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Acute aortic occlusion as a result of extrinsic compression from peritoneal encapsulation
CASE REPORTS
Acute aortic occlusion as a result of extrinsic compression from peritoneal encapsulation Michael B. Silva, Jr., M D , M a r k M. Connolly, M D , Adrienne B u r f o r d - F o g g s , M D , and William R . Flinn, M D , Chicago, Ill. Acute aortic occlusion frequently occurs with catastrophic visceral, spinal, or lower extremity ischemia and is most often caused by embolic or thrombotic events in older individuals with known cardiovascular disorders. This case describes the rapid development of the clinical signs of acute aortic occlusion in a young and completely healthy individual. Aortic occlusion was produced by extrinsic compression o f the juxtarenal aorta from a closed-loop small intestinal obstruction contained within a peritoneal encapsulation, an extremely rare intraabdominal developmental anomaly. (J VAsc SURG 1992;16: 286-9.)
Acute occlusion o f the abdominal aorta is a rare but potentially catastrophic vascular emergency that most often produces profound limb ischemia and significant lower extremity neuromotor dysfunction including even paraplegia. Acute infrarenal aortic occlusion is most commonly caused by a "saddle" embolus or thrombosis o f an atherosclerotic aorta or an aortic aneurysm. 1"7 Occlusion o f the aorta as a sequella o f extrinsic compression alone has not previously been described. Peritoneal encapsulation is a rare developmental anomaly wherein a portion o f the small bowel is contained within an accessory intraperitoneal membrane that is presumed to be the remnant o f the embryologic yolk sac. Since its initial description by Cleland 8 in 1868, 10 cases have been described in the world literature. 9-16 The present case describes our experience with abdominal aortic occlusion produced by extrinsic compression from dilated small bowel confined within a peritoneal encapsulation. CASE REPORT A 29-year-old man who was an aerobics instructor was admitted with a recent history of colicky periumbilical abdominal pain radiating to his back. He had two episodes of bilious emesis that morning but had a normal bowel
From the Department of Surgery and the Center for Vascular Disease, Columbus Hospital, Chicago. Reprint requests: W. R. Flinn, MD, Center for Vascular Disease, Columbus Hospital, 2520 N. Lakeview, Chicago, IL 60614. 24/4/36162 286
movement the day before admission. The patient described similar episodes of pain that had occurred on numerous occasions previously but had always been of lesser intensity and had resolved spontaneously. Physical examination revealed a muscular man who was most comfortable in a semi-Fowler's position. He was a_febrileand his vital signs were normal. His abdomen was scaphoid and tender in the periumbilical region but without signs of peritoneal irritation. His rectal examination was normal, and stool culture was negative for occult blood. Neuromotor and vascular examinations of his lower extremities were normal. Blood glucose, urea nitrogen, serum electrolytes, and urine were normal. His hemoglobin was 14.1 gm/di, hematocrit 40%, and white blood cell count 13,000, with 29 segmented neutrophils, 1 banded neutrophil, 65 lymphocytes, and 5 monocytes. Abdominal radiography revealed dilated loops of small bowel with gas noted throughout the colon. An unprepared barium enema was performed which showed normal colon anatomy and demonstrated filling of the appendix. Reflux of contrast into the terminal ileum, showed thickened folds of mucosa with considerable irregularity, suggesting the possibility of terminal ileitis or lymphomatous involvement. Over the ensuing hours the patient's pain worsened, and an associated sensation of uncoordination developed in his lower extremities, which progressed from numbness and weakness to a complete loss of muscular function and sensation to the level of his umbilicus. This was accompanied by mild distention of his abdomen, mottling and coolness in his lower body, with absent femoral, popliteal, and pedal pulses. A Foley catheter was placed, and the patient was found to be oliguric. An emergency abdominal CT scan performed during this period showed dilated loops of small bowel. The suprarenal aorta was normal but the
Volume 16 Number 2 Augxtst 1992
Acute aortic occlusion caused by extrinsic compression 287
Fig. 1. A, Selected image from CT scan ofabdorrlen near superior poles of kidneys (K) reveals aorta to be of normal caliber (arrow). B, CT scan cuts of infrarenal aorta (arrow) show flattening and almost complete obliteration of aortic lumen. Residual contrast seen in anatomically normal ascending colon (AC) and descending colon (DC) from previous barium enema. Margins of peritoneal encapsulation of dilated small bowel noted by small arrows.
