Case 1 is a 55 year-old healthy man who was brought to the ER after co-workers witnessed him slump down while seated and lose consciousness for 30 seconds. The patient recalled feeling “uneasy” prior to the episode. There were no tonic-clonic movements or loss of bowel or bladder function. Upon awakening, the patient vomited once. In the ER, the patient’s vital signs were normal as were EKG and basic laboratory testing, including troponin. He was admitted to the observation unit to evaluate for cardiac syncope.
On further review of systems, it was revealed that the patient had been feeling unwell for the past 2 days as if “about to come down with something.” He endorsed headache, sore throat and malaise. He denied fever or cough though subsequently became febrile on the unit. In light of his symptoms, a flu swab was sent and returned positive for Influenza A. Orthostatic vital signs were within normal range. A cardiac etiology for syncope was thought to be unlikely. The patient was given intravenous hydration and discharged on oseltamavir.
Case 2 is a 44 year-old healthy man who presented to the ER after two witnessed syncopal episodes. The first episode occurred while eating breakfast when he suddenly felt unwell with a cold sweat. He subsequently lost consciousness for a few seconds as witnessed by family. He promptly regained consciousness with no sequela and went to see his primary care physician. In the office, he again lost consciousness for 30 seconds, this time with mild hand twitches witnessed by office staff. His blood pressure at that time was 50/20 with a normal blood glucose.
The patient was sent to the ER where his blood pressure had normalized to 119/64 without intervention. Vitals, EKG and routine labs, including troponin, were unremarkable. On review of systems, he reported 3 days of malaise associated with chills, sneezing and a mild cough. He was given intravenous hydration and admitted to the observation unit for work-up of syncope. A flu swab was requested prior to bed assignment which resulted positive for Influenza B. The patient was started on oseltamavir and monitored for 24 hours with no further hypotension noted. The suspicion for cardiac syncope or sepsis was low and he was discharged in stable condition.
Discussion: Syncope as a presenting symptom of influenza infection has rarely been reported in the adult literature though cases have been seen in the pediatric population, particularly during the H1N1 pandemic in Asia. In each of the cases described above, the patients had a vague prodromal illness for 2 to 3 days; this was followed by a syncopal episode which prompted medical evaluation. While influenza myocarditis is known to cause arrhythmia and resultant syncope, the cases reported here do not seem to represent direct cardiac involvement by the virus. Instead, the mechanism of syncope in both cases appears to be neurocardiogenic (vasovagal/situational) in the setting of underlying malaise and viral illness. Further investigation of the pathophysiologic basis of syncope in influenza infection is warranted.
Conclusions: In patients presenting with syncope, a thorough review of systems may reveal associated symptoms characteristic of underlying influenza infection. Testing for influenza in such patients may allow for early diagnosis and initiation of appropriate measures including hydration, anti-viral agents, and transmission control. Moreover, identification of an underlying viral infection may prevent unnecessary testing for alternate causes of syncope.