| OCR Text |
Show Optic Atrophy Following Jejunoileal Bypass JEFFREY R. HAAG, f\1.D. J LAWTON SMITH, M.D. JOHN O. SUSAC. M.D. SANDRA FRAZIER BYRNE Abstract A 38-year-old woman presented with a bilateral, chronic, progressive optic neuropathy following jejunoileal bypass surgery for morbid obesity. Standardized A-scan orbital echography revealed grossly swollen optic nerve sheaths with a positive 30° test, indicating increased subarachnoid fluid. Review of reported complications of jejunoileal bypass surgery revealed no similar case of what might be termed the "optic nerve ascites syndrome." Introduction Complications are common following jejunoileal bypass surgery. J 0 However, ocular involvement has been reported in only six cases. IO - 14 In this report. we describe a patient who developed a bilateraL chronic. progressive optic neuropathy following jejunoileal bypass for morbid obesity. Case Report A 38-year-old, right-handed white female was first seen on November 14, 1983, with a chief complaint of loss of peripheral visual field in both eves for 8 Years. . On August 13, 1973, the patient underwent a jeJunoileal bypass for morbid obesity. Before the operation, she weighed 287 Ibs. and had hypertension and diabetes mellitus. Within 9 months following surgery, the hypertension and diabetes resolved, she lost approximately 100 Ibs., and her weight stabilized at 190 lbs. One year after the operation, transient blurring of the central vision in both eyes occurred, but cleared within 1 day after a Lasix injection. She noted no further visual difficulties until From the t'uru-uphthalmologl' ",·rvin·. B,hCl'm Palme'. h": Institute, D,'partment llf Ophthalmology, UniVl'r~ilv ot M,ami School of Medicint'. Miami. Florid,l. March 1985 1976, when she began to stumble over objects in her lower visual field. Corrected visual acuity was 20/20 in both eyes at that time, but the question uf optic disc pallor was raised. As a result, she was hospitalized in June 1976, and blood tests, brain scan, skull films, and a right transfemoral arteriogram were normal. Over the ensuing years, a steady, painless, essentially symmetrical progressive loss of visual field in both eyes occurred, but central visual acuity remained remarkably spared. On follow-up examination in 1978 and 1980, although visual acuity remained excellent, optic atrophy was described. Although she noted no problem with dark adaptation, a modest impairment in her ability to distinguish colors became evident. By August 1983, the visual field was compromised even further, prompting a CT scan and lumbar puncture, which were normal. A "borderline" reactive serum FTA-ABS test was obtained on four occasions, although serum VORL was nonreactive. The patient was then referred to the Bascom Palmer Eye Institute. Dietary history revealed a more than adequate caloric intake with six feedings per day. She experienced seven to ten watery, foul-smelling stools daily. In addition, bouts of diarrhea occurred about once a month and lasted for 2-1 hours, during which time she might have up to 15 stools per day. She \Vas not on medication or on vitamin replacement therapy. Past history revealed that she had hepatitis at age 7 and infectious mononucleosis in 1967. HepattlOlt'galy \V,15 noted in 1977, and a liver biopsy on October 5, 1977, demonstrated moderate fatty mL'tanHlrphosis. F,lmily history was noncontributory. On examination, November 14, 1983, the corfected visual acuity was 20/20 +4 and 11 in the right eye and 20/15 and 11 in the left eye. She missed seven of 15 color plates with both eyes. Slight dermatochalasis and a few whitish-gray lashes were noted on the upper lids of both eyes. Ocular motility was intact, the pupils were equal 9 T •• , ob)ec" Y" OP __-~.