pararenal and infrarenal aortas appeared compressed against the lumbar spine (Fig. 1). The patient was heparinized and taken to the operating room for exploratory laparotomy. When the abdomen was opened in operation gangrenous small bowel was encountered displaced to the right of the midline by an apparent retroperitoneal mass measuring approximately 15 cm by 18 cm bordered laterally by a normal appearing descending colon and cephalad by the mesentery of the transverse colon. Mobilization of the mass away from the left colon and off the aorta resulted in an immediate return of normal flow through the distal aorta, which was soft and then had
a strong pulse. Mthough the patient had been atmost anuric since the time of CT scanning, the return of renal perfusion after aortic decompression resulted in a prompt resumption of normal urine output. Flow into the lower extremities also returned as evidenced by normal femoral pulses. Further exploration of the mass revealed it to be an anomalous intraperitoneal sac with a closed loop gangrenous obstruction of the majority of the small bowel, which was contained within the sac. The accessory peritoneal membrane (Fig. 2) was reflected superiorly" and laterally on the normally placed left colon mesentery and posteriorly to the parietal peritoneum. The small bowel
288
5ournal of VASCULAR SURGERY
Silva et al.
Fig. 2. Intraoperative appearance of a portion of accessory intraperitoneal sac anchored to retroperitoneum along the course of the aorta-diagnostic of peritoneal encapsulation.
entered and exited through a small opening in the sac just distal to the ligament of Treitz. The positions of all other abdominal viscera were normal. Superior mesenteric artery, exploration was undertaken; however, no thrombus was found. Resection of all gangrenous small bowel was accomplished with the formation of a jejunoileal anastomoses. Lower extremity perfusion renamed to normal, but bilateral fasciotomies were required. The following day reexploration was performed to assess the viability of the remaining bowel. He was found to have had progression of the initial ischemic insult with a nonviable terminal ileum and multiple segments of ischemic sigmoid colon and rectum. His condition deteriorated rapidly, and he died approximately 4 hours after his second operation. Postmortem examination revealed a completely normal aorta and no other developmental abnormalities of the cardiovascular or gastrointestinal tract. DISCUSSION
Acute occlusion of the abdominal aorta has a variety of causes, including in order of decreasing frequency, embolism of cardiac origin, thrombosis of preexisting aortoiliac occlusive disease, thrombosis of an aortic aneurysm, acute aortic dissection, and abdominal trauma. ~The clinical presentation of acute aortic occlusion may reflect the sequential loss of visceral (renal or mesenteric), spinal, and lower extremity arterial perfusion. The severity of symptoms depends on the cephalad extension of the occlusion, the presence of collaterals, and on whether total or partial occlusion is present. Occlusion of the abdominal aorta in a previously
healthy young individual with no preexistent arterial collateralization would be expected to produce profound ischemia of the abdominal viscera and lower extremities as seen with our patient. However, published reviews of acute aortic occlusion have not reported this problem occurring in adults under 35 years of age) 7 In addition, extrinsic compression of the abdominal aorta has not been previously described as a cause of aortic occlusion. When considering possible sources of extrinsic compression of the aorta, one might speculate that expanding visceral or lymphatic tumors be suspected; however, these would be expected to cause gradual rather than acute o&lusion. Similarly, bowel dilation from mechanical obstruction generally produces significant abdominal distention rather than retroperitoneal compression. In this patient the obstruction was confined within the anomalous peritoneal encapsulation, which was anatomically attached to the retroperitoneum. As boweJ distention progressed, pressure within this sac was apparently directed posteriorly, compressing the normal soft wall of the aorta against the vertebral bodies. Peritoneal encapsulation is an exceedingly rare entity that has been thoroughly described but infrequently reported and, as noted above, there have been only 10 cases previously described. It has been proposed that the peritoneal sheath seen in this anomaly arises during embryonic development during the twclfth week of gestation as the midgut which has been contained within the umbilical sac is withdrawn into the abdominal cavity. 1° If the neck of
