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Ketan R Vagholkar
Associate Professor, Department of Surgery, Padmashree Dr. DY Patil Medical College and Rajawadi Municipal General Hospital, Ghatkopar, Mumbai - 400 077.

Background : Gastrointestinal anastomosis is one of the commonest procedures performed on the intestinal tract. Despite refinements in the field of gastrointestinal surgery yet anastomotic leakage and dehiscence still remains a frequent and serious problem associated with very high morbidity and mortality. A retrospective analysis of 35 patients undergoing anastomosis at various levels in the GI tract was done with the aim of studying the factors influencing healing of the anastomosis in the GI tract.

Methods :
Indoor case records of 35 patients who underwent gastrointestinal anastomosis in a single unit by the same surgeon over a period of four years were analyzed retrospectively.

Results :
Out of the 35 patients analyzed 16 had undergone small bowel anastomosis, 17 had a large bowel anastomosis, one had a biliaryenteric (Choledochoduodenostomy) and one had a gastrojejunostomy. There were three anastomotic failures (8.5%).

Conclusion :
Adequate attention should be paid to the various preoperative, intraoperative and postoperative factors which influence healing of anastomosis in the GI tract in order to keep the morbidity and mortality associated with the procedure to a bare minimum.


Healing in the intestinal tract is rapid when free of complications unlike cutaneous healing in which progress can be observed on a daily basis and intervention instituted early if necessary. Healing of the intestinal anastomosis is anatomically observed from inspection, allowing the surgeon only to judge the success of operation by assessing the patient’s parameters of general well being. For the same reason, complications usually warrant re-exploration, with associated morbidity and mortality. This places great responsibility on the surgeon to be aware of all the pre-operative, intra-operative and postoperative factors relating to anastomotic healing that might compromise the healing process. Awareness of all these factors is pivotal in limiting complications to a bare minimum. Hence the aim of the retrospective study was to evaluate the factors influencing the healing of anastomosis in the GI tract.


The indