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Hemangiomas of the small bowel in children
The Journal of P E D I A T R I C S
243
Hemangiomas of the small bowel in children Report o f a case a n d revie~v o f the literature
Peggy J. Copple, M.D.,* and Richard A. Kingsbury, M.D. PORTLAND,
ORE.
V A S Cl U L A R t u m o r s o f t h e s m a l l intestine are comparatively rare and are uncommonly seen in childhood. They are almost universally benign in their cellular structure but are dangerous because they may produce gastrointestinal bleeding or obstruction of the intestinal lumen. The following case is presented as an illustration of the repeated examinations and procedures which may be necessary to detect such lesions as one of the causes of gastrointestinal bleeding in children. The patient was a 5-year-old white raale who entered Doernbecher Memorial Hospital for Children on Aug. 19, 1960, for evaluation of persistent anemia of 2 years' duration. The first episode of bleeding occurred in December, 1957, with epistaxis which ceased spontaneously, followed by melena. Later the same month, the patient had hematemesis of more than 1 cup of bright red blood. The hemoglobin was 4 Gm. per cent, so the pa-
From the Department o[ Pediatrics, Doernbecher Memorial Hospital [or Children and the University o[ Oregon Medical School Hospital. "X'Address, Department o[ Pediatrics, University o] Oregon Medical School, 3181 $. W. Sara Jackson Park Road, Portland 1, Ore.
tient was hospitalized and given a transfusion of whole blood. Barium contrast x-ray studies of the esophagus, stomach, and duodenum were normal. The prothrombin time was normal. Two months later, a bout of tonsillitis was followed by vomiting of blood. The hemoglobin was 5 Gm. per cent, so the patient was given 1 unit of whole blood and transferred to Doernbecher Hospital for evaluation. Physical examination showed congenital shortening of the right forearm, a left supernumerary digit, and a Grade 3 systolic m u r m u r in the aortic area. The heart murmur and quality of the peripheral pulses were thought to be characteristic of congenital aortic stenosis. No skin hemangiomas were noted. A complete examination of the nose and throat was negative. The hemoglobin was 8.2 Gm. per cent, the white blood count and differential were normal, and the reticulocyte count was 4 per cent. A survey of the adequacy of coagulation, including bleeding time, coagulation time, clot retraction, tourniquet test, prothrombin time, partial thromboplastin time, prothrombin-proconvertin time, and proacce!erin time revealed no abnormalities. Examination of the bone marrow showed only hyperplasia of the erythrocytic series. Complete barium x-ray
244
Copple and Kingsbury
examination of the esophagus, stomach, duodenum, and intestine was negative. Examination of a string swallowed by the patient showed no locus of bleeding. Sigmoidoscopy was negative. The patient continued to pass 2 to 4 plus guaiac-positive stools ahd the hemoglobin remained low; hence on March 3, 1958, exploratory laparotomy was performed. The serosal surface of the entire gastrointestinal tract was examined and no abnormalities were seen. The gastric mucosa was visualized through a gastrotomy incision, and sigmoidoscopic examination from the cardioesophageal junction to the duodenum revealed no site of bleeding. The postoperative course was uneventful and without further bleeding. The hemoglobin remained around 9 Gm. per cent and the patient was discharged 1 month following operation. There were no interim symptoms of gastrointestinal bleeding. The patient was readmitted in October, 1959, because of recurrent syncopal attacks. Surgical correction of the aortic stenosis was performed without difficulty. T h e postoperative course was complicated by the passage of tarry stools and persistent anemia. On Nov. 17, 1959, the patient vomited bright red blood on two occasions, lowering the hematocrit to 26 per
August 1961
cent; a blood transfusion was given. Three days later, spontaneous epistaxis occurred and responded promptly to bilateral compression of the nares. Five days later, a recurrence of the epistaxis ceased spontaneously. A thorough examination of the nasopharynx again revealed no site of bleeding and no telangiectasia was seen. Two weeks later, on Dec. 9, 1959, the patient experienced massive epistaxis from the left nostril with an estimated blood loss of 750 to 1,000 c.c. The mucosa of the left nasal septum was cauterized with silver nitrate, a Gelfoam pack inserted, and the blood loss replaced. Following these procedures, the stools became negative for occult blood. The hemoglobin remained approximately 12 Gm. per cent, and the patient was discharged. A second upper gastrointestinal series done prior to discharge was normal. Following discharge, the stools remained black; however, the patient was taking oral iron medication. Hemoglobin levels gradually fell, and in early August, 1960, blood transfusion was required to raise the hemoglobin to 12 Gin. per cent. The iron was discontinued and the stools became normal until Aug. 16, 1960, 3 days prior to admission, when the onset of melena and a fall in hemoglobin to 5.5 Gm. per cent caused re-
Fig. 1. Photograph of upper jejunum showing the two hemangiomas.
