Paroxysmal spells are non-epileptic, paroxysmal events that may mimic epileptic seizures but are not associated with rhythmic discharges of cortical neurons typical of seizures. They clinically manifest as a transient loss of consciousness, often occurring suddenly, with or without a prodrome. Paroxysmal spells can be caused by psychological disorders such as substance abuse and psychiatric disease or physiological events such as hypoglycemia, traumatic brain injury, and syncope.
Data suggest that men with psychiatric disease have an increased incidence of syncope or paroxysmal events of unknown etiology. This data should lead clinicians to consider screening for psychiatric disorders in patients with transient loss of consciousness they cannot identify with a clear etiology.
Among patients with a history of substance use disorder, 45% have been found to have unexplained syncope. This suggests that prior and current substance use is also associated with increased incidence of transient loss of consciousness of unknown etiology. Patients evaluated in the emergency department or even hospitalized with syncope of unknown etiology may benefit from toxicology screening and possible detoxification referral.
Hypoglycemia is defined as low blood sugar with associated symptoms. In patients without diabetes mellitus, this is usually manifested at glucose levels below 50 mg/dl. To diagnose hypoglycemia, symptoms and blood sugar must improve with exogenous glucose. Hypoglycemia can affect the central nervous system, leading to lightheadedness, nausea, flashes of light, focal neurological deficits, transient loss of consciousness, and seizure. It is, therefore, paramount that patients with any paroxysmal spell or syncope receive a fingerstick glucose.
Traumatic Brain Injury
Traumatic brain injury is an intracranial impairment, often due to external forces. These forces may include blunt or penetrating trauma to the head, causing acceleration/deceleration injury to the cerebral cortex. Intracerebral bleeding, lacerations, and diffuse axonal injuries may result. Injuries, such as an epidural hematoma, may cause a brief state of loss of consciousness, with rapid return of, usually, altered consciousness. Other injuries, such as large subdural hematoma or diffuse axonal injury may cause worsening mentation and coma over hours to days. This is a result of increased intracranial pressure, leading to decreased cerebral perfusion pressure, and finally, neuronal ischemia. Diagnosis is by clinical history and CT imaging, although MRI may be more specific for secondary trauma. Management is to reduce intracranial pressure and edema.
As most paroxysmal events are syncopal, the remainder of this discussion will focus primarily on syncope. Physiologically, syncope is a transient loss of consciousness as a result of cerebral hypoperfusion. As such, syncope varies from other etiologies of loss of consciousness in that it does not include head trauma or a post-ictal state. Syncope instead results in complete and rapid resolution of mental status. It may have myoclonic jerking, but no generalized tonic-clonic movement. Rather than a disease, syncope is a symptom of an underlying pathology ranging from benign to life-threatening. Patients are often divided into "low-risk" and "high-risk" groups. The etiology, epidemiology, evaluation, treatment, and management of these patients vary greatly. In the United States, hospitalization costs for syncope are estimated to be $5300 per admission and more than $2 billion annually. These costs are higher than those of chronic obstructive pulmonary disease and asthma combined. As extensive workups can be costly, time-consuming, and often unnecessary, a growing cadre of management tools has been devised to evaluate patients with syncope. These tools are tailored to determining the etiology of the syncopal event and treating dangerous, high-risk, syncope patients.
The etiology of syncope varies greatly. Benign causes include dehydration and vasovagal, known as neurocardiogenic syncope. Vasovagal syncope is the predominant cause of syncope worldwide, particularly in young patients. More worrisome etiologies of syncope include dysrhythmias, cardiac conduction disease, valvular heart disease, congenital heart disease (such as Brugada, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, and long QT syndrome), acute anemia or gastrointestinal bleed, and pulmonary embolism. All of these etiologies result in the hypoperfusion of the brain and require evaluation in the emergency department.
The prevalence of syncope is approximately 20% in the general population. The risk of recurrence is approximately 13.5%. Females have a greater prevalence than men. In retrospective studies, the etiology of syncope is undetermined in 37% of cases. Most cases of syncope, especially in young patients, are reflex-mediated neurocardiogenic and benign.
The pathophysiology of syncope varies by its etiology. In benign syncope, as vasovagal syncope, the vagus nerve is often over-stimulated, thus causing a transient loss of consciousness. The most common causes are classically due to fear, excitement, or temperature intolerances.
The other etiologies, listed above, require a careful history, physical, and evaluation, as the etiology is most-often cardiac and may be a predictor of a dangerous, life-threatening pathology.
A history and a physical exam are the most important aspects of the workup for syncope. In fact, health care costs and time can be substantially reduced with a proper history. Multiple decision support guidelines have been developed and compared. The Boston Syncope Pathway has a negative predictive value approaching 100%. Specifically, a history should include evaluation of prodrome, including chest pain, obtaining a tailored personal and family history of cardiac disease and cardiac death, and a thorough physical exam, including auscultation for a murmur.
Evaluation of syncope should focus on risk stratifying between low-risk and high-risk syncope. As noted, a complete history and physical exam will help assist with risk stratification. New medications, such as beta-blockers, nitrates, diuretics, and antiarrhythmics, should be carefully considered as possible contributors. A family history of sudden cardiac death is a dangerous predictor of adverse outcome.
