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Repair of congenital atresia of the colon in a foal
REPAIR OF CONGENITAL ATRESIA OF THE COLON IN A FOAL J. E. Schneider, DVM; H. W. Leipold, DVM, PhD; S. L. White, DVM and E. Korsgaard , DVM
SUMMARY A foal with congenital atresia of the left dorsal colon was repaired surgicaIly. After the successful repair, a search of the literature was conducted to determine the factors necessary for a repair and for the possible inheritance factor. Theories of etiology, development, and repair in animals and man a re reported. No successful repair in the foal has been previously reported.
CASE REPORT An 18 hours old Quarter Horse foal was referred to Dykstra Veterinary Hospital with anorexia and a distended abdomen which was painful upon palpation. Abdominal discomfort began six hours after birth and had progressed in severity during the next twelve hours prior to entry. The foal would stand with some urging after which she would lie down and immediately roll over on her back with her legs in a flex position. The foal had been treated twice with a soapy warm water enema prior to entry but no fecal passage had occurred. On entry the temperature was 10I 0 F, the pulse 1601 min., respirations 34/min . and the mucous membrances were slightly congested. Abdominal auscultation revealed no intestinal sounds and fluid could not be discerned upon ballotment of the abdomen. A digital rectal examination revealed some clear, pasty material around the anus and perineal area. Results obtained on blood submitted showed hemoglobin 17.8 g/dl, a packed cell volume 47.5% blood urea nitrogen 42.5 tug] dl and total protein of 8.7 gl dl. The total WBC was 4,700/mm3, with34% band,and 55% mature neurophils, 9% lymphocytes, and 2% monocytes. Blood pH , creatinine, and electrolytes were all within normal limits. An abdominal paracentesis revealed a clear fluid with slight amber color. Abdominal radiographs taken after barium was administered orally indic ated that the intestinal tract was patent to the right ventral colon, but barium could not he followed past this area. Because the foal's signs progressively worsened, surgery was elected.
Author's Address : Department of Surgery & Medicine, Department of Pathology, College of Veterinary Medicine, Kansas State University, Man hattan , Kansas 66506. EaUINE VETERINARY SCIENCE
After induction with 500 mg of Thiamylal Sodium,' anesthesia was maintained with Halothane." Lactated Ringer 's solution was dripped intravenously during the surgical procedure for maintenance of blood pressure and to correct the dehydration revealed from the hemogram. The foal was placed in dorsal recumbency and a midline laparotomy performed through a 22 em incision which curved around the umbilical stump which was dissected free. Upon opening the abdominal cavity, a greatly distended left ventral colon and pelvic flexure were visualized. The left dorsal colon consisted of a fibrous band and was not patent at the pelvic flexure (Figure I). The blue distended ventral colon had become dilated 13 em while the dorsal colon was -2 cm across. Both dorsal and ventral colons were relieved from the abdominal cavity, packed off with sterile plastic and cloth dr apes in preparation for an enter anastomosis. The atretic left dorsal colon was removed by scissors dissection staying as close to the fibrous band as possible. This was done to retain the normal vessels and nerves of the intercolic ligaments between the two colons. Fluid contents of the distended left ventral colon and pelvic flexure were aspirated through an eight gauge needle. After decompression, intestinal forceps were applied to the diaphragmatic and pelvic flexures and the ends cut. The ventral colon was folded back onto itself and an anastomosis performed using #0 surgical gut placed in a crushing type pattern after which a reinforcing continuous Lembert pattern was placed with #0 surgical gut. The mesentery was united by #0 surgical gut placed in a simple continuous pattern (Figure 2). Special care was taken to avoid the vessels and nerves as the mesentery was sutured. Upon completion of the anastomosis and the suturing of the intercolic ligament, the intestine was thoroughly washed with a I% solution of Neomycin" in sterile physiological saline solution. The remainder of the digestive tract was examined to determine whether any other abnormalities existed, and all appeared to be normal. The left ventral colon returned to normal color and with pressure applied to the colonic contents, the strength of the anastomosis was confirmed. Two grams of Neomycin sulfate were deposited in the abdominal cavity prior to closure of the incision. Closure was 'Surital - Parke-Davis, Oetro it, Michigan. bUalothane - Halocarbon Labs Inc., Hackensack, New Jersey.
