- Email: [email protected]
Intraoperative Fibrinolysis of Submacular Hemorrhage With Tissue Plasminogen Activator and Surgical Drainage
4. Kokame GT. Recurrence of macular holes. Ophthalmology 1995;102:172-3.
Intraoperative Fibrinolysis of Submacular Hemorrhage With Tissue Plasminogen Activator and Surgical Drainage EDITOR: IN THE ARTICLE, "INTRAOPERATIVE FIBRINOLYSIS OF SUB-
macular hemorrhage with tissue plasminogen activator and surgical drainage" by H. Lewis (Am. J. Ophthalmol. 118:559-68, November 1994), the author assumed that the visual prognosis for eyes with submacular hemorrhage and age-related macular degeneration was destined to be poor because of destructive effect produced by the fibrin portion of the clot. That assumption requires clarification. The presence of an underlying choroidal neovascular membrane, the sine qua non for such cases, and the pigment epithelial destruction that follows activation of a neovascular membrane provide the explanation for the poor visual outcome of such eyes. The degree to which the hemorrhagic component contributes to the mechanical injury sustained by the macula has not received adequate study, it is true, and Dr. Lewis is to be commended for his efforts in that regard. But for the purpose of his study, the question is whether or not the hemorrhagic component markedly decreases the visual prognosis beyond that which results from the development of the choroidal neovascular membrane alone. The necessity for clarification becomes apparent when one analyzes the results of the study. Only six (26%) of the 23 eyes that were examined by fluorescein angiography in the postoperative period showed evidence of a choroidal neovascular membrane. That finding elicits two responses. First, what happened to the choroidal neovascular membrane in the 17 eyes? Second, did the presumed disappearance of the choroidal neovascular membrane, in the 17 eyes, affect the overall visual results? Dr. Lewis contends that the visual outcome for his series of cases was improved, in comparison to no treatment at all, by the pharmacologie lysis procedure. If so, to what should we credit the improvement? He 550
focuses on the extraction of the hemorrhage. Conversely, I would attribute whatever improvement that was realized, in large part, to the disappearance of the choroidal neovascular membrane. Dr. Lewis concluded that the operative procedure caused regression of the choroidal neovascular membrane for the 17 eyes. The commonly accepted notion is that a contracted and inactive submacular choroidal neovascular membrane continues to exhibit a prominent degree of hyperfluorescence. A n alternate explanation is that the choroidal neovascular membrane was removed during the procedure, for the 17 eyes. Perhaps, those choroidal neovascular membranes with a glial component of minimal severity were aspirated, in some manner, along with the liquified blood. Perhaps some of the choroidal neovascular membranes with a more substantial glial component were mechanically extracted along with, and while attached to, the submacular blood clot. Whatever the explanation, we are left with an inability to reconcile the results of Dr. Lewis's study. Was the visual improvement primarily the result of the removal of the hemorrhage, the disappearance of the choroidal neovascular membrane, or both? The supplied information is not sufficient to provide an answer. The degree to which submacular hemorrhage extraction, by pharmacologie method or otherwise, affects the macular recovery and the visual potential for an eye remains unknown. As a final comment, I take exception to the angiographie interpretation supplied for Dr. Lewis for Figure 7 in his article. The preoperative angiogram (Fig. 7, top right) shows hyperfluorescence immediately superonasal to the fovea, a finding Dr. Lewis failed to acknowledge in the legend. It would seem fair to assume, at that initial time in the evaluation process, that the choroidal neovascular membrane responsible for the submacular hemorrhage extended beneath the superonasal portion of the macula, at the very least. The postoperative angiogram (Fig. 7, bottom left and right) demonstrated, for the postinjection interval photographed, prominent hyperfluorescence immediately inferotemporal to the fovea. Dr. Lewis classified the choroidal neovascular membrane as extrafoveal. Analysis of the postoperative photographs discloses, however, a subpigment epithelial
AMERICAN JOURNAL OF OPHTHALMOLOGY
OCTOBER 1995
corona of red blood cells that encircle not only an extrafoveal choroidal neovascular membrane, but also a subfoveal portion of the membrane as well. One can confidently conclude, even without the assistance of indocyanine green angiography, that laser coagulation of the prominently fluorescent extrafoveal site for such an eye would, in the long run, be doomed to failure. W. REX HAWKINS, M.D.
