Ocular Bottles

Injuries

From

Beverage

To the Editor.\p=m-\Therecent article in the Archives entitled "Ocular Injuries From Exploding Beverage Bottles" by Mondino et al (96:2040-2041, 1978) is of interest to me, because I happened to see two cases of similar injuries with considerable damage to the eyes, in the summer of 1977. The first case was in a young girl who had been trying to remove the cap from one of the new unbreakable plastic bottles, when the cap hit her left eye, causing corneoscleral laceration, vitreous prolapse, and cataract formation. The second case also occurred when the cap of a bottle hit the

patient's eye while she was working in the kitchen; it caused a corneal opacity without affecting her vision.

If I small

injuries in a community of 25,000 people, in one summer, I must conclude that beverage-bottle injuries of the eyes must not be very infrequent, but probably most of them go unreported. Even if the bottle is unbreakable, the cap remains a hazard. Perhaps the larger the bottle, the more hazardous it is, because of the pressure inside the bottle. The authors of the article in the Archives are to be commended for bringing this hazard to the attention of the ophthalmic community. Jila S. Waikhom, MD Xenia, Ohio see

two serious eye

To the Editor.\p=m-\Inregard to a recent article in the Archives by Mondino et al (96:2040-2041, 1978), I have personally seen nearly half a dozen injuries related to "exploding" carbonated beverage bottles in 1978. I would concur that the incidence is surely higher than that suggested by infrequent reports in the literature; however, I would suggest that this may be so because serious injury may be rare, relative to incidence of all such injuries. For example, on Feb 3, 1978, I was asked to see a 26-year-old woman who had sustained an explosion injury to her right eye that day, from a carbonated beverage bottle. The injury was

said to be spontaneous, having occurred with a chilled bottle that had not been shaken, and had undergone only normal cap removal. Although her vision was initially only hand motion in the injured eye, within four weeks her visual acuity had improved to 6/6 (20/20). She sustained a 100% cellular hyphemia and traumatic iritis. Both cleared within one month with

mydriatic therapy, topically applied. patient also sustained a corneal abrasion, which healed within two days with patching and antibiotic ointment. She had no angle alteration, retinal damage, orbital changes, or other ocular sequelae of the injury, except a slightly peaked and irregular pupil, which has persisted to date. There was no sign of cataractous change, no posterior segment hemor¬ rhage, no iridodialysis, and no disrup¬ tion of globe integrity. The

None of my other

this year the one described here; I conclude that rela¬ tively inconsequential injuries from exploding bottle tops may commonly be minor. I certainly agree with the safety precautions recommended in the article by Mondino et al. Kenneth R. Fox, MD Falls Church, Va were even

equally

cases

severe as

Corneal Edema After Use of Carbachol

To the Editor.\p=m-\In a recent issue of the Archives (96:1897-1901,1978) Vaughn et al described their experimental data on the perfusion of the anterior chamber of rabbits with carbachol. They noted transitory but reversible swelling of the cornea, which implied some transitory endothelium dysfunction. However, they advised caution in using this solution in humans in whom the cornea has already compromised endothelial cells. In the past two years, the National Registry of Drug-Induced Ocular Side Effects has had numerous reports of patients having transitory and even persistent corneal edema after the use of this drug intraocularly to induce miosis. In the majority of cases of persistent corneal edema that have

been reported to the registry, the surgeon reformed the anterior chamber at the end of the procedure with this solution. This procedure is not intended by the manufacturer and should not be performed. That this is, indeed, a drug-related event is most difficult to prove, since in any operative procedure, inadvertent endothelium trauma can occur with resultant corneal edema, and the drug might incorrectly be implicated. However, there are a number of cases in the registry that suggest a possible rela¬ tionship. This drug is commonly used and only a rare adverse reaction has been reported; however, with in¬ creased procedures that have a poten¬ tial of endothelial trauma during the

operation (intraocular lenses, phacoemulsification) or in surgical proce¬

dures with more endothelial trauma than usual, bathing these cells with a solution with a pH of 5.2 theoretically may not be in the patient's best inter¬ est. Therefore, we agree with the above authors that carbachol should be used with caution in patients with increased endothelial trauma, Fuchs' dystrophy, or in corneal transplant surgery. Frederick T. Fraunfelder Portland, Ore Name and Trademarks of Drug

Nonproprietary

Carbachol-Caròacei Bufopto, Carbamiotin, Miostat, Mistura C, P.V. Carbachol.

