Subarachnoid Hemorrhage

Case Presentation

A 49 year old male experienced a sudden onset severe headache followed by a syncopal episode at work. Colleagues called EMS. When they arrived, the patient was awake but confused. He was transported to the ED and arrived within one hour of the event. The patient had no past medical history and was on no medications. On exam, he was a well developed, well nourished male who appeared uncomfortable. His head exam was atraumatic, cervical spine nontender, heart and lungs normal. He was alert but oriented to person only. The right pupil was dilated and the right eye was deviated down and out. No other cranial nerve deficits were noted and the rest of the neurologic exam was normal. His ECG showed II, III, and aVF T wave inversions.

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Subarachnoid Hemorrhage

Introduction

Subarachnoid hemorrhage is a relatively uncommon cause of headache.   Most patients with headache who visit Emergency Departments (EDs) or physicians' offices have more benign tension‑type, sinus-related or migraine headaches.  Among all patients with headache who presented to EDs, retrospective studies have found that approximately 1 to 4 percent had SAH.   Prospective studies found that if only patients with the "worst headache" of their lives and a normal neurologic exam were considered, 12‑33% percent of such patients had SAH.(1)  This proportion increased to 25% when patients whose examinations were abnormal were included. Of the 30,000 patients found to have nontraumatic SAH in the United States annually, roughly 80% have ruptured saccular aneurysms causing acute bleeding into the subarachnoid space primarily at the base of the brain.  Among the remaining 20%, about half have nonaneurysmal peri-mesencephalic hemorrhages.

Despite considerable advances in diagnostic, surgical and perioperative management, the overall outcome remains poor.  One of four patients will suffer a fatal initial hemorrhage and many of the survivors will be severely disabled.  In a population study in Rochester, MN, Ingall and Wiebers noted that 12% of patients with ruptured aneurysms died before receiving medical attention.(2)  Among patients who reach a medical center within 3 days of SAH, approximately 25% die within 3 months despite medical and surgical therapies.(3) Approximately 40% of survivors will have residual neurological deficits including cognitive disturbances.(3)

The leading causes of death or disability include the effects of the initial hemorrhage, rebleeding, and vasospasm.  Management of patients with recent subarachnoid hemorrhage should emphasize therapies to limit the acute effects of the hemorrhage, prevent rebleeding and halt or reverse vasospasm.  Early surgery to repair the aneurysm, aggressive blood and intracranial pressure control and the careful use of antifibrinolytic and antihypertensive drugs with the early use of calcium channel blocking drugs reduces short‑term complications such as recurrent bleeding and vasospasm and improves outcomes.  The importance of early treatment is equal to the importance of early diagnosis.  An early Portuguese study demonstrates the impact of physician misdiagnoses in the treatment of patients with SAH.  Presumably because of the severity of the headache and the associated symptoms, most patients will seek medical attention.(4)  However, many of these patients do not have neurological impairments and do not appear critically ill, and physicians often do not consider the diagnosis.(4)  These diagnostic errors mean that patients are not treated during the critical first days after SAH and they are often made in patients with the greatest potential of benefiting from early aneurysm detection and surgery.

Diagnosis of SAH requires a thorough history and a very high index of suspicion.  Once considered, an accurate diagnosis also requires an understanding of the role of diagnostic CT, lumbar puncture as well as magnetic resonance imaging and cerebral angiography.

What is the prognosis of a patient with a “warning” headache and unrecognized SAH?

The clinical features of subarachnoid hemorrhage are often stereotyped.  The premier symptom of subarachnoid hemorrhage is a sudden, unusually severe headache.  The headache is often instantaneous or cataclysmic in onset.  It can be located anywhere in the head and can be of any quality (throbbing, pressure, etc).  It is often described as the “worst in my life” and has been written about as a “thunderclap” headache that is an intense, acute headache with peak intensity at its onset.  Transient loss of consciousness and seizures commonly occur and frequently happen at the time of hemorrhage.  Occipital or neck pain is relatively common and pain in the eye, face, or back may develop.  

The signs of subarachnoid hemorrhage are often more subtle.   Many alert patients present only with headache.  Most patients with SAH do not have focal neurologic signs. They may have only subtle or no neurologic abnormalities and may not have meningeal signs.   More common focal neurologic signs include a III nerve palsy with an internal carotid-posterior communicating artery aneurysm, hemiparesis with a middle cerebral artery aneurysm, or paraparesis/neurogenic bladder/encephalopathy with an anterior communicating artery aneurysm.

Roughly half of all patients with SAH have atypical symptoms features.  Without focal neurologic deficit or a disturbance of consciousness and perhaps a minor headache, the diagnosis of subarachnoid hemorrhage is often missed.  Overall, there is a delay in diagnosis leading to delays in treatment in approximately 25% of patients who have only a headache.(5,6)  These “minor” headaches are often retrospectively diagnosed as warning leaks or minor or “sentinel” hemorrhage.(7)  In one series, it was diagnostic error rather than failure to see a physician or a delay in transfer that accounted for over 70% of delay in treatment of SAH. (4)

Patients later found to have SAH are often diagnosed as having other causes of headache, in particular migraine or tension headaches. (8) Also, concomitant vomiting, nausea, photophobia, and phonophobia often lead to the diagnosis of migraine or a viral illness.  Headache and stiff neck are often seen as viral meningitis.  Young patients with acute confusion or mental status changes without other signs of stroke may be diagnosed as having an intoxication from drugs or alcohol or considered to have a primary psychiatric illness.  (9) Hypertension is very common after subarachnoid hemorrhage and may lead to the misdiagnosis of hypertensive encephalopathy.  It is presumably due to high levels of circulating catecholamine released at the time of hemorrhage. A markedly elevated blood pressure and headache may prompt the diagnosis of a hypertensive crisis or hypertensive encephalopathy. (6,8) Many patients with SAH have cardiac dysrhythmia and electrocardiographic patterns that resemble myocardial ischemia or infarction.  These patients are often diagnosed with a primary cardiac disorder. (6,8,10) 

Misdiagnosed “warning” headaches are generally followed by major aneurysmal SAH in approximately 50% of patients. Between 20 and 50% of patients with documented subarachnoid hemorrhage report a distinct, unusually severe headache in the days or weeks before the index episode of bleeding.  These headaches are considered to be limited hemorrhages or “sentinel” leaks.  The pathophysiology is similar to the larger hemorrhage that occurs with complete rupture of the aneurysm.  “Warning” headaches are serious and, when considered, should serve as an opportunity to screen the patient for very treatable pathology before a full-blown hemorrhage occurs.

