1. INTRACRANIAL HAEMORRHAGEBY
DR DENNIS PRABHU DAYAL

2. INTRACEREBRAL HAEMORRHAGE (10%)
SUBARACHNOID HAEMORRHAGE (SAH) (5%)

3. INTRACEREBRAL HAEMORRHAGE
AETIOLOGY AND PATHOLOGY
CLINICAL PRESENTATION
INVESTIGATIONS
MANAGEMENT

4. AETIOLOGY AND PATHOLOGY
CHRONIC SYSTEMIC HYPERTENSION
(Degeneration of vessel walls or microaneurysms by lipohyalinosis)
MALIGNANT TUMOUR NEOVASCULATURE
VASCULITIS
MYCOTIC ANEURYSMS
AMYLOIDOSIS
SARCOIDOSIS
MALIGNANT HYPERTENSION
PRIMARY HAEMORRHAGIC DISORDERS
OVER ANTICOAGULATION
OCCASIONALLY CEREBRAL ANEURYSMS OR AVM`S
(WITHOUT SAH)
VASCULAR ABNORMALITIES (YOUNG PATIENTS)
COCAINE ABUSE
(SYMPATHOMIMETIC ACTIVITY)

5. COMMON SITES OF HAEMORRHAGE
(The rupture of microaneurysms tend to occur at the bifurcation of small perforating arteries)
PUTAMEN 55%
CEREBRAL CORTEX 15%
THALAMUS 10%
PONS 10%
CEREBELUM 10%
CORTICAL HAEMORRHAGES TEND TO BE LARGER THAN PONTINE BLEEDS
BUT LATTER MORE FATAL

6. CLINICAL PRESENTATION
NO PRODROMAL SYMPTOMS
FOCAL NEUROLOGY (SUDDEN ONSET)
DEPRESSED CONSCIOUS LEVELS (SUDDEN ONSET)
(20% patient has GCS drop of 2 or more points between initial onset of symptoms and arrival to emergency department )
HEADACHE / NECK STIFFNESS IN CONSCIOUS PATIENT
(Occurs if there is subarachnoid extension by haemorrhage into the ventricles)
PROGRESSIVE FALL OF GCS
(Secondary hydrocephalus due to intraventricular extension of bleed resulting in)
OCULAR PALSIES (SUNSET EYES)
Focal neurology will depend on the area of brain involved. All symptoms relate to tissue destruction, compression, raised ICP which if progressive will result in Braistem ischaemia, and death.

7. INVESTIGATIONS
(Generally similar to ishaemic stroke)
HISTORY
EXAMINATION
BLOOD TESTS
FULL BLOOD COUNT
FULL COAGULATION SCREEN
(PATIENT ON WARFARIN /ACITROM FOR AF / VALVE REPLACEMENT ETC)
ECG
(AF, ARRYHMIAS)
ECHOCARDIOGRAPHY

8. CT/MRI
SCAN TO BE PERFORMED AT THE EARLIEST
(Early deterioration due to active bleed. Repeat CT after 3 hours reveals significant enlargement)
CT/MRI ANGIOGRAPHY/MRI VENOGRAPHY
(Arteriovenous Malformations /Aneurysm / Tumour Neovasculature)
LUMBAR PUNCTURE
( If not contraindicated,to exclude infection if mycotic aneurysm is suspected)

9. MANAGEMENT
SIMILAR TO ISHAEMIC STROKE
REVERSAL OF ANTICOAGULATION THERAPY ON URGENT BASIS
(VIT K / FRESH FROZEN PLASMA/ CRYOPRECIPITATE)
EMERGENCY DECOMPRESSIVE SURGERY ( if indicated)
(prothrombin complex concentrate used to correct warfarin induced coagulopathy)
EXTRAVENTRICULAR DRAIN (EVD)
(secondary hydrocephalus)
SURGICAL DECOMPRESSION
(Cerebellar ICH > 3cms in diameter/ brainstem compression / secondary hydrocephalus)

10. HYPERTENSION MANAGEMENT
HIGH BP (provoke bleeding) VS LOW BP (ischaemia) DILEMMA
CEREBRAL PERFUSSION PRESSURE (CPP) - >60 mmHg
(CPP = MAP - ICP)
Normal ICP – 7 to 12 mm Hg
>20 mm Hg (requires active management )
If no evidence of increase ICP than MAP to be reduced to 110 mm Hg
Or a target BP of 160/90 mmHg
STEROIDS / HYPERVENTILATION
(no role as it has detrimental effects on cerebral blood flow in other areas of the brain)

