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Focal lesions of the small intestine
Focal Lesions of the Small Intestine j o l t ~ L. KISER, M.D., St. Louis, Missouri
From the Departments of Surgery and Pathology, Washington University, St. Louis, Missouri.
were treated successfully by segmental intestinal resection. Two patients with an acute illness of brief duration had ulcers due to strangulation of the bowel in an inguinal Richter's hernia. One of these patients had an incarcerated hernia which was reduced in the emergency room. Twelve hours later generalized peritonitis developed from an acutely perforated ulcer of the midileum measuring 1.5 era. in diameter. A perforation of the jejunum occurred in the second patient. Grossly and microscopically these ulcers could not be differentiated from the others. In one woman massive diarrhea and vomiting suddenly developed a few hours before admission. Operation showed three acute ulcers in the proximal jejunum. The diarrhea and dehydration progressed in severity and she died. The cause of these lesions v?as not recognized until large amounts of arsenic were demonstrated in the liver, kidney, and other organs post mortem. This patient presented with an acute fulminant illness which was obviously different from t h a t of the others, although jejunal ulceration was similar to the other focal inflammatory lesions of intestine. She also had acute gastritis which was noted at operation and at autopsy. Unidentified. An etiologic agent was not identified in eight of the nineteen cases. T h e y remain nonspecific ulcerations of the small bowel. The age and sex of these patients are not compatible with an arteriosclerotic cause. Four of the eight patients were less than forty years old and five were female patients. Ages ranged from twenty-two months through eighty-eight years. Duration of s y m p t o m s varied from three days to one year. Five of these lesions involved the ileum and three the jejunum. T h e only perforation was observed in the mesentery of the proximal
HE REPORTS of ulcers of the small intestine by the combination of entericcoated potassium and hydrochlorothiazide [1-3] have p r o m p t e d a careful review of all focal lesions of the small bowel which required operation at the Washington University Medical Center between 1955 and 1964. The literature concerning these lesions has been reviewed.
T produced
MATERIAL
The records concerning focal inflammatory lesions of the small intestine encountered by the Division of Surgical Pathology at Washington University between 1955 and 1964 were re-examined. Those lesions due to adhesions, radiation therapy, gastroenterostomy, Meckel's diverticulum, ectopic gastric mucosa, and other specific causes were excluded. Nineteen focal inflammatory lesions remained to be discussed herein. ETIOLOGIC FACTORS
Identified. A definite etiologic agent was established in eleven of the nineteen patients. Seven persons had been receiving the diuretic potassium-hydrochlorothiazide combination implicated recently as the cause of ulceration of the small bowel. An intestinal ulcer occurred in an eighth patient who had been taking a diuretic of an unknown type. All eight lesions were annular stenotic ulcers of the ileum. Five patients had solitary lesions while the remaining three had multiple annular ulcers a few centimeters apart in the terminal ileum. The only perforation in this group was an unsuspected finding at cesarean section for a full term, twin pregnancy. Three patients had had previous abdominal operations. S y m p t o m s were those of partial intestinal obstruction of two days' to five years' duration. All eight patients
48
American Journal of Surgery
F o c a l L e s i o n s of S m a l l I n t e s t i n e jejunum of a thirty-four year old woman. One forty-six year old m a n with obstruction due to a proximal jejunal ulcer had had a nondiagnostic jejunal biopsy three years previously. Although the jejunum was dilated to twice the normal size, no microscopic abnormality was demonstrated. This m a n died on the third postoperative day. Autopsy did not explain the ulceration or the sudden death. Fibrosis with varying degrees of acute and chronic inflammation was the predominant histologic feature in five of these ulcers of undetermined cause. In three specimens an unusual inflammatory response contained eosinophils and abundant lymphocytes. Acid-fast