Most patients with SAH have more typical symptoms but many will have atypical ones and may have subtle findings.  The Emergency Physician must appreciate the wide spectrum of clinical presentations.  A careful history and targeted physical examination must be done to identify patients who should be evaluated for SAH.

What is the mini-mental status exam and how is it helpful in assessing patients with altered mental status?

Patients with SAH often have headache and, at times, this is accompanied only with changes in mental status.  The assessment of the mental state in patients in the Emergency Department can be very difficult.  The physician generally does not know the patient’s baseline mental state, whether alcohol or drugs are clouding the patient’s sensorium, or whether the patient is suffering an electrolyte abnormality or infection that may contribute to changes in mental state.

The Mini‑Mental State Exam (MMSE) is generally considered a test of organic brain disease and dementia.  The MMSE asks the patient to answer questions and perform tasks that evaluate cognitive skills of attention, short‑term or working memory and gross orientation.  These more subtle abnormalities are often the only deficits found with brain injury including SAH.

The assessment of mental status can be particularly challenging in elderly patients in the Emergency Department.  The prevalence of mental status abnormalities, particularly alterations in consciousness, in the elderly is high among ED patients.  Alterations in mental status are present in 40 to 66% (11) and delirium has been found in 24% of these patients over 70 years who visit the ED.  It is even more common in yet older patients with more severe illness. (12)

Nonetheless, the test seem to be reliable. And, importantly, the abnormalities detected with the use of the MMSE are more likely to go unnoticed when mental status is assessed without using such standardized testing. (11) 

Formal mental status testing in the ED to assess cognitive function is often limited by the amount of time necessary to apply the test.   However, abbreviated versions of mental status examinations have been studied that can be administered within five minutes by nursing personnel. Merigian and Hedges used an Abbreviated Mental Status Examination (AMSE) to evaluate ED patients with normal neurologic function as well as acute drug overdose patients.  They concluded that the AMSE might be useful for stratifying cognitive function in acute drug overdose patients and for identifying patients at increased risk for an adverse outcome from their overdose. (13)  A six‑item Brief Mental Status Examination (BMSE) was administered to ED patients to assess their mental status (normal, mildly impaired, or severely impaired) and competence to refuse emergency care. In this study, BMSE scores correlated significantly with physicians' assessments of patients' mental status and competence to refuse care.   They found it useful in decision-making 98% of the time.(14)

Traditional mental status screens have limited sensitivity in detection of focal brain damage.  They are generally considered tests of organic brain disease and dementia.  And yet, the MMSE has been used to test cognitive skills in patients who have had traumatic brain injury. (15) Also, when clock drawing, a measure of constructional ability, was added to the MMSE, it became a sensitive indicator of functional outcome when applied during the recovery phase of right hemisphere stroke. (16) The MMSE has been used to identify cognitive dysfunction after left hemispheric stroke and has been used as an outcome measure to assess the effects of pharmacologic therapies after stroke. 

The MMSE has been used in the assessment of mental status in the acutely injured patient in the Emergency Department.  Mental status testing is not sensitive or accurate enough to identify focal disease in head trauma. Even if refined, it is unlikely that clinical evaluation will result in diagnostic accuracy comparable with that of CT scanning. Accordingly, any patient who has suffered a loss of consciousness or amnesia following head injury should have an urgent cranial CT scan. (17)  However, patients that have sustained head injuries can have subtle cognitive dysfunction even when apparently recovering well.  Gross measures of mental status such as the Glasgow Coma Scale are insensitive in detecting subtle cognitive and memory function abnormalities.   For this reason, some suggest that all patients with injury significant enough to warrant hospitalization need formal psychological evaluation.(18)  Patients with milder forms of brain injury might also have more subtle functional abnormalities that require more extensive mental status testing to detect.

Patients with nonfocal, extensive, or generalized brain injury are more likely to have memory and cognitive dysfunction and alterations in consciousness.  The findings may be very subtle in SAH, particularly if the amount of bleeding is small and the patient presents long after symptom onset.  One of the emergency physician’s greatest challenges is to detect not only the larger, more obvious, subarachnoid hemorrhage but also the smaller bleed.  A thorough physical and mental status exam can help to improve the likelihood of detecting SAH.  This may be particularly important when the symptoms or the amount of bleeding are mild.

The MMSE has good test-retest reliability.  It can, then, be used repeatedly to monitor the patient’s progress and guide therapy throughout the patient’s hospitalization and rehabilitation.  

What are the ECG changes found with intracranial events and why do they occur?

