A case: syncope

Syncope and Palpitation: A Case

A 37-year-old woman with a history of anxiety disorder presents to the emergency department (ED) with concern for panic attack. She describes a sensation of chest-pounding palpitations, racing heart rate, severe dyspnea, and lightheadedness. She is beginning to feel some chest heaviness. She has a several-year history of these intermittent symptoms, which she ascribes to her "panic attacks." These paroxysms often last for 10-15 minutes and spontaneously subside before her arrival to the ED. In the past, she had an extensive but essentially normal cardiac work-up, which included electrocardiography, exercise treadmill test, 24-hour Holter monitor, and echocardiography. She notes that she was asymptomatic at the time that the studies were being conducted. Her primary care provider diagnosed her with anxiety disorder with panic attacks and prescribed a selective serotonin reuptake inhibitor (SSRI). Despite treatment, she has had several episodes per year. They do not appear to be associated with anything in particular. Her current episode began while she was playing water polo with her community league team and, to her surprise, it did not spontaneously subside. She began to feel drained of her usual energy and stamina and thought that she would pass out. She immediately got out of the pool and was quickly rushed to the ED by her friends.

On initial physical examination, the patient is a young woman in athletic condition who appears pale and diaphoretic. In general, she is somewhat lethargic and in mild respiratory distress. Her heart rate is irregular and tachycardic, ranging from 170 to 300 bpm. Her blood pressure is 80/46 mm Hg. Her respiratory rate is 18 breaths/min, with an oxygen saturation of 99% on 2 L. Her heart sounds include an S1 and S2, with an irregular tachycardic rhythm. The patient's lung sounds are clear to auscultation bilaterally. Her extremities are free of edema, but they are cool and with faint distal pulses.

The initial electrocardiogram (ECG, see Figure 1) reveals an irregular, wide complex tachycardia at a rate of 224 bpm. Because of her altered mentation and significant hypotension, the American Heart Association's (AHA's) Advanced Cardiac Life Support (ACLS) algorithm^[1] is initiated by the ED staff, and a synchronized cardioversion is performed. The patient converts to a normal sinus rhythm at a heart rate of 58 bpm. A repeat 12-lead ECG is obtained (see Figure 2).

On the basis of the clinical presentation and the first ECG, what is the diagnosis?

Hint: The key to diagnosis is combining the rate and morphology of the QRS complex with an understanding of whether the rhythm is regular, irregular, or irregularly irregular. The ECG in Figure 1 is unique and considered pathognomonic

Diagnosis: Wolff-Parkinson-White syndrome with atrial fibrillation

Syncope and Palpitation: Managment of WPW syndrome with Atrial fibrillation

The diagnosis of Wolff-Parkinson-White (WPW) syndrome with atrial fibrillation was made on the basis of the patient's history in conjunction with the classic ECG findings in both figures. The history of previously undiagnosed paroxysms of palpitations, lightheadedness, and shortness of breath is common in cases of supraventricular tachycardia. The subtle findings on the baseline ECG are often overlooked, and young patients can be diagnosed with other disorders, such as anxiety. This patient's baseline ECG (see Figure 2) contains a short (<120 msec) P-R interval. There is subtle widening of the QRS complex to >120 msec. The initial portion of the QRS complex is slurred, with a slow upward slope immediately before the sharp upstroke. This initial slur is known as a delta wave. The arrhythmia (see Figure 1) is irregularly irregular; this is an important fact in recognizing atrial fibrillation. The wide complex tachycardia represents activation of the ventricles through a pathway outside of the normal conduction system. The heart rates of 170-300 bpm are consistent with the cycle of atrial fibrillation, with almost 1:1 activation of the ventricles through this accessory pathway. It is important to remember that because these rapid heart rates lack the decremental conduction (an intrinsic protective mechanism) from the atrioventricular node, the ventricular rhythm can degrade into ventricular fibrillation, resulting in sudden cardiac death. This is a life-threatening event and requires immediate intervention, even if the patient appears hemodynamically stable. In this case, the ED staff made use of the AHA's ACLS algorithms because of the patient's hemodynamic instability.^[1] Synchronized cardioversion is a reasonable option for treatment of this rhythm. Alternatively, if the patient is a bit more stable, a bolus of amiodarone, which is also part of the ACLS algorithm, could selectively decrease conduction through the bypass tract relative to the atrioventricular node, resulting in a break in the rhythm. This can help avoid cardioversion, though there may be concerns over transient hypotension. If the rhythm is recognized immediately, procainamide is another, more effective option for stopping the arrhythmia. After cardioversion, the patient was started on procainamide in consultation with the cardiovascular medicine service.

