Jejunal obstructions

Jejunal RKHARD

Obstructions

MARTORELL, M.D., Tampa,

Florida

intraperitonea1 nitrogen mustard, radioactive goId and other cancerostatic agents for carcinomatosis, the incidence of obstructions in this category will probably increase in the coming years.

BSTRUCTIONS of the jejunum are Iess common than obstructions of the ileum in a ratio of about one to six. Differences from other types of intestinal obstructions are so distinct as to permit them to be classified separately from other small intestinal obstruc. tions. No cIear cut morphoIogic division exists between the jejunum and iIeum; therefore, obstructions which occur within four to six feet distance from the ligament of Treitz or in the proximal two-fifths of the small bowel are considered to occur in the jejunum.

0

INTERNAL HERNIA This interesting group accounts for approximately a twentieth of a11 jeiunal obstructions. Most of these hernial defects are congenital in origin and are numerous. The paraduodenal fossae occasionally entrap a loop of jejunum. Defects in the mesosigmoid or in the faIciform ligament have also been known to permit internal herniation of a jejunaI loop. Herniation may occur through congenital defects in the omentum or if defects in the omentum have been left as a resuIt of surgery. Other less common causes of interna herniation are through the foramen of Winslow, the broad the pericecal fossae or through Iigament, defects in the mesentery.

CAUSES Adhesions account for a half of jejunal obstructions or about 57 per cent. Most frequently noted types of adhesions are late sequelae of gastrectomies or gastroenterostomies. Early laparotomy obstructions accounted for about a third of the obstructions due to adhesions. Compromise of the upper part of the smaI1 intestine may occur when a Ioop of jejunum is densely aggIutinated to an inflamed viscera or in the waI1 of an abscess as has been noted in sigmoid diverticulitis, appendicitis, cholecystitis or pancreatitis and the like. Approximately a fifth of high obstructions occur because of externa1 hernia. Ventral hernias are the most common cause of jejunal obstructions in this group; umbiIica1 hernias are the next most common cause. Rarely does cause hernia incarceration in an inguinal jejunal obstruction. Secondary carcinoma is not an unusual cause for jejunal obstruction, whereas, primary carcinomas of the small intestine are rare. Secondary carcinomas or metastatic carcinomas, most frequently of ovarian origin, account for about a fifth of these cases. Perforating carcinomas of the transverse and descending coIon also cause mechanical obstruction of the jejunum caused by secondary invoIvement. With the increasing usage of

MESENTERIC THROMBOSIS Mesenteric thrombosis with the proximal limit of demarcation in the jejunum accounts for a small percentage of jejunal obstructions. Of course, this is the most IethaI type of obstruction. When mesenteric thrombosis involves the jejunum, the most proxima1 portion of the superior mesenteric artery or vein is involved and carries a grave prognosis. MISCELLANEOUS OBSTRUCTIONS Less common causes of obstructions are tumors, congenital atresias, intussusception, regional ileitis invoIving the jejunum and jejuna1 diverticulitis. Botsford et al. [r] reviewing I I 5 case reports of primary tumors of the small intestine found 32 occurring in the jejunum. Ten were primary adenocarcinomas, six were adenomatous poIypi and six were Ieiomyomata. Others were Iipomas, tibromas and Iymphomas. The clinical manifestations 433

American

Journal

of Surgery,

Volume

rod,

September

1~61

MartoreII Intraluminal pressures are not as high when there is not a closed loop of jejunum. Encroachment on the lumen of the jejunum resuhs in distention of the Ioop proximal to the site of obstruction. Hyperactive and retrograde peristalsis begins as the patient experiences severe cramping. Edema and hyperemia of the mucosa occur proximal to the obstruction. As edema and swelling increase at the obstruction, distention increases in the proxima1 loop. If distention is not relieved the venous return is impaired and strangulation or perforation will ensue. As has been shown in early postoperative obstructions, if the proximal loop can be decompressed before circulation is impaired, edema and swelling at the site of obstruction is reversibIe and patency of the lumen may be restored. Fluid and electrolyte imbaIances are more profound than in Iow obstructions. Loss of copious secretions from the upper part of the gastrointestinal tract produce severe imbaIantes within twelve to twenty-four hours of onset. Loss of sodium, chloride and potassium from gastric juice, bicarbonate from biIe and pancreatic juice are roughly parallel; consequentIy, the acid-base balance is maintained. Severe dehydration may give normal concentrations of extracellular determinations, but when rehydration is accomplished, hyponatremia, hypopotassemia and hypochIoremia are often severe. Potassium repIacement therapy is instituted to restore osmolarity to the extraceIIular compartments. Most frequently employed are isotonic sodium chloride, o. I 67 M. sodium lactate and potassium chloride as repIacement therapy. Some authors report replacement of 8,000 to 10,000 cc. of electrolyte solution in preoperative preparation of severely depleted patients; but such large quantities are rarely necessary in a twelve hour period. The replacement of potassium preoperatively is an important factor in reducing anesthetic risk. Severe hypopotassemia increases the likelihood of cardiac arrest. Normally, little absorption of water or saIts occurs in the jejunum, but high obstruction results in loss of water and electrolyte. The distention factor which endangers the anesthetic caused by elevation of the diaphragm is not great because the jejunum partially decompresses itself by vomiting, and the distal alimentary tract is collapsed. In summary, the principa1 factors con-