Electrocardiographic alterations in the course of subarachnoid hemorrhage have long been recognized.  ECG changes occur in 50% to 100% of patients during the acute stage of SAH.  The most frequent anomalies reported have been elevation or depression of the ST segment, very negative or positive deep T waves, lengthening of the QT interval and the presence of U waves. (19-21)  In most cases, these abnormalities are clinically inconsequential and are attributed to neurally mediated electrophysiologic effects.   Studies show that, even in patients with SAH who have ECG findings consistent with ischemia or myocardial infarction, the risk of death resulting from cardiac causes is low.  Rather, early ECG abnormalities have been correlated with the severity of the neurologic injury.  Patients with more intracranial or an intracerebral clot seen on computed tomography were more likely to have ECG abnormalities. (22) And, significant QT interval prolongation and arrhythmias were observed after rats were given subarachnoid injections of packed red blood cells. (23)   Certain ECG abnormalities, in particular prolongation of the QT interval (especially if associated with hypokalemia), is frequently found in patients with life-threatening arrhythmias such as ventricular flutter /fibrillation and torsade de pointes. (22)

There are two mechanisms that might mediate ECG changes in patients with SAH, ie, autonomic neural stimulation from the hypothalamus or elevated levels of circulating catecholamine.  Hypothalamic stimulation may cause ECG changes without associated myocardial damage whereas elevated catecholamine levels have been correlated with QT interval prolongation and myocardial damage. (23)

Some SAH patients do show evidence of structural cardiac damage.  Plasma levels of creatine kinase myocardial isoenzyme (CK-MB) are mildly elevated in 20% to 50% of patients (21-22).   A characteristic form of myocardial pathology, contraction band necrosis, is commonly found at autopsy (25) and has been produced in experimental SAH models.(26) More recently, echocardiography studies have demonstrated reversible abnormalities of left ventricular contraction and, in severely affected patients, reductions in cardiac output after SAH.(27) And, important in the acute setting, are the findings that symmetrical T wave inversion and severe QTc segment prolongation can identify patients at risk for myocardial dysfunction.(21) These findings suggest that abnormal early ECG findings or elevations of CK-MB should be pursued with echocardiography.   Echocardiography can identify those patients with wall motion abnormalities.  These structural cardiac abnormalities can lead to reductions in cardiac output resulting in lowered blood pressure and cerebral perfusion.  Reductions in cerebral blood flow, intracerebral volume and perfusion can increase the risk of vasopasm and cerebral ischemia.  These patients are more likely to benefit from antiischemic medications.  The potential impact of neurogenic cardiac injury on left ventricular performance after SAH may have important implications because some 30% of patients develop delayed cerebral ischemia related to vasospasm.  Vasospasm is generally associated with a loss of autoregulation.  Cerebral blood flow in ischemic area can vary passively with changes in blood pressure and cardiac output.  Hypovolemia can, then, cause of symptomatic vasospasm, echocardiography can identify those patients likely to benefit from blood pressure and cardiac output augmentation.(22)

 

How valuable is a negative CT scan in SAH? Is a lumbar puncture still indicated with the new “high-resolution” CT scanners?

Computed tomography  is the single most important diagnostic test in the evaluation of a patient with suspected SAH.  Its yield on the day of the ictus approaches 95%.  It is noninvasive and generally available at most hospitals in the United States. 

The value of CT depends on the quality of the study, the timing of the study, the severity of the hemorrhage, and on the skill level of the reader.  The technique used is important.  It is recommended that very thin cuts (3 mm in thickness) be done through the base of the brain because thicker cuts (10 mm) miss small collections of blood.   The plane of scanning should be parallel to the hard palate.  Blood and adjacent bone, which both appear white, can be difficult to distinguish from one another, especially in small hemorrhages.  Artifacts of motion in the scans of restless patients can render such scans technically suboptimal and obscure the diagnosis.  Also, because the visualization of blood on CT is a function of the hemoglobin concentration, the subarachnoid blood of anemic patients may appear isodense rather than white.

The sensitivity of CT decreases over time from the onset of symptoms.  The process of clearing the blood and clot lysis begins early after hemorrhage making the detection of small amounts of blood more difficult over a short period of time.  Studies using modern third‑generation CT scanners have shown decreases in sensitivity for SAH from as high as 98% to 100% when studies were done within the first 12 hours after the onset of symptoms to 93% when done between 12 and 24 hours after the start of symptoms. (27-30)

The sensitivity of any diagnostic test that requires interpretation such as CT also depends on the skill level of the reader.  It is important to note that the studies sited assessing the value of CT scanning in SAH were interpreted by a radiologist or, more often, by a neuroradiologist.  Many hospitals do not have these consultants immediately available and CT scans are initially interpreted by Emergency physicians.  Skill levels among emergency physicians, neurologists and general radiologists and between individual physicians vary greatly.  The impetus is on the Emergency Physician to understand the limitations of diagnostic tests, particularly those that require interpretation.  

The sensitivity of CT to detect blood is also correlated with the amount of blood present which is at least somewhat correlated with the severity of symptoms and signs.  As such, more alert patients with subtler signs are more likely to have normal CT scans than those with diminished mental status (3). In the International Cooperative Study, 15% of 638 alert patients had normal scans.   Patients with small hemorrhage, who are the most likely to receive an incorrect clinical diagnosis, are also more likely to have negative results on CT.

Lumbar puncture to obtain CSF for examination remains an important diagnostic tool when the clinical presentation suggests SAH and a CT scan is negative, equivocal, or technically inadequate. (5,28).

In patients suspected of SAH, the CSF is tested for the presence of persistent blood and/or xanthochromia.  CSF obtained from patients with SAH having symptoms of less than about 12 hours duration will be persistently bloody.  In order to help differentiate a “traumatic” lumbar puncture from truly bloody CSF, the CSF should be centrifuged and examined as quickly as possible looking for xanthochromia. It should be done immediately after lumbar puncture to avoid hemolysis of red blood cells following the procedure, which will confuse the diagnosis. (5)

When the lumbar puncture is delayed several days following the subarachnoid hemorrhage, CSF findings will be only xanthochromia or perhaps an inflammatory reaction similar to aseptic meningitis.  Xanthochromia is the discoloration caused by the presence of pigmented oxyhemoglobin (reddish pink) and bilirubin (yellow) that result as hemoglobin, released from lysed erythrocytes, is metabolized. Oxyhemoglobin can be detected within hours but bilirubin generally takes up to 12 hours or so to manifest.  This makes the timing important when interpreting the results of a lumbar puncture. (31)  

In general, the findings of negative CT and CSF studies in a patient with symptoms of recent SAH effectively eliminate the diagnosis.  However, if these procedures are not performed within a few days of the ictus, these negative studies may not eliminate the possibility of a ruptured aneurysm, and other tests, including arteriography, may be required. 

