Hemorrhagic Stroke: SAH & ICH

Introduction

Hemorrhagic stroke occurs due to mechanical compression of brain tissue and local toxicity from blood breakdown products.
Hemorrhagic stroke can occur within the brain parenchyma (ie, intracerebral) or subarachnoid space (ie, between the arachnoid and pia mater).
Incidence: Intracerebral hemorrhage is more common than SAH, accounting for 10% to 15% of all strokes. SAH accounts for around 5% of all strokes. 

What is Risk factors for Hemorrhagic stroke?

1. Chronic hypertension is the strongest risk factor for stroke and is present in most stroke patients. Many patients with ICH are dramatically hypertensive on presentation; however, acute elevations of ICP from the hemorrhage may actually precipitate HTN (part of Cushing’s triad)
2. Advanced age and heavy alcohol consumption increase the risk of intraparenchymal hemorrhage. 
3. Cigarette smoking: increases the risk of SAH and ischemic infarction but probably does not increase the risk of ICH
4. Cocaine is one of the main causes of stroke in young patients. ICH, ischemic stroke, and SAH are all associated with cocaine use.

What is Cushing’s triad? 

The Cushing reflex is a physiological nervous system response to acute elevations of intracranial pressure (ICP), resulting in the Cushing triad:

1. Widened pulse pressure (increasing systolic, decreasing diastolic) 
2. Bradycardia
3. Irregular respirations.

Causes of Hemorrhagic stroke

Three lesions account for the majority of intracranial and intracerebral hemorrhage: “berry” or saccular aneursyms; microaneursyms of Charcot and Bouchard; and cerebral amyloid angiopathy (CAA).

1. Rupture of a “berry” aneurysm is the usual cause of subarachnoid hemorrhage. Polycystic kidney disease and coarctation of the aorta are predisposing diseases.
2. The microaneursyms of Charcot and Bouchard are important causes of intracerebral hemorrhage. These tiny aneurysms originate from very small arteries most commonly in the region of the basal ganglia (lenticulostriate arteries) and are associated with chronic hypertension
3. Cerebral amyloid angiopathy (CAA) is an important cause of intracerebral hemorrhage in the elderly. It is the usual cause in patients who have no history of hypertension.

Clinical features of Hemorrhagic stroke

• Hemorrhagic stroke tends to be more variable in presentation because the area of injury often crosses multiple vascular territories. Unlike ischemic infarct: smooth progressive onset over minutes to hours, often with severe headache, vomiting, and alterations in level of consciousness
• The patient usually presents with severe headache, vomiting, convulsion, followed by unconsciousness
• Drop Attacks: Although often confused with syncope, drop attacks classically refer to an abrupt fall to the ground without loss of consciousness. They occur predominantly in the elderly and reflect vertebrobasilar insufficiency, frequently the consequence of cervical spondylosis.

Hemorrhagic stroke is associated with higher morbidity and mortality in the acute poststroke period compared with ischemic stroke with a 30-day mortality rate approaching 50% (5 times greater than ischemic stroke)

Subarachnoid Hemorrhage (SAH)

Definition and overview 

Subarachnoid Hemorrhage: it's blood in the subarachnoid space (i.e., between the arachnoid membrane and the pia mater). 
Subarachnoid Hemorrhage may be posttraumatic or spontaneous. Most cases of spontaneous SAH are due to aneurysmal rupture. 

Trauma is also a common cause—most cases of traumatic SAH are mild and do not require specific treatment.

Ruptured saccular (berry) aneurysms

Ruptured saccular (berry) aneurysms are the most common cause of SAH—has higher morbidity and mortality than other causes. 

• Mortality rate can be as high as 40% to 50% at 30 days. Death—25% to 50% of patients die with the first rupture. Those who survive will recover consciousness within minutes.
• Peak age for aneurysmal SAH is 55–60 years, ≈ 20% of cases occur between ages 15–45 yrs
• Locations—Saccular (berry) aneurysms occur at bifurcations of arteries of the circle of Willis.

Common Sites of SAH 

1. Junction of anterior communicating artery with anterior cerebral artery 
2. Junction of posterior communicating artery with the internal carotid artery
3. Bifurcation of the MCA

Features of SAH 

Subarachnoid hemorrhage is associated with severe (“thunderclap”) headache, nuchal rigidity, and, frequently, reduced level of consciousness.

