Kapoor WN, N Engl J Med, 2000;343(25):1856
Syncope is defined as a sudden and brief transient loss of consciousness associated with a loss of postural tone. Patients by definition return spontaneously to their baseline status with no therapeutic intervention and do not experience prolonged confusion. The pathophysiology of all forms of syncope consists of a sudden decrease in or brief cessation of cerebral blood flow.
The first important issue is distinguishing syncope from several other symptoms. Dizziness, presyncope, and vertigo do not result in a loss of consciousness or postural tone. Patients who require cardioversion to regain consciousness have survived a cardiac arrest, not syncope. Sometimes it's difficult to distinguish syncope from seizure. A loss of consciousness that is precipitated by pain, exercise, micturition, defecation, or other stressful event is usually syncope rather than seizure.
Symptoms such as sweating and nausea that occur prior to or during the event are usually syncope, while aura is typical of seizure. Rhythmic movements such as generalized tonic or clonic convulsions are consistent with seizures, but short-lived jerking (myoclonic) movements may be consistent with syncope. Disorientation after the event and unconsciousness lasting more than five minutes suggests seizure.
The differential diagnosis of a syncopal event is as broad as any in the field of medicine. Most studies have found that the most commonly diagnosed cause of syncope is the vasovagal attack, but “no cause of syncope” is found in approximately 34 percent of the patients in these studies. According to studies that rely heavily on tilt table testing, approximately 50 to 66 percent of patients with previously diagnosed “unexplained syncope” actually have neurally mediated (also called neurocardiogenic or vasovagal) syncope.
The exact mechanism of neurally mediated syncope is poorly understood, but is mostly caused by increased vagal efferent activity with associated sympathetic withdrawal. Examples of vasovagal syncope include emotional fainting, situational syncope (i.e., in response to micturition, defecation, cough), and carotid-sinus syncope.
Orthostatic hypotension, another important cause of syncope, may be due to volume depletion (i.e., GI bleed, leaking AAA, ruptured ectopic pregnancy, dehydration), medications (i.e., alpha-blockers, anti-psychotics), secondary autonomic dysfunction (i.e., diabetes), or primary forms of autonomic failure.
In the evaluation of syncope, the presence of a structural heart disease (coronary artery disease, congestive heart failure, valvular heart disease, or congenital heart disease) has emerged as the single most important factor for predicting the risk of death, as well as the likelihood of arrhythmias. Patients with heart disease or an abnormal ECG have an increased risk of death within one year.
A thorough history and physical examination are extremely important in diagnosing or suggesting the cause of syncope that can be evaluated with direct testing. An ECG is recommended for virtually all patients despite its low yield because the findings can lead to decisions about the immediate management of underlying disease or can help in planning further testing. Routine use of basic laboratory tests is not recommended because of their low yield, and should be done only when specifically indicated by the history and physical examination.
When a thorough initial evaluation does not lead to or suggest a diagnosis, the patient has unexplained syncope, and decisions about further testing should be based on an assessment of the patient's risk factors.
In patients with structural heart disease or abnormalities on the ECG, the chief concern is arrhythmias. If the presence of structural heart disease cannot be confirmed clinically, if syncope is associated with exercise, or if there is known structural heart disease of undetermined severity, echocardiography and stress testing are recommended. Electrocardiographic monitoring for 24 hours is recommended, as is consultation with a cardiologist to plan the evaluation and management of disease in these patients. The relevant findings on monitoring are symptoms that occur in conjunction with arrhythmias and symptoms that occur without accompanying arrhythmias. In the remaining patients, electrophysiologic studies are recommended.
The use of the tilt table testing and carotid massage may be useful, especially in patients with recurrent syncope with negative evaluations to diagnose neurally mediated syncope and carotid-sinus syncope, respectively. Other diagnostic tests that rarely help but may be of some small utility in diagnosing the cause of a syncopal event include ambulatory (Holter) monitoring, continuous-loop event monitors, electroencephalograms, and computed tomographic scans of the head.
Comment: Syncope is a common presentation to the emergency department that accounts for one percent to 1.5 percent of annual visits and up to six percent of hospital admissions in the U.S. Because it's so common, ACEP originally published syncope guidelines in 2001 that were recently revised in January 2007 to assist emergency physicians in evaluating and ultimately helping dispose these patients.
On the question, “What diagnostic testing data help to risk-stratify patients with syncope?” a Level A recommendation was given to obtaining a standard 12-lead ECG in patients with syncope. On the question, “Who should be admitted after a syncopal event?” the guideline gives a “Level B” recommendation to admitting patients with evidence of heart failure or structural heart disease and those with other factors that lead to stratification as high-risk for adverse outcome (i.e., old age and associated comorbidities; ECG abnormalities such as acute ischemia, dysrhythmias, or significant conduction abnormalities; hematocrit less than 30 [if obtained]; history or presence of heart failure, coronary artery disease, or structural heart disease).
In a recent retrospective study of patients presenting to an ED with syncope, the 2001 ACEP level B recommendations were found to be 100% sensitive and 81% specific in diagnosing cardiogenic syncope. Additionally, if the 2001 ACEP level B recommendations had been followed, the admission rate would have been 28.5 percent rather than the 57.5 percent who were admitted based on physician judgment alone. (Am Heart J 2005;149:826.)