Preexcitation, or WPW syndrome, is an abnormality recognized on the surface ECG that represents an early activation of the ventricle outside the normal conduction pathway.^[2] As normal atrial conduction occurs, there is inherent delay in the atrioventricular node prior to activation of the ventricles. With preexcitation, a communication or "accessory pathway" exists between the atria and ventricle that bypasses normal atrioventricular node conduction delay and activates some portion of the ventricle. The resultant beat is a fusion of early and normal ventricular activation. The bundle of Kent, a communicating tract between the left atrial appendage and left ventricle, is a classic example of a preexcitation pathway. Localization of the various types of accessory pathways can often be achieved through the baseline ECG.^[3] For example, in Figure 2, the delta wave is positive in V₁ (moves toward V₁) and negative in aVL (moves away from aVL), suggesting that this pathway is located in the left ventricle along the lateral wall.

Atrioventricular accessory pathways are not the only mechanism of early ventricular activation. There are rare reports of atrio-Hisian (from atria to bundle of His) pathways, a condition known as Lown-Ganong-Levine (LGL) syndrome.^[2] In LGL syndrome, the ECG demonstrates a short P-R interval (usually <0.12 sec) without a delta wave and with a normal QRS complex.

Preexcitation is believed to have an estimated prevalence of 0.1-0.3% in the general population. As in the original descriptions, preexcitation syndromes predispose patients (often otherwise young and healthy) to paroxysmal tachydysrhythmias, specifically atrioventricular reentrant tachycardias. Initially, these syndromes were thought to be benign until the recognition that atrial fibrillation in these patients can precipitate ventricular fibrillation.^[4,5] Luckily, this patient presented prior to having such a lethal event. As many as 80% of patients with WPW syndrome have reentrant tachycardia, 15-30% have atrial fibrillation, and 5% have atrial flutter.^[2] Ventricular fibrillation is estimated to occur in patients with recurrent tachycardia at about 0.1% of the time.

The initial treatment for acute tachycardia is as described in the AHA's ACLS protocol.^[1] In many cases of narrow complex tachycardia, adenosine can be helpful in both the diagnosis and, depending on the underlying arrhythmia, the treatment to stop the cycle of the arrhythmia; however, patients who have the typical narrow-complex atrioventricular reentrant tachycardia associated with WPW can theoretically be at risk for harm. This is not just because adenosine can prolong conduction and refractory time in the atrioventricular node, promoting conduction down the accessory pathway, but also because there is a small risk of precipitating atrial fibrillation with adenosine. Digoxin is absolutely contraindicated when there is atrial fibrillation because it may shorten the refractory period and enhance conduction over the bypass tract, resulting in even faster conduction to the ventricles and increasing the risk for ventricular fibrillation. If the diagnosis is made early, the American College of Cardiology (ACC)/AHA guidelines for the management of atrial fibrillation in WPW syndromes list direct-current (DC) cardioversion, ibutilide to break the atrial fibrillation, and procainamide as class I treatment options.^[6] Amiodarone has a class IIb indication. Digoxin and nondihydropyridine calcium channel blockers are listed as class III agents because of the potential harm that they can cause.

