Hemorragia cerebral.


Published on

Published in: Health & Medicine
  • Be the first to comment

  • Be the first to like this

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Hemorragia cerebral.

  1. 1. Stroke, Hemorrhagic
  2. 3. <ul><li>accounts for 10-15% of all strokes </li></ul><ul><li>associated with higher mortality. </li></ul><ul><li>similar focal neurologic deficits but tend to be more ill than patients with ischemic stroke. </li></ul><ul><li>Patients with intracerebral bleeds are more likely to have headache, altered mental status, seizures, nausea and vomiting, and/or marked hypertension; </li></ul><ul><li>however, none of these findings reliably distinguishes between hemorrhagic stroke and ischemic stroke </li></ul>
  3. 4. Pathophysiology <ul><li>bleeding occurs directly into the brain parenchyma. </li></ul><ul><li>The usual mechanism is thought to be leakage from small intracerebral arteries damaged by chronic hypertension. </li></ul><ul><li>Other mechanisms include bleeding diatheses, iatrogenic anticoagulation, cerebral amyloidosis , and cocaine abuse. </li></ul><ul><li>Intracerebral hemorrhage has a predilection for certain sites in the brain, including the thalamus, putamen, cerebellum, and brainstem. </li></ul><ul><li>In addition to the area of the brain injured by the hemorrhage, the surrounding brain can be damaged by pressure produced by the mass effect of the hematoma. </li></ul><ul><li>A general increase in intracranial pressure may occur. </li></ul>
  4. 5. Mortality/Morbidity <ul><li>Stroke is a leading killer and disabler. Combining all types of stroke, it is the third leading cause of death and the first leading cause of disability. </li></ul><ul><li>Morbidity is more severe and mortality rates are higher for hemorrhagic stroke than for ischemic stroke. Only 20% of patients regain functional independence. </li></ul><ul><li>The 30-day mortality rate for hemorrhagic stroke is 40-80%. Approximately 50% of all deaths occur within the first 48 hours . </li></ul><ul><li>A independent predictors of death were high age, central and brainstem hemorrhage location, </li></ul><ul><li>intraventricular hemorrhage, increased </li></ul><ul><li>volume, and decreased level of consciousness. </li></ul>
  5. 6. <ul><li>Race </li></ul><ul><li>African Americans have a higher incidence of hemorrhagic and ischemic strokes than other races in the United States. </li></ul><ul><li>The incidence of hemorrhagic stroke in the Japanese population is increased. </li></ul><ul><li>Age </li></ul><ul><li>The risk of stroke increases with age. </li></ul>
  6. 7. <ul><li>History </li></ul><ul><li>Patients' symptoms vary depending on the </li></ul><ul><li>area of the brain affected and the extent of the bleeding. </li></ul><ul><li>Hemorrhagic strokes are more likely to exhibit symptoms of increased intracranial pressure than other types of stroke. </li></ul><ul><ul><li>Headache, often severe and sudden onset </li></ul></ul><ul><ul><li>Nausea and/or vomiting </li></ul></ul><ul><li>Seizures are more common in hemorrhagic stroke than in ischemic stroke. They occur in up to 28% of hemorrhagic strokes and generally occur at the onset of the intracerebral hemorrhage (ICH) or within the first 24 hours. </li></ul>
  7. 8. <ul><li>Physical </li></ul><ul><li>ICH may be clinically indistinguishable from ischemic stroke. </li></ul><ul><li>Hypertension is commonly a prominent finding. </li></ul><ul><li>An altered level of consciousness or coma is more common with hemorrhagic </li></ul><ul><li>Meningismus may result from blood in the ventricles. </li></ul><ul><li>Focal neurologic deficits </li></ul><ul><ul><li>The type of deficit depends upon the area of brain involved. </li></ul></ul><ul><ul><li>If the dominant hemisphere (usually left) is involved, a syndrome consisting of right hemiparesis, right hemisensory loss, left gaze preference, right visual field cut, and aphasia may result. </li></ul></ul><ul><ul><li>If the nondominant (usually right) hemisphere is involved, a syndrome of left hemiparesis, left hemisensory loss, right gaze preference, and left visual field cut may result. Nondominant hemisphere syndrome may also result in neglect when the patient has a left-sided hemi-inattention and ignores the left side. </li></ul></ul><ul><ul><li>If the cerebellum is involved, the patient is at high risk of herniation and brainstem compression. Herniation may cause a rapid decrease in the level of consciousness, apnea, and death. </li></ul></ul>