Treatment of

Malignant Melanoma

To the Editor.\p=m-\Ina

recently published

article, Zimmerman

et al1 of the Armed Forces Institute of Pathology challenge the standard oncologic treatment of a malignancy, that is, en bloc excision. In a study of malignant melanoma of the choroid and ciliary body, they suggest that the enucleation of the affected eye actually may be the cause of the dissemination of tumor cells, resulting in metastatic disease. This conclusion is based on two observations. First, citing sub-

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stantial data, Zimmerman et al state that "the mortality rate before enucleation is low, estimated at 1% per year, and that [it] rises abruptly

following enucleation, reaching a peak

of about 8% during the second year after enucleation." Second, they observe that "uveal melanomas . are rarely observed to have metastasized before that patient is referred for treatment for the primary tumor."1 While I do not argue with the observations of Zimmerman et al, I most emphatically question their conclusion. I suggest that the high mortality observed by them in the second year after enucleation is merely the normal biologic activity of a tumor as noted in other types of malignancies, specifi¬ cally that of the breast. Interestingly, in a study of 505 patients with breast cancer, Eggers et al,2 as noted by Park and Lees,3 found a similar type of mortality curve as that observed by Zimmerman et al. Their data corre¬ spond almost exactly to those noted by Zimmerman et al. They found that the number of deaths from a malignancy peaks at two years after diagnosis, whether or not there is surgical inter¬ vention. I suggest that the 8% mortal¬ ity will occur not because of enuclea¬ tion but as a result of the natural development of the tumor. The second major observation on which Zimmerman et al base their theory pertains to the low percentage of patients with overt métastases at the time that the choroidal melanoma is diagnosed. Similarly, we found a very low incidence of métastases in patients with choroidal melanoma at our institution (Ohio State University Hospitals, Columbus). We studied a series of 95 patients who had a complete medical workup prior to enucleation. Only one patient (1.05%) manifested signs of overt métastases. Zimmerman et al theorize that the development of metastatic disease after enucleation is a direct result of the enucleation. We believe that an alternative explanation for the in¬ crease in métastases after the proce¬ dure is that we are dealing with a growing tumor, and subclinical metastases have occurred prior to surgery. To test this theory, I reviewed the last 100 patients who were diagnosed with choroidal melanoma and whose eye was subsequently enucleated. In only 9% of these patients was a diagnosis made as a result of a routine eye examination. The rest were referred as a result of definite patient symp¬ toms, ie, decreased vision, flashers and floaters, and blurred vision. In fact, three of the nine patients who .

.

