Ophthalmic Surgery, Lasers and Imaging Retina

Case Report 

Severe Worsening of Diabetic Retinopathy Following Bariatric Surgery

Ruwan A. Silva, MD; John M. Morton, MD, MPH, MHA; Darius M. Moshfeghi, MD

Abstract

Intensive glycemic control results in long-term reduction of diabetic retinopathy, although initial short-term worsening of retinopathy is not uncommon. The authors report a patient with a history of stable diabetic retinopathy who, despite achieving abrupt glycemic control following laparoscopic Roux-en-Y gastric bypass surgery, suffered rapid worsening of her retinopathy within 1 month of surgery. Hemoglobin A1c levels were 8.8 preoperatively and declined to 7.2 at 3.5 months postoperatively. Although visual function in the left eye was spared, useful visual acuity was lost in the right eye. Retinal evaluation is recommended in all patients with diabetes mellitus who are considering bariatric surgery, with close follow-up as warranted.

[Ophthalmic Surg Lasers Imaging Retina. 2013;44:E11–E14.]

From the Byers Eye Institute, Department of Ophthalmology, Stanford University School of Medicine, Stanford, California (RAS, DMM); and the Department of General Surgery, Stanford University School of Medicine, Stanford, California (JMM).

The authors have no financial or proprietary interest in the materials presented herein.

Address correspondence to Darius M. Moshfeghi, MD, Byers Eye Institute, Department of Ophthalmology, Stanford University School of Medicine, 2452 Watson Court, Palo Alto, CA 94303.

Received: April 12, 2013
Accepted: June 19, 2013
Posted Online: October 18, 2013

Abstract

Intensive glycemic control results in long-term reduction of diabetic retinopathy, although initial short-term worsening of retinopathy is not uncommon. The authors report a patient with a history of stable diabetic retinopathy who, despite achieving abrupt glycemic control following laparoscopic Roux-en-Y gastric bypass surgery, suffered rapid worsening of her retinopathy within 1 month of surgery. Hemoglobin A1c levels were 8.8 preoperatively and declined to 7.2 at 3.5 months postoperatively. Although visual function in the left eye was spared, useful visual acuity was lost in the right eye. Retinal evaluation is recommended in all patients with diabetes mellitus who are considering bariatric surgery, with close follow-up as warranted.

[Ophthalmic Surg Lasers Imaging Retina. 2013;44:E11–E14.]

From the Byers Eye Institute, Department of Ophthalmology, Stanford University School of Medicine, Stanford, California (RAS, DMM); and the Department of General Surgery, Stanford University School of Medicine, Stanford, California (JMM).

The authors have no financial or proprietary interest in the materials presented herein.

Address correspondence to Darius M. Moshfeghi, MD, Byers Eye Institute, Department of Ophthalmology, Stanford University School of Medicine, 2452 Watson Court, Palo Alto, CA 94303.

Received: April 12, 2013
Accepted: June 19, 2013
Posted Online: October 18, 2013

Introduction

Bariatric surgery results in a surgical cure of type 2 diabetes mellitus in approximately 80% of patients, with subsequent alterations of glucose homeostasis, pancreatic function, and insulin sensitivity implicated.1–4 Data from the Diabetes Control and Complications Trial (DCCT) demonstrated that intensive control of blood glucose delays the onset and progression of diabetic retinopathy, nephropathy, and neuropathy in patients with type 1 diabetes mellitus, with similar benefits demonstrated in patients with type 2 diabetes mellitus who underwent intensive glycemic control.5,6

Interestingly, patients in the DCCT with preexisting retinopathy experienced an increased risk of a three-step progression in retinopathy during the first year after institution of intensive glycemic control.5 This phenomenon of early worsening of diabetic retinopathy was previously noted in smaller studies of patients with type 1 diabetes mellitus undergoing intensive glycemic control.7–9 While this is mostly a transient phenomenon, some patients were noted to experience loss of visual acuity.7,10–12 Similar early worsening of retinopathy following intensive glycemic control has been reported in patients with type 2 diabetes mellitus.13–15 To date, this phenomenon has not been reported in patients undergoing bariatric surgery who experience a surgical cure of their type 2 diabetes mellitus.

