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Background Nonspecific orbital inflammation (NSOI) is a rare idiopathic ocular pathology characterized by unilateral, painful orbital swelling without identifiable infectious or systemic disorders, which can be complicated by optic nerve compromise. Case Report A 50-year-old man presented to the Emergency Department with recurring, progressive painless left eye swelling, decreased visual acuity, and binocular diplopia in the absence of trauma, infection, or known malignancy. His physical examination was notable for left-sided decreased visual acuity, an afferent pupillary defect, severe left eye proptosis and chemosis, and restricted extraocular movements; his dilatated funduscopic examination was notable for ipsilateral retinal folds within the macula, concerning for a disruption between the sclera and the retina. Ocular examination of the right eye was unremarkable. Laboratory data were unrevealing. Gadolinium-enhanced magnetic resonance imaging showed marked thickening of the left extraocular muscles associated with proptosis, dense inflammatory infiltration of the orbital fat, and characteristics consistent with perineuritis. The patient was diagnosed with NSOI with optic neuritis and admitted for systemic steroid therapy; he was discharged on hospital day 2 after receiving high-dose intravenous (i.v.) methylprednisolone with significant improvement. Why Should an Emergency Physician Be Aware of This? NSOI is a rare and idiopathic ocular emergency, with clinical mimicry resembling a broad spectrum of systemic diseases such as malignancy, autoimmune diseases, endocrine disorders, and infection. Initial work-up for new-onset ocular proptosis should include comprehensive laboratory testing and gadolinium-enhanced magnetic resonance imaging. Timely evaluation by an ophthalmologist is crucial to assess for optic nerve involvement. Signs of optic nerve compromise include decreased visual acuity, afferent pupillary defect, or decreased color saturation. Patients with optic nerve compromise require admission for aggressive anti-inflammatory therapy with i.v. steroids in an attempt to reduce risk of long-term visual sequelae. Our case demonstrates a severe presentation of this disorder and exhibits remarkable visual recovery after 48 h of systemic i.v. steroid treatment.

Background Acute infarctions of the spinal cord are rare events characterized by sudden paralysis or sensory deficits below the level of injury. Etiologies include spinal cord trauma, vascular injury, arterial dissection, thromboembolic disease, chronic inflammatory conditions, or mass effect on the spinal cord. Case Report A 63-year-old male presented to the emergency department with sudden-onset bilateral leg numbness and weakness. His physical examination was notable for decreased light touch and temperature sensation and bilateral lower-extremity paresis. Initial magnetic resonance imaging (MRI) of his spine did not show cord injuries. Computed tomography angiography of his chest, abdomen, and pelvis demonstrated a 7.5-cm non-ruptured infrarenal abdominal aortic aneurysm (AAA) extending into bilateral iliac arteries. The patient was diagnosed with clinical spinal cord infarction secondary to a thromboembolic event from his AAA. A repeat MRI 15 h later showed spinal cord infarction from T8 down to the conus. He received an endovascular aortic repair and was ultimately discharged to rehabilitation with slightly improved lower-extremity strength. Why Should an Emergency Physician Be Aware of This? Atraumatic cord syndrome is exceedingly rare and is associated with dissection or complication of aortic aneurysm repair. There are very few reported cases of thrombotic events leading to ischemic cord syndrome. When presented with a patient with symptoms consistent with cord syndrome in the absence of trauma or mass effect on the spinal cord, providers should work up for vascular etiology.

Background Scopolamine is a potent anticholinergic compound used commonly for the prevention of postoperative nausea and vomiting. Scopolamine can cause atypical anticholinergic syndromes due to its prominent central antimuscarinic effects. Case Report A 47-year-old female presented to the emergency department (ED) 20 h after hospital discharge for a right-knee meniscectomy, with altered mental status (AMS) and dystonic extremity movements that began 12 h after her procedure. Her vital signs were normal and physical examination revealed mydriasis, visual hallucinations, hyperreflexia, and dystonic movements. Laboratory data, lumbar puncture, and computed tomography were unrevealing. The sustained AMS prompted a re-evaluation that revealed urinary overflow with 500 mL of retained urine discovered on ultrasound and a scopolamine patch hidden behind her ear. Her mental status improved shortly after patch removal and physostigmine, with complete resolution after 24 h with discharge diagnosis of scopolamine-induced anticholinergic toxicity. Why Should an Emergency Physician Be Aware of This? Although therapeutically dosed scopolamine transdermal patches rarely cause complications, incomplete toxidromes can be insidiously common in polypharmacy settings. Providers should thoroughly evaluate the skin of intoxicated patients for additional adherent medications that may result in a delay in ED diagnosis and curative therapies. Our case, as well as rare case reports of therapeutic scopolamine-induced anticholinergic toxicity, demonstrates that peripheral anticholinergic effects, such as tachycardia, dry mucous membranes, and hyperpyrexia are often not present, and incremental doses of physostigmine may be required to reverse scopolamine's long duration of action. This further complicates identification of the anticholinergic toxidrome and diagnosis.