sponse amplitude of about 5% to 10% of normal, the rod was severely impaired. There is no possible vascular insult that could destroy simultaneously all the rods in both eyes while largely sparing the cones. The other findings were also classic for RP. The patient's final dark-adapted threshold was elevated. The visual fields were not shown, but they were described as constricted with what sounds like partial-ring scotomata, which are typical, again, of RP and not vascular insufficiency. The arteries were narrow, of course, which the authors explained as "hypertension." But the patient was not hypertensive! The "sudden" onset of impaired night vision in the patient was, certainly, a sudden awareness of impaired night vision, which, again, is a common phenomenon in RP. Cynthia J. MacKay, MD New York, NY 1. DuBois LG, Sadun AA, Lawton TB. Inner retinal layer loss in complicated migraine. Arch Ophthalmol. 1988;106:1035-1037.
Reply.\p=m-\Weappreciate Dr MacKay's interest and suggestion that our patient had early RP. It is true that RP, especially sine pigmento, may be difficult to diagnose. As noted in our case report,1 we, too, were initially confounded by the abnormal ophthalmologic findings in the absence of an observable cause. However, the diagnosis of RP was considered and rejected. In response to Dr MacKay, we can add that there was never a question of a faulty patient history. Now an attorney, the patient was a truck driver at presentation and often drove at night. He was an excellent recorder of his visual changes; he complained that "swirling designs" and poor contrast developed during a period of about 1 month. There was no family history of nyctalopia or degenerative retinal diseases. We agree that the electrophysiologic changes were highly suggestive of peripheral retinal impairment from congenital nyctalopia, yet there were no observable retinal changes. The vascular attenuation was attributable to the patient's hypertension; pig¬ mentary changes were not noted in the retina, nor was pig¬ ment dusting found in the vitreous. The visual field in the right eye demonstrated a partial superior arcuate scotoma; the field in the left eye showed a pericentral, donut-shaped In
scotoma 5° to 20° from fixation. Moreover, the deficits in contrast sensitivity functions were characteristic of inner retinal or optic nerve dysfunction. The contrast sensitivity functions and electroretinograms of the eyes improved af¬ ter initiating prophylactic therapy for migraine.
Interestingly, shortly after our article was published, Berson and Lessell2 reported a case with an almost identi¬ cal clinical picture in a patient with cutaneous malignant melanoma and suggested a paraneoplastic cause for the oc¬ ular findings. Two years after our patient's initial presen¬ tation, he informed us that he had just had an axillary cu¬ taneous and lymph node malignant melanoma excised. This is an attractive explanation for the loss of rod function in our patient. However, improved ophthalmologic findings and cessation of migraines preceded the excision of the ma¬ lignant melanoma. Thus, we remain perplexed. However, the lack of family history, tempo of onset, partial resolution
of symptoms, examination, laboratory studies, and followup are all inconsistent with RP. Lindreth G. DuBois, MEd Alfredo A. Sadun, MD PhD Los Angeles, Calif 1. DuBois LG, Sadun AA, Lawton TB. Inner retinal layer loss in complicated migraine. Arch Ophthalmol. 1988;106:1035-1037. 2. Berson EL, Lessell S. Paraneoplastic night blindness with malignant melanoma. Am J Ophthalmol. 1988;106:307-311.
Suture Removal After Blepharoplasty
To the Editor.\p=m-\Inthe April 1990 issue of the Archives, Glatt et al1 reported on discomfort during suture removal after blepharoplasty. They described the removal of a running of 6-0 silk suture 4 days after blepharoplasty. I found it interesting that their patients were experiencing so much discomfort that they felt compelled to try to minimize this with proparacaine hydrochloride. When I perform blepharoplasty surgery, I use a 6-0 polypropylene (Prolene) suture and knot it on itself and either end so that at the time of removal one need only cut in the middle of the running suture and then pull on the two loops that are formed on either end. This avoids the need to find the knot that would be buried in the skin if it had not been looped on itself. Most patients tell me they are amazed that they do not feel any pain or discomfort when the sutures are removed in this manner. Prolene is a much smoother suture than silk; perhaps that is why there is little or no discomfort with this removal. Janet M. Neigel, MD West Orange, NJ 1. Glatt HJ, Putterman AM, Farber MD. Topical proparacaine and suture removal after blepharoplasty. Arch Ophthalmol. 1990;108:476.
Reply.\p=m-\We prefer silk to polypropylene (Prolene) for cutaneous wound closure because of its superior handling properties. Discomfort during removal of silk sutures has generally been a problem only after blepharoplasty and not after a vast array of other oculoplastic procedures. We can think of two reasons for this difference between our patients who have undergone blepharoplasty and the rest of our patients. First, it is our impression that many patients who have undergone blepharoplasty have very low pain thresh-
In
olds compared with other patients. Second, one of us (A.M.P.) removes sutures 4 days after blepharoplasty, compared with 5 to 7 days after most other procedures. Patients may be a little more tender at this earlier time.
