Ed Legal Letter December 1997

Aneurysmal Subarachnoid Hemorrhage: More than Just a Headache

By Michael Gibbs MD, FACEP, Clinical Instructor, Department of Emergency Medicine, University of North Carolina at Chapel Hill, Department of Emergency Medicine, Carolinas Medical Center, Medical Director, MedCenter Air; Andrew Perron, MD, Chief Resident, Department of Emergency Medicine, Carolinas Medical Center; Daniel J. Sullivan, MD, JD, FACEP, Chairman, Department of Emergency Medicine, Ingalls Memorial Hospital

When assessing the patient with headache, the emergency physician is charged with identifying the estimated 5% of this group harboring serious intracranial pathology.1 Included in the differential diagnosis is subarachnoid hemorrhage (SAH), a neurosurgical emergency afflicting up to 30,000 Americans each year.2 Although the incidence of other types of stroke has declined substantially over the past three decades, the incidence of aneurysmal SAH has remained unchanged.3,4,5 Despite considerable advances in diagnostic and therapeutic techniques, the outcome from SAH remains disappointing: 8-60% of patients die before reaching the hospital.3,6 Of those who reach medical attention, the mortality rate is 37%, with significant morbidity affecting more than 50% of survivors.3-8 Fewer than 40% of patients stricken with SAH ultimately return to a functional lifestyle despite aggressive modern treatment.9

Traditional teaching stresses that whenever SAH is considered, the diagnosis should be pursued until SAH has been definitively proven or excluded. Despite this axiom, SAH is missed in between 15% and 51% of patients.10-12 Because the clinical presentation is seldom "classic," SAH is not always considered. When the diagnosis is delayed there is a high risk of rebleeding, and both morbidity and mortality increase substantially.11,13 The emergency physician must always consider SAH in the differential diagnosis of headache. On the other hand, it is neither practical, possible, nor necessary to perform a "CT-LP" workup in every ED patient with headache. Instead, we should target those at risk and pursue a well thought-out diagnostic algorithm.

Epidemiology of Aneurysmal SAH

The prevalence of intracranial aneurysms in the general population is estimated to be between 1-6%, based on large autopsy series.14,15Extrapolation of these numbers to current population estimates would suggest that 10-15 million Americans currently harbor intracranial aneurysms. Each year, approximately 30,000 Americans will suffer a non-traumatic SAH, based on a rate of 7.5-10 per 100,000 population.2-4,16The peak age for aneurysmal SAH is 55-60 years,8but approximately 20% of cases occur between the ages of 15-45 years.17The female-to-male ratio of unruptured aneurysms is 5:3, while the incidence of SAH favors men slightly.8,18

Pathophysiology of Aneurysmal SAH

The pathophysiology of saccular aneurysm development is still incompletely understood, and it is likely that aneurysms arise from a complex, multifactorial set of circumstances involving a congenital anatomic predisposition enhanced by both local and systemic environmental factors that further weaken the arterial wall. Aneurysms arising from intracranial arteries are much more common than those arising from extracranial arteries of similar size. Most intracranial aneurysms (> 80%) arise in the anterior cerebral circulation vessels.19,20

It is known that intracranial arteries have an attenuated tunica media and lack an external elastic lamina.21 The vast majority of aneurysms occur at points of arterial bifurcation, implicating turbulent blood flow in their formation.17,21 Considerable evidence also supports a role for genetic factors in the formation of intracranial aneurysms. There is a strong association of aneurysms with a number of heritable connective tissue disorders (polycystic kidney, Ehlers-Danlos type II, neurofibromatosis type I, and Marfan’s syndrome).22,23 Although the inheritance pattern is not completely elucidated, it is also known that among first-degree relatives of patients with aneurysmal SAH, the risk of ruptured aneurysm is nearly four times higher than the risk for the general population. (See Case # 5.)22-24

Environmental Risk Factors for Aneurysmal SAH

Of the environmental risk factors that have been implicated, cigarette smoking is the only one that has consistently been correlated with SAH.8The estimated risk of aneurysmal SAH is 3-10 times greater in smokers as compared to non-smokers.8,25Hypertension has been shown to be a relative risk factor for both aneurysm formation and rupture in some but not all population-based studies.8,25The data on hyper-cholesterolemia as an independent risk factor for aneurysm formation is inconclusive.5A moderate to high level of alcohol use is another independent risk factor for aneurysmal SAH, and recent heavy use of alcohol (binge drinking) in particular has been shown to increase the risk of subarachnoid hemorrhage.

Can Patients with SAH Be Identified Clinically?

Yes and no. Classically, the patient with SAH complains of acute onset of severe diffuse headache that may be associated with nausea, vomiting, neck pain or stiffness, and altered mental status. Indeed, when this constellation of symptoms is present, the likelihood of SAH approaches 90%.26However, in the majority of cases, signs and symptoms are much less dramatic.

Headache is indeed the most common symptom, although it is clearly not seen in all cases (range, 75-85%).12,27 The location and quality of the headache have not been found to be accurate discriminators for SAH. Nausea, vomiting, or both occur in roughly two-thirds of patients and may be present in the absence of headache. Neck pain and stiffness is seen in no more than one-third of patients.28 Less common symptoms include coma, confusion, and seizures.13,27,28 One recurring observation is that the signs and symptoms of SAH, whatever they might be, usually begin acutely.12,27 When a patient describes abrupt onset of any of the above-mentioned symptoms, the diagnosis of SAH should be strongly considered.