Volume 16 Number 2 August 1992
the peritoneum of the physiologic umbilical hernia adheres to the duodenum as it is returned into the abdominal cavity it develops as an anomalous peritoneal sheath covering the small bowel in the presence of normally rotated abdominal viscera. Both the preoperative barium enema and the findings at operation documented normal intestinal rotation in this case. Initially, peritoneal encapsulation was thought to be an anatomic curiosity of little clinical significance, and earlier authors suggested that it should be ignored if discovered incidentally during laparotomy. ~4 More recent reports suggest that it may be the source of chronic abdominal pain and acute intestinal obstruction, and should, therefore, be removed when encountered. ~5a6 Peritoneal encapsulation may be mistaken for another tmusual condition, abdominal cocoon, 14 but this latter' abnormality involves a diffuse fibrinous sheath covering the entire small bowel within the peritoneal cavity'. Abdominal cocoon is also rare but has been previously reported only in "women, where an infectious origin has been proposed. The case presented clearly suggests that peritoneal encapsulation may not be a benign congenital conclifton, and this case documents the catastrophic results of a dilating closed-loop obstruction constrained within the peritoneal encapsulation. This type of obstruction did not initially distend anteriorly in the peritoneal cavity as bowel obstructions typically do, but instead was forced posteriorly against the abdominal aorta, causing its acute progressive occlusion, and manifesting itself by isclhemia of the spinal cord with resultant paraplegia, renal artery compromise with acute onset of antlria, loss of lower extremity perfusion with subsequent myonecrosis, and ultimately, by fatal visceral ischemia from compromise of the mesenteric circulation. CT scanning was helpful in this case to correlate the preoperative appearance of the juxtarenal aorta with the clinical observation of return of distal perfusion after decompression of the intestinal obstruction, which resulted from mobilizing the encapsulation off of the aorta.
Acute ao~¢icocclusion caused by extrinsic compression 289
Peritoneal encapsulation is far too rare to expect that CT scanning will provide accurate diagnosis; however, it greatly facilitated an understanding of the pathophysiologic mechanism of the ischemic events in this case. REFERENCES
1. Kornmesser TW, Tripple OH, Haid SP. Acute occlusion of the abdominal aorta. In: Bergan JJ, Yao JST, eds. Surgery of the aorta and its body branches. New York: Grtme and Stratton, 1979:329-36. 2. Littooy FN, Baker WH. Acute aortic occlusion-a multifaceted catastrophe. I VAse SURe 1986;4:211-6. 3. Webb IGH, Jacocks/VIA. Acute aortic occlusion. Am I Surg 1988;155:405-7. 4. Drager SB, Riles TS, Imparato AM. Management of acute aortic occlusion. Am I Surg 1979;138:293-5. 5. Matolo NM, Cheung L, Albo D, Lazarus HM. Acute occlusion of the infrarenal aorta. Am I Surg 1973;t26:78893. 6. Danto LA, Fry WI, Kraft RO. Acute aortic thrombosis. Arch Surg 1972;104:569-72. 7. Harris RW, Andros G, Dulawa LB, Oblath RW. Malignant melanoma embolus as a cause of acute aortic occlusion: report of a case. 1 VAsc St3R~ 1986;3:550-3. 8. Cleland J. On an abnormal arrangement of the peritoneum with remarks on the development of the mesocoion. 1 ,~nat Physiol 1868;2:201-6. 9. Licldey JD, Cameron 1. Note on a case of abnormal disposition of the peritoneum. 1Anat Pbysio11907;41:88-90. 10. Papez ~rw. A rare intestinal anomaly of embryonic origin. Anat Rec 1907;53:197-215. 11. Thorlakson PHT, Monie IW, Thorlakson TK. Anomalous peritoneal encapsulation of the small intestine. Br I Surg 1953;40:490-3. 12. Lewin I(, McCarthy LJ. Peritoneal encapsulation of the small intestine. Gastroenterology 1970;59:270-2. 13. Sayfan I, Adam YG, Reif R. Peritoneal encapsulation in childhood. Am J Surg 1979;138:725-7. 14. SieckJO, Cowgill R, Larkworthy W. Peritoneal encapsulation and abdominal cocoon. Gastroenterology 1983;84:1597601. 15. Lifscbitz O, Tin 1, Sumeruk RA. Peritoneal encapsulation of small intestine. S Aft Med I 1987;71:452. 16. Huddy SPJ, Bailey ME. SmaU bowel obstruction due to peritoneal encapsulation. Br J Surg 1988;75:262.
