- Email: [email protected]
Sacral nerve stimulation as a treatment for fecal incontinence
GASTROENTEROLOGY 2001;121:536 –541
Sacral Nerve Stimulation as a Treatment for Fecal Incontinence HARALD R. ROSEN, CHRISTINA URBARZ, BRIGITTE HOLZER, GABRIELE NOVI, and RUDOLF SCHIESSEL Department of Surgery and Ludwig Boltzmann Research Institute for Surgical Oncology, Danube Hospital/SMZ-Ost, Vienna, Austria
Background & Aims: Sacral nerve stimulation is a proven therapeutic option for the treatment of some forms of urinary incontinence. Very recently, preliminary reports have given evidence for its efficacy in fecal incontinence (FI) too. Methods: Since November 1998, 20 patients have been treated for severe FI. The cause of FI was mainly neurologic (n ⴝ 15), and was idiopathic in 5 patients. After temporary (subchronic) external stimulation over a period of 10 –14 days, patients whose continence status improved underwent implantation of a permanent quadripolar lead and a subcutaneously implanted pulse generator. Results: Acute (needle) testing revealed a positive pelvic floor response in 16 patients who underwent subsequent permanent implantation. The median number of incontinence episodes decreased from 6 episodes (3–15/21 days) to 2 (0 – 5/21 days). The time period of retention of a volume of saline causing an urge until definitive defecation was 2 minutes (range, 0 –5 minutes) preoperatively and increased to 7.5 minutes (2–15 minutes) postoperatively. Results of preoperative and postoperative (3 months) anal manometry showed a statistically significant increase in maximal resting and squeeze pressures. Conclusions: Sacral nerve stimulation seems to be a new and promising modality for patients with certain types of FI in whom conventional treatment options have failed to achieve an improvement.
ost patients with fecal incontinence (FI) caused by a simple defect of the external anal sphincter will benefit from direct (overlapping) sphincter repair. Larger sphincter defects resulting from obstetric, surgical, or other trauma are candidates for new treatment options such as skeletal muscle transposition1,2 or the application of an artificial bowel sphincter,3 which markedly improve the situation in up to 75%– 80% of patients. However, a considerable number of patients with severe FI do not show a structural defect of the external or internal anal sphincter on endoanal ultrasonography or magnetic resonance imaging and in the past have been considered to have idiopathic incontinence. In this group with primary degeneration and weakness of the anal
M
sphincter and the pelvic floor as well as in patients with FI caused by spinal injury and other neurologic disorders, treatment options have been limited. Long-term sacral nerve stimulation (SNS) has been proposed for treatment of selected forms of non-neurogenic and neurogenic bladder dysfunction, mainly caused by reduction of the contractility of the detrusor during electrostimulation.4,5 During stimulation, 2 different reflex arcs are believed to be activated via excitation of S2–S4 afferents. Sympathetic hypogastric activity is increased, and parasympathetic activity of the lower motoneuron of the bladder is reduced. This dual effect is used for the treatment of detrusor hyperactivity. Based on various studies in the past, SNS is an accepted treatment modality for urge incontinence as well as the pelvic pain syndrome.6 Additionally, electrostimulation has been researched extensively for improvement of micturition in patients with spinal cord injuries.7 Anorectal side effects during this treatment for urinary incontinence consisted of increases in anal sphincter as well as colonic motility. Because intramuscular stimulation of an insufficient anal sphincter had been attempted as late as in the 1960s,8 the application of SNS in patients with incontinence caused by a weak anal sphincter or of neurologic origin appeared to be an interesting new therapeutic approach. Preliminary reports showed promising data for SNS in patients with therapy-refractory FI9 –11; therefore, this treatment was introduced at our institution.
Patients and Methods From November 1998 to December 2000, 20 patients (14 female, 6 male) with a median age of 50.1 years (range, 11–79 years) were accepted as candidates for SNS. The cause of FI was neurologic in 15 patients and idiopathic in 5 (Table 1). Two patients with idiopathic incontinence had undergone postanal repair procedures with no improvement, and in 3 Abbreviations used in this paper: FI, fecal incontinence; QOL, quality of life; SNS, sacral nerve stimulation. © 2001 by the American Gastroenterological Association 0016-5085/01/$35.00 doi:10.1053/gast.2001.27120
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Table 1. Patient Characteristics Cause of incontinence
n
Idiopathic Neurologic Spinal cord injury Spinal cord surgery Meningomyelocele Multiple sclerosis Friedreich ataxia Spinal stroke Total
5 15 6 4 2 1 1 1 20
Age ( yr) median (range)
History of incontinence ( yr) median (range)
64 (32–69) 50 (11–79)
3 (0.5–5) 5 (1–15)
50 (11–79)
5 (0.5–15)
patients SNS was the first surgical treatment for their incontinence. Inclusion criteria for this treatment included a minimum of 1 incontinence episode per week for solid stool (incontinence diary); an intact external sphincter documented by endoanal ultrasonography and/or magnetic resonance imaging, which has been proven to be an appropriate instrument for evaluation for the pelvic floor anatomy12,13; a minimum history of FI of 1 year after a neurologic event (surgery, trauma, stroke); informed consent about the experimental nature of this treatment; failure of a 6-week course of a standardized biofeedback protocol during which patients had to undergo 2 training sessions per week under the guidance of our medical technician (C.U.) by use of an audiovisual biofeedback device (Polygram Lower GI; Gastrosoft, Irving, TX) and were instructed how to perform these exercises at home regularly; and no evidence of diabetes or connective tissue disorders. This new treatment was presented to the local ethical committee and was approved under the condition that informed consent include information about the limited clinical experience with this method. Furthermore, patients with idiopathic incontinence had to be advised about alternative conventional therapeutic options (i.e., postanal repair, irrigation, stoma, etc.) if they had not previously undergone any other treatment.
Preoperative Evaluation All patients had to undergo extensive preoperative evaluation, including clinical inspection, completion of a standardized incontinence diary over a period of 3 weeks, anal sphincter manometry, and endoanal ultrasonography and/or magnetic resonance imaging. Anal manometry was performed using an 8-channel waterperfusion catheter (Zinetics Medical, Salt Lake City, UT) connected to an analog digital computer (Polygraph) and a Synectics computer interface (Synectics Medical, Krainer Comp., Vienna, Austria) and included a specific software program (Polygram Lower GI; Gastrosoft). The maximal resting and contraction pressures (measured during 30 seconds of contraction) were documented, and rectal sensory threshold, sensation of urgency, and maximum tolerated rectal volume to balloon distention with air were recorded. A saline retention test after the application of saline at a volume causing the first urge to defecate was performed, and
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the maximal time span from the end of instillation to the first evacuation of saline was documented.
