Publication Exclusive: Infant presents with tearing, discharge from both eyes

A 4-month-old previously healthy full-term infant presented to her pediatrician with tearing and discharge from both eyes. The mother noted this had been present since birth and did not note any associated symptoms. On exam, the pediatrician noted normal development and bilateral tearing. The infant was diagnosed with nasolacrimal duct obstruction. Warm compresses and nasolacrimal massage were recommended.

The patient was sent home; however, a week later she returned to the emergency department with right eye injection and mild edema around the right eye. She was playful on exam and had appropriate intake/output for her age. The emergency department prescribed polymyxin B-trimethoprim eye drops, and the patient was again discharged. A week later, she returned to the emergency department with bilateral ocular discharge and injection in both eyes. Again, she had no change in activity or appetite. She was prescribed erythromycin ointment. She was referred to our clinic for non-resolution of symptoms. The mother noted near complete improvement of symptoms; however, she noted that the right eye “looked smaller than normal.” The patient had no change in activity, appetite, or urination and stool output and had no fevers. Medical history was noncontributory.

Examination

The patient was noted to fix and follow objects in each eye separately. On pupillary examination, pupils were noted to be 1 mm on the right and 2.5 mm on the left in photopic conditions and 3 mm on the right and 6 mm on the left in scotopic conditions. She was also noted to have ptosis on the right, with a marginal reflex distance-1 of 3 mm on the right and 5 mm on the left. Pupils were briskly reactive, and there was no afferent pupillary defect noted. The rest of the anterior segment and posterior segment exam was within Before dilation, the options for testing the etiology of the anisocoria were discussed with the family. Given studies documenting extreme drowsiness, unresponsiveness, bradycardia, hypertension and decreased oxygen saturation in infants, the decision was made to defer Iopidine (apraclonidine, Alcon) testing. Topical cocaine testing was discussed with the mother; however, given the length of time necessary for compounding the agent at our institution, the mother declined testing with topical cocaine. Photographs of the child from 1 month prior were requested but did not show any ptosis or anisocoria at that time.

What is your diagnosis?

Anisocoria, unilateral ptosis

The differential diagnosis of Horner’s syndrome is broad because it can be caused by a disruption anywhere along the oculosympathetic pathway. This includes both congenital and acquired causes. The oculosympathetic pathway originates in the hypothalamus and descends through the midbrain, pons and medulla to the cervical spinal cord where it synapses in the spinal cord. From there, it courses through the stellate ganglion to synapse at the superior cervical ganglion. It then courses along the internal carotid artery through the cavernous sinus to innervate the orbit. An injury or mass at any point along this tract causes damage to the sympathetic nervous system, ultimately resulting in a Horner’s syndrome characterized by unilateral ptosis, miosis and anhidrosis.

Acquired etiologies include carotid injury or dissection, injury to the brachial plexus, stroke, tumor, brainstem injury and apical lung tumors. In a young child, congenital etiologies are most common, most frequently caused by damage to the brachial plexus during delivery. We requested prior photos of the child, and it was noted that the ptosis and anisocoria were indeed present since birth.

Click here to read the full publication exclusive, Grand Rounds at the New England Eye Center, published in Ocular Surgery News U.S. Edition, February 25, 2016.