As mentioned above, some patients with WPW syndrome are at risk for sudden death. In these patients, a cardiac electrophysiology study and radiofrequency catheter ablation may be definitive and curative. ACC/AHA guidelines for radiofrequency ablation (RFA) list symptomatic patients with drug-resistant accessory pathway arrhythmias or atrial fibrillation in preexcitation syndromes as class I indications for RFA.^[7] A family history of sudden cardiac death in patients with accessory pathways has a class IIa indication. Because of the association with family history, there is a great deal of active research in identifying the underlying molecular and genetic mechanisms that result in the development of such accessory pathways.^[8,9] It is therefore important to review family history in patients who present with these syndromes. The patient in this case did not have an immediate family history of sudden cardiac death. There is also data to support radiofrequency ablation in asymptomatic patients who may be at high risk for atrial arrhythmia as recognized by electrophysiology studies.^[10] ACC/AHA guidelines include a class IIa recommendation for asymptomatic patients whose jobs, livelihood, or safety may be adversely affected by arrhythmia.^[7]

Given this patient's history of severe symptoms and her presentation with atrial fibrillation, the cardiovascular electrophysiology service recommended radiofrequency ablation. She underwent the procedure during her admission and had no complications. At 3-month follow-up, she was free of any need for antiarrhythmic medication. In addition, she noted that she did not have any further "panic attacks" in that timeframe, and her primary care provider was planning to wean her off of the SSRI.

References

1. American Heart Association. Management of symptomatic bradycardia and tachycardia. Circulation. 2005;112:IV-67-IV-77.
2. Olgin JE, Zipes DP. Specific arrhythmias: diagnosis and treatment. In: Libby P, Bonow RO, Mann DL, Zipes DP, eds. Braunwald's Heart Disease. Philadelphia, Penn.:Saunders Elsevier;2008:863-931.
3. Arruda MS, McClelland JH, Wang X et al. Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome. J Cardiovasc Electrophysiol. 1998;9:2-12.
4. Wolff L, Parkinson J, White PD. Bundle-branch block with short P-R interval in healthy young people prone to paroxysmal tachycardia. Am Heart J. 1930;5:685-704.
5. Mazur A, Meisel S, Shotan A, et al. The mechanism of sudden death in the Wolff-Parkinson-White syndrome. J Cardiovasc Electrophysiol. 2005;16:1393.
6. European Heart Rhythm Association; Heart Rhythm Society, Fuster V, Rydén LE, Cannom DS, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation). J Am Coll Cardiol. 2006;48:854-906.
7. Zipes DP, DiMarco JP, Gillette PC, et al. Guidelines for clinical intracardiac electrophysiological and catheter ablation procedures. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Clinical Intracardiac Electrophysiologic and Catheter Ablation Procedures), developed in collaboration with the North American Society of Pacing and Electrophysiology. J Am Coll Cardiol. 1995;26:555-73.
8. Basson CT. A molecular basis for Wolff-Parkinson-White syndrome. N Engl J Med. 2001;344:1861-64.
9. Gollob MH, Green MS, Tang AS, et al. Identification of a gene responsible for familial Wolff-Parkinson-White syndrome. N Engl J Med. 2001;344:1823-31.
10. Pappone C, Santinelli V, Manguso F, et al. A randomized study of prophylactic catheter ablation in asymptomatic patients with the Wolff-Parkinson-White syndrome. N Engl J Med. 2003;349:1803-11.

Syncope and Palpitation: A Case

A 37-year-old woman with a history of anxiety disorder presents to the emergency department (ED) with concern for panic attack. She describes a sensation of chest-pounding palpitations, racing heart rate, severe dyspnea, and lightheadedness. She is beginning to feel some chest heaviness. She has a several-year history of these intermittent symptoms, which she ascribes to her "panic attacks." These paroxysms often last for 10-15 minutes and spontaneously subside before her arrival to the ED. In the past, she had an extensive but essentially normal cardiac work-up, which included electrocardiography, exercise treadmill test, 24-hour Holter monitor, and echocardiography. She notes that she was asymptomatic at the time that the studies were being conducted. Her primary care provider diagnosed her with anxiety disorder with panic attacks and prescribed a selective serotonin reuptake inhibitor (SSRI). Despite treatment, she has had several episodes per year. They do not appear to be associated with anything in particular. Her current episode began while she was playing water polo with her community league team and, to her surprise, it did not spontaneously subside. She began to feel drained of her usual energy and stamina and thought that she would pass out. She immediately got out of the pool and was quickly rushed to the ED by her friends.

