs hydrocephalus due to ventricular obstruction
Supratentorial ICH evacuation: Controversial
STICH trial: patients assigned to early (within 24hr) surgical hematoma evacuation were slightly more likely to have a favorable outcome at six months compared with initial conservative treatment, but trend did not reach statistical significance.
It should only be considered as a life saving procedure to treat refractory increases in ICP
American and Best practice canadian guidelines for stroke management

40. Surgical Indications
Favoring surgery: obtunded-stupor patients, recent onset of hemorrhage, ongoing clinical deterioration, involvement the nondominant hemisphere, location of the hematoma near the cortical surface.
For patients presenting with lobar clots >30 mL and within 1 cm of the surface evacuation of supratentorial ICH by standard craniotomy might be considered
No clear evidence at present indicates that ultra-early removal of supratentorial ICH improves functional outcome or mortality rate.
American and Best practice canadian guidelines for stroke management

41. Intra-ventricular Hemorrhage
EVD
Intra- ventricular rtpa (CLEAR)

42. Case 55F presented with Headache and LOC

43. PROGNOSIS
Mortality 35-52% in the first 30 days and half of them in the first 2 days

44. Factors Affecting Prognosis
Volume of hemorrhage
Hematoma growth
Early Neurological deterioration within 48hr
Oral Anticoaglants
GCS on presentation
Age
Hemorrhage location
Intraventricular hemorrhage

45. Summary ICH Management
Early control of elevated BP
Correction of coagulopathy and platelet abnormalities
Identification and control of urgent surgical issues, such as threatening mass effect, intracranial HTN and hydrocephalus
Definitive diagnosis of the cause of the hemorrhage and definitive treatment of the underling cause

46. Questions

47. Modified Rankin Scale