What is the role of MRI/MRA in SAH?

Because of its wide availability, relatively low cost, and convenience for ill patients, and because there is more experience with its interpretation as compared to more advanced magnetic resonance (MRI) technology, CT remains the imaging method of choice for detecting SAH. Although it is continually advancing and can detect aneurysms, standard MRI is considered inferior to CT for the detection of acute subarachnoid hemorrhage.  However, as MR imaging is becoming more available and MR angiography is becoming an attractive alternative to angiography, more and more clinicians encourage the use of MRI/MRA in SAH.  MRI is attractive over CT in that it does not rely on ionizing radiation.  Also, MRI can delineate infarction, often better and earlier than CT. Because of the lack of MRI signal from bone and thus the lack of transverse artifact from bone often seen with CT, lesions in the posterior fossa are very well visualized. With MRI it is possible to obtain images in the transverse, coronal, and sagittal planes, which provides for good evaluation of lesion size.

MRI can distinguish vascular malformations and can detect subdural hematoma.  However, for detection of intracerebral hemorrhage and subarachnoid hemorrhage, MRI is, at most, comparable and may actually be inferior to CT at the present time. (32,33)  The sensitivity of MRI alone has been found to be quite high in the diagnosis of subarachnoid hemorrhage.  However, the images are at times obscured by flow artifacts.  Nonetheless, there is a general sense that as the modality is perfected, it will provide information not only about the anatomy but also about the dynamic status of the brain and go beyond the capability of CT. (34)

The value of magnetic resonance imaging (MRI) that includes angiography (MRA) is in its ability to demonstrate ruptured and unruptured intracranial aneurysm. Since excellent recovery is not expected in patients with severe subarachnoid hemorrhage, management of unruptured aneurysms is essential in reducing the overall mortality and morbidity rates.  Less invasive imaging tools such as magnetic resonance angiography have been used to screen large groups of people for unruptured intracranial aneurysms.  This practice is widespread in Japan where it is believed that early detection and prophylactic surgery for unruptured aneurysms will improve the overall outcome of aneurysm treatment in the future. (35)

Koegh and Vhora found that MR imaging and angiography could adequately identify and characterize lesions so as to enable early surgery on ruptured intracranial aneurysms without resorting to intra‑arterial digital subtraction in the acute phase of the illness.  Over a 25‑month period, sixty‑three aneurysms in 122 patients were demonstrated and 55 of these were surgically corrected.  The authors concluded that, in view of the multiple images obtained from MRI/MRA, it may often be superior to conventional digital subtraction angiography.  The fact that it avoids radiation, is non‑invasive, and is relatively easily obtained makes this modality very attractive in the acute phase of care to help plan early aneurysm clipping after SAH. (37)

One study found MRA to be as sensitive and specific a test for intracranial aneurysm as selective intra‑arterial digital subtraction angiography (IA‑DSA) in patients with SAH. (38)  But, generally, MRA lacks the sensitivity of IA-DSA and of conventional angiography. (39,40) One report suggested that, while MRA was able to detect 19 of 22 aneurysms, that at least one-third of the studies in their series were limited by flow artifacts and poor resolution. (41)

The 3D display of the intracranial vessels obtained with MRA sometimes demonstrates the aneurysms better than DSA. However, due to its high spatial resolution, DSA more clearly defines the overall anatomy of the walls of the normal and abnormal vessels. (42) It is possible that the future will show us the progressive replacement of the invasive technologies by MRA.  However, at the present stage of Magnetic Resonance development there is still an important, if not crucial, role for catheter angiography in the diagnosis of most of the diseases producing stroke syndromes including SAH. (43)

Using a combination of diffusion‑weighted (DW) and hemodynamically weighted (HW) MRI can identify tissue ischemia and early ischemic injury in patients with vasospasm after SAH.  By analyzing the passage of an intravenous contrast bolus through the brain a multislice map of relative cerebral blood volume (rCBV), relative cerebral blood flow (rCBF), and tissue mean transit time (tMTT) can be constructed.   Ischemic lesions on DW images were seen encircled by a large area of decreased rCBF and increased tMTT in all patients with symptomatic vasospasm.  Importantly, MRI images were normal in the asymptomatic patient with angiographic vasospasm and the patient with normal angiogram and no clinical signs of vasospasm. If  DW/HW MRI can detect early changes in tissue hemodynamics associated with  ischemic injury and can identify those patients with vasospasm at risk for ischemia, the technique could become a useful tool in the clinical management of patients with SAH. (44)

What is the role of nimodipine in the management of patients with subarachnoid hemorrhage?

Just after the patient is beyond the complications that surround the initial hemorrhage and beyond the risk of early rebleeding, the risk of arterial vasospasm and ischemic injury becomes most important.  Vasospasm is a leading cause of death or disability after subarachnoid hemorrhage.  It occurs in approximately 70% of persons with ruptured aneurysms and produces symptoms in 20-30%. (45,46)  Vasospasm is rarely identified in the first 3 to 4 days after the hemorrhage.  It peaks at one week and then resolves over the next 2 to 3 weeks.  Vasospasm can be localized or involve several intracranial arteries.  Factors released at the time of the bleeding induce vasoconstriction that decreases cerebral blood flow.  The reduction in blood flow leads to brain ischemia and stroke.

The symptoms of vasospasm gradually evolve with waxing and waning of signs such as new headache, seizures, or decreased alertness. 

