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Re: Urological Complications of Sickle Cell Disease in a Pediatric Population, by W. F. Tarry, J. W. Duckett, Jr. and H. McC. Snyder, III, J. Urol., 138: 592–594, 1987
1554
LETTERS TO THE EDITOR
contrary, we believe that these manipulations complicate the surgical maneuver rather than simplify it. We are not opposed to the suggestion that revascularization of an anencephalic kidney should be done by a vascular surgeon at hospitals where there may be special circumstances that dictate the necessity but by no means is this absolutely necessary at all hospitals to date. Mixed teams of vascular and urological surgeons did have justification in the "early days" of transplants but the training programs of the new generation of urologists include periods of intense practical experience and theoretical instruction in several surgical departments. The urological teams of a Renal Transplant Center at a large regional hospital collectively treat successfully a large number of cases each year and many of the interventions involve a multiplicity of vascular corrections with standard microsurgical techniques. These techniques are rehearsed in the laboratory during a series of supervised and successful renal transplant operations on rats whose vessels are considerably smaller than those of the neonate. RE: PREDICTIVE CRITERIA FOR FAILED SPHINCTEROTOMY IN SPINAL CORD INJURY PATIENTS
J. K. Light, A. Eerie and P. G. Wise J. Urol., 138: 1201-1204, 1987
To the Editor. I was surprised that the authors considered a large post-void residual urine their criterion for failure of sphincterotomy in spinal cord injury patients. The purpose of sphincterotomy in these patients is to decrease bladder outlet resistance so that the patient will be capable of evacuating urine from the bladder at low pressure. Low bladder storage and micturition pressures are related to preservation of normal upper tract function and freedom from febrile urinary tract infection. 1 This is the actual goal of the surgery and, therefore, this alone should be used to judge the success or failure of the procedure. Examination of the maximum intravesical pressures before voiding reveals excellent reduction to 40 cm. water pressure in 8 of their 9 patients. The remaining patient had a reduction from 68 to 45 cm. water pressure. If concern persists regarding a large post-void residual urine level then low pressure Crede's maneuvercan be performed. Reflex vesical activity does not continue until bladder emptying because bladder activity following spinal cord injury is typically nonfacilitated. 2 The "subtle dysfunction of the lumbosacral area" described by the authors suggests an etiology for unsustained bladder contractions after spinal cord injury. Their hypothesis is reasonable and objective electromyographic data are presented for substantiation. Nevertheless, these poorly facilitated bladder contractions and resultant large post-void residual urines should be expected by urologists performing this surgery. Total sphincterotomy with Crede's expression voiding is necessary to induce complete bladder emptying in most patients with suprasacral spinal cord injury. 3 It would be interesting to know how many other spinal cord injury patients the authors treated by sphincterotomy during this same period. These patients who obtained a presumably normal post-void residual urine were their surgical success group and not reported. My suspicion is that with long-term followup they will fare no differently than the failed sphincterotomy group. This study presents urodynamic data that serve to elucidate a mechanism for nonfacilitated bladder contractions following spinal cord injury. However, the success of sphincterotomy should be based on the elimination of febrile urinary tract infections and the long-term survival of renal units rather than post-void residual urine levels. I considered the operation successful in the patients reported because it produced acceptable maximum intravesical pressures as required. Respectfully, Eric J. Zeidman Department of Surgery/Urology Service Brooke Army Medical Center San Antonio, Texas 78234 The opinions expressed herein are those of the author and do not necessarily reflect those of the Department of the Army or the Department of Defense.
r,
"'."oo~side, ,!- R. a~d Borden, T. A.: Upper urinary tract deterioration m patients with myelodysplasia and detrusor hyp~rtonia: a followup study. J. Urol., 129: 823, 1983. 2. McGuire, E. J. and Brady, S.: Detrusor-sphincter dyssynergia. J. Urol., 121: 774, 1979. 1. McGuire, E.
3. Perkash, I.: An attempt to understand and to treat voiding dysfunctions during rehabilitation of the bladder in spinal cord injury patients. J. Urol., 115: 36, 1976.