SNS Technique Under general anesthesia, 4 – 6 needles were positioned into the foramina S2 to S4 bilaterally, and stimulation was performed using an external pulse generator (Screener model 3625; Medtronic, Minneapolis, MN). The muscular response of the pelvic floor and the anal sphincters was evaluated visually with both buttocks fixed firmly to differentiate pelvic floor response from a possible gluteal contraction. Additionally, intraoperative anal manometry was performed using a “solid-state catheter” with 4 pressure receptors (Ko¨nigsberg catheter; Ko¨nigsberg Instruments, Pasadena, CA), which was connected to a computer (Digitrapper; Synectics-Medical, Stockholm, Sweden). After a positive stimulation response of the pelvic floor and/or the anal sphincters (i.e., contraction of the pelvic floor in a cranial-ventral direction and circular contraction of the anal sphincter and an increase of 20 mm Hg in the manometry during stimulation), subchronic stimulation was performed as follows: to evaluate the functional relevance of a positive electric stimulation, a percutaneous nerve evaluation was performed by application of a temporary stimulation wire (model 3057 CL test stimulation lead; Medtronic, Minneapolis, MN) that was introduced into the stimulation needle and fixed to the skin (patients 1 and 2). Alternatively, a permanent quadripolar stimulation electrode (Quadlead model 3886; Medtronic, Minneapolis, MN) was inserted via a 7–10cm-long sacral incision into the foramen, where the stimulation needle was left in place. After the positive stimulation response had been reproduced again by external stimulation, this lead was sutured to the sacral periosteum with nonabsorbable sutures (Prolene 2/0; Ethicon, Vienna, Austria) and connected to an extension cable (extension kit; Medtronic, Minneapolis, MN). After closure of the sacral wound, this extension cable was brought out subcutaneously through the skin and connected to the external test stimulator (patients 3–10). External stimulation (either via stimulation wires or via a terminal stimulation electrode) was begun on the first postoperative day in a continuous stimulation mode, with a pulse width of 210 microseconds, a frequency of 20 pps, and a stimulation amplitude of 1.5– 4.5 V (median, 2.7 V). The functional result of stimulation was recorded over a period of 10 days, followed by a final saline retention test. Patients whose continence status improved underwent permanent implantation of a pulse generator (Interstim; Medtronic, Kerkrade, Netherlands). During this procedure, either the permanent electrode was implanted at the site of the external stimulation wire and then connected to the subcutaneous pulse generator by application of the extension kit, or the previously implanted extension kit, which had been used for temporary external stimulation, was removed and the new sterile extension kit was connected to the permanent lead and guided by a contralateral route to the pulse generator. All patients who received permanent implants were stimulated in a continuous mode beginning with a stimulation amplitude at which they
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reported feeling the stimulation around or in the anal canal, starting on the first postoperative day. Follow-up was performed at monthly intervals, and continence diaries were collected. Results of saline retention tests and anal manometry, rectal sensory threshold, sensation of urgency, and maximum tolerated volume as well as anal canal length were documented after 3 months. Quality of life (QOL) questionnaires administered according to the recommendations of the American Society of Colorectal Surgeons were evaluated preoperatively and 6 months after permanent implantation. This validated scale is composed of 29 items from which 4 scales (lifestyle, coping behavior, depression/self-perception, and embarrassment) are formed.14
Statistics Results were documented by their median values as well as their minima and maxima. Statistical analysis of measured preoperative versus postoperative (3 months after implantation) anal physiology values and QOL scales were performed by use of the Wilcoxon paired ranks test. A P value of ⬍0.01 was considered statistically significant.
Results The median follow-up of all patients who had received permanent implants was 15 months (range, 3–26 months) at the control date (March 1, 2001). Acute (needle) testing showed a typical positive visual response (i.e., contraction of the pelvic floor in a cranialventral direction and circular contraction of the anal sphincter) in 16 patients who subsequently underwent permanent implantation. In 4 patients (2 with FI caused by spinal cord trauma after a car accident, 1 with spinal stroke, and 1 with meningomyelocele), acute testing failed to show any response. Functional Results All patients who had shown a positive visual response during acute testing and who had received a permanent implant revealed a marked reduction in their incontinence episodes as well as an increase in the time span during saline retention tests. The median number of incontinence episodes for solid or liquid stool per 21 days decreased from 6 (3–15/21 days) to 2 (0 –5/21 days) in the total series of 16 implanted patients. The 4 patients with idiopathic incontinence had 3, 3, 4, and 6 episodes preoperatively compared with 0, 0, 0, and 2 episodes postoperatively. The median numbers of incontinence episodes in the 12 patients with neurologic events were 7 (4 –15) preoperatively and 2 (0 –5) postoperatively (P ⬍ 0.01). The time of retention of a volume of saline causing an urge until definitive defecation was 2 minutes (0 –5 minutes) preoperatively and increased to 7.5 minutes
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(2–15 minutes) postoperatively. In patients with idiopathic incontinence, retention times were 2, 2, 5, and 7 minutes preoperatively and 2, 10, 10, and 15 minutes, respectively, postoperatively. In the group with neurologic incontinence, the preoperative retention test revealed a median time of 2 minutes (0 –5 minutes) compared with 7 minutes (2–15 minutes; P ⬍ 0.01). QOL Evaluation Assessment of QOL scales using the American Society of Colorectal Surgeons questionnaire after 6 months showed significant improvement compared with preoperative values on all scales in patients with permanent implantation (Table 2). Anorectal Physiologic Testing Results of preoperative and postoperative (3 months) anal manometry are shown in Table 3, revealing a statistically significant increase in the maximal resting and squeeze pressures in the group of patients with neurologic incontinence but did not reach statistical significance in the group with idiopathic incontinence (probably because of the small number of patients in this group). As the most prominent observation, patients with neurologically induced incontinence and 2 patients with idiopathic incontinence reported restoration of anal sensory function, consisting of improvement in the sensory capacity of the rectum ampulla and restoration of sensory function perianally and of the perineal skin. This improvement was nicely shown by 2 patients in the idiopathic group who did not report any feeling in the rectum up to the maximal distention of the balloon (300 mL) and reported complete recovery of sensory function after SNS (Table 4). However, evaluation of the volumes of inflated air into the rectum in the total series failed to prove these observations on the statistical level (Table 4). The median values for anal canal length in the idiopathic group was 2.5 cm (1.0 –3.5 cm) before and 3.75 cm (2– 4 cm) after SNS (P ⫽ 0.066). In the neurologic Table 2. Results of QOL Evaluation 6 Months After Permanent Implantation
Scale
Baseline; median (range) n ⫽ 20
6 Months after SNS; median (range) n ⫽ 12
Lifestyle Coping/behavior Depression/self-perception Embarrassment
2.1 (1.0–2.8) 2.0 (1.3–2.5) 2.6 (1.7–3.1) 1.7 (1.0–2.2)
3.9 (2.7–4.4)a 3.7 (3.0–4.1)a 3.7 (3.2–4.3)a 3.8 (3.0–4.6)a
aP
⬍ 0.01.