Transcranial Doppler ultrasonography is an effective screening tool for detection of vasospasm. (47-49)  Doppler can noninvasively measure cerebral flow velocities which have been correlated with the severity of arterial narrowing.  It can detect changes in flow velocities that precede the appearance of neurological signs by 24-48 hours, and therapies to prevent ischemia can be started before ischemia begins.

Several measures can help prevent ischemia and the complications of vasospam after SAH. (45,46)  Treating hypovolemia, generally by avoiding dehydration, will improve circulation.  Lowering increased intracranial pressure will also improve cerebral perfusion pressure.  Careful administration of antifibrinolytic and antihypertensive medications and, in particular, calcium channel blocking drugs, will also lessen the likelihood of ischemic injury.

Calcium channel blocking agents work by reducing intracellular and transmembrane calcium movement.  Transmembrane fluxes of calcium play an important role in the contraction of vascular smooth muscle and platelet aggregation.  Calcium fluxes are also an important factor in cell ischemia.  Drugs that block calcium channels will limit transmembrane fluxes, which may be effective in the prevention of ischemic stroke following subarachnoid hemorrhage.   The ideal calcium channel blocking agent is one that has selective cerebrovascular effects, crosses the blood-brain barrier, and has limited cardiovascular effects.  Early administration of a specific 'cerebral' calcium antagonist like nimodipine after SAH protects neural cells and prevents Ca2+‑induced smooth‑muscle contraction of cerebral vessels by preventing intracellular calcium overloading which encourages ischemic deficits after SAH. Clinical studies of nimodipine, a cerebrovascular-specific calcium channel blocker, have shown an improvement in outcome after SAH with a decrease in the number of deaths due to delayed ischemic deterioration. (50-55) A four center study in the UK of oral nimodipine versus placebo administered 4 hours after SAH showed a reduction in the incidence of cerebral infarction from 33% in those given placebo to 22% in those given nimodipine. (54)  Poor outcomes were also significantly reduced by 40% with nimodipine. (54,55)

Interestingly, while the drug improves survival and functional outcome after SAH, it seems to be due to its antihypertensive effects and its neuron protective effects rather than on any demonstrable change on vessel caliber or on vasospasm. (56)

Nimodipine is routinely used after SAH. Clinical studies have shown that it can induce mild hypotension so that blood pressure must be carefully monitored during its use.  Nonetheless, despite side effects, early administration of oral or intravenous nimodipine is indicated to help prevent delayed cerebral ischemia after SAH.

 

Take Home Points/Conclusions

§         While classic symptoms of SAH have been stereotyped, many patients present with atypical symptoms and subtle signs often attributed to other causes.  The impetus on the clinician is to identify these “warning” bleeds before the patient has a larger, more catastrophic hemorrhage.

§         Despite the advances in CT, there is a small but important percentage of patients with SAH that have negative CT.  To optimally screen for intracranial hemorrhage,  the clinician needs a thorough understanding of the role of CT, lumbar puncture as well as the more recently developed MRI/MRA technology.

§         Early therapy includes management of the patient’s immediate needs and making an effort to prevent potential post-SAH complications.  This requires attending to the basic ABC’s and recognizing and treating arrhythmias.  Nimodipine should be administered early in the course to help improve outcome.  Doppler or magnetic resonance angiography can be used to monitor cerebral blood flow so that vasospasm can be recognized and treated as quickly as possible to decrease the high degree morbidity and the mortality associated with SAH. 

   

Outcome of Case

The patient was placed on a monitor and found to have a variety of nonsustained atrial arrhythmias.   CT scan showed subarachnoid hemorrhage.  Neurosurgical consultation was obtained and oral Nimodipine administration was suggested.  During the hospital course, he underwent angiography that revealed a ruptured right posterior communicating artery aneurysm.  He underwent aneurysm clipping and developed symptomatic vasospasm 4 days post op.  After rehab, he was left with only a mild right hemiparesis. 

 

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Subarachnoid Hemorrhage

Reference List

 

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32. DeWitt LD: Clinical use of nuclear magnetic resonance imaging in stroke.Stroke 1986 Mar; 17(2):328‑31.

33. Chrysikopoulos H, Papanikolaou N, Pappas J: Acute subarachnoid hemorrhage: detection with magnetic resonance imaging. Br J Radiol 1996 Jul; 69(823):601‑9

34. Wiesmann M, Mayer TE, Medele R, et. al: Diagnosis of acute subarachnoid hemorrhage at 1.5 Tesla  using proton‑density weighted FSE and MRI sequences. Radiology 1999;39(10):860‑5

35. Yoshimoto T, Mizoi K: Importance of management of unruptured cerebral aneurysms.   Surg Neurol 1997 Jun; 47(6):522‑5; discussion 525‑6.

36. Raaymakers TW: Aneurysms in relatives of patients with subarachnoid hemorrhage:      frequency and risk factors. MARS Study Group. Magnetic Resonance Angiography in Relatives of patients with Subarachnoid hemorrhage. Neurology 1999 Sep; 53(5):982‑8

37. Keogh AJ, Vhora S: The usefulness of magnetic resonance angiography in surgery for intracranial aneurysms that have bled. Surg Neurol 1998 Aug; 50(2):122‑7; discussion 127‑9.