Reply by Authors. Doctor Zeidman is correct when he states that a decreased bladder pressure resulting from a decrease in bladder outlet resistance is the aim of sphincterotomy. However, the purpose of the operation is to decrease post-void residuals and, thus, to decrease episodes of dysreflexia and symptomatic urinary tract infections. As indicated in the article large post-void residuals persisted in this particular group of patients despite an adequate surgical result. This has clinical significance, since 6 of the 9 patients continued to have precisely the same symptomatology that resulted in the sphincterotomy, that is recurrent symptomatic urinary tract infections and repeated episodes of autonomic dysreflexia. This necessitated the insertion of permanent tube drainage, a solution, which if it could have been predicted, would have saved the patient an unnecessary operation. In addition, the majority of patients suffering from a distinct separate lumbosacral dysfunction are inevitably quadriplegics in whom the Crede maneuver is not possible. This particular syndrome, that is the development of detrusor hypocontractility following sphincterotomy, appears to be peculiar to the high thoracic or low cervical spinal cord injuries. We have not observed this with mid or low thoracic lesions. It was this very observation that led us to evaluate further this particular group of patients. Further experience has revealed that approximately 30 per cent of the patients with cervical spinal cord injuries will have some degree of lumbosacral dysfunction. The neurophysiological evaluation of these patients is important, not only to understand further the abnormal physiology following spinal cord injury, but also from a clinical viewpoint.
RE: UROLOGICAL COMPLICATIONS OF SICKLE CELL DISEASE IN A PEDIATRIC POPULATION
W. F. Tarry, J. W. Duckett, Jr. and H. McC. Snyder, III J. Urol., 138: 592-594, 1987
To the Editor. The urological complications of sickle cell disease in a pediatric population are addressed well by the authors of this article. However, we must differ with their statement that for priapism in the sickle cell patient the "management rarely is surgical". Of their 10 reported patients 2 ultimately underwent surgical attempts to correct this problem. This 20 per cent rate of surgical intervention can hardly be considered rare. We reported previously our experience with a large population of patients with sickle cell disease and, in particular, the management of priapism within this group. 1 We have continued to add to the original numbers and are convinced that shunting procedures, that is the glandular cavernosal shunt, do, indeed, have a role in the management of priapism in the sickle cell patient. Although the authors cite the potential for a high rate of surgical and anesthetic complications, such has not been our experience even in our expanded series. We have had no anesthetic or surgical complications and the shunting procedure has enjoyed a high success rate in our hands. We believe that with proper anesthetic management, particularly in the well prepared child who has undergone preoperative hypertransfusion, shunting appears to be a safe and reliable measure to relieve priapism in a sickle cell patient. Emond and associates found that 20 per cent of their sickle cell patients had partial impotence and 16 per cent had total impotence, which, if this holds true in the sickle cell population, provides a tremendous challenge to prevent this disorder when possible.2 Our successful surgical experience apparently also has been shared by others in attempts to reach this goal. 3 Given the increasing survival rate of patients with sickle cell disease, it is highly likely that the problem with impotence also will be an increasing problem in this population. None of our original patients is impotent. However, we have participated in the followup management of 3 patients who, because of prior episodes of prolonged untreated priapism, suffered fibrosis of the corpora and secondary impotence. These patients are extremely difficult to treat in terms of placing a penile prosthesis. In 1 instance the procedure for implantation had to be abandoned because no discernible plane or cavity could be developed in which to place the prosthesis. This appears to be the experience of a number of prosthetic surgeons, and it further highlights the need for aggressive early treatment of
LETTERS TO T~lE EDITOR priapism in this population to prevent importance and the difficulties in treatment in the adult years. In addition to consideration of the possible problem of impotence, other factors, such as shortened hospital stay and patient comfort, in our experience have been provided by earlier shunting, since we have become convinced that it is a safe procedure in our hands. We do not disagree with the authors in attempting first to hydrate the patient and next to transfuse them in an attempt to reduce viscosity and increase oxygen-carrying capacity and so forth. After these initial steps are performed, we disagree with observing patients with continuedpriapism for as long as the stated 12 days because we believe that this increases the later chances of corporeal fibrosis and impotence. Although it is true that only a minority of sickle cell patients with priapism have impotence, it is clear from our experience that when impotence with this etiology occurs it can be disastrous. For the aforementioned reasons, we believe that shunting in the management of priapism has an important role. It certainly is not the first line of treatment but it is by no means rarely indicated. Even the authors' description of the surgical intervention confirms this. To withhold shunting procedures completely from these patients would perhaps be doing them a tremendous disservice that cannot be rectified easily by current techniques to treat impotence in adults. Another consideration is that additional procedures as an adult have a higher risk than the early shunting procedure. Respectfully, H. Norman Noe and Gerald R. Jerkins Department of Pediatric Urology University of Tennessee Health Sciences Center 848 Adams Avenue, Suite 403 Memphis, Tennessee 38103 1. Noe, H. N., Wilimas, J. and Jerkins, G. R.: Surgical management of priapism in children with sickle cell anemia. J. Urol., 126: 770, 1981. 2. Emond, A. M., Holman, R., Hayes, R. J. and Serjeant, G. R.: Priapism and impotence in homozygous sickle cell disease. Arch. Intern. Med., 140: 1434, 1980. 3. Howe, G. E., Prentiss, R. J., Cole, J. W. and Masters, R. H.: Priapism: a surgical emergency. J. Urol., 101: 576, 1969.