and fungus stains in all cases for which material was available gave negative results. T h e submucosal infiltrate and granulomatous reaction characteristic of regional enteritis were not observed in any of these cases. In reviewing small bowel lesions prior to selection of these cases no patient was encountered with an initial presentation as nonspecific ulcer and subsequent manifestations of regional enteritis. Arteriosclerotic changes in the bowel wall were not more common than in other cases. Arteriosclerotic changes were graded 0 to 4 microscopically in all specimens. On this basis no microscopic difference was observed between the cases of known and the cases of unknown cause. Thrombosis of blood vessels in the bowel wall or mesentery was observed in two cases due to diuretics and three due to unknown cause. Thrombosis of blood vessels was also seen in several cases with a specific diagnosis t h a t were excluded from this review. This was observed in two patients with focal ulceration due to adhesions and in several patients previously given x-ray therapy to the abdomen and pelvis. No evidence of noxious agents, infection, arteritis, or ectopic mucosa was elicited in these cases. Four of the patients had previously undergone abdominal surgery but adhesions were not present about the lesions. Follow-up information is not available in two patients. Of the remaining six, one died, one had a return of lower abdominal pain eight months postoperatively, and four are asymptomatic. COMMENTS
Traditionally, the earliest reference on priVol. 112, J u l y 1966
49
m a r y nonspecific ulceration of the small bowel is t h a t of the English physician Baillie [4] in 1795. T h e one criterion for inclusion in this group has been the absence of an etiologic agent. In the past 160 years m a n y new causative agents have become manifest. Several discussions of these possibilities have been published [5]. Even before the introduction of the thiazide diuretics i n 1961, similar ulcers were being reported with increasing frequency. In 1930 Morrin [6] was able to find only eightyfive published cases while t o d a y several hundred have been reported. Variability characterizes the group of people in whom these ulcers develop and the course of the illness. Persons in whom nonspecific ulcers of the small intestine develop are of both sexes and include the very young to the very old. I n the review of Barnett [7] the average age was forty-three years, and 9 of the 129 patients were less t h a n twenty years old. Similarly the history varies from acute perforation to partial chronic intestinal obstruction. T h e first signs presented b y some have been guaiac-positive stools and anemia. A large number of etiologic agents produce lesions which m a y be similar clinically or histologieally. Syphilis, tuberculosis, and typhoid fever were the first infections recognized as producing these lesions [5]. Sturim, Kouchoukos, and Ahlvin [8] reported two cases of small bowel ulceration due to histoplasmosis from autopsy data in this medical center. Others have reported ulceration as a presenting sympt o m in histoplasmosis [9 ]. T h e signifcance of peptic ulcers in the jejunum remains uncertain. Jejunal ulcers m a y occur with either gastroenterostomy or ectopie gastric mueosa. Ulcers of the proximal jejunum have been reported which required five operations and because of their persistent nature were thought to be of peptic origin [10]. Markedly elevated overnight gastric acid secretion has been demonstrated in a few cases. Zollinger and Ellison [11] first reported the syndrome in two patients with high gastric acid secretion, p r i m a r y jejunal ulceration, and islet cell tumor. T h e y cited four additional cases, three in patients with ulcers in the second portion of the duodenum and one in a patient with an ulcer in the third portion of the duodenum. The combination of enteric-coated hydrochlorothiazide and potassium was introduced
50
Kiser