of tumors of the jejunum are obstruction, bleeding and cramping abdominal pain. River et al. [2] reported that intussusception was the most common form of obstruction associated with benign tumors of the small bowel and tumors are the most common cause of intussusception in adults. (Fig. I .) PATHOLOGIC

PHYSIOLOGY

The norma secretions of the upper gastrointestinal tract exceed 3,000 cc. for twenty-four hours (1,000 cc. saliva, 3,000 cc. gastric juice, 300 cc. bile, 500 cc. pancreatic juice) excluding the secretion of succus enteritis which is over Retrograde peristaIsis 2,000 cc. per day. originating at the obstructed loop will eject this much vomitus daiIy; whereas, in low obstructions a large amount of this fluid and gas is retained in the obstructed Ioops. The intramural pressures are higher in obstructions of the ileum than in jejunal obstructions except in cIosed loop obstructions. CIosed loop obstructions of the jejunum have an intramural pressure several times greater than that of a closed loop of ileum because of the copious secretion of the jejunum, as has been shown by Morton and Sullivan [?I. A closed loop of jejunum, therefore, will attain a high intramural pressure more rapidly which will cause compression of the intramura1 circulation and resultant strangulation. As the pressure within increases, the intramural capillaries are compressed, hypoxia and ischemia progress to cause necrosis of the bowel waI1. As the intramural circulation is impaired an increase occurs in permeabiIity of the bowe1 wall and certain toxic substances, believed to be endotoxins of Clostridium Welchii by Cohn [a], Barnett [T] and others, are reIeased into the peritoneal cavity from which they are then absorbed into the systemic circuIation. HyaIuronidase produced by bacteria in the strangulated loop is believed to also contribute to the permeability of the bowel walI. A dark, bloody fluid (transudate) escapes into the peritoneal cavity and is lethal within twelve to twentyfour hours as has been demonstrated in experimental animals. Barnett [5], Cohn [4] and co-workers have shown that antibiotics pIaced into the lumen of strangulated bowel aIter the character of this peritoneal fluid so as to render it nontoxic and as this fluid is steribzed by the introduction of antibiotics, the fluid Ioses its toxicity. 434

AMIESIONS

S 7%

HERNIA r8

a

FIG. I. Causes and percentage of each in jejunal obstruction.

EXTERNAt

Martorell tributing to mortality are toxic absorption and depIetion of fluid and eIectroIyte reservoirs. CLINICAL