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Table 3. Anal Manometry Cause of incontinence Idiopathic Neurologic Total
Resting pressure before SNS
P
Resting pressure after SNS
Squeeze pressure before SNS
P
Squeeze pressure after SNS
36.3 (19–39) 21.4 (16–37) 27.7 (16–39)
0.1 0.01 0.005
54.2 (46–76) 49.7 (29.9–75) 50.2 (29–76)
50 (30–61) 68 (28–87) 59.2 (28–87)
0.10 0.01 0.005
110 (57–115) 126 (81–193) 120.2 (57–193)
Data represent median (range) maximum resting and squeeze pressures (mm Hg).
group, anal canal length measurement showed a median length of 3.0 cm (2– 4) before and 3.5 cm (3– 4) after SNS (P ⫽ 0.041). The total series showed a median anal canal length of 3.0 cm (1.0 – 4) before and 3.5 cm (2– 4) after SNS (P ⫽ 0.007). One patient who had undergone implantation because of a permanent rectal urge and multiple sclerosis as the basic disease reported a marked decrease in defecation episodes per day and in incontinence episodes per week. Postoperative Complications Three patients (1 with meningomyelocele, 1 with Friedreich ataxia, and 1 with idiopathic incontinence) who had seen marked improvement of their continence situations had severe infections of the implanted systems that had to be treated by explantation of the leads and the generator and drainage of the wounds 0 –3 months after implantation. These patients reported immediate deterioration of continence after explantation of the system. After consolidation of the infectious situation, all of them were rated as candidates for renewed SNS. Until the control date (March 1, 2001), 1 patient underwent successful reimplantation and regained satisfying continence function, and 2 others are still waiting for new SNS. Retrospective evaluation of the course of these 3 patients had inflammation at the site of the external stimulation cable before permanent implantation of the pulse generator. After SNS for incontinence of neurologic origin, 1 patient had dislocation of the permanent electrode that led to reintervention and new placement. When a second dislocation occurred 3 months later, the permanent electrode was explanted and a dynamic graciloplasty using the already implanted pulse generator was performed.
No complications were observed in the remaining patients, and postoperative pain was easily controlled by the administration of mild analgetics (e.g., diclofenac). Of 20 total patients, 16 (80%) reported improvement of continence after acute testing and in the early postoperative period after permanent implantation. After explantation because of infection or dislodgement, 12 patients (60% of the total series) with functioning systems and improved continence status are still under follow-up.
Discussion In contrast to the extensive experience gained with SNS for urologic indications, reports concerning the application of this modality for FI are limited. The largest series published so far consists of 9 evaluable patients and was presented by Vaizey et al.10 Most of the patients were treated for FI caused by weakness of the anal sphincters, and 1 patient was treated for incontinence following a pull-through procedure after anal atresia; a significant reduction in the number of incontinence episodes was registered in 7 of 9 patients. Contrary to this report, the main indication in our series was incontinence of neurologic origin (n ⫽ 15), usually following spinal cord trauma or as a complication after spinal cord surgery for protrusion. Although 4 patients had no pelvic floor and/or anal sphincter response during acute testing, 15 patients achieved marked improvement or even complete restoration of continence, as shown by a reduction in the number of incontinence episodes per week as well as by an increase in retention time.
Table 4. Threshold, Urge, and Maximum Tolerated Rectal Volumes to Balloon Distention Cause of incontinence
Threshold before SNS
Threshold after SNS
Urge before SNS
Urge after SNS
Maximal volume before SNS (mL air)
Maximal volume after SNS
Idiopathic (n ⫽ 4) Neurologic (n ⫽ 12) Total (n ⫽ 16)
115 (54–300) 90 (15–300) 90 (15–300)
50 (10–60) 77 (40–300) 60 (10–300)
140 (50–120) 100 (60–300) 100 (20–300)
105 (80–300) 100 (60–300) 100 (50–300)
180 (80–300) 220 (35–300) 180 (35–300)
142 (70–170) 180 (80–300) 160 (70–300)
Data presented as median (range) milliliters of air.
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The positive stimulation response during acute testing was confirmed visually by the typical contraction features of the pelvic floor and the anal sphincters, and significant changes in postoperative anal manometry (3 months postoperatively) were observed. Contrary to other reports,9,10 we were able to demonstrate a significant increase in sphincter pressures and anal canal length, which we attribute to the larger number of patients (compared with previous publications) in our series. Neuromodulation of sacral reflexes and regulation of rectal sensitivity appear to be the major reasons for the functional improvement in our neurologic patients after SNS. Although difficult to objectify by diagnostic instruments, all patients showed a successful response and reported marked improvement in rectal sensory function as well as in perianal and perineal sensitivity. Especially after spinal cord trauma in the lumbar region (L1–L5), the notion of overcoming the neurologic defect by a more distally applied stimulation is a novel approach. Neurophysiologic investigations such as measurement of pudendal nerve latency, which might be able to show the effects of SNS, were not performed in our series. Besides the lack of equipment for these procedures at our institutions, these investigations have always been restricted to specialized departments and have been criticized for their interobserver variability as well as their limited clinical relevance. For research purposes, it could be interesting to evaluate whether preoperative pudendal nerve latency values could serve as predictors for functional outcome after SNS. Furthermore, more thorough evaluations of the muscular conditions of the sphincter and pelvic floor muscles by endoanal ultrasonography and magnetic resonance imaging techniques with regards to muscle atrophy could offer additional information. Our preliminary experience showed that the surgical treatment of patients with FI might differ considerably from that of urologic patients. Although an effective influence of SNS on the urinary bladder can be evaluated only during an observation period of 2–3 weeks involving repeated measurements of the residual bladder volume,4,6 a typical positive response to external stimulation during acute testing in FI was associated with improved function in almost all of our patients reported in this series. Furthermore, 3 patients developed severe infection of the implanted material, which led to explantation of the stimulation system despite a positive influence on continence function; the infection had probably occurred during the external stimulation process. Therefore, we altered our concept to an immediate implant during a
GASTROENTEROLOGY Vol. 121, No. 3
one-stage procedure following a positive pelvic floor and/ or sphincter response after needle stimulation. Referring to concerns about the implantation of a cost-intensive system and the potentially inadequate functional outcome, it should be emphasized that all patients in the present series had severe FI that was refractory to other treatment modalities. In the past, most patients with such severe incontinence had been candidates for dynamic graciloplasty at our institution.15 In cases of unsatisfactory functional outcome despite a positive pelvic floor response during acute testing, the patient would be a candidate for graciloplasty, which could be applied using the previously implanted pulse generator. In conclusion, in our preliminary experience, SNS has shown promising results in the treatment of FI of neurologic etiology as well as due to an idiopathic diffuse weakness of the pelvic floor. Although a longer follow-up is needed to assess the long-term efficacy of this method, the initial promising results warrant further clinical studies focusing on this new modality.