Submitted Oct: 21, 1991; accepted Jan. 10, 1992.
Acute aortic occlusion as a result of extrinsic compression from peritoneal encapsulation Michael B. Silva, Jr., M D , M a r k M. Connolly, M D , Adrienne B u r f o r d - F o g g s , M D , and William R . Flinn, M D , Chicago, Ill. Acute aortic occlusion frequently occurs with catastrophic visceral, spinal, or lower extremity ischemia and is most often caused by embolic or thrombotic events in older individuals with known cardiovascular disorders. This case describes the rapid development of the clinical signs of acute aortic occlusion in a young and completely healthy individual. Aortic occlusion was produced by extrinsic compression o f the juxtarenal aorta from a closed-loop small intestinal obstruction contained within a peritoneal encapsulation, an extremely rare intraabdominal developmental anomaly. (J VAsc SURG 1992;16: 286-9.)
Acute occlusion o f the abdominal aorta is a rare but potentially catastrophic vascular emergency that most often produces profound limb ischemia and significant lower extremity neuromotor dysfunction including even paraplegia. Acute infrarenal aortic occlusion is most commonly caused by a "saddle" embolus or thrombosis o f an atherosclerotic aorta or an aortic aneurysm. 1"7 Occlusion o f the aorta as a sequella o f extrinsic compression alone has not previously been described. Peritoneal encapsulation is a rare developmental anomaly wherein a portion o f the small bowel is contained within an accessory intraperitoneal membrane that is presumed to be the remnant o f the embryologic yolk sac. Since its initial description by Cleland 8 in 1868, 10 cases have been described in the world literature. 9-16 The present case describes our experience with abdominal aortic occlusion produced by extrinsic compression from dilated small bowel confined within a peritoneal encapsulation. CASE REPORT A 29-year-old man who was an aerobics instructor was admitted with a recent history of colicky periumbilical abdominal pain radiating to his back. He had two episodes of bilious emesis that morning but had a normal bowel
From the Department of Surgery and the Center for Vascular Disease, Columbus Hospital, Chicago. Reprint requests: W. R. Flinn, MD, Center for Vascular Disease, Columbus Hospital, 2520 N. Lakeview, Chicago, IL 60614. 24/4/36162 286
movement the day before admission. The patient described similar episodes of pain that had occurred on numerous occasions previously but had always been of lesser intensity and had resolved spontaneously. Physical examination revealed a muscular man who was most comfortable in a semi-Fowler's position. He was a_febrileand his vital signs were normal. His abdomen was scaphoid and tender in the periumbilical region but without signs of peritoneal irritation. His rectal examination was normal, and stool culture was negative for occult blood. Neuromotor and vascular examinations of his lower extremities were normal. Blood glucose, urea nitrogen, serum electrolytes, and urine were normal. His hemoglobin was 14.1 gm/di, hematocrit 40%, and white blood cell count 13,000, with 29 segmented neutrophils, 1 banded neutrophil, 65 lymphocytes, and 5 monocytes. Abdominal radiography revealed dilated loops of small bowel with gas noted throughout the colon. An unprepared barium enema was performed which showed normal colon anatomy and demonstrated filling of the appendix. Reflux of contrast into the terminal ileum, showed thickened folds of mucosa with considerable irregularity, suggesting the possibility of terminal ileitis or lymphomatous involvement. Over the ensuing hours the patient's pain worsened, and an associated sensation of uncoordination developed in his lower extremities, which progressed from numbness and weakness to a complete loss of muscular function and sensation to the level of his umbilicus. This was accompanied by mild distention of his abdomen, mottling and coolness in his lower body, with absent femoral, popliteal, and pedal pulses. A Foley catheter was placed, and the patient was found to be oliguric. An emergency abdominal CT scan performed during this period showed dilated loops of small bowel. The suprarenal aorta was normal but the
Volume 16 Number 2 Augxtst 1992
Acute aortic occlusion caused by extrinsic compression 287
Fig. 1. A, Selected image from CT scan ofabdorrlen near superior poles of kidneys (K) reveals aorta to be of normal caliber (arrow). B, CT scan cuts of infrarenal aorta (arrow) show flattening and almost complete obliteration of aortic lumen. Residual contrast seen in anatomically normal ascending colon (AC) and descending colon (DC) from previous barium enema. Margins of peritoneal encapsulation of dilated small bowel noted by small arrows.