Volume 59 Number 2
Fig. 2. Roentgenogram taken following injection of 50 per cent Urokon solution into major vessel supplying one of the hemangiomas.
ferral for readmission. There was no history of recent hematemesis or epistaxis, but there had been occasional mild epigastric pain unrelated to ingestion of food. There was no family history of hemangiomas. Two maternal uncles were said to have had recurrent epistaxis without other hemorrhagic manifestations. Physical examination on admission revealed no abnormalities except for the anomalies previously mentioned. The hemoglobin was 4.9 Gm. per cent and the hematocrit was 18 per cent. Repeat coagulation survey and complete examination of the nasopharynx again were unremarkable. An upper gastrointestinal x-ray series with small bowel follow-through films, and barium enema with air contrast study were negative. Oral iron therapy was instituted and the hemoglobin initially rose to 7.4 Gm. per cent, but again recurrent melena was noted. On Sept. 21, 1960, vomiting of guaiac-negatire material occurred on three occasions. On
Hemangiomas o[ small bowel
24 5
the following day, the hemoglobin was 3.4 Gm. per cent, and a blood transfusion was given. Melena persisted and on Sept. 29, 1960, a second exploratory laparotomy revealed two hemangiomas of the upper jejunum, about 24 inches apart. The two dark red lesions encircled the entire circumference of the jejunum for a distance of 1.5 cm. each (Fig. 1). The vascular supply of the lesions was from large dilated vessels extending from the root of the jejunal mesentery (Fig. 2). T h e serosal surface of the bowel including the hemangiomas and the intervening area was removed and a primary bowel anastomosis was performed. The patient tolerated the operation well and there was no untoward bleeding during the procedure. On the second postoperative day hematemesis and melena occurred with a fall in hemoglobin. A blood transfusion was given. No further bleeding was noted and the patient was discharged 2 weeks following operation. At reevaluation 3 months later, the patient had had a single episode of epistaxis related to direct trauma but no further gastrointestinal bleeding had taken place. Microscopic sections of the involved bowel revealed the presence of numerous large dilated blood vessels in the submueosa, muscularis, and subserosa of the involved jejunmn, as well as in the mesenteric attachment. Elastic staining demonstrated that most of the vessels were veins. One area showed penetration of one of these large vessels through the mucosa. DISCUSSION
The hemangiomas were not seen during the first exploratory laparotomy. It m a y be assumed, therefore, that they grew remarkably in the 2 year interim. It remains possible that small and undetected hemangiomas were left which accounted for the postoperative bleeding and that these will later increase in size. Small lesions limited to the mucosa and not visible externally might have been made visible by passing a sigmoidoscope through muItiple smalI incisions in the small intestine. Such a technique would have been
2 4 6 CoppIe and Kingsbury