38. Gouliamos A, Gotsis E, Vlahos L, et al: Magnetic resonance angiography compared to intra‑arterial digital subtraction angiography in patients with subarachnoid hemorrhage. Neuroradiology 1992; 35(1):46‑9

39. Wilcock D, Jaspan T, Holland I, et al: Comparison of magnetic resonance angiography with conventional angiography in the detection of intracranial aneurysms in patients presenting with subarachnoid hemorrhage.  Clin Radiol 1996 May; 51(5):330‑4

40. Schuierer G, Huk WJ, Laub G: Magnetic resonance angiography of intracranial aneurysms: comparison with intra‑arterial digital subtraction angiography. Neuroradiology 1992; 35(1):50‑4

41. Tamatani S, Sasaki O, Takeuchi S, et al: Detection of delayed cerebral vasospasm, after rupture of intracranial aneurysms, by magnetic resonance angiography [see comments] Neurosurgery 1997 Apr; 40(4):748‑53; discussion 753‑4

42. Anzalone N, Triulzi F, Scotti G: Acute subarachnoid hemorrhage: 3D time‑of‑flight MR angiography versus intra‑arterial digital angiography.  Neuroradiology 1995 May; 37(4):257‑61

43. ManaJas R, Cerqueira L: Angiography in the diagnosis of cerebrovascular pathology.  Current indications and controversies.  Acta Med Port 1993 Aug; 6(8‑9):411‑20

44. Rordorf G, Koroshetz WJ, Copen WA, et al: Diffusion‑ and perfusion‑weighted imaging in vasospasm after subarachnoid hemorrhage. Stroke 1999 Mar; 30(3):599‑605

45. Heros RC, Zervas NT, Varsos V: Cerebral vasospasm after subarachnoid hemorrhage: an update.  Ann Neurol. 1983;14:599-608

46. Kassell NF, Sasaki T, Colohan AR, Nazar G: Cerebral vasospasm following aneurysmal subarachnoid hemorrhage.  Stroke 1985;16:562-572

47. Aaslid R, Huber P, Nornes H: Evaluation of cerebrovascular spasm with transcranial Doppler ultrasound.  J.Neurosurg. 1984;60:37-41.

48. Harders A, Gilsbach J: Haemodynamic effectiveness of nimodipine on spastic brain vessels after subarachnoid hemorrhage evaluated by the transcranial Doppler method. A review of clinical studies. Harders and Gilsbach.  Acta Neurochir Suppl (Wien) 1988; 4:21‑28.

49. Sloan MA, Haley EC, Kassell NF, et al: Sensitivity and specificity of transcranial Doppler ultrasonography in the diagnosis of vasospasm following subarachnoid hemorrhage.  Neurology 1989;39:1514-1518

50. Allen GS, Ahn HS, Preziosi TJ, et al: Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage.  N.Engl.J.Med. 1983;308:619-624

51. Feigin VL, Rinkel GJ, Algra A, et al.: Calcium antagonists in patients with aneurysmal subarachnoid hemorrhage: a systematic review [see comments]  Neurology 1998: 50(4):876‑83

52. Philippon J, Grob R, Dagreou F et al.: Prevention of vasospasm in subarachnoid hemorrhage. A controlled study with nimodipine.  Acta Neurochir (Wien) 1986; 82(3‑4):110‑4

53. Grotenhuis JA, Bettag W: Prevention of symptomatic vasospasm after SAH by constant venous infusion of nimodipine. Neurol Res. 1986;8:243-246.

54. Pickard JD, Murray GD, Illingworth R et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid hemorrhage: British aneurysm nimodipine trial. BMJ. 1989;298:636-642.

55. Ohman J, Heiskanen O: Effect of nimodipine on the outcome of patients after aneurismal subarachnoid hemorrhage and surgery. J Neurosurg 1988;69(5):683‑686.

56. Sahlin C, Brismar J, Delgado T et al.: Cerebrovascular and metabolic changes during the delayed vasospasm following experimental subarachnoid hemorrhage in baboons, and treatment with a calcium antagonist. Brain Res 1987; 403(2):313‑332.

 

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Subarachnoid Hemorrhage

Annotated Bibliography

1.         Ferro J, Lopes J, Melo T, et al: Investigation into the causes of delayed diagnosis of subarachnoid hemorrhage. Cerebrovasc dis 1991;1:160‑4. 

This Portuguese study demonstrates the impact of physician misdiagnosis in the treatment of patients with recent subarachnoid hemorrhage.  Because of the severity of the headache and associated symptoms, most patients will seek medical attention.  However, many of these patients do not have neurologic impairments and do not appear ill, and physicians often do not consider the diagnosis.  In this study, only 4 of 63 (6%) of patients failed to see a physician whereas 94% suffered a delay in treatment as a result of a diagnostic error (73%) or a delay in transfer (20%).  The authors suggest that these diagnostic errors mean that patients are not treated during the critical first days after subarachnoid hemorrhage. 

 

2.         Edlow JA, Caplan LR: Avoiding the pitfalls in the diagnosis of subarachnoid hemorrhage. NEJM January 2000;342(1):29‑36.

This recent review of the literature emphasizes the need for the Emergency Physician and Primary Care physician to understand the pitfalls in the diagnosis of subarachnoid hemorrhage.  They provide strategies for identifying those patients who warrant evaluation and for establishing the diagnosis.  The authors warn that, in the absence of more “typical” symptoms and signs, clinicians often miss the diagnosis.  The authors emphasize how properly performed and interpreted CT and lumbar puncture in patients with acute, severe headaches will identify the vast majority of patients with SAH.  Symptomatic treatment of headache, discharge, and outpatient follow‑up are a safe practice in patients whose results are normal. An important exception would be a patient who presents more than two weeks after the onset of symptoms, who may often have negative CT findings and may have normal CSF.  There is also a group of patients in whom diagnostic test results are ambiguous or are at particularly high risk for aneurysm.  They should undergo neurologic or neurosurgical consultation and vascular imaging by MRI, CT or conventional angiography.

 

3.         Mayer, P.L., et al: Misdiagnosis of symptomatic cerebral aneurysm: prevalence and correlation with outcome at four institutions. Stroke; September 1996 27(9):1558.