Herbert J. Glatt, MD Knoxville, Tenn Allen M. Putterman, MD Marilyn D. Farber, MD Chicago, Ill
Endophthalmitis Therapy: Changing Antibiotic Sensitivity Patterns and Current Therapeutic Recommendations
To the Editor.\p=m-\Martinand associates' reported vitreous cefazolin levels in a rabbit model of experimental endophthalmitis. These authors used heat-killed Staphylococcus epidermidis organisms to induce intraocular inflammation and then measured the penetration of systemically administered cefazolin. Meredith and associates2 reported further rabbit model studies of S epidermidis endophthalmitis and observed no significant difference in inflammatory scores between the placebo-treated group and the group treated with 2.25 mg of intravitreal cefazolin. However, there were more eyes with clear media at the end of week 3 in the group treated with vitrectomy, 2.25 mg of intravitreal cefazolin, and either systemic or intravitreal corticosteroids. Although cefazolin does penetrate the eye from systemic administration and also may be used intravitreally, it is important to recognize that frequent resistance will occur among organisms commonly encountered in clinical endophthalmitis. Davis and associates3 reported a series of
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Reply.\p=m-\Weappreciate Dr MacKay's interest and suggestion that our patient had early RP. It is true that RP, especially sine pigmento, may be difficult to diagnose. As noted in our case report,1 we, too, were initially confounded by the abnormal ophthalmologic findings in the absence of an observable cause. However, the diagnosis of RP was considered and rejected. In response to Dr MacKay, we can add that there was never a question of a faulty patient history. Now an attorney, the patient was a truck driver at presentation and often drove at night. He was an excellent recorder of his visual changes; he complained that "swirling designs" and poor contrast developed during a period of about 1 month. There was no family history of nyctalopia or degenerative retinal diseases. We agree that the electrophysiologic changes were highly suggestive of peripheral retinal impairment from congenital nyctalopia, yet there were no observable retinal changes. The vascular attenuation was attributable to the patient's hypertension; pig¬ mentary changes were not noted in the retina, nor was pig¬ ment dusting found in the vitreous. The visual field in the right eye demonstrated a partial superior arcuate scotoma; the field in the left eye showed a pericentral, donut-shaped In
scotoma 5° to 20° from fixation. Moreover, the deficits in contrast sensitivity functions were characteristic of inner retinal or optic nerve dysfunction. The contrast sensitivity functions and electroretinograms of the eyes improved af¬ ter initiating prophylactic therapy for migraine.
Interestingly, shortly after our article was published, Berson and Lessell2 reported a case with an almost identi¬ cal clinical picture in a patient with cutaneous malignant melanoma and suggested a paraneoplastic cause for the oc¬ ular findings. Two years after our patient's initial presen¬ tation, he informed us that he had just had an axillary cu¬ taneous and lymph node malignant melanoma excised. This is an attractive explanation for the loss of rod function in our patient. However, improved ophthalmologic findings and cessation of migraines preceded the excision of the ma¬ lignant melanoma. Thus, we remain perplexed. However, the lack of family history, tempo of onset, partial resolution
of symptoms, examination, laboratory studies, and followup are all inconsistent with RP. Lindreth G. DuBois, MEd Alfredo A. Sadun, MD PhD Los Angeles, Calif 1. DuBois LG, Sadun AA, Lawton TB. Inner retinal layer loss in complicated migraine. Arch Ophthalmol. 1988;106:1035-1037. 2. Berson EL, Lessell S. Paraneoplastic night blindness with malignant melanoma. Am J Ophthalmol. 1988;106:307-311.
Suture Removal After Blepharoplasty
To the Editor.\p=m-\Inthe April 1990 issue of the Archives, Glatt et al1 reported on discomfort during suture removal after blepharoplasty. They described the removal of a running of 6-0 silk suture 4 days after blepharoplasty. I found it interesting that their patients were experiencing so much discomfort that they felt compelled to try to minimize this with proparacaine hydrochloride. When I perform blepharoplasty surgery, I use a 6-0 polypropylene (Prolene) suture and knot it on itself and either end so that at the time of removal one need only cut in the middle of the running suture and then pull on the two loops that are formed on either end. This avoids the need to find the knot that would be buried in the skin if it had not been looped on itself. Most patients tell me they are amazed that they do not feel any pain or discomfort when the sutures are removed in this manner. Prolene is a much smoother suture than silk; perhaps that is why there is little or no discomfort with this removal. Janet M. Neigel, MD West Orange, NJ 1. Glatt HJ, Putterman AM, Farber MD. Topical proparacaine and suture removal after blepharoplasty. Arch Ophthalmol. 1990;108:476.
Reply.\p=m-\We prefer silk to polypropylene (Prolene) for cutaneous wound closure because of its superior handling properties. Discomfort during removal of silk sutures has generally been a problem only after blepharoplasty and not after a vast array of other oculoplastic procedures. We can think of two reasons for this difference between our patients who have undergone blepharoplasty and the rest of our patients. First, it is our impression that many patients who have undergone blepharoplasty have very low pain thresh-
In
olds compared with other patients. Second, one of us (A.M.P.) removes sutures 4 days after blepharoplasty, compared with 5 to 7 days after most other procedures. Patients may be a little more tender at this earlier time.
Herbert J. Glatt, MD Knoxville, Tenn Allen M. Putterman, MD Marilyn D. Farber, MD Chicago, Ill
Endophthalmitis Therapy: Changing Antibiotic Sensitivity Patterns and Current Therapeutic Recommendations
To the Editor.\p=m-\Martinand associates' reported vitreous cefazolin levels in a rabbit model of experimental endophthalmitis. These authors used heat-killed Staphylococcus epidermidis organisms to induce intraocular inflammation and then measured the penetration of systemically administered cefazolin. Meredith and associates2 reported further rabbit model studies of S epidermidis endophthalmitis and observed no significant difference in inflammatory scores between the placebo-treated group and the group treated with 2.25 mg of intravitreal cefazolin. However, there were more eyes with clear media at the end of week 3 in the group treated with vitrectomy, 2.25 mg of intravitreal cefazolin, and either systemic or intravitreal corticosteroids. Although cefazolin does penetrate the eye from systemic administration and also may be used intravitreally, it is important to recognize that frequent resistance will occur among organisms commonly encountered in clinical endophthalmitis. Davis and associates3 reported a series of
Downloaded From: http://archopht.jamanetwork.com/ by a University of Edinburgh Library User on 06/21/2015