--
---accomplished by suturing the linea alba with #2 polyglycolic acid" using a simple interrupted pattern, the subcutaneous fascia with #0 polyglycolic acid in a simple continuous pattern and the skin.with #00 nylon using a horizontal mattress pattern. The foal recovered uneventfully one hour after surgery. She stood and nursed and showed no abdominal distress thereafter. Tetanus antitoxin was administered after surgery and 400 mg Ampicillin- were administered two times a day for six days following surgery. The day after surgery hemogram revealed WBe 6000/mm,3 with 122
Figure I. A . L ef t ventral co lon (1) and I~fl dor / ('010" (2) d elivered fr om the abdom en along with C ' um (3) . H. I.ef t ventr co/a" (1) an "'11 dorsal colon (2) elevated [o r o bserv lion alar with ecum (3) and rna / intestine (4). , 'ote ban s on ventral colon (5). C. ~ me as R except c Ions h VI' been turned [o r obser vation oj bands ( J) and engor tement of VI' SSl'l.f • • 'ott aboence of mes cnt erytl}:
3% metamyelocytes , 54% bands, 19% mature neutrophils, 15% lymphocytes, and 17% monocytes. Blood urea nitrogen remained at 43 tug] dl, but the total protein had dropped to 6.4 g/ dl. The hemogram on succeeding days returned to normal and the blood urea nitrogen decreased to 30.8 mg/ dl on day three 'to 7.1 mg/ dl on day four. The foal was discharged from the hospital II days after surgery. dDexon - American Cyanamid Co.• Pearl River. New York.
Figure 2. A. Engorged le]t ventral colon (1) with atretic left dorsal colon as a fibrous band (2), B. Packing off with towelsfor aspiration with a 12 gauge needle. C. Aspiration site identified, It will later be ill the transected portion. D, Collapsed left ventral colon (I), E. Relative size of empty left ventral colon (I) with the fibrous left dorsal colon (2). EQUINE VETERINARY SCIENCE
123
DISCUSSION A search of the literature re vealed that intestinal atresia has been reported in man,' :" pigs, 25.26 sheep.":" dogs.P-" and cattle. 34•35 Atresia coli in foals has been suggested as a lethal autosomal recessive inheritable defect with little supportive evidence." The lethal white foal syndrome is a distinctly separate entity which has neither agenesis nor atresia. but a thinning of the muscular walls and paucity of myenteric plcxcs.:" The term atresia implies a closure from the previously normally formed lumen while agenesis implies a failure of the development of a part of the intestine. All parts of the colon in this case were present, but were not united. There are various theories why congential atresia develops. Atresia ani in pigs is considered an inheritable trait. 2s.26 Atresia jejunae in Jersey calves is reported to be an inheritable autosomal recesive trait. 36 Atresia ilei in Swedish Highland cattle is compatible with an autosomal recessive inheritance." There have also been some reports in the human literature of single and multiple level intestinal atresias in the same families suggesting a probable inheritance factor. 5.15.16 The developmental arrest theory that was first proposed 1.8.10.20 states that atresia of the intestine is generally considered to be an embryonal malformation due to lack of recanalization of the intestinal tube at the end of the second month of fetal life. This assumes the intestine initially is open; then is plugged by mucous, then closes, then recanalizes. Some earlier reports which supported that theory also cited cases ofjejunal and ileal atresia in humans in which the total length of the small intestine was far less than the normal.' In a report" that refuted that theory, it was observed that in multiple areas of atresia of the jejunum and ileum, there were gross meconium, microscopic squamous epithelial cells, lanugo hair, and bile droplets. found distal to the point of atresia and even between segments of multiple atresias. Since excretion of bile begins about the I Ith week, the squamous epithelial cells swallowed from the vernix caseosa are found in the intestine after the twelfth week. Recanalization of the intestinal tube usually occurs at the end of the second month of fetal life. Therefore, if the recanalization theory were a valid argument, the bile pigments and the squamous epithelium would not be found distal to the atresia. Experimental work has shown that if blood supply is interrupted to any portion of the intestinal tract, subsequent atresia can develop in that area at the point of interrupted blood supply to the gut (Figure 3). This work was done in puppies/-'! in utero 10 days pre-partum and also in chicken embryos." An observation was also reported from a case of lack of blood supply and atresia coli in a calf,"? Interruptiorr'-" of the blood supply can be caused by fetal herniation, kinks, intussusception, torsions, or primary vascular accidents. Depending on the severity of the vascular insult, three distinct types of atresia occur: I) a complete occlusion by a small 124
.B A
Figure 3. Various forms of atresia: A. Simple occlusion by a diaphragm-type closure. B. Intestine ending in a blindpouch connected to caudal segment by aflbrous band(arrow). C. Complete occlusion by a separation of intestine and mesentery.
diaphragm-type closure, 2) a complete occlusion of the lumen with intestine terminating in a blind segment, or 3) a complete occlusion without any connection between two segments with a corresponding V-shaped defect in the mesentery (Figure 3). Intestinal atresia can occasionally be associated with defects in other systems as well. The urogenital system is most commonly involved; therefore, evaluation of this system prior to and during surgery is necessary.6.7.27.JO.JI Intestinal atresia is a surgical emergency requiring early diagnosis and treatment to obtain a successful result. In humans the signs arc those of a low intestinal obstruction resulting in vomiting of bile along with acute abdominal distention usually occurring within 24-36 hours after birth, and there have been few survivals in infants treated beyond the fourth day of life." Failure to pass meconium on the first day of life is viewed with suspicion and radiographs arc used to help diagnose the problem. Delay in diagnosis, inadequate supportive care, and presence of associated anomalies all lend to the grave prognosis in intestinal atresia. There are many factors which could contribute to the high mortality of atresia such as delay in diagnosis, delay in correction, inadequate supportive care both before and after surgery, associated anomalies, and improper assessment of the intestinal tract during the surgical procedure. An aggressive approach to the maintenance of the blood volume with fluid and electrolye therapy and maintenance of the acid base balance cannot be over emphasized. Thorough evaluation of the dilated viscus cranial to the atresia is a very important consideration and intestinal decompression prior to anastomosis is mandatory. EQUINE VETERINARY SCIENCE
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Figure 4. Tire essential features. of a closure of a gut of different sizes: A. A tretlc segment resected. Cranial segment is incised longitudinally at tire antimesenteric border sufficiently to create similar sizes to anastamose. B. A continuous seromuscular suture is placed and long ends left on tire posterior row for stabilization. C. Series of Lembert-type sutures for completion of closure on tire anterior row.