• Before the major bleeding event, some patients with SAH experience a sentinel headache, which is described as sudden in onset and unusually severe. 
• The sentinel headache typically occurs within 2 weeks before SAH, with a peak incidence within 1 day.
• Seizures may occur in up to 20% of patients after SAH, most commonly in the first 24 hours, and are associated with ICH, HTN, and aneurysm location (MCA)

How SAH is diagnosed?  

1) Noncontrast CT scan—identifies the majority of subarachnoid hemorrhages (SAHs). However, CT scan may be negative in up to 10% of cases.
2) Perform lumbar puncture (LP) if the CT scan is unrevealing or negative and clinical suspicion is high. LP is diagnostic. 

• Blood in the CSF is a hallmark of SAH (Be certain that it is not blood from a traumatic spinal tap.) 
• Xanthochromia (yellow color of the CSF) is the gold standard for diagnosis of SAH. Xanthochromia results from RBC lysis. Xanthochromia implies that blood has been in CSF for several hours and that it is not due to a traumatic tap.

3) Once SAH is diagnosed, order a cerebral angiogram. It is the definitive study for detecting the site of bleeding (for surgical clipping).

Treatment of SAH

1) Surgical—consult neurosurgery. Surgically clip the aneurysm to prevent rebleeding. Recent studies have shown endovascular coiling to have better outcomes than surgical clipping.

2) Medical—therapy reduces the risks of rebleeding and cerebral vasospasm. 

1. Bed rest in a quiet, dark room. Stool softeners to avoid straining (increases ICP and risk of rerupture). 
2. Analgesia for headache (acetaminophen). IV fluids for hydration. 
3. Control of HTN—lower the BP gradually because the elevation in BP may be a compensation for the decrease in cerebral perfusion pressure (secondary to increased ICP or cerebral arterial narrowing). 
4. Calcium channel blocker (nimodipine) for vasospasm—lowers the incidence of cerebral infarction by one-third.

Intracerebral Hemorrhage (ICH)

Intracerebral hemorrhage (ICH) is a hemorrhage within the brain parenchyma. It's the second most common form of stroke (15–30% of strokes) and is associated with a 50% case fatality rate. 
The incidence increases significantly after age 55 years and doubles with each decade of age until age > 80 yrs where incidence is 25 times that during previous decade.

Causes of Intracerebral hemorrhage (ICH)

Hypertension, trauma and cerebral amyloid angiopathy cause the majority of intraparenchymal hemorrhage.

1) Hypertension HTN (particularly a sudden increase in BP) is the most common cause (50% to 60% of cases)

• Acute hypertension (HTN): as may occur in eclampsia or with certain drugs, e.g. cocain
• Chronic HTN: possibly causes degenerative changes within blood vessels

2) Microaneurysms of Charcot-Bouchard: Occur primarily at bifurcation of small perforating branches of lateral lenticulostriate arteries in basal ganglia (found in 46% of hypertensive patients over age 66). 

3) Cerebral amyloid angiopathy (Congophilic angiopathy): Pathologic deposition of beta amyloid protein within the media of small meningeal and cortical vessels (especially those in white matter) without evidence of systemic amyloidosis.

• CAA should be suspected in patients with recurrent hemorrhages (uncommon with “hypertensive hemorrhages”) that are lobar in location.
• Patients with CAA may present with a TIA-like prodrome
• MRI may identify petechial hemorrhages (microbleeds) or hemosiderin deposits from small cortical hemorrhages.

4) Hemorrhagic brain tumors: Malignant tumors most commonly associated with ICH: Glioblastoma, Lymphoma, Metastatic tumors (Melanoma, Choriocarcinoma).

5) Anticoagulation preceding ICH: 10% of patients on warfarin (Coumadin®) develop a significant bleeding complication per year (not all are intracranial), including ICH (65% mortality in this group). 

• The risk of hemorrhagic complications was increased with the length and also the variability of the PT, and during the first three months of anticoagulation.
• Patients with cerebral amyloid angiopathy (CAA) are also at increased risk of ICH following administration of antiplatelet drugs or anticoagulants.

6) Trauma: Approximately one-half of patients with traumatic brain injury will develop some type of intracranial hemorrhage

Features of ICH

• Hemorrhage presents as abrupt onset of focal neurologic deficit that worsens steadily over 30 to 90 minutes with a diminishing level of consciousness & signs of raised ICP (headache/vomiting). Seizures are uncommon.
• H/A may not be more prevalent than in embolic stroke, but it is often a first and prominent symptom.

Intracerebral hemorrhages almost always occur in awake state.

