VALSALVA'S RETINOPATHY

Signs and Symptoms

Small, superficial hemorrhages resulting from Valsalva maneuver.

The Valsalva's maneuver was named after the Italian anatomist Antonio Maria Valsalva, who defined the Valsalva ligaments and anatomy related to the forcible exhalation effort against a closed glottis. This increases the intrathoracic pressure and interferes with venous return to the heart.1,2 The clinical calling card of the Valsalva's hemorrhage is its well-encased appearance between the retina and the posterior hyaloid face of the vitreous humor. Patients often complain of a sudden, painless change in vision. Depending upon its location, these contained pockets of hemorrhage may cause variable loss of acuity, the perception of floating spots, metamorphopsia and visual field loss.3-8

Pathophysiology

Valsalva retinopathy occurs secondary to increased intra-thoracic or intra-abdominal pressure that is transmitted or transferred to the eye and its systems.1,3­8 Valsalva-induced pre-retinal hemorrhage typically presents in the macula and can be observed positioned between the internal limiting membrane and the rest of the neurosensory retina. These hemorrhages have the potential to be unilateral or bilaterally asymmetric. Valsalva maneuvers occur from natural phenomena such as coughing, sneezing, vomiting, strenuous bowel movements and sexual intercourse. Other strenuous activity such as heavy lifting, fighting, singing or screaming can also cause this retinopathy.5

Management

Massive preretinal hemorrhage secondary to Valsalva maneuver.

Most cases of Valsalva's retinopathy resolve spontaneously, leaving little or no residual visual sequelae. Following the diagnosis, patients should be instructed to avoid strenuous activity, to sleep sitting up and to avoid agents that affect coagulation. As resolution evolves, gravity will cause the blood to settle, with the thinnest portion of the hemorrhage clearing first. The hemorrhage will undergo a specific color change, from red to yellow to white. More often than not, when resolution is complete there is no evidence of injury or the event.3­8

In cases of persistent hemorrhage or if speedier resolution is desired, the Nd:YAG laser can be used, in a procedure called Nd:YAG membranotomy, to create a posterior vitreal hyaloidotomy, enabling diffusion of the hemorrhage into the vitreous gel. This procedure has been proven effective, especially in cases of Valsalva pre-retinal hemorrhage.6­8 It usually results in an improvement in vision within one month. The two-step procedure incorp orates two stretch burns to make the membrane stable and taut and penetration burns to create the conduit into the vitreous. In most cases, visual improvement is immediate.5,7 The procedure is not without mild risks, including macular hole formation and retinal detachment.6

Clinical Pearls

  • In most cases, the history does most of the work in unveiling the ultimate diagnosis.
  • In cases where the patient denies contributing behaviors, the differential diagnosis can be difficult. Pre-retinal hemorrhage that is well encased between the neuro-sensory retina and the posterior hyaloid face of the vitreous may be precipitated by blunt trauma, neovascularization, hypertensive retinopathy, retinal macro-aneurysm, posterior vitreous detachment, Terson's syndrome and shaken-baby syndrome.5
  • Although vitreous bleeding seen secondary to retinal detachments is diffuse and not typically well encased, any case of vitreous hemorrhage should prompt one to consider the etiology to be a retinal break until proven otherwise.

 

  1. Friel, J.P. Valsalva's maneuver. Dorlands Illustrated Medical Dictionary, 26th ed. Philadelphia, PA: W.B. Saunders Co., 1985: 774.
  2. Friel, J.P. Valsalva's ligaments, maneuver . Dorlands Illustrated Medical Dictionary, 26th ed. Philadelphia, PA: W.B. Saunders Co., 1985:1435.
  3. Friedman NJ, Pineda R, Kaiser PK. Retina / Choroid: Valsalva retinopathy. In: Friedman NJ, Pineda R, Kaiser PK. The Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology. Philadelphia, PA: W.B. Saunders Co., 1998: 248-250.
  4. Regillo CD. Distant trauma with posterior segment effects. In: Yanoff M, Duker JS. Ophthalmology. Philadelphia, PA: Mosby Co 1999: 8.44.1­8,44.6.
  5. Puthalath S, Chirayath A, Shermila MV, et al. Frequency-doubled Nd:YAG laser treatment for premacular hemorrhage. Ophthalmic Surg Lasers Imaging 2003; 34(4):284-90.
  6. Ulbig MW, Mangouritsas G, Rothbacher HH, et al. Long-term results after drainage of premacular subhyaloid hemorrhage into the vitreous with a pulsed Nd:YAG laser. Arch Ophthalmol 1998; 116(11):1465-9.
  7. Ladjimi A, Zaouali S, Messaoud R, et al. Valsalva retinopathy induced by labour. Eur J Ophthalmol 2002; 12(4):33 6-8.
  8. Chapman-Davies A, Lazarevic A. Valsalva maculopathy. Clin Exp Optom 2002; 85(1): 42-5.