The neurosurgical literature emphasizes the importance of "warning symptoms" that occur days, weeks, or months before a major hemorrhage. A review of the seven largest series of patients with warning signs of intracranial aneurysms29-35 shows that about 50% (range, 28-60%) of patients admitted with SAH had a symptomatic premonitory warning leak. Headache was the warning symptom in the majority of patients (range, 86-97%), and was associated with nausea and vomiting, neck pain, visual disturbances, or brief loss of consciousness.26,29-35 Because these data are retrospective, it is difficult to place the importance of warning symptoms into clinical context. This information, when present, should be considered a small piece of the clinical puzzle.

It should also be remembered that intracranial aneurysms may cause symptoms prior to rupture.36,37 This results either from expansion and compression of adjacent structures, or regional ischemia due to intrasaccular thrombosis or distal emboli. Rap et al reviewed the clinical course of 111 symptomatic patients with 132 unruptured aneurysms.36 Clinical presentations included acute severe headache, seizures, cranial nerve palsies, facial pain, hemiparesis, hemianesthesia, and hemianopsia. Therefore, a cataclysmic headache, seizure, or focal neurologic deficit may serve as the telltale sign not only of SAH but also of acute aneurysmal expansion or thrombosis. Special attention should be paid to this group of patients who, in the presence of a normal CT and lumbar puncture, may still harbor an expanding intracranial aneurysm.

When the diagnosis of SAH is missed, a large number of incorrect clinical impressions are made, including tension and migraine headache, viral infection, hypertensive crisis, vaso occlusive stroke, cervical radiculopathy, sinusitis, temporal arteritis, eye strain, acute myocardial infarction, meningitis, and alcohol intoxication.8-13,26,27 It certainly makes good clinical sense to at least consider SAH in the differential diagnosis, as we are poised to disposition a patient with any of the above-mentioned presumed diagnoses.

Case # 2

The patient was a 29-year-old female who came to the hospital with a severe headache and complaints of nausea, vomiting, and sensitivity to light. The headache started abruptly and was quite severe. The defendant, Dr. T, saw the woman in the ED but never asked her about the severity of the headache and failed to order a CT scan.

The patient was released but returned 24 hours later after she quit breathing at her home. She was declared brain dead, removed from the respirator, and died 48 hours after her initial visit to the hospital. The cause of death was SAH.

The plaintiff claimed the CT scan would have shown a SAH. Dr. T felt that the headache might have been due to general malaise or a urinary tract infection. Dr. T did admit that the SAH was in his differential diagnosis and admitted that he did not do anything to rule out the hemorrhage as a possibility.

The defendant indicated that he did not feel that an SAH was high on his list and he thought the patient suffered from a migraine. He admitted that it was his duty to rule out life-threatening diseases. The defendants maintained, however, that the SAH did not cause her death, and that it was due to a heart attack or trauma because the autopsy showed a contusion on her head, and there was evidence of blood in her ears. The plaintiff’s expert pathologist indicated that the post-mortem findings of contusion and hematoma were not located in the same area as the SAH and had no relation.

The parties reached an $800,000 settlement.38

The physician’s deposition would look something like this:

Plaintiff’s attorney: Did you consider SAH in your differential diagnosis?

Emergency Physician: Yes, I certainly considered the diagnosis.

Plaintiff’s attorney: Well, Doctor, once you consider a diagnosis in your differential, isn’t it your duty to rule it out, particularly if this is a life threatening problem?"

Your answer will, of course, be "No," or you might as well throw in the towel. There is an obvious logic to the plaintiff’s position. Once the emergency physician gives serious consideration to this diagnosis, a work-up should follow or the chart should include meticulous documentation why that course was not followed. The plaintiff’s line of reasoning plays very well to a jury. The correct answer to the attorney’s question is, "No, following my history, physical examination, management, and further observation, SAH was not on my differential diagnosis, and therefore there was no duty to rule that diagnosis out."

You may even consider placing your reasoning into the medical record. For example, "Patient presented with a severe headache with a rapid onset. However, on physical examination, the neurologic examination was completely normal, the patient had an excellent clinical course with complete pain relief, the patient has had similar episodes in the past . . . "

Does a Negative CT Scan Exclude SAH?

To answer this question, we should first consider the implications of missing the diagnosis. Given the high morbidity and mortality associated with SAH, which is higher still when the diagnosis is delayed, it is not rational to settle for a diagnostic test with less than 100% sensitivity.

Early studies using CT scanning in the diagnosis of SAH demonstrated a sensitivity of 85-95%.39-42 With the advent of third-generation CT technology, the diagnostic accuracy has increased substantially. It is clear that the sensitivity of CT is highest when performed shortly after the ictus, decreasing progressively thereafter as blood is gradually cleared from the subarachnoid space. Recent studies demonstrate a sensitivity of 98-100% when CT is performed within the first 12 hours43,44 and 93% when it is performed within the first 24 hours.45 Sensitivity decreases steadily to 80% by day 3, 50% by day 7, and 20% by day 9.46

MRI is not sensitive in detecting acute hemorrhage, and its role in the early evaluation of SAH is limited.47

Although the results of early CT scanning are very encouraging, it is clear this is not a perfect test. When the clinical suspicion for SAH is high, and the CT scan is negative, lumbar puncture should always be performed, regardless of the duration of symptoms.

Case # 3

A 42-year-old female presented to the ED with a complaint of feeling dizzy, with her right face, shoulder, neck, and clavicle hurting. The triage nurse noted the vital signs: BP 120/70; P 72; Respiratory 18. The patient was alert and oriented. In the ED, the nurse noted that the patient had had a right-sided headache, neck, and shoulder pain since noon. The patient was alert but drowsy, with weak speech, and was slumping in the wheelchair. She had no known history of trauma.

