• Definisi Perdarahan Subarachnoid
• Perdarahan Subarachnoid

Definisi Perdarahan Subarachnoid

Komplikasi tersering dari perdarahan subarachnoid adalah: Hipertensi Vasospasm.000 populasi/tahun (6. Perdarahan yang menumpuk dalam ruang subarachnoid dapat mencetuskan terjadinya stroke. Kejang dan komplikasi lainnya. Dalam hal ini tampaknya ada faktor-faktor diet. Herediter dan keadaan ekonomi yang berperan dalam patogenesisnya.

TRANSCRIPT

Perdarahan Subarachnoid

• Tinjauan Pustaka

  Maj Kedokt Indon, Volum: 59, Nomor: 1, Januari 2009

  The Characteristics ofSubarachnoid Hemorrhage

  Harsono

  Department of Neurology, Faculty of Medicine Gadjah Mada University/Dr. Sardjito Hospital Yogyakarta, Indonesia

  Abstract: Spontaneous or non-traumatic subarachnoid hemorrhage (SAH) accounts for about80% of cases and has a high rate of death and complications. Diagnosis of SAH can be challeng-ing and critical. Delayed cerebral ischemia (DCI) due to cerebral vasospasm and acute hydro-cephalus after SAH are major complications and continue to be the leading causes of death anddisability following SAH. Characteristics of spontaneous SAH are diverse, comprise clinicalmanifestations, diagnostic procedure, specific complications, principles of management, defi-nite treatment to the aneurysm, and prognosis. Spontaneous SAH is a major life experience thatleads to additional morbidity in up to 25% of surviving patients.Keywords: subarachnoid hemorrhage, cerebral ischemia, acute hydrocephalus, diagnostic pro-cedure, morbidity

  Karakteristik Perdarahan Subaraknoid

  Harsono

  Bagian Ilmu Penyakit Saraf, Fakultas Kedokteran Universitas Gadjah Mada/SMF Penyakit Saraf RS Dr. Sardjito Yogyakarta, Indonesia

  Abstrak: Perdarahan subaraknoid spontan atau non-traumatik meliputi 80% dari seluruh kasusperdarahan subaraknoid, mempunyai tingkat kematian dan komplikasi yang tinggi. DiagnosisPSA bersifat sangat menantang karena berkaitan erat dengan komplikasi dan outcome. Iskemiaserebral karena vasospasme serta hidrosefalus akut merupakan penyebab utama kematian dandisabilitas. Karakteristik perdarahan subaraknoid cukup beragam, mencakup perspektif klinik,prosedur diagnostik, komplikasi, prinsip manajemen, terapi definitif terhadap aneurisma danprognosis. Para penderita perdarahan subaraknoid yang bertahan hidup akan mengalamimorbiditas yang sangat mengganggu aktivitas sehari-hari; proporsi penderita dengan morbiditasini mencapai 25%.Kata kunci: perdarahan subaraknoid, iskemia serebral, hidrosefalus akut, prosedur diagnostik,morbiditas

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  The Characteristics of Subarachnoid Hemorrhage

  IntroductionSubarachnoid hemorrhage (SAH) is a neurologic emer-

  gency characterized by the extravasation of blood into thespaces covering the central nervous system that are filledwith cerebrospinal fluid. The causes of subarachnoid hem-orrhage are rupture of an intracranial aneurysm and non-aneurysmal bleeding. Rupture of an intracranial aneurysmaccounts for about 80% of cases and has a high rate ofdeath and complications. Nonaneurysmal subarachnoid hem-orrhage, including traumatic and isolated perimesencephalicsubarachnoid hemorrhage, occurs in about 20% of casesand carries a good prognosis with uncommon neurologiccomplications.1,2

  In patients with aneurysmal SAH, delayed cerebral is-chemia (DCI) is an important cause of poor outcome. Thepathogenesis of DCI is still poorly understood. Intracranialvasospasm, which results from the release of vasoactivesubstances, has often been incriminated. Vasospasm is of-ten used as a synonym but is not sufficient factor becauseeven severe vasospasm does not always lead to secondaryischemia. Platelet aggregation probably plays a role also.Activation of platelet aggregation and the associated re-lease of thromboxane B2 are increased from day 3 after theonset of SAH. This increase is larger in patients who actu-ally develop DCI than in patients without DCI. Data fromanimal research further support the involvement of plateletaggregation. Both rupture of an artery and the presence ofblood at the abluminal side of an intact artery activate plate-let aggregation. Moreover, antiplatelet activity of the endot-helium is reduces after SAH.3 Sudden death from a massiveincrease in intracranial pressure occurs in approximately 1 of10 patients (with 40% in a posterior circulation aneurysm),and another 10% to 20% of patients who arrive at the emer-gency department are comatose and need immediate respi-ratory support.4