employed at the time of the second operation if no overt lesion had been found. The hematemesis and epistaxis have not been explained by the bowel hemangiomas. One hundred years ago, Gascoyen I reported the first case of hemangiomas of the small intestine, called "naevi of the viscera," in a man aged 40. Since that time, a total of 15 cases have been reported in children under the age of 16. T M The age range has been from 2 months to 15 years, with 6 of the patients under 10 months of age. Seven of the patients were female, 6 were male, and the sex of 2 was not stated. The predominant symptoms were fatigue, listlessness, and intermittent melena and cramping abdominal pain. The initial clinical picture in 4 of the cases was that of intestinal obstruction; 2 presented as intussusception. In 6 of the cases there were visible hemangiomas or telangiectasia of the skin, but other congenital anomalies were not mentioned. Anemia was a prominent finding in all the patients; in most of them, it was of gradual onset. In 2, sudden collapse occurred, associated with massive rectal bleeding. In 9 of the cases reviewed, the hemangiomas occurred singly, in 6 the lesions were multiple. Of the 13 children who underwent laparotomy, 7 died, mainly from postoperative intestinal obstruction or peritonitis. Five of the patients made an uneventful recovery without further bleeding being noted; however, the longest follow-up reported was 2 years. This case is reported because of its unusual nature and the fact that a second laparotomy was necessary to establish the diagnosis. Although the diagnosis of hemangioma of the small intestine can rarely be made preoperatively, the possibility should be considered in any child who presents with recurrent melena, anemia, absence of any bIeeding tendency, and hemanglomatous lesions elsewhere on the body. Pathologically, the lesions usually consist, as in our case, of dilated venous channels with poorly differentiated connective tissue stroma. It is generally believed that the lesions are congenital and have their origin
August 1961
in embryonic sequestrations of mesodermal tissue. 5 Hemangiomatous lesions have also been found in the esophagus, stomach, large bowel, and the rectum. Vascular lesions of the small bowel cannot always be ruled out by a series of normal roentgenograms, as the lesions often are not demonstrable by roentgen studies. The findings that m a y be noted in some cases on barium studies include intraluminal filling defects, disordered motility, stenosis or angular narrowing of the lumen, regional dilatation, and intussusception. Numerous blood transfusions m a y be necessary, as in our case, to restore adequate hemoglobin levels and circulating blood volume. Other conditions which may produce rectal bleeding but which usually can be distinguished from hemangiomas by other features include Meckel's diverticulum, intestinal polyps, intestinal duplication, intussusception, peptic ulcer, Henoch's purpura, ulcerative colitis, and bacterial dysenteries. The most common cause of rectal bleeding in childhood, anal fissure, usually can be ruled out by careful anorectal examination. It may be emphasized that if a child presents with repeated melena and continued anemia, and if preliminary studies as performed in our case are negative, a laparotomy is justified. As Bockus states, "The physician must be 'small bowel conscious' when confronted with an unexplained anemia and positive occult blood reactions in the stools. ''19 SUMMARY
A case of hemangiomas of the small intestine in a 5-year-old boy is presented. Historical, clinical, surgical, and pathologic features of the condition are discussed. The value of a repeat laparotomy is illustrated in delineation of the cause of persistent gastrointestinal bleeding in childhood.
REFERENCES
1. Gascoyen, M.: Case of Naevus Involving the Parotid Gland, and Causing Death from Suffocation: Naevi of the Viscera, Tr. Path. Soc. Lond. ll: 267, 1860. 2. Sussig, L.: Ein Fall yon blastomat6sem
Volume 59 Number 2
3. 4. 5. 6. 7.
8. 9. 10. 11.