PICTURE

It is interesting to note the extremes in the variation in the Iength of time between onset of iIIness and diagnosis or operation. A deIay of two to four days is frequent in the diagnosis of a high intestina1 obstruction. The absence of distention of the abdomen and passage of ffatus per rectum are found to be pitfaIIs in the diagnosis. The relatively coIIapsed dista1 smaI1 bowel and coIon accommodate for the distended obstructed jejunum; hence, the abdomen does not appear strikingIy distended. RareIy is a history of compIete obstipation obtained. Hibbard and Wangensteen [6] observed that 68 per cent of gas in the smaI1 intestine is swaI1owed and 32 per cent is formed in the body. Anderson and Ringstead in 1945 concIuded that swaIIowed air is the excIusive source of gas in a11 types of obstruction. However, it is probabIe that gas forms in the Iower alimentary tract for several days after onset of a high obstruction and arises from gaseous exchange with the circuIation and as a byproduct of bacteria1 fermentation in the coIon. This gas is nitrogen, oxygen, carbon dioxide and methane. The duration of the obstruction is known to be the chief factor affecting the mortality. The deIay in diagnosis is frequently caused by the Iack of distention of the abdomen which is caused by the coIIapsed dista1 smaI1 bowe1 and coIon and because of the jejunum partiaIIy decompressing itseIf through vomiting. The characteristic symptoms are intense, cramping pain in the upper part of the abdomen, the vomiting of biIe stained Iiquid in copious quantities and a nondistended abdomen. Dehydration, thirst, tachycardia, Iow grade fever, weakness, paIlor, Ioss of tissue turgor and frequentIy hiccoughs resuIt from the decrease in volume of the extracelIuIar ffuid. When stranguIation obstruction or mesenteric infarction is present, the signs of the toxic phase predominate, such as shock, fever, leukocytosis and exquisite abdomina1 tenderness. NeedIe aspiration of the peritonea1 cavity is not necessary to determine the presence of strangulation obstruction. Other physical signs and Iaboratory aids wiI1 assist in determining the viabiIity of smal1 bowe1 without subjecting a critically III patient to a needIess and hazardous test. 436

Fiat and erect roentgenograms of the abdomen are indispensabIe to the diagnosis. The presence or absence of obstruction is verified and even the severity of the Iesion can be determined by a competent radiologist. Thickening and edema of the jejuna1 waI1 can be noted from a pIain fiIm of the abdomen. The finding of a cIosed loop by the radioIogist wil1 indicate prompt operative intervention as stranguIation, if not already present, wiI1 occur within hours. The most vaIuabIe single too1 in the diagnosis of obstruction of the smaI1 bowel is a roentgenogram of the abdomen. TREATMENT

Decompression therapy shouId aIways be instituted preoperativeIy as it facihtates IocaIization of the obstruction; it decreases intestina manipuIation at the time of surgery, aids in cIosure of the abdomina1 wound and decreases pressure on the suture Iine if resection is necessary. The use of Iong tube decompression has become the subject of much controversy. Its use in conjunction with operation has greatIy reduced the morbidity and mortality in the past twenty years. When empIoyed as a substitute for operation, however, intubation is fraught with danger. BolIinger and FowIer [7] have reported a directIy proportional rise in mortaIity rate corresponding with the duration of unsuccessfu1 tube decompression. This Iatter practice has been condemned by Becker et a1. [S] and others as a misuse of tube decompression. The principa1 use of the MiIIerAbbott tube or Cantor tube, as a definitive measure for the reIief of obstruction, is restricted to early postoperative adhesions; wherein, the nature of the obstruction is known and the absence of stranguIation is certain. In instances in which tube intubation is difficult or is not making satisfactory progress, conservative measures shouId be abandoned, and operative intervention becomes necessary. When one is certain that no stranguIation and no cIosed Ioop obstruction exists, then Iong tube decompression is justifiabIe if the patient is re-evaIuated at intervals of twelve hours. The passage of an intestina1 tube may be of assistance to the ffuoroscopic instaIIation of radiopaque oi1 when the diagnosis is obscured, as in poIypi, stenosis, iIeitis and the Iike. EarIy postoperative obstructions occurring within seven to ten days of abdomina1 surgery can be treated successfuIIy with long tube de-

JejunaI

Obstructions

compression, and only in rare instances does reoperation become necessary. In this group of patients surgical re-exploration shouId be done only when conservative measures fail. Electrolyte imbalances are more severe, the patient is debilitated from recent surgery and signs of strangulation are masked. These factors make the decision, as to when to abandon conservative measures, more difficult. Congenital atresias of the upper part of the intestinal tract should be operated upon as early as the diagnosis is made. The neonatal patient’s condition will progressiveIy deteriorate from the standpoint of water and eIectroiytcs, as surgery is delayed. At surgical exploration a systematic approach to the obstruction is recommended rather than complete evisceration of the distended proximal loops. It is recommended that distal collapsed loops be “run” in a proximal direction to the point of obstruction. This reduces the operative trauma to a minimum. Once the obstruction is reIeased distention equalizes to the ileum and colon. The aseptic &compression technic popularized by Wangensteen [9] is rarely necessary in jejunal obstructions once the mechanica obstruction is released. Conversely, in ilea obstructions aseptic decompression is frequently necessary to facilitate closure of the abdominal wound and to allow intestinal muscuIature to resume its tonicity and peristaltic powers. When resection of jejunum becomes necessary, extreme care is recommended in the handling of the mesentery. Mesenteric vessels shouId be dissected and Iigated individually rather than serially clamping and ligating bulks of mesenteric fat with the vessels. Although a rich arcade of cohateral vesseIs was noted the mesentery was shorter and propagation of mesenteric vein thrombosis was more ominous. The jejunal wall is thicker and more vascular than the iIea1 and aIso has a greater diameter, therefore, anastomosis is more easily accomplished. An end to end anastomosis is preferable when practicable. COMMENTS