Houston, Texas
AUTHOR REPLY I THANK DR. HAWKINS FOR HIS INTEREST IN MY ARTICLE.
Submacular hemorrhage is associated with a poor visual prognosis caused by multiple factors, which were listed in the third paragraph of the discussion of my article. One of these factors is indeed fibrinmediated retinal damage as it was elegantly demonstrated by Toth and associates.1 Dr. Hawkins states that an underlying choroidal neovascular membrane and retinal pigment epithelial destruction, rather than the hemorrhage itself, is the cause for the poor visual outcome, and that it is not possible to determine postoperatively if the visual improvement is the result of the removal of the hemorrhage or the disappearance of the choroidal neovascular membrane, or both. Rather than the choroidal neovascular membrane itself, it is the leaky substances such as blood, lipid, plasma, fibrin, and the like, that damage the sensory retina and lead to a poor visual outcome. Not all patients with subfoveal choroidal neovascularization have a poor prognosis. These patients can sometimes enjoy good visual function, particularly when the choroidal neovascular membrane is not leaking or when it is located under the retinal pigment epithelium and there is apposition of the retinal pigment epithelium to the sensory retina.2,3 Clinicopathologic studies of laser-treated choroidal neovascularization have demonstrated that choroidal neovascularization can still be present despite that we cannot visualize it clinically or angiographically (involuted or obliterated choroidal neovascularization).4 Dr. Hawkins also states that the degree to which the hemorrhagic component contributes to the mechanical injury sustained by the macula has not received adequate study. Although we all would like more studies to be VOL.UO, No. 4
available, I would point to the existing literature on this topic listed as references 1 to 4 of the original article.1,5'7 Dr. Hawkins questions "whether or not the hemorrhagic component markedly decreases the visual prognosis beyond that which results from the development of the choroidal neovascular membrane alone." According to the Macular Photocoagulation Study, patients with classic subfoveal choroidal neovascularization in age-related macular degeneration without treatment had an average visual acuity of 20/400 after two years.8 Eyes with occult subfoveal choroidal neovascularization have a better visual prognosis.2,3 In a study by Soubrane and associates,2 60% of the eyes had an initial visual acuity of 20/50 or better and 36% of the eyes had a final ( 12 to 95 months) visual acuity of 20/50 or better. In another study of occult subfoveal choroidal neovascularization, 25% of the eyes had a visual acuity of 20/40 or better, and the average final (six to 53 months) visual acuity was 20/250.3 In contrast, a study of eyes with submacular hemorrhage secondary to age-related macular degeneration demonstrated a markedly worse visual prognosis with patients having an average final visual acuity of 20/1700.7 I do not have a better explanation than the one I gave in paragraph 12 of the discussion regarding the failure to visualize choroidal neovascularization angiographically after removal of the submacular hemorrhage. I have been able to review the fluorescein angiograms of five patients before the development of the submacular hemorrhage, and they all demonstrate occult choroidal neovascularization caused by leakage of an undetermined source. To date, we do not have much information of the histopathologic factors or behavior of occult choroidal neovascularization because of leakage of the undetermined source, and we could only speculate on the mechanisms that lead to involution of these membranes. Glaser and associates9 have suggested that factors and substances released by stimulated retinal pigment epithelium or other cells may play a role in containment and resolution of choroidal neovascularization. Experimental studies by Miller, Miller, and Ryan10 suggest that involution of choroidal neovascularization with cessation of visible fluorescein leakage is the result of retinal pigment epithelium proliferation that envelopes the choroidal neovascular membrane and probably resorbs the
CORRESPONDENCE
551
Intraoperative Fibrinolysis of Submacular Hemorrhage With Tissue Plasminogen Activator and Surgical Drainage EDITOR: IN THE ARTICLE, "INTRAOPERATIVE FIBRINOLYSIS OF SUB-