Case Report

A 57-year-old Caucasian woman with a body mass index of 44.2, hypertension, and type 2 diabetes mellitus (HbA1c 8.8, first diagnosed 8 years prior) underwent laparoscopic Roux-en-Y gastric bypass surgery. The patient’s previous ophthalmologist had diagnosed very severe nonproliferative diabetic retinopathy in both eyes and clinically significant macular edema in the left eye 2 years prior to her surgery. Her clinically significant macular edema was treated with focal laser photocoagulation 4 months prior to gastric bypass surgery as per the Early Treatment Diabetic Retinopathy Study.16 Fundus photography at the time of the laser treatment demonstrated very severe nonproliferative diabetic retinopathy in both eyes and clinically significant macular edema in the left eye (Figure 1, page E12). One month prior to bariatric surgery, her best corrected visual acuity (BCVA) was 20/20 in each eye.

Fundus photographs of the right (A) and left (B) eyes 4 months prior to Roux-en-Y gastric bypass surgery. Visual acuity is 20/20 in each eye although very severe nonproliferative diabetic retinopathy is evident in both eyes. Exam reveals microaneurysms, intraretinal hemorrhages and nerve fiber layer infarcts (“cotton-wool spots”) in all four quadrants, venous beading in all four quadrants, and exudate in the parafovea of each eye. The left eye also demonstrates retinal thickening within 500 μm of the fovea (arrow).

Figure 1.

Fundus photographs of the right (A) and left (B) eyes 4 months prior to Roux-en-Y gastric bypass surgery. Visual acuity is 20/20 in each eye although very severe nonproliferative diabetic retinopathy is evident in both eyes. Exam reveals microaneurysms, intraretinal hemorrhages and nerve fiber layer infarcts (“cotton-wool spots”) in all four quadrants, venous beading in all four quadrants, and exudate in the parafovea of each eye. The left eye also demonstrates retinal thickening within 500 μm of the fovea (arrow).

Two weeks after successful laparoscopic Roux-en-Y gastric bypass, the patient noted a decline in visual acuity in her right eye and presented to her ophthalmologist for evaluation. Her BCVA was 20/50 and 20/20 in the right and left eyes, respectively. Fundus examination demonstrated high-risk proliferative diabetic retinopathy in the right eye with tractional changes and clinically significant macular edema in the both eyes (Figure 2). Per the Diabetic Retinopathy Study,16 she received panretinal laser photocoagulation to the right eye. However, her vision continued to decline, and 1 month later she was referred to a vitreoretinal surgeon for evaluation. At the time of that evaluation, her BCVA was counting fingers at 5 feet in the right eye and 20/50 in the left eye. Progressive proliferative diabetic retinopathy was noted in both eyes, with the development of a vitreous hemorrhage in the right eye and preretinal hemorrhage in the left eye. Panretinal laser photocoagulation was therefore performed in the left eye, with the patient’s vitreous hemorrhage precluding repeat laser photocoagulation of the right eye. On follow-up examination 1 month later (3.5 months after Roux-en-Y gastric bypass), her HbA1c level was noted to decline to 7.2 and she was noted to have stable visual acuity in the left eye. However, she was diagnosed with a macula-involving tractional retinal detachment behind her vitreous hemorrhage in the right eye. She therefore underwent pars plana vitrectomy, membrane peel, air-fluid exchange, endolaser photocoagulation, peripheral cryoretinopexy, and 10% C3F8 gas tamponade in the right eye with successful reattachment of the retina. During her postoperative course, her vision remained light perception in the right eye with her retina remaining attached until postoperative month 5, when B-scan ultrasonography demonstrated a total combined rhegmatogenous and tractional retinal detachment in the right eye. She underwent pars plana vitrectomy, lensectomy, membrane peel, silicone oil insertion, iridectomy, endolaser photocoagulation, posterior retinotomy, and scleral buckle procedure in the right eye.

Fundus photographs of the right (A) and left (B) eyes 2 weeks after Roux-en-Y gastric bypass surgery. There is interval development of proliferative retinopathy involving the optic discs (arrowheads) in both eyes with an associated (nasal) tractional retinal detachment in the right eye. Both eyes also demonstrate exudative changes with associated retinal thickening within 500 μm of the fovea.