With atresia there is usualIy a disparity between the size of bowel and the distended cranial portion is much larger than the portion caudal to the atresia. It has been shown that a higher percentage of recoveries occur when the hypertrophied dilated blind pouch is excised because the chronic dilation reduces blood to the area. Leaving the acutely distended blind pouch results in the failure of some anastomoses. Post-operatively this pouch may become necrotic resulting in leakage, peritonitis, and subsequent death. The anastomosis should be performed with the intestines in normal continuity. In some cases where side-to-side anastomosis was performed in the jejuno-ileo atresia, obstruction and a "blind loop" syndrome were frequent sequela.t-'? The anastomosis, therefore, should be made either end to oblique or end to end. On some occasions, even with perfect anastomosis, there is a failure of propulsion of the meconium in the caudal segments and because of this, it is recommended that the dilated portion cranial to the atresia be resected a July/August 1981
distance of approximately 15-20 cm.P-" All remaining fecal material should be flushed out of the intestine cranial to the transection. In this case, it would have been difficult because the dilation extended completely around the sternal flexure to the right ventral colon area. A technique illustrated in Figure 4 could solve the problem of disparity closure. EsentialIy, it involves a one layer closure using either #00 surgical gut, #00 polyglycolic acid or polyglactin 91O[ as the suture of choice. The posterior layer is placed as a continuous seromuscular suture with each end being retained as a guide suture. An anterior layer is made next as a series of Lernbert-type sutures. This permits one to place the interrupted sutures where they are under ready vision. Incising the intestines, as demonstrated in Figure 4A can
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Ethicon, Inc., Somerville. New Jersey.
125
be done prior to the suturing to correct the disparity. In this case reported, a crushing type s ut ure was used with a continuous Lcmbert ovcrsew. Neomycin was used to wash the inte stines in this case. Aminoglycosides can cause a neuromuscular blockage and respiratory depression or arrest. cardiovascular depression, kidney degeneration or vestibular degeneration. Care must be given to dosage of the drug and monitoring of the patient.
CONCLUSIONS Mo st domestic animals and man arc susceptible to intestinal atrcsias ranging from duodenal to anal atresias. Some of th e reasons why they occur may be: I) inheritance, 2) development arrest with failure of recanalization of a part, and 3) vascular accidents during fetal development. Surgery is possible in most cases , but delay in diagnosis and surgery lessens the recovery rate. Associated anomalies must be considered in the diagnostic work up , and should always be checked at the time of surgery. Fluids, electrolytes, and whole blood mu st be regul ated to effect a cure. End to end or end to oblique anastomosis is preferred to allow normal continuity of the intestine and to prevent th e "blind loop" syndrome. Resection of the severely dilated cranial po rtion is recommended to obtain a normal vascularized functional intestine. Two other foals have been sur gica lly explored. One foal with a congenital atresia of the left dorsal colon was corrected, but expired four days after surgery with renal failure . One kidney was absent and the second was one-half normal size. The other foal could not be corrected surgically as the entire diaphragmatic flexure was atretic to the transverse colon. Radiographic studies were not useful in locating the site of atresia in any of these three cases.
REFERENCES I. Arcy, LB: Developmcnral anatomy. 6th ed. Ph iladelphia. \VB Saunders Co . 1954. pp 249-250 . 2. Barnard. CN : The gen esis of intestinal a tres ia. Surg Forum. 42nd Clin Congress. Amer Coli Surg, 7: 393 . 1956. . 3. Barnard. CN : The genesis o f intest inal atresia . Minn sted 39:745. 1956. 4. Benson. CD. Lofti, MW, Brough. AJ : Congenital atresia a nd stenosis of the colon. J Ped Surg 3 (2): 253. 1968. 5. Berant, M, Kah a na. 0: Familial duodenal atresia. Arch Dis Child 45: 28/ . /970. 6. Dykstra, G. Sieber. WK. Ki eswetter, \VB: Intestinal artesia. Arch Surg 97: 175. 1968. 7. Fronkalsrud, EW, de Lorirnier, AA . Hays. OM : Congen ital artesia and stenosis of the duodenum. Ped 43: 79. 1969. 8. Forssner, H: D ie Angeborenen darm-und oesophagusatres ian, eine entwicklungsgeschichtliche un pathologisch-anatornische studie. Anat lIeJte. Wiesbodell.34: I. 1907. 9. Hand elsman. JC. Abrams. S. Corry. RJ : Improvement of therapy for congcnital jejunoileal atres ia surgery. Gyn & Ob, 691, 1963. 10. Johnson. FP: The development of the mucous membrane of the esophagus. stomach. and small intestine in th e human embryo. Allier J Allot 10: 521.1910. II. Louw, J II. Barnard. CN : Co ngen ital intes t ina l atresia , ob servat ions on its origin. Lancet 2: 1065. 1955.
