Syncope is a transient loss of consciousness due to global cerebral hypoperfusion. It’s incredibly common with 11% of patients in the Framingham study experiencing syncope, and this incidence increases with age (as high as 20% in women >80 years of age). Certain causes of syncope (cardiac, neurologic, and unknown) portend a poor prognosis. Additionally, syncopal episodes cause significant anxiety and reduction in quality of life for the patients affected, particularly those who have recurrent episodes.
For all of these reasons, we should take it seriously and pursue an appropriate diagnostic work up. Causes of syncope can be divided into causes of global cerebral hypoperfusion (issues with cardiac output, systemic vascular resistance, or the glucose or oxygen that the brain needs) and syncope mimics (neuro causes such as TIA, Stroke, Seizure, and Psych) as shown:
A helpful mnemonic is PASSOUT:
- P – Pressure (Hypotension)
- A – Arrhythmias
- S – Seizures
- S – Sugar
- O – Output (Cardiac) or Oxygen
- U – Unusual Causes (Psych)
- T – TIAs, Strokes
Based on the findings in the Framingham study, the most common identified cause is typically vasovagal syncope (20%) followed by cardiac causes (10%), and orthostatic hypotension (10%). In almost 40% of patients in this cohort study, no cause was identified. In the Italian PESIT Study, 1/6 patients presenting with a first episode of syncope were found to have pulmonary emboli. However, this study was criticized for lack of a control group, potential selection bias due to exclusion of 81% of initially eligible patients (primarily due to discharge from ED), and concern that PEs may have been incidentally identified and not the cause of syncope in many patients.
Work up of syncope should always include a thorough history and physical exam and EKG. History and physical will lead to identification of a cause in almost half of patients. Additional work up depends on initial findings. Our patient’s initial history of no known prodrome, no witnessed seizure activity, and immediate return to normal mental status led our differential toward cardiac causes such as arrhythmia. Structural cardiac causes were also considered a strong possibility given his history of MVP and moderate mitral regurgitation. Exam revealed an irregularly irregular rhythm and the EKG below:
TTE was performed with the following findings:
Ultimately, the patient’s syncopal episode was attributed to progression of mitral regurgitation (now severe) which led to worsening left atrial dilation and new onset atrial fibrillation. Cardiology was consulted, and he underwent mechanical mitral valve replacement while in the hospital.
References:
Soteriades ES et al. Incidence and Prognosis of Syncope. The New England Journal of Medicine. 2002; 347(12): 878-885.
Prandoni P et al. Prevalence of Pulmonary Embolism among Patients Hospitalized for Syncope (PESIT). The New England Journal of Medicine. 2016; 375(16): 1524-31.
Kapoor WN. Syncope. The New England Journal of Medicine. 2000; 343: 1856-1862.
Weiner RB et al. Case 25-2018: A 63-Year-Old Man with Syncope. The New England Journal of Medicine. 2018; 379: 670-80.
THIS. IS. AMAZING. Thank you for doing this. This blog will definitely contribute to the learning that can be gleaned from afternoon delight for second and third year residents who should be moving past differential diagnosis into evidence past medicine and journal articles. LOVE IT.