Other recent noteworthy studies include the derivation and validation of the San Francisco Syncope Rule. (Ann Emerg Med 2004;43:224; Ann Emerg Med 2006;47:448.) This decision rule was created to assist physicians in predicting which patients were at greatest risk for short-term (seven-day) serious outcome. Patients with abnormal ECGs (defined as not sinus rhythm or new changes compared with a previous ECG), a history of CHF, shortness of breath, systolic blood pressure less than 90 mm Hg, or hematocrit less than 30% were considered “high risk.” The authors created a mnemonic, CHESS (CHF, HCT<30%, ECG abnormal, SOB, SBP<90), to assist in remembering the decision algorithm. The San Francisco Syncope Rule was found to be 98% sensitive and 56% specific for predicting short-term serious outcome.
One final important paper, published in 2003, derived and validated a risk score to predict arrhythmias in patients with unexplained syncope. (Acad Emer Med 2003;10:1312.) I won't go too much into the paper because it's one of the 2006 LLSA articles, but basically it found three important predictors of arrhythmia: history of CHF, age older than 65, and an abnormal ECG.
Dexamethasone in Adults with Bacterial Meningitis, deGans J, van de Beek D, N Eng J Med, 2002;347(20):1549
The mortality rate among adults with acute bacterial meningitis and the frequency of neurologic sequelae among those who survive are high, especially among patients with pneumococcal meningitis. Unfavorable neurologic outcomes are not the result of treatment with inappropriate antimicrobial agents because cerebrospinal fluid (CSF) cultures are usually sterile 24 to 48 hours after starting antimicrobial therapy. Bacterial lysis, induced by treatment with antibiotics, leads to inflammation in the subarachnoid space. Anti-inflammatory agents such as dexamethasone reduce CSF inflammation and neurologic sequelae in animal models. Additionally, adjunctive dexamethasone therapy decreases severe hearing loss in children with H. influenzae type b meningitis.
This study by deGans and van de Beek was a prospective, randomized, double-blind, multicenter, European trial of adjunctive treatment with dexamethasone, as compared with placebo, in adults with acute bacterial meningitis. In the dexamethasone group, a dose of 10 mg was given intravenously every six hours for four days, administered 15 to 20 minutes prior to the parenteral administration of antibiotics. A total of 301 patients were randomly assigned to a treatment group: 157 to the dexamethasone group and 144 to the placebo group.
The baseline characteristics of the two groups were similar. Classic symptoms and signs were present in a large proportion of patients: headache in 94 percent, fever in 81 percent, and neck stiffness in 94 percent. There was no doubt about the diagnosis of bacterial meningitis in this study: 78 percent had CSF positive cultures, 65 percent had positive blood cultures, opening pressures were about 35 cm of water, and the mean white blood cell count was about 8,000 cells per cubic millimeter.
Predictors of unfavorable outcome during the study were coma on admission, hypotension, and meningitis due to Streptococcus pneumoniae. The percentage of patients with an unfavorable outcome was significantly less in the dexamethasone group compared with the placebo group (15% vs. 25%). Among patients with pneumococcal meningitis, 26 percent in the dexamethasone group and 52 percent in the placebo group suffered an unfavorable outcome, and 14 percent vs. 34 percent died, respectively. There were no differences in the groups when patients were infected with N. meningitidis. Adverse events were similar in the two groups.
Comment: This was a landmark study that really changed how physicians treat meningitis. No confirmatory study has followed, but it certainly appears to heavily suggest that any adult patient who may have meningitis (especially pneumococcal) be treated with 10 mg of intravenous dexamethasone 15 to 20 minutes prior to or with the first dose of antibiotics (and then every six hours for four days).
For the purposes of the study, treatment was not started unless the diagnosis was certain: the CSF was cloudy, bacteria were in the CSF on Gram's stain, or the CSF leukocyte count was greater than 1,000 cells per cubic millimeter. Because delaying antibiotic administration may increase morbidity and mortality, emergency physicians should not follow this study protocol. If meningitis is highly suspected, the appropriate antibiotics with adjunctive dexamethasone therapy should be given as soon as possible and not delayed if a lumbar puncture is difficult or a CT scan of the head is deemed necessary.
One concern that some physicians have in giving dexamethasone to patients with pneumococcal meningitis is that it appears to reduce blood-brain permeability, and thus impedes the penetration of vancomycin into the subarachnoid space. In the U.S. there is a greater concern for drug resistant S. pneumoniae, so high-dose ceftriaxone and vancomycin are usually given until culture results with sensitivities are reported. Would the results of this study be different if done in the U.S. current day? No one knows, but because this disease is so devastating and the results of this study are so impressive, physicians should not wait for further data before deciding whether to use this therapy. Dexamethasone therapy, along with appropriate antibiotics, should be considered the standard of care in treating adults with bacterial meningitis, especially if S. pneumoniae is the suspected infectious agent.
About the LLSA
As part of its continuous certification program, the American Board of Emergency Medicine has developed the Life-long Learning and Self-Assessment (LLSA) program to promote continuous education of diplomates. Each year, beginning in 2004, 16 to 20 articles are chosen based on the Emergency Medicine Model. A list of these articles can be found on the ABEM web site, www.abem.org.
ABEM is not authorized to confer CME credit for the successful completion of the LLSA test, but it has no objection to physicians participating in such activities. EMN's CME activity, Learning to Live with the LLSA, is not affiliated with ABEM's LLSA program, and reading this article and completing the quiz does not count toward ABEM certification. Rather, participants may earn 1 CME credit from the Lippincott Continuing Medical Education Institute, Inc., for each completed EMN quiz.