References 1. Madoff RD, Baeten CGMI, Christiansen J, Rosen HR, Williams NS, Heine JA, Lehur PA, Lowry AC, Lubowski DZ, Matzel KE, Nicholls RJ, Seccia M, Thorson AG, Wexner SD, Wong WD. Standards for anal sphincter replacement. Dis Colon Rectum 2000; 43:135–141. 2. Baeten CGMI, Geerdes BP, Adang EMM, Heineman E, Konsten J, Engel GL, Kester AD, Spaans F, Soeters PB. Anal dynamic graciloplasty in the treatment of intractable fecal incontinence. N Engl J Med 1995;332:1600 –1605. 3. Wong WD, Jensen LL, Bartolo DCC, Rothenberger DA. Artificial anal sphincter. Dis Colon Rectum 1996;39:1345–1351. 4. Thon WF, Baskin LS, Jonas U. Neuromodulation of voiding dysfunction and pelvic pain. World J Urol 1991;9:138 –141. 5. Bosch JLHR, Groen J. Sacral (S3) segmental nerve stimulation as a treatment for urge incontinence in patients with detrusor instability: results of chronic electrical stimulation using an implantable neural prosthesis. J Urol 1995;154:504 –507. 6. Weil EHJ, Riuz-Cerda JL, Eerdmans PHA, Janknegt RA, Van Kerrebroeck PE. Clinical results of sacral neuromodulation for chronic voiding dysfunction using unilateral sacral foramen electrodes. World J Urol 1998;16:313–321. 7. Ishigooka M, Suzuki T, Hashimoto I, Sasagawa I, Nakada T, Handa Y. A new technique for sacral nerve stimulation: a percutaneous method for urinary incontinence caused by spinal cord injury. Br J Urol 1998;81:315–318. 8. Caldwell KPS. The electrical control of sphincter incompetence. Lancet 1963;2:174 –177. 9. Matzel KE, Stadelmaier U, Hohenfellner M, Gall FP. Electrical stimulation of spinal nerves for treatment of fecal incontinence. Lancet 1995;346:1124 –1127. 10. Vaizey CJ, Kamm MA, Turner I, Nicholls RJ, Woloszko J. Effects of short term sacral nerve stimulation on anal and rectal function in patients with anal incontinence. Gut 1999;44:407– 412. 11. Malouf AJ, Vaizey CJ, Nicholls J, Kamm MA. Permanent sacral nerve stimulation for fecal incontinence. Ann Surg 2000;232: 143–148. 12. Urban M, Rosen HR, Ho¨lbling N, Feil W, Hochwarther G, Hruby W,
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Schiessel R. MR imaging for the preoperative planning of sphincter-saving surgery of tumors of the lower third of the rectum: use of intravenous and endorectal contrast material. Radiology 2000; 214:503–508. 13. Holzer B, Rosen HR, Urban M, Anzbo¨ck W, Schiessel R, Hruby W. Magnetic resonance imaging of perianal fistulas: predictive value for Parks classification and identification of the inner opening. Colorectal Dis 2000;2:340 –345. 14. Rockwood TH, Church JM, Fleshman JW, Kane RL, Mavrantonis C, Thorson AG, Wexner SD, Bliss D, Lowry AC. Fecal incontinence quality of life scale: quality of life instrument for patients with fecal incontinence. Dis Colon Rectum 2000;43:9 –16.
15. Rosen HR, Novi G, Zo¨ch G, Feil W, Urbarz C, Schiessel R. Restoration of anal sphincter function by single-stage dynamic graciloplasty with a modified (split sling) technique. Am J Surg 1998;175:187–193.
Received January 4, 2001. Accepted May 2, 2001. Address requests for reprints to: Harald R. Rosen, M.D., Department of Surgery, Danube Hospital/SMZ-Ost, Langobardenstrasse 122, A-1220 Vienna, Austria. e-mail: [email protected]; fax: (43) 1 288-02-3380.
Mallory and Weiss of the Mallory-Weiss Syndrome George Kenneth Mallory (1900 –1986) was born in Boston, the son of the famed pathologist Frank Burr Mallory (1862–1941) for whom Mallory bodies are named. Kenneth Mallory received his M.D. degree from Harvard Medical School in 1926, then pursued postgraduate work in pathology in Hamburg and Vienna. He became professor of pathology at Boston University.
Soma Weiss (1898 –1941) was born in Bestereze, Hungary, the son of a civil engineer. A brilliant student, in 1920 he emigrated to the United States to escape the turmoil of Europe following World War I. He attended Columbia University, then obtained his M.D. degree at the Cornell Medical College in 1923. He began his academic career at the Thorndike Laboratory in Boston, then while still a youth became physician-in-chief at the Peter Bent Brigham Hospital. An inspiring teacher and astute investigator, his most notable contributions were to clarification of cardiovascular pathophysiology. His meteoric career was cut short by fatal rupture of a cerebral aneurysm, a catastrophic event he diagnosed himself while on his deathbed. An irony of eponymy is that Kenneth Mallory and Soma Weiss are remembered today chiefly because of a brief report (Hemorrhage from laceration of the cardiac orifice of the stomach due to vomiting. Am J Med Sci 1929;178:506) that doubtlessly they both deemed relatively trivial at the time. —Contributed by WILLIAM S. HAUBRICH, M.D. Scripps Clinic and Research Foundation, La Jolla, California Copyright holder unknown. Photo obtained from the National Library of Medicine Website (http:///www.nlm.nih.gov).