Figure 2.

Fundus photographs of the right (A) and left (B) eyes 2 weeks after Roux-en-Y gastric bypass surgery. There is interval development of proliferative retinopathy involving the optic discs (arrowheads) in both eyes with an associated (nasal) tractional retinal detachment in the right eye. Both eyes also demonstrate exudative changes with associated retinal thickening within 500 μm of the fovea.

One month after the procedure, the patient sought vitreoretinal surgery consultation from the department of ophthalmology at Stanford University. During this visit (8.5 months after bariatric surgery), the patient’s HbA1c level was 6.3 and her BCVA was hand motion in the right eye and 20/50 in the left eye. Intraocular pressures were 10 and 16 mm Hg in the right and left eyes, respectively. Anterior segment examination was notable for neovascularization of the iris in the right eye and early cataract formation in the left eye. Dilated fundus examination of the right eye demonstrated 1+ optic nerve pallor, dilated and tortuous retinal vessels, silicone oil tamponade, an encircling scleral buckle effect for 360°, and inferonasal proliferative vitreoretinopathy with an associated retinal detachment (Figure 3A). The left eye had an inferior vitreous hemorrhage, florid neovascularization of the disc extending for 3 clock hours nasally, four quadrants of vascular tortuosity and dilatation, incomplete scatter laser photocoagulation, and exudates in the macula (Figure 3B). Panretinal laser photocoagulation was therefore performed in the left eye, with the patient returning to her initial vitreoretinal surgeon for continued management of her right eye. During the subsequent 2 months of follow-up, her BCVA remained hand motion in the right and 20/40 in the left eye. She developed a total retinal detachment in the right eye, and the neovascularization of the left eye continued to regress with staged panretinal photocoagulation. Fluorescein angiography demonstrated a severely ischemic fundus in the right eye and diffuse macular edema in the left eye, which was corroborated on optical coherence tomography. Surgical intervention was deferred in the right eye given its poor visual potential, while the patient declined any intervention (focal laser treatment or intravitreal triamcinolone acetonide) in the left eye given her monocular status and poor response of diffuse macular edema to laser photocoagulation.

Fundus photographs of the right (A) and left (B) eyes 8.5 months after Roux-en-Y gastric bypass surgery. Six months after vitrectomy of the right eye and 1 month after scleral buckle, vitrectomy, silicone oil insertion, and lensectomy of the right eye, there is pallor of the optic nerve head, four quadrants of vascular tortuosity, retinal opacification, inferior retinal detachment, scattered intraretinal hemorrhages, and evidence of laser photocoagulation in the right eye (A). The left eye (B) demonstrates a florid neovascularization of the disc extending nasally (between arrowheads), with exudate and thickening of the superotemporal macula. The peripheral retina demonstrated prior laser photocoagulation.

Figure 3.

Fundus photographs of the right (A) and left (B) eyes 8.5 months after Roux-en-Y gastric bypass surgery. Six months after vitrectomy of the right eye and 1 month after scleral buckle, vitrectomy, silicone oil insertion, and lensectomy of the right eye, there is pallor of the optic nerve head, four quadrants of vascular tortuosity, retinal opacification, inferior retinal detachment, scattered intraretinal hemorrhages, and evidence of laser photocoagulation in the right eye (A). The left eye (B) demonstrates a florid neovascularization of the disc extending nasally (between arrowheads), with exudate and thickening of the superotemporal macula. The peripheral retina demonstrated prior laser photocoagulation.

Discussion

We present a case of severe worsening of diabetic retinopathy after laparoscopic Roux-en-Y gastric bypass surgery. This phenomenon has not been previously reported following treatment of type 2 diabetes mellitus with bariatric surgery, although it is known to occur after institution of tight glycemic control in both type 1 and type 2 diabetes mellitus.7–9,13–15 This patient had a preoperative HbA1c level of 8.8 with known history of nonproliferative diabetic retinopathy, which was stable for 2 years prior to bariatric surgery. Within 2 weeks of surgery, she manifested proliferative retinopathy in the right eye, which assumed an accelerated, unrelenting course despite numerous surgical interventions. Disease in her left eye, although aggravated, was eventually stabilized with laser photocoagulation.