Hamartom des Diinndarmes als Ursache einer Invagination im S~iuglingsalter, Beitr. klin. Chir. 130: 353, 1923-1924. Merchant, F. T.: Intussusception Due to Hemangioma of the Jejunum, Arch. Surg. 39: 1031, 1939. Jaffa, R. H.: Multiple Hemangiomas of the Skin and Internal Organs, Arch. Path. 7: 44, 1929. Kalsjer, R.: l~ber Hamangiome des Tractus gastrointestinalis, Arch. klin. Chir. 187: 351, 1936. Brown, A. J.: Vascular Tumors of the Intestine, Surg. Gynec. & Obst. 39: 191, 1924. Michaelsson, E.: Case of Cavernoma Ilei, Simulating Intussusception, in a Child, Aged Three Months, Acta chit. scandlnav. 61: 570, 1927. Peyton, W. T.: Hemangioma and Its Treatment, Minnesota Med. 21: 590, 1938. White, R. J.: Hemangioma of the Terminal Ileum With Recurrent Hemorrhages From the Rectum, South. Surgeon 10: 886, 1941. Blahd, M. E., Mashke, A. S., and Karsner, H. T.: A Case of Hemangioendothelioma of the Ileum, Am. J. Dis. Child. 26: 379, 1923. Wollsteln, M.: Malignant Hemangioma of the
Hemangiomas o[ small bowel
12. 13. 14. 15. 16. 17.
18. 19.
247
Lung With Multiple Visceral Foci, Arch. Path. 12: 562, 1931. Konjetzny, G. E.: Zur Pathologic der Angiome, Muenchen rned. Wchnschr. 1: 241, 1912. Rickham, P. P.: A Case of Haemangiomatosis of the Small Intestine, Brit. J. Surg. 39: 462, 1952. Heycock, J. B., and Dickinson, P. H.: Haemangiomata of the Intestine, Brit. M. J. 1: 620, 1951. Marine, R., and Lattomus, W. W.: Cavernous Hemangioma of the Gastrointestinal Tract, Radiology 70: 860, 1958. Weddle, R. H., and Snyder, C. D.: Hemangiomas of the Ileum With Intussusception, Surgery 25: 749, 1949. Gentry, R. W., Dockerty, M. B., and Clagett, O. T.: Vascular Malformations of the Intestinal Tract, Surg. Gynec. & Obst. 88: 281, 1949. Ochsner, S., and Penick, R. M.: Hemangioma of the Small Intestine, Radiology 68: 845, 1957. Bockus, H. L., et al.: Gastro-Enterology. Vol. 2, The Small and Large Intestine and Peritoneum, Philadelphia, 1944, W. B. Saunders Company, p. 124.
243
Hemangiomas of the small bowel in children Report o f a case a n d revie~v o f the literature
Peggy J. Copple, M.D.,* and Richard A. Kingsbury, M.D. PORTLAND,
ORE.
V A S Cl U L A R t u m o r s o f t h e s m a l l intestine are comparatively rare and are uncommonly seen in childhood. They are almost universally benign in their cellular structure but are dangerous because they may produce gastrointestinal bleeding or obstruction of the intestinal lumen. The following case is presented as an illustration of the repeated examinations and procedures which may be necessary to detect such lesions as one of the causes of gastrointestinal bleeding in children. The patient was a 5-year-old white raale who entered Doernbecher Memorial Hospital for Children on Aug. 19, 1960, for evaluation of persistent anemia of 2 years' duration. The first episode of bleeding occurred in December, 1957, with epistaxis which ceased spontaneously, followed by melena. Later the same month, the patient had hematemesis of more than 1 cup of bright red blood. The hemoglobin was 4 Gm. per cent, so the pa-
From the Department o[ Pediatrics, Doernbecher Memorial Hospital [or Children and the University o[ Oregon Medical School Hospital. "X'Address, Department o[ Pediatrics, University o] Oregon Medical School, 3181 $. W. Sara Jackson Park Road, Portland 1, Ore.