This retrospective study examined the records of 217 patients with symptomatic subarachnoid hemorrhage (SAH) to determine the frequency of initial misdiagnosis and the influence of misdiagnosis on outcome.  Twenty-five percent of cases later found to have SAH were initially misdiagnosed.  Almost all of these patients had minimal findings other than headache at the time of their initial presentation.  The cases were most commonly diagnosed as viral meningitis (15%), migraine (13%) and headache of uncertain etiology (13%).  There was a relatively high rate of false negative CT scans among patients misdiagnosed on initial presentation (20%) half of which were retrospectively read as SAH.   The outcome of patients who were misdiagnosed was poorer than in patients correctly diagnosed with SAH.  Almost 50% of “misdiagnosed” patients had recurrent bleeding before aneurysm surgery compared with 2% of those receiving a correct initial diagnosis.  The overall functional outcome was much better (91%) when patients presented in good clinical condition and were correctly identified as having SAH than patients who were initially misdiagnosed (53%).  This study confirms the need to maintain a high suspicion for SAH and to pursue the appropriate diagnostic testing in order to identify small bleeding episodes that so often are precede larger hemorrhages.

 

4.         Jakobsson KE et al: Warning leak and management outcome in aneurysmal subarachnoid hemorrhage, J Neurosurg December 1996 85(6):995.

This multicenter study examined frequency of warning leaks and their impact on outcome.   A warning leak was reported for approximately 20% of the 422 patients presenting with SAH.   These episodes occurred a mean of eleven days prior to the onset of clinically apparent SAH.  Roughly half of the patients with warning leaks (41%) presented for medical attention, and none were correctly diagnosed.  CT scans were negative in the three patients undergoing this diagnostic test, and no patient had a lumbar puncture.  Sixty-three percent of patients without warning leaks compared with 54% of those with warning leaks were considered to have a good neurologic recovery.  In contrast,  88% of the patients without warning leaks had a good six-month neurologic recovery.  The authors argue that correct identification of patients with warning leaks could improve the rate of favorable outcomes after SAH by 28%.   They suggest an aggressive approach using both CT and lumbar puncture to lower the rate of misdiagnosis.

 

5.         Mayer SA, Lin J, Homma S, et al: Myocardial injury and left ventricular performance after subarachnoid hemorrhage . Stroke. 1999;30:780-786.

Electrocardiographic abnormalities are commonplace after SAH.  And, in most cases, these abnormalities are clinically inconsequential.  However, up to half of patients with SAH suffer a characteristic form of myocardial pathology called contraction band necrosis.  This study questioned the clinical relevance of this cardiac injury.  They measured wall motion in 72 patients with elevations in CK-MB levels.  They found that abnormal left ventricular wall motion occurred only in patients with CK-MB levels >2%, had poor neurological grade (Hunt and Hess III to V).  The authors suggest that CK-MB could be a useful marker of subsequent cardiac compromise that rendered the patient at higher risk for hemodynamic deterioration and as a marker for the development of vasospasm after SAH. 

 

6.         Mayer SA, LiMandri G, Sherman D, et al: Electrocardiographic markers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage.  J Neurosurg 1995; 83(5):889-896. 

This study assesses the relationship between serial electrocardiograms and echocardiograms in SAH patients without preexisting cardiac disease.  They found that 5 of 57 (8%) patients with SAH had wall motion abnormalities by echocardiography and that most of these patients suffered hypotension or pulmonary edema within 6 hours of the SAH as compared to none of the 52 patients without wall motion abnormalities.  They found that patients with abnormal wall motion were much more likely to have symmetrical T-wave inversion (5/5 vs 7/52) or severe QTc segment prolongation (5/5 vs 3/52) on their ECGs.  The authors suggest that these ECG abnormalities might, especially if associated with CK-MB elevations and a poor neurologic grade, serve as useful indicators of myocardial dysfunction and as a signal for more aggressive monitoring and therapy.

 

7.         Sames TA, et al: Sensitivity of new‑generation computed tomography in subarachnoid hemorrhage. Acad Emerg Med January 1996; 3(1):16.

This retrospective study examined the sensitivity of newer‑generation CT scanning for SAH.  The initial radiology interpretation made by either a neuroradiologist, a general radiologist or a radiology resident was reviewed.  Among 181 patients in whom acute nontraumatic SAH was ultimately diagnosed, the sensitivity of the initial CT scan was 91.2% overall, 93.1% in patients with symptoms for less than 24 hours, and 83.8% in those with symptoms for more than 24 hours.  Lumbar puncture was diagnostic for SAH in all patients with "normal" CT scans.  The authors suggest that LP should be performed in all patients with normal CT scans and symptoms suggestive of SAH. 


8.         The International Study of Unruptured Intracranial Aneurysm Investigators.  Unruptured Intracranial Aneurysms -- Risk of Rupture and Risks of Surgical Intervention.  NEJM 1998;339(24):336-342.

This large, multicenter study was undertaken to assess the relative risks of aneurysmal rupture among asymptomatic patients and the risk of surgery to repair these unruptured aneurysms.  The authors noted that, while the morbidity and mortality of aneurysmal hemorrhage is high, the incidence of their rupture in the general population is very low.  They estimated that cumulative rate of rupture of aneurysms less than 10 mm in diameter was less than 0.5% per year and 6% for the first year for “giant (25 mm in diameter)” aneurysms.  On the other hand, there was between a 13% and 17.5% overall rate of surgery-related morbidity and mortality among the over 700 patients who had prior aneurysmal repair after suffering a SAH. The authors argue that, on the basis of the rupture rates and treatment risks in their study, surgery is unlikely to reduce the morbidity or mortality of patients with unruptured intracranial aneurysms less than 10 mm in diameter.