~)l_l_J__ LE. VISUAL FIELDS (Perlpharal,) C DLr I) ___l:!\~<..l~v~e;.!!mb~e:!r--ll.:!.4~,~1:z.928Jl_.3 _Date Te H ob j to t L. _ I~ OD~ _ Figure 1. Visual field examination showing that field defects bru\...e <..lut of the blind spot in size and reacted crisply tulight, and nu afferent pupillary defect was present. Krahn exophthalmometry measured 23 mm in the right eye and 22 mm in the left eye at base 100. Blulld pressure 10 was 130/75, right arm, sitting. Visual field examination demonstrated a rather symmetrical concentric contraction of the fields in both eyes, but with a definite lower altitudinal component. Journal of Clinical Neuro-ophthalmology Iiaag, Smith, Susac, Byrne Figure 3. CT sc~n "I the br~in ~nd orbits, December 19R3. ott' enlargenwnt ,'f ri~ht "rl" n,'f"". On tangent screen examination, it was apparent that the field defects broke out of the blind spot (Figs. 1 and 2). Slit lamp biomicroscopy of the anterior segments was normal. No vitreous cells "'ere seen. Applanation tensions were 13 mm Hg in the right eye and 14 mm Hg in the left eye. Dilated fundus examination revealed bilateral optic atrophy. Both discs were diffusely pale with small cups. The remainder of the fundus was nl)rmal. Laboratorv studies revealed a normal ERG, serum vitamin B1: level of 409 pg/ml (11 1801,000), and serum vitamin A of 74 J.Lg/ml (11 3095), although a quantitative serum carotene level was definitely low at 20 J.Lg/ml (n 70-250). Serum \,'as sent to Dr. Collarl's laboratory in Paris, France, for TPI, FTA-ABS, TPHA, and VORL, all of which were nonreactive. Serum and urine studies for trace metals including zinc, copper, and manganese were normal. The patient was started on a Theragran-M tablet, three times/day, and 1 cc of hydroxy-cobalamin intramuscularly/ week for 10 weeks. A CT scan of the brain and orbits was made in December 1983. The orbital portion of the right optic nerve was definitely enlarged, and the question was raised as to whether the left optic nerve might not also be larger than normal (Figs. 3 and 4). Follow-up visit on January 12, 1984, found the visual acuity and fields unchanged. Standardized A-scan orbital echography revealed that both optic nerves were diffusely enlarged, with a positive 30° test, indicating increased subarachnoid fluid (Fig. 5, Table 1). A left optic nerve sheath decompression was performed on January 13, 1984. March 1985 On the first postoperative day, visual acuity was 20/20 +4, and the visual field was slightly larger to the 10/330 white isopter. A definite spontaneous venous pulse was present in the left eye. A spontaneous venous pulse was not present in the right eye. At follow-up 5 weeks later, she reported improvement in the left eye following surgery until 2 weeks prior to her visit. At that time, she noted a loss of clarity and believed the field became somewhat constricted again. On February 21, 1984, visual acuity was 20/20 in both eyes. However, the visual field in the left eye was slightly more constricted than on the first day after surgery. No spontaneous venous pulse was seen in the right eye as before. The left eye, on careful observation, at times appeared to have a spontaneous venous pulse and at other times did not. A repeat ultrasound examination 5 weeks after surgery showed essentially no change in the left optic nerve (Table 1). It was suspected that the window in the left optic nerve sheath had closed off 2 weeks earlier when the visual