INTRODUCTION: Stroke following sclerotherapy appears to be a rare complication–only two case reports have been published [1,2]. This report describes a well documented case of ischemic stroke following sclerotherapy for esophageal varices. Clinicians should be aware of this possibility when evaluating patients with neurologic disturbances after sclerotherapy.
CASE PRESENTATION: A 50-year old man with alcoholic and Hepatitis C cirrhosis was transferred to our medical center because of recurrent esophageal variceal bleeding. Over the preceding month, he had three episodes of variceal bleeding—controlled each time by endoscopic placement of esophageal variceal bands. On the day of transfer to our hospital, he presented to his local emergency department with a fourth episode of hematemesis. He was intubated for airway protection. A subclavian central venous catheter was placed uneventfully. He was resuscitated with blood products and crystalloid. Emergent endoscopy revealed bleeding grade IV esophageal varices. Because of his recent banding procedures, the gastroenterologist performed intralesional sclerotherapy with sodium morrhuate to hemostatic effect. The patient was then transferred to our hospital for consideration of transvenous intrahepatic portocaval shunt. Upon arrival at our hospital, the patient was hemodynamically stable. He had abdominal distention and dull percussion suggesting abdominal ascites. Initial neurologic exam was non-focal. Arterial blood gas on FiO2 1.0 was: pH 7.33, PaCO2 39, and PaO2 255. A chest radiograph showed clear lungs. Repeat endoscopy showed adherent clot, prior banding, sclerotherapy injection sites, and portal gastropathy without acute bleeding. No interventions were performed. The following day, the patient was observed to have no spontaneous movement of his left side. Motor responses of his left arm and leg were absent. Noncontrast head CT revealed a right hemispheric infarct involving both anterior cerebral artery and middle cerebral artery territories. MRI confirmed several acute infarcts in different vascular distributions, suggesting an embolic etiology. Transcranial doppler ultrasound (TCD) of the cerebral vessels showed hyperdynamic flow, and intravenous injection of agitated saline showed multiple bubbles in the middle cerebral arteries. Doppler ultrasound of his internal carotid arteries and lower extremities were unremarkable. Transthoracic echocardiogram with agitated saline contrast failed to demonstrate an intracardiac shunt. After aggressive rehabilitation, the patient was discharged home but continues to have residual left-sided weakness.
DISCUSSIONS: Neurologic complications following sclerotherapy are rare, but at least two cases of stroke following sclerotherapy have been reported. Both of those patients received injections with polydocanol. Our patient suffered a stroke within 36 hours of sclerotherapy with sodium morrhuate. The presence of cerebrovascular bubbles on the agitated saline portion of his TCD suggests he had an anatomic shunt that permitted paradoxical emboli. The fact that no intracardiac shunt could be identified suggests he may have anatomic intrapulmonary shunts, possibly due to type II hepatopulmonary syndrome. This possibility is further supported by the large alveolar arterial oxygen difference while FiO2 was 1.0.
CONCLUSION: This report describes a well-documented case of stroke following sclerotherapy. Thorough evaluation failed to identify another potential cause of stroke, and both vascular imaging and blood gas data suggested he had anatomic intrapulmonary shunt allowing paradoxical embolization of either sclerosant material, sclerosant-induced thrombus, or sclerotherapy-associated intravariceal air. Although rare, this complication can be devastating. Some authors have suggested pre-sclerotherapy screening for intracardiac shunts to identify at-risk patients , but in an emergent situation this may not be feasible. Stroke should be considered in patients with neurologic disturbances following sclerotherapy. Optimal ways to screen for patients at risk and to prevent this complication remain unknown.
DISCLOSURE: Carrie Chun, None.