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Sacral Nerve Stimulation as a Treatment for Fecal Incontinence HARALD R. ROSEN, CHRISTINA URBARZ, BRIGITTE HOLZER, GABRIELE NOVI, and RUDOLF SCHIESSEL Department of Surgery and Ludwig Boltzmann Research Institute for Surgical Oncology, Danube Hospital/SMZ-Ost, Vienna, Austria
Background & Aims: Sacral nerve stimulation is a proven therapeutic option for the treatment of some forms of urinary incontinence. Very recently, preliminary reports have given evidence for its efficacy in fecal incontinence (FI) too. Methods: Since November 1998, 20 patients have been treated for severe FI. The cause of FI was mainly neurologic (n ⴝ 15), and was idiopathic in 5 patients. After temporary (subchronic) external stimulation over a period of 10 –14 days, patients whose continence status improved underwent implantation of a permanent quadripolar lead and a subcutaneously implanted pulse generator. Results: Acute (needle) testing revealed a positive pelvic floor response in 16 patients who underwent subsequent permanent implantation. The median number of incontinence episodes decreased from 6 episodes (3–15/21 days) to 2 (0 – 5/21 days). The time period of retention of a volume of saline causing an urge until definitive defecation was 2 minutes (range, 0 –5 minutes) preoperatively and increased to 7.5 minutes (2–15 minutes) postoperatively. Results of preoperative and postoperative (3 months) anal manometry showed a statistically significant increase in maximal resting and squeeze pressures. Conclusions: Sacral nerve stimulation seems to be a new and promising modality for patients with certain types of FI in whom conventional treatment options have failed to achieve an improvement.
ost patients with fecal incontinence (FI) caused by a simple defect of the external anal sphincter will benefit from direct (overlapping) sphincter repair. Larger sphincter defects resulting from obstetric, surgical, or other trauma are candidates for new treatment options such as skeletal muscle transposition1,2 or the application of an artificial bowel sphincter,3 which markedly improve the situation in up to 75%– 80% of patients. However, a considerable number of patients with severe FI do not show a structural defect of the external or internal anal sphincter on endoanal ultrasonography or magnetic resonance imaging and in the past have been considered to have idiopathic incontinence. In this group with primary degeneration and weakness of the anal
M
sphincter and the pelvic floor as well as in patients with FI caused by spinal injury and other neurologic disorders, treatment options have been limited. Long-term sacral nerve stimulation (SNS) has been proposed for treatment of selected forms of non-neurogenic and neurogenic bladder dysfunction, mainly caused by reduction of the contractility of the detrusor during electrostimulation.4,5 During stimulation, 2 different reflex arcs are believed to be activated via excitation of S2–S4 afferents. Sympathetic hypogastric activity is increased, and parasympathetic activity of the lower motoneuron of the bladder is reduced. This dual effect is used for the treatment of detrusor hyperactivity. Based on various studies in the past, SNS is an accepted treatment modality for urge incontinence as well as the pelvic pain syndrome.6 Additionally, electrostimulation has been researched extensively for improvement of micturition in patients with spinal cord injuries.7 Anorectal side effects during this treatment for urinary incontinence consisted of increases in anal sphincter as well as colonic motility. Because intramuscular stimulation of an insufficient anal sphincter had been attempted as late as in the 1960s,8 the application of SNS in patients with incontinence caused by a weak anal sphincter or of neurologic origin appeared to be an interesting new therapeutic approach. Preliminary reports showed promising data for SNS in patients with therapy-refractory FI9 –11; therefore, this treatment was introduced at our institution.
Patients and Methods From November 1998 to December 2000, 20 patients (14 female, 6 male) with a median age of 50.1 years (range, 11–79 years) were accepted as candidates for SNS. The cause of FI was neurologic in 15 patients and idiopathic in 5 (Table 1). Two patients with idiopathic incontinence had undergone postanal repair procedures with no improvement, and in 3 Abbreviations used in this paper: FI, fecal incontinence; QOL, quality of life; SNS, sacral nerve stimulation. © 2001 by the American Gastroenterological Association 0016-5085/01/$35.00 doi:10.1053/gast.2001.27120
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Table 1. Patient Characteristics Cause of incontinence
n
Idiopathic Neurologic Spinal cord injury Spinal cord surgery Meningomyelocele Multiple sclerosis Friedreich ataxia Spinal stroke Total
5 15 6 4 2 1 1 1 20
Age ( yr) median (range)
History of incontinence ( yr) median (range)
64 (32–69) 50 (11–79)
3 (0.5–5) 5 (1–15)
50 (11–79)
5 (0.5–15)
patients SNS was the first surgical treatment for their incontinence. Inclusion criteria for this treatment included a minimum of 1 incontinence episode per week for solid stool (incontinence diary); an intact external sphincter documented by endoanal ultrasonography and/or magnetic resonance imaging, which has been proven to be an appropriate instrument for evaluation for the pelvic floor anatomy12,13; a minimum history of FI of 1 year after a neurologic event (surgery, trauma, stroke); informed consent about the experimental nature of this treatment; failure of a 6-week course of a standardized biofeedback protocol during which patients had to undergo 2 training sessions per week under the guidance of our medical technician (C.U.) by use of an audiovisual biofeedback device (Polygram Lower GI; Gastrosoft, Irving, TX) and were instructed how to perform these exercises at home regularly; and no evidence of diabetes or connective tissue disorders. This new treatment was presented to the local ethical committee and was approved under the condition that informed consent include information about the limited clinical experience with this method. Furthermore, patients with idiopathic incontinence had to be advised about alternative conventional therapeutic options (i.e., postanal repair, irrigation, stoma, etc.) if they had not previously undergone any other treatment.
Preoperative Evaluation All patients had to undergo extensive preoperative evaluation, including clinical inspection, completion of a standardized incontinence diary over a period of 3 weeks, anal sphincter manometry, and endoanal ultrasonography and/or magnetic resonance imaging. Anal manometry was performed using an 8-channel waterperfusion catheter (Zinetics Medical, Salt Lake City, UT) connected to an analog digital computer (Polygraph) and a Synectics computer interface (Synectics Medical, Krainer Comp., Vienna, Austria) and included a specific software program (Polygram Lower GI; Gastrosoft). The maximal resting and contraction pressures (measured during 30 seconds of contraction) were documented, and rectal sensory threshold, sensation of urgency, and maximum tolerated rectal volume to balloon distention with air were recorded. A saline retention test after the application of saline at a volume causing the first urge to defecate was performed, and
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the maximal time span from the end of instillation to the first evacuation of saline was documented.