  Characteristics of SAH are diverse; whether clinicalperspective, diagnostic procedure, specific complications,principles of management, definite treatment to the aneu-rysm, and prognosis. The purpose of the following discus-sion on such characteristics is to describe the phenomenol-ogy related to the rupture of an intracranial aneurysm and itsclinical as well as pathological consequences. The impor-tance of the description is to increase the physicians alert-ness while handling SAH, in line with the attempt to de-crease morbidity as well as mortality rate.

  Clinical PerspectiveBlood in the subarachnoid space is a powerful me-

  ningeal irritant, which irritation that causes most of the ini-tial signs and symptoms of SAH. Findings vary from insig-nificant to serious depending on the extent of hemorrhage.The characteristic initial symptoms of patients with SAH issudden headache described as the most painful ever experi-enced.5

  A ruptured cerebral aneurysm causes an unexpected,sudden headache and may lead to loss of consciousness.Patients describe a thunderclap headache (an unfortunateterm because no sound is heard). The patient reports theworst headache of his or her life, more precisely, a split sec-ond, extremely intense, and overwhelming headache that failto subside. Many patients report feeling as if the top of myhead is blown off or as though someone hit me in the headwith a hammer, but these key elements in medical historymay be difficult to elicit in confused patients. Rarely, thereare other nonaneurysmal causes of thunderclap headachepresent. These disorders include pituitary apoplexy, arterialdissection, cerebral venous thrombosis, and hypertensiveencephalopathy. Also, thunderclap headache may be idio-pathic.6

  When the patient is seen hours after onset of symp-toms, neurologic examination may reveal nuchal rigidity, cra-nial neuropathy (third or sixth cranial nerve most commonly),or other localized neurologic deficit (aphasia, hemiparesis);however, major neurologic signs generally are absent. Sei-zures may occur in a small percentage of surviving patients,and epilepsy may develop in less than 10%, particularly inthose who had subdural hematoma or cerebral infarctionduring their hospital course.7

  DiagnosisSpontaneous SAH should always be suspected in pa-

  tients with a typical presentation, which includes a suddenonset of severe headache (frequently described as the worstever), with nausea, vomiting, neck pain, photophobia, andloss of consciousness. Physical examination may reveal reti-nal hemorrhages, meningismus, a diminished level of con-sciousness, and localizing neurologic signs. The latter find-ings usually includes third-nerve palsy (posterior communi-cating aneurysm), sixth-nerve palsy (increased intracranialpressure), bilateral lower-extremity weakness or abulia (ante-rior communicating aneurysm), and the combination of hemi-paresis and aphasia or visuospatial neglect (middle cerebralartery aneurysm). Retinal hemorrhages should be differenti-ated from the preretinal hemorrhages of Tersons syndrome,which indicates a more abrupt increase in intracranial pres-sure and increased mortality.2

  Diagnosis SAH can be challenging. Computed tomog-raphy is the first-line diagnostic procedure in patients withsuspected SAH. Historically, CT has 90% to 95% sensitivityfor recent SAH; with modern CT equipment, sensitivity iscloser to 98%. On CT, an aneurysm is rarely seen but whenpresent indicates large size (more than 10 cm).1 Head CTscanning can also demonstrate intraparenchymal hemato-mas, hydrocephalus, and cerebral edema and can help pre-dict the site of aneurysm rupture, particularly in patients withaneurysms in the anterior cerebral or anterior communicat-ing arteries. Head CT scanning is also the most reliable testfor predicting cerebral vasospasm and poor outcome. Be-

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  The Characteristics of Subarachnoid Hemorrhage

  cause of rapid clearance of blood, delayed head CT scan-ning may be normal despite a suggestive history, and sensi-tivity drops to 50% at the seven days.2

  Lumbar puncture should be performed in any patientwith suspected subarachnoid hemorrhage and negative orequivocal results on head CT scanning. Cerebrospinal fluid(CSF) should be collected in four consecutive tubes, withred cell count determined in tubes 1 and 4. Findings consis-tent with subarachnoid hemorrhage include an ele-vatedopening pressure, an elevated red-cell count that does notdiminish from tube 1 to tube 4, and xanthochromia (owingto red-cell breakdown detected by spectrophotometry), whichmay require more than 12 hours to develop.2

