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Case 57: Positional Vertigo in the ED With Incidental Interatrial Shunt on Bubble Study

Carmon Controy, Akash Desai

44 y.o. male, brought by EMS from an outpatient procedure suite after sudden onset vertigo and gait instability following a right TMJ/ CNIII V3 injection. Patient experienced abrupt dizziness described as imbalance with ataxic gait, nausea, and one episode of emesis. The symptoms worsen with head movement/position change and improve at rest. No focal weakness, speech change, or headache reported. 

Pertinent PMHx: HIV on ART; cognitive impairment on donepezil/memantine; lumbar stenosis s/p L5–S1 decompression. Prior episodes concerning for TIAs/CVAs. 

Pertinent FHx: Patient states his father had a “hereditary hole in his heart” which was an incidental finding in his adult life, corrected with surgery.  

Vitals on Arrival: BP 146/88, HR 91, RR 16, SpO₂ 98% RA, afebrile 

Physical Examination:

  • General: No distress. 
  • Neuro: Alert/oriented; cranial nerves grossly intact; strength/sensation intact; left-beating nystagmus noted initially; abnormal ataxic gait on arrival. 
  • Cardiopulmonary/Abdomen: Unremarkable. 

ED Imaging and Tests:

  • CT/CTA Head & Neck (stroke protocol): No hemorrhage, large territorial infarct, LVO, or significant stenosis. 
  • MRI Brain (DWI): “Questionable subtle punctate” diffusion restriction in the left thalamocapsular region—artifact favored; tiny acute ischemic focus possible. No hemorrhage or mass effect. 
  • Neurology Consult: Vertigo most consistent with peripheral cause (positional trigger, brief episodes, improvement). HINTS/Dix-Hallpike negative when re-examined after symptom improvement. 
  • Labs: CBC/BMP/coags unremarkable. 
  • Cardiac Ultrasound: Transthoracic Echo with Agitated Saline (Bubble Study)
    • Normal LV size and EF ~54%; mild concentric LVH; normal RV size/function; no significant valvular disease. 
    • Bubble study positive: At rest, microbubbles appeared after 6–7 cardiac cycles; with Valsalva, a large, uncountable shower of bubbles traversed to the left heart—consistent with an interatrial shunt (e.g., PFO/ASD).

ED Course

Symptomatic therapy was provided (e.g., meclizine). Neurological symptoms improved during observation. Neurology judged low suspicion for central vertigo; recommended Epley if recurrent and discharge if symptoms resolved. Comprehensive stroke labs and imaging obtained. TTE with bubble study was positive for interatrial shunt as above, prompting recommendation for outpatient follow-up (stroke clinic/cardiology) to risk-stratify and discuss closure versus medical management in the context of prior suspected cerebrovascular events. 

Clinical course and neurology consultant assessment favored positional peripheral vertigo (likely posterior canal BPPV precipitated by head positioning during the OP nerve block procedure) over central causes; neuroimaging was equivocal for a tiny thalamocapsular DWI focus. However, the positive bubble study establishes an interatrial right-to-left shunt, providing a plausible pathway for paradoxical embolism. In a patient with a reported history of likely TIAs/CVAs (including possible TIA at the time of current evaluation), this finding heightens stroke risk considerations and may influence long-term secondary prevention (antithrombotic strategy) and candidacy for shunt closure after more thorough outpatient stroke-neurology/cardiology evaluation. 