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12. Louw, JII : Congenital inte stinal atresia and steno sis in the ne wbo rn . Ob servations on its pathogenesis and treatment. Ann Rov Coli Surg Eng 25: 209. 1959. . 13. Louw, J II : Inve st igat ions into the etiology of congenital atresia o f the colon. Dis oj Colon and Rectum, 7: 471, 1964. 14. Magnu s. RV: Rectal atresia as distingu ished from rectal agenesis. J oj Peel Surg 3: 593. 1968. 15. Mishalany, IlG. Najjar, FB : Familial jejunal a tr esia: Threccases in one famil y. J Peel 73: 753. 1968. 16. M ishal any, IlG. Der Kaloustian, VM. Ghandour, M: Familial congenital duodenal atresia. Peel 46: 629. 1970. 17. Nixon. 1I11: I ntest in al obstruct ion in th e newborn. Arch Dis Child 30: 13. 1955. 18. Santull i. TV. Blanc. \VA: Con genital a t resia of the intest ine: Pathogenesis and treatment. ..11111 oj Surg 154: 939. 1961. 19. Sukarochana, K. Kiesewetter. WB: Imperforate anus . 38: 89, 1968. 20. Tandler, J : Zur entwicklungsgeschichte des men schlichen duodenum im fruhen embryonal stadien . Gegenbau Morph, Jahrbuch 29: 187. 1900. 21. Tosov sky, VV. Novak, K: Congenital intest inal atresia. Internat ional Surger y 51: 438. 1969. 22. Weitzman. J. Vanderhoof. RS : Jejunal atres ia with agenesis of the dorsal mesentery. Alii J oj Surg III: 143. 1966. 23. Wilmore, OW: Factors correlating with a successful outcome following extensive intest inal resecti on in newborn infants. J oj Ped80: 88, 1972. 24. Zwi rcn , GT. Andrews. IIG. Ahman, P: J ejunal atresia with a genesis of th e dorsal mesentery. J oj Ped Surg 7: 414. 1972. 25. Norrish , JG. Rennie, JC: Observations on the inheritance of at res ia ani in swine. J llcred 59: 186-1 87. 1968. 26. Vogt , OW: Chromosome cond ition of two atresia ani pigs. J Allim Sci 26: 1002-1004. 1967. 27. Dennis. SM Leipold. IIW: Atresia ani in sheep. Vet Rec91: 219224. 1972. 28. Hancock, J: Atresia ani in sheep. Proc /Oth Amlll COIIJNZ. A nim al Produ ction, 91. 1950. 29. Hartley, WJ . Kater. JC: Perin atal disease co nd it ion s of sheep in New Zealand . N Z eal Vet J 12: 49 . 1964. 30. Leipold , II W: Atresia jejuni in a la m b. Vet Rec 93: 644. 1973. 31. Safford. JW. 1I0vcrsland. AS : A study of lamb mortality in a western range flock. I Autopsy findings on 1051 Iambs. JAil S ci 19: 265. 1960. 32. Ladd s, PW. And erson. "'V: Atresi a ilei in a pup. JA V.\fA 158: 20 7 1-2072. 1971. 33. Rawlings. CA. Capps. WF. Jr: Recto vaginal fistula and imperforate anus in a dog. JAV.\fA 159: 320-3 26, 1971. 34. Greene. IIJ et 31: Congeni tal d efe cts in cattle. Irish Vet J 27: 37 45. 1973. 35. Hunter, AG : Atresia ilei in a calf. Vet Rec 94 : 170. 1974. 36. Jubb, KVF, Kennedy, PC: Pathologyof Domestic Animals. Vol. 2. 5th ed., Academic Press. New York. i'\.W., 1970. 37. Kernkamp, IICII. Legates, JE: Duo-cecum - An intestinal anomaly in Calves, JA VMA 139: 1207. 1961. 38. Leipold. IIW. S aperstein. G . Johnson, DO. Dennis, SM: Int estinal atrcsti a in calves. I'M/SAC 1037. 1976. 39. Len gh aus, C .. Wh ite, WE: Int estinal atresia in calves. A /lSI Vet J 49: 587-588. 1973. 40. ~lcG eady. TA ct al: Atres ia coli in a calf: A note on its Pathogenesis. Irish Vet J 21: 148-150. 1967. 41. Nair, S : Atresia ani with rcctovaginal fistula in a calf - a case report. Indian Vet J 49 : 528-529, 1972. 42. Nihl een , B. Eriksson. K: A hereditary lethal defect in calves atresia ilei . Nord Vet Med 10: 113-127, 1958. 43. Osborne. JC, Legates. JE: Six cas es of bovine intestinal anoma ly. JA V,\/A 142: 1104, 1963 . 44. Schlouhauer, CF: Congen ital atresi a of the co lo n in a calf. JAVMA 127: 339.1955. 45. Sk ewe s. AR: Bovine intestinal anomaly. Vet ,\/ed 57: 133-134, 1962. 46 . Cohrs. P: Nieb erle and Cohrs' Textbook of the special pathological anatomy ofdomestic animals. Peragamon Press. Oxford. 1967. pp 389. 47. Earlarn, RJ: A study of th e a eti ol og y of congenital sten osi s of th e gut. Anll Roy Surg Ellg151 : 126. 1972. 48. Schn ieider, J E. Leipold. HW : Rece ssive leth al wh ite in two foal s. J £q sted and Sur g 2 (Ill: 479. 1978. .