Reply by Authors. We emphasized the favorable results that we and others have seen with hypertransfusion of sickle cell patients with priapism. We have not resorted to a shunt since 1975. Perhaps we have just been fortunate. Actually, there is no statistical difference between our 2 of 10 patients shunted and the 5 of 9 reported on by Noe and associates (reference 1 in Letter). It is not surprising that untreated priapism, as in the cases of Emond and associates (reference 2 in Letter) and the 3 older patients described by Noe and associates, should produce more severe corporeal fibrosis and a higher impotence rate. However, such patients often have had multiple episodes ofpriapism during the years. A question that remains unanswered is whether a shunt in childhood remains patent for life and protects against recurrent priapism in the patient so predisposed after no treatment or medical management. We agree with Leiter's Editorial Comment to the article by Noe and associates that "the logical treatment ... must rest on the treatment of the underlying abnormality rather than the surgical resolution of the secondary priapism. Nevertheless ... should nonoperative methods, such as hydration and hypertransfusion, fail to result in resolution of the erection then a prompt shunting procedure is indicated."
parenchyma over the deep surface of the tunica during the filling of the vascular spaces with blood and the establishment of erection".' This paragraph at no point suggests that such a suspected sliding contributes to the cause of erection but only that it could be a consequence of the erecting corpora cavernosa. Kiss described the sub-albugineal veins and venous plexuses. 2 He conceived the idea that during erection these veins are compressed against the deep surface of the tunica albuginea, thus slowing down or obstructing the outflow of blood from the corpora cavernosa during erection. He also suggests the possible mechanism that the cavernosal spaces in the sub-albugineal area are small and flat. During erection and the filling of the corpora cavernosa with blood the more axially located sinusoids, which are the larger capillaries that start filling first, increase pressure against the sub-albugineal sinusoids, thus slowing down the outflow of blood. Braus adopted the same concepts 3 but later Stieve, based on his anatomical experiments, disagreed with them. 4 The authors performed cavernosography and cavernosometry in dogs and, while they injected intracavernosally different vasodilators, some substances resulted in intracavernosal pressures of greater than 450 mm. Hg. Their rates are similar to those obtained by us using a noninvasive pressure measuring technique in young men with strong erections produced by mental stimulation. 5 While trying to explain obstructive mechanisms for the outflow of blood from the corpora cavernosa during erection, the authors do not attempt to explain the mechanism that prevents reflux into the arteries when high intracavernosal pressures develop. It is probably a misconception to refer to smooth muscle in the sinusoidal walls. The smooth muscle of the corpora does not form walls around the sinusoids. The intracorporocavernosal muscle is arranged in bundles that establish insertions to the deep surface of the tunica albuginea, its fibrous columns and on all of the fibrous elements of the fibrous skeleton of the corpora cavernosa. 6 The radiographic proof that during erection blood does not penetrate the perialbugineal veins possibly could be the result of several associated mechanisms, such as compression of sub-albugineal sinusoids and veins, contraction of circumflex veins that contain strong muscular "polsters" and possibly some participation of complex valves located in the circumflex veins. The article indicates that there is much to learn about the micro-architecture of the corpora and their intrinsic physiology.
1.
2. 3.
4. 5. 6.