Discussion 

This presentation is most consistent with peripheral, positional vertigo; the positive agitated-saline study is therefore best viewed as incidental to today’s symptoms.¹,² That said, a PFO is common (~20–25% of adults) and provides a plausible conduit for paradoxical embolism (especially when shunting becomes prominent with Valsalva), so its relevance is probabilistic and depends on clinical context rather than timing alone.³,² Frameworks like the Risk of Paraxodical Embolism (RoPE) score weigh age, event phenotype, and vascular risk factors to estimate whether a PFO is likely pathogenic versus incidental.⁴,⁵ Larger shunt burden and high-risk anatomy (e.g., atrial septal aneurysm) increase suspicion, while alternative mechanisms (occult AF, atherosclerosis, dissection, thrombophilia) must be assessed in parallel.⁶,⁵ 

For secondary cerebrovascular prevention, guideline-concordant work-up (e.g., rhythm monitoring for AF; targeted DVT evaluation; selective hypercoagulability testing) should inform therapy.⁷,⁶ In carefully selected patients 18–60 with a recent non-lacunar ischemic stroke of undetermined cause and a high-risk PFO, randomized trials (RESPECT long-term, CLOSE, REDUCE) show reduced recurrent stroke with percutaneous closure plus antiplatelet therapy compared with antiplatelet therapy alone, albeit with a small increase in atrial arrhythmias;⁸,⁹,¹⁰,¹¹ outside these criteria, optimized medical therapy is appropriate and decisions should be shared between stroke neurology and cardiology.⁶ Bottom line: (1) the PFO is likely incidental to this vertigo episode; (2) given prior TIAs/CVAs without a clear alternative mechanism, the PFO may have contributed to earlier events; and (3) the finding warrants formal risk stratification and guideline-based discussion of closure vs. medical therapy.⁴,⁵,⁶ 

References

  1. Collins S, Guntheroth WG, Raghu G, et al. Agitated saline contrast echocardiography: Contraindications, complications, and safety. J Am Soc Echocardiogr. 2022;35(1):13-21. doi:10.1016/j.echo.2021.10.016 
  1. Abdelmoneim SS, Mulvagh SL, Porter TR, et al. The clinical applications of ultrasonic enhancing agents in echocardiography: 2018 American Society of Echocardiography guidelines update. J Am Soc Echocardiogr. 2018;31(3):241-274. doi:10.1016/j.echo.2017.11.013 
  1. Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc. 1984;59(1):17-20. doi:10.1016/S0025-6196(12)60336-X 
  1. Kent DM, Ruthazer R, Weimar C, et al. An index to identify stroke-related vs incidental patent foramen ovale in cryptogenic stroke. Ann Intern Med. 2013;158(5):285-292. doi:10.7326/0003-4819-158-5-201303050-00004 
  1. Kent DM, Dahabreh IJ, Ruthazer R, et al. Device closure of patent foramen ovale in patients with cryptogenic stroke: RoPE-estimated attributable fraction and treatment effect. Stroke. 2020;51(7):2143-2150. doi:10.1161/STROKEAHA.119.028966 
  1. Kleindorfer DO, Towfighi A, Chaturvedi S, et al. 2021 Guideline for the prevention of stroke in patients with stroke and transient ischemic attack. Stroke. 2021;52(7):e364-e467. doi:10.1161/STR.0000000000000375 
  1. Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45(7):2160-2236. doi:10.1161/STR.0000000000000024 
  1. Saver JL, Mattle HP, Thaler DE. Patent foramen ovale closure versus medical therapy for cryptogenic ischemic stroke: a topical review. Stroke. 2018;49(6):1541-1548. doi:10.1161/STROKEAHA.117.018153 
  1. Saver JL, Carroll JD, Thaler DE, et al. Long-term outcomes of patent foramen ovale closure or medical therapy after stroke. N Engl J Med. 2017;377(11):1022-1032. doi:10.1056/NEJMoa1610057 
  1. Mas J-L, Derumeaux G, Guillon B, et al. Patent foramen ovale closure or anticoagulation vs. antiplatelet therapy after stroke (CLOSE). N Engl J Med. 2017;377(11):1011-1021. doi:10.1056/NEJMoa1705915 
  1. Søndergaard L, Kasner SE, Rhodes JF, et al. Patent foramen ovale closure or antiplatelet therapy for cryptogenic stroke (REDUCE). N Engl J Med. 2017;377(11):1033-1042. doi:10.1056/NEJMoa1707404 

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