StranguIation is comparatively infrequent in high obstructions when compared to iIea1 obstructions; consequentIy, the mortality rate is lower than it is for acute smaII bowe1 obstructions in general. ExcIuding those instances of mesenteric thrombosis, patients with jejunal

obstructions have a mortality rate of 5 per cent which is comparativeIy lower than the rate for all small intestinal obstructions which is 8 to 16 per cent. The larger diameter of the jejunum as compared to the ileum probably accounts for the much greater frequency of ileal obstructions. The jejunum has a larger absorptive function and its wails are thicker, more vascular and the circular folds of its mucous membrane arc more numerous. The mesentery is somewhat shorter than the mesentery of the ileum and its limited mobility decreases the likelihood of becoming obstructed. The lower incidence of strangulation is probably caused by the short mesentery of the jejunum, its short blood supply and its great vascularity. An additional factor to be considered when comparing the incidences of jejunal and ileal obstructions is the relatively sheltered position of the jejunum beneath the mesocolon, transverse colon and omentum. MilIer [IO] reported a mortality rate of 65 per cent in 1929 at Charity Hospital in New Orleans. Tendler and Cartwright [I I] reported mortality rates for all obstructions of the intestine as 51 per cent from 1923 to 1932, then 26 per cent from 1933 to 1946 and 8 per cent from 1947 to 1953. Turner et al. [rz] rrportecl IOO consecutive cases from each of three decades and found a mortality rate of 2- per cent in 1929, 21 per cent in 1939 and _I per cent in

19+$

A mortality rate of 16 per cent for small bowel obstructions was reported by hlichel et al. [I ?] in 1950. Moses [14] in 1946 reported an 8 per cent mortality rate for all small bowel obstructions excepting atresias. Wrest and Schethn [IY] in 1950 reported 16.3 per cent exclusive of atresias and mesenteric thromboses. The remarkable reductions in mortality rates in the preceding three decades have been attributed to: (I) the popularization of parenteral solutions, (2) the introduction of tube decompression and (3) in the past decade, improved methods of anesthesia. To this list of great contributions should be added the fourth, that is, the role of antibiotics in strangulation obstruction as has been advocated by Poth [IY], Cohn [4] and Barnett [r] in the past seven years. This should further reduce the mortality rate. Mesenteric thromboses continue to be a lethal disease. Although in recent years principles of vascular surger?

MartoreII study of 205 consecutive cases. Arch. Surg., 66: 888, ‘953. 8. BECKER, W. F., DAVIS, C. E., JR. and LEHMAN, E. P. IntestinaI obstruction. Ann. Surg., 131:

have been apphed to mesenteric vascuIar emno appreciabIe aIteration rebarrassment, mains in the mortahty rate from mesenteric thrombosis. SUMMARY

JejunaI obstructions are Iess common than ileal obstructions in a ratio of one to six. 2. Adhesions are the most common causative factor with externa1 hernia the next most common factor. 3. The principIe factors contributing to the mortality are toxic absorption and depletion of the fluid and eIectroIyte reserves. 4. CIinical findings are: (a) undistended abdomen, (b) pain in the upper part of the abdomen and (c) passage of ffatus for severa days after onset. 5. Fluid and eIectroIyte therapy are the most important adjuncts to surgical treatment. 6. The treatment of jejunal obstructions is primarily operative and the use of Iong intestina tubes as a substitute for operation is condemned. Judicious, cautious use of intestinal tubes is justifiabIe in certain instances. 7. The Iarger diameter of the jejunum, its restricted mobility, its sheItered position and its shorter mesentery probably account for its lower incidence of obstruction and stranguIation. 8. The recent eIaboration of the roIe of antibiotics in stranguIation obstruction shouId further reduce the mortality rate, aIthough the mortality from mesenteric vascuIar 0ccIusions remains unaltered. REFERENCES