RE: THE VENO-OCCLUSIVE MECHANISM OF THE CANINE CORPUS CAVERNOSUM: ANGIOGRAPHIC AND PHARMACOLOGIC STUDIES
K. Valji and J. J. Bookstein
J. Urol., 138: 1467-1470, 1987 To the Editor. In their discussion of the different concepts regarding the intrinsic mechanism of erection the authors cite our article. 1 However, they have misread our concept. After our discussion of a possible mechanism of erection we added the following paragraph of pure anatomical interest: "The thin layer of loose connective tissue between the parenchyma and the corpora cavernosa and the deep surface of the tunica albuginea possibly facilitates some sliding of the corporeal
1555
Respectfully, A. M. B. Goldstein, J.P. Meehon, R. Zakhary, P. A. Buckley and F. A. Rogers Department of Surgery, Division of Urology University of Southern California Medical Center 1200 North State Street Los Angeles, California 90033 Goldstein, A. M. B., Meehan, J.P., Zakhary, R., Buckley, P.A. and Rogers, F. A.: New observations on microarchitecture of corpora cavernosa in man and possible relationship to mechanism of erection. Urology, 20: 259, 1982. Kiss, F.: Anatomisch-histologische Untersuchungen iiber die Erektion. Ztschr. ges. Anat., 61: 455, 1921. Braus, H.: Anatomie des Menschen. Berlin: Verlag von Julius Springer, vol. 2, pp. 441-447, 1924. Stieve, H.: Handbuck der Mikroskopischen. Anatomie des Menschen. Berlin: Springer von Julius Springer, vol. 7, pp. 321339, 1930. Meehan, J.P. and Goldstein, A. M. B.: High pressure within corpus cavernosum in man during erection. Its probable mechanism. Urology, 21: 385, 1983. Goldstein, A. M. B., Meehan, J.P., Morrow, J. W., Buckley, P.A. and Rogers, F. A.: The fibrous skeleton of the corpora cavernosa and its probable function in the mechanism of erection. Brit. J. Urol., 57: 574, 1985.
Reply by Authors. We agree that the article by Doctor Goldstein and associates does not directly state that a sliding mechanism might be responsible for veno-occlusion; perhaps that conclusion was largely our own. At any rate, we believe that Doctor Goldstein and associates deserve credit for postulating the presence of a sliding mechanism on the basis of their anatomical observations, regardless of any possible veno-occlusive role, and that their postulate deserved further study. Therefore, we carefully observed the position and angulation of cavernosal septations and venous perforators with respect to each other and with respect to adjacent fixed bony landmarks before and after canine
LETTERS TO THE EDITOR
contrary, we believe that these manipulations complicate the surgical maneuver rather than simplify it. We are not opposed to the suggestion that revascularization of an anencephalic kidney should be done by a vascular surgeon at hospitals where there may be special circumstances that dictate the necessity but by no means is this absolutely necessary at all hospitals to date. Mixed teams of vascular and urological surgeons did have justification in the "early days" of transplants but the training programs of the new generation of urologists include periods of intense practical experience and theoretical instruction in several surgical departments. The urological teams of a Renal Transplant Center at a large regional hospital collectively treat successfully a large number of cases each year and many of the interventions involve a multiplicity of vascular corrections with standard microsurgical techniques. These techniques are rehearsed in the laboratory during a series of supervised and successful renal transplant operations on rats whose vessels are considerably smaller than those of the neonate. RE: PREDICTIVE CRITERIA FOR FAILED SPHINCTEROTOMY IN SPINAL CORD INJURY PATIENTS
J. K. Light, A. Eerie and P. G. Wise J. Urol., 138: 1201-1204, 1987
To the Editor. I was surprised that the authors considered a large post-void residual urine their criterion for failure of sphincterotomy in spinal cord injury patients. The purpose of sphincterotomy in these patients is to decrease bladder outlet resistance so that the patient will be capable of evacuating urine from the bladder at low pressure. Low bladder storage and micturition pressures are related to preservation of normal upper tract function and freedom from febrile urinary tract infection. 1 This is the actual goal of the surgery and, therefore, this alone should be used to judge the success or failure of the procedure. Examination of the maximum intravesical pressures before voiding reveals excellent reduction to 40 cm. water pressure in 8 of their 9 patients. The remaining patient had a reduction from 68 to 45 cm. water pressure. If concern persists regarding a large post-void residual urine level then low pressure Crede's maneuvercan be performed. Reflex vesical activity does not continue until bladder emptying because bladder activity following spinal cord injury is typically nonfacilitated. 2 The "subtle dysfunction of the lumbosacral area" described by the authors suggests an etiology for unsustained bladder contractions after spinal cord injury. Their hypothesis is reasonable and objective electromyographic data are presented for substantiation. Nevertheless, these poorly facilitated bladder contractions and resultant large post-void residual urines should be expected by urologists performing this surgery. Total sphincterotomy with Crede's expression voiding is necessary to induce complete bladder emptying in most patients with suprasacral spinal cord injury. 3 It would be interesting to know how many other spinal cord injury patients the authors treated by sphincterotomy during this same period. These patients who obtained a presumably normal post-void residual urine were their surgical success group and not reported. My suspicion is that with long-term followup they will fare no differently than the failed sphincterotomy group. This study presents urodynamic data that serve to elucidate a mechanism for nonfacilitated bladder contractions following spinal cord injury. However, the success of sphincterotomy should be based on the elimination of febrile urinary tract infections and the long-term survival of renal units rather than post-void residual urine levels. I considered the operation successful in the patients reported because it produced acceptable maximum intravesical pressures as required. Respectfully, Eric J. Zeidman Department of Surgery/Urology Service Brooke Army Medical Center San Antonio, Texas 78234 The opinions expressed herein are those of the author and do not necessarily reflect those of the Department of the Army or the Department of Defense.