SNS Technique Under general anesthesia, 4 – 6 needles were positioned into the foramina S2 to S4 bilaterally, and stimulation was performed using an external pulse generator (Screener model 3625; Medtronic, Minneapolis, MN). The muscular response of the pelvic floor and the anal sphincters was evaluated visually with both buttocks fixed firmly to differentiate pelvic floor response from a possible gluteal contraction. Additionally, intraoperative anal manometry was performed using a “solid-state catheter” with 4 pressure receptors (Ko¨nigsberg catheter; Ko¨nigsberg Instruments, Pasadena, CA), which was connected to a computer (Digitrapper; Synectics-Medical, Stockholm, Sweden). After a positive stimulation response of the pelvic floor and/or the anal sphincters (i.e., contraction of the pelvic floor in a cranial-ventral direction and circular contraction of the anal sphincter and an increase of 20 mm Hg in the manometry during stimulation), subchronic stimulation was performed as follows: to evaluate the functional relevance of a positive electric stimulation, a percutaneous nerve evaluation was performed by application of a temporary stimulation wire (model 3057 CL test stimulation lead; Medtronic, Minneapolis, MN) that was introduced into the stimulation needle and fixed to the skin (patients 1 and 2). Alternatively, a permanent quadripolar stimulation electrode (Quadlead model 3886; Medtronic, Minneapolis, MN) was inserted via a 7–10cm-long sacral incision into the foramen, where the stimulation needle was left in place. After the positive stimulation response had been reproduced again by external stimulation, this lead was sutured to the sacral periosteum with nonabsorbable sutures (Prolene 2/0; Ethicon, Vienna, Austria) and connected to an extension cable (extension kit; Medtronic, Minneapolis, MN). After closure of the sacral wound, this extension cable was brought out subcutaneously through the skin and connected to the external test stimulator (patients 3–10). External stimulation (either via stimulation wires or via a terminal stimulation electrode) was begun on the first postoperative day in a continuous stimulation mode, with a pulse width of 210 microseconds, a frequency of 20 pps, and a stimulation amplitude of 1.5– 4.5 V (median, 2.7 V). The functional result of stimulation was recorded over a period of 10 days, followed by a final saline retention test. Patients whose continence status improved underwent permanent implantation of a pulse generator (Interstim; Medtronic, Kerkrade, Netherlands). During this procedure, either the permanent electrode was implanted at the site of the external stimulation wire and then connected to the subcutaneous pulse generator by application of the extension kit, or the previously implanted extension kit, which had been used for temporary external stimulation, was removed and the new sterile extension kit was connected to the permanent lead and guided by a contralateral route to the pulse generator. All patients who received permanent implants were stimulated in a continuous mode beginning with a stimulation amplitude at which they
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reported feeling the stimulation around or in the anal canal, starting on the first postoperative day. Follow-up was performed at monthly intervals, and continence diaries were collected. Results of saline retention tests and anal manometry, rectal sensory threshold, sensation of urgency, and maximum tolerated volume as well as anal canal length were documented after 3 months. Quality of life (QOL) questionnaires administered according to the recommendations of the American Society of Colorectal Surgeons were evaluated preoperatively and 6 months after permanent implantation. This validated scale is composed of 29 items from which 4 scales (lifestyle, coping behavior, depression/self-perception, and embarrassment) are formed.14
Statistics Results were documented by their median values as well as their minima and maxima. Statistical analysis of measured preoperative versus postoperative (3 months after implantation) anal physiology values and QOL scales were performed by use of the Wilcoxon paired ranks test. A P value of ⬍0.01 was considered statistically significant.
Results The median follow-up of all patients who had received permanent implants was 15 months (range, 3–26 months) at the control date (March 1, 2001). Acute (needle) testing showed a typical positive visual response (i.e., contraction of the pelvic floor in a cranialventral direction and circular contraction of the anal sphincter) in 16 patients who subsequently underwent permanent implantation. In 4 patients (2 with FI caused by spinal cord trauma after a car accident, 1 with spinal stroke, and 1 with meningomyelocele), acute testing failed to show any response. Functional Results All patients who had shown a positive visual response during acute testing and who had received a permanent implant revealed a marked reduction in their incontinence episodes as well as an increase in the time span during saline retention tests. The median number of incontinence episodes for solid or liquid stool per 21 days decreased from 6 (3–15/21 days) to 2 (0 –5/21 days) in the total series of 16 implanted patients. The 4 patients with idiopathic incontinence had 3, 3, 4, and 6 episodes preoperatively compared with 0, 0, 0, and 2 episodes postoperatively. The median numbers of incontinence episodes in the 12 patients with neurologic events were 7 (4 –15) preoperatively and 2 (0 –5) postoperatively (P ⬍ 0.01). The time of retention of a volume of saline causing an urge until definitive defecation was 2 minutes (0 –5 minutes) preoperatively and increased to 7.5 minutes
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(2–15 minutes) postoperatively. In patients with idiopathic incontinence, retention times were 2, 2, 5, and 7 minutes preoperatively and 2, 10, 10, and 15 minutes, respectively, postoperatively. In the group with neurologic incontinence, the preoperative retention test revealed a median time of 2 minutes (0 –5 minutes) compared with 7 minutes (2–15 minutes; P ⬍ 0.01). QOL Evaluation Assessment of QOL scales using the American Society of Colorectal Surgeons questionnaire after 6 months showed significant improvement compared with preoperative values on all scales in patients with permanent implantation (Table 2). Anorectal Physiologic Testing Results of preoperative and postoperative (3 months) anal manometry are shown in Table 3, revealing a statistically significant increase in the maximal resting and squeeze pressures in the group of patients with neurologic incontinence but did not reach statistical significance in the group with idiopathic incontinence (probably because of the small number of patients in this group). As the most prominent observation, patients with neurologically induced incontinence and 2 patients with idiopathic incontinence reported restoration of anal sensory function, consisting of improvement in the sensory capacity of the rectum ampulla and restoration of sensory function perianally and of the perineal skin. This improvement was nicely shown by 2 patients in the idiopathic group who did not report any feeling in the rectum up to the maximal distention of the balloon (300 mL) and reported complete recovery of sensory function after SNS (Table 4). However, evaluation of the volumes of inflated air into the rectum in the total series failed to prove these observations on the statistical level (Table 4). The median values for anal canal length in the idiopathic group was 2.5 cm (1.0 –3.5 cm) before and 3.75 cm (2– 4 cm) after SNS (P ⫽ 0.066). In the neurologic Table 2. Results of QOL Evaluation 6 Months After Permanent Implantation
Scale
Baseline; median (range) n ⫽ 20
6 Months after SNS; median (range) n ⫽ 12
Lifestyle Coping/behavior Depression/self-perception Embarrassment
2.1 (1.0–2.8) 2.0 (1.3–2.5) 2.6 (1.7–3.1) 1.7 (1.0–2.2)
3.9 (2.7–4.4)a 3.7 (3.0–4.1)a 3.7 (3.2–4.3)a 3.8 (3.0–4.6)a
aP
⬍ 0.01.