in 1961. A several-fold increase in small bowel ulceration has followed over the past three years. Nine of the present cases occurred in the past two years. Lindholmer, Nyman, and Raf [3] were the first to report this relationship. A recent survey of this problem in 440 hospitals showed t h a t 57 per cent of 484 patients in whom these ulcers developed were previously treated with either diuretic or potassium [2]. Animal experiments showed t h a t entericcoated potassium preparations alone or in combination caused ulceration of the intestine whereas thiazides alone did not cause ulcers. Arteriosclerosis has been frequently suggested as an etiologic factor [12-14], and it well m a y account for p a r t of the cases by either focal thrombosis or embolization from other diseased areas. As in this study, the microscopic changes of vascular disease can be produced b y an acute inflammatory process or by other agents. In no series is the age and sex distribution typical of arteriosclerosis. Only a few patients with nonspeeifie ulceration have had other organ systems involved b y arteriosclerosis. Several investigators have presented cases of ulcerated stenosing lesions due to emboli from an endocardial thrombus with emboli lodged in multiple organs [15,16]. Another positive manifestation of atheromatous embolization is the demonstration of cholesterol clefts in the embolus as shown b y Taylor, Gueft, and Lebowieh [17]. Similar vascular lesions and focal stenosing ulcers m a y be the first evidence of periarteritis nodosa [18,19]. Mechanical factors can produce focal ulceration. This m a y result from strangulation or adhesions [20]. Other authors have suggested t h a t an intraluminal foreign body m a y even erode the intestinal wall and then pass on through the intestine [21 ]. Toxic agents such as roentgen rays, systemic 6-mereaptopurine [22], steroids, and arsenic [23-25] m a y produce similar lesions [26]. Ulcer and perforation in pediatric patients is an especially difficult problem. Along with m a n y of the aforementioned agents, septic embolus is probably an i m p o r t a n t cause [27]. Idiopathic perforation of the intestine is relatively common in newborn infants. CONCLUSIONS
Careful s t u d y of nineteen patients with focal ulceration of the small intestine has clarified the cause of eleven ulcers. T h e y were due to
parenteral diuretics, arsenic poisoning, and incarcerated hernia. In previously reported series of patients a marked variation is present in the ages of patients, duration of symptoms, and presenting complaint. Numerous agents seem to have a documented role in the production of such ulcers. Ulceration, fibrosis, and stricture are a common response of the intestine to m a n y different injuries. In addition to the more well established causes, histoplasmosis and focally toxic agents can produce such lesions. With the development of medical knowledge over the past 160 years, etiologic factors have been assigned to m a n y ulcers of the small intestine, thus removing t h e m from the nonspecific category. By history and all other diagnostic criteria the remaining group is still heterogeneous and probably represents motley causes. REFERENCES 1. BAKER, D. R., SCHRADER, W., and HITCHCOCK, C. Small bowel ulceration apparently associated with thiazide and potassium therapy. J.A.M.A., 190: 586, 1964. 2. LAWRASON, F. D., ALBERT, E., MOHR, F. L., and McMAHoN, F. G. Ulcerative-obstructive lesions of the small intestine. J.A.M.A., 191: 116, 1965. 3. LINDHOLMER, B., NYMAN, E., and RAF, L. Nonspecific stenosing ulceration of the small bowel. Acta chir. scandinav., 128: 310, 1964. 4. BAILLIE, M. The Morbid Anatomy of Some of the Most I m p o r t a n t Parts of the H u m a n Body. Albany, 1795. Barber & Southwiek. 5. GRASSMAN, M. Zur Frage des Uleus simples des Dunndarnes. Arch. klin. Surg., 136: 449, 1925. 6. MORRIS, J. C. Spontaneous perforation of primary jejunal ulcers. Irish J. M. Sci., p. 198, 1931. 7. BARNETT, W. O. Primary nonspecific ulcerations of the small intestine. Am. J. Surg., 96: 679, 1958. 8. STURIM, H. S., KOUCHOUKOS, N. T., and AItLVIN, R. C. Gastrointestinal manifestations of disseminated histoplasmosis. Am. f . Surg., 110:435, 1965. 9. HENDBRSON, R. G., PINKERTON, H., and MOORE, L. T. Itistoplasma capsulatum as a cause of chronic ulcerative enteritis. J . A . M . A . , 118: 885, 1942. 10. LEVITT, S. and SAINT, t~. G. Primary peptic ulceration of the jejunum. Lancet, 1 : 77, 1955. 11. ZOLLINGER, R. M. and ELLISON, ]~. H. Pepti c ulceration of the jejunum associated with an islet cell tumor of the pancreas. Ann. Surg., 142: 709, 1955. 12. GREI~NBLATT,M. and GOODMAN, H. Segmental jejunal stenosis of ischemic origin. New England J. Med., 261: 754, 1959. 13. LITWIN, M. S. and CRANE, C. Primary nonspeeific ulcer of the jejunum. Ann. Surg., 151 : 594, 1960.