  Moreover, examination of CSF is necessary when CT isnormal and has been reviewed for subtle areas of subarach-noid blood (posterior horns, sylvian fissure, and sulci).Prompt ascertainment of diagnosis of SAH is warranted be-cause a ruptures aneurysm has the highest rate of rerupturewithin the initial 48 hours. However, no evidence suggeststhat lumbar puncture increases the risk of aneurismalrebleeding. Testing CSF for the presence of xanthochromia,the yellow tinge in CSF caused by the breakdown productsof hemoglobin is the gold standard for diagnosis of SAH,with sensitivity greater than 99%. Xanthochromia is presentas early as 6 hours after SAH and along with bilirubin re-mains detectable until about 2 to 3 weeks after SAH. Whengross blood is present in initial CSF specimen tube, a de-crease in the quantity of red blood cells in successive speci-men tubes is a frequently used (albeit unreliable) marker forthe absence of SAH. The medicolegal implications can besubstantial if cerebral angiography id deferred on the basisof this loose criterion.6,8

  Determining the presence of xanthochromia is the bestmethod to document disintegrated erythrocytes, but vialsshould be held against a bright light and white backgroundto appreciate the discoloration. Visual inspection is far fromperfect. Spectrophotometry of CSF may document oxyhe-moglobin or bilirubin if visual assessments of the vial withcentrifuged CSF are conflicting. Bilirubin absorbance at 473lis diagnostic (note that iodine used during the proceduremay lead to a false-positive effects).8

  The experience of an aneurysmal SAH often promptsother family members to seek advice on screening for aneu-rysm. If screened on a large scale, aneurysms would be foundin approximately 7% of first degree relatives (parents, sib-lings, and children), with higher chance of an unrupturedaneurysm in a sibling. Screening for aneurysm is compli-cated and unresolved issue. The rupture risk of incidentallydetected aneurysm is low (less than 0.5% annually), but themorbidity of surgical or endovascular repair (5%) is poten-tially substantial. Moreover, noninvasive imaging tests aresuboptimal for detecting unruptured aneurysm.6,9

  ComplicationsCerebral Vasospasm

  Vasospasm has been described as a sustained arterialcontraction unresponsive to vasodilator drugs. This condi-tion is commonly classified as either angiographic or clinical.Angiographic vasospasm refers to visible narrowing of thedye column in an artery, as shown on cerebral angiograms.Clinical vasospasm is the functional manifestation of cere-bral ischemia produced by this arterial narrowing.5

  Cerebral vasospasm is a major complication and contin-ues to be one of the leading causes of death and disabilityfollowing SAH. Vasospasm usually manifests in the first 3 to4 days after the hemorrhage, peaks at one week, and gener-ally resolves over the next 2 to 3 weeks. Blood products thatcollect after SAH and remain in prolonged contact with thecerebral vessel walls induce vasospasm, resulting in narrow-ing of the vessel lumen and compromised cerebral bloodflow and oxygenation. This can result in ischemic sequelaemanifested by the onset of confusion, a decreased level ofconsciousness, speech and motor impairments, increasingblood pressure, and a worsening headache. Approximately7% of patients who reach neurosurgical referral centers willdie of vasospasm and another 7% will be seriously injuredbecause of this condition. The diagnosis of cerebral vasos-pasm is based on both angiographic changes and clinicalchanges. Although 70% of patients may experienceangiographic vasospasm, only 20 to 30% will exhibit delayedischemic neurological deficits or DCI.10

  The etiology and pathophysiology of cerebral vasos-pasm after SAH are complex and are only partially under-stood. Precise molecular mechanisms of vasospasm remainto elucidated, but they include a combination of both in-creased dilator functions. Several theories have been offeredto explain the multifaceted process known to be involved.Considerable evidence supports the hypothesis that oxyhe-moglobin plays a primary role in the development of cerebralvasospasm associated with aneurysmal SAH. After the ini-tial hemorrhage, erythrocytes trapped in the subarachnoidcisterns slowly hemolize, releasing oxyhemoglobin and otherby-products of red cell lysis (e.g., bilirubin and methemoglo-bin) to circulate within the subarachnoid space. Thesespasminogens increase the influx calcium into the vascularsmooth muscle, altering myocyte function and causing pro-longed contraction and vessel constriction.11 SpontaneousSAH increases production of vascular extra-cellular super-oxide anion. Meanwhile endogenous overexpression of ex-tra-cellular superoxide dismutase (EC-SOD) attenuated va-sospasm and oxidative stress but failed to reduce neurologi-cal deficits after SAH. Extra-cellular superoxide anion likelyplays a direct role in the etiology of vasospasm.12

  Transcranial doppler ultrasonography is a noninvasivemethod for monitoring development of cerebral vasospasm.