Most reports of early worsening of diabetic retinopathy are confined to the 12-month period after institution of tight glycemic control, with overall reduction in retinopathy grading being seen by 36 months.1,12,14,15,17 Notably, the visual consequences of such early worsening are typically negligible,1,5,14,17 with only a subgroup of these patients experiencing any visual deficits.11,18 Risk factors for early worsening include younger age, 10- to 15-year duration of diabetes mellitus, elevated HbA1c, and existing diabetic retinopathy.19 As in the right eye of our patient, laser photocoagulation may be futile.20 Prior reports have implicated serum insulin-like growth factor (IGF-1) upregulation,20–22 with consequent recommendations then advocating less stringent glycemic control during episodes of early worsening.19 Given this putative role of IGF-1 in enhancing ischemia-induced VEGF expression23 and consequently worsening diabetic retinopathy, the relatively recent advent of intravitreal anti-VEGF therapy may provide a more effective as well as feasible strategy in patients with worsening diabetic retinopathy after bariatric surgery. Alternative pharmacologic interventions (aside from more lax glycemic control) are also being pursued,24,25 which may provide yet another avenue to combat what, as demonstrated above, can be intractable visual decline.

This severe visual consequence of early worsening of retinopathy in type 2 diabetes mellitus warrants further investigation, particularly with regard to patients undergoing surgical treatment for their disease. In the interim, patients with type 2 diabetes mellitus who are contemplating bariatric surgery should be advised of possible early worsening of retinopathy following surgery and should additionally be referred for retinal evaluation prior to bariatric surgery to document the baseline level of disease, particularly if they have had long-standing type 2 diabetes mellitus with poor control (as evidenced by elevated HbA1c) and preexisting retinopathy.21 Follow-up should occur frequently during the first year after bariatric surgery to monitor for subclinical disease progression because this represents the highest risk period for potentially devastating worsening of diabetic retinopathy.