function had subjectively worsened. Optic nerve sheath decompression on the right eye was therefore postponed in order to evaluate further the outcome of surgery on the left eye. In the meantime, she was advised to continue vitamin replacement therapy, and reported no subjective change in visual function by June 1984. Discussion Morbid obesity may be defined as a condition in which body weight is maintained at more than twice the ideal for at least 5 years, despite per- 11 kjul1llill'al Bypass Figure 4. CT scan taken at the same time It appeafed that the left optic nefve mi!\hl also be enl.nged. 1l0N I , , \ "\ I'.r:.ll II ~ (I~ II II L '\~ ,'I , 'i 1, . ,I~ Figure 5. St,lndMd'/l'd A-",lI1 llfb.t,ll l'(hllp,lphl' IIld'(,ltlll~ l·nl.H~l'nll'nt l,f bl,th l'ptiC ner\'es, with incfeased ,ub.u,lChntl,d flUid sistent weight reduction efforts.' Affected individuals Me predispllsed to ,1 number eli serillUS illnessl's including hypertension, insulin-resistant diabetes mellitus, cardiovascular and (l'rebnlVas- 12 CUlM disease, pulmonary insufficiency, gallbladder disease, and osteoarthritis, all of which contribute to a reduced life expectancy, ~ Nonsurgical treatment approaches to this seri- Journal of Clinical Neuro-ophthalmology Haag, Smith, Susac, Byrne till' p,lssage of time. However, in a review of 100 p,ltients followed carefully after jejunoileal byp, bS, 5R~!;, had more than three stools per day, 5 yeMs after surgery." Chronic diarrhea to the extent of seven to ll'n stuols per day, as our patient has experienced, most certainly predisposes to electrolyte imbalance and malabsurption uf vitamins, minerals, and uther nutrients which may be essential for normal uptic nerve function. Approximately 5'1,1 of ;ejunuileal bypass patients develup some degree uf liver failure postoperatively, and 0.5-2% die frum liver failure or cirrhosis, 5-24 munths after surgery' Indeed, the must commun reason for reanastomosis of the buwel is liver failure. I' Liver biopsy demonstrates fatty metamorphosis in 65-9/3% uf obese patients even before jejunoileal bypass. lh The cause uf this is believed to be relative protein insufficiency, which may be aggravated by further reduction in protein intake following jejunoileal bypass. Fortunately, our patient demonstrated only moderate fatty metamorphosis on liver biopsy in 1977, and has shown no evidence of progressive liver involvement. Liver disease may have been the cause of her falsely positive serum FTA-ABS test. Arthritis has been reported in 6-30% of patients17 It tends to be transient, migratory, and asymmetric, involving both large and small joints. Joint effusions are uncommon, and generally there is no joint deformity. Serologic tests are repeatedly negative; however, the erythrocyte sedimentation rate may be elevated during exacerbation. It has been likened to the arthritis associated with inflammatory bowel disease.; Some patients have developed a skin rash associated with arthritis, and erythema nodosum has been described' 7 Affected pa tien ts often respond well to nonsteroidal anti-inflammatory agents, as our patient did. Our patient was treated with Motrin, which has itself been reported to cause optic neuritis. Is However, the onset of her uptic neuropath\' antedated treatment with Mlltrin, and sht> tllllk this medicine for only a brief peril1d llf time 1 year prior to presentation. Therefure, Motrin can be excluded as an etiologic agent in our patient. Pertinent to the case under discussion is the fact that optic nt>rvt> involvement has been reported in inflammatory bowel diseast>. Knox rt>counts two patients with