The physician noted the presence of right temporal cephalgia, with nausea and photophobia. There was no previous history of headache, no trauma. The headache was progressive from frontal to temporal. On his dictated history, the physician noted that she had headaches around menstruation but had previously never had a headache like this. The patient admitted to being under more stress than usual due to some financial difficulties.

Findings on physical examina showed that the patient was alert and oriented times 3; speech was soft; and her neck was supple. Her pupils were equal and reacted to light. She had normal coratid pulses without bruits. On neurologic exam, her wrist strength was normal, reflexes were normal and there was no cerebellar drift. Cranial nerves were intact. The emergency physician concluded that the patient had an intact neurological examination.

The physician ordered a CT of the head. The radiologist interpreted the CT as a "normal study." The physician ordered 2 fiorinal tablets, and later during the visit, 800 mg of ibuprofen. The physician diagnosed "cephalgia," etiology unclear. He discharged the patient to home, off work, bed rest , on fiorinal with codeine. The physician also noted that the patient was to follow up with the private physician, without a designated time frame. She was to "return to the ER if necessary."

The patient returned to the same ED 13 days later with vertigo, a feeling that her ears were clogged, and she had pressure behind the right eye. She was alert and oriented, with normal vital signs at triage. The ED nurse noted the patient complained of weakness, dizziness, and a headache over the right eye and down the back of the right side of the neck. Patient said she had been seeing her private physician for the same complaints for three weeks. Patient in no acute distress.

The physician examined the patient, again diagnosed "cephalgia," and discharged her on naprosyn and bedrest with the instructions to see her private physician the next day.

The patient returned by ambulance three days later, following a syncopal episode. She presented with dilated pupils, diaphoresis, and was slow to respond. She would initially follow commands. At that point, the diagnosis of an intracranial injury was apparent. Repeat CT revealed a SAH with ventriculomegaly. The patient died within 48 hours.

In the discharge summary, the private physician wrote that this woman was in the ED two weeks ago with the worst headache of her life, with a negative CT scan. She was found comatose outside her bathroom on the day of admission and CT scan showed a large SAH.

Emergency physicians must recognize the "rule out subarachnoid" presentation. The sudden and severe headache, the worst headache of a patient’s life, or an unusual headache with subtle or obvious neurologic signs or symptoms should trigger the "rule out" workup for subarachnoid. It is impossible to know which sudden, severe, or unusual headache is the result of a cerebral arterial aneurysm, or a sentinal or subarachnoid bleed. Therefore, the emergency physician must maintain a low threshold for the work-up.

The facts of this case suggest that the patient presented with the worst headache of her life’ during the first ED visit. If, in fact, that is true, then the negative CT should have been followed by a lumbar puncture. The physician noted that she had never had a headache like this one before. That information, plus the nurses documentation suggesting an altered mental status, strongly suggests the need for a complete work-up to rule out a subarachnoid.

How Should the Lumbar Puncture Be Interpreted?

Lumbar puncture is still considered to be the "gold standard" in the evaluation of SAH. Yet, there are several potential pitfalls in the interpretation of cerebrospinal fluid (CSF) results.

It is a widely held belief that collecting the CSF in sequential tubes and comparing the red cells in consecutive tubes makes the distinction between SAH and a traumatic tap possible. A decrease in the red cell count is said to indicate a traumatic tap, while the red cell count remains unchanged in SAH. Studies have shown that this method is unreliable, and although a decrease in the red cell count is more likely in traumatic punctures, it may also occur in patients with SAH.48,49

The most reliable method in the detection of SAH is the demonstration of xanthochromia in the CSF. Xanthochromia reflects the degradation of pigments released by lysed red blood cells. It takes a few hours for the red cells to lyse, and, therefore, the pigments that cause xanthochromia of the CSF are not immediately present. In patients with SAH, xanthochromia is present in 100% of cases 12 hours after symptom onset, and it remains present in 70% of patients for up to four weeks.50 The presence or absence of xanthochromia should always be determined using spectrophotometry and not direct vision. The latter method is very unreliable and may yield false-negatives in up to 50% of cases.51,52

Several additional CSF assays have been evaluated in the diagnosis of SAH, including bilirubin, ferritin, D-dimers, and erthyrophages. The detection of D-dimer offers the most promise, although studies to date have been small, and false-positive as well as false-negative results have been described.53-55


The plaintiff’s attorney will bring any cause of action that relates to the missed diagnosis. The obvious cause of action is the medical malpractice suit. However, the Emergency Medical Treatment and Active Labor Act (EMTALA) creates a duty to provide emergency department patients with a medical screening examination, and a duty to stabilize an emergency medical condition.56The law also gives an injured party the right to sue the hospital, in federal court, for damages related to a breach of the obligation to screen and/or stabilize. Plaintiff’s attorneys have increasingly used EMTALA to set forth a cause of action in "missed diagnosis" cases, alleging both a failure to provide an adequate screening examination and to adequately stabilize the patient prior to discharge. It is important to note that EMTALA does not provide the injured party a right to sue the physician in civil court for these alleged violations.

Case # 4

A 35-year-old woman presented to a community hospital ED with a chief complaint of "migraine headache." An emergency nurse triaged the patient and called the patient’s private physician, who told the nurse to send the patient to his office. The patient was not examined by the emergency physician on duty; nor did the nurse inform the physician of the patient’s presence prior to sending the patient to the private physician’s office.