 

NEW TECHNOLOGY: OPTICAL COHERENCE TOMOGRAPHY

OPTICAL COHERENCE TOMOGRAPHY (OCT) is a relatively new technique for two and three-dimensional imaging of tissues at the histological level.1­7 The technique is based on optical technology and commercially available fiber-optic components adapted for ophthalmic use. OCT is a non-invasive technique that does not utilize ionizing radiation to provide in vivo images. OCT has numerous potential clinical applications and, in effect, creates "optical biopsies" of tissues. It has also been used in the detection, characterization and management of skin tumors and other dermatological diseases, cardiology and intravascular disease. OCT may be able to contribute to early diagnosis of vulnerable atherosclerotic lesions.2

Stratus OCT (Carl Zeiss Meditec, Dublin, Calif.) completes a transverse scanning of tissue to 2mm in depth using infrared light over a one to two second period without requiring pupil dilation. The propagation of light through the tissue in combination with the time-of-flight delay of the reflected light received from the biological tissues produces false­color images of the microstructure.3 Stratus OCT has impressive spatial resolution (10 microns), with additional differentiation possible in transparent tissues. Analogous to a sort of "optical ultrasound" the technology has been documented as capable of imaging single cells in living systems via a surface, intravascular or endoscopic approach. Stratus OCT has a smaller footprint, can scan four times faster, and store 10 times the data than previous models.1

Stratus OCT has a normative database containing age­matched reference values for retinal nerve fiber layer thickness (NFL) that aids in identifying NFL defects secondary to glaucoma and other neuropathies, as well as an analysis change package that gives one the ability to compare the data from left and right eyes from successive visits and over time.4 Radial line scans through the optic disc provide cross-sectional information regarding cupping and neuroretinal rim area.4 Unlike other instruments, the optic disc margin is objectively determined by the interpretation of the signals received from the end of the retinal pigment epithelium in the retina.4 Stratus OCT also provides a volumetric and area assessment in tabular format.4

Stratus OCT has demonstrated reliability and consistency in its determination of NFL thickness in both normal and glaucomatous subjects.5 A study by Guedes and coworkers, which included 534 eyes in 367 subjects (166 eyes of normal subjects, 83 eyes of glaucoma suspects, 196 eyes of early glaucoma patients and 89 eyes of advanced glaucoma patients), determined the presence of a correlation between the macular and NFL thickness measurements, concluding that OCT has usefulness in the clinical assessment of glaucoma.6

Unstundag and researchers7 and Wirbelauer and associates8 have used the instrument to examine the use of optical coherence tomography for the purpose of evaluating anatomical changes in the anterior segment. Unstungad's team used OCT after laser in situ keratomileusis (LASIK) to observe complications related to the interface and corneal flap.7 Wirbelauer used the instrument to observe and monitor the healing process before and after excimer laser phototherapeutic keratectomy (PTK) for recurrent epithelial erosions. Both groups concluded that OCT appears to be a promising method for evaluating anatomical changes within the cornea.7,8 However, the Stratus OCT does not incorporate the anterior segment application into its programming, and this device is not FDA approved or intended for this use.

Stratus OCT has also been evaluated as a adjunctive instrument for the diagnosis and management of posterior segment diseases such as macular edema, choroidal neovascularization (CNV) and macular hole.9-13 Kim and researchers examined the classification, size and activity of CNV by optical coherence tomography as compared with data obtained by fluorescein angiography (FA) and Indocyanine green angiography (ICG). They concluded that retinal thickness, as affected by factors such as retinal edema and CNV, was proportional and consistent to lesion size, making OCT, when used in combination with FA and ICG, a valuable tool for increasing the specificity of diagnosis of neovascular disease.9

OCT technology has been used to measure and quantify macular holes.10 Spaide used the device to examine patients with branch retinal vein occlusion (BRVO) and found a significant number within his sample had sustained serous retinal detachment (SRD) not detectable with standard ophthalmoscopy.11 As few patients with BRVO are discovered to have SRD by ophthalmoscopy, the entity has been considered to be an uncommon occurrence. However, OCT may show that this is a rather common complication of retinal vascular occlusion. In addition, they offered that subretinal hemorrhage may also occur in the context of BRVO, proposing that blood gravitates through the subretinal fluid to settle behind the retina.11

