LAUSR

A 71-year-old woman developed dyspnea, tachycardia, and hypoxia 4 days after an open reduction and internal fixation of an ankle fracture. Contrast-enhanced chest computed tomography (CT) showed bilateral pulmonary emboli (PE). Transthoracic echocardiogram demonstrated severe right ventricular dysfunction and pulmonary hypertension. Laboratory evaluation demonstrated a markedly elevated cardiac troponin. She subsequently underwent ultrasound-facilitated, catheter-based, lowdose fibrinolysis via the right internal jugular vein. Approximately 18 hours after sheath removal, the patient was noted to have anisocoria, with her left pupil 6 mm in diameter and her right pupil 4 mm (Panels A and B). Both pupils were briskly reactive to light without afferent pupillary defect. The remainder of the neurologic exam was normal and no ptosis was noted. The patient had no history of physiologic anisocoria. One drop of 0.5% apraclonidine was administered to each eye, resulting in dilation of the right pupil and slight constriction of the left pupil 30 minutes later, and confirmed the diagnosis of Horner’s syndrome. To investigate the cause of the Horner’s syndrome, CT angiography of the neck was completed. Imaging demonstrated fat stranding circumferentially around the right internal jugular vein with extension to the posterolateral margin of the common carotid artery (arrows in Panels C and D). Sympathetic fibers from the hypothalamus synapse at C8–T2, then exiting the spinal cord to pass superior to the lung apices and ascend through the cervical sympathetic chain in the neck which lies outside the carotid sheath behind the common carotid artery, ultimately innervating the levator palpebrae superioris and dilator pupillae muscles. The exam findings suggested a right Horner’s syndrome due to trauma associated with catheter placement or removal. A Horner pupil lacks sympathetic innervation, leading to supersensitivity of the alpha-1 receptor and thus resulting in pupillary dilatation with administration of apraclonidine, which is a weak alpha-1 and strong alpha-2 agonist. In the normal eye, the stronger alpha-2 stimulation by apraclonidine causes the pupil to constrict slightly. Previous studies suggest the incidence of traumatic Horner’s syndrome after central venous catheter placement ranges from 0.2% to 5%.1 The mechanism of traumatic Horner’s syndrome most commonly occurs due to hematoma formation or direct needle trauma. Risk of traumatic Horner’s increases when turning the head to the left more than 40 A case of Horner’s syndrome after catheter-based fibrinolysis for pulmonary embolism