 

9.         Keogh AJ, Vhora S: The usefulness of magnetic resonance angiography in surgery for intracranial aneurysms that have bled. Surg Neurol 1998 Aug; 50(2):122‑7; discussion 127‑9.2

This prospective study was set up to establish whether satisfactory magnetic resonance imaging (MRI) including angiography (MRA) could demonstrate intracranial aneurysm images that could be used to plan and execute early surgery on ruptured intracranial aneurysms without intra‑arterial digital subtraction angiography (IA/DSA) in the acute phase SAH.  The protocol included a three‑dimensional time‑of‑flight with T1 and T2‑weighted sagittal and axial images.  If an aneurysm was demonstrated and early surgery was undertaken they were entered into the study. Over a 25‑month period, 55 patients were found to have aneurysms who were clinically suitable for early surgery. Sixty‑three aneurysms in all were demonstrated and 55 of these were surgically dealt with.  There were two false positives.  The authors suggest that MRI is the investigation of choice to plan surgery in those patients presenting with an SAH who, on clinical grounds, would be considered suitable for early surgery. The imaging is easily obtained, non‑invasive, avoids radiation, and in view of the multiple images obtained is often superior to conventional DSA.

 

10.       Pickard JD, Murray GD, Illingworth R et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid hemorrhage: British aneurysm nimodipine trial. BMJ. 1989;298:636-642.

This is a large, prospective, randomized clinical trial conducted in the United Kingdom to assess the effects of oral nimodipine initiated early in the course of SAH.  The impact of nimodipine administered every 4 hours on cerebral infarct size, functional outcome, and mortality was compared to placebo.  They found that nimodipine affected a 34% reduction in infarct size, a 40% reduction in “poor outcome” and 18% increase in “good recovery” while reducing the mortality by 29%.  This study gives support to several other studies that evidence the efficacy on nimodipine in patients with subarachnoid hemorrhage. 

               

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Subarachnoid Hemorrhage

Questions

1. Of patients who present to the Emergency Department with headache, which of the following is TRUE? 

a. Most have primary headache disorders such as migraine or tension‑type headaches.

b. Over half will have treatable secondary causes that threaten life, limb, or brain such as subarachnoid hemorrhage.

c. Roughly 20% of patients with nontraumatic SAH have ruptured saccular or fusiform aneurysms.

d. Approximately 80% have non-aneurysmal perimesenphalic hemorrhages.

 

2.  Subarachnoid hemorrhage is often misdiagnosed because of the which of the following?

a. There is no “typical” presentation of SAH.

b. Misdiagnosis often results from the failure to correctly interpret the CT.

c. Misdiagnosis often results from failure to appreciate the spectrum of clinical presentation.

d. Surgery is unlikely to be offered to an alert patient with a very small bleed that is difficult to detect.

 

3. A 45-year-old male presents with head and neck pain for 2 days.  He has a normal sensory, motor, cerebellar exam.  Which of the following is FALSE about this patient?

a. He has a 12-33% chance of having a subarachnoid hemorrhage.

b. If he has SAH, his CT scan has a 97% likelihood of being positive for blood.

c. If he turns out to have a subarachnoid hemorrhage, there is a 20 and 50 % chance that he had a distinct, unusually severe headache in the last several days or weeks.

d. A mental status test may reveal subtle abnormalities.

 

4. The differential diagnosis of an unusually severe headache of sudden onset includes all of the following EXCEPT:

a. Exertional / coital headache

b. SAH

c. New onset migraine

d. Benign thunderclap headache

e. Central venous thrombosis

  

5. The initial management of SAH includes attention to “the ABCs”.  Which of the following is true regarding the early management of SAH? 

a. Most patients with SAH require intubation and hyperventilation to reduce ICP.

b. Since autoregulation is a significant problem after SAH, the mean blood pressure should be maintained at <80 mm Hg.

c. Aspiration may occur in patients who are vomiting and particularly if they are drowsy.

d. Hyponatremia should be treated with fluid restriction.

e. Cardiac arrhythmias are common and should be treated aggressively with antiarrhythmics.            

 

 

6. Which of the following is not an acute complication of SAH?

a. Seizure

b. SIADH

c. Dehydration

d. Hydrocephalus

 

7. Which of the following statements is true regarding electrcardiographic abnormalities occurring with SAH?

a. Symmetrical T-wave inversion and prolonged Qtc are associated with wall motion abnormalities.

b. The most common ECG abnormality is sinus tachycardia.

c. The presence of ventricular arrhythmias and torsades de pointe is associated with more severe myocardial dysfunction.

d. Contraction band necrosis has been found in almost all patients with SAH at autopsy.

8. Which is FALSE regarding CT scanning for SAH?

a. A noncontrast CT scan should be done because we are looking for blood.

b. The dynamics of the CSF and spontaneous lysis result in rapid clearing of CSF blood.

c. The sensitivity of CT scanning increases over time from the onset of symptoms.

d. CT is less sensitive in detecting posterior fossa bleeding and generally requires thinner cuts in that area.

 

9. Which of the following is FALSE regarding vasospasm after SAH?

a. Its peak occurrence is between 1 and 2 weeks after the bleeding.

b. Its occurrence can be prevented to some extent by early management of hemodynamic dysfunction.

c. Is reversed by calcium channel blocker.

d. Leads to tissue ischemia and infarction.

e. Can be detected by Doppler Ultrasonography or MRA.

 

10. Lumbar puncture should be performed in a patient whose clinical presentation suggests SAH and whose CT scan is negative, equivocal, or technically inadequate.  Which of the following is TRUE? 

a. A decreasing number of RBCs in subsequent tubes suggests a nontraumatic tap.

b. Since we are looking for signs of bleeding, opening pressures need not be measured.

c. Traumatic taps occur in less that 5% of lumbar punctures.

d. The presence of xanthochromia is not detectable until about 12 hours after the bleeding.


Answers

 

1.         a.

2.         c.

3.         b.

4.         c.

5.         c.

6.         b.

7.         a.

8.         c.

9.         c.

10.       d.

 

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