Numerous researchers have expounded on the value of OCT in reporting applications for evaluation of diffuse diabetic macular edema (DME) before and after vitrectomy,12 while Browning cautions that there are pitfalls associated with OCT technology, creating the potential for inaccurate treatment of diabetic macular edema. Massin and associates found that OCT was beneficial in identifying eyes with diffuse DME combined with vitreomacular traction. In these cases, the instrument allowed diagnosis of subtle vitreomacular traction and provided precise preoperative and postoperative assessments of macular thickness.13 Lattanzio and his group14 and Goebel and Kretzchmar­Gross15 assessed the relationships between macular thickness and the stage of diabetic retinopathy along with macular edema, quantifying the changes before and after laser treatment. Lattanzio determined that macular thickness was greater in diabetic patients than in controls, and that it tended to increase with the severity of the diabetic retinopathy and macular edema.14 Both teams concluded OCT is a sensitive technique for detecting early diabetic macular abnormalities and that OCT was well suited for quantifying macular thickness reduction after laser treatment.14,15

Stratus OCT is a powerful tool that deserves recognition as the newest member of the diagnostic armamentarium for early diagnosis, differential diagnosis and more sensitive monitoring of a variety of ocular abnormalities, including glaucoma, retinal and anterior eye diseases.1-13 The OCT technology is also being developed in other clinical areas and is expected to become integrated in a range of clinical situations in the future.1,2,4

  1. Kent C. Creating a "virtual biopsy": improvements in technology make it possible to "see" more internal tissue than ever before. Ophthalmology Management 2002; 6(5):111-2.
  2. Andersen PE, Thrane L, Bjerring P, et al. Optical coherence tomography. Ugeskr Laeger 2003; 165(15):546-50.
  3. Wang M, Luo R, Liu Y. Optical coherence tomography and its application in ophthalmology. Yan Ke Xue Bao 1998; 14(2):116-20.
  4. Zeiss Instruments. Add depth to your diagnosis: Direct cross ­ sectional imaging. Dublin, CA, Carl Zeiss Meditec Inc. Press 2003: 1­6.
  5. Carpineto P, Ciancaglini M, Zuppardi E, et al.. Reliability of nerve fiber layer thickness measurements using optical coherence tomography in normal and glaucomatous eyes. Ophthalmology 2003; 110(1):90­5.
  6. Guedes V, Schuman JS, Hertzmark E, et al. Optical coherence tomography measurement of macular and nerve fiber layer thickness in normal and glaucomatous human eyes. Ophthalmology 2003; 110(1):177-89.
  7. Ustundag C, Bahcecioglu H, Ozdamar A, et al. Optical coherence tomography for evaluation of anatomical changes in the cornea after laser in situ keratomileusis. J Cataract Refract Surg 2000; 26(10):1458-62.
  8. Wirbelauer C, Scholz C, Haberle H, et al. Corneal optical coherence tomography before and after phototherapeutic keratectomy for recurrent epithelial erosions. J Cataract Refract Surg 2002; 28(9):62-35.
  9. Kim SG, Lee SC, Seong YS, et al. Choroidal neovascularization characteristics and its size in optical coherence tomography. Yonsei Med J. 2003; 44(5):821-7.
  10. Liu X, Ling Y, Gao R, et al. Optical coherence tomography's diagnostic value in evaluating surgical impact on idiopathic macular hole. Chin Med J 2003; 116 (3):444-7.
  11. Spaide RF, Lee JK, Klancnik JK Jr, et al. Optical coherence tomography of branch retinal vein occlusion. Retina 2003; 23(3):343-7.
  12. Browning DJ. Potential pitfalls from variable optical coherence tomograph displays in managing diabetic macular edema. Am J Ophthalmol 2003; 136 (3):555-7.
  13. Massin P, Duguid G, Erginay A, et al. Optical coherence tomography for evaluating diabetic macular edema before and after vitrectomy. Am J Ophthalmol 2003; 135(2):169-77.
  14. Lattanzio R, Brancato R, Pierro L, et al. Macular thickness measured by optical coherence tomography (OCT) in diabetic patients. Eur J Ophthalmol 2002; 12 (6):482-7.
  15. Goebel W, Kretzchmar ­ Gross T. Retinal thickness in diabetic retinopathy: a study using optical coherence tomography (OCT). Retina 2002; 22(6):59-67.