Crohn's dist>ase who presenll'd with visual loss and optic disc swelling that respunded tu systemic prednisune, and one patient with ulcerative colitis whu had severe bilateral papillitis which improved only after colectumy.'" He alsu states that papilledema has been present in two patients with Whipple's disease. Sedwick et al. e" have recently reported five cases uf optic neuritis occurring in patients with inflammatory bowel disease. h_~ .I" h.J 37 100"" 3[1"; 17_·U::f'~ ,,-JOr ; 5-20r ;, 1O-15 r " lOr" 5r ; 2-1l1 r , I\I~hl Il'Il l )plll" Nl'l"\'l' l lplll Nl'l\ t' ['I.lerl",.l E!<',tr,'kte ImbJI,m,c' ()~h..·l'n,.\I.ll.'-l.l .\rlhr,II~I,1 L nn,H\ ',lkuh Ch,'Il'inhIJ'" Inlt>,tlnJI prc'blem,; LI\ er fJIIure \!,'rlJht\· Bt'lc'fl' It'll c'ptlC' l1l'rlc' ,hc',11h de l"\,.)nlF'rl·~:'olll" :\nh.'fl\\r dl.lI11l'tl'r. IHIn Jl)...... t\':,,-I I\l~tl'rhlr I..h.1I1h.'kr. In III 3[10 lc',t Fi\ l' wl...~ .lttl'r It-ft IlFltll "en'l' :'ohl'.lth lhll-llnlprl'~~h'll :\nll'fl\.'[ l..il.l111c..'ICf nun Jl' ...... h.·.... t I\l~krh'r dl.lIlll'tl'f n"n Jl) ...., k;-.t ous health problem are generally ineffective, The success rate is estimated to be less than 5%.' As a result. attempts to reduce weight by surgical means were first introduced in the 1950s. By the late 19605, the jejunoileal bypass became established as an effective treatment for morbid obesitv, resulting in a stable weight reduction of 25 ·fO'C( in most patients. 4 ; Since the jejunoileal bypass was introduced, many thousands of patients have submitted to this procedure, and numerous reports of postoperative complications have appeared in the literature"-'" (Table 2). In the early postoperative period, thromboembolism and wound infection are encountered. Later, serious medical problems include hepatic dysfunction and liver failure, nephrolithiasis, electrolyte imbalance, cholelithiasis, and arthritis. The procedure has an estimated 50% morbidity, in addition to a postoperative mortality rate of up to 10%.' The patient presented in this report manifestt-d several reported medical comphcatlOns of )ejUnoileal bypass surgery-namely, chronic diarrhea, liver disease, arthralgias, and a low serum carotene. Diarrhea is an expected complication in the early postoperative period following jejunoileal bypass that it generally reported to abate With TABLE I. Ullrasound Measurements of Optic Nerves L\BLl' 2 \Iedical Complications of Jejunoileal Bypass· March 1985 13 IAHII J Ocular Complications of J~junoil~al Bypass Laboratury Studies 2 C"nJunctlviti', ''Pi'clL'ntl' NVLlal"pla Blt"t" 'p"h ("n,tnLled field, 2t1/2t10 0 U with central .... t-(lh..Jma Nntal"plil 'Stlppllng" uf rl'llnill pigment <'pithellum Fluurescein angiugram showed retinal vasculitis in one patient Dark adaptatiun abnormal Serum vitamin A 18 mg/dl (11 30-95) Dark adaptation abnormal ERG abnormal Serum carotene 6 mg/dl (11 60-260) Anemia Hgb 80 g/dl Hypoproteinemia Total protein 3.8 Albumin 1.6 ERG abnurmal Vitamin A 10.2 mg/dl (11 > 20) Carotene 25 mg/dl (II 50-150) TABLE .. Orbital Ultrasound of Optic N~rv~ Dis~as~ Dlagnusls In Patients wIth posltl\'e 30° test Optll n<'unttS (.. ) Optic n<,n'e ,heath menlngll'ma (2 I Hvperupla and macular [,,1&; (2) Pseudupapdled<'ma (1 I Papilledema (II Optic' atwph\ (5) method for measuring the diameter of the orbital optic nerve to within 0,5 mm 21. The nerve is enlarged if it measures greater than 4,2 mm in diameter. In addition, the 30° test can be employed to differentiate solid nerve sheath thickening from distension of the sheaths by subarachnoid tluid. The diameter of the nerve is first measured in primary