On initial physical examination, the patient is a young woman in athletic condition who appears pale and diaphoretic. In general, she is somewhat lethargic and in mild respiratory distress. Her heart rate is irregular and tachycardic, ranging from 170 to 300 bpm. Her blood pressure is 80/46 mm Hg. Her respiratory rate is 18 breaths/min, with an oxygen saturation of 99% on 2 L. Her heart sounds include an S1 and S2, with an irregular tachycardic rhythm. The patient's lung sounds are clear to auscultation bilaterally. Her extremities are free of edema, but they are cool and with faint distal pulses.

The initial electrocardiogram (ECG, see Figure 1) reveals an irregular, wide complex tachycardia at a rate of 224 bpm. Because of her altered mentation and significant hypotension, the American Heart Association's (AHA's) Advanced Cardiac Life Support (ACLS) algorithm^[1] is initiated by the ED staff, and a synchronized cardioversion is performed. The patient converts to a normal sinus rhythm at a heart rate of 58 bpm. A repeat 12-lead ECG is obtained (see Figure 2).

On the basis of the clinical presentation and the first ECG, what is the diagnosis?

Hint: The key to diagnosis is combining the rate and morphology of the QRS complex with an understanding of whether the rhythm is regular, irregular, or irregularly irregular. The ECG in Figure 1 is unique and considered pathognomonic

Diagnosis: Wolff-Parkinson-White syndrome with atrial fibrillation

Emergency Medicine: Syncope Diagnostic Flow Chart

Emergency Medicine: Syncope History taking Pointer

Table 2

History taking pointers in syncope

Features from history	Suggested diagnosis
The “5Ps”
Precipitants:
Warm or  crowded environments, pain, emotional distress, fear, exercise, dehydration (as a result of drugs or illness), specific activities (coughing, laughing, micturition, eating)	Vasovagal syncope, orthostatic hypotension, situational syncope
Head  movements, tight collars, shaving	Carotid sinus syndrome
During  exercise, or no obvious precipitant	Arrhythmia, structural heart disease
Prodrome:
Light  headedness, dizziness, blurred vision	Vasovagal syncope, orthostatic hypotension
Nausea,  sweating, abdominal pain	Vasovagal syncope
None	Vasovagal syncope in older people, cardiac syncope
Chest pain,  shortness of breath, or no prodrome	Cardiac syncope
Déjà vu,  jamais vu	Seizure
Palpitations	Arrhythmia
Position:
Prolonged  standing	Vasovagal syncope, orthostatic hypotension
Sudden changes  in posture	Orthostatic hypotension
Supine	Arrhythmia, structural heart disease
Post-event phenomena:
Nausea,  vomiting, fatigue	Vasovagal syncope
Immediate  complete recovery	Any cause, common in arrhythmia
Appearance:
Pallor,  sweating	Syncope rather than seizure
“Blue”	Seizure
Abnormal movements:
Minor  twitching but floppy while unconscious (myoclonic jerks)	Syncope (any cause)
Rhythmic  jerking preceded by rigidity or abnormal posturing	Seizure
Eyes:
Open	Seizure or syncope
Closed	Pseudoseizure, psychogenic syncope
Mental state:
Prolonged  confusion, retrograde amnesia	Seizure
Transient  disorientation	Common in neurally mediated syncope
Amnesia  concerning loss of consciousness	Neurally mediated syncope in older people
Other:
Incontinence	Non-specific, but unusual in syncope
Tongue  biting	Seizure
Chronic medical problems
Pre-existing heart disease	Cardiac syncope
Diabetes, Parkinson’s disease, Parkinson plus syndromes, alcohol dependence, renal replacement therapy	Orthostatic hypotension
Hypertension	Drug related neurally mediated syncope, orthostatic hypotension
Family history of sudden cardiac death
	Hereditary long and short QT syndromes, Brugada, arrhythmogenic right ventricular dysplasia, structural heart disease

case of the week:Acute Onset of Headache and Blurred Vision in a 16-Year-Old Girl