An hour later the patient returned, and the private physician called the ED with orders to give the patient 75 mg of meperidine IM and 75 mg of Vistaril IM for her headache. The nursing staff administered the medication and allowed the patient to leave the ED without being seen by the emergency physician. Six hours later the patient returned by EMS after a seizure and died from an SAH. The family brought a wrongful death and a COBRA action against the hospital and the emergency physician for failure to provide the patient with an appropriate medical screening exam.

Under EMTALA, the stated purpose of the medical screening examination (MSE) is to determine whether an emergency medical condition (EMC) exists.38 The hospital should conduct whatever examination is necessary and "reasonably calculated" to make that determination. It may take only a visual glance to rule out an EMC in a patient with a rash. But, if it takes a CT scan and a lumbar puncture to decide whether a patient with the "worst headache of my life" has an SAH, then those tests and procedures are part of the MSE. Also, the federal court will not allow this action to proceed against the emergency physician. The EMTALA civil suit is allowed only against the hospital.

Risk Management Recommendations

Any patient presenting with a potential neurologic problem should receive a complete history and physical examination with particular focus on the neurologic system. The standard of care mandates a relevant history and physical examination. Documentation of that examination is generally not a standard-of-care issue. It is performance of the exam, not documentation of the exam, that relates to the standard of care. However, documentation of the relevant exam may assist subsequent providers and may be critical evidence to challenge allegations of substandard practice in any resulting litigation.

A review of the legal literature indicates that "missed SAH" cases fall into one of just a few categories. Often, the clinician simply fails to recognize the signs or symptoms of an obvious bleed or apparent intracranial pathology. These cases are difficult to defend. In other cases, the patient has had a small leak from the aneurysm or possibly a small bleed into the wall of the aneurysm, resulting in a headache of mild to moderate severity, or perhaps some subtle neurologic changes such as dizziness, photophobia, etc. In many cases, the hemorrhage is not apparent, patients respond to minor analgesics, and are discharged in good condition. In fact, in retrospect, it is not clear whether the patient had a sentinel event or had a tension headache, migraine, or some other type of headache unrelated to the aneurysm.

Unless there are obvious signs of intracranial pathology on examination, or the patient is in extreme pain, it is impossible to determine which "headache" patient is having a sentinel or minor bleed from intracranial aneurysm. The emergency physician must take the same, conservative, risk-managed approach in every "headache" case and carefully document a textbook neurologic review of systems and neurologic physical examination. Documentation of the patient’s condition over a period of observation in the ED is also extremely helpful in the event of litigation. Close and careful follow-up of "headache" patients discharged from the ED is good patient care and strong risk management.

The emergency group should work with the nursing staff to perform a "headache" chart review on a regular basis. Check for appropriate documentation of attention to issues such as: rate of onset of the headache; severity of the headache; appropriate use of CT and LP; documentation of history and physical exam with a "neurologic" focus; condition after a period of observation; and short term follow-up by phone or with the private physician. The busy EP often neglects to document the pertinent negatives. In the event of a lawsuit, the pertinent negatives are as important as the positive findings on review of systems and physical exam.

Case # 5

The patient was a 48-year-old female who presented to the ED with a chief complaint that she had worked all day and then 30 minutes prior to arrival at the ED, she developed a severe headache, neck pain, and leg cramps. The triage nurse also noted diaphoresis and a small emesis. The initial vital signs were a temperature of 95.2°F, pulse 73, BP 189/88, respiration 24. The presenting cardiac rhythm was a normal sinus rhythm. Forty-five minutes after arrival, the patient complained of increased pain in the legs, and she was moaning. The emergency physician examined the patient and then ordered Toradol 30 mg IV push for pain and Procardia 10 mg sublingual for her elevated blood pressure. The patient was discharged and the discharge nurse noted that the patient was stable.

The emergency physician dictated his history and physical examination. He noted the chief complaint was weakness and numbness. He noted that the patient had an argument and afterward started complaining that her head felt funny and her legs felt weak. The patient was supposed to be on three Naprosyn a day, and she had only taken one. The emergency physician noted that the patient’s legs hurt and that she thought it was related to not taking enough naprosyn. He noted that she "also has a headache."

The emergency physician noted that the patient was not in acute distress. Physical examination was essentially unremarkable. The documented neurological examination was limited to an eye examination, hand grasp, biceps and triceps, flexors and extensors, and hips; knees and ankles were 5/5 bilaterally. The patient was discharged with a diagnosis of headache.

The patient returned to the ED approximately six hours after discharge. The triage nurse noted that the patient had been seen that afternoon, had apparently gotten into an argument with her sister, and returned to the ED complaining of leg pain, received IV toradol, and was sent home. Prior to this second ED visit, the patient was apparently not speaking normally. She was very sleepy, according to the family, and she came in by ambulance.

The patient’s diagnosis of SAH was apparent at that point. She was admitted, and she died a short time following surgery.

The emergency physician did not document a complete neurologic examination. He did not check the neck for meningismus. He did not document the rate of onset of the headache or a neurologic review of systems. He did not document the patient’s response to treatment. He did not document the severity of her headache either on arrival or on discharge from the ED.

That is not to say that the emergency physician did not perform the appropriate history or physical examination. It is quite possible that he asked all the correct questions and performed the appropriate physical examination, but failed to document the results. The patient’s presentation certainly suggests the need for complete history taking, a complete examination of the neurologic system, and a search for meningeal signs. Also, if the pain was, in fact, as severe as documented by the triage nurse, the emergency physician would be expected to document resolution or improvement of her condition. Discharge from the ED would occur only if the patient were stable and in good condition. Stability and condition were not documented by the emergency physician.