r,
"'."oo~side, ,!- R. a~d Borden, T. A.: Upper urinary tract deterioration m patients with myelodysplasia and detrusor hyp~rtonia: a followup study. J. Urol., 129: 823, 1983. 2. McGuire, E. J. and Brady, S.: Detrusor-sphincter dyssynergia. J. Urol., 121: 774, 1979. 1. McGuire, E.
3. Perkash, I.: An attempt to understand and to treat voiding dysfunctions during rehabilitation of the bladder in spinal cord injury patients. J. Urol., 115: 36, 1976.
Reply by Authors. Doctor Zeidman is correct when he states that a decreased bladder pressure resulting from a decrease in bladder outlet resistance is the aim of sphincterotomy. However, the purpose of the operation is to decrease post-void residuals and, thus, to decrease episodes of dysreflexia and symptomatic urinary tract infections. As indicated in the article large post-void residuals persisted in this particular group of patients despite an adequate surgical result. This has clinical significance, since 6 of the 9 patients continued to have precisely the same symptomatology that resulted in the sphincterotomy, that is recurrent symptomatic urinary tract infections and repeated episodes of autonomic dysreflexia. This necessitated the insertion of permanent tube drainage, a solution, which if it could have been predicted, would have saved the patient an unnecessary operation. In addition, the majority of patients suffering from a distinct separate lumbosacral dysfunction are inevitably quadriplegics in whom the Crede maneuver is not possible. This particular syndrome, that is the development of detrusor hypocontractility following sphincterotomy, appears to be peculiar to the high thoracic or low cervical spinal cord injuries. We have not observed this with mid or low thoracic lesions. It was this very observation that led us to evaluate further this particular group of patients. Further experience has revealed that approximately 30 per cent of the patients with cervical spinal cord injuries will have some degree of lumbosacral dysfunction. The neurophysiological evaluation of these patients is important, not only to understand further the abnormal physiology following spinal cord injury, but also from a clinical viewpoint.
