Sclerotherapy is a venous ablation technique used to manage chronic venous insufficiency, particularly in varicose veins, reticular veins, and telangiectasias. Although liquid-injection sclerotherapy is the criterion standard, foam sclerotherapy is becoming a popular alternative because of its efficacy and success rate.¹ A potential complication of foam sclerotherapy is the formation of gas microemboli in the brain, which can lead to neurologic deficits.^2,3 In a study of 1025 patients who underwent sclerotherapy, 2.6% reported visual disturbances, migraines, or transient ischemic attacks (TIAs) developing after the procedure.¹ A study of 500 patients reported the incidence of transient visual disturbances after sclerotherapy as 0.09% to 2.0%, with most cases involving foam sclerotherapy.³ 

We present a case of neurologic sequelae after foam sclerotherapy in a patient with an undiagnosed patent foramen ovale (PFO). In patients with PFO, when the pressure in the right atrium increases, such as with the Valsalva maneuver, an asymptomatic PFO may open, thus increasing the risk of microemboli traveling into the left atrium and then traveling systemically. 

A 55-year-old woman presented to the emergency department with visual disturbances, confusion, and dysarthria. Earlier in the day, she had undergone foam sclerotherapy, with no apparent complications. She noticed her symptoms while driving home after the procedure, which prompted her to return to the hospital. All of the symptoms resolved within 30 minutes of onset. Before the procedure, her medical and social history were found to be unremarkable aside from self-reported migraines. Her family history did not indicate that she was at risk for thrombus formation or other contraindications for the procedure. She was taking ibuprofen as needed and levothyroxine for hypothyroidism. 

In the emergency department, the patient was evaluated for a potential stroke, including computed tomography of the head, the results of which were unremarkable. She denied any chest pain, shortness of breath, palpitations, photophobia, phonophobia, or calf pain. She reported taking ibuprofen and levothyroxine. Osteopathic examination showed no cervical tenderness or tissue texture changes. Findings from the remainder of the physical examination, including cardiac and neurologic examinations, were unremarkable. T2-Fluid-attenuated inversion recovery magnetic resonance imaging showed no signs of an acute infarction, but multiple scattered areas of hyperintense white matter signal abnormalities in the periventricular left parietal lobe measuring 12 mm were observed and interpreted as nonspecific findings (Figure 1). The Neurology Department also performed magnetic resonance imaging of the cervical and thoracic spine to rule out any acute abnormalities. Transthoracic echocardiographic imaging while performing the Valsalva maneuver revealed a PFO (Figure 2). Electrocardiographic telemetry showed a normal sinus rhythm, and carotid Doppler ultrasonography did not show plaque formation. 

Consultation with a neurologist led to a diagnosis of TIA due to a microembolism caused by the foam sclerotherapy in the setting of a PFO. Given the timing of the symptoms arising shortly after the procedure, her self-diagnosed migraines were not thought to contribute to her symptoms. The patient followed up with a cardiologist several months later and reported no recurrent episodes. 

Assessing contraindications for sclerotherapy is vital given the potential complications of this procedure. Figure 3 lists conditions in which patients should avoid foam sclerotherapy because of a hypercoaguable state that could lead to thrombus or microemboli formation. Migraine headaches and heart defects, such as a PFO, put patients at risk for microembolisms leading to TIAs or other neurologic conditions.⁴ 

The existence of a PFO could be unknown in a large number of patients, as it is largely asymptomatic.⁵ An autopsy study of 965 hearts from cadavers evenly distributed in age and sex showed the existence of a PFO in 25% to 30% of the hearts.⁵ The rather high incidence of PFO suggests the need to screen patients for PFO before sclerotherapy given the risks for neurologic sequelae. 

A systematic review examined 69 studies to assess the risks for complications of sclerotherapy in the management of varicose veins. The median rates of pulmonary embolism and deep venous thrombosis were less than 1.0%. Rates for visual disturbances were 1.4%; headaches, 4.2%; thrombophlebitis, 4.7%: skin pigmentation or matting, 17.8%: and pain at injection site, 25.6%.⁶ Figure 3 lists the potential complications of sclerotherapy, most of which are consequences of thrombus or emboli formation. 

The patient in the current case did not meet any contraindications for sclerotherapy on presentation for treatment, and her reported headaches did not meet the clinical criteria for migraine. The undiagnosed PFO created a right-to-left shunt, which allowed microemboli to escape into the left atrium and enter the cerebral vasculature. One study⁶ examined cerebrovascular gas microemboli in 82 patients undergoing foam sclerotherapy. The patients were monitored with transcranial Doppler ultrasonography, and within 15 minutes of the procedure, a right-to-left shunt developed in 61 patients, allowing gas microemboli to flow into the middle cerebral artery.⁷ Knowledge of a PFO would allow proper guidance for patients who are considering sclerotherapy. For patients with a known PFO, liquid sclerotherapy may be the preferred method of treatment because it has fewer complications. 

With the rise in popularity of foam sclerotherapy, it benefits physicians and patients to understand the risks of neurologic sequelae after this procedure. Our patient did not have obvious risk factors for complications of the procedure; however, she had visual and neurologic disturbances shortly after the procedure. It may be beneficial, therefore, to monitor patients for any symptoms before discharge from the medical office. Because neurologic complications are relatively rare, screening all patients for PFO may not be justified; however, a discussion with patients about potential complications may be warranted. Educating patients on stroke signs and symptoms and contraindications such as a PFO as a part of informed consent, for example, should be communicated in case a patient has an undiagnosed PFO or another undiagnosed risk factor that could lead to complications from foam sclerotherapy.