tient was hospitalized and given a transfusion of whole blood. Barium contrast x-ray studies of the esophagus, stomach, and duodenum were normal. The prothrombin time was normal. Two months later, a bout of tonsillitis was followed by vomiting of blood. The hemoglobin was 5 Gm. per cent, so the patient was given 1 unit of whole blood and transferred to Doernbecher Hospital for evaluation. Physical examination showed congenital shortening of the right forearm, a left supernumerary digit, and a Grade 3 systolic m u r m u r in the aortic area. The heart murmur and quality of the peripheral pulses were thought to be characteristic of congenital aortic stenosis. No skin hemangiomas were noted. A complete examination of the nose and throat was negative. The hemoglobin was 8.2 Gm. per cent, the white blood count and differential were normal, and the reticulocyte count was 4 per cent. A survey of the adequacy of coagulation, including bleeding time, coagulation time, clot retraction, tourniquet test, prothrombin time, partial thromboplastin time, prothrombin-proconvertin time, and proacce!erin time revealed no abnormalities. Examination of the bone marrow showed only hyperplasia of the erythrocytic series. Complete barium x-ray
244
Copple and Kingsbury
examination of the esophagus, stomach, duodenum, and intestine was negative. Examination of a string swallowed by the patient showed no locus of bleeding. Sigmoidoscopy was negative. The patient continued to pass 2 to 4 plus guaiac-positive stools ahd the hemoglobin remained low; hence on March 3, 1958, exploratory laparotomy was performed. The serosal surface of the entire gastrointestinal tract was examined and no abnormalities were seen. The gastric mucosa was visualized through a gastrotomy incision, and sigmoidoscopic examination from the cardioesophageal junction to the duodenum revealed no site of bleeding. The postoperative course was uneventful and without further bleeding. The hemoglobin remained around 9 Gm. per cent and the patient was discharged 1 month following operation. There were no interim symptoms of gastrointestinal bleeding. The patient was readmitted in October, 1959, because of recurrent syncopal attacks. Surgical correction of the aortic stenosis was performed without difficulty. T h e postoperative course was complicated by the passage of tarry stools and persistent anemia. On Nov. 17, 1959, the patient vomited bright red blood on two occasions, lowering the hematocrit to 26 per
August 1961
cent; a blood transfusion was given. Three days later, spontaneous epistaxis occurred and responded promptly to bilateral compression of the nares. Five days later, a recurrence of the epistaxis ceased spontaneously. A thorough examination of the nasopharynx again revealed no site of bleeding and no telangiectasia was seen. Two weeks later, on Dec. 9, 1959, the patient experienced massive epistaxis from the left nostril with an estimated blood loss of 750 to 1,000 c.c. The mucosa of the left nasal septum was cauterized with silver nitrate, a Gelfoam pack inserted, and the blood loss replaced. Following these procedures, the stools became negative for occult blood. The hemoglobin remained approximately 12 Gm. per cent, and the patient was discharged. A second upper gastrointestinal series done prior to discharge was normal. Following discharge, the stools remained black; however, the patient was taking oral iron medication. Hemoglobin levels gradually fell, and in early August, 1960, blood transfusion was required to raise the hemoglobin to 12 Gin. per cent. The iron was discontinued and the stools became normal until Aug. 16, 1960, 3 days prior to admission, when the onset of melena and a fall in hemoglobin to 5.5 Gm. per cent caused re-
Fig. 1. Photograph of upper jejunum showing the two hemangiomas.
Volume 59 Number 2
Fig. 2. Roentgenogram taken following injection of 50 per cent Urokon solution into major vessel supplying one of the hemangiomas.