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  A handled probe is used to transmit and receive a low-fre-quency pulsed wave through the temporal bone of the skull.This ultrasonic wave is both range gated and directionallysensitive, which allows for insonation of the cerebral ves-sels at varying depths and directions. Elevated blood flowvelocities in the middle cerebral artery are correlated withangiographic narrowing of this vessel, although the correla-tion of angiographic vessel narrowing with other cerebralvessels is less reliable.6

  In contrast to the above description, several lines ofevidence cast doubt on angiographically confirmed vasos-pasm as the sole cause of delayed ischemic neurologicaldeficits (DINDs). These include the following: i) the rela-tively limited role that large arteries play in control of cere-bral blood flow, ii) a lack of correspondence between thesites and severity of angiographically confirmed vasospasmand cerebral ischemia, iii) the appearance of cerebral infarctsat autopsy, and iv) the disappointing clinical effects of va-sospasm therapy. On the other hand, SAH also causes con-siderable injury to the vascular endothelium, resulting indesquamation. This accompanied by the appearance of mark-ers of endothelial activation in blood, cerebral dialisate, andcerebrospinal fluid, blood-brain barrier dysfunction, andplatelet accumulation. The fate of microthrombi created byeither mechanic, depends on vessel size. In large arteries,microclots are likely to embolize. Small arterioles would bemore liable to thrombose. Several investigators have dem-onstrated that micro-emboli can indeed cause cerebral inf-arction and symptomatic ischemia in animal and humans.Hence, vasospasm and thrombo-embolism play interrelatedand additive roles in the development of DINDs, and thisinteraction provides opportunities for novel therapeutic ap-proaches.13

  Acute HydrocephalusNormal CSF circulation may become obstructed sec-

  ondary to intraventricular blood due to a thick clot in thebasal cisterns or a clot at the level of the arachnoid villi.Certain clinical and radiographic features may predict theoccurrence of acute hydrocephalus: intracerebral extensionof hemorrhage, posterior circulation aneurysm, and reducedGlasgow Coma Scale score on admission.6

  Acute hydrocephalus after SAH is a necessary consid-eration in patients presenting with altered consciousness;by CT criteria, it is present in 20% of patients. Acute neuro-logic deterioration in the setting of progressive ventricularenlargement on CT is a clear indication for external ventricu-lar drainage. However, the treatment of patients who arriveat the hospital in a comatose state with ventricular enlarge-ment on CT is more controversial because the neurologyimpairment may be a result of the effect of the initial hemor-rhage rather than due to hydrocephalus. Such patients canbe observed initially for 24 hours, and some will improveclinically without intervention. If serial CT scans reveal pro-

  gressive ventricular enlargement or if the neurologic condi-tion deteriorates, external ventricular drainage is indicated.Other clinicians may advocate early placement of externalventricular drains and then observation for possible improve-ment. The most recent data suggest that external ventriculardrainage does not increase the likelihood of aneurismalrehemorrhage when drainage is performed at moderate pres-sure (130 mmHg. If mean arterial pressure

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  General ApproachBlood pressure should be maintained within normal lim-

  its, and if necessary, intravenous antihypertensive agentssuch as labetolol and nicardipine can be used. Once theaneurysm is secured, hypertension is allowed, but there isno agreement on the range. Analgesia is often required, andreversible agents such as narcotics are indicated. Two im-portant factors that are associated with poor outcome arehyperglycemia and hyperthermia, and both should be cor-rected.19-21

  Prophylaxis of deep venous thrombosis should be in-stituted early with sequential compressive devices, and sub-cutaneous heparin should be added after the aneurysmis treated. Calcium antagonists reduce the risk of poor out-come from ischemic complications, and oral nimodipine iscurrently recommended. Prolonged administration of anti-fibrinolytic agents reduces rebleeding but is associated withan increased risk of cerebral ischemia and systemic throm-botic events. Early treatment of aneurysms has become themainstay of rebleeding prevention, but antifibrinolyitictherapy may be used in the short term before aneurysm treat-ment.22,23