American Journal of Surgery
Focal Lesions of Small Intestine 14. ROSI~NMANN, L. D. and GROPPER, A. N. Small intestine stenosis caused by infarction; an unusual sequel of mesenteric artery embolism. Ann. Surg., 141: 254, 1955. 15. HAWKINS, C. F. Jejunal stenosis following mesenteric artery occlusion. Lancet, 2: 121, 1957. 16. PoP~, C. H. and O'NEAL, R. M. Incomplete infarction of the ileum simulating regional enteritis. J-.A.M.A., 161: 963, 1956. 17. TAYLOR, 2q. S., GUI~'T, B., and LEBOWICH, R. J. Atheromatous embolization, a cause of gastric ulcers and small bowel necrosis. Gastroenterology, 47: 97, 1964. 18. MCKEOWN, K. C. and GARGULI, A. K. Gastrointestinal symptoms in periarteritis nodosa; report of a case. Brit. J. Surg., 44: 308, 1956. 19. PUGH, J. H. and STRINgeR, P. Abdominal periarteritis nodosa: report of a case. Brit. or. SuPg., 44: 302, 1956. 20. RAW, S. Stricture of small bowel following strangulated hernia. Lancet, 1 : 460, 1963. 21. BEARSE, C. Fish bones as a cause o f intestinal
Vol. 112, July 1966
22.
23. 24.
25.
26.
27.
51
perforations. New England J. .~ed., 2 0 1 : 8 8 5 1929. CLARK, P. A., HSIA, Y. E., and HUNTSMAN, R. G. Toxic complications of therapy with 6-mercaptopurine: two cases with hepatic necrosis and intestinal ulceration. Brit. M. J., 1 : 393, 1960. FISHER, R. C. Metallic poisoning simulating acute surgical abdomen. Am. J. Surg., 26: 175, 1934, GONZALt~S, A. and VANCE, M. Legal Medicine, Pathology and Toxicology, p. 737. New York, 1954. Appleton-Century-Crofts, Inc. HANSI~N, F. and MOLLER, K. Arsenic contents of human organs after fatal poisoning with arsenic trioxide and other arsenical compounds, with some remarks on the manifestations of arsenic poisoning. Acta pharmacol, et toxicol., 5: 135, 1949. MARKOWlTZ, A. M. The less common perforations of the small bowel. Ann. Sufg., 152: 240, 1960. HYDE, G. A. and SANTULLI, T. V. Idiopathic perforation of the small intestine in the neonatal period. Pediatrics, 26: 261, 1960.
From the Departments of Surgery and Pathology, Washington University, St. Louis, Missouri.
were treated successfully by segmental intestinal resection. Two patients with an acute illness of brief duration had ulcers due to strangulation of the bowel in an inguinal Richter's hernia. One of these patients had an incarcerated hernia which was reduced in the emergency room. Twelve hours later generalized peritonitis developed from an acutely perforated ulcer of the midileum measuring 1.5 era. in diameter. A perforation of the jejunum occurred in the second patient. Grossly and microscopically these ulcers could not be differentiated from the others. In one woman massive diarrhea and vomiting suddenly developed a few hours before admission. Operation showed three acute ulcers in the proximal jejunum. The diarrhea and dehydration progressed in severity and she died. The cause of these lesions v?as not recognized until large amounts of arsenic were demonstrated in the liver, kidney, and other organs post mortem. This patient presented with an acute fulminant illness which was obviously different from t h a t of the others, although jejunal ulceration was similar to the other focal inflammatory lesions of intestine. She also had acute gastritis which was noted at operation and at autopsy. Unidentified. An etiologic agent was not identified in eight of the nineteen cases. T h e y remain nonspecific ulcerations of the small bowel. The age and sex of these patients are not compatible with an arteriosclerotic cause. Four of the eight patients were less than forty years old and five were female patients. Ages ranged from twenty-two months through eighty-eight years. Duration of s y m p t o m s varied from three days to one year. Five of these lesions involved the ileum and three the jejunum. T h e only perforation was observed in the mesentery of the proximal
HE REPORTS of ulcers of the small intestine by the combination of entericcoated potassium and hydrochlorothiazide [1-3] have p r o m p t e d a careful review of all focal lesions of the small bowel which required operation at the Washington University Medical Center between 1955 and 1964. The literature concerning these lesions has been reviewed.
