the red blood cells to be metabolized into bilirubin. ecg ecg changes resembling those of an stemi in a woman who had an acute cns injury from a subarachnoid hemorrhage electrocardiographic changes are relatively common in subarachnoid hemorrhage, occurring in 40–70 percent of cases. they may include qt prolongation, q waves, cardiac dysrhythmias, and st elevation that mimics a heart attack. also one of the characteristic ecg changes that could be found in patients with subarachnoid hemorrhage, is the j waves or osborn waves, which are positive deflections that occur at the junction between qrs complexes and st segments, where the s point, also known as the j point, has a myocardial infarction-like elevation. j waves or osborn waves, which represent an early repolarization and delayed depolarization of the heart ventricles, are thought to be caused by the high catecholamines surge released in patients with subarachnoid hemorrhage or brain damage, the issue that might lead to ventricular fibrillation and cardiac arrest in unmanaged patients. classification there are several grading scales available for sah. the glasgow coma scale (gcs) is ubiquitously used for assessing consciousness. its three specialized scores are used to evaluate sah; in each, a higher number is associated with a worse outcome. these scales have been derived by retrospectively matching characteristics of people with their outcomes. the first widely used scale for neurological condition following sah was published by botterell and cannell in 1956 and referred to as the botterell grading scale. this was modified by hunt and hess in 1968: grade signs and symptoms survival 1 asymptomatic or minimal headache and slight neck stiffness70% 2 moderate to severe headache; neck stiffness; no neurologic deficit except cranial nerve palsy60% 3 drowsy; minimal neurologic deficit50% 4 stuporous; moderate to severe hemiparesis; possibly early decerebrate rigidity and vegetative disturbances20% 5 deep coma; decerebrate rigidity; moribund10% the fisher grade classifies the appearance of subarachnoid hemorrhage on ct scan. grade appearance of hemorrhage 1 none evident 2 less than 1 mm thick 3 more than 1 mm thick 4 diffuse or none with intraventricular hemorrhage or parenchymal extension this scale has been modified by claassen and coworkers, reflecting the additive risk from sah size and accompanying intraventricular hemorrhage (0 – none; 1 – minimal sah w/o ivh; 2 – minimal sah with ivh; 3 – thick sah w/o ivh; 4 – thick sah with ivh);. the world federation of neurosurgeons (wfns) classification uses glasgow coma score and focal neurological deficit to gauge severity of symptoms. grade gcs focal neurological deficit 1 15absent 2 13–14absent 3 13–14present 4 7–12present or absent 5 <7present or absent a comprehensive classification scheme has been suggested by ogilvy and carter to predict outcome and gauge therapy. the system consists of five grades and it assigns one point for the presence or absence of each of five factors: age greater than 50; hunt and hess grade 4 or 5; fisher scale 3 or 4; aneurysm size greater than 10 mm; and posterior circulation aneurysm 25 mm or more. screening and prevention screening for aneurysms is not performed on a population level; because they are relatively rare, it would not be cost-effective. however, if someone has two or more first-degree relatives who have had an aneurysmal subarachnoid hemorrhage, screening may be worthwhile. autosomal dominant polycystic kidney disease (adpkd), a hereditary kidney condition, is known to be associated with cerebral aneurysms in 8 percent of cases, but most such aneurysms are small and therefore unlikely to rupture. as a result, screening is only recommended in families with adpkd where one family member has had a ruptured aneurysm. an aneurysm may be detected incidentally on brain imaging; this presents a conundrum, as all treatments for cerebral aneurysms are associated with potential complications. the international study of unruptured intracranial aneurysms (isuia) provided prognostic data both in people having previously had a subarachnoid hemorrhage and people who had aneurysms detected by other means. those having previously had a sah were more likely to bleed from other aneurysms. in contrast, those having never bled and had small aneurysms (smaller than 10 mm) were very unlikely to have a sah and were likely to sustain harm from attempts to repair these aneurysms. on the basis of the isuia and other studies, it is now recommended that people are considered for preventive treatment only if they have a reasonable life expectancy and have aneurysms that are highly likely to rupture. moreover, there is only limited evidence that endovascular treatment of unruptured aneurysms is actually beneficial. treatment management involves general measures to stabilize the person while also using specific investigations and treatments. these include the prevention of rebleeding by obliterating the bleeding source, prevention of a phenomenon known as vasospasm, and prevention and treatment of complications. stabilizing the person is the first priority. those with a depressed level of consciousness may need to be intubated and mechanically ventilated. blood pressure, pulse, respiratory rate, and glasgow coma scale are monitored frequently. once the diagnosis is confirmed, admission to an intensive care unit may be preferable, especially since 15 percent may have further bleeding soon after admission. nutrition is an early priority, mouth or nasogastric tube feeding being preferable over parenteral routes. in general, pain control is restricted to less-sedating agents such as codeine, as sedation may impact on the mental status and thus interfere with the ability to monitor the level of consciousness. deep vein thrombosis is prevented with compression stockings, intermittent pneumatic compression of the calves, or both. a bladder catheter is usually inserted to monitor fluid balance. benzodiazepines may be administered to help relieve distress. antiemetic drugs should be given to awake persons. people with poor clinical grade on admission, acute neurologic deterioration, or progressive enlargement of ventricles on ct scan are, in general, indications for the placement of an external ventricular drain by a neurosurgeon. the external ventricular drain may be inserted at the bedside or in the operating room. in either case, strict aseptic technique must be maintained during insertion. in people with aneurysmal subarachnoid hemorrhage the evd is used to remove cerebrospinal fluid, blood, and blood byproducts that increase intracranial pressure and may increase the risk for cerebral vasospasm. preventing rebleeding arteriogram