A 16-year-old girl presents to the emergency department with an acute-onset severe headache as well as nausea, vomiting, and intermittent diplopia. She feels dizzy while walking and cannot walk independently. She also complains of blurred vision. This is her first physician's visit for the headaches, which have been episodic during the past 2 weeks. The headaches involve her entire head. They are not throbbing and are not associated with an aura or a certain time of the day. The severity increases while coughing or straining. She has photophobia and phonophobia during these episodes. The headaches previously responded to over-the-counter analgesics, but now she has intolerable pain unrelieved by medications. She has no significant medical history, except for minor head trauma while cycling 1 month ago. Her only medication is an oral contraceptive that she has taken for 2 years. She denies any illicit drug use. The family history is positive for atypical migraine headaches; her mother has been treated with medications for this condition for years.

On physical examination, the patient is a normal-appearing teenager, but she is agitated due to her headache. She has a regular heart rate of 65 bpm, her blood pressure is 165/95 mm Hg, and her oral temperature is normal at 98.6°F (37°C). The general physical examination reveals no abnormalities in the head, neck, chest, abdomen, or extremities. A thorough neurologic examination is performed, which reveals decreased visual acuity in each eye to 6/10 (or about 20/30 US Standard). Ophthalmoscopy reveals papilledema, venous engorgement, and a diminished venous pulse. Bilateral sixth cranial nerve palsy is evident. Other neurologic examinations, including sensory and motor examinations, deep tendon reflexes, and cerebellar tests, are all within normal range.

During the initial assessment of the patient in the emergency department, she develops a generalized tonic-clonic seizure, which is immediately controlled with intravenous diazepam. Her blood pressure rises to 175/100 mm Hg, and her heart rate is 60 bpm after the convulsion. A repeat neurologic examination reveals bilateral extensor plantar reflexes and midsized pupils with slight reaction to light. After initiating a loading dose of intravenous phenytoin, an urgent computed tomography (CT) scan of the head is performed.

What is your diagnosis?

Discussion

The new onset of headache with nausea, vomiting, blurred vision, and diplopia were strongly suggestive of increased intracranial pressure in this patient. The presence of bilateral sixth nerve palsy and bilateral papilledema on neurologic examination confirmed this suspicion. Laboratory tests revealed normal electrolytes, renal function, and complete blood count findings. The CT scan of the brain revealed acute lateral ventricular hydrocephalus, with periventricular edema and a hyperdense round mass within the third ventricle causing obstruction of the foramen of Monro. The most likely diagnosis was colloid cyst of the third ventricle.

Colloid cysts of the third ventricle account for 10%-15% of intraventricular tumors. They are the most common masses of the third ventricle found in adults. Controversy exists over whether these cysts can be classified as brain neoplasms. The cysts are considered to be congenital in origin, and there are some reports of familial occurrence of the disease^[1,2]; however, no specific gene has been identified. Autosomal dominant inheritance is the proposed mechanism in such cases.^[2] Some believe that the cysts originate from the neuroepithelium, but other sources, such as endoderm or ectopic respiratory tissue, have also been hypothesized. The cysts are thin-walled benign masses with a gelatinous content.^[3] They are located in the anterior third ventricular area and are connected to the rostral aspect of its roof, projecting inferiorly close to the foramina of Monro. The inner epithelium with simple cuboidal and columnar cells secretes a mucinous content, which accumulates under pressure. Most cysts are asymptomatic and rarely are a cause of headache. In symptomatic cysts, headache is the most common presentation. Persistent or intermittent obstruction of the foramina of Monro is believed to be the cause of headache.^[4] Symptomatic cysts typically present in mid-adulthood with headache, signs of increased intracranial pressure, and acute lateral ventricular hydrocephalus, although atypical presentations -- such as hemorrhagic cysts -- have been described during childhood as well.^[3] Other symptoms may include altered mental status, nausea and vomiting, seizure, vertigo, and sudden attacks of leg weakness.^[2] The latter might be rarely associated with other brain tumors and may be due to stretching of corticospinal nerve fibers to the legs after acute hydrocephalus. The most severe presentation is sudden death. The cause of this rare phenomenon is debatable, but it may be secondary to reflex cardiac effects due to the cyst compressing of the hypothalamus.^[2] Acute blockage of cerebrospinal fluid with instant herniation or decompensation in chronic hydrocephalus has also been postulated.^[5]

