2. Dr. Hashemi MD
Hemorrhagic stroke

3. Hemorrhagic stroke

4. Intracerebral Hemorrhage (ICH)

5. What Is ICH?
A hemorrhagic stroke is bleeding (hemorrhage) that suddenly interferes with the brain's function. This bleeding can occur either within the brain or between the brain and the skull.

6. ICH background 10-18% of strokes. Mortality rate : 25% and 60%.
Mortality is strongly dependent on hematoma size and, to a lesser extent, location.
The main cause of ICH is hypertension~ 60-70%
In both hypertensive and nonhypertensive patients, the circadian rhythm of ICH onset, with peaks at 8 AM and 8 PM, coincides with the physiological daily peaks of blood pressure, pointing to the importance of blood pressure rises in the pathogenesis of ICH.

7. Subarachnoid hemorrhage
Bleeding from a damaged blood vessel causes blood to accumulate at the surface of the brain.
As blood flows into the cerebral spinal fluid, it increases pressure on the brain, which causes an immediate headache.
In the days immediately following the bleeding, chemical irritation from clotted blood can cause brain arteries near to the clot to go into spasm. Artery spasm can damage brain tissue.
Most often, a subarachnoid hemorrhage happens because of a saccular aneurysm, but it also can occur because of leakage from an AVM.

8. Ischemic versus hemorrhagic stroke

9. VASCULAR ANATOMY

10. anatomy
Knowledge of cerebrovascular arterial anatomy and the brain regions supplied by the arteries is useful in determining which vessels are involved in acute stroke. Atypical patterns that do not conform to a vascular distribution may indicate another diagnosis, such as venous infarction.
The cerebral hemispheres are supplied by 3 paired major arteries: the anterior, middle, and posterior cerebral arteries. The anterior and middle cerebral arteries are responsible for the anterior circulation and arise from the supraclinoid internal carotid arteries. The posterior cerebral arteries arise from the basilar artery and form the posterior circulation, which also supplies the thalami, brainstem, and cerebellum. The angiograms in the images below demonstrate some portions of the circulation involved in hemorrhagic strokes.

11. Anterior circulation

12. Posterior circulation

13. Territories of the principle cerebral arteries
Posterior circulation
Vertebral
PICA
Medulla, lower cerebellum
Basilar
AICA
Lower and midpons, mid cerebellum
SCA
Upper pons, lower midbrain, upper cerebellum
Posterior cerebral
Medial occipital and temporal cortex and subjacent white matter, posterior corpus callosum, upper midbrain
Thalamoperforate branches
Thalamus
Thalamogeniculate branches
Artery
Territory
Anterior circulation
Internal carotid
Anterior choroidal
Hippocampus, globus pallidus, lower internal capsule
Anterior cerebral
Medial frontal and parietal cortex and subjacent white matter, anterior corpus callosum
Middle cerebral
Lateral frontal, parietal, occipital, and temporal cortex and subjacent white matter
Lenticulostriate branches
Caudate nucleus, putamen, upper internal capsule

14. Distribution of major supratentorial arterial territories

15. Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery illustrates the anterior circulation. The anterior cerebral artery consists of the A1 segment proximal to the anterior communicating artery with the A2 segment distal to it. The middle cerebral artery can be divided into 4 segments: the M1 (horizontal segment) extends to the limen insulae and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches), and M4 (distal cortical branches on the lateral hemispheric convexities)

16. Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery (ACA) and sylvian triangle. The pericallosal artery has been described as arising distal to the anterior communicating artery or distal to the origin of the callosomarginal branch of the ACA. The segmental anatomy of the ACA has been described as follows: (1) the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery, (2) A2 extends to the junction of the rostrum and genu of the corpus callosum, (3) A3 extends into the bend of the genu of the corpus callosum, and (4) A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The sylvian triangle overlies the opercular branches of the middle cerebral artery, with the apex representing the sylvian point.

17. Frontal projection from a right vertebral artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the basilar artery. The posterior inferior cerebellar arteries (PICA) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICA) arise from the proximal basilar artery. The superior cerebellar arteries (SCA) arise distally from the basilar artery before its bifurcation into the posterior cerebral arteries.

18. Diagnosis
Brain imaging is a crucial step in the evaluation of suspected hemorrhagic stroke and must be obtained on an emergent basis.
Brain imaging aids in excluding ischemic stroke, and it may identify complications of hemorrhagic stroke such as intraventricular hemorrhage, brain edema, and hydrocephalus.
Either noncontrast computed tomography (NCCT) scanning or magnetic resonance imaging (MRI) is the modality of choice.

19. Risk factors
The risk of hemorrhagic stroke is increased with the following factors:
Advanced age
Hypertension (up to 60% of cases)
Previous history of stroke
Alcohol abuse
Use of illicit drugs (cocaine, other sympathomimetic drugs)

20. Hypertension
Hypertensive small-vessel disease results from tiny lipohyalinotic aneurysms that subsequently rupture and result in intraparenchymal hemorrhage. Typical locations include the basal ganglia, thalami, cerebellum, and pons.