Benign or low-risk characteristics include age younger than 40, syncope after standing from a sitting position, warmth, nausea, cough, or micturition before syncope, and an individualized trigger for syncope (such as pain or emotional distress). In children, these triggers are known as psychogenic. A history of recurring syncope in a young patient in the setting of these benign events indicates a low-risk factor. Dehydration is a common cause of syncope in young patients, and orthostatic evaluation can be considered as part of the workup. Rarely, a cerebrovascular accident, such as an intracranial bleed, can cause a reflex-mediated syncope. Features that indicate high-risk include exertional syncope, chest pain, history of congestive heart failure, aortic stenosis, left ventricular outflow tract disease, dilated cardiomyopathy, coronary artery disease, congenital heart disease, past myocardial infarction, and implantable cardioverter-defibrillator placement. Of note, recurrence of syncope multiple times in 6 months should warrant further evaluation, regardless of age.
Vital sign abnormalities, such as hypotension, may indicate an acute bleed. In older patients and menstruating females, an exam looking for pallor or gastrointestinal bleed should be considered as this can lead to cerebral hypoperfusion, causing syncope. Hemoglobin or hematocrit is indicated in such patients. Other vital sign abnormalities, such as bradycardia, may indicate arteriovenous (AV) dissociation. Hypoxia can indicate a pulmonary embolism. Physical exam findings of a new murmur can indicate dangerous valvular pathologies, such as aortic stenosis or mitral regurgitation.
All patients should receive a screening electrocardiogram (ECG). ECG features, such as a new left bundle branch block, Brugada pattern, arrhythmogenic RV dysplasia, prolonged QTc, and hypertrophic cardiomyopathy patterns, suggest high risk and indicate a need for further workup. Similarly, sinus bradycardia, dysrhythmias, and second or third-degree AV blocks should all warrant further workup.
Patients with low-risk syncope, as evaluated by history, physical, and screening ECG, can be discharged home. Without any high-risk features, the likely cause of the syncope is benign; vasovagal and dehydration are the most common. Orthostatic in young patients often delineate between vasovagal and dehydration. Patients can be rehydrated and discharged if symptoms resolve. If the young patient has recurrent syncope without high-risk features, a non-emergent echocardiogram can be scheduled for the patient as an outpatient. Management may include beta-blocker, compression stockings, or fludrocortisone.
Patients with high-risk syncope require further observation or workup. Specifically, studies have been conducted to investigate the utility of observation units in the emergency department for patients with syncope as a means to decrease health care expenditures. These studies have shown similar outcomes, adverse events, and a reduction in costs when compared to inpatient hospitalizations.
Testing done in observation units or as inpatient should be tailored to the patient’s syncopal evaluation and etiology. If there are signs and symptoms of acute coronary syndrome, such as chest pain or ECG ischemic changes, serial troponins should be done. Exercise stress testing may also be useful.
Patients with a worrisome cardiac history, such as significant coronary artery disease, congestive heart failure, or hypertrophic cardiomyopathy, are at high-risk for structural abnormalities and arrhythmia. These patients should have an echocardiogram to evaluate for worsening structural abnormalities that would decrease left ventricular outflow. The treatment may include an implantable cardioverter defibrillator (IDC). Patients with a history of ventricular dysrhythmias are at high risk for recurrence. Recurrence of syncope in six months may also indicate a dysrhythmia. Patients with an ICD or pacemaker already in place should have their device interrogated to determine further if a dysrhythmia occurred.
All patients with worrisome cardiac history should have 24-hour telemetry observation and evaluation for ICD placement. Patients with conduction disease on ECG, a new murmur on physical exam, or a concerning family history of sudden cardiac death should be evaluated for structural and valvular disorders with an echocardiogram, telemetry, and home telemetry. Often, these patients may require a pacemaker or ICD.
All patients with anemia as the cause of hypovolemia should have a complete blood count (CBC), type and screen, and evaluation for the etiology of the bleed.
Patients with concern for acute intracranial bleed as the cause of syncope should have a CT of their head and likely neurosurgical consultation.
Finally, patients with hypoxia should undergo a workup for pulmonary embolism.
There are many causes of syncope, and thus, the condition is best managed by an interprofessional team that includes an emergency department physician, primary care physician, nurse practitioner, cardiologist, neurologist, pharmacist, and specialty trained nurses.
The etiology of syncope varies greatly. Benign causes include dehydration and vasovagal, known as neurocardiogenic syncope. Vasovagal syncope is the predominant cause of syncope worldwide, particularly in young patients. More worrisome etiologies of syncope include dysrhythmias, cardiac conduction disease, valvular heart disease, congenital heart disease (such as Brugada, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, and long QT syndrome), acute anemia or gastrointestinal bleed, and pulmonary embolism. All of these etiologies result in the hypoperfusion of the brain and require evaluation in the emergency department. The prognosis depends on the cause.
Nurses are involved in triage, patient monitoring, patient education including discharge instructions. Pharmacists should review prescribed medications, check for drug-drug interactions, and counsel patients on side effects and the importance of compliance. [Level 5]
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