s
EQUINE VETERINARY SCIENCE
SUMMARY A foal with congenital atresia of the left dorsal colon was repaired surgicaIly. After the successful repair, a search of the literature was conducted to determine the factors necessary for a repair and for the possible inheritance factor. Theories of etiology, development, and repair in animals and man a re reported. No successful repair in the foal has been previously reported.
CASE REPORT An 18 hours old Quarter Horse foal was referred to Dykstra Veterinary Hospital with anorexia and a distended abdomen which was painful upon palpation. Abdominal discomfort began six hours after birth and had progressed in severity during the next twelve hours prior to entry. The foal would stand with some urging after which she would lie down and immediately roll over on her back with her legs in a flex position. The foal had been treated twice with a soapy warm water enema prior to entry but no fecal passage had occurred. On entry the temperature was 10I 0 F, the pulse 1601 min., respirations 34/min . and the mucous membrances were slightly congested. Abdominal auscultation revealed no intestinal sounds and fluid could not be discerned upon ballotment of the abdomen. A digital rectal examination revealed some clear, pasty material around the anus and perineal area. Results obtained on blood submitted showed hemoglobin 17.8 g/dl, a packed cell volume 47.5% blood urea nitrogen 42.5 tug] dl and total protein of 8.7 gl dl. The total WBC was 4,700/mm3, with34% band,and 55% mature neurophils, 9% lymphocytes, and 2% monocytes. Blood pH , creatinine, and electrolytes were all within normal limits. An abdominal paracentesis revealed a clear fluid with slight amber color. Abdominal radiographs taken after barium was administered orally indic ated that the intestinal tract was patent to the right ventral colon, but barium could not he followed past this area. Because the foal's signs progressively worsened, surgery was elected.
Author's Address : Department of Surgery & Medicine, Department of Pathology, College of Veterinary Medicine, Kansas State University, Man hattan , Kansas 66506. EaUINE VETERINARY SCIENCE
After induction with 500 mg of Thiamylal Sodium,' anesthesia was maintained with Halothane." Lactated Ringer 's solution was dripped intravenously during the surgical procedure for maintenance of blood pressure and to correct the dehydration revealed from the hemogram. The foal was placed in dorsal recumbency and a midline laparotomy performed through a 22 em incision which curved around the umbilical stump which was dissected free. Upon opening the abdominal cavity, a greatly distended left ventral colon and pelvic flexure were visualized. The left dorsal colon consisted of a fibrous band and was not patent at the pelvic flexure (Figure I). The blue distended ventral colon had become dilated 13 em while the dorsal colon was -2 cm across. Both dorsal and ventral colons were relieved from the abdominal cavity, packed off with sterile plastic and cloth dr apes in preparation for an enter anastomosis. The atretic left dorsal colon was removed by scissors dissection staying as close to the fibrous band as possible. This was done to retain the normal vessels and nerves of the intercolic ligaments between the two colons. Fluid contents of the distended left ventral colon and pelvic flexure were aspirated through an eight gauge needle. After decompression, intestinal forceps were applied to the diaphragmatic and pelvic flexures and the ends cut. The ventral colon was folded back onto itself and an anastomosis performed using #0 surgical gut placed in a crushing type pattern after which a reinforcing continuous Lembert pattern was placed with #0 surgical gut. The mesentery was united by #0 surgical gut placed in a simple continuous pattern (Figure 2). Special care was taken to avoid the vessels and nerves as the mesentery was sutured. Upon completion of the anastomosis and the suturing of the intercolic ligament, the intestine was thoroughly washed with a I% solution of Neomycin" in sterile physiological saline solution. The remainder of the digestive tract was examined to determine whether any other abnormalities existed, and all appeared to be normal. The left ventral colon returned to normal color and with pressure applied to the colonic contents, the strength of the anastomosis was confirmed. Two grams of Neomycin sulfate were deposited in the abdominal cavity prior to closure of the incision. Closure was 'Surital - Parke-Davis, Oetro it, Michigan. bUalothane - Halocarbon Labs Inc., Hackensack, New Jersey.
