Spontaneous Subarachnoid and Intracerebral Hemorrhage PDF

Spontaneous Subarachnoid and Intracerebral Hemorrhage Tamar Saria SAH  SAH About 75% of subarachnoid hemorrhages are caused by a ruptured aneu rysm. In about 20%, a cause is not identified  Risk Factors for Subara...

Spontaneous Subarachnoid and Intracerebral Hemorrhage Tamar Saria SAH  SAH About 75% of subarachnoid hemorrhages are caused by a ruptured aneu rysm. In about 20%, a cause is not identified  Risk Factors for Subarachnoid Hemorrhage Hypertension Smoking Excessive alcohol consumption Polycystic kidney disease Family history of subarachnoid hemorrhage Coarctation of the aorta Marfan’s syndrome Ehlers-Danlos syndrome type IV α1-Antitrypsin deficiency  CLINICAL FEATURES severe headache of acute onset (termed a “thunderclap” head ache) that reaches maximal intensity within minutes Even if a patient is not experiencing the “worst ever” headache, a headache that is different in intensity or quality from past headaches raises concern for subarachnoid hemorrhage. Headaches associated with loss of con sciousness, seizure, diplopia or other neurologic signs, or nuchal rigid ity also require clinical investigation Approximately 20% of patients develop their symptoms while engaged in activities that cause increased blood pressure, such as exercise, sexual intercourse, or defecation.  DX Noncontrast CT of the head, which sensitivity is highest shortly after symptoms begin and is estimated to be 98% within 6 to 12 hours of the onset of symptoms. Differential Diagnosis of Subarachnoid Hemorrhage Vascular (other intracranial hemorrhage, ischemic stroke or transient ischemic attack, arterial dissection, venous thrombosis) Drug toxicity Infection (meningitis, encephalitis) Intracranial tumor Intracranial hypotension Metabolic derangements Primary headache syndromes (benign thunderclap headache, migraine, cluster headache) Hypertensive disorders  Lumbar Puncture Most authorities recommend CSF analysis when a patient with suspected subarachnoid hemorrhage has a normal result on head CT Advantage of LP is the ability to identify other causes of headache such as meningitis or idiopathic intracranial hypertension Xanthochromia and increased RBC count.  Hunt-Hess Scale I - Mild headache, normal mental status, no cranial nerve or motor findings II II - Severe headache, normal mental status, may have cranial nerve deficit III III - Somnolent, confused, may have cranial nerve or mild motor deficit IV - Stupor, moderate to severe motor deficit, may have intermittent reflex posturing V - Coma, reflex posturing or flaccid  TREATMENT The risk of rebleeding is greatest in the first 24 hours and can be reduced by adequate blood pressure control; Labetalol and nicardipine are most often used, with neither showing clear superi ority. Avoid nitroprusside and nitroglycerin because they increase cerebral blood volume and intracranial pressure Vasospasm is most common 2 days to 3 weeks after subarachnoid hemorrhage  Treatment of vasospasm A modest protective benefit is seen with administration of nimodipine, 60 milligrams PO every 4 hours, therapy should be initiated within 96 hours of symptom onset unless contraindicated due to allergy, nonfunctioning GI tract, or hepatic disease.  DISPOSITION AND FOLLOW-UP Admit all patients diagnosed with subarachnoid hemorrhage to an intensive care unit in consultation with a neurosurgeon INTRACEREBRAL HEMORRHAGE  PATHOPHYSIOLOGY Risk factors for intracerebral hemorrhage include long-standing hypertension, arteriovenous malformations, arterial aneurysm, Anticoagulant therapy, Use of sympathomimetic drugs (particularly cocaine and phenylpropanolamine), intracranial tumors, and amyloid angiopathy in the elderly  CLINICAL FEATURES Intracerebral hemorrhage may be clinically indistinguishable from cerebral infarction, subarachnoid hemorrhage, and ischemic stroke. In intracerebral hemorrhage - headache, nausea, and vomiting often precede the neurologic deficit, and in contrast to subarachnoid hemorrhage, the headache onset is usually more insidious. In hypertensive intracerebral hemorrhage, bleeding is usually localized to the putamen, thalamus, pons, or cerebellum (in decreasing order of frequency), and clinical examination findings may be relatable to those areas. Cerebellar hemorrhage is commonly associated with dizziness, vomiting, marked  TREATMENT The INTERACT2 study demonstrated no reduction in the rate of death or severe disability among patients assigned to rapid (within 1 hr) reduction of blood pressure to