21. Nonhypertensive Causes of Intracerebral Hemorrhage
Vascular malformations (saccular or mycotic aneurysms, arteriovenous malformations, cavernous angiomas)
Intracranial tumors
Bleeding disorders, anticoagulant and fibrinolytic treatment
Cerebral amyloid angiopathy
Granulomatous angiitis of the central nervous system and other vasculitides, such as polyarteritis nodosa
Sympathomimetic agents (including amphetamine and cocaine)
Hemorrhagic infarction
Trauma

22. Arteriovenous malformations
Numerous genetic causes may predispose to AVMs in the brain, although AVMs are generally sporadic. Hereditary hemorrhagic telangiectasia (HHT), previously known as Osler-Weber-Rendu syndrome, is an autosomal dominant disorder that causes dysplasia of the vasculature.
HHT is most frequently diagnosed when patients present with telangiectasias on the skin and mucosa or with chronic epistaxis from AVMs in the nasal mucosa. Additionally, HHT can result in AVMs in any organ system or vascular bed.

23. Arteriovenous malformations

24. Intracranial tumors

25. Noncontrast CTscan of acute left putaminal intracerebral hemorrhage (CT done 3 hours after symptom onset) with a large amount of surrounding hypodensity edema and mass effect. Biopsy of tissue adjacent to the hemorrhage at the time of surgical drainage revealed typical features of gliobastoma multiform.

26. Amyloidosis
Cerebral amyloidosis affects people who are elderly and may cause up to 10% of intracerebral hemorrhages. Rarely, cerebral amyloid angiopathy can be caused by mutations in the amyloid precursor protein and is inherited in an autosomal dominant fashion.
80-year-old woman with numerous punctate foci of hypointensity (black dots) on MRI gradient-echo (GRE) sequence (left), suggesting multiple lobar microbleeds caused by cerebral amyloid angiopathy.

27. Coagulopathies
Coagulopathies may be acquired or inherited. Liver disease can result in a bleeding diathesis. Inherited disorders of coagulation such as factor VII, VIII, IX, X, and XIII deficiency can predispose to excessive bleeding, and intracranial hemorrhage has been seen in all of these disorders.

28. Hemorrhagic transformation of ischemic stroke
Hemorrhagic transformation represents the conversion of a bland infarction into an area of hemorrhage (20-40% of patients with ischemic infarction).
Mechanisms:
Reperfusion of ischemically injured tissue, either from recanalization of an occluded vessel or from collateral blood supply to the ischemic territory
Disruption of the blood-brain barrier

29. Hemorrhagic transformation of ischemic stroke
Hemorrhagic transformation of an ischemic infarct occurs within 2-14 days postictus, usually within the first week. It is more commonly seen following cardioembolic strokes and is more likely with larger infarct size.
Hemorrhagic transformation is also more likely following administration of tissue plasminogen activator (tPA) in patients whose noncontrast computed tomography (CT) scans demonstrate areas of hypodensity.

30. Noncontrast computed tomography scan (left) obtained in a 75-year-old man who was admitted for stroke demonstrates a large right middle cerebral artery distribution infarction with linear areas of developing hemorrhage. These become more confluent on day 2 of hospitalization (middle image), with increased mass effect and midline shift. There is massive hemorrhagic transformation by day 6 (right), with increased leftward midline shift and subfalcine herniation. Obstructive hydrocephalus is also noted, with dilatation of the lateral ventricles, likely due to compression of the foramen of Monroe. Intraventricular hemorrhage is also noted layering in the left occipital horn.

31. CLINICAL FEATURES
The clinical presentation of ICH has two main elements: symptoms that reflect the effects of intracranial hypertension and those that are specific for the location of the hematoma.
The general clinical manifestations of ICH related to increased intracranial pressure (lCP) (headache, vomiting, and depressed level of consciousness) vary in their frequency at onset of ICH.
A characteristic of ICH at presentation is the frequent progression of the focal neurological deficits over periods of hours . This early course reflects the progressive enlargement of the hematoma.
Seizures at the time of presentation of ICH are rare, except for lobar ICH, in which they occur in as many as 28% of patients.

32. Symptoms of a hemorrhagic stroke
ICH —Symptoms worsen over a period of 30 to 90 minutes. Symptoms can include:
Sudden weakness
Paralysis or numbness in any part of the body
Inability to speak
Inability to control eye movements correctly
Vomiting
Difficulty walking
Irregular breathing
Stupor
Coma
SAH — When caused by a ruptured aneurysm, symptoms can include:
A very severe headache that starts suddenly (thunderclap)
Loss of consciousness
Nausea and vomiting
Inability to look at bright light
Stiff neck
Dizziness
Confusion
Seizure

33. Patients with hemorrhagic stroke present with focal neurologic deficits similar to those of ischemic stroke but tend to be more ill than are patients with ischemic stroke. However, though patients with intracerebral bleeds are more likely to have headache, altered mental status, seizures, nausea and vomiting, and/or marked hypertension, none of these findings reliably distinguishes between hemorrhagic and ischemic stroke.