  8. 9. <ul><ul><li>Other signs of cerebellar or brainstem involvement include the following: </li></ul></ul><ul><ul><ul><li>Gait or limb ataxia </li></ul></ul></ul><ul><ul><ul><li>Vertigo or tinnitus </li></ul></ul></ul><ul><ul><ul><li>Nausea and vomiting </li></ul></ul></ul><ul><ul><ul><li>Hemiparesis or quadriparesis </li></ul></ul></ul><ul><ul><ul><li>Hemisensory loss or sensory loss of all 4 limbs </li></ul></ul></ul><ul><ul><ul><li>Eye movement abnormalities resulting in diplopia or nystagmus </li></ul></ul></ul><ul><ul><ul><li>Oropharyngeal weakness or dysphagia </li></ul></ul></ul><ul><ul><ul><li>Crossed signs (ipsilateral face and contralateral body) </li></ul></ul></ul>
  9. 10. <ul><li>Causes </li></ul><ul><li>Hypertension 60% of cases </li></ul><ul><li>Advanced age (risk factor) </li></ul><ul><li>Cerebral amyloidosis may cause up to 10% of ICH </li></ul><ul><li>Coagulopathies </li></ul><ul><li>Anticoagulant therapy </li></ul><ul><li>Thrombolytic therapy for acute myocardial infarction (MI) and acute ischemic stroke </li></ul><ul><li>Abuse of cocaine and other sympathomimetic drugs </li></ul><ul><li>Arteriovenous malformation </li></ul><ul><li>Intracranial aneurysm </li></ul><ul><li>Vasculitis </li></ul><ul><li>Intracranial neoplasm </li></ul><ul><li>History of prior stroke (risk factor </li></ul>
  10. 11. Treatment <ul><li>Emergency Department Care </li></ul><ul><li>Assess the ABCs </li></ul><ul><li>Establish intravenous (IV) access. </li></ul><ul><li>Obtain bedside glucose determination.  </li></ul><ul><ul><li>Hypoglycemia may mimic stroke. </li></ul></ul><ul><ul><li>Hyperglycemia has been associated with poorer outcomes in patients experiencing stroke. </li></ul></ul><ul><li>Institute cardiac monitoring and obtain an ECG. </li></ul><ul><li>Intubation should be performed for patients who demonstrate potential loss of airway protective mechanisms or signs of brainstem dysfunction. </li></ul>
  11. 12. <ul><li>Careful blood pressure (BP) monitoring is important. </li></ul><ul><ul><li>No controlled studies define optimum BP levels. </li></ul></ul><ul><ul><li>Greatly elevated BP is thought to lead to rebleeding and hematoma expansion. </li></ul></ul><ul><ul><li>Patients who have had a stroke may lose their cerebral autoregulation of cerebral perfusion pressure. </li></ul></ul><ul><ul><li>Rapid or aggressive BP lowering may compromise cerebral perfusion. </li></ul></ul><ul><ul><li>Nicardipine, labetalol, esmolol, and hydralazine are agents that may be used when necessary for BP control. Avoid nitroprusside because it may raise intracranial pressure. </li></ul></ul>
  12. 13. <ul><ul><li>The American Heart Association guidelines for treating elevated BP are as follows: 1 </li></ul></ul><ul><ul><ul><li>If systolic BP is >200 mm Hg or mean arterial pressure (MAP) is >150 mm Hg, then consider aggressive reduction of BP with continuous intravenous infusion with frequent BP (every 5 min) checks. </li></ul></ul></ul><ul><ul><ul><li>If systolic BP is >180 mm Hg or MAP is >130 mm Hg and there is evidence or suspicion of elevated intracranial pressure (ICP), then consider monitoring of ICP and reducing BP using intermittent or continuous intravenous medications to maintain cerebral perfusion pressure >60-80 mm Hg. </li></ul></ul></ul><ul><ul><ul><li>If systolic BP is >180 or MAP is >130 mm Hg and there is NOT evidence or suspicion of elevated ICP, then consider modest reduction of BP (target MAP of 110 mm Hg or target BP of 160/90 mm Hg) with BP checks every 15 minutes. </li></ul></ul></ul>
