Journal of Neuro-Ophthalmology, March 1994, Volume 14, Issue 1

Temporary blindness in the TUR syndrome.

The TUR syndrome is a clinical disorder consisting of circulatory, gastrointestinal, and neurologic signs that are infrequently seen in some patients undergoing endoscopic surgery of the prostate gland with the use of nonconductive irrigating fluids. Several theories of its pathogenesis have been proposed. The condition may occasionally be associated with bilateral profound loss of vision. We report a patient with the TUR syndrome who suffered bilateral temporary blindness and speculate on the etiology of the visual loss and localization of the dysfunction along the visual pathway.

Journal of Ncuro- Ophthalmology 14( 1): 6- 8, 1994. © 1994 Raven Press, Ltd., New York Temporary Blindness in the TUR Syndrome John P. Barletta, M. D., Maher M. Fanous, M. D., and Latif M. Hamed, M. D. The TUR syndrome is a clinical disorder consisting of circulatory, gastrointestinal, and neurologic signs that are infrequently seen in some patients undergoing en­doscopic surgery of the prostate gland with the use of nonconductive irrigating fluids. Several theories of its pathogenesis have been proposed. The condition may occasionally be associated with bilateral profound loss of vision. We report a patient with the TUR syndrome who suffered bilateral temporary blindness and speculate on the etiology of the visual loss and localization of the dysfunction along the visual pathway. Key Words: Transurethral resection of prostate- Endoscopic fluid absorption- Hyperammonemia- glycine toxicity. The TUR syndrome refers to a constellation of symptoms and signs that can develop during transurethral resection of the prostate. It is charac­terized by irritability, confusion, bradycardia, nau­sea, hypertension, dyspnea, convulsions, and blindness ( 1- 4). It is speculated to be due to exces­sive absorption of the nonelectrolyte irrigating fluid through the prostatic venous sinuses into the general circulation ( 2- 4). The resulting metabolic disturbance includes a dilutional hyponatremia, hyperglycinemia, and subsequent hyperammone­mia ( 2,5- 8). Visual disturbances such as blurred vision or temporary blindness have occasionally been re­ported as a consequence of the TUR reaction ( 1, 9- 12). We describe a patient undergoing transure­thral resection of the prostate who experienced blindness as the first presenting manifestation of the TUR syndrome. From the Department of Ophthalmology, University of Flor­ida College of Medicine, Gainesville, Florida, U. S. A. This work was supported in part by an unrestricted depart­mental grant from Research to Prevent Blindness, Inc., New York, New York. Address correspondence and reprint requests to Dr. Latif M. Hamed, Department of Ophthalmology, University of Florida College of Medicine, P. O. Box 100284, JHMHC, Gainesville, FL 32610- 0284, U. S. A. CASE PRESENTATION A 61- year- old man underwent transurethral re­section of the prostate under spinal anesthesia. Ir­rigating fluid was 1.5% glycine. At 45 minutes into the operation the patient experienced sudden blindness, acute nausea and vomiting, altered mental status, and, shortly thereafter, seizure ac­tivity. Stat laboratory studies revealed the serum sodium concentration to have dropped precipi­tously from 138 mEq/ L to 120 mEq/ L ( normal: 135- 145 mEq/ L) and the serum ammonia was 708 | xmol/ L ( normal: 11- 35 ixmol/ L). The patient was started on 3% normal saline and furosemide, and the procedure was terminated. An electrocardiogram showed normal sinus rhythm. The patient responded favorably, becom­ing oriented but lethargic within 1 hour. Ophthal­mologic examination displayed no light perception vision OU, with sluggish but reactive pupils and no relative afferent pupillary defects. The fundus TEMPORARY BLINDNESS IN TUR SYNDROME 7 examination was normal as was the neurologic ex­amination. Computed tomography of the brain was normal. Therapy with intravenous pyridoxine and L- argi-nine HC1 was begun for treatment of the hyper­ammonemia. Four hours later, the ammonia level dropped to 456 u- mol/ L and the visual acuity grad­ually improved to 20/ 800 in each eye over the same time period. The ocular examination was other­wise unchanged. The patient's vision continued to improve over the next 12 hours, returning to nor­mal in 24 hours. DISCUSSION The TUR reaction was first described in 1947 ( 3) as a complication of transurethral resection of the prostate characterized by severe neurologic, circu­latory, and gastrointestinal disturbances. Death may occasionally result. Visual loss has been de­scribed as one of the earliest, and, rarely, the sole symptom of the TUR reaction ( 1,9,11). The exact etiology of the visual loss remains unclear, but has been generally attributed to the rapid absorption of large amounts of irrigating fluid into the systemic circulation, inducing metabolic disturbances. The choice of irrigating fluid during endoscopic surgery has evolved since the late 1920s. Many of the severe complications derived from the earlier use of hypotonic irrigants were eliminated with the introduction of isotonic glycine solution. How­ever, with excessive absorption of the glycine so­lution, acute hyponatremia still occasionally oc­curs. Blindness was first described when glycine was used as an irrigating solution ( 4). Historically, the most widely accepted hypothe­sis regarding the development of vision loss