The patient presented to the triage nurse and stated that 30 minutes prior to arrival she developed a severe headache and neck pain. The SAH classically presents with a sudden onset of a severe headache and often causes neck pain or meningeal signs. The patient did not tell the triage nurse she had a sudden onset of pain. However, there does appear to be a discrepancy between the patient’s statement to the triage nurse, and the emergency physician’s history that "her head felt funny." He also noted that she "has a headache." He did not note that she had a severe headache nor that she had pain in the neck.

The nurses’ triage statement is certainly suggestive of SAH type pain. If the emergency physician were to give strong testimony regarding the patient’s presentation, he may be able to explain away this apparent discrepancy between the nursing notes and the physician’s history. The stronger position would have been to review the nursing notes and squarely address the discrepancy on the record.

Case # 6

The patient presented to the ED with a headache. The triage nurse noted the patient’s vital signs: pulse 80, respiration 16, BP 180/90. The nurse documented the chief complaint: "pain in back of head and front of head. Head pain in front went away—back of head still hurts—when coughs has pain in epigastric area."

The physician’s history indicates that the patient was 54 years old and was playing a video game when she began to have frontal and occipital pressure and mild pain. She had no other signs and symptoms, but she was concerned because she had two siblings that died from cerebral aneurysm.

On physical exam, the physician noted the following: "No apparent distress. Pupils equal, round, and reactive to light. Tympanic membranes benign. Mild mastoid and occipital tenderness. Neck with a full range of motion. Lungs were clear to auscultation."

The emergency physician ordered ibuprofen. He also ordered an icepack. At some later time, the physician noted the patient was "much better." The diagnosis was occipital cephalgia. The patient was discharged, with follow-up to see her private physician for any problems. There were no other apparent discharge instructions.

The patient returned to the ED one week later with a complaint of severe headache and low back pain. On arrival the patient had a pulse of 80, respirations were 24, and BP was 170/88.

The emergency physician’s dictated report indicates that the patient had presented one week prior with a severe headache and lower back pain. That headache had gone away with ibuprofen. She continued to have headaches off and on, but had done better in the last few days. The headache prior to this visit awoke her. She had some nausea and vomiting after riding in the ambulance. He also noted the strong family history for aneurysms: a brother and sister died of brain stem aneurysms and her mother had strokes. On physical exam the pupils were equal, round, and reactive to light. Extraocular movements were normal. The neck was supple without pain. The patient was awake, alert and oriented times 4. Cranial nerves 2-12 were intact. Motor and sensory exams were normal.

The emergency physician noted that while he was trying to get in contact with the private physician, the patient developed neurologic changes. She became confused, suggesting neurologic deterioration. He ordered an immediate transfer via helicopter. Just prior to transfer, the patient became unresponsive and was intubated on the second attempt. She had an episode where her heart rate when down into the 40s. She was hyperventilated and transferred.

The radiologist’s formal interpretation of the CT scan indicates that there was a left-sided subarachnoid bleed. This reading is consistent with SAH in the distribution of the left middle cerebral artery.

The physician’s documentation was not perfect. He noted that the patient had frontal and occipital pressure and mild pain, and no other signs and symptoms. Hopefully, the physician asked about changes in the patient’s level of consciousness, any loss of consciousness, and the presence of nausea or vomiting. He did make a general statement that there were "no other signs and symptoms," which may be adequate. During the process of litigation, he will certainly be asked those questions.

During the first visit, the emergency physician did not document a neurologic examination. This is a common problem when reviewing litigation involving emergency physicians. The chart is often deficient in that one organ system that is the dead focus of the case. There may be a great lung examination and a great back examination, but they aren’t particularly helpful in a headache presentation. In this case, the physician should have documented a textbook neurologic examination, leaving no doubt to any subsequent reviewer that he had done a full-blown, heavy duty, Sears and Roebuck neurologic examination. In fact, the physician probably did a thorough neurologic examination, and will be kicking himself all the way to the courtroom.

Causation is on of the four critical elements in any medical malpractice action, and is particularly important in missed subarachnoid cases. The plaintiff must prove not only that the physician breached a standard of care, but also that the breach resulted in injury to the patient. Subarachnoid hemorrhage is a lethal entity, and in many cases, a missed or delayed diagnosis does not change the ultimate outcome. The defense team typically takes a two pronged approach in this type of case: 1) there was no breach in a standard of care; and 2) if there was a breach in a standard of care, it did not cause the patient’s injury. That is, the patient would have been injured anyway, unrelated to the breach.

The literature suggests, in general, that patients with fewer symptoms at presentation have a better prognosis. Some authorities recommend a grading system for the clinical presentation of the subarachnoid bleed.57 The lower grades (i.e. fewer signs and symptoms) have a better prognosis than the higher grades. In this case, if the patient had a bleed during the first visit, it was a low-grade bleed, and she returned with a high-grade presentation a week later. Therefore, based on the grading system, the patient’s prognosis changed between the first and second visit. This would compromise the defense teams causation arguments.

Case # 7

A 57-year-old female presented to the ED and gave the following complaint to the triage nurse: "headache, back of neck, and off balance for 24 hours." She had a history of hypertension and presenting vital signs of: BP, 170/100; pulse, 80; and respiration, 20. The physician noted that "yesterday began strong aching in the back and neck when bent over to wash hair—lasted two hours then moved to frontal part of head. Vomited once at noon and once today—the headache today has stayed in frontal region and some relief with two Tylenol." The patient had No significant headache history.

On physical exam, the neck was supple, repeat BP was 180/96. Eye exam was normal, including funduscopic. Sinuses were nontender. Neurologic exam included normal muscle strength and reflexes bilaterally. There was no additional neurologic exam documented.