pararenal and infrarenal aortas appeared compressed against the lumbar spine (Fig. 1). The patient was heparinized and taken to the operating room for exploratory laparotomy. When the abdomen was opened in operation gangrenous small bowel was encountered displaced to the right of the midline by an apparent retroperitoneal mass measuring approximately 15 cm by 18 cm bordered laterally by a normal appearing descending colon and cephalad by the mesentery of the transverse colon. Mobilization of the mass away from the left colon and off the aorta resulted in an immediate return of normal flow through the distal aorta, which was soft and then had
a strong pulse. Mthough the patient had been atmost anuric since the time of CT scanning, the return of renal perfusion after aortic decompression resulted in a prompt resumption of normal urine output. Flow into the lower extremities also returned as evidenced by normal femoral pulses. Further exploration of the mass revealed it to be an anomalous intraperitoneal sac with a closed loop gangrenous obstruction of the majority of the small bowel, which was contained within the sac. The accessory peritoneal membrane (Fig. 2) was reflected superiorly" and laterally on the normally placed left colon mesentery and posteriorly to the parietal peritoneum. The small bowel
288
5ournal of VASCULAR SURGERY
Silva et al.
Fig. 2. Intraoperative appearance of a portion of accessory intraperitoneal sac anchored to retroperitoneum along the course of the aorta-diagnostic of peritoneal encapsulation.
entered and exited through a small opening in the sac just distal to the ligament of Treitz. The positions of all other abdominal viscera were normal. Superior mesenteric artery, exploration was undertaken; however, no thrombus was found. Resection of all gangrenous small bowel was accomplished with the formation of a jejunoileal anastomoses. Lower extremity perfusion renamed to normal, but bilateral fasciotomies were required. The following day reexploration was performed to assess the viability of the remaining bowel. He was found to have had progression of the initial ischemic insult with a nonviable terminal ileum and multiple segments of ischemic sigmoid colon and rectum. His condition deteriorated rapidly, and he died approximately 4 hours after his second operation. Postmortem examination revealed a completely normal aorta and no other developmental abnormalities of the cardiovascular or gastrointestinal tract. DISCUSSION
Acute occlusion of the abdominal aorta has a variety of causes, including in order of decreasing frequency, embolism of cardiac origin, thrombosis of preexisting aortoiliac occlusive disease, thrombosis of an aortic aneurysm, acute aortic dissection, and abdominal trauma. ~The clinical presentation of acute aortic occlusion may reflect the sequential loss of visceral (renal or mesenteric), spinal, and lower extremity arterial perfusion. The severity of symptoms depends on the cephalad extension of the occlusion, the presence of collaterals, and on whether total or partial occlusion is present. Occlusion of the abdominal aorta in a previously
healthy young individual with no preexistent arterial collateralization would be expected to produce profound ischemia of the abdominal viscera and lower extremities as seen with our patient. However, published reviews of acute aortic occlusion have not reported this problem occurring in adults under 35 years of age) 7 In addition, extrinsic compression of the abdominal aorta has not been previously described as a cause of aortic occlusion. When considering possible sources of extrinsic compression of the aorta, one might speculate that expanding visceral or lymphatic tumors be suspected; however, these would be expected to cause gradual rather than acute o&lusion. Similarly, bowel dilation from mechanical obstruction generally produces significant abdominal distention rather than retroperitoneal compression. In this patient the obstruction was confined within the anomalous peritoneal encapsulation, which was anatomically attached to the retroperitoneum. As boweJ distention progressed, pressure within this sac was apparently directed posteriorly, compressing the normal soft wall of the aorta against the vertebral bodies. Peritoneal encapsulation is an exceedingly rare entity that has been thoroughly described but infrequently reported and, as noted above, there have been only 10 cases previously described. It has been proposed that the peritoneal sheath seen in this anomaly arises during embryonic development during the twclfth week of gestation as the midgut which has been contained within the umbilical sac is withdrawn into the abdominal cavity. 1° If the neck of