T produced
MATERIAL
The records concerning focal inflammatory lesions of the small intestine encountered by the Division of Surgical Pathology at Washington University between 1955 and 1964 were re-examined. Those lesions due to adhesions, radiation therapy, gastroenterostomy, Meckel's diverticulum, ectopic gastric mucosa, and other specific causes were excluded. Nineteen focal inflammatory lesions remained to be discussed herein. ETIOLOGIC FACTORS
Identified. A definite etiologic agent was established in eleven of the nineteen patients. Seven persons had been receiving the diuretic potassium-hydrochlorothiazide combination implicated recently as the cause of ulceration of the small bowel. An intestinal ulcer occurred in an eighth patient who had been taking a diuretic of an unknown type. All eight lesions were annular stenotic ulcers of the ileum. Five patients had solitary lesions while the remaining three had multiple annular ulcers a few centimeters apart in the terminal ileum. The only perforation in this group was an unsuspected finding at cesarean section for a full term, twin pregnancy. Three patients had had previous abdominal operations. S y m p t o m s were those of partial intestinal obstruction of two days' to five years' duration. All eight patients
48
American Journal of Surgery
F o c a l L e s i o n s of S m a l l I n t e s t i n e jejunum of a thirty-four year old woman. One forty-six year old m a n with obstruction due to a proximal jejunal ulcer had had a nondiagnostic jejunal biopsy three years previously. Although the jejunum was dilated to twice the normal size, no microscopic abnormality was demonstrated. This m a n died on the third postoperative day. Autopsy did not explain the ulceration or the sudden death. Fibrosis with varying degrees of acute and chronic inflammation was the predominant histologic feature in five of these ulcers of undetermined cause. In three specimens an unusual inflammatory response contained eosinophils and abundant lymphocytes. Acid-fast and fungus stains in all cases for which material was available gave negative results. T h e submucosal infiltrate and granulomatous reaction characteristic of regional enteritis were not observed in any of these cases. In reviewing small bowel lesions prior to selection of these cases no patient was encountered with an initial presentation as nonspecific ulcer and subsequent manifestations of regional enteritis. Arteriosclerotic changes in the bowel wall were not more common than in other cases. Arteriosclerotic changes were graded 0 to 4 microscopically in all specimens. On this basis no microscopic difference was observed between the cases of known and the cases of unknown cause. Thrombosis of blood vessels in the bowel wall or mesentery was observed in two cases due to diuretics and three due to unknown cause. Thrombosis of blood vessels was also seen in several cases with a specific diagnosis t h a t were excluded from this review. This was observed in two patients with focal ulceration due to adhesions and in several patients previously given x-ray therapy to the abdomen and pelvis. No evidence of noxious agents, infection, arteritis, or ectopic mucosa was elicited in these cases. Four of the patients had previously undergone abdominal surgery but adhesions were not present about the lesions. Follow-up information is not available in two patients. Of the remaining six, one died, one had a return of lower abdominal pain eight months postoperatively, and four are asymptomatic. COMMENTS
Traditionally, the earliest reference on priVol. 112, J u l y 1966
49
m a r y nonspecific ulceration of the small bowel is t h a t of the English physician Baillie [4] in 1795. T h e one criterion for inclusion in this group has been the absence of an etiologic agent. In the past 160 years m a n y new causative agents have become manifest. Several discussions of these possibilities have been published [5]. Even before the introduction of the thiazide diuretics i n 1961, similar ulcers were being reported with increasing frequency. In 1930 Morrin [6] was able to find only eightyfive published cases while t o d a y several hundred have been reported. Variability characterizes the group of people in whom these ulcers develop and the course