The patient was treated for her pain, observed for approximately two hours, and discharged with a diagnosis of "headache." The patient died the following day of a SAH.

This patient presented with enough historical factors to consider SAH in the differential diagnosis. Although there was no "sudden onset" and no complaint of the "worst headache of my entire life," there were complaints of "off-balance for 24 hours," movement of the pain from the back and neck to the frontal area, and vomiting. These complaints are not specific for SAH, nor do they rule out migraine or other headache disorders; however, they should increase the emergency physician’s concern that there may be an intracranial event.

Looking at the history, the emergency physician could have questioned the patient further regarding her complaint of being "off balance." Off balance can mean a wide range of things from a little lightheadedness, to several episodes of falling to the floor. The latter would obviously be far more important and would very likely result in a thorough evaluation for an intracranial event. Also, whenever presented with a similar case, the emergency physician would be well-served by documenting some pertinent negatives. Specifically, the emergency physician should ask and document whether this pain came on suddenly or whether this is the "worst" headache of the patient’s life. The act of documenting these facts does nothing to assist the emergency physician in patient care, however, in the event of a complication and subsequent care by another provider or in the event of peer review or litigation, it is important to demonstrate that history taking was thorough. You can be absolutely certain that these particular pertinent negatives will be an area of focus in every case of missed SAH.

Looking at the physical examination, the neurologic exam is incomplete. The patient’s presentation is clearly neurologic. Therefore, the emergency physician should document a complete, textbook, neurologic examination. For example, in this case, based on the patient’s presentation, the patient could have had a cerebellar bleed. There is no documentation of cerebellar signs. The emergency physician should understand that when he or she testifies at deposition and trial, the plaintiff’s attorney will have a field day with what wasn’t documented. The plaintiff will say the emergency physician never did the exam, and the emergency physician will testify that she did do the exam. Veteran defense attorneys commonly feel that it is difficult, often impossible, to convince a jury that the emergency physician did a complete exam but failed to document it.

Case # 8

A 36-year-old female presented to the ED and complained to the nurse of neck stiffness, headache, dizziness, and vomiting the previous day. The patient said that she had a sudden onset of a headache with vomiting while watching TV. She was unable to sleep for three days. She was unable to turn her head from side to side or up or down without discomfort. She experienced sudden onset of the headache while sitting in a chair, unable to eat.

The physician noted that the patient complained of a headache, neck pain, and stiffness. He noted that she had bilateral nasal congestion. The neck was supple. The emergency physician did not document a neurologic exam. The emergency physician noted that x-ray of the sinuses revealed a sinusitis. He diagnosed "paranasal sinusitis," treated her with Demerol and Vistaril, ordered antibiotics, and discharged her with follow up to her primary physician.

The patient returned to the same ED four days later complaining of nausea, vomiting, and a headache. She stated she had not been feeling well for one week. The physician noted that her appetite was markedly decreased, she was unable to hold down fluids without vomiting. On exam, head, ears, eyes, nose, and throat were normal, lungs were clear, neck was supple, adenopathy was not present, and heart sounds were regular.

The patient returned within eight hours with facial asymmetry, a weak left upper extremity and mild weakness of the left lower extremity. CT revealed a SAH.

The physician’s diagnosis is convenient, but does not explain the patient’s presentation. The emergency physician should carefully review the triage and other nursing notations. In this case, the nursing notes read like a chapter on subarachnoid hemorrhage. If the emergency physician agreed with these statements, she was obligated to rule out a subarachnoid hemorrhage. If she disagreed with the statements, she must address this on the ED record.

This case presents another significant documentation problem. The EP did not document a neurologic examination. Based on the patient’s presentation, it will be immediately apparent to any jury, that the physician’s focus should have been on the neurologic system. The physicians’ assessment may have been reasonable. However, the lack of documentation of this exam will make the case difficult to defend.


SAH is a devastating neurosurgical emergency for which prompt diagnosis and definitive therapy are essential. The diagnosis should be strongly suspected in patients with acute onset of headache, nausea, vomiting, neck pain, seizures, or altered mental status. Because the clinical presentation of SAH may be subtle, misdiagnosis is common. Frequently described incorrect diagnoses include tension or migraine headache, viral syndrome, hypertensive crisis, cervical radiculopathy, and sinusitis. When delays in diagnosis occur, both morbidity and mortality increase substantially.

When the diagnosis is entertained, unenhanced CT of the brain should be performed emergently. Although the diagnostic accuracy of third-generation CT-scanners is excellent, the emergency physician must not be satisfied by a normal study, and lumbar puncture is always indicated when the suspicion of SAH is high. Analysis of spinal fluid for xanthochromia by spectrophotometry as well as the red cell count accurately confirms or excludes the diagnosis.

Any patient presenting with a headache, or a potential neurologic problem, should receive a complete history and physical examination with particular focus on the neurologic system. Documentation of the relevant exam, including the pertinent negatives, may be critical evidence to challenge allegations of substandard practice in resulting litigation, peer review or disciplinary review.

Unless there are obvious signs of intracranial pathology on examination, or the patient is in extreme pain, it is impossible to determine which "headache" patient is having—a sentinel or minor bleed from or into an intracranial aneurysm. Therefore, the emergency physician must take the same, conservative, risk-managed approach in every case.


1. Laight MJ. Non-traumatic headache in the emergency department.Ann Emerg Med1980; 9:404-409.

2. Mayberg MR, Batjer HH, Day R, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage. A statement for healthcare professionals from a special writing group of the stroke council, American Heart Association. Stroke 1994;25:2315-2328.

3. Phillips LH II, Whisnant JP, O’Fallon WM, et al. The unchanging pattern of subarachnoid hemorrhage in the community. Neurology 1980;30:1034-1040.

