Stroke Prognosis & Intracerebral Hemorrhage

• The material discusses stroke prognosis, intracerebral hemorrhage, hypertensive hemorrhage, and related topics.

Prognosis

• Stroke outcome is influenced by the severity of the neurological deficit, patient age, and the cause of the stroke.
• About half of stroke survivors go directly home from the hospital, while the rest need inpatient rehabilitation.
• Roughly 50% of patients return to work within 6-12 months of having a stroke.
• Post-stroke mortality is about 10% at 30 days, 20% at 1 year, and 40% at 5 years.

Intracerebral Hemorrhage

• Intracerebral hemorrhage is bleeding in the brain parenchyma, unlike bleeding in the epidural, subdural, or subarachnoid spaces.
• It usually presents as a focal stroke and is hard to distinguish from ischemic stroke without imaging.
• Epidural, subdural, and subarachnoid hemorrhages cause headache and altered consciousness, while focal signs are not very obvious.
• Imaging studies are essential for definitively diagnosing these hemorrhages.
• Cerebral macrobleeds are macroscopic, symptomatic hemorrhages and often caused by head trauma or chronic hypertension.
• Cerebral microbleeds are small (1-10 mm), reflect small vessel disease and are usually found via imaging studies.
• Hypertension is associated with microbleeds in the deep subcortical gray matter and brainstem.
• Cerebral amyloid angiopathy tends to cause lobar microbleeds at the cortical gray matter-white matter junction.
• Microbleeds can also be caused by CADASIL, moyamoya, and infective endocarditis, fat embolism and malaria.
• Microbleeds correlate to cognitive function problems and risk of large intracerebral bleeds.
• Nonlobar microbleeds are predictive of ischemic stroke.
• Treatment of microbleeds focuses on controlling hypertension and their presence does not mean antiplatelet agents, anticoagulants, thrombolytics, or statins can't be used for concurrent ischemic cerebrovascular disease.

Hypertensive Hemorrhage

• Intracerebral hemorrhage causes about 10% of strokes.
• Hypertension is the most common cause of nontraumatic hemorrhage.

Pathophysiology of Chronic Hypertension

• Chronic hypertension changes the walls of small cerebral arteries in the subcortical white matter, basal ganglia, thalamus, pons, and cerebellum.
• These changes include lipohyalinosis and fibrinoid necrosis.
• This can cause ischemic stroke and lead to miliary aneurysms which predispose hemorrhage.

Acute Hypertension

• The role of acute elevation of blood pressure in intracerebral hemorrhage is uncertain.
• Most patients are hypertensive after intracerebral hemorrhage, but this may be because of baseline chronic hypertension and the vasopressor response to increased intracranial pressure (Cushing reflex).
• Some patients lack history of hypertension, suggesting that acute hypertension could be a precipitant, triggered by sympathomimetic drugs like amphetamine or cocaine.

Hematoma Effects

• Hypertensive hemorrhage causes tissue injury from both destruction and compression.
• Breakdown products of extravasated blood can cause inflammation and secondary injury.
• Perihematoma edema is correlated to hematoma size and predicts a poor outcome.
• Increased intracranial pressure from the rupture can lead to brain herniation and even death.

Hydrocephalus

• Hydrocephalus may be due to hematomal compression of the ventricular system or obstruction by intraventricular or subarachnoid blood.
• This is especially common after cerebellar hemorrhage.

Rebleeding

• Occurs in up to 15% of cases and is associated with clinical worsening.

Clinical Findings

• Hypertensive hemorrhage occurs without warning, often when awake, with headache in about 50% of cases, and possibly vomiting.
• Elevated blood pressure is present, so normal or low pressure in a patient with stroke challenges hypertensive hemorrhage diagnosis
• Increasing edema can produce clinical worsening, and clinical features will depend on where the hemorrhage occurred in the brain.

Deep Cerebral Hemorrhage

• The most common sites are the putamen and thalamus, which are separated by the posterior limb of the internal capsule.
• Pressure from a putaminal or thalamic hematoma produces a contralateral sensorimotor deficit.
• Putaminal hemorrhage typically leads to more severe motor deficit and thalamic hemorrhage to more marked disturbances in sensory function.
• Putaminal hemorrhage produces tonic eye deviation toward the affected side of the brain
• Thalamic hemorrhage may cause tonic downward and medial eye deviation.

Clinical Features of Hypertensive Intracerebral Hemorrhage

• Putamen hemorrhage involves the Ipsilateral deviation of the eyes and Contralateral hemiparesis neurological disturbance
• Thalamus hemorrhage involves a downward deviation of the eyes and Contralateral hemisensory neurological disturbance
• Lobar hemorrhage involves normal or Ipsilateral eye deviation and a Contralateral hemiparesis or deficits in sensory and is less common
• Pons hemorrhage involves a Absent horizontal eye movement and Quadriparesis neurological disturbance.
• Cerebellum hemorrhage involves Impaired eye movement when tested late and Gait ataxia disturbance in neurological symptoms

Symptoms of Cerebellar Hemorrhage

• Headache, vomiting, dizziness, and can't stand or walk.
• Patients may be alert or confused, with large hemorrhages leading to coma within 12-24 hours.
• Coma at onset can be hard to distinguish from pontine hemorrhage.
• Can cause impaired gaze, skew deviation, small pupils, and impaired upgaze.
• Ipsilateral facial weakness may occur, but limb strength is usually normal.
• Limb ataxia doesn't happen, but stance and gait need to be tested.