RE: UROLOGICAL COMPLICATIONS OF SICKLE CELL DISEASE IN A PEDIATRIC POPULATION
W. F. Tarry, J. W. Duckett, Jr. and H. McC. Snyder, III J. Urol., 138: 592-594, 1987
To the Editor. The urological complications of sickle cell disease in a pediatric population are addressed well by the authors of this article. However, we must differ with their statement that for priapism in the sickle cell patient the "management rarely is surgical". Of their 10 reported patients 2 ultimately underwent surgical attempts to correct this problem. This 20 per cent rate of surgical intervention can hardly be considered rare. We reported previously our experience with a large population of patients with sickle cell disease and, in particular, the management of priapism within this group. 1 We have continued to add to the original numbers and are convinced that shunting procedures, that is the glandular cavernosal shunt, do, indeed, have a role in the management of priapism in the sickle cell patient. Although the authors cite the potential for a high rate of surgical and anesthetic complications, such has not been our experience even in our expanded series. We have had no anesthetic or surgical complications and the shunting procedure has enjoyed a high success rate in our hands. We believe that with proper anesthetic management, particularly in the well prepared child who has undergone preoperative hypertransfusion, shunting appears to be a safe and reliable measure to relieve priapism in a sickle cell patient. Emond and associates found that 20 per cent of their sickle cell patients had partial impotence and 16 per cent had total impotence, which, if this holds true in the sickle cell population, provides a tremendous challenge to prevent this disorder when possible.2 Our successful surgical experience apparently also has been shared by others in attempts to reach this goal. 3 Given the increasing survival rate of patients with sickle cell disease, it is highly likely that the problem with impotence also will be an increasing problem in this population. None of our original patients is impotent. However, we have participated in the followup management of 3 patients who, because of prior episodes of prolonged untreated priapism, suffered fibrosis of the corpora and secondary impotence. These patients are extremely difficult to treat in terms of placing a penile prosthesis. In 1 instance the procedure for implantation had to be abandoned because no discernible plane or cavity could be developed in which to place the prosthesis. This appears to be the experience of a number of prosthetic surgeons, and it further highlights the need for aggressive early treatment of
LETTERS TO T~lE EDITOR priapism in this population to prevent importance and the difficulties in treatment in the adult years. In addition to consideration of the possible problem of impotence, other factors, such as shortened hospital stay and patient comfort, in our experience have been provided by earlier shunting, since we have become convinced that it is a safe procedure in our hands. We do not disagree with the authors in attempting first to hydrate the patient and next to transfuse them in an attempt to reduce viscosity and increase oxygen-carrying capacity and so forth. After these initial steps are performed, we disagree with observing patients with continuedpriapism for as long as the stated 12 days because we believe that this increases the later chances of corporeal fibrosis and impotence. Although it is true that only a minority of sickle cell patients with priapism have impotence, it is clear from our experience that when impotence with this etiology occurs it can be disastrous. For the aforementioned reasons, we believe that shunting in the management of priapism has an important role. It certainly is not the first line of treatment but it is by no means rarely indicated. Even the authors' description of the surgical intervention confirms this. To withhold shunting procedures completely from these patients would perhaps be doing them a tremendous disservice that cannot be rectified easily by current techniques to treat impotence in adults. Another consideration is that additional procedures as an adult have a higher risk than the early shunting procedure. Respectfully, H. Norman Noe and Gerald R. Jerkins Department of Pediatric Urology University of Tennessee Health Sciences Center 848 Adams Avenue, Suite 403 Memphis, Tennessee 38103 1. Noe, H. N., Wilimas, J. and Jerkins, G. R.: Surgical management of priapism in children with sickle cell anemia. J. Urol., 126: 770, 1981. 2. Emond, A. M., Holman, R., Hayes, R. J. and Serjeant, G. R.: Priapism and impotence in homozygous sickle cell disease. Arch. Intern. Med., 140: 1434, 1980. 3. Howe, G. E., Prentiss, R. J., Cole, J. W. and Masters, R. H.: Priapism: a surgical emergency. J. Urol., 101: 576, 1969.
Reply by Authors. We emphasized the favorable results that we and others have seen with hypertransfusion of sickle cell patients with priapism. We have not resorted to a shunt since 1975. Perhaps we have just been fortunate. Actually, there is no statistical difference between our 2 of 10 patients shunted and the 5 of 9 reported on by Noe and associates (reference 1 in Letter). It is not surprising that untreated priapism, as in the cases of Emond and associates (reference 2 in Letter) and the 3 older patients described by Noe and associates, should produce more severe corporeal fibrosis and a higher impotence rate. However, such patients often have had multiple episodes ofpriapism during the years. A question that remains unanswered is whether a shunt in childhood remains patent for life and protects against recurrent priapism in the patient so predisposed after no treatment or medical management. We agree with Leiter's Editorial Comment to the article by Noe and associates that "the logical treatment ... must rest on the treatment of the underlying abnormality rather than the surgical resolution of the secondary priapism. Nevertheless ... should nonoperative methods, such as hydration and hypertransfusion, fail to result in resolution of the erection then a prompt shunting procedure is indicated."