References

  1. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med. 1993;329(14):977–986.
  2. Ballantyne GH, Gumbs A, Modlin IM. Changes in insulin resistance following bariatric surgery and the adipoinsular axis: role of the adipocytokines, leptin, adiponectin and resistin. Obes Surg. 2005;15(5):692–699. doi:10.1381/0960892053923789 [CrossRef]
  3. Greenway SE, Greenway FL 3rd, Klein S. Effects of obesity surgery on non-insulin-dependent diabetes mellitus. Arch Surg. 2002;137(10):1109–1117. doi:10.1001/archsurg.137.10.1109 [CrossRef]
  4. Varela JE. Bariatric surgery: a cure for diabetes?Curr Opin Clin Nutr Metab Care. 2011;14(4):396–401. doi:10.1097/MCO.0b013e3283468e50 [CrossRef]
  5. Diabetes Control and Complications Trial Research Group. The effect of intensive diabetes treatment on the progression of diabetic retinopathy in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial. Arch Ophthalmol. 1995;113(1):36–51.
  6. Diabetes Control and Complications Trial Research Group. Progression of retinopathy with intensive versus conventional treatment in the Diabetes Control and Complications Trial. Ophthalmology. 1995;102(4):647–661.
  7. The Kroc Collaborative Study Group. Blood glucose control and the evolution of diabetic retinopathy and albuminuria. A preliminary multicenter trial. N Engl J Med. 1984;311:365–372.
  8. The Kroc Collaborative Study Group. Diabetic retinopathy after two years of intensified insulin treatment. Follow-up of the Kroc Collaborative Study. JAMA. 1988;260(1):37–41.
  9. Lauritzen T, Frost-Larsen K, Larsen HW, Deckert T. Effect of 1 year of near-normal blood glucose levels on retinopathy in insulin-dependent diabetics. Lancet. 1983;1(8318):200–204. doi:10.1016/S0140-6736(83)92585-0 [CrossRef]
  10. Agardh CD, Eckert B, Agardh E. Irreversible progression of severe retinopathy in young type I insulin-dependent diabetes mellitus patients after improved metabolic control. J Diabetes Complications. 1992;6(2):96–100. doi:10.1016/1056-8727(92)90018-G [CrossRef]
  11. Dandona P, Bolger JP, Boag F, Fonesca V, Abrams JD. Rapid development and progression of proliferative retinopathy after strict diabetic control. Br Med J (Clin Res Ed). 1985;290(6472):895–896. doi:10.1136/bmj.290.6472.895 [CrossRef]
  12. Jennings AM, Lewis KS, Murdoch S, Talbot JF, Bradley C, Ward JD. Randomized trial comparing continuous subcutaneous insulin infusion and conventional insulin therapy in type II diabetic patients poorly controlled with sulfonylureas. Diabetes Care. 1991;14(8):738–744. doi:10.2337/diacare.14.8.738 [CrossRef]
  13. Four risk factors for severe visual loss in diabetic retinopathy. The third report from the Diabetic Retinopathy Study. The Diabetic Retinopathy Study Research Group. Arch Ophthalmol. 1979;97(4):654–655.
  14. DeWitt DE, Hirsch IB. Outpatient insulin therapy in type 1 and type 2 diabetes mellitus: scientific review. JAMA. 2003;289(17):2254–2264. doi:10.1001/jama.289.17.2254 [CrossRef]
  15. Henricsson M, Berntorp K, Berntorp E, Fernlund P, Sundkvist G. Progression of retinopathy after improved metabolic control in type 2 diabetic patients. Relation to IGF-1 and hemostatic variables. Diabetes Care. 1999;22(12):1944–1949. doi:10.2337/diacare.22.12.1944 [CrossRef]
  16. The Diabetic Retinopathy Study Research Group. Photocoagulation treatment of proliferative diabetic retinopathy. Clinical application of Diabetic Retinopathy Study (DRS) findings, DRS Report Number 8. Ophthalmology. 1981;88(7):583–600.
  17. Early worsening of diabetic retinopathy in the Diabetes Control and Complications Trial. Arch Ophthalmol. 1998;116(7):874–886.
  18. Moskalets E, Galstyan G, Starostina E, Antsiferov M, Chantelau E. Association of blindness to intensification of glycemic control in insulin-dependent diabetes mellitus. J Diabetes Complications. 1994;8(1):45–50. doi:10.1016/1056-8727(94)90010-8 [CrossRef]
  19. Chantelau E, Meyer-Schwickerath R. Reversion of ‘early worsening’ of diabetic retinopathy by deliberate restoration of poor metabolic control. Ophthalmologica. 2003;217(5):373–377. doi:10.1159/000071355 [CrossRef]
  20. Chantelau E. What may be gained from standard photocoagulation during early worsening of diabetic retinopathy? An observational study in type-1 diabetic patients after tightening of glycaemic control. Diabetes Metab. 2001;27(3):366–371.
  21. Chantelau E. Evidence that upregulation of serum IGF-1 concentration can trigger acceleration of diabetic retinopathy. Br J Ophthalmol. 1998;82(7):725–730. doi:10.1136/bjo.82.7.725 [CrossRef]
  22. Henricsson M, Berntorp K, Fernlund P, Sundkvist G. Progression of retinopathy in insulin-treated type 2 diabetic patients. Diabetes Care. 2002;25(2):381–385. doi:10.2337/diacare.25.2.381 [CrossRef]
  23. Chantelau E, Kimmerle R, Meyer-Schwickerath R. Insulin, insulin analogues and diabetic retinopathy. Arch Physiol Biochem. 2008;114(1):54–62. doi:10.1080/13813450801900553 [CrossRef]
  24. Chantelau E, Frystyk J. Progression of diabetic retinopathy during improved metabolic control may be treated with reduced insulin dosage and/or somatostatin analogue administration -- a case report. Growth Horm IGF Res. 2005;15(2):130–135. doi:10.1016/j.ghir.2004.12.005 [CrossRef]
  25. Grant MB, Mames RN, Fitzgerald C, et al. The efficacy of octreotide in the therapy of severe nonproliferative and early proliferative diabetic retinopathy: a randomized controlled study. Diabetes Care. 2000;23(4):504–509. doi:10.2337/diacare.23.4.504 [CrossRef]

10.3928/23258160-20131009-01

Sign up to receive

Journal E-contents