4. Ingall TJ, Whisnant JP, Wiebers DO, et al. Has there been a decline in subarachnoid hemorrhage mortality? Stroke 1989; 20:718-720.

5. Schievink WI. Intracranial aneurysms. N Engl J Med 1997;336:28-39.

6. Kiyohara Y, Ueda K, Hasuo Y, et al. Incidence and prognosis of subarachnoid hemorrhage in a Japanese rural community. Stroke 1989; 20:1150-1155.

7. Sahs AL, Nibbenlink DW, Torner JC, Editors. Aneurysmal Subarachnoid Hemorrhage: Report of the Cooperative Study. Baltimore: Urban & Schwarzenberg; 1981.

8. Sacco RL, Wolf PA, Bharucha NE, et al. Subarachnoid and intracranial hemorrhage: Natural history, prognosis, and precursive factors in the Framingham Study. Neurology 1984;34:847-854.

9. Kassell NF, Drake CG. Timing of aneurysm surgery. Neurosurgery 1982;10:514-519.

10. Adams HP, Jergenson DD, Kassell NF, et al. Pitfalls in the recognition of subarachnoid hemorrhage. JAMA 1980, 244:794-796.

11. Dwyer N, Lang D. Brain attack’-aneurysmal subarachnoid haemorrhage: Death due to delayed diagnosis. J R Coll Physicians Lond 1997;31:49-52.

12. Fontanarosa P. Recognition of subarachnoid hemorrhage. Ann Emerg Med 1989;18:1199-1205.

13. Kassell NF, Kongable GL, Torner JC, et al. Delay in referral of patients with ruptured aneurysms to neurosurgical attention. Stroke 1985;16:587-590.

14. McCormick WF, Nofzinger JD. Saccular intracranial aneurysms: An autopsy study. J Neurosurg 1965; 22:155-159.

15. Inagawa T, Hirano A. Autopsy study of unruptured incidental intracranial aneurysms. Surg Neurol 1990;34:361-365.

16. Brown RD, Whisnant JP, Sicks JD, et al. Stroke incidence, prevalence, and survival. Secular trends in Rochester, Minnesota, through 1989. Stroke 1996;27:373-380.

17. Biller J, Toffol GJ, Kassell NF, et al. Spontaneous subarachnoid hemorrhage in young adults. Neurosurgery 1987;21:664-667.

18. Sarti C, Tuomilehto J, Salomaa V, et al. Epidemiology of subarachnoid hemorrhage in Finland from 1983-1985. Stroke 1991;22:848-853.

19. Fox JL, ed. Intracranial Aneurysms. vol. 1. New York: Springer-Verlag; 1983:19-117.

20. Batjer HH. Intracranial aneurysms. In: Rengachary SS, Wilkins RH, eds.: Principles of Neurosurgery. London: Wolfe Publishing; 1993.

21. Stehbens WE. The pathology of intracranial arterial aneurysms and their complications. In: Fox JL, ed. Intracranial Aneurysms. Vol. 1. New York: Springer-Verlag, 1983: 272-357.

22. Schievink WI, Michaels VV, Piepgras DG. Neurovascular manifestations of heritable connective tissue disorders: a review. Stroke 1994;25:889-903.

23. Schievink WI, Schaid DJ, Michaels VV, et al. Familial aneurysmal subarachnoid hemorrhage: A community based study. J Neurosurg 1995;83:426-429.

24. Bromberg JC, Rinkel GF, Algra A, et al. Subarachnoid hemorrhage in first and second degree relatives of patients with subarachnoid hemorrhage. BMJ 1995;311:288-289.

25. Bonita R. Cigarette smoking, hypertension, and the risk of subarachnoid hemorrhage: A population-based case-control study. Stroke 1986;17:831-835.

26. Duffy GP. The warning leak in spontaneous subarachnoid hemorrhage. M J Aust 1983;1:514-516.

27. Adams HP, et al. CT and clinical correlation in recent aneurysmal subarachnoid hemorrhage: A preliminary report of the Cooperative Aneurysm Study. Neurology 1983;33:981-988.

28. Sarner M, Rose FC. Clinical presentation of ruptured intracranial aneurysm. J Neurol Neurosurg Psychiatry 1967; 30:67-70.

29. Jakobsson K, Saveland H, et al. Warning leak and management outcome in aneurysmal subarachnoid hemorrhage. Neurosurgery 1996;85:995-999.

30. Ostergaard JR. Headache as a warning symptom of impending subarachnoid haemorrhage. Cephalgia 1991;11:53-55.

31. Verweij RD, Wijdicks EFM, Van Gijn J. Warning headache in aneurysmal subarachnoid hemorrhage: A case-control study. Arch Neurol 1988;45:1019-1020.

32. King RB, Saba MI. Forewarning of major subarachnoid hemorrhage. NY State J Med 1974;74:638-639.

33. Okawara SH. Warning signs prior to rupture of an intracranial aneurysm. J Neurosurg 1973;38:575-580.

34. Waga S, Ohtsubo K, Handa H. Warning signs in intracranial aneurysms. Surg Neurol 1973;3:15-20.

35. Leblanc R. The minor leak preceding subarachnoid hemorrhage. J Neurosurg 1987;66:35-39.

36. Raps ED, Rogers JD, Galetta SL, et al. The clinical spectrum of unruptured intracranial aneurysms. Arch Neurol 1993; 50:265-268.