11. SUBARACHNOID HAEMORRHAGE (SAH)
SAH refers to bleeding that occurs principally into the subarachoind space and not into the brain parenchyma.
SAH PREDISPOSITION IS FOUND IN THE FOLLOWING:
YOUNGER POPULATION PEAKING 6TH DECADE
FEMALE TO MALE RATIO OF 1.24:1
AFRO –CARIBBEAN ANCESTRY
(twice the risk than whites )
FAMILY HISTORY
(5% TO 20% PATIENTS )

12. MODIFIABLE RISK FATORS
SMOKING
HEAVY DRINKING
COCAINE ABUSE
HYPERTENSION

13. SUBARACHNOID HAEMORRHAGE (SAH)
AETIOLOGY AND PATHOLOGY
CLINICAL MANIFESTATION
COMPLICATIONS
INVESTIGATIONS
MANAGEMENT

14. AETIOLOGY AND PATHOLOGY
RUPTURED (BERRY) SACCULAR ANEURYSM (85%)
PERIMESENCEPHALIC H`GH (10%)
RARE CAUSES
ARTERIAL DISSECTION
CEREBRAL OR DURAL AVM
MYCOTIC ANEURYSM
PITUITARY APOPLEXY
VASCULAR LESIONS
COCAINE ABUSE

15. CLINICAL PRESENTATION
CLASSICAL THUNDERCLAP HEADACHE
DEPRESSED CONSCIOUSNESS FOR LESS THAN HOUR (50%)
FOCAL NEUROLOGY (30%)
MENINGISM
(neck stiffness, photophobia, vomiting, positive kernig sign)

17. COMPLICATIONS
REBLEEDING
ACUTE HYDROCEPHALUS
DELAYED CEREBRAL ISCHAEMIA (DCI)
PARENCHYMAL HAEMATOMA
SEIZURES
MEDICAL COMPLICATIONS

18. REBLEEDING
(Depends on site, presence of clot,degree of vasospasm,age, sex,)
Tranexamic acid (antifibrinolytic)
ACUTE HYDROCEPHALUS
Occurs within 24 hours
Drop in GCS
Sluggish pupillary responses
Bilateral downward deviation of the eyes (sunset eyes)
CT to be repeated if sunset sign present and if large intraventricular bleed noted then a ventricular drain may be inserted.

19. DELAYED CEREBRAL ISCHAEMIA (DCI)
VASOSPASM (70%)
Not all patients have symptoms
DCI refers to Focal neurological deficit, drop in GCS by 2, and or cerebral infarction occurs 4 to 12 days post SAH unrelated to aneurysm treatment or other causes of neurological deficit such as hydrocephalus, cerebral odema, or metabolic disorder.
TRANSCRANIAL DOPPLER (VELOCITY > 120 cm/s) indicates vasospasm
Not all patients with high velocities have symptoms

20. Depressed level of conscious, evidence of DCI clinically, on TCD or angiogram, and in absence of rebleed, hydrocephalus, or metabolic disturbances.
VASOSPASM DURING COILING OR ANGIOGRAPHY
Papaverine or nimodipine (intravascular vasodilators)
CTA (imaging choice for vasospasm unless intracerebral therapy is planned)
DIGITAL SUBTRACTION ANGIOGRAPHY (INTRACEREBRAL THERAPY)

21. PARENCHYMAL HAEMATOMA
occurs in 30% SAH following aneurysm rupture and has a much worst prognosis than SAH alone.
MEDICAL COMPLICATIONS
The mortality due to medical complication, almost same as that due to combined effects of initial bleed, rebleeds, and delayed cerebral ischaemia

22. MEDICAL COMPLICATIONS

23. INVESTIGATIONS
CT/MRI SCAN
LUMBAR PUNCTURE (if no contraindicated)
When high suspicion of SAH despite negative CT
To detect xanthochromia
ANGIOGRAPHY
Angiography via arterial catheterization still most commonly used investigation for localizing the aneurysm or other vascular abnormalities prior to surgery. Generally performed on patient who remain or become conscious after SAH. Risk of aneurysm rupture present.
CT/MRA/
DSA – DIAGNOSTIC TOOL OF CHOICE WHERE CTA INCONCLUSIVE
ICP MONITORING
(Limited use in SAH)
Hydrocephalus Or Parenchymal Haematoma Increases ICP
Early Detecting Of Increased Icp Indication For Drainage Or Decompressive Surgery
TRANSCRANIAL DOPPLER
DETECTING VASOSPASM OR IMPAIRED AUTOREGULATION