ferral for readmission. There was no history of recent hematemesis or epistaxis, but there had been occasional mild epigastric pain unrelated to ingestion of food. There was no family history of hemangiomas. Two maternal uncles were said to have had recurrent epistaxis without other hemorrhagic manifestations. Physical examination on admission revealed no abnormalities except for the anomalies previously mentioned. The hemoglobin was 4.9 Gm. per cent and the hematocrit was 18 per cent. Repeat coagulation survey and complete examination of the nasopharynx again were unremarkable. An upper gastrointestinal x-ray series with small bowel follow-through films, and barium enema with air contrast study were negative. Oral iron therapy was instituted and the hemoglobin initially rose to 7.4 Gm. per cent, but again recurrent melena was noted. On Sept. 21, 1960, vomiting of guaiac-negatire material occurred on three occasions. On
Hemangiomas o[ small bowel
24 5
the following day, the hemoglobin was 3.4 Gm. per cent, and a blood transfusion was given. Melena persisted and on Sept. 29, 1960, a second exploratory laparotomy revealed two hemangiomas of the upper jejunum, about 24 inches apart. The two dark red lesions encircled the entire circumference of the jejunum for a distance of 1.5 cm. each (Fig. 1). The vascular supply of the lesions was from large dilated vessels extending from the root of the jejunal mesentery (Fig. 2). T h e serosal surface of the bowel including the hemangiomas and the intervening area was removed and a primary bowel anastomosis was performed. The patient tolerated the operation well and there was no untoward bleeding during the procedure. On the second postoperative day hematemesis and melena occurred with a fall in hemoglobin. A blood transfusion was given. No further bleeding was noted and the patient was discharged 2 weeks following operation. At reevaluation 3 months later, the patient had had a single episode of epistaxis related to direct trauma but no further gastrointestinal bleeding had taken place. Microscopic sections of the involved bowel revealed the presence of numerous large dilated blood vessels in the submueosa, muscularis, and subserosa of the involved jejunmn, as well as in the mesenteric attachment. Elastic staining demonstrated that most of the vessels were veins. One area showed penetration of one of these large vessels through the mucosa. DISCUSSION
The hemangiomas were not seen during the first exploratory laparotomy. It m a y be assumed, therefore, that they grew remarkably in the 2 year interim. It remains possible that small and undetected hemangiomas were left which accounted for the postoperative bleeding and that these will later increase in size. Small lesions limited to the mucosa and not visible externally might have been made visible by passing a sigmoidoscope through muItiple smalI incisions in the small intestine. Such a technique would have been
2 4 6 CoppIe and Kingsbury
employed at the time of the second operation if no overt lesion had been found. The hematemesis and epistaxis have not been explained by the bowel hemangiomas. One hundred years ago, Gascoyen I reported the first case of hemangiomas of the small intestine, called "naevi of the viscera," in a man aged 40. Since that time, a total of 15 cases have been reported in children under the age of 16. T M The age range has been from 2 months to 15 years, with 6 of the patients under 10 months of age. Seven of the patients were female, 6 were male, and the sex of 2 was not stated. The predominant symptoms were fatigue, listlessness, and intermittent melena and cramping abdominal pain. The initial clinical picture in 4 of the cases was that of intestinal obstruction; 2 presented as intussusception. In 6 of the cases there were visible hemangiomas or telangiectasia of the skin, but other congenital anomalies were not mentioned. Anemia was a prominent finding in all the patients; in most of them, it was of gradual onset. In 2, sudden collapse occurred, associated with massive rectal bleeding. In 9 of the cases reviewed, the hemangiomas occurred singly, in 6 the lesions were multiple. Of the 13 children who underwent laparotomy, 7 died, mainly from postoperative intestinal obstruction or peritonitis. Five of the patients made an uneventful recovery without further bleeding being noted; however, the longest follow-up reported was 2 years. This case is reported because of its unusual nature and the fact that a second laparotomy was necessary to establish the diagnosis. Although the diagnosis of hemangioma of the small intestine can rarely be made preoperatively, the possibility should be considered in any child who presents with recurrent melena, anemia, absence of any bIeeding tendency, and hemanglomatous lesions elsewhere on the body. Pathologically, the lesions usually consist, as in our case, of dilated venous channels with poorly differentiated connective tissue stroma. It is generally believed that the lesions are congenital and have their origin
August 1961
in embryonic sequestrations of mesodermal tissue. 5 Hemangiomatous lesions have also been found in the esophagus, stomach, large bowel, and the rectum. Vascular lesions of the small bowel cannot always be ruled out by a series of normal roentgenograms, as the lesions often are not demonstrable by roentgen studies. The findings that m a y be noted in some cases on barium studies include intraluminal filling defects, disordered motility, stenosis or angular narrowing of the lumen, regional dilatation, and intussusception. Numerous blood transfusions m a y be necessary, as in our case, to restore adequate hemoglobin levels and circulating blood volume. Other conditions which may produce rectal bleeding but which usually can be distinguished from hemangiomas by other features include Meckel's diverticulum, intestinal polyps, intestinal duplication, intussusception, peptic ulcer, Henoch's purpura, ulcerative colitis, and bacterial dysenteries. The most common cause of rectal bleeding in childhood, anal fissure, usually can be ruled out by careful anorectal examination. It may be emphasized that if a child presents with repeated melena and continued anemia, and if preliminary studies as performed in our case are negative, a laparotomy is justified. As Bockus states, "The physician must be 'small bowel conscious' when confronted with an unexplained anemia and positive occult blood reactions in the stools. ''19 SUMMARY
A case of hemangiomas of the small intestine in a 5-year-old boy is presented. Historical, clinical, surgical, and pathologic features of the condition are discussed. The value of a repeat laparotomy is illustrated in delineation of the cause of persistent gastrointestinal bleeding in childhood.