--
---accomplished by suturing the linea alba with #2 polyglycolic acid" using a simple interrupted pattern, the subcutaneous fascia with #0 polyglycolic acid in a simple continuous pattern and the skin.with #00 nylon using a horizontal mattress pattern. The foal recovered uneventfully one hour after surgery. She stood and nursed and showed no abdominal distress thereafter. Tetanus antitoxin was administered after surgery and 400 mg Ampicillin- were administered two times a day for six days following surgery. The day after surgery hemogram revealed WBe 6000/mm,3 with 122
Figure I. A . L ef t ventral co lon (1) and I~fl dor / ('010" (2) d elivered fr om the abdom en along with C ' um (3) . H. I.ef t ventr co/a" (1) an "'11 dorsal colon (2) elevated [o r o bserv lion alar with ecum (3) and rna / intestine (4). , 'ote ban s on ventral colon (5). C. ~ me as R except c Ions h VI' been turned [o r obser vation oj bands ( J) and engor tement of VI' SSl'l.f • • 'ott aboence of mes cnt erytl}:
3% metamyelocytes , 54% bands, 19% mature neutrophils, 15% lymphocytes, and 17% monocytes. Blood urea nitrogen remained at 43 tug] dl, but the total protein had dropped to 6.4 g/ dl. The hemogram on succeeding days returned to normal and the blood urea nitrogen decreased to 30.8 mg/ dl on day three 'to 7.1 mg/ dl on day four. The foal was discharged from the hospital II days after surgery. dDexon - American Cyanamid Co.• Pearl River. New York.
Figure 2. A. Engorged le]t ventral colon (1) with atretic left dorsal colon as a fibrous band (2), B. Packing off with towelsfor aspiration with a 12 gauge needle. C. Aspiration site identified, It will later be ill the transected portion. D, Collapsed left ventral colon (I), E. Relative size of empty left ventral colon (I) with the fibrous left dorsal colon (2). EQUINE VETERINARY SCIENCE
123
DISCUSSION A search of the literature re vealed that intestinal atresia has been reported in man,' :" pigs, 25.26 sheep.":" dogs.P-" and cattle. 34•35 Atresia coli in foals has been suggested as a lethal autosomal recessive inheritable defect with little supportive evidence." The lethal white foal syndrome is a distinctly separate entity which has neither agenesis nor atresia. but a thinning of the muscular walls and paucity of myenteric plcxcs.:" The term atresia implies a closure from the previously normally formed lumen while agenesis implies a failure of the development of a part of the intestine. All parts of the colon in this case were present, but were not united. There are various theories why congential atresia develops. Atresia ani in pigs is considered an inheritable trait. 2s.26 Atresia jejunae in Jersey calves is reported to be an inheritable autosomal recesive trait. 36 Atresia ilei in Swedish Highland cattle is compatible with an autosomal recessive inheritance." There have also been some reports in the human literature of single and multiple level intestinal atresias in the same families suggesting a probable inheritance factor. 5.15.16 The developmental arrest theory that was first proposed 1.8.10.20 states that atresia of the intestine is generally considered to be an embryonal malformation due to lack of recanalization of the intestinal tube at the end of the second month of fetal life. This assumes the intestine initially is open; then is plugged by mucous, then closes, then recanalizes. Some earlier reports which supported that theory also cited cases ofjejunal and ileal atresia in humans in which the total length of the small intestine was far less than the normal.' In a report" that refuted that theory, it was observed that in multiple areas of atresia of the jejunum and ileum, there were gross meconium, microscopic squamous epithelial cells, lanugo hair, and bile droplets. found distal to the point of atresia and even between segments of multiple atresias. Since excretion of bile begins about the I Ith week, the squamous epithelial cells swallowed from the vernix caseosa are found in the intestine after the twelfth week. Recanalization of the intestinal tube usually occurs at the end of the second month of fetal life. Therefore, if the recanalization theory were a valid argument, the bile pigments and the squamous epithelium would not be found distal to the atresia. Experimental work has shown that if blood supply is interrupted to any portion of the intestinal tract, subsequent atresia can develop in that area at the point of interrupted blood supply to the gut (Figure 3). This work was done in puppies/-'! in utero 10 days pre-partum and also in chicken embryos." An observation was also reported from a case of lack of blood supply and atresia coli in a calf,"? Interruptiorr'-" of the blood supply can be caused by fetal herniation, kinks, intussusception, torsions, or primary vascular accidents. Depending on the severity of the vascular insult, three distinct types of atresia occur: I) a complete occlusion by a small 124
.B A
Figure 3. Various forms of atresia: A. Simple occlusion by a diaphragm-type closure. B. Intestine ending in a blindpouch connected to caudal segment by aflbrous band(arrow). C. Complete occlusion by a separation of intestine and mesentery.