parenchyma over the deep surface of the tunica during the filling of the vascular spaces with blood and the establishment of erection".' This paragraph at no point suggests that such a suspected sliding contributes to the cause of erection but only that it could be a consequence of the erecting corpora cavernosa. Kiss described the sub-albugineal veins and venous plexuses. 2 He conceived the idea that during erection these veins are compressed against the deep surface of the tunica albuginea, thus slowing down or obstructing the outflow of blood from the corpora cavernosa during erection. He also suggests the possible mechanism that the cavernosal spaces in the sub-albugineal area are small and flat. During erection and the filling of the corpora cavernosa with blood the more axially located sinusoids, which are the larger capillaries that start filling first, increase pressure against the sub-albugineal sinusoids, thus slowing down the outflow of blood. Braus adopted the same concepts 3 but later Stieve, based on his anatomical experiments, disagreed with them. 4 The authors performed cavernosography and cavernosometry in dogs and, while they injected intracavernosally different vasodilators, some substances resulted in intracavernosal pressures of greater than 450 mm. Hg. Their rates are similar to those obtained by us using a noninvasive pressure measuring technique in young men with strong erections produced by mental stimulation. 5 While trying to explain obstructive mechanisms for the outflow of blood from the corpora cavernosa during erection, the authors do not attempt to explain the mechanism that prevents reflux into the arteries when high intracavernosal pressures develop. It is probably a misconception to refer to smooth muscle in the sinusoidal walls. The smooth muscle of the corpora does not form walls around the sinusoids. The intracorporocavernosal muscle is arranged in bundles that establish insertions to the deep surface of the tunica albuginea, its fibrous columns and on all of the fibrous elements of the fibrous skeleton of the corpora cavernosa. 6 The radiographic proof that during erection blood does not penetrate the perialbugineal veins possibly could be the result of several associated mechanisms, such as compression of sub-albugineal sinusoids and veins, contraction of circumflex veins that contain strong muscular "polsters" and possibly some participation of complex valves located in the circumflex veins. The article indicates that there is much to learn about the micro-architecture of the corpora and their intrinsic physiology.
1.
2. 3.
4. 5. 6.
RE: THE VENO-OCCLUSIVE MECHANISM OF THE CANINE CORPUS CAVERNOSUM: ANGIOGRAPHIC AND PHARMACOLOGIC STUDIES
K. Valji and J. J. Bookstein
J. Urol., 138: 1467-1470, 1987 To the Editor. In their discussion of the different concepts regarding the intrinsic mechanism of erection the authors cite our article. 1 However, they have misread our concept. After our discussion of a possible mechanism of erection we added the following paragraph of pure anatomical interest: "The thin layer of loose connective tissue between the parenchyma and the corpora cavernosa and the deep surface of the tunica albuginea possibly facilitates some sliding of the corporeal
1555
Respectfully, A. M. B. Goldstein, J.P. Meehon, R. Zakhary, P. A. Buckley and F. A. Rogers Department of Surgery, Division of Urology University of Southern California Medical Center 1200 North State Street Los Angeles, California 90033 Goldstein, A. M. B., Meehan, J.P., Zakhary, R., Buckley, P.A. and Rogers, F. A.: New observations on microarchitecture of corpora cavernosa in man and possible relationship to mechanism of erection. Urology, 20: 259, 1982. Kiss, F.: Anatomisch-histologische Untersuchungen iiber die Erektion. Ztschr. ges. Anat., 61: 455, 1921. Braus, H.: Anatomie des Menschen. Berlin: Verlag von Julius Springer, vol. 2, pp. 441-447, 1924. Stieve, H.: Handbuck der Mikroskopischen. Anatomie des Menschen. Berlin: Springer von Julius Springer, vol. 7, pp. 321339, 1930. Meehan, J.P. and Goldstein, A. M. B.: High pressure within corpus cavernosum in man during erection. Its probable mechanism. Urology, 21: 385, 1983. Goldstein, A. M. B., Meehan, J.P., Morrow, J. W., Buckley, P.A. and Rogers, F. A.: The fibrous skeleton of the corpora cavernosa and its probable function in the mechanism of erection. Brit. J. Urol., 57: 574, 1985.
Reply by Authors. We agree that the article by Doctor Goldstein and associates does not directly state that a sliding mechanism might be responsible for veno-occlusion; perhaps that conclusion was largely our own. At any rate, we believe that Doctor Goldstein and associates deserve credit for postulating the presence of a sliding mechanism on the basis of their anatomical observations, regardless of any possible veno-occlusive role, and that their postulate deserved further study. Therefore, we carefully observed the position and angulation of cavernosal septations and venous perforators with respect to each other and with respect to adjacent fixed bony landmarks before and after canine