routinely did have some transient symptoms, which subsided before the time of examination. These data suggest that in at least 91% of the patients, sufficient change had occurred within the tumor to cause symptoms. It is logical to assume that a growing tumor is more likely to metastasize than one that exhibits no evidence of growth. Certainly, one cannot ignore the relationship be¬ tween tumor growth and métastases before enucleation. The 1% incidence of métastases found at the time of diagnosis may simply reflect our inability to detect early metastatic involvement. This theory, of course, is not new and is supported by Brennan in his study of breast carcinoma, when he reports on incidence of recurrent disease: "Almost certainly such hematogenous spread existed at the time of primary treatment but was subclinical and undetectable."4 Reese also states that "hematogenous dissemination of tumor cells is very likely to have occurred at the time the diagnosis is made."5 Ideally, of course, the surgeon should remove the tumor burden if it has the potential to metastasize but has not yet done so. The removal of a tumor after it has metastasized is of little value. Nevertheless, since the eventuality of metastatic spread is impossible to predict and occult mé¬ tastases are impossible to detect, it is important to consider the available information about the neoplasm when considering treatment. Clinical evi¬ dence clearly demonstrates a more favorable survival rate for patients with small tumors (less than 10 mm in diameter and less than 3 mm in height) than for patients with large ones. Five-year mortalities for pa¬ tients with small melanomas were found to be 6.1% as compared with a 35.8% mortality in patients with large tumors. Comparison of ten-year mor¬ talities showed 22.7% for patients with small melanomas to 46.0% for patients with larger tumors." The lethality of the tumor also depends on variables such as cell type and mitotic activity. In spite of sophisticated clinical and laboratory studies on melanomas, it is impossible to detect the difference between spindle cell tumors and epithelial cell tumors in vivo. Clearly, therefore, some malignant melano¬ mas are potentially lethal tumors; large tumors are more lethal than small tumors. Failure to enucleate theoretically allows a tumor to grow and metastasize, which would ulti¬ mately result in the patient's death. Certainly, enucleation is not the were seen

indicated

malignant

procedure

in all

cases

of

menanoma; many factors

influence the physician's decision. Age and the patient's general health are two important factors. For exam¬ ple, an 85-year-old patient with a malignant melanoma only has an average life expectancy of six years.7 To subject this patient to a procedure that would almost assuredly not increase his survival would not be a prudent choice. A 60-year-old patient,

however, presents a more philosophi¬ cal problem to the physician, since this patient's life expectancy is 19 years.7 This fact must be weighed against the mortality for patients with ocular melanoma when deciding whether to enucleate.

Finally, a word must be said about the so-called conservative treatment of choroidal malignant melanomas. Before one becomes too enthusiastic about the favorable survival rates in these patients, it must be remembered that most of these tumors measure 10 mm in diameter or less and generally have a more favorable prognosis than larger tumor. Therefore, any com¬ parison between conservative treat¬ a

ment and enucleation must be based on

patients with small large ones.

mortalities for

tumors and not

The basic concept of cancer surgery is to eliminate the tumor burden from the body. It is the goal of enucleation to achieve this end. While I do not deny the possibility that some tumors do not have metastatic potential, until we can unquestionably isolate them from those tumors that do, for all but very small tumors, enucleation must be the indicated procedure. For many patients, the failure to perform such procedures may mean the develop¬ ment of avoidable metastatic disFrederick H. Davidorf, MD Columbus, Ohio 1. Zimmerman LE, McLean IW, Foster WD: Does enucleation of the eye containing a malignant melanoma prevent or accelerate the dissemination of tumor cells? Br J Ophthalmol 62:420\x=req-\ 425, 1978. 2. Eggers C, deCholnoky T, Jessup DSD: Cancer of the breast. Ann Surg 113:321-340, 1941. 3. Park WW, Lees JC: The absolute curability of cancer of the breast. Surg Gynecol Obstet 93:129-152, 1951. 4. Brennan MJ: Breast cancer, in Holland JF, Frei E III (eds): Cancer Medicine. Philadelphia, Lea & Febiger Publishers, 1974, p 1778. 5. Reese AB: Tumors of the Eye. New York, Harper & Row Publishers, 1963, p 241. 6. Davidorf FH, Lang JR: The natural history of malignant melanoma of the choroid: Small vs large tumors. Trans Am Acad Ophthalmol Otolaryngol 79:310-320, 1975. 7. Newspaper Enterprise Association Inc: The World Almanac and Book of Facts 1978. New York, Doubleday & Co, 1978, p 955.

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Treatment of malignant melanoma.

Ocular Bottles Injuries From Beverage To the Editor.\p=m-\Therecent article in the Archives entitled "Ocular Injuries From Exploding Beverage Bott...
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