 

NEW MANAGEMENT: INTRAVITREAL STEROID INJECTION FOR EDEMATOUS MACULAR DISEASE

CYSTOID MACULAR EDEMA (CME) and macular edema in general typically manifest as either decreased visual acuity, metamorphopsia, visible retinal thickening, or leakage seen upon fluorescein angiography. It is the result of vascular compromise with leakage of serous fluid out of incompetent intraretinal capillaries into the macular outer plexiform layer of Henle.1 Depending on the cause (post surgical, venous occlusion, retinal infection, retinal inflammation, trauma), the prognosis ranges from good (where patients recover spontaneously, with full restoration of visual acuity over the course of one year) to guarded (where patients recover incompletely over a one- to two-year period) to poor (where patients do not recover any lost acuity).1­9 In fact, in approximately one-third of patients, macular edema persists indefinitely, accompanied by decreased visual acuity.1

Once established, CME has been treated with oral acetazolamide, topical corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), or posterior sub-Tenon's injection of long-acting cortico-steroids. The results have been mixed. Over the last three years, intravitreal steroid injection has received much attention for its perceived and often verified ability to reduce or resolve this sometimes chronic, debilitating condition.2­9

In two papers, researchers reported success investigating the treatment of CME associated with central retinal vein occlusion (CRVO) with intravitreal triamcinolone acetonide.2,3 Park and coworkers evaluated 10 eyes of nine patients with perfused CRVO with visual acuity of 20/50 or worse and macular edema. Following baseline evaluation, including best-corrected visual acuity, intraocular pressure (IOP), optical coherence tomography (OCT) and fluorescein angiography, triamcinolone acetonide (4mg in 0.1ml) was injected into the vitreous cavity. Over the course of 15.4 months, all 10 eyes demonstrated ophthalmoscopic improvement in cystoid macular edema with corresponding improvement in OCT measurements of macular thickness. In this sample, the mean best-corrected visual acuity improved from 58 letters at baseline to 78 letters. The visual acuity improvement was statistically significant with six eyes (60 %) greater or equal to 20/50. More importantly, there were no significant complications. Three eyes (30%) without previous history of glaucoma required initiation of a topical aqueous suppressant for IOP elevation. One eye with a previous history of open-angle glaucoma required trabeculectomy. Intravitreal injection of triamcinolone acetonide appears to be an effective treatment in reducing cystoid macular edema associated with central retinal vein occlusion.2

In their retrospective review of eight patients with macular edema secondary to CRVO that were treated with an intravitreal injection of triamcinolone acetonide, Ip and associates reported the mean visual acuity at the three-month follow up was an average gain of 3.3 lines.3 No patient had a decrease in visual acuity. Seven of eight patients had complete resolution of macular edema on clinical examination and no adverse effects such as cataract, glaucoma, retinal detachment or endophthalmitis were noted. They, too, concluded that intravitreal injection of triamcinolone acetonide appeared to be a safe and effective treatment for selected patients with macular edema due to CRVO.3

In another study, researchers set out to determine if intravitreal injection of triamcinolone acetonide was an effective option for treating severe persistent macular edema unresponsive to other treatments.4 Here, 15 eyes with severe macular edema of long duration (nine­30 months) were injected with 4mg of intravitreal triamcinolone acetonide. The visual acuity and anatomic responses were monitored with pre- and postoperative fluorescein angiography and optical coherence tomography. Remarkably, the central macular thickness, as evaluated by OCT, decreased by 50%. This beneficial effect was correlated with a significant improvement in visual acuity. Ten of 15 patients (66%) experienced improved visual acuity by more than two Snellen lines. On the negative side, a significant increase in intraocular pressure was observed and attributed to the corticosteroid medication. No injection-related complications occurred. One patient had to be retreated after three months due to recurrence of the macular edema. The study concluded that intravitreal triamcinolone acetonide is a promising therapeutic option deserving of some consideration for severe, chronic, leakage.4

Another report investigated the efficacy of intravitreal triamcinolone acetonide in refractory pseudophakic cystoid macular edema.5 Three eyes of three patients with longstanding pseudophakic cystoid macular edema following uncomplicated cataract surgery, refractory to medications, were treated with 8mg of intravitreal triamcinolone acetonide. One month after intravitreal triamcinolone acetonide injection, there was a documented dramatic decrease in macular thickness as measured by optical coherence tomography in all three eyes. In this sample, mean improvement in visual acuity was 3.7 Snellen lines. Unfortunately, the edema recurred in all cases with a relapse of the decreased vision. Two eyes underwent a second injection. The macular thickness decreased again, but only temporarily. The edema recurred three months after the injection leading this group to conclude that intravitreal injection of triamcinolone in cases such as these induces a striking, short-term regression that appears to be transient even in the presence of a second injection.5

