Key words: General anesthesia; ocular complications; pupil dilation.
DURING general anesthesia bilateral nonreactive mydriasis is a rare finding. Here we report a case of a 22-yr-old patient who during an orthopedic operation in the prone position revealed marked bilateral dilated pupils that completely recovered normal diameter and reactivity to light a few hours after surgery.
A 22-yr-old American Society of Anesthesiologists (ASA) physical status I woman was admitted to the orthopedic department for elective surgical reduction of a pelvic fracture that had occurred 6 months previously. She had also suffered a fracture of her right wrist, of the T5 vertebral body, and a linear fracture of the right temporal region. After the trauma the patient sustained a brief loss of consciousness and a state of psychomotor agitation that lasted about 24 h. Otherwise her recovery was unremarkable.
On admission, she was not taking any medications. Neurologic examination was normal. Pupils were bilaterally isochoric, isocyclic, and reactive to light. A computed tomography scan showed a 5-mm diameter hypodensity in the right temporal lobe, which was interpreted as a posttraumatic lesion. Electroencephalography was unremarkable.
The patient underwent osteosynthesis of a sacroiliac fracture in the prone position, with her head resting on a horseshoe headrest. General anesthesia was induced with fentanyl, 5 [micro sign]g/kg, thiopental, 3 mg/kg, and isoflurane, 1.8% in oxygen. Intubation was facilitated by administration of vecuronium, 0.08 mg/kg; surgical anesthesia was maintained with isoflurane, 0.5-1%, and 66% nitrous oxide in oxygen, fentanyl, and vecuronium. Routine monitoring included arterial blood pressure via a radial artery catheter, pulse oximetry, electrocardiography, urine output, end tidal CO2, and volatile agent concentration. Surgery lasted approximately 8 h. After anesthesia induction, routine eye examination revealed bilateral nonreactive 2-mm pupils. Arterial blood pressure remained stable around 120/70 mmHg, heart rate (HR) was 70 beats/min, hematocrit was 32%, and neither inotropic or parasympathetic drugs were administered. The patient received 15.000 ml of intravenous fluids (10.000 ml crystalloids, 2.250 ml colloids, 2.700 ml blood), and fluid losses were estimated to be about 4.400 ml (1.900 ml urine, 2.500 ml blood).
Two hours after intubation both eyes were noted to be edematous, and chemosis was seen. Three hours later we observed the pupils to be dilated and showed no reactivity to light. Bilateral instillation of 1% pilocarpine in the conjunctival sacs did not modify pupil diameters.
A wake-up test excluded major neurologic complications; the operation was then completed.
After surgery the prone position was reversed, and the patient was transferred to the intensive care unit (ICU) for routine monitoring. On admission blood pressure (BP) was 170/110 mmHg, HR was 90 beats/min, hematocrit was 30%, temperature was 35.2[degree sign]C, arterial blood gas analysis at a FiO(2) of 0.5 showed a pH of 7.398, PCO(2) of 31 mmHg, and a PO(2) of 243 mmHg. Eye examination revealed eyelid edema and conjunctival chemosis. Both pupils were fixed, and their diameter was 8 mm. The most striking ophthalmoscopic feature was a grayish appearance of the entire retina caused by edema in both eyes. The retinal arteries and veins were dilated, but the optic disc was well outlined and normally pink in color. Fluid restriction and diuretic therapy were started; 2 h after surgery the patient was completely awake, and her trachea was extubated. On arousal she complained only of transient blurred vision and accommodation disturbances. Five hours after extubation, after diuresing 5.200 ml from the time of admission in the ICU, her pupils showed a complete functional recovery, with reduction of eyelid edema and conjunctival chemosis. The next day the patient was discharged from the ICU.
In the past with the administration of diethyl ether or fluroxene during general anesthesia, bilateral, persistent, reversible mydriasis was frequently seen. With drugs like isoflurane or sevoflurane associated with opiates, such a finding is uncommon, which forces us to perform a differential diagnosis to exclude the presence of cerebral mass lesions.
However, persistent pupil dilation can also be found in those with other conditions, such as pheochromocytoma, during the administration of drugs such as adrenergic agonists or ganglioplegics or during "total spinal anesthesia." In addition, many systemic diseases are frequently associated with pupil diameter disturbances: ocular infections such as herpes zoster, orbital tumors, syphilis, and Adie's syndrome. These disorders determine parasympathetic postganglion denervation of the intraocular muscles, revealing consequently disappearance of the light reflex. 
In the case we observed, edema, determined by prolonged prone decubitus, might be the cause of damage to the efferent neurons of the pupillary light reflex. Transient parasympathetic denervation of the sphincter of the pupil could explain: (1) the presence of a medium mydriatic fixed pupil with accommodation disturbances and no response to pilocarpine; and (2) the total recovery of the light reflex and of a normal pupil diameter together with the disappearance of conjunctival chemosis and periorbital tissue edema. The normal visual acuity we observed excluded a deficit of the afferent arch observed by several authors during general anesthesia (improper application of the mask, direct ocular compression in the prone position). [2-4]
In conclusion, we report a case of prolonged, perfectly reversible fixed mydriasis in a patient who underwent osteosynthesis surgery in the prone position after a pelvic fracture. The absence of any reduction of visual acuity together with the complete functional recovery may lead us to consider, in this case, the appearance of nonreactive mydriasis during general anesthesia a sign of a transient postganglionic denervation of the pupillary sphincter occurring in orbital tissue edema, resulting from the prolonged prone decubitus. Procedures directed to prevent orbital edema, such as fluid restriction, diuretic therapy, and maintenance of intravascular colloid osmotic pressure, may have a role in avoiding such a complication.