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Table 3. Anal Manometry Cause of incontinence Idiopathic Neurologic Total
Resting pressure before SNS
P
Resting pressure after SNS
Squeeze pressure before SNS
P
Squeeze pressure after SNS
36.3 (19–39) 21.4 (16–37) 27.7 (16–39)
0.1 0.01 0.005
54.2 (46–76) 49.7 (29.9–75) 50.2 (29–76)
50 (30–61) 68 (28–87) 59.2 (28–87)
0.10 0.01 0.005
110 (57–115) 126 (81–193) 120.2 (57–193)
Data represent median (range) maximum resting and squeeze pressures (mm Hg).
group, anal canal length measurement showed a median length of 3.0 cm (2– 4) before and 3.5 cm (3– 4) after SNS (P ⫽ 0.041). The total series showed a median anal canal length of 3.0 cm (1.0 – 4) before and 3.5 cm (2– 4) after SNS (P ⫽ 0.007). One patient who had undergone implantation because of a permanent rectal urge and multiple sclerosis as the basic disease reported a marked decrease in defecation episodes per day and in incontinence episodes per week. Postoperative Complications Three patients (1 with meningomyelocele, 1 with Friedreich ataxia, and 1 with idiopathic incontinence) who had seen marked improvement of their continence situations had severe infections of the implanted systems that had to be treated by explantation of the leads and the generator and drainage of the wounds 0 –3 months after implantation. These patients reported immediate deterioration of continence after explantation of the system. After consolidation of the infectious situation, all of them were rated as candidates for renewed SNS. Until the control date (March 1, 2001), 1 patient underwent successful reimplantation and regained satisfying continence function, and 2 others are still waiting for new SNS. Retrospective evaluation of the course of these 3 patients had inflammation at the site of the external stimulation cable before permanent implantation of the pulse generator. After SNS for incontinence of neurologic origin, 1 patient had dislocation of the permanent electrode that led to reintervention and new placement. When a second dislocation occurred 3 months later, the permanent electrode was explanted and a dynamic graciloplasty using the already implanted pulse generator was performed.
No complications were observed in the remaining patients, and postoperative pain was easily controlled by the administration of mild analgetics (e.g., diclofenac). Of 20 total patients, 16 (80%) reported improvement of continence after acute testing and in the early postoperative period after permanent implantation. After explantation because of infection or dislodgement, 12 patients (60% of the total series) with functioning systems and improved continence status are still under follow-up.
Discussion In contrast to the extensive experience gained with SNS for urologic indications, reports concerning the application of this modality for FI are limited. The largest series published so far consists of 9 evaluable patients and was presented by Vaizey et al.10 Most of the patients were treated for FI caused by weakness of the anal sphincters, and 1 patient was treated for incontinence following a pull-through procedure after anal atresia; a significant reduction in the number of incontinence episodes was registered in 7 of 9 patients. Contrary to this report, the main indication in our series was incontinence of neurologic origin (n ⫽ 15), usually following spinal cord trauma or as a complication after spinal cord surgery for protrusion. Although 4 patients had no pelvic floor and/or anal sphincter response during acute testing, 15 patients achieved marked improvement or even complete restoration of continence, as shown by a reduction in the number of incontinence episodes per week as well as by an increase in retention time.
Table 4. Threshold, Urge, and Maximum Tolerated Rectal Volumes to Balloon Distention Cause of incontinence
Threshold before SNS
Threshold after SNS
Urge before SNS
Urge after SNS
Maximal volume before SNS (mL air)
Maximal volume after SNS
Idiopathic (n ⫽ 4) Neurologic (n ⫽ 12) Total (n ⫽ 16)
115 (54–300) 90 (15–300) 90 (15–300)
50 (10–60) 77 (40–300) 60 (10–300)
140 (50–120) 100 (60–300) 100 (20–300)
105 (80–300) 100 (60–300) 100 (50–300)
180 (80–300) 220 (35–300) 180 (35–300)
142 (70–170) 180 (80–300) 160 (70–300)
Data presented as median (range) milliliters of air.
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The positive stimulation response during acute testing was confirmed visually by the typical contraction features of the pelvic floor and the anal sphincters, and significant changes in postoperative anal manometry (3 months postoperatively) were observed. Contrary to other reports,9,10 we were able to demonstrate a significant increase in sphincter pressures and anal canal length, which we attribute to the larger number of patients (compared with previous publications) in our series. Neuromodulation of sacral reflexes and regulation of rectal sensitivity appear to be the major reasons for the functional improvement in our neurologic patients after SNS. Although difficult to objectify by diagnostic instruments, all patients showed a successful response and reported marked improvement in rectal sensory function as well as in perianal and perineal sensitivity. Especially after spinal cord trauma in the lumbar region (L1–L5), the notion of overcoming the neurologic defect by a more distally applied stimulation is a novel approach. Neurophysiologic investigations such as measurement of pudendal nerve latency, which might be able to show the effects of SNS, were not performed in our series. Besides the lack of equipment for these procedures at our institutions, these investigations have always been restricted to specialized departments and have been criticized for their interobserver variability as well as their limited clinical relevance. For research purposes, it could be interesting to evaluate whether preoperative pudendal nerve latency values could serve as predictors for functional outcome after SNS. Furthermore, more thorough evaluations of the muscular conditions of the sphincter and pelvic floor muscles by endoanal ultrasonography and magnetic resonance imaging techniques with regards to muscle atrophy could offer additional information. Our preliminary experience showed that the surgical treatment of patients with FI might differ considerably from that of urologic patients. Although an effective influence of SNS on the urinary bladder can be evaluated only during an observation period of 2–3 weeks involving repeated measurements of the residual bladder volume,4,6 a typical positive response to external stimulation during acute testing in FI was associated with improved function in almost all of our patients reported in this series. Furthermore, 3 patients developed severe infection of the implanted material, which led to explantation of the stimulation system despite a positive influence on continence function; the infection had probably occurred during the external stimulation process. Therefore, we altered our concept to an immediate implant during a
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one-stage procedure following a positive pelvic floor and/ or sphincter response after needle stimulation. Referring to concerns about the implantation of a cost-intensive system and the potentially inadequate functional outcome, it should be emphasized that all patients in the present series had severe FI that was refractory to other treatment modalities. In the past, most patients with such severe incontinence had been candidates for dynamic graciloplasty at our institution.15 In cases of unsatisfactory functional outcome despite a positive pelvic floor response during acute testing, the patient would be a candidate for graciloplasty, which could be applied using the previously implanted pulse generator. In conclusion, in our preliminary experience, SNS has shown promising results in the treatment of FI of neurologic etiology as well as due to an idiopathic diffuse weakness of the pelvic floor. Although a longer follow-up is needed to assess the long-term efficacy of this method, the initial promising results warrant further clinical studies focusing on this new modality.