  13. 14. <ul><li>Intracranial pressure control: </li></ul><ul><ul><li>Elevated intracranial pressure (ICP) may result from the hematoma itself, surrounding edema, or both. The frequency of increased ICP in patients with intracerebral hemorrhage (ICH) is not known. </li></ul></ul><ul><ul><li>Elevate the head of the bed to 30 degrees. This improves jugular venous outflow and lowers ICP. The head should be midline and not turned to the side. </li></ul></ul><ul><ul><li>Provide analgesia and sedation as needed. </li></ul></ul><ul><ul><li>More aggressive therapies such as osmotic therapy (mannitol, hypertonic saline), barbiturate anesthesia. </li></ul></ul><ul><ul><li>Hyperventilation is not recommended. Its effect is transient, it decreases cerebral blood flow, and it may result in rebound elevated intracranial pressure. 1 </li></ul></ul><ul><ul><li>Glucocorticoids are not effective and result in higher rates of complications with poorer outcomes. </li></ul></ul><ul><ul><li>Ventriculostomy is often used in the setting of obstructive hydrocephalus. Obstructive hydrocephalus is a common complication of thalamic hemorrhage with third ventricle compression and of cerebellar hemorrhage with fourth ventricle compression. Ventriculostomies are associated with high rates of complications including bacterial meningitis. </li></ul></ul>
  14. 15. <ul><li>Seizures: </li></ul><ul><ul><li>Early seizure activity occurs in 4-28% of patients with intracerebral hemorrhage, and these seizures are often nonconvulsive seizures. </li></ul></ul><ul><ul><li>Seizure activity should be rapidly controlled with a benzodiazepine, such as lorazepam or diazepam, accompanied by either phenytoin or fosphenytoin loading. </li></ul></ul><ul><ul><li>Prophylactic anticonvulsant therapy is recommended in patients with lobar hemorrhages to reduce the risk of early seizures. </li></ul></ul><ul><ul><li>However, the use of prophylactic anticonvulsant therapy in all cases of intracerebral hemorrhage is controversial, as no prospective controlled trials have demonstrated a clear benefit. </li></ul></ul>
  16. 18. <ul><li>Intracranial aneurysms are common lesions; </li></ul><ul><li>Prevalence in the adult population between 1 and 5 percent, </li></ul><ul><li>10 million to 12 million persons in the United States. </li></ul><ul><li>Fortunately, most aneurysms are small, </li></ul><ul><li>and an estimated 50 to 80 percent of all aneurysms do not rupture during the course </li></ul><ul><li>of a person’s lifetime. </li></ul><ul><li>Intracranial aneurysms are considered to be sporadically acquired lesions, </li></ul><ul><li>Associated conditions include autosomal dominant polycystic kidney disease, fibromuscular dysplasia, Marfan’s syndrome, Ehlers–Danlos syndrome type IV, and arteriovenous malformations of the brain. </li></ul><ul><li>An estimated 5 to 40 percent of patients with autosomal dominant polycystic kidney disease have intracranial aneurysms </li></ul><ul><li>and 10 to 30 percent of patients have multiple aneurysms. </li></ul>
  17. 19. <ul><li>The estimated incidence of SAH in the United States is 1 case per 10,000 persons, </li></ul><ul><li>yielding approximately 27,000 new cases of subarachnoid hemorrhage each year. </li></ul><ul><li>Subarachnoid hemorrhage is more common in women than in men (2:1); </li></ul><ul><li>Incidence is in persons 55 to 60 years old. </li></ul><ul><li>An estimated 5 to 15% of cases of stroke are related to </li></ul><ul><li>ruptured intracranial aneurysms. </li></ul><ul><li>Has a 30-day mortality rate of 45%. </li></ul><ul><li>An estimated 30% of survivors will have moderate-to-severe disability. </li></ul>
  18. 20. <ul><li>Little is known about the cause of intracranial aneurysms or the process by which they form, grow, and rupture, although hypertension and smoking-induced vascular changes are thought to have a major role. </li></ul><ul><li>The most common histologic finding is a decrease in the tunica media, the middle muscular layer of the artery, causing structural defects. </li></ul><ul><li>These defects, combined with hemodynamic factors, lead to aneurysmal outpouchings at arterial branch points in the subarachnoid space at the base of the brain. </li></ul>
