The oculocardiac reflex during strabismus surgery: its relationship to preoperative clinical eye findings and subsequent postoperative emesis.

PURPOSE: To compare the occurrence of significant bradycardia due to the oculocardiac reflex (OCR) during strabismus surgery and its relationship to preoperative clinical eye findings and subsequent development of postoperative emesis. METHODS: The medical records of consecutive patients who underwent strabismus surgery August 2006 to June 2009 were retrospectively reviewed. OCR was defined as presence of dysrhythmia or a sudden heart rate decrease ≥ 20% after traction on the extraocular muscle. OCR incidence was compared between the first, second, and third (if any) extraocular muscles in patients who had multiple-muscle strabismus surgery and also between specific muscles (eg, medial rectus vs lateral rectus muscle). Associations with OCR were compared for different strabismus types. Vomiting was considered postoperative if it occurred before discharge of the patient at noon on the day following surgery. Risk factors for OCR and postoperative vomiting were evaluated by logistic regression analysis. RESULTS: A total of 111 records were reviewed; 41 patients (37%) experienced OCR. Incidence of OCR and absence of OCR during traction of the first muscle were significantly associated with events during traction of the second (χ(2) = 36.681, P < 0.001) and third muscles (Fisher exact test, P = 0.030). The best predictors of OCR were the absence of fine stereopsis and a larger number of surgically treated muscles. Of the 111 patients, 30 (27%) who had postoperative vomiting, the best predictors were female sex and young age. CONCLUSIONS: In our cohort, patients experiencing intraoperative OCR when the first extraocular muscle was manipulated during multiple-muscle strabismus surgery were likely to experience it again during traction of additional muscles. More severe postoperative vomiting was common in these patients. OCR was associated with the preoperative absence of fine stereopsis.

Neuroprotective effects of recombinant human granulocyte colony-stimulating factor (G-CSF) in neurodegeneration after optic nerve crush in rats.

The purpose of the present study was to investigate the effects of granulocyte colony-stimulating factor (G-CSF) on neurodegeneration of optic nerve (ON) and retinal ganglion cells (RGCs) in a rat model of ON crush. The ONs of adult male Wistar rats (150-180 g) were crushed by a standardized method. The control eyes received a sham operation. G-CSF (100 microg/kg/day in 0.2 ml phosphate-buffered saline) or phosphate-buffered saline (PBS control) was immediately administered after ON crush for 5 days by subcutaneous injection. Rats were euthanized at 1 or 2 weeks after the crush injury. RGC density was counted by retrograde labeling with FluoroGold application to the superior colliculus, and visual function was assessed by flash visual evoked potentials (FVEP). TUNEL assay, Western blot analysis and immunohistochemistry of p-AKT in the retina and ED1 (marker of macrophage/microglia) in the ON were conducted. 2 weeks after the insult, the RGC densities in the central and mid-peripheral retinas in ON-crushed, G-CSF-treated rats were significantly higher than that of the corresponding ON-crushed, PBS-treated rats (survival rate was 60% vs. 19.6% in the central retina; 46.5% vs. 23.9% in mid-peripheral retina, respectively; p<0.001). FVEP measurements showed a significantly better preserved latency of the p1 wave in the ON-crushed, G-CSF-treated rats than the ON-crushed, PBS-treated rats (78+/-9 ms in the sham operation group, 98+/-16 ms in the G-CSF-treated group, and 174+/-16 ms in the PBS-treated group; p<0.001). TUNEL assays showed fewer apoptotic cells in the retinal sections in the ON-crushed, G-CSF-treated rats. p-AKT immunoreactivity was up-regulated in the retinas of the ON-crushed, G-CSF-treated rats at 1 and 2 weeks. In addition, the number of ED1-positive cells was attenuated at the lesion site of the optic nerve in the ON-crushed, G-CSF-treated group. From these results, we gather that administration of G-CSF is neuroprotective in the rat model of optic nerve crush, as demonstrated both structurally by RGC density and functionally by FVEP. G-CSF may work by being anti-apoptotic involving the p-AKT signaling pathway as well as by attenuation of the inflammatory responses at the injury site, as evidenced by less ED1-positive cell infiltration in the optic nerve.