  Treatment of Cerebral Vasospasma. Triple H Therapy

  The foundation for prevention and treatment of vasos-pasm is maintaining euvolemia or mild hypovolemia andnormotension or moderate hypertension.6 For patients whobecome symptomatic with DCI due to vasospasm, more ag-gressive intravascular volume expansion (hypervolemia),hemodilution and induced hypertension which is calledtriple H therapy, are used. A hypertensive state is main-tained through the use of vasopressors. Hypervolemia sub-sequently produces hemodilution. These maneuvers are alldesigned to increase cerebral perfusion pressure, improveblood flow to the brain, and decrease the risk of ischemia.5,24

  Triple H therapy is generally started soon as the aneu-rysm has been secured or clipped. Occasionally, a modifiedversion of triple H therapy is used before securement of theaneurysm in order to prevent rebleeding or rupture. Therapyis continued for at least 14 days after the initial hemorrhage,the most common period for vasospasm. Induced hyperten-sion is designed to increase cerebral blood flow and thusenhance perfusion pressure. In order to accomplish this goal,target systolic blood pressure may be as high as 200 mmHg.In addition to fluids, vasopressor and inotropic agents suchas dopamine, phenylephrine, and dobutamine are generallyrequired to maintain systolic blood pressure at this elevatedlevel. Epsxe 1.9.0 full bios and plugin. Therapeutic hypertension is only initiated once theaneurysm has been surgically clipped or coiled. If the aneu-rysm has not yet been repaired surgically or is consideredinoperable, systolic blood pressure is kept between 120 and150 mmHg to minimize the risk of rupture and rebleeding.5, 25

  Hypervolemia is produced by infusing intravenouscrystalloids or colloids sufficient to optimize a patients Star-ling curve. To ensure appropriate intravascular volume andcardiac output in symptomatic patients, invasive monitoringin the form of right atrial or pulmonary artery catheterizationis recommended. Determining the point at which optimiza-tion occurs requires careful hemodynamic assessment. Gen-eral parameters include pulmonary artery wedge pressure of14 to 20 mmHg, cardiac index (calculated as cardiac output inliters per minute divided by body surface area in squaremeters) of 2.2 or greater, and central venous pressure of 10 to12 mmHg.5

  b. NimodipineNimodipine is a calcium channel antagonist of the 1,4-

  dihydripiridine class. It acts primarily by preventing the fluxof calcium ions through voltage-dependent and receptoroperated slow channels of the cell membrane and hencerelaxes vascular smooth muscle. Compared with nifedipine,nimodipine is more lipophilic, a more potent cerebral vasodi-lator and more rapidly and widely distributed in cerebral tis-sue, and can lead to improvement in long-term outcomesafter SAH.5,26 Nimodipine, a calcium channel antagonists witha relatively selective vasodilatory effect on cerebral bloodvessels, has been approved for improvement of neurologicdeficits due to spasm following SAH. Nimodipine has loworal bioavailability (2.7-27.9%), a short half-life (2 hours), ishighly protein bound (98-99%), and is hepatically metabo-lized.27

  Because nimodipine is lipid soluble, it easily crossesthe blood-brain barrier. This leads to decreased smooth-muscle contraction as well as decreased release of vasoac-tive substances from the endothelium, resulting in reducedarterial narrowing. Nimodipine may also have some directneuroprotective properties, including blockage of free-radi-cal attack on the intraneuronal mitochondria, improvementof carbon dioxide reactivity and cerebral oxygen metabolism,or reduction of tissue damaged caused by calcium overloadin ischemic neurons.26

  Nimodipine has been used extensively in the treatmentof the prevention of vasospasm related to SAH. After hem-orrhage, patients are prophylactically given oral nimodipineat a dosage of 60 mg, every 4 hours, for 21 days. Of note, thedrug does not increase the caliber of narrowed cerebral arter-ies on cerebral angiography. Several randomized controlledtrials have been conducted. In a meta-analysis of a numberof published randomized trials, the evidence in favor of rou-tine prophylactic use of nimodipine is strong. Nicardipinehas also been the subject of several controlled trials. Al-though the largest trial showed a considerably lower rate ofischemic deficits secondary to cerebral vasospasm, the overalloutcome was not improved.5, 24,28

  In a rabbit model of chronic cerebral vasospasm, theresults indicate that selective intra-arterial (IA) nimodipine