Lobar Hemorrhage

• Hypertensive hemorrhages occur in subcortical white matter of the frontal, parietal, temporal, and occipital lobes.
• Causes headache, vomiting, hemiparesis, hemisensory deficits, aphasia, and visual field defects depending on the location.
• Seizures are more frequent than with other locations, coma is less so.

Pontine Hemorrhage

• Bleeding into the pons causes coma and death within 48 hours.
• Key findings are pinpoint pupils, horizontal eye movements are absent or impaired, with vertical eye movements preserved.
• Patients are quadriparetic, and hyperthermia may be present.
• Pontine hemorrhage ruptures into the fourth ventricle.

Investigative Studies

• A noncontrast CT scan is obtained to confirm intracerebral hemorrhage and assess underlying cause other than hypertension.
• Lobar hemorrhage, deep hemorrhage in an atypical location, or disproportionate brain bleeding suggests other causes.
• CT angiography or MR angiography can reveal intracranial aneurysm or arteriovenous malformation.
• Blood tests identify coagulopathy or thrombocytopenia, while blood glucose detects hyperglycemia or hypoglycemia.
• Lumbar puncture yields bloody CSF, not performed if brain herniation risk.

Differential Diagnosis

• Hypertensive hemorrhages are hard to distinguish from infarction.
• Severe headache, nausea, vomiting, and impaired consciousness suggest hemorrhage, which CT or MRI can diagnose.
• Brainstem stroke and cerebellar infarction can mimic cerebellar hemorrhage, the tests will easily show the difference

Treatment

• Initial management includes airway support with ventilatory assistance if required.
• Reduce systolic blood pressure to 140-179 mm Hg via intravenous nicardipine and labetalol.
• Coagulopathy reversed by clotting factor replacement with prothrombin complex concentrate or fresh frozen plasma.
• Discontinue warfarin and administer vitamin K if from anticoagulation with warfarin.
• Thrombocytopenia corrected via platelet transfusion.
• Hyper/hypoglycemia should be avoided and managed via insulin or glucose, as needed.
• Suppress fever with antipyretics; fever may be from inflammation.
• Do not treat brain edema with corticosteroids or osmotic agents.
• Seizures may occur with lobar hemorrhages, but prophylactic anticonvulsants are not recommended.
• Neurologic deterioration, brainstem compression, and hydrocephalus are indications for decompressive surgery on cerebellar hemorrhages, best in conscious patients.
• Lobar hematomas especially those larger than 30 mL in volume and located within approximately 1 cm of the brain surface are treated with Surgical evacuation.
• Patients with deep hemorrhage is not beneficial with surgery.

Complications

• Are the same related to ischemic strokes, except for no prophylaxis of deep vein thrombosis with subcutaneous heparin is recommended in the acute phase.

Rehabilitation

• Rehabilitation is described for ischemic stroke.

Prognosis

• Return of neurologic function can occur based on location and size of intracerebral hemorrhage, location and size.
• Mortality is 30-40% at 1 month; most deaths occur in the first few days.
• About 75% of patients have significant disability at discharge.

Other Causes

• Traumatic hemorrhages may occur at the site of impact or directly opposite (coup or contrecoup), with the frontal and temporal lobes being locations for Traumatic hemorrhages that are diagnosed by CT or MRI

Hemorrhagic Transformation of Cerebral Infarcts

• Hemorrhage into a cerebral infarct is common factors for hemorrhagic transformation thrombolytic therapy, anticoagulation, cardioembolic stroke, massive infarction, cortical gray matter infarction, and thrombocytopenia.
• Treatment is stopping thrombolytic or anticoagulant drugs when possible

Anticoagulation & Thrombolytic Therapy

• Using anticoagulants or thrombolytic agents can increase the risk of intracerebral hemorrhage .

Coagulopathy

• Intracerebral hemorrhage can occur due to clotting factors (eg, hepatic failure, hemophilia, disseminated intravascular coagulopathy) or platelets (eg, immune thrombocytopenic purpura).

Cerebral Amyloid Angiopathy

• The condition mostly affects the wall of Leptomeningeal patients Risk factors apolipoprotein E 84 and 2 alleles, anticoagulation or antiplatelet therapy, head trauma, and hypertension. A rare form is hereditary cases and inherited in autosomal dominant fashion

Vascular Malformations

• Cerebrovascular malformations can be arteries (saccular, or berry, aneurysms), veins (cavernous malformations), or their interconnections (arteriovenous malformations, or AVMs),.
• AVMs consist of tortuous arteries and dilated veins and may develop or cause hemorrhage, seizures, headache, or focal neurologic deficits.
• Treatment consists of Anticonvulsants for AVMs that present with seizures and Surgical resection, endovascular embolization, or radiosurgery can prevent rebleeding,
• Cavernous are sporadic or familial and caused by autosomal dominant mutations. Treatment includes either anticonvulsants patients presenting seizures,microsurgical resection, and radiosurgery.
• Saccular aneurysms are acquired lesions and bleed into brain

Amphetamine or Cocaine Abuse

• Amphetamine or cocaine use can cause intracerebral hemorrhage and ruptures blood pressure

Hemorrhage into Tumors

• Bleeding into brain tumors can association with the melanoma, lung