gaze, and then on 30° eccentric gaze, If the diameter decreases by 25% or nwre with this maneuver, the 30° test is positive, indicating distension of the nerve sheath by fluid .md nl)t sl)lid nerve sheath enlargement. The causes of a positive test include increased intracranial pressure, optic nerve hematoma, arachnoid Cyst of the optic nerve, anterior to an optic nerve tuml)r, and retrobulbar optic neuritis.:':' Since the 30° test has been available at the Bascom Palmer Eye Institute, 27 patients have been referred for ultrasound examination of the l)ptiC nerves from this office (Table 4). Fifteen of these have had positive 30° tests. Four of these patients had optic neuritis. Two patients had optic nerve sheath meningiomas with fluid anterior to 15 12 311 0 Te" Pt.lSltln' 'egatJve 27 Ocular complications following jejunoileal bypass have been reported in only six patients (Table 3). In four of these, abnormal visual function has been attributed to vitamin deficiency. Three cases of vitamin A deficiency resulting in nyctal- opia have been descn. bed. 1\ 1"'.14 Inone 0 f th ese, the visual fields, dark adaptation, and ERG returned to normal after only 3 days of vitamin replacement therapy. A second report describes resolution of nyctalopia following treatment with vitamin A, but notes persistent retinal pigment epithelial abnormalities on funduscopic examination. In the third case, there is no mention of treatment for an abnormally low serum vitamin A level. It is pertinent to recall that our patient had a low serum carotene, although her serum vitamin A and ERG were normal. Thompson and Felton J 1 reported a patient with nutritional amblyopia following jejunoileal bvpass. Visual acuity was reduced to 20/200 in both eves with bilateral central scotomas, and anemia a~d hypoproteinemia were present. After multivitamin therapy and surgical reanastomosis of the bypass, visual acuity returned to 20/30. Fagan et al]1I reported two patients whu developed conjunctivitis and episcleritis during an e:\acerbation of polyarthritis with skin rash following jejunoileal bypass. One of these patients had a fluorescein angiogram which demonstrated retinal vasculitis. Standardized A-scan orbital echographv was an extremely valuable aid in defining the nature of the optic nerve disease in this patient. The presence of bilaterally enlarged optic nerve sheaths with a positive 30° test, indicating increased subarachnoid fluid, was the indication for a left optic nerve sheath decumpressiun. Standardized A-scan echographv is an accurate 14 Journal of Clinical Neuro-ophthalrnology the tumur. One patient had malignant hypertensiun with papilledema. In the remaining patients, the etiuk)gy ui the tluid is unclear. Twu patients had hypermetwpia, macular iulds, and ,111 anomaluus appearance ui the uptic discs, but normal visual iunctilH1. Anuther p,ltient vvith normal visual iunctilm had unly minim,ll hyperopia ,lIld no macular iulds. but the uptic discs had the ,lppearance l)i ·pseudup,lpilledema.· Thl' remaining patients have h,ld l)ptiC atwphy ui undetl'rmined cause and a variable reductiun in visual iunctiun. We believe that the patient described in this repl)rt h,lS a pn,'\'ilHlslv ulueCllgnized cumplicatilm lli lejunl1ileal bypass surgery, which Dr. Norman J. Sdl.ltl h,lS termed the "llptiC nerve ascites s\'ndrlH11e.