of the illness. Persons in whom nonspecific ulcers of the small intestine develop are of both sexes and include the very young to the very old. I n the review of Barnett [7] the average age was forty-three years, and 9 of the 129 patients were less t h a n twenty years old. Similarly the history varies from acute perforation to partial chronic intestinal obstruction. T h e first signs presented b y some have been guaiac-positive stools and anemia. A large number of etiologic agents produce lesions which m a y be similar clinically or histologieally. Syphilis, tuberculosis, and typhoid fever were the first infections recognized as producing these lesions [5]. Sturim, Kouchoukos, and Ahlvin [8] reported two cases of small bowel ulceration due to histoplasmosis from autopsy data in this medical center. Others have reported ulceration as a presenting sympt o m in histoplasmosis [9 ]. T h e signifcance of peptic ulcers in the jejunum remains uncertain. Jejunal ulcers m a y occur with either gastroenterostomy or ectopie gastric mueosa. Ulcers of the proximal jejunum have been reported which required five operations and because of their persistent nature were thought to be of peptic origin [10]. Markedly elevated overnight gastric acid secretion has been demonstrated in a few cases. Zollinger and Ellison [11] first reported the syndrome in two patients with high gastric acid secretion, p r i m a r y jejunal ulceration, and islet cell tumor. T h e y cited four additional cases, three in patients with ulcers in the second portion of the duodenum and one in a patient with an ulcer in the third portion of the duodenum. The combination of enteric-coated hydrochlorothiazide and potassium was introduced
50
Kiser
in 1961. A several-fold increase in small bowel ulceration has followed over the past three years. Nine of the present cases occurred in the past two years. Lindholmer, Nyman, and Raf [3] were the first to report this relationship. A recent survey of this problem in 440 hospitals showed t h a t 57 per cent of 484 patients in whom these ulcers developed were previously treated with either diuretic or potassium [2]. Animal experiments showed t h a t entericcoated potassium preparations alone or in combination caused ulceration of the intestine whereas thiazides alone did not cause ulcers. Arteriosclerosis has been frequently suggested as an etiologic factor [12-14], and it well m a y account for p a r t of the cases by either focal thrombosis or embolization from other diseased areas. As in this study, the microscopic changes of vascular disease can be produced b y an acute inflammatory process or by other agents. In no series is the age and sex distribution typical of arteriosclerosis. Only a few patients with nonspeeifie ulceration have had other organ systems involved b y arteriosclerosis. Several investigators have presented cases of ulcerated stenosing lesions due to emboli from an endocardial thrombus with emboli lodged in multiple organs [15,16]. Another positive manifestation of atheromatous embolization is the demonstration of cholesterol clefts in the embolus as shown b y Taylor, Gueft, and Lebowieh [17]. Similar vascular lesions and focal stenosing ulcers m a y be the first evidence of periarteritis nodosa [18,19]. Mechanical factors can produce focal ulceration. This m a y result from strangulation or adhesions [20]. Other authors have suggested t h a t an intraluminal foreign body m a y even erode the intestinal wall and then pass on through the intestine [21 ]. Toxic agents such as roentgen rays, systemic 6-mereaptopurine [22], steroids, and arsenic [23-25] m a y produce similar lesions [26]. Ulcer and perforation in pediatric patients is an especially difficult problem. Along with m a n y of the aforementioned agents, septic embolus is probably an i m p o r t a n t cause [27]. Idiopathic perforation of the intestine is relatively common in newborn infants. CONCLUSIONS
Careful s t u d y of nineteen patients with focal ulceration of the small intestine has clarified the cause of eleven ulcers. T h e y were due to