The differential diagnosis of colloid cyst includes a wide range of tumors of the anterior third ventricle. These lesions usually originate outside the third ventricle and deform the ventricle by encroachment of the surrounding parenchyma; however, intraventricular tumors may also be the source of cerebrospinal fluid pathway blockage. Choroid plexus papillomas usually present during the first 2 decades of life. Although 10%-30% are found within the third ventricle, mobile tumors may slip from lateral ventricles into the foramina of Monro and become trapped in the third ventricle, thereby causing hydrocephalus.^[6] Neurocytomas are intraventricular tumors that are seen in young adults and may be found in the lateral and third ventricular regions. These tumors are frequently misdiagnosed as oligodendroglioma or ependymoma under light microscopy, and the true incidence of this condition may be more than expected. Intraventricular meningiomas account for 15%-17% of meningiomas in pediatric patients, but only 1.6% of meningiomas in adults.^[6] Only 50 reported cases of third ventricle meningioma exist in the literature, and the majority of these lesions are found within lateral ventricles.^[6] They commonly present as basal tumors with extension up into the floor of the third ventricle.

As described earlier, most other lesions encroach on the third ventricle from the surrounding parenchyma. The majority of these lesions are glial tumors, including juvenile pilocytic astrocytoma, fibrillary astrocytoma, protoplasmic astrocytoma, subependymal giant cell astrocytoma, glioblastoma multiforme, and ependymoma. Metastatic neoplasms may involve the third ventricle via its roof, floor, lateral wall, or choroid plexus. Metastases from the lungs, colon, kidneys, and breasts are most common. In these cases, the prognosis is poor, and death is often due to progressive systemic disease. Suprasellar germinomas and craniopharyngiomas can invade the floor of the third ventricle from below. Suprasellar extension of pituitary macroadenomas may also involve the third ventricle. Decreased visual acuity or visual field, endocrinopathy, and headache are the main symptoms in these cases.

Other cystic lesions in the anterior third ventricular area include epidermoid cyst, dermoid cyst, and neurocysticercosis. Epidermoid and dermoid cysts are rarely found in the third ventricle, and neurocysticercosis is endemic to Mexico, Eastern Europe, Asia, Central and South America, and Africa. Fenestration into the third ventricle has occurred in 15%-25% of cases with ensuing hydrocephalus.^[7] Inflammatory lesions, such as pyogenic abscesses, and granulomatous diseases, such as tuberculosis or fungal infection, may rarely impinge on the third ventricle. Other lesions, such as sarcoidosis and histiocytosis, may involve the third ventricle via its floor and hypothalamus. Finally, vascular lesions, such as cavernous malformations and arteriovenous malformations, should be added to the differential diagnosis of third ventricular mass lesions.

The contents of the colloid cyst determine its appearance on imaging studies. The cyst may be found incidentally on CT scanning or when the patient presents with symptoms and signs of increased intracerebral pressure suggestive of acute obstructive hydrocephalus. It is generally a round homogeneous hyperdense mass within the third ventricle at the level of the foramina of Monro.^[5] Acute lateral hydrocephalus with periventricular edema might be seen due to the blockage of the cerebrospinal fluid pathway into the third ventricle. On T2-weighted magnetic resonance imaging (MRI), the cyst might be either hypo- or hyperintense, and fluid-attenuated inversion recovery (FLAIR) shows periventricular edema in the acute stage of hydrocephalus as hyperintensity surrounding the lateral ventricle.