34. Differences between ICH and hemorrhagic stroke
Hemorrhagic infarct
Clinical
Onset
Raised ICP
Embolic source
Sudden, with progression
Prominent No
Maximal from onset
Absent
Yes
CT scan
High attenuation
Mass effect
Location
Distribution
Enhancement
Ventricular blood
Dense, homogeneous
Subcortical, deep
Beyond arterial territory
Ring- type
Spotted, mottled
Absent or mild
Cortex > subcortical WM
Along branch distribution
Gyral- type
MRI
Hypo intense blood
Hyper intense edema
Homogeneous
Thin peripheral halo
Patchy, mottled
Extensive, territorial
Angiography
Mass effect, avascular
Branch occlusion

35. Putaminal Hemorrhage
A wide spectrum of clinical severity relates to hematoma size, from minimally symptomatic cases presenting with pure motor hemiparesis, or slight hemiparesis and dysarthria, to the extreme of coma with decerebrate rigidity in instances of massive hematomas with rupture into the ventricles.
Modern CT series of putaminal hemorrhage document a mortality rate of 37%.
Ventricular extension carries an invariably poor prognosis in putaminal hemorrhage.

36. Putaminal Hemorrhage
The most common variety of ICH, putaminal hemorrhage, represents approximately 35% of the cases.

37. Lobar hemorrhage
Nonhypertensive mechanisms, including AVMs, sympathomimetic agents (in young patients), and CAA (in elderly patients) are frequent causes.
The clinical features reflect location : hemiparesis of upper limb predominance in frontal hematomas, sensorimotor deficit and hemianopia in parietal hemorrhages, fluent aphasia with relatively preserved repetition in dominant temporal hematomas, and homonymous hemianopia in occipital lobe hemorrhages.

38. Lobar Hemorrhage
Lobar hemorrhage is second to putaminal hemorrhage in frequency, accounting for approximately 25% of the cases.

39. Thalamic Hemorrhage 10% to 15% of the cases of ICH
Its onset tends to be more abrupt than that of putaminal hemorrhage, and slow progression of deficits is less common.
Early communication of the medially located hematoma with the third ventricle
The prognosis in thalamic hemorrhage relates to hematoma size and level of consciousness at presentation, presence of hydrocephalus, a complication that occasionally occurs abruptly, as a result of aqueductal obstruction by an intraventricular clot.
ventriculostomy may result in a reversal of symptoms.

40. Right thalamic hemorrhage with ventricular extention

41. Cerebellar Hemorrhage
5% to 10% of the cases
Its clinical presentation is characteristic, with abrupt onset of vertigo, headache, vomiting, and inability to stand and walk, with absence of hemiparesis or hemiplegia.
Triad of appendicular ataxia, horizontal gaze palsy, and peripheral facial palsy, all ipsilateral to the hemorrhage.
There is a notorious tendency for abrupt deterioration to coma and death after a period of clinical stability under hospital observation.

42. Large midline and left sided hemispheric cerebellar hemorrhage

43. GENERAL MANAGEMENT OF STROKE
Control of HTN
Surgical treatment
Nutritional status and fluid requirements
Prevention of hyperthermia
Prevention of pulmonary complications
DVT prophylaxis
Pressure sores
Rehabilitation
Treatment of depression

44. Prognosis
About 30% to 60% of people with an intracerebral hemorrhage die. In those who survive long enough to reach an emergency room, bleeding usually has stopped by the time they are seen by a doctor. Many people with ruptured aneurysms or subarachnoid hemorrhages also do not survive long enough to reach a hospital. Of those who do, about 50% die within the first month of treatment. However, in people with subarachnoid hemorrhages resulting from arteriovenous malformations, the risk of death is only about 15%.

45. Prognosis
Among the 25% of people who survive an intracerebral hemorrhage, many experience a major improvement in their symptoms as their bodies naturally and gradually reabsorb the clotted blood within the brain. Among those who survive a bleeding aneurysm, about 50% suffer long-term neurological problems. People who bleed from an aneurysm or AVM and do not have this problem treated are at risk for having a repeat bleeding event. If the blood vessel is not repaired or removed, one out of 5 survivors of subarachnoid hemorrhage have bleeding again within 14 days if the abnormal blood vessel was not repaired or removed. 50% who do not have surgical treatment have a repeat bleed within 6 months. When surgery is used to clip a bleeding aneurysm, there is a good chance of success, but there is also a 5% risk of death or long-term disability after surgery.

46. Thank you