showing a partially coiled aneurysm (indicated by yellow arrows) of the posterior cerebral artery with a residual aneurysmal sac. the person was a 34-year-old woman initially treated for a subarachnoid hemorrhage. efforts to keep a person's systolic blood pressure somewhere between 140 and 160 mmhg is generally recommended. medications to achieve this may include labetalol or nicardipine. people whose ct scan shows a large hematoma, depressed level of consciousness, or focal neurologic signs may benefit from urgent surgical removal of the blood or occlusion of the bleeding site. the remainder are stabilized more extensively and undergo a transfemoral angiogram or ct angiogram later. it is hard to predict who will have a rebleed, yet it may happen at any time and carries a dismal prognosis. after the first 24 hours have passed, rebleeding risk remains around 40 percent over the subsequent four weeks, suggesting that interventions should be aimed at reducing this risk as soon as possible. some predictors of early rebleeding are high systolic blood pressure, the presence of a hematoma in the brain or ventricles, poor hunt-hess grade (iii-iv), aneurysms in the posterior circulation, and an aneurysm >10 mm in size. if a cerebral aneurysm is identified on angiography, two measures are available to reduce the risk of further bleeding from the same aneurysm: clipping and coiling. clipping requires a craniotomy (opening of the skull) to locate the aneurysm, followed by the placement of clips around the neck of the aneurysm. coiling is performed through the large blood vessels (endovascularly): a catheter is inserted into the femoral artery in the groin and advanced through the aorta to the arteries (both carotid arteries and both vertebral arteries) that supply the brain. when the aneurysm has been located, platinum coils are deployed that cause a blood clot to form in the aneurysm, obliterating it. the decision as to which treatment is undertaken is typically made by a multidisciplinary team consisting of a neurosurgeon, neuroradiologist, and often other health professionals. in general, the decision between clipping and coiling is made on the basis of the location of the aneurysm, its size and the condition of the person. aneurysms of the middle cerebral artery and its related vessels are hard to reach with angiography and tend to be amenable to clipping. those of the basilar artery and posterior cerebral artery are hard to reach surgically and are more accessible for endovascular management. these approaches are based on general experience, and the only randomized controlled trial directly comparing the different modalities was performed in relatively well people with small (less than 10 mm) aneurysms of the anterior cerebral artery and anterior communicating artery (together the "anterior circulation"), who constitute about 20 percent of all people with aneurysmal sah. this trial, the international subarachnoid aneurysm trial (isat), showed that in this group the likelihood of death or being dependent on others for activities of daily living was reduced (7.4 percent absolute risk reduction, 23.5 percent relative risk reduction) if endovascular coiling was used as opposed to surgery. the main drawback of coiling is the possibility that the aneurysm will recur; this risk is extremely small in the surgical approach. in isat, 8.3 percent needed further treatment in the longer term. hence, people who have undergone coiling are typically followed up for many years afterwards with angiography or other measures to ensure recurrence of aneurysms is identified early. other trials have also found a higher rate of recurrence necessitating further treatments. vasospasm vasospasm, in which the blood vessels constrict and thus restrict blood flow, is a serious complication of sah. it can cause ischemic brain injury (referred to as "delayed ischemia") and permanent brain damage due to lack of oxygen in parts of the brain. it can be fatal if severe. delayed ischemia is characterized by new neurological symptoms, and can be confirmed by transcranial doppler or cerebral angiography. about one third of people admitted with subarachnoid hemorrhage will have delayed ischemia, and half of those have permanent damage as a result. it is possible to screen for the development of vasospasm with transcranial doppler every 24–48 hours. a blood flow velocity of more than 120 centimeters per second is suggestive of vasospasm. the pathogenesis of cerebral vasospasm following subarachnoid hemorrhage is attributed to the higher levels of endothelin 1, a potent vasoconstrictor, and the lower levels of endothelial nos (enos), a potent vasodilator. both of which are produced from a series of events that begin from the inflammatory reaction caused by the products released from erythrocytes' degradation. following subarachnoid hemorrhage, different clotting factors and blood products are released into the surrounding perivascular spaces known as (virchow-robin spaces). the released clotting factors like; fibrinopeptides, thromboxane a2 and others lead to microthrombosis around near vessels that leads to extrinsic vasoconstriction of these vessels. besides that extrinsic vasoconstriction, the erythrocytes' degradation products like; bilirubin and oxyhemoglobin lead to neuroinflammation that in turn increases the production of reactive oxygen species (ros) which increases and decreases the production of endothelin 1 and endothelial nos, respectively, the issue that yields in intrinsic vasoconstriction of the neighboring blood vessels and results in cerebral ischemia if left untreated. the use of calcium channel blockers, thought to be able to prevent the spasm of blood vessels by preventing calcium from entering smooth muscle cells, has been proposed for prevention. the calcium channel blocker nimodipine when taken by mouth improves outcome if given between the fourth and twenty-first day after the bleeding, even if it does not reduce the amount of vasospasm detected on angiography. it is the only food and drug administration (fda)-approved drug for treating cerebral vasospasm. in traumatic subarachnoid hemorrhage, nimodipine does not affect long-term outcome, and is not recommended. other calcium channel blockers and magnesium sulfate have been studied, but are not presently recommended; neither is there any evidence that shows benefit if nimodipine is given intravenously. nimodipine is readily authorized in the form of tablets and solution for infusion for the prevention and treatment of complications due to vasospasm following subarachnoid hemorrhage. another sustained formulation of nimodipine administered via an external ventricular drain (evd), called eg-1962, is also