diaphragm-type closure, 2) a complete occlusion of the lumen with intestine terminating in a blind segment, or 3) a complete occlusion without any connection between two segments with a corresponding V-shaped defect in the mesentery (Figure 3). Intestinal atresia can occasionally be associated with defects in other systems as well. The urogenital system is most commonly involved; therefore, evaluation of this system prior to and during surgery is necessary.6.7.27.JO.JI Intestinal atresia is a surgical emergency requiring early diagnosis and treatment to obtain a successful result. In humans the signs arc those of a low intestinal obstruction resulting in vomiting of bile along with acute abdominal distention usually occurring within 24-36 hours after birth, and there have been few survivals in infants treated beyond the fourth day of life." Failure to pass meconium on the first day of life is viewed with suspicion and radiographs arc used to help diagnose the problem. Delay in diagnosis, inadequate supportive care, and presence of associated anomalies all lend to the grave prognosis in intestinal atresia. There are many factors which could contribute to the high mortality of atresia such as delay in diagnosis, delay in correction, inadequate supportive care both before and after surgery, associated anomalies, and improper assessment of the intestinal tract during the surgical procedure. An aggressive approach to the maintenance of the blood volume with fluid and electrolye therapy and maintenance of the acid base balance cannot be over emphasized. Thorough evaluation of the dilated viscus cranial to the atresia is a very important consideration and intestinal decompression prior to anastomosis is mandatory. EQUINE VETERINARY SCIENCE
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Figure 4. Tire essential features. of a closure of a gut of different sizes: A. A tretlc segment resected. Cranial segment is incised longitudinally at tire antimesenteric border sufficiently to create similar sizes to anastamose. B. A continuous seromuscular suture is placed and long ends left on tire posterior row for stabilization. C. Series of Lembert-type sutures for completion of closure on tire anterior row.
With atresia there is usualIy a disparity between the size of bowel and the distended cranial portion is much larger than the portion caudal to the atresia. It has been shown that a higher percentage of recoveries occur when the hypertrophied dilated blind pouch is excised because the chronic dilation reduces blood to the area. Leaving the acutely distended blind pouch results in the failure of some anastomoses. Post-operatively this pouch may become necrotic resulting in leakage, peritonitis, and subsequent death. The anastomosis should be performed with the intestines in normal continuity. In some cases where side-to-side anastomosis was performed in the jejuno-ileo atresia, obstruction and a "blind loop" syndrome were frequent sequela.t-'? The anastomosis, therefore, should be made either end to oblique or end to end. On some occasions, even with perfect anastomosis, there is a failure of propulsion of the meconium in the caudal segments and because of this, it is recommended that the dilated portion cranial to the atresia be resected a July/August 1981
distance of approximately 15-20 cm.P-" All remaining fecal material should be flushed out of the intestine cranial to the transection. In this case, it would have been difficult because the dilation extended completely around the sternal flexure to the right ventral colon area. A technique illustrated in Figure 4 could solve the problem of disparity closure. EsentialIy, it involves a one layer closure using either #00 surgical gut, #00 polyglycolic acid or polyglactin 91O[ as the suture of choice. The posterior layer is placed as a continuous seromuscular suture with each end being retained as a guide suture. An anterior layer is made next as a series of Lernbert-type sutures. This permits one to place the interrupted sutures where they are under ready vision. Incising the intestines, as demonstrated in Figure 4A can
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be done prior to the suturing to correct the disparity. In this case reported, a crushing type s ut ure was used with a continuous Lcmbert ovcrsew. Neomycin was used to wash the inte stines in this case. Aminoglycosides can cause a neuromuscular blockage and respiratory depression or arrest. cardiovascular depression, kidney degeneration or vestibular degeneration. Care must be given to dosage of the drug and monitoring of the patient.
CONCLUSIONS Mo st domestic animals and man arc susceptible to intestinal atrcsias ranging from duodenal to anal atresias. Some of th e reasons why they occur may be: I) inheritance, 2) development arrest with failure of recanalization of a part, and 3) vascular accidents during fetal development. Surgery is possible in most cases , but delay in diagnosis and surgery lessens the recovery rate. Associated anomalies must be considered in the diagnostic work up , and should always be checked at the time of surgery. Fluids, electrolytes, and whole blood mu st be regul ated to effect a cure. End to end or end to oblique anastomosis is preferred to allow normal continuity of the intestine and to prevent th e "blind loop" syndrome. Resection of the severely dilated cranial po rtion is recommended to obtain a normal vascularized functional intestine. Two other foals have been sur gica lly explored. One foal with a congenital atresia of the left dorsal colon was corrected, but expired four days after surgery with renal failure . One kidney was absent and the second was one-half normal size. The other foal could not be corrected surgically as the entire diaphragmatic flexure was atretic to the transverse colon. Radiographic studies were not useful in locating the site of atresia in any of these three cases.
