Mechanisms of Visual Dysfunction

Proposed mechanisms of the visual changes include cerebral edema, ^[250] hyponatremia,^[249] glycine toxicity involving the retina and cerebral cortex,^[251] ammonia toxicity,^{[270] [272]} increased IOP as a result of water absorption,^[273] and cranial nerve dysfunction secondary to spinal anesthesia.

Glycine Toxicity

Glycine, the smallest amino acid, enters cells primarily through a carrier-mediated process, but its rate of transport is relatively slow. As long as glycine remains in the extracellular space, it acts as an effective osmole. The glycine solution generally used, which has an osmolarity of 200 mOsm/L, contains 300 mL/L free water, and two thirds of it will enter cells whereas one third enters the extracellular fluid.^[257]

Glycine easily crosses the blood-brain barrier, and it depresses the spontaneous and evoked activity of retinal neurons and hyperpolarizes cells through blockade of chloride channels.^{[274] [275]} The highest glycine concentration is present in the amacrine cells, inner plexiform, and ganglion cell layers of the retina.^[251] When injected into the vitreous in rabbits, glycine has inhibitory action on the ERG, which reverses spontaneously within 24 hours. Similar effects were seen in the ERG of patients with TURP syndrome and glycine toxicity.^[253] Because of a profound effect on oscillatory potentials of the ERG, the predominant site of action may be amacrine cells,^[276] although other inner retinal cells are probably involved as well. Moreover, glycine altered VEPs in dogs and in humans, thus suggesting an effect on the ON as well.^{[277] [278]} The threshold for visual symptoms is a plasma glycine concentration over 4000 µmol/L.^[277] Glycine concentrations do not correlate well with the presence of visual symptoms, which suggests that perhaps its metabolites, such as serine,^[279] play an important role in causing visual changes. A γ-aminobutyric-like antianxiety effect of glycine may account for the inappropriate

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Glycine metabolism may produce ammonia, serine, glucose, proteins, creatinine, hippurate, and glyoxylate. Hyperammonemia with toxicity has been reported to result from glycine absorption during TURP.^{[270] [272]} Ammonia levels are increased in many, but not all patients after glycine administration. Correlation between CNS changes and ammonia levels has been lacking, however. Preexisting liver disease has been suggested as a risk factor for the development of significant hyperammonemia during glycine administration.^[280] Serine, a major metabolite, has inhibitory effects on the retina that are similar to those of glycine.^[281] These metabolites may also play a role, by unknown mechanisms, in visual dysfunction after TURP.^{[255] [279]}

Cerebral Edema

It has been suggested that the hyponatremia/hypo-osmolality occurring during TURP produces occipital cortical edema, but such an association has not been confirmed. Perhaps segmental vascular disease in the blood supply to the occipital cortex placed that portion of the brain more at risk for swelling.^[252]

Hyponatremia

Absorption of irrigant fluid by damaged blood vessels or leakage into the retroperitoneal space is the cause of symptoms from hypo-osmolality and decreased serum sodium.^[282] The osmolal gradient causes water to move into the brain. The amount of CNS dysfunction is related to the rapidity and degree of fall in sodium concentration.^[283] Symptoms include hallucinations, psychosis, seizures, and focal neurologic signs. Hyponatremia and glycine toxicity may occur independently.

Increased Intraocular Pressure

Ocular hypertension causes enlarged blind spots and paracentral scotoma. In the presence of water overload, it seemed logical that an increase in IOP could be involved in TURP syndrome. However, in a prospective study of 22 patients undergoing TURP, Peters and colleagues found no change in IOP in the affected patients. ^[273]

Spinal Anesthesia

TURP is frequently performed under spinal anesthesia. Cranial nerve palsies, particularly of the sixth nerve, have been reported as a complication of spinal anesthesia, theoretically because of a reduction in intracranial pressure from loss of cerebrospinal fluid. These palsies occur several hours after the procedure, along with post-dural puncture headache. However, a cranial nerve dysfunction does not explain complete blindness. In addition, the visual disturbance seen with TURP has occurred after general anesthesia as well, and regional techniques are unlikely to be causative.