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  treatment is effective in reversing vasospasm in experimen-tal SAH. IA nimodipine infusion was found more effectivethan its intrathecal (IT) application in basilar artery. Thisprobably due to the limited diffusion of the drug in IT appli-cation. IA and IT applications of nimodipine were equallyeffective in vertebral artery, which demonstrates the potentvasodilator effect of the drug. IA nimodipine infusion wasfound more effective than IA papaverine infusion in bothvertebral and basilar arteries. Selective IA nimodipine treat-ment can be considered as an alternative technique for thetreatment of vasospasm due to SAH. However, further stud-ies are needed to implement this treatment option into clini-cal practice.29

  Treatment Options for AneurysmCurrently, the two main therapeutic options for secur- The marshall mathers lp 2000 zip code.

  ing a ruptured aneurysm are microvascular neurosurgicalclipping and endovascular coiling. Historically, microsurgi-cal clipping has been the preferred method of treatment. Al-though the timing of surgery has been debated, most neu-rovascular surgeon recommends early operation. Evidencefrom clinical trials suggests that patients undergoing earlysurgery have a lower rate of rebleeding and tend to farebetter than those treated later. Securing the ruptured aneu-rysm will also facilitate the treatment of complications suchas cerebral vasospasm. Although many neurovascular sur-geons use mild hypothermia during microsurgical clippingof aneurysms, it has not proved to be beneficial in patientswith lower grades of subarachnoid hemorrhages.30

  When vasospasm becomes refractory to maximal medi-cal management consisting of induced hypertension, hyper-volemia, and administration of calcium channel antagonists,endovascular therapies should be considered. Endovasculartreatment of aneurysm has been available as an alternativeto surgical therapy for the past 15 years. Coils are made ofplatinum and are attached to a delivery wire. Once properposition within the aneurysm is achieved, coils are detachedfrom the wire. Multiple coils of various length and diameterare often packed into the aneurysm to exclude it from thecirculation.2,10

  The International Subarachnoid Aneurysm Trial (ISAT)prospectively examined patients with ruptured aneurysmswho were considered equally suitable for either endovascularcoiling or microsurgical clipping. The authors found that forthis particular subgroup of patients, a favorable outcome,which was defined as survival free of disability at one year,occurred significantly more often in patients treated withendovascular coiling than with surgical placement clips. Therisk of epilepsy was substantially lower in patients who un-derwent endovascular coiling, but the risk of rebleeding washigher. Also, in patients who underwent follow-up cerebralangiography, the rate of complete occlusion of the aneu-rysm was greater with surgical clipping.31,32

  Outcomes in SurvivorsOptimal outcome after aneurysmal SAH depends on

  careful assessment and management of patients throughoutthe course of hospitalization. Critical care nurses play a cru-cial role in this process. Efforts continue to understand thecascade of events that lead to cerebral vasospasm and todevelop more effective treatment.5

  Spontaneous SAH is a major life experience that leadsto additional morbidity in up to 25% of surviving patients.Many patients do not return to work, retire early, and areunable to function at the same intellectual level as before therupture. Numerous clinical factors may influence outcomeafter SAH, including the presenting clinical condition of thepatient, age older than 65 years, presence of posterior distri-bution aneurysms, rupture, intracerebral extension, and de-velopment of cerebral vasospasm or cerebral infarctions.Pre-existing medical conditions and aneurysm size do notappear to affect outcome. Recovery in young patients maybe protracted and better than expected. The most importantclinical factor in predicting poor patient outcome after SAHis the presenting level of consciousness. The natural his-tory of such patients is dismal with higher than 90% mortal-ity. Population-based studies that eliminate the selection biasof referral centers have estimated that approximately 30% ofpatients have poor outcome after SAH.6

  SummarySubarachnoid hemorrhage should always be suspected

  in patients with a sudden onset of typical presentation,which includes a sudden onset of severe headache (fre-quently described as the worst ever or a thunderclapheadache), with nausea, vomiting, neck pain, photophobia,and loss of consciousness. Diagnosis of SAH can be chal-lenging. Computed tomography is the first-line diagnosticprocedure in patients with suspected SAH. However, lum-bar puncture should be performed in any patient with sus-pected subarachnoid hemorrhage and negative or equivocalresults on head CT scanning

  The most dangerous complications of SAH are cerebralvasospasm and acute hydrocephalus. These complicationsshould be kept on mind and predicted earlier, soon after theonset. Triple H therapy is generally started soon as the an-eurysm has been secured or clipped. The calcium channelantagonist nimodipine has strong evidence in preventingcerebral vasospasm related to SAH. When vasospasm be-comes refractory to maximal medical management,endovascular therapies should be considered.

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