Surgical intervention is indicated after considering certain factors, such as the patient's age, symptoms, and cyst size. Because of the threat of sudden death, surgery is recommended for cysts exceeding 1.5 cm in diameter in young patients, even in asymptomatic cases.^[8] Symptomatic patients should always receive treatment.^[9] Options for treatment include endoscopic removal of the cyst^[10] and open surgery with different approaches, such as transcortical or interhemispheric transcallosal approaches.^[4,9]

In this case, MRI revealed a round mass with high signal intensity on T1-weighted imaging, low signal intensity on T2-weighted imaging, and high signal intensity on FLAIR images. The patient was taken to the operating room. Bilateral external ventricular drainage was inserted in the frontal horns of the lateral ventricles. Bilateral drainage was performed because unilateral ventricular drainage may fail to reduce intracranial pressure when a third ventricular mass simultaneously obstructs both foramina of Monro. Unilateral drainage may also result in selective enlargement (or "trapping") of the contralateral lateral ventricle. The tumor was totally resected via a interhemispheric transcallosal approach under a surgical microscope. The macroscopic appearance of the tumor was a creamy soft cyst suggestive of colloid cyst. Histopathology revealed a fibrous wall lined by inner ciliated columnar epithelium and colloid and cell ghosts, confirming the diagnosis. On the first postoperative day, the patient's diplopia and headache resolved. The patient had an uneventful postoperative course and was discharged from the hospital 6 days after surgery. She was on phenobarbital for 6 months, which was tapered and discontinued after a normal EEG. Gradual improvement in visual acuity was observed, and she regained her full vision 5 months later.

(Source: Medscape)

Emergency Medicine: Syncope Rule

Am J Emerg Med. 2010 May;28(4):432-9. Epub 2010 Jan 28.

San Francisco Syncope Rule, Osservatorio Epidemiologico sulla Sincope nel Lazio risk score, and clinical judgment in the assessment of short-term outcome of syncope.

Dipaola F, Costantino G, Perego F, Borella M, Galli A, Cantoni G, Barbic F, Casella F, Duca PG, Furlan R; STePS investigators.

Unità Sincopi, Medicina Interna II, Ospedale L. Sacco, Università degli Studi di Milano, 20157 Milano, Italy.

Abstract

OBJECTIVE: The study aimed to compare the efficacy of the Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL) risk score, San Francisco Syncope Rule, and clinical judgment in assessing the short-term prognosis of syncope.
METHODS: We studied 488 patients consecutively seen for syncope at the emergency department of 2 general hospitals between January and July 2004. Sensitivity, specificity, predictive values, and likelihood ratios for short-term (within 10 days) severe outcomes were computed for each decision rule and clinical judgment. Severe outcomes comprised death, major therapeutic procedures, and early readmission to hospital.
RESULTS: Clinical judgment had a sensitivity of 77%, a specificity of 69%, and would have admitted less patients (34%, P < .05 vs decision rules). The OESIL risk score was characterized by a sensitivity of 88% and a specificity of 60% (admission 43%). San Francisco Syncope Rule sensitivity was 81% and specificity was 63% (admission 40%). According to both clinical rules, no discharged patient would have died. With combined OESIL risk score and clinical judgment, the probability of adverse events was 0.7% for patients with both low risk scores, whereas that for both high risk scores was roughly 16%.
CONCLUSION: Because of a relatively low sensitivity, both risk scores were partially lacking in recognizing patients with short-term high-risk syncope. However, the application of the decision rules would have identified all patients who subsequently died, and OESIL risk score and clinical judgment combined seem to improve the decision-making process concerning the identification of high-risk patients who deserve admission.
(c) 2010 Elsevier Inc. All rights reserved.