Volume 16 Number 2 August 1992
the peritoneum of the physiologic umbilical hernia adheres to the duodenum as it is returned into the abdominal cavity it develops as an anomalous peritoneal sheath covering the small bowel in the presence of normally rotated abdominal viscera. Both the preoperative barium enema and the findings at operation documented normal intestinal rotation in this case. Initially, peritoneal encapsulation was thought to be an anatomic curiosity of little clinical significance, and earlier authors suggested that it should be ignored if discovered incidentally during laparotomy. ~4 More recent reports suggest that it may be the source of chronic abdominal pain and acute intestinal obstruction, and should, therefore, be removed when encountered. ~5a6 Peritoneal encapsulation may be mistaken for another tmusual condition, abdominal cocoon, 14 but this latter' abnormality involves a diffuse fibrinous sheath covering the entire small bowel within the peritoneal cavity'. Abdominal cocoon is also rare but has been previously reported only in "women, where an infectious origin has been proposed. The case presented clearly suggests that peritoneal encapsulation may not be a benign congenital conclifton, and this case documents the catastrophic results of a dilating closed-loop obstruction constrained within the peritoneal encapsulation. This type of obstruction did not initially distend anteriorly in the peritoneal cavity as bowel obstructions typically do, but instead was forced posteriorly against the abdominal aorta, causing its acute progressive occlusion, and manifesting itself by isclhemia of the spinal cord with resultant paraplegia, renal artery compromise with acute onset of antlria, loss of lower extremity perfusion with subsequent myonecrosis, and ultimately, by fatal visceral ischemia from compromise of the mesenteric circulation. CT scanning was helpful in this case to correlate the preoperative appearance of the juxtarenal aorta with the clinical observation of return of distal perfusion after decompression of the intestinal obstruction, which resulted from mobilizing the encapsulation off of the aorta.
Acute ao~¢icocclusion caused by extrinsic compression 289
Peritoneal encapsulation is far too rare to expect that CT scanning will provide accurate diagnosis; however, it greatly facilitated an understanding of the pathophysiologic mechanism of the ischemic events in this case. REFERENCES
1. Kornmesser TW, Tripple OH, Haid SP. Acute occlusion of the abdominal aorta. In: Bergan JJ, Yao JST, eds. Surgery of the aorta and its body branches. New York: Grtme and Stratton, 1979:329-36. 2. Littooy FN, Baker WH. Acute aortic occlusion-a multifaceted catastrophe. I VAse SURe 1986;4:211-6. 3. Webb IGH, Jacocks/VIA. Acute aortic occlusion. Am I Surg 1988;155:405-7. 4. Drager SB, Riles TS, Imparato AM. Management of acute aortic occlusion. Am I Surg 1979;138:293-5. 5. Matolo NM, Cheung L, Albo D, Lazarus HM. Acute occlusion of the infrarenal aorta. Am I Surg 1973;t26:78893. 6. Danto LA, Fry WI, Kraft RO. Acute aortic thrombosis. Arch Surg 1972;104:569-72. 7. Harris RW, Andros G, Dulawa LB, Oblath RW. Malignant melanoma embolus as a cause of acute aortic occlusion: report of a case. 1 VAsc St3R~ 1986;3:550-3. 8. Cleland J. On an abnormal arrangement of the peritoneum with remarks on the development of the mesocoion. 1 ,~nat Physiol 1868;2:201-6. 9. Licldey JD, Cameron 1. Note on a case of abnormal disposition of the peritoneum. 1Anat Pbysio11907;41:88-90. 10. Papez ~rw. A rare intestinal anomaly of embryonic origin. Anat Rec 1907;53:197-215. 11. Thorlakson PHT, Monie IW, Thorlakson TK. Anomalous peritoneal encapsulation of the small intestine. Br I Surg 1953;40:490-3. 12. Lewin I(, McCarthy LJ. Peritoneal encapsulation of the small intestine. Gastroenterology 1970;59:270-2. 13. Sayfan I, Adam YG, Reif R. Peritoneal encapsulation in childhood. Am J Surg 1979;138:725-7. 14. SieckJO, Cowgill R, Larkworthy W. Peritoneal encapsulation and abdominal cocoon. Gastroenterology 1983;84:1597601. 15. Lifscbitz O, Tin 1, Sumeruk RA. Peritoneal encapsulation of small intestine. S Aft Med I 1987;71:452. 16. Huddy SPJ, Bailey ME. SmaU bowel obstruction due to peritoneal encapsulation. Br J Surg 1988;75:262.
Submitted Oct: 21, 1991; accepted Jan. 10, 1992.