References 1. Madoff RD, Baeten CGMI, Christiansen J, Rosen HR, Williams NS, Heine JA, Lehur PA, Lowry AC, Lubowski DZ, Matzel KE, Nicholls RJ, Seccia M, Thorson AG, Wexner SD, Wong WD. Standards for anal sphincter replacement. Dis Colon Rectum 2000; 43:135–141. 2. Baeten CGMI, Geerdes BP, Adang EMM, Heineman E, Konsten J, Engel GL, Kester AD, Spaans F, Soeters PB. Anal dynamic graciloplasty in the treatment of intractable fecal incontinence. N Engl J Med 1995;332:1600 –1605. 3. Wong WD, Jensen LL, Bartolo DCC, Rothenberger DA. Artificial anal sphincter. Dis Colon Rectum 1996;39:1345–1351. 4. Thon WF, Baskin LS, Jonas U. Neuromodulation of voiding dysfunction and pelvic pain. World J Urol 1991;9:138 –141. 5. Bosch JLHR, Groen J. Sacral (S3) segmental nerve stimulation as a treatment for urge incontinence in patients with detrusor instability: results of chronic electrical stimulation using an implantable neural prosthesis. J Urol 1995;154:504 –507. 6. Weil EHJ, Riuz-Cerda JL, Eerdmans PHA, Janknegt RA, Van Kerrebroeck PE. Clinical results of sacral neuromodulation for chronic voiding dysfunction using unilateral sacral foramen electrodes. World J Urol 1998;16:313–321. 7. Ishigooka M, Suzuki T, Hashimoto I, Sasagawa I, Nakada T, Handa Y. A new technique for sacral nerve stimulation: a percutaneous method for urinary incontinence caused by spinal cord injury. Br J Urol 1998;81:315–318. 8. Caldwell KPS. The electrical control of sphincter incompetence. Lancet 1963;2:174 –177. 9. Matzel KE, Stadelmaier U, Hohenfellner M, Gall FP. Electrical stimulation of spinal nerves for treatment of fecal incontinence. Lancet 1995;346:1124 –1127. 10. Vaizey CJ, Kamm MA, Turner I, Nicholls RJ, Woloszko J. Effects of short term sacral nerve stimulation on anal and rectal function in patients with anal incontinence. Gut 1999;44:407– 412. 11. Malouf AJ, Vaizey CJ, Nicholls J, Kamm MA. Permanent sacral nerve stimulation for fecal incontinence. Ann Surg 2000;232: 143–148. 12. Urban M, Rosen HR, Ho¨lbling N, Feil W, Hochwarther G, Hruby W,
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Schiessel R. MR imaging for the preoperative planning of sphincter-saving surgery of tumors of the lower third of the rectum: use of intravenous and endorectal contrast material. Radiology 2000; 214:503–508. 13. Holzer B, Rosen HR, Urban M, Anzbo¨ck W, Schiessel R, Hruby W. Magnetic resonance imaging of perianal fistulas: predictive value for Parks classification and identification of the inner opening. Colorectal Dis 2000;2:340 –345. 14. Rockwood TH, Church JM, Fleshman JW, Kane RL, Mavrantonis C, Thorson AG, Wexner SD, Bliss D, Lowry AC. Fecal incontinence quality of life scale: quality of life instrument for patients with fecal incontinence. Dis Colon Rectum 2000;43:9 –16.
15. Rosen HR, Novi G, Zo¨ch G, Feil W, Urbarz C, Schiessel R. Restoration of anal sphincter function by single-stage dynamic graciloplasty with a modified (split sling) technique. Am J Surg 1998;175:187–193.
Received January 4, 2001. Accepted May 2, 2001. Address requests for reprints to: Harald R. Rosen, M.D., Department of Surgery, Danube Hospital/SMZ-Ost, Langobardenstrasse 122, A-1220 Vienna, Austria. e-mail: [email protected]; fax: (43) 1 288-02-3380.
Mallory and Weiss of the Mallory-Weiss Syndrome George Kenneth Mallory (1900 –1986) was born in Boston, the son of the famed pathologist Frank Burr Mallory (1862–1941) for whom Mallory bodies are named. Kenneth Mallory received his M.D. degree from Harvard Medical School in 1926, then pursued postgraduate work in pathology in Hamburg and Vienna. He became professor of pathology at Boston University.
Soma Weiss (1898 –1941) was born in Bestereze, Hungary, the son of a civil engineer. A brilliant student, in 1920 he emigrated to the United States to escape the turmoil of Europe following World War I. He attended Columbia University, then obtained his M.D. degree at the Cornell Medical College in 1923. He began his academic career at the Thorndike Laboratory in Boston, then while still a youth became physician-in-chief at the Peter Bent Brigham Hospital. An inspiring teacher and astute investigator, his most notable contributions were to clarification of cardiovascular pathophysiology. His meteoric career was cut short by fatal rupture of a cerebral aneurysm, a catastrophic event he diagnosed himself while on his deathbed. An irony of eponymy is that Kenneth Mallory and Soma Weiss are remembered today chiefly because of a brief report (Hemorrhage from laceration of the cardiac orifice of the stomach due to vomiting. Am J Med Sci 1929;178:506) that doubtlessly they both deemed relatively trivial at the time. —Contributed by WILLIAM S. HAUBRICH, M.D. Scripps Clinic and Research Foundation, La Jolla, California Copyright holder unknown. Photo obtained from the National Library of Medicine Website (http:///www.nlm.nih.gov).
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