37. Day JW, Raskin NH. Thunderclap headache: Symptom of unruptured cerebral aneurysm. Lancet 1986;2:1247-1248.

38. Declue and His Four Minor Children v. Taylor and Emergency Medical Care, Inc. Jefferson County (Mo) Circuit Court, No. CV190-4898-CC-J4.

39. Kendall BE, Lee BDP, Claveria E. Computerized tomography and angiography in subarachnoid hemorrhage. Br J Radiol 1976;49:483-501.

40. Liliequist B, Linqvist M, Valdimarsson E. Computed tomography and subarachnoid hemorrhage. Neuroradiology 1977;14:21-26.

41. Modesti LM, Binet EF. Value of computed tomography in the diagnosis and management of subarachnoid hemorrhage. Neurosurgery 1978;3:151-156.

42. Adams HP Jr, Kassell NF, Torner JC, et al. CT and clinical correlations in recent aneurysmal subarachnoid hemorrhage: a preliminary report of the Cooperative Aneurysm Study. Neurology 1983;33:981-988.

43. Sidman R, Connoly E, Lemke T. Subarachnoid hemorrhage diagnosis: lumbar puncture is still needed when the computed tomography scan is normal. Acad Emerg Med 1996; 3:827-831.

44. van der Wee N, Rinkel GJE, Hasan D, et al. Detection of subarachnoid haemorrhage on early CT: Is lumbar puncture will needed after a negative scan? J Neurol Neurosurg Psychiatry 1995;58:357-359.

45. Sames TA, Storrow AB, Finkelstein JA, et al. Sensitivity of new- generation computed tomography in subarachnoid hemorrhage. Acad Emerg Med 1996;3:16-20.

46. Brouwers PJAM, Wijdicks EFM, Van Gijn J. Infarction after aneurysm rupture does not depend on the distribution or clearance rate of blood. Stroke 1992;23:374-379.

47. Ogawa T, Inugami A, Fujita H, et al. MR diagnosis of subacute and chronic subarachnoid hemorrhage: Comparison with CT. AJR Am J Roentgenol 1995;165:1257-1262.

48. Buruma OJS, Janson HLF, Den Bergh FAJ, et al. Blood-stained cerebrospinal fluid: traumatic puncture of haemorrhage? J Neurol Neurosurg Psychiatry 1981;44:144-147.

49. Vermeulen M. Subarachnoid hemorrhage: Diagnosis and treatment. J Neurol 1996;243:496-501.

50. Vermeulen M, Hasan D, Blijenberg BG, et al. Xanthochromia after subarachnoid haemorrhage needs no revisitation. J Neurol Neurosurg Psychiatry 1989;52:826-828.

51. Soderstrom CE. Diagnostic significance of CSF spectophotometry and computed tomography in cerebrovascular disease. A comparative study in 231 cases. Stroke 1977;5:606-612.

52. MacDonald A, Mendelow AD. Xanthochromia revisited: a re-evaluation of lumbar puncture and CT scanning in the diagnosis of subarachnoid hemorrhage. J Neurol Neurosurg Psychiatry 1988;51:342-344.

53. Lang DT, Berberian LB, Lee S, et al. Rapid differentiation of subarachnoid hemorrhage from traumatic lumbar puncture using the D-dimer assay. Am J Clin Pathol 1990; 93(3):403-405.

54. Wick M, Fink W, Pfister W, et al. Ferritin in cerebrospinal fluid differentiation between central nervous system haemorrhage and traumatic spinal puncture. J Clin Pathol 1988; 41:809-814.

55. Page KB, Howell SJ, Smith CML, et al. Bilirubin, ferritin, D-dimers an erythrophages in the cerebrospinal fluid of patients with suspected subarachnoid haemorrhage but negative computed tomography scans. J Clin Pathol 1994; 47:986-989.

56. 42 USC 1395dd

57. Rosen, P, et al. Emergency Medicine Concepts and Clinical Practice. 3rd ed. St. Louis: Mosby-Year Book; 1992:1835.

Physician CME Questions

8. All of the following are risk factors for the development of intracranial aneurysmsexcept:

a. a family’s history of intracranial aneurysms.

b. Marfan’s syndrome.

c. cigarette smoking.

d. coronary artery disease.

e. polycystic kidney disease.

9. During the past three decades, the incidence of aneurysmal subarachnoid hemorrhage has:

a. increased.

b. decreased.

c. remained unchanged.

10. What percentage of survivors of SAH will have a good functional outcome?

A. 90%

B. 75%

C. 60%

D. Less than 40%

E. Less than 25%

11. All patients with subarachnoid hemorrhage will complain of headache.

a. True

b. False

12. When questioning a patient with headache about the nature of their symptoms, which piece of historical information is most often associated with SAH?

a. The severity of headache

b. Abrupt onset of symptoms

c. The location of headache

d. The presence of associated neck pain

e. The presence of associated nausea and vomiting.

13. Signs and symptoms of unruptured intracranial aneurysms may include:

a. headache.

b. cranial nerve palsies.

c. seizures.

d. hemiparesis and/or hemianesthesia.

e. all of the above

14. A patient presents to the ED following the acute onset of a severe headache associated with nausea and vomiting. A CT scan of the brain (read by your best neuroradiologist) is normal. You should:

a. discharge patient after appropriate analgesics are given.

b. repeat the CT scan in 12-24 hours.

c. perform an MRI.

d. perform a lumbar puncture.

e. None of the above

15. The most accurate spinal fluid study in the detection of subarachnoid hemorrhage is:

a. the absolute RBC count in the last tube.

b. a persistently elevated RBC count in all tubes.

c. the presence of xanthochromia by direct vision.

d. the presence of xanthochromia by spectrophotometry.

e. the D-dimer assay.