in­criminated the dilutional hypervolemia with hy­ponatremia that develops as a consequence of a rapid fluid absorption through open venous si­nuses during prostatectomy. It has been postu­lated that changes in serum sodium levels may produce alterations in the central nervous system function as a result of cerebral edema. Involve­ment of the occipital cortex would cause vision loss ( 2). Although hyponatremia develops, serum os­molality remains near normal ( 6,13,14). In a study of 72 patients, 19% of whom had marked diminu­tion in serum sodium, only two had reduced se­rum osmolality ( 5). Thus hyponatremia has been thought to be an unlikely etiology of the transient visual loss. Another possible cause of vision loss may be am­monia, which becomes elevated by oxidative deamination of glycine in the liver. Hyperam­monemia in hepatic encephalopathy is well-known, but the mechanism for central nervous system ( CNS) depression is unknown. A partial deficiency of the urea cycle enzyme, arginosucci-nate synthetase, has been postulated in patients with hyperammonemia ( 8). Infusion of L- arginine prevents the rise in blood ammonia in patients re­ceiving intravenous glycine ( 17). Serum ammonia levels have been described as the most accurate marker for delayed awakening from general anes­thesia ( 7). Ryder reported two patients whose re­covery from coma after TUR more closely followed a drop in ammonia level than a rise in serum so­dium ( 8). In four patients with TUR syndrome who showed elevated glycine and abnormal elec-troretinograms, two had normal ammonia levels, rendering it unlikely that hyperammonemia plays a significant role in the vision loss ( 15). Another putative etiology for the transient blindness is hyperglycinemia and direct glycine toxicity. Glycine, a nonessential amino acid, is a known inhibitory neurotransmitter that readily crosses the blood- brain barrier. It causes mem­brane hyperpolarization with a concomitant fall in membrane resistance and increase in chloride per­meability. Light has been shown to evoke the re­lease of glycine from cat and rabbit retinas, which in turn has an inhibitory effect on the electroretin-ogram and visual evoked potential in rabbits ( 19). Because high serum levels of glycine and vision loss have been shown to coexist in affected pa­tients, glycine may be the cause due to its inhibi­tory action in the retina and/ or the CNS. Further­more, an association between the normalization of serum glycine levels and visual recovery have been demonstrated in some patients with the TUR syn­drome who suffered visual loss ( 12). In support of the theory of glycine toxicity to the retina ( as op­posed to a generalized toxic effect on the CNS), Burkhart and colleagues ( 16) described a case of transient visual blindness during arthroscopy, us­ing 1.5% glycine as the irrigating solution. The pa­tient had no other symptoms and a normal sen-sorium. In a study of 17 patients who underwent transurethral resection of the prostate, four pa­tients described visual disturbances coincident with elevated serum glycine and decreased serum sodium levels. Electroretinograms consistently demonstrated complete loss of the oscillatory po­tentials on the ascending limb of the b- wave and abolition of the 30- Hz flicker response ( 15). Hy­ponatremia does not appear to be a confounding factor in the etiology as sodium has little effect on retinal physiologic functions in contrast to glycine ( 18). / Neuro- Ophthalmol, Vol. 14, No. 1, 1994 /. P. BARLETTA ET AL. Year 1956 1975 1979 1982 1984 1985 1990 Present TABLE" Reference Harrison et al. ( 4) Defalque et al. ( 11) Appelt et al. ( 9) Ovassapian et al. ( 12) Kaiser et al. ( 10) Gillett et al. ( 1) Burkhart et al. ( 16) case I. Visual examination and Va NLP LP NLP LP LP LP LP LP LP NLP NLP NLP NLP NLP [ Sod [ Nm ium m Eq/ L] 11 135- 145] 111 110 107 106 114 115 121 107 111 125 116 118 N. A. 120 ' laboratory values in [ Glycine [ Nml 13 N. A. N. A. N. A. N. A. N. A. N. A. N. A. N. A. 1,029 1,374 N. A. N. A. N. A. N. A. [ NH3 = Nml 11- 708 - 35 ( mg/ L] - 17] Ixmol/ L] xrnol/ L the TUR syndrome Pupils N. A. Normal N. A. Normal Nonreact N. A. N. A. N. A. N. A. Nonreact N. A. N. A. Sluggish Sluggish Systemic Yes None Yes None None None Yes None Yes None None None None Yes Recovery time N. A. 4 h Several hours Several hours 48 h 24 h 8 h 12 h 24 h 24 h 12 h 12 h 30 min 12 h N. A., not available; Nml, normal. The site of dysfunction along the visual path­ways that is responsible for the visual loss remains elusive. The loss of vision has been commonly at­tributed to cortical edema, but the clinical cases reported to date do not support a cortical localiza­tion of the vision loss in all cases. While the pres­ence of normal pupillary light reflexes in some pa­tients with severe vision loss would support a cor­tical localization, other cases with sluggish or nonreactive pupils would suggest an anterior pathway disturbance ( Table 1). Documentation of the pupillary response and the presence or ab­sence of associated neurologic disease in future cases may help delineate the exact localization of the dysfunction along the visual pathway. On the basis of available evidence, glycine toxicity appears to correlate best with the clinical picture. REFERENCES 1. Gillett W, Grossman HB, Lee R. Visual disturbances in TUR reaction. Urology 1985; 25: 573- 1. 2. Henderson DJ, Middleton RG. 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