· We wlluld be interested tu knuw ii ,lIlV similar cases h,l\'e been enCllunkred by any lli the readers lli this report. Alsu, we wuuld ad\'ise peripheral iield examinatiuns un jejunuileal b\'pass patients, as the visual acuity in uur patient remained nurmal in the presence ui marked constriction l)i the visual iield. Finally, ii llptiC neurupathv iulluwing jejunuileal bypass clmtinues tu pwgress despite all uther therapeutic attempts, surgical reanastumusis ui the bypass WLluld have tu be considered beiure the uptic nerye disease pwgressed tu blindness. References Joffe,S\:. A re\'lew: Surgery for morbid obesity. I 5l1rg Res 33: 74-88, 1982. 2 \\'robel. SB, et al.. The surgIcal treatment of morbid obesity Economic, psychosocial. ethical. pre\' enti\'e, medical aspects of health care. Yale I BioI. Med. 56: 231-241. 1983 3 Griffen, \\'0, Bivens, BA., and Bell, R.M.: The decline and fall of the lelunoileal bypass. SlIrg. Gl/Ilecol Obstet 157: 301-308,1983 4. Payne, JH, and DeWind, LT.: Surgical treatment of obeSIty Am I SlIrg 118: 141-147, 1969. 5 Reynolds, T. B Medical complications of intestinal bypass surgery Adu. Intem. Med. 23: 47-59,1978. 6. Hah'erson, JD, Wise, L, Wazna, MF, and Ballinger, WF.. jelunolleal bypass for morbid obesity: A critical approach Am I Med. 64: 461-475, 1978. 7. Lipner, A.: Symptomatic magnesium deficiency after small-intestmal bypass for obesity. Br. Med. I 1: 148, 1977 8. DeWind, LT., and Payne, j.H.: Intestinal bypass surgery for morbid obesity: Long-term results. IA.M.A. 236: 2298-2301, 1976. 9. Hocking, MD, Duerson, M.e., O'Leary, jr, and March 1985 Haag, Smith, Susac, Byrne WlllldwMd, LIt: klunoileal bypass for morbid obeslly: Latl' fllllow-up in 100 cases. N. Engl. I Me,r 308: 945-499, 1983. Ill. F,lgan, E. A., d aI.: Systemic inflammatory compllc. ltillns fllllowlllg Jejuno-ileal bypass. Q. I Med. 204: 445-4hO, 19H2. II. I'.Htamian, LG., Sidrys, L.A, and Tripathl, R.e.: 1,ltrugl'nic night blindness and keratoconjunctival xerusis. N. ElIgll Med. 301: 943-944,1979. 12. Brown, G.e., Felton, SM., and Benson, WE.: Revl'rsib1l' night blindness associated with intestinal bypass surgery. Am. I Op/llhalmol. 89: 776-779, 19HO. 13. Thompson. r~.E. and Felton, jL. Nutritional amblyopi, 1 associated with Il'lunoileal bypass surgery. Anll. Ophthalmol. 14: 84H-H50, 19H2. 14. YMborough, G.W., et aI.: Retinopathy following je)unoileal bypass surgery: Report of a case Int I O/Jesill/ 6: 253-248. 1981. 15 Halverson, j.D.: Obesity surgery in perspective. Surgery 87: 119-127, 1980. 16. Hocking, M.P., Duerson, M.e., Alexander, R.W, and Woodward, E.R.: Late hepatic histopathology after JeJunoileal bypass for morbid obesity. Am. I SlIrg. 141: 159-163, 1981. 17. Leff, R.D., Towles, W., Aldo-Benson, MA., Modura, J., and Biegel, A.A.: A prospective analysis of the arthritis syndrome and immune function in jejunoileal bypass patients. I Rhellmatol. 10: 612618,1983. 18. Hamburger, H.A., Beckman, H., and Thompson, R.: Visual evoked potentials and ibuprofen (Motrin) toxicity. All/I. Ophthalmol. 16: 328-329,1984. 19. Knox, D.L: Optic nerve manifestations of systemic disease. TrailS. Am. Acad. Ophthalmol. Otolaryngol. 83: 743-750,1977. 20. Sedwick, LA, et aI.: Optic neuritis in intlammatory bowel disease. I Clw. Nellro-Ophthalmol. 4: 3-6, 1984. 21. Ossoinig, K.e., Cennamo, G., and Frazier-Byrne, S.: Echographic differential diagnosis of 'optic nerve lesions. Oocllm. Ophthalmol. Proc 29: 327332,1981. 22. Byrne, S.F., and Glaser, j.5.: Orbital tissue differentiation with standardized echography. Ophthalmology 90: 1071-1090, 1983. Acknowledgments The authors thank the assistance llf Dr July PllS!, who reviewed the patient's CT scan; and Dr Richard Tenzel. who performed the optic nerve sheath decompression. Writ" for rel'rlIIts tIl.' I L1\\'tl)I) Smith, M.D., 9820 SW /12nd Cllurt, Mhlmi, Flurid,l 3315/1. 15 |