Scott, Flynn and Rosenfeld reported on the use of intravitreal triamcinolone acetonide for the management of idiopathic cystoid macular edema (ICME).6 Two patients with ICME were treated with intravitreal triamcinolone acetonide. In one patient, the best-corrected acuity was 20/70 before treatment, improving to 20/30 six months post-treatment. Foveal thickness was also measurably reduced following the injection. In the second patient, best-corrected acuity was 20/200 before treatment, improving to 20/50 five months post-treatment. There, too, foveal thickness could be measured to demonstrate resolution of the swelling. While recurrence of leakage responded well to repeat injection, the study supported the contention that the effects of intravitreal triamcinolone acetonide may be transient.5,6

Martidis et al, experimented with intravitreal injection of triamcinolone acetonide to determine its profile for treating diabetic macular edema unresponsive to laser photocoagulation.7 In their study, the mean improvement in visual acuity was 2.4, 2.4 and 1.3 Snellen lines at the one-, three- and six-month follow-up intervals, respectively. The central macular thickness as measured by OCT decreased by 55%, 57.5% and 38%, respectively, over these same intervals. The panel concluded that intravitreal triamcinolone is a promising therapeutic method for treating diabetic macular edema unresponsive to conventional laser photocoagulation.7

The procedure is not without potential complications. Jonas and coworkers and Moshfeghi and researchers both acknowledge potential complications, including the possibility of IOP elevation in approximately 50% of eyes one to two months after a 25mg injection.8,9 The majority of IOP elevation can be normalized using topical medications, returning to pretreatment/normal values without the need for topical medications six months after the procedure.8

Moshfeghi and researchers in their retrospective, multicenter, case series investigated the incidence of acute postoperative endophthalmitis following intravitreal triamcinolone acetonide injection at seven academic clinical centers.9 In their study, a total of 922 procedures were reviewed. Eight eyes of eight patients with acute postoperative endophthalmitis were identified within a six-week time period following the injection for an incidence of 0.87%. From this data, it appears this complication is rare; however, when it does occur, it ensues rapidly and can result in severe loss of vision.9

Research is underway to address other refractory conditions with intravitreal steroid injection. Anecortave acetate is being investigated as an intravitreal steroid for the treatment of choroidal neovascular membranes in age-related macular degeneration. Early research has shown that anecortave acetate is safe and clinically efficacious at one year for maintaining vision, preventing severe vision loss, and inhibiting subfoveal CNV lesion growth.10

Intravitreal steroid injection is a relatively new modality designed to treat an old, often stubborn problem. While it is not without risk and may only be transiently helpful in some cases, it can offer limited hope to patients who would otherwise surely suffer visual losses. Its refinement may yet prove to be revolutionary.

  1. Ahmed I, Ai E. Cystoid macular edema. In : Yanoff M, Duker JS. Ophthalmology. Philadelphia, PA: Mosby 1999:8.34.1­8.34.6.
  2. Park CH, Jaffe GJ, Fekrat S. Intravitreal triamcinolone acetonide in eyes with cystoid macular edema associated with central retinal vein occlusion. Am J Ophthalmol 2003; 136(3):419-25.
  3. Ip M, Kahana A, Altaweel M. Treatment of central retinal vein occlusion with triamcinolone acetonide: an optical coherence tomography study. Semin Ophthalmol 2003; 18(2):67-73.
  4. Rakic JM, Zelinkova M, Comhaire­Poutchinian Y, et al. Treatment of Graves macular edema with intravitreal injection of corticosteroids. Bull Soc Belge Ophtalmol 2003; (288):43-8.
  5. Benhamou N, Massin P, Haouchine B, et al. Intravitreal triamcinolone for refractory pseudophakic macular edema. Am J Ophthalmol 2003; 135(2):246-9.
  6. Scott IU, Flynn HW Jr., Rosenfeld PJ. Intravitreal triamcinolone acetonide for idiopathic cystoid macular edema. Am J Ophthalmol 2003; 136(4):737-9.
  7. Martidis A, Duker JS, Greenberg PB, et al. Intravitreal triamcinolone for refractory diabetic macular edema. Ophthalmology 2002; 109(5):920-7.
  8. Jonas JB, Kreissig I, Degenring R. Intraocular pressure after intravitreal injection of triamcinolone acetonide. Br J Ophthalmol 2003; 87(1):24-7.
  9. Moshfeghi DM, Kaiser PK, Scott IU, et al. Acute endophthalmitis following intravitreal triamcinolone acetonide injection. Am J Ophthalmol 2003; 136 (5):791-6.
  10. Slakter JS, Anecortave Acetate Clinical Study Group. Anecortave acetate as monotherapy for treatment of subfoveal neovascularization in age-related macular degeneration: twelve-month clinical outcomes. Ophthalmology 2003;110(12):2372-83.


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