macular hemorrhage with tissue plasminogen activator and surgical drainage" by H. Lewis (Am. J. Ophthalmol. 118:559-68, November 1994), the author assumed that the visual prognosis for eyes with submacular hemorrhage and age-related macular degeneration was destined to be poor because of destructive effect produced by the fibrin portion of the clot. That assumption requires clarification. The presence of an underlying choroidal neovascular membrane, the sine qua non for such cases, and the pigment epithelial destruction that follows activation of a neovascular membrane provide the explanation for the poor visual outcome of such eyes. The degree to which the hemorrhagic component contributes to the mechanical injury sustained by the macula has not received adequate study, it is true, and Dr. Lewis is to be commended for his efforts in that regard. But for the purpose of his study, the question is whether or not the hemorrhagic component markedly decreases the visual prognosis beyond that which results from the development of the choroidal neovascular membrane alone. The necessity for clarification becomes apparent when one analyzes the results of the study. Only six (26%) of the 23 eyes that were examined by fluorescein angiography in the postoperative period showed evidence of a choroidal neovascular membrane. That finding elicits two responses. First, what happened to the choroidal neovascular membrane in the 17 eyes? Second, did the presumed disappearance of the choroidal neovascular membrane, in the 17 eyes, affect the overall visual results? Dr. Lewis contends that the visual outcome for his series of cases was improved, in comparison to no treatment at all, by the pharmacologie lysis procedure. If so, to what should we credit the improvement? He 550
focuses on the extraction of the hemorrhage. Conversely, I would attribute whatever improvement that was realized, in large part, to the disappearance of the choroidal neovascular membrane. Dr. Lewis concluded that the operative procedure caused regression of the choroidal neovascular membrane for the 17 eyes. The commonly accepted notion is that a contracted and inactive submacular choroidal neovascular membrane continues to exhibit a prominent degree of hyperfluorescence. A n alternate explanation is that the choroidal neovascular membrane was removed during the procedure, for the 17 eyes. Perhaps, those choroidal neovascular membranes with a glial component of minimal severity were aspirated, in some manner, along with the liquified blood. Perhaps some of the choroidal neovascular membranes with a more substantial glial component were mechanically extracted along with, and while attached to, the submacular blood clot. Whatever the explanation, we are left with an inability to reconcile the results of Dr. Lewis's study. Was the visual improvement primarily the result of the removal of the hemorrhage, the disappearance of the choroidal neovascular membrane, or both? The supplied information is not sufficient to provide an answer. The degree to which submacular hemorrhage extraction, by pharmacologie method or otherwise, affects the macular recovery and the visual potential for an eye remains unknown. As a final comment, I take exception to the angiographie interpretation supplied for Dr. Lewis for Figure 7 in his article. The preoperative angiogram (Fig. 7, top right) shows hyperfluorescence immediately superonasal to the fovea, a finding Dr. Lewis failed to acknowledge in the legend. It would seem fair to assume, at that initial time in the evaluation process, that the choroidal neovascular membrane responsible for the submacular hemorrhage extended beneath the superonasal portion of the macula, at the very least. The postoperative angiogram (Fig. 7, bottom left and right) demonstrated, for the postinjection interval photographed, prominent hyperfluorescence immediately inferotemporal to the fovea. Dr. Lewis classified the choroidal neovascular membrane as extrafoveal. Analysis of the postoperative photographs discloses, however, a subpigment epithelial
AMERICAN JOURNAL OF OPHTHALMOLOGY
OCTOBER 1995
corona of red blood cells that encircle not only an extrafoveal choroidal neovascular membrane, but also a subfoveal portion of the membrane as well. One can confidently conclude, even without the assistance of indocyanine green angiography, that laser coagulation of the prominently fluorescent extrafoveal site for such an eye would, in the long run, be doomed to failure. W. REX HAWKINS, M.D.