Emergency Medicine:Accuracy and quality of clinical decision rules for syncope in the emergency department

Ann Emerg Med. 2010 Oct;56(4):362-373.e1.

Accuracy and quality of clinical decision rules for syncope in the emergency department: a systematic review and meta-analysis.

Serrano LA, Hess EP, Bellolio MF, Murad MH, Montori VM, Erwin PJ, Decker WW.

Department of Emergency Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA. serrano.luis@mayo.edu

Abstract

STUDY OBJECTIVE: We assess the methodological quality and prognostic accuracy of clinical decision rules in emergency department (ED) syncope patients.
METHODS: We searched 6 electronic databases, reviewed reference lists of included studies, and contacted content experts to identify articles for review. Studies that derived or validated clinical decision rules in ED syncope patients were included. Two reviewers independently screened records for relevance, selected studies for inclusion, assessed study quality, and abstracted data. Random-effects meta-analysis was used to pool diagnostic performance estimates across studies that derived or validated the same clinical decision rule. Between-study heterogeneity was assessed with the I(2) statistic, and subgroup hypotheses were tested with a test of interaction.
RESULTS: We identified 18 eligible studies. Deficiencies in outcome (blinding) and interrater reliability assessment were the most common methodological weaknesses. Meta-analysis of the San Francisco Syncope Rule (sensitivity 86% [95% confidence interval {CI} 83% to 89%]; specificity 49% [95% CI 48% to 51%]) and the Osservatorio Epidemiologico sulla Sincope nel Lazio risk score (sensitivity 95% [95% CI 88% to 98%]; specificity 31% [95% CI 29% to 34%]). Subgroup analysis identified study design (prospective, diagnostic odds ratio 8.82 [95% CI 3.5 to 22] versus retrospective, diagnostic odds ratio 2.45 [95% CI 0.96 to 6.21]) and ECG determination (by evaluating physician, diagnostic odds ratio 25.5 [95% CI 4.41 to 148] versus researcher or cardiologist, diagnostic odds ratio 4 [95% CI 2.15 to 7.55]) as potential explanations for the variability in San Francisco Syncope Rule performance.
CONCLUSION: The methodological quality and prognostic accuracy of clinical decision rules for syncope are limited. Differences in study design and ECG interpretation may account for the variable prognostic performance of the San Francisco Syncope Rule when validated in different practice settings.
Copyright © 2010 American College of Emergency Physicians. Published by Mosby, Inc. All rights reserved

Emergency Medicine : Predictors of 30-Day Serious Events in Older Patients with Syncope

Study objective

We identify predictors of 30-day serious events after syncope in older adults.

Methods

We reviewed the medical records of older adults (age ≥60 years) who presented with syncope or near syncope to one of 3 emergency departments (EDs) between 2002 and 2005. Our primary outcome was occurrence of a predefined serious event within 30 days after ED evaluation. We used multivariable logistic regression to identify predictors of 30-day serious events.

Results

Of 3,727 potentially eligible patients, 2,871 (77%) met all eligibility criteria. We excluded an additional 287 patients who received a diagnosis of a serious clinical condition while in the ED. In the final study cohort (n=2,584), we identified 173 (7%) patients who experienced a 30-day serious event. High-risk predictors included age greater than 90 years, male sex, history of an arrhythmia, triage systolic blood pressure greater than 160 mm Hg, abnormal ECG result, and abnormal troponin I level. A low-risk predictor was a complaint of near syncope rather than syncope. A risk score, generated by summing high-risk predictors and subtracting the low-risk predictor, can stratify patients into low- (event rate 2.5%; 95% confidence interval [CI] 1.4% to 3.6%), intermediate- (event rate 6.3%; 95% CI 5.1% to 7.5%), and high-risk (event rate 20%; 95% CI 15% to 25%) groups.

Conclusion

We identified predictors of 30-day serious events after syncope in adults aged 60 years and greater. A simple score was able to stratify these patients into distinct risk groups and, if externally validated, might have the potential to aid ED decisionmaking.