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12. Louw, JII : Congenital inte stinal atresia and steno sis in the ne wbo rn . Ob servations on its pathogenesis and treatment. Ann Rov Coli Surg Eng 25: 209. 1959. . 13. Louw, J II : Inve st igat ions into the etiology of congenital atresia o f the colon. Dis oj Colon and Rectum, 7: 471, 1964. 14. Magnu s. RV: Rectal atresia as distingu ished from rectal agenesis. J oj Peel Surg 3: 593. 1968. 15. Mishalany, IlG. Najjar, FB : Familial jejunal a tr esia: Threccases in one famil y. J Peel 73: 753. 1968. 16. M ishal any, IlG. Der Kaloustian, VM. Ghandour, M: Familial congenital duodenal atresia. Peel 46: 629. 1970. 17. Nixon. 1I11: I ntest in al obstruct ion in th e newborn. Arch Dis Child 30: 13. 1955. 18. Santull i. TV. Blanc. \VA: Con genital a t resia of the intest ine: Pathogenesis and treatment. ..11111 oj Surg 154: 939. 1961. 19. Sukarochana, K. Kiesewetter. WB: Imperforate anus . 38: 89, 1968. 20. Tandler, J : Zur entwicklungsgeschichte des men schlichen duodenum im fruhen embryonal stadien . Gegenbau Morph, Jahrbuch 29: 187. 1900. 21. Tosov sky, VV. Novak, K: Congenital intest inal atresia. Internat ional Surger y 51: 438. 1969. 22. Weitzman. J. Vanderhoof. RS : Jejunal atres ia with agenesis of the dorsal mesentery. Alii J oj Surg III: 143. 1966. 23. Wilmore, OW: Factors correlating with a successful outcome following extensive intest inal resecti on in newborn infants. J oj Ped80: 88, 1972. 24. Zwi rcn , GT. Andrews. IIG. Ahman, P: J ejunal atresia with a genesis of th e dorsal mesentery. J oj Ped Surg 7: 414. 1972. 25. Norrish , JG. Rennie, JC: Observations on the inheritance of at res ia ani in swine. J llcred 59: 186-1 87. 1968. 26. Vogt , OW: Chromosome cond ition of two atresia ani pigs. J Allim Sci 26: 1002-1004. 1967. 27. Dennis. SM Leipold. IIW: Atresia ani in sheep. Vet Rec91: 219224. 1972. 28. Hancock, J: Atresia ani in sheep. Proc /Oth Amlll COIIJNZ. A nim al Produ ction, 91. 1950. 29. Hartley, WJ . Kater. JC: Perin atal disease co nd it ion s of sheep in New Zealand . N Z eal Vet J 12: 49 . 1964. 30. Leipold , II W: Atresia jejuni in a la m b. Vet Rec 93: 644. 1973. 31. Safford. JW. 1I0vcrsland. AS : A study of lamb mortality in a western range flock. I Autopsy findings on 1051 Iambs. JAil S ci 19: 265. 1960. 32. Ladd s, PW. And erson. "'V: Atresi a ilei in a pup. JA V.\fA 158: 20 7 1-2072. 1971. 33. Rawlings. CA. Capps. WF. Jr: Recto vaginal fistula and imperforate anus in a dog. JAV.\fA 159: 320-3 26, 1971. 34. Greene. IIJ et 31: Congeni tal d efe cts in cattle. Irish Vet J 27: 37 45. 1973. 35. Hunter, AG : Atresia ilei in a calf. Vet Rec 94 : 170. 1974. 36. Jubb, KVF, Kennedy, PC: Pathologyof Domestic Animals. Vol. 2. 5th ed., Academic Press. New York. i'\.W., 1970. 37. Kernkamp, IICII. Legates, JE: Duo-cecum - An intestinal anomaly in Calves, JA VMA 139: 1207. 1961. 38. Leipold. IIW. S aperstein. G . Johnson, DO. Dennis, SM: Int estinal atrcsti a in calves. I'M/SAC 1037. 1976. 39. Len gh aus, C .. Wh ite, WE: Int estinal atresia in calves. A /lSI Vet J 49: 587-588. 1973. 40. ~lcG eady. TA ct al: Atres ia coli in a calf: A note on its Pathogenesis. Irish Vet J 21: 148-150. 1967. 41. Nair, S : Atresia ani with rcctovaginal fistula in a calf - a case report. Indian Vet J 49 : 528-529, 1972. 42. Nihl een , B. Eriksson. K: A hereditary lethal defect in calves atresia ilei . Nord Vet Med 10: 113-127, 1958. 43. Osborne. JC, Legates. JE: Six cas es of bovine intestinal anoma ly. JA V,\/A 142: 1104, 1963 . 44. Schlouhauer, CF: Congen ital atresi a of the co lo n in a calf. JAVMA 127: 339.1955. 45. Sk ewe s. AR: Bovine intestinal anomaly. Vet ,\/ed 57: 133-134, 1962. 46 . Cohrs. P: Nieb erle and Cohrs' Textbook of the special pathological anatomy ofdomestic animals. Peragamon Press. Oxford. 1967. pp 389. 47. Earlarn, RJ: A study of th e a eti ol og y of congenital sten osi s of th e gut. Anll Roy Surg Ellg151 : 126. 1972. 48. Schn ieider, J E. Leipold. HW : Rece ssive leth al wh ite in two foal s. J £q sted and Sur g 2 (Ill: 479. 1978. .
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