Pupillary findings in ICH and corresponding level of involvement: 

1. Pinpoint pupils—pons 
2. Poorly reactive pupils—thalamus 
3. Dilated pupils—putamen

Location of the lesions

The most common sites of hypertensive intraparenchymal hemorrhage are basal ganglia (esp. putamen), thalamus, cerebellum and pons.

1) Putaminal hemorrhage (The MC site for ICH): In putaminal hypertensive hemorrhage, contralateral hemiparesis is the sentinel sign. Eyes deviate away from the side of hemiparesis. Papilledema and subhyaloid preretinal hemorrhage are rare.
Contralateral hemiparesis, may progress to hemiplegia or even coma or death.

2) Thalamic hemorrhage: Classically, contralateral hemisensory loss. Also hemiparesis when the internal capsule is involved. 

• Thalamic hemorrhages may extend inferiorly into upper midbrain and cause deviation of eyes downward and inward.
• Prominent sensory deficit involving all modalities is usually present.
• Hydrocephalus may occur from compression of CSF pathways.
• In patients, when hemorrhage > 3.3cm on CT, all died. Smaller hematomas usually caused permanent disability.

3) Pontine hemorrhages: In pontine hemorrhages, there is impairment of reflex horizontal eye movements evoked by head turning (doll’s head or oculocephalic maneuver).

• In pontine hemorrhages, deep coma with quadriplegia usually occurs over a few minutes with prominent decerebrate rigidity.

4) Cerebellar hemorrhage: 

1. Symptoms of increased ICP: due to hydrocephalus
2. Direct compression of brainstem may produce: Facial palsy: due to pressure on the facial colliculus 
3. These patients classically become comatose without first having hemiparesis, unlike many supratentorial etiologies

Acute cerebellar hemorrhage is a medical emergency; prompt recognition followed by surgical evacuation of the hematoma is lifesaving

Lobar Hemorrhage:

• Clinical syndromes associated with ICH in each of the cerebral lobes. 
• Accounts for 10–32% of nontraumatic ICHs.
• Lobar hemorrhages are more likely to be associated with structural abnormalities than deep hemorrhages.
• They may also be more common in patients with high alcohol consumption.
• TIA-like symptoms may precede lobar hemorrhages in patients with CAA; Unlike typical TIAs, these usually consist of numbness, tingling, or weakness (corresponding to the area where the hemorrhage will subsequently occur)
  
• Lobar hemorrhages may also have a more benign outcome than ganglionic-thalamic hemorrhages.

Causes of Lobar Hemorrhage:

1. Cerebral amyloid angiopathy: the most common cause of lobar ICH in elderly normotensive patients
2. Hemorrhagic transformation of an ischemic infarct
3. Hemorrhagic tumor: Multiple lobar hemorrhages may occur with metastases.
4. Cerebrovascular malformation (especially AVM)

Management of ICH

NB: Intracerebral hemorrhage typically appears as a round or oval hyperattenuating lesion on noncontrast CT imaging
 
1) Admission to the ICU 
2) ABC’s (airway, breathing, and circulation)—airway management is important due to altered mental status and decreased respiratory drive. Patients often require intubation.
3) BP reduction: Elevated BP increases ICP and can cause further bleeding. However, hypotension can lower cerebral blood flow, worsening the neurologic deficits. Therefore, BP reduction must be gradual. 

• Treatment is indicated if systolic BP is >180 or the MAP is >130. 
• Common IV agents used include nicardipine, labetalol, nitroprusside, and others.

4) Initial management of elevated ICP includes:

1. Elevating the head of the bed to 30 degrees and appropriate sedation and pain control.
2. Mannitol (osmotic agent) is often used to lower ICP; other options include hyperventilation, barbiturates, neuromuscular blockade, and CSF drainage.

5) If the patient is on anticoagulation or an antiplatelet agent, reversal agents (e.g., vitamin K for warfarin, protamine sulfate for heparin, prothrombin complex concentrate for warfarin and the newer oral anticoagulants, etc.).
6) Rapid surgical evacuation of cerebellar hematomas can be lifesaving. However, surgery is not helpful in most cases of ICH.

Use of steroids is harmful and is not recommended.

Delayed deterioration:

Deterioration after the initial hemorrhage is usually due to any combination of the following: 

1. Rebleeding: Rebleeding (more so in basal ganglion hemorrhages than in lobar hemorrhages)
2. Edema: Edema and ischemic necrosis around the hemorrhage may cause delayed deterioration.
3. Hydrocephalus, Seizures, Increased ICP