Houston, Texas
AUTHOR REPLY I THANK DR. HAWKINS FOR HIS INTEREST IN MY ARTICLE.
Submacular hemorrhage is associated with a poor visual prognosis caused by multiple factors, which were listed in the third paragraph of the discussion of my article. One of these factors is indeed fibrinmediated retinal damage as it was elegantly demonstrated by Toth and associates.1 Dr. Hawkins states that an underlying choroidal neovascular membrane and retinal pigment epithelial destruction, rather than the hemorrhage itself, is the cause for the poor visual outcome, and that it is not possible to determine postoperatively if the visual improvement is the result of the removal of the hemorrhage or the disappearance of the choroidal neovascular membrane, or both. Rather than the choroidal neovascular membrane itself, it is the leaky substances such as blood, lipid, plasma, fibrin, and the like, that damage the sensory retina and lead to a poor visual outcome. Not all patients with subfoveal choroidal neovascularization have a poor prognosis. These patients can sometimes enjoy good visual function, particularly when the choroidal neovascular membrane is not leaking or when it is located under the retinal pigment epithelium and there is apposition of the retinal pigment epithelium to the sensory retina.2,3 Clinicopathologic studies of laser-treated choroidal neovascularization have demonstrated that choroidal neovascularization can still be present despite that we cannot visualize it clinically or angiographically (involuted or obliterated choroidal neovascularization).4 Dr. Hawkins also states that the degree to which the hemorrhagic component contributes to the mechanical injury sustained by the macula has not received adequate study. Although we all would like more studies to be VOL.UO, No. 4
available, I would point to the existing literature on this topic listed as references 1 to 4 of the original article.1,5'7 Dr. Hawkins questions "whether or not the hemorrhagic component markedly decreases the visual prognosis beyond that which results from the development of the choroidal neovascular membrane alone." According to the Macular Photocoagulation Study, patients with classic subfoveal choroidal neovascularization in age-related macular degeneration without treatment had an average visual acuity of 20/400 after two years.8 Eyes with occult subfoveal choroidal neovascularization have a better visual prognosis.2,3 In a study by Soubrane and associates,2 60% of the eyes had an initial visual acuity of 20/50 or better and 36% of the eyes had a final ( 12 to 95 months) visual acuity of 20/50 or better. In another study of occult subfoveal choroidal neovascularization, 25% of the eyes had a visual acuity of 20/40 or better, and the average final (six to 53 months) visual acuity was 20/250.3 In contrast, a study of eyes with submacular hemorrhage secondary to age-related macular degeneration demonstrated a markedly worse visual prognosis with patients having an average final visual acuity of 20/1700.7 I do not have a better explanation than the one I gave in paragraph 12 of the discussion regarding the failure to visualize choroidal neovascularization angiographically after removal of the submacular hemorrhage. I have been able to review the fluorescein angiograms of five patients before the development of the submacular hemorrhage, and they all demonstrate occult choroidal neovascularization caused by leakage of an undetermined source. To date, we do not have much information of the histopathologic factors or behavior of occult choroidal neovascularization because of leakage of the undetermined source, and we could only speculate on the mechanisms that lead to involution of these membranes. Glaser and associates9 have suggested that factors and substances released by stimulated retinal pigment epithelium or other cells may play a role in containment and resolution of choroidal neovascularization. Experimental studies by Miller, Miller, and Ryan10 suggest that involution of choroidal neovascularization with cessation of visible fluorescein leakage is the result of retinal pigment epithelium proliferation that envelopes the choroidal neovascular membrane and probably resorbs the
CORRESPONDENCE
551