A patient presents with a headache which he describes as the worst of his life. NCCT was done. All are true about the condition except:
OPTION C) CAUSES OF DELAYED NEUROLOGICAL DEFICIT IN SAH 1)Rerupture 2)Hydrocephalus 3)Delayed cerebral ischemia- vasospasm is norrowing of aretries at the base of the brain following SAH. This may cause symptomatic ischemia and infarction in ~30% of patients and is the major cause of delayed morbidity and death. Signs of DCI appear 4-14 days after the hemorrhage, most often at 7 days. The severity and distribution of vasospasm determine whether infarction will occur.DCI (DELAYED CEREBRAL ISCHEMIA)due to vasospasm remains the leading cause of morbidityand moality following aneurysmal SAH. 4)Hyponatremia OPTION A)MECHANISM OF XANTHOCHROMIC CSF-Lysis of the red blood cells subsequent conversion of hemoglobin to bilirubin stains the spinal fluid yellow within 6-12 h.The xanthochromic csf peaks in intensity at 48 h and lasts for 1-4 weeks, depending on the amount of subarachnoid blood. OPTION B)1)-frequently shows ST-segment and T-wave changes similar to those associated with cardiac ischemia. 2)A prolonged QRS complex,increased QT interval, and prominent"peaked" or deeply inveed symmetric T waves are usually secondary to the intracranial hemorrhage. There is evidence that circulating catecholamines and excessive discharge of sympathetic neurons may occur after SAH, causing structural myocardial lesions , these ECG changes and a reversible cardiomyopathy sufficient to cause shock or congestive hea failure. OPTION D) Management of SAH 1) Surgical 2 )Medical management A)ANTIHYPEENSIVE B)ANALGESIC C)ANTIEIPELTICS D)STEROIDS E)ANTIFIBRINOLYTIC AGENT Treatment with the calcium channel antagonist nimodipine (60 mg PO every 4 h) improves outcome, perhaps by preventing ischemic injury rather than reducing the risk of vasospasm.
Xanthochromic CSF
Prolonged QT interval
Most common cause of death is re-bleeding
Nimodipine is drug of choice
Headache And Migraine