I. BOTSFORD,T. W., CROWE, P. and CROCKER, D. W. Tumors of the smaII intestine. Am. J. Surg., 103: 358, 1962. 2. RIVER, L., SILVERSTEIN,J. and TOPE, J. W. Benign neoplasms of the smaI1 intestine. Internat. Abstr. Surg., 102: I, 1956. 3. MORTON, J. J. and SULLIVAN, W. C. A comparison between simuhaneous equa1 sized cIosed obstruction of duodenum and iIeum. Arch. Surg., 21: 531, 1930. 4. COHN, I., JR. Bacteria1 factors in stranguIation obstruction: review of experimenta work. Am. Surgeon, 22: 836, 1956. 5. BARNETT, W. 0. StranguIation obstruction. Experimenta1 findings with experimental impIications. Am. Surgeon, 27: 230, 1961. 6. HIBBARD, J. S. and WANGENSTEEN, 0. H. Character of gaseous distention in mechanica obstruction of small intestine. Proc. Sot. Exper. Biol. ti Med., 31: 1063, 1934. 7. BOLLINGER, J. A. and FOWLER, E. F. Results of treatment of smaI1 bowe1 obstruction, clinica

438

3859 1950. o. WANGENSTEEN.0. H. IntestinaI Obstructions, 3rd. ed. Springheld, III., 1955. CharIes C Thomas: IO. MILLER, C. J. A study of 343 surgica1 cases of intestina1 obstruction. Ann. Surg., 89: 91, 1929. II. TENDLER, M. J. and CARTWRIGHT, R. S. Acute intestina1 obstruction. A re-evaIuation of 31 years at a university hospita1 (19281953). J. Louisiana M. Sot., 108: 4, 1956. 12. TURNER, J. C., JR., DEARING, W. H. and JUDD, E. S. Postoperative morbidity and mortality in intestina1 obstruction: comparative study of IOO consecutive cases from each of the past three decades. Ann. Surg., 147: 33, 1958. 13. MICHEL, M. L., JR., KNAPP, L. and DAVIDSON, A. Acute intestina1 obstruction. Surgery, 28: go, ‘950. 14. MOSES, W. R. Acute obstructions of the smaI1 intestine. New England J. Med., 134: 78, 1946. 15. WEST, J. P. and SCHETLIN, C. F. Acute mechanica obstruction of smaI1 intestine. Am. J. Surg., 79: 432, 1950. 16. POTH, E. J., MILLER, T. E. and DUNLAP, W. The protection of contaminated deep wounds against infection by intraperitonea1 neomycin soIutions. Am. J. Surg., IOI: 766, 1961.

Additional

References

BECKER, W. F. IntestinaI obstruction: anaIysis of 1007 cases. South. M. J., 48: 41, 1955. CANTOR, M. 0. StranguIation obstruction: experimenta Iindings with cIinica1 implications. Am. Surgeon, 27: 230, 1961. COHN, I., JR. CoIIective review; strangulation obstruction. Abstr. Surg., Surg. Gynec. Ed Obst., 103: 5, 1956. HALPERIN, P. H., AKS, D. and SMITH, 0. D. JejunaI diverticuIa: a reappraisa1 of its importance and report of three cases. Am. Surgeon, 23: 703, 1957. JENSEN, C. B. and SMITH, G. A. CIinicaI study of 51 cases of mesenteric infarction. Surgery, 40: 930, 156. LAUFMAN, H. and NOA, P. F. PhysioIogicaI probIems underlying intestina1 stranguIation obstruction. S. Clin. Nortb America, 42: 219, 1962. MARTORELL, R. A. JejunaI obstruction. Am. Surgeon, 26: 481, 1960. MICHEL, M. L., JR., TYLER, L. T., LEPERE, R. H. and MARTORELL, R. A. Intestinal obstruction. Mississippi Doctor, 33: I, 1955. MOORE, T. C. JejunaI obstruction as compIication of acute hemorrhagic pancreatitis. Arch. Surg., 73: 977, 1956. MOORE, R. M. Role of intestina1 decompression in treating acute mechanica obstruction. Texas J. Med., 53: 71, 1957. NOER, R. J. IntestinaI obstruction. Postarad. Med.. 20: 268, 1956. WELCH, C. E. Intestinal Obstruction. Chicago, 1958. Year Book PubIishers. Inc. WILSON, H. IntestinaI obstruction in infants and children. South. M. J., 50: 1288, 1957.