parenteral diuretics, arsenic poisoning, and incarcerated hernia. In previously reported series of patients a marked variation is present in the ages of patients, duration of symptoms, and presenting complaint. Numerous agents seem to have a documented role in the production of such ulcers. Ulceration, fibrosis, and stricture are a common response of the intestine to m a n y different injuries. In addition to the more well established causes, histoplasmosis and focally toxic agents can produce such lesions. With the development of medical knowledge over the past 160 years, etiologic factors have been assigned to m a n y ulcers of the small intestine, thus removing t h e m from the nonspecific category. By history and all other diagnostic criteria the remaining group is still heterogeneous and probably represents motley causes. REFERENCES 1. BAKER, D. R., SCHRADER, W., and HITCHCOCK, C. Small bowel ulceration apparently associated with thiazide and potassium therapy. J.A.M.A., 190: 586, 1964. 2. LAWRASON, F. D., ALBERT, E., MOHR, F. L., and McMAHoN, F. G. Ulcerative-obstructive lesions of the small intestine. J.A.M.A., 191: 116, 1965. 3. LINDHOLMER, B., NYMAN, E., and RAF, L. Nonspecific stenosing ulceration of the small bowel. Acta chir. scandinav., 128: 310, 1964. 4. BAILLIE, M. The Morbid Anatomy of Some of the Most I m p o r t a n t Parts of the H u m a n Body. Albany, 1795. Barber & Southwiek. 5. GRASSMAN, M. Zur Frage des Uleus simples des Dunndarnes. Arch. klin. Surg., 136: 449, 1925. 6. MORRIS, J. C. Spontaneous perforation of primary jejunal ulcers. Irish J. M. Sci., p. 198, 1931. 7. BARNETT, W. O. Primary nonspecific ulcerations of the small intestine. Am. J. Surg., 96: 679, 1958. 8. STURIM, H. S., KOUCHOUKOS, N. T., and AItLVIN, R. C. Gastrointestinal manifestations of disseminated histoplasmosis. Am. f . Surg., 110:435, 1965. 9. HENDBRSON, R. G., PINKERTON, H., and MOORE, L. T. Itistoplasma capsulatum as a cause of chronic ulcerative enteritis. J . A . M . A . , 118: 885, 1942. 10. LEVITT, S. and SAINT, t~. G. Primary peptic ulceration of the jejunum. Lancet, 1 : 77, 1955. 11. ZOLLINGER, R. M. and ELLISON, ]~. H. Pepti c ulceration of the jejunum associated with an islet cell tumor of the pancreas. Ann. Surg., 142: 709, 1955. 12. GREI~NBLATT,M. and GOODMAN, H. Segmental jejunal stenosis of ischemic origin. New England J. Med., 261: 754, 1959. 13. LITWIN, M. S. and CRANE, C. Primary nonspeeific ulcer of the jejunum. Ann. Surg., 151 : 594, 1960.
American Journal of Surgery
Focal Lesions of Small Intestine 14. ROSI~NMANN, L. D. and GROPPER, A. N. Small intestine stenosis caused by infarction; an unusual sequel of mesenteric artery embolism. Ann. Surg., 141: 254, 1955. 15. HAWKINS, C. F. Jejunal stenosis following mesenteric artery occlusion. Lancet, 2: 121, 1957. 16. PoP~, C. H. and O'NEAL, R. M. Incomplete infarction of the ileum simulating regional enteritis. J-.A.M.A., 161: 963, 1956. 17. TAYLOR, 2q. S., GUI~'T, B., and LEBOWICH, R. J. Atheromatous embolization, a cause of gastric ulcers and small bowel necrosis. Gastroenterology, 47: 97, 1964. 18. MCKEOWN, K. C. and GARGULI, A. K. Gastrointestinal symptoms in periarteritis nodosa; report of a case. Brit. J. Surg., 44: 308, 1956. 19. PUGH, J. H. and STRINgeR, P. Abdominal periarteritis nodosa: report of a case. Brit. or. SuPg., 44: 302, 1956. 20. RAW, S. Stricture of small bowel following strangulated hernia. Lancet, 1 : 460, 1963. 21. BEARSE, C. Fish bones as a cause o f intestinal
Vol. 112, July 1966
22.
23. 24.
25.
26.
27.
51
perforations. New England J. .~ed., 2 0 1 : 8 8 5 1929. CLARK, P. A., HSIA, Y. E., and HUNTSMAN, R. G. Toxic complications of therapy with 6-mercaptopurine: two cases with hepatic necrosis and intestinal ulceration. Brit. M. J., 1 : 393, 1960. FISHER, R. C. Metallic poisoning simulating acute surgical abdomen. Am. J. Surg., 26: 175, 1934, GONZALt~S, A. and VANCE, M. Legal Medicine, Pathology and Toxicology, p. 737. New York, 1954. Appleton-Century-Crofts, Inc. HANSI~N, F. and MOLLER, K. Arsenic contents of human organs after fatal poisoning with arsenic trioxide and other arsenical compounds, with some remarks on the manifestations of arsenic poisoning. Acta pharmacol, et toxicol., 5: 135, 1949. MARKOWlTZ, A. M. The less common perforations of the small bowel. Ann. Sufg., 152: 240, 1960. HYDE, G. A. and SANTULLI, T. V. Idiopathic perforation of the small intestine in the neonatal period. Pediatrics, 26: 261, 1960.