24. MANAGEMENT
Initial management of SAH influenced by :
GRADING OF SAH
MEDICAL CO MORBIDITIES OR COMPLICATIONS
LOW GCS – EARLY INTUBATION AND VENTILATION
NORMAL GCS – NEUROLOGICAL OBSERVATION, ANALGESIA FOR HEADACHE, AND BEDREST
OTHER MEASURES
STRESS ULCER PROPHYLAXIS
DEEP VEIN THROMBOSIS
(COMPRESSION STOCKINGS OR BOOTS)
SEIZURE CONTROL
(WITH PHENYTOIN AND BARBITURATES )

25. HYPONATRAEMIA
(Adequate fluid therapy with normal saline is required with electrolyte levels maintained in normal range)
BLOOD PRESSURE CONTROL
IDEAL SYSTOLIC PRESSURE - <160 mmHg
Mean arterial pressure - <110 mmHg
Beta adrenergic blockers or calcium antagonists

26. DELAYED CEREBRAL ISCHAEMIA (DCI)
Vasospasm Prevention
Oral Nimodipine at 60 mg given 4hrly for 21 days
Nicardipine
AT877 (experimental drug)
STATINS
HYPOMAGNESAEMIA SHOULD BR PREVENTED

27. TREATMENT of SAH
Low cerebral blood flow is known to worsen outcome and this resulted in development of prophylactic - TRIPLE H THERAPY - HYPERTENSIVE HYPERVOLAEMIC HAEMODILUTION
HYPERTENSIVE HYPERVOLAEMIC HAEMODILUTION X 21 DAYS
Therapy involves use of fluid loading to achieve haemodilution and vasopressor therapy to increase cerebral blood flow, combined with surgery within 24 hours if possible.
This therapy is continued for 21 days and patients remain neurologically stable in the absence of vasospasm.
The Focus now is normovolemia and if indicated hypertension is induce with vasopressors (if BP not already raised.)
If DCI symptoms not reversing with induced hypertension, cerebral angioplasty or direct intracerebral vasodilators to be considered after excluding rebleeding, hydrocephalus and metabolic disturbances.
Poor grade SAH patients who are sedated or have low GCS are clinically difficult to assess:
Multimodal monitoring is recommended to look for deterioration.

28. SEIZURES
26 % SAH patient have seizures.
Prophylactic anticonvulsants not recommended
Indicators for development of seizures:
Increased cerebral bleed
Poor grade SAH
Rebleeding Infarction
MCA aneurysm
Patient who is poor grade SAH and deteriorating neurologically from an unknown cause should have continuous EEG monitoring.

29. SURGERY
Clipping of aneurysm is the surgical treatment of choice, with wrapping, proximal ligation or bypass grafting being used if the aneurysm is inaccessible to Yasargil clipping.
Timing of surgery:
Early surgery within 3 days of bleed beneficial but technically difficult due to friability of associated tissues.
Delayed surgery 10 – 12 days post bleed gives better operating condition but risk of rebleed increases
AHA recommendations is to secure the aneurysm as early as possible.
Large ICH with SAH with MCA aneurysms should be strongly considered for surgery.
Hypotension and hyperglycemia to be avoided.
No good level one evidence for induced hypertension or hypothermia during clipping but can be considered in certain patients

30. ENDOVASCULAR COILING
Platinum detachable microcoils used in endovascular embolization of aneurysms or AVMs by interventional radiology.
The International Subarachnoid Aneurysm Trial (ISAT) favours Coiling rather than open surgical technique in ruptured intracranial aneurysm.
Complications of coiling include:
Rupture of aneurysm or adjacent vessel occlusion causing ischaemia
Rupture during catheter placement, coil embolization, and vasospasm.
If patient are elderly (>70 years) or have poor grade SAH than coiling is preferred.
Stenting of acute SAH carries worst prognosis

31. NEUROPROTECTIVE THERAPY
A great deal of research has been done on cellular and biochemical responses to brain injury.
The 21 amino steroid - TIRILAZAD, NICARAVEN AND EBSELEN all free radical scavengers have been widely investigated. None has been shown to improve outcome consistently in all types of patients with SAH.

32. THERAPY FOR MEDICAL COMPLICATIONS
This is obviously specific to the type of medical
complication.
Pneumonia, ARDS, arrthymias, neurogenic pulmonary odema, cardiogenic shock, hypo/hypernatremia, blood glucose levels, fever and shivering, deep vein thrombosis, and anaemia.
All the above conditions require specific medical management and other supportive measures at a tertiary level centre.

33. THANK YOU