Effect of gestational age and birth weight on the risk of strabismus among premature infants.

IMPORTANCE: Strabismus causes irreversible vision loss if not detected and treated early. It is unclear whether birth weight (BW) and gestational age (GA) are risk factors for strabismus. OBJECTIVE: To estimate the effect of BW and GA on the likelihood of premature infants developing strabismus. DESIGN, SETTING, AND PARTICIPANTS: In this longitudinal cohort analysis, we monitored a group of premature children from birth to determine the proportion that developed strabismus and the timing of the first strabismus diagnosis. Multivariable Cox regression analyses assessed the relationships of BW and GA with the development of strabismus. Regression models were adjusted for other risk factors for strabismus, sociodemographic factors, and ocular comorbidities. The analysis included 38,055 otherwise healthy children born prematurely who were enrolled for more than 6 months in a nationwide US managed care network between 2001 and 2011 in communities throughout the United States. EXPOSURES: Birth weight less than 2000 g or GA of 32 weeks or less. MAIN OUTCOMES AND MEASURES: Hazard ratios (HRs) for strabismus with 95% CIs. RESULTS: Of 38,055 otherwise healthy children who were born prematurely, 583 received a diagnosis of strabismus later in life. The cumulative incidence of strabismus was 3.0% at 5 years. Controlling for GA and other covariates, infants born with BW less than 2000 g had a 61% increased hazard (HR, 1.61; 95% CI, 1.22-2.13) of developing strabismus. Controlling for BW and other covariates, there was no significant association between strabismus and GA (HR, 0.98; 95% CI, 0.69-1.38). Among premature infants with BW of less than 2000 g, a GA of 32 weeks or less conveyed no additional increased risk for developing strabismus relative to infants born after 32 weeks (HR, 1.27; 95% CI, 0.86-1.88). In contrast, among infants with a GA of 32 weeks or less, BW of less than 2000 g conveyed a 14-fold increase in the risk of strabismus relative to BW of 2000 g or more (HR, 14.39; 95% CI, 1.99-104.14). CONCLUSIONS AND RELEVANCE: Independent of GA, very low BW conferred a large increase in strabismus risk among premature infants. In contrast, independent of BW, GA did not significantly affect the risk of strabismus. Updates to existing guidelines in the pediatric and ophthalmic literature should be considered, highlighting the importance of BW rather than GA and alerting clinicians about the need for careful monitoring of premature infants with low BW for strabismus.

Cerebrospinal fluid leak presenting as oculorrhea after blunt orbitocranial trauma.

Cerebrospinal fluid (CSF) leak is an uncommon but well-documented occurrence after blunt head trauma, typically manifesting as otorrhea or rhinorrhea. Blunt cranio-orbital trauma also may cause CSF leak into the orbit, manifesting as orbitocele, blepharocele, chemosis, or tearing ("oculorrhea"). We report a patient who developed oculorrhea after blunt head trauma, and neuroimaging disclosed comminuted fractures of the left frontal, greater sphenoid wing, nasal, and maxillary bones. Because he also displayed chemosis and markedly reduced ocular ductions and periocular pain, carotid-cavernous fistula was suspected but appropriate vascular imaging was negative. Aspiration of subconjunctival fluid was positive for beta-2 transferrin, a specific marker for CSF. Chemosis lessened and the oculorrhea ceased spontaneously within 6 days of the trauma. This manifestation of CSF leak must not be overlooked because of the threat of meningitis.

Relapsing dorsal midbrain syndrome following interventions for hydrocephalus in aqueductal stenosis.

Dorsal midbrain syndrome (DMS) is a recognized clinical manifestation of increased intracranial pressure (ICP) associated with ventricular enlargement, especially in shunt malfunction, but the mechanism by which DMS occurs in this setting is unsettled. We report a patient with triventriculomegaly attributed to aqueductal narrowing by a tectal mass who went through 2 cycles of developing and resolving DMS promptly after undergoing interventions that altered the size of the posterior third ventricle and proximal aqueduct but probably did not markedly alter ICP. This case provides additional evidence that DMS in this setting is caused by deformation of the dorsal midbrain region produced by rapid expansion of the posterior third ventricle or proximal aqueduct.