  19. 21. <ul><li>An unruptured aneurysm may be asymptomatic and thus be found incidentally, or it may be diagnosed on the basis of symptoms. </li></ul><ul><li>Unruptured aneurysms cause symptoms by </li></ul><ul><li>exerting a mass effect, leading to cranial-nerve </li></ul><ul><li>palsies or brain-stem compression. </li></ul><ul><li>One common aneurysm-related syndrome is rapid onset of a third-nerve palsy caused by enlargement of an aneurysm of the posterior communicating artery. </li></ul>
  20. 22. Pericallosal artery, 4% Anterior communicating artery, 30% Internal carotid artery bifurcation, 7.5% Middle cerebral artery, 20% Posterior communicating artery, 25% Basilar tip, 7% Posterior inferior cerebellar artery, 3%
  21. 23. <ul><li>2-4 % hemorrhage again within the first 24 hours after the initial episode, </li></ul><ul><li>and approximately 15 to 20% bleed a second time within the first two Weeks. </li></ul><ul><li>Persons with intracranial aneurysms presenting with symptoms of compression such as cranial-nerve palsies or brain-stem dysfunction should be evaluated and treated promptly because of the increased risk of rupture (6 % per year). </li></ul><ul><li>The risk of rupture of an intracranial aneurysm that has not bled but is found incidentally is much less certain, and these intracranial aneurysms are generally managed electively. </li></ul><ul><li>Unruptured intracranial aneurysms were viewed as posing a high risk, with an estimated risk of rupture of approximately 1 to 2 percent per year. </li></ul>
  22. 24. MEDICAL DIAGNOSIS <ul><li>An acute onset of severe headache, often described by patients as the “worst headache of my life.” </li></ul><ul><li>However, an estimated 10 percent die before reaching medical attention, and many others present in a coma or with severe neurologic compromise. </li></ul><ul><li>Clinical grading scales such as the Hunt and Hess Scale are used to describe the neurologic condition on admission and are considered good predictors of ultimate outcome. </li></ul><ul><li>Computed tomography (CT) of the head without the administration of contrast material is the initial diagnostic test of choice for suspected subarachnoid hemorrhage. </li></ul><ul><li>Lumbar puncture is reserved for the approximately 5% of patients in whom cranial CT reveals no abnormalities, despite a history suggesting a subarachnoid hemorrhage. </li></ul>
  23. 25. Hunt and Hess Grading Scale for Subarachnoid Hemorrhage. <ul><li>Grade Clinical Description </li></ul><ul><li>1 Asymptomatic or minimal headache and slight nuchal rigidity </li></ul><ul><li>2 Moderate-to-severe headache, nuchal rigidity, and </li></ul><ul><li>no neurologic deficit other than cranial-nerve </li></ul><ul><li>palsy </li></ul><ul><li>3 Drowsiness, confusion, or mild focal deficit </li></ul><ul><li>4 Stupor, moderate-to-severe hemiparesis, and </li></ul><ul><li>possibly, early decerebrate rigidity and vegetative </li></ul><ul><li>disturbances </li></ul><ul><li>5 Deep coma, decerebrate rigidity, and moribund </li></ul><ul><li>appearance </li></ul>
  24. 26. <ul><li>Acute Effects of Subarachnoid Hemorrhage </li></ul><ul><li>Hydrocephalus develops in about 15 to 20 % of patients </li></ul><ul><li>Symptomatic hydrocephalus is usually treated with ventriculostomy and drainage of cerebrospinal fluid. </li></ul><ul><li>Cerebral vasospasm , a major cause of morbidity-mortality, refers to the intracranial vasoconstriction that may occur between 3 and 12 days after a subarachnoid hemorrhage. </li></ul><ul><li>The cause of vasospasm is unknown; </li></ul><ul><li>even with maximal therapy, vasospasm can cause strokes and death. </li></ul><ul><li>Transcranial Doppler ultrasonography is a useful noninvasive method to detect vasospasm </li></ul>
  25. 27. <ul><li>Evidence of cardiac abnormalities after subarachnoid hemorrhage is common and includes electrocardiographic changes (25 to 100% of cases) </li></ul><ul><li>Elevations of cardiac enzymes (troponin in 17 to 28% and creatine kinaseMB isoenzyme in 37% of cases) </li></ul><ul><li>And left ventricular dysfunction (8 to 30% of cases) </li></ul>