REFERENCES
1. Gascoyen, M.: Case of Naevus Involving the Parotid Gland, and Causing Death from Suffocation: Naevi of the Viscera, Tr. Path. Soc. Lond. ll: 267, 1860. 2. Sussig, L.: Ein Fall yon blastomat6sem
Volume 59 Number 2
3. 4. 5. 6. 7.
8. 9. 10. 11.
Hamartom des Diinndarmes als Ursache einer Invagination im S~iuglingsalter, Beitr. klin. Chir. 130: 353, 1923-1924. Merchant, F. T.: Intussusception Due to Hemangioma of the Jejunum, Arch. Surg. 39: 1031, 1939. Jaffa, R. H.: Multiple Hemangiomas of the Skin and Internal Organs, Arch. Path. 7: 44, 1929. Kalsjer, R.: l~ber Hamangiome des Tractus gastrointestinalis, Arch. klin. Chir. 187: 351, 1936. Brown, A. J.: Vascular Tumors of the Intestine, Surg. Gynec. & Obst. 39: 191, 1924. Michaelsson, E.: Case of Cavernoma Ilei, Simulating Intussusception, in a Child, Aged Three Months, Acta chit. scandlnav. 61: 570, 1927. Peyton, W. T.: Hemangioma and Its Treatment, Minnesota Med. 21: 590, 1938. White, R. J.: Hemangioma of the Terminal Ileum With Recurrent Hemorrhages From the Rectum, South. Surgeon 10: 886, 1941. Blahd, M. E., Mashke, A. S., and Karsner, H. T.: A Case of Hemangioendothelioma of the Ileum, Am. J. Dis. Child. 26: 379, 1923. Wollsteln, M.: Malignant Hemangioma of the
Hemangiomas o[ small bowel
12. 13. 14. 15. 16. 17.
18. 19.
247
Lung With Multiple Visceral Foci, Arch. Path. 12: 562, 1931. Konjetzny, G. E.: Zur Pathologic der Angiome, Muenchen rned. Wchnschr. 1: 241, 1912. Rickham, P. P.: A Case of Haemangiomatosis of the Small Intestine, Brit. J. Surg. 39: 462, 1952. Heycock, J. B., and Dickinson, P. H.: Haemangiomata of the Intestine, Brit. M. J. 1: 620, 1951. Marine, R., and Lattomus, W. W.: Cavernous Hemangioma of the Gastrointestinal Tract, Radiology 70: 860, 1958. Weddle, R. H., and Snyder, C. D.: Hemangiomas of the Ileum With Intussusception, Surgery 25: 749, 1949. Gentry, R. W., Dockerty, M. B., and Clagett, O. T.: Vascular Malformations of the Intestinal Tract, Surg. Gynec. & Obst. 88: 281, 1949. Ochsner, S., and Penick, R. M.: Hemangioma of the Small Intestine, Radiology 68: 845, 1957. Bockus, H. L., et al.: Gastro-Enterology. Vol. 2, The Small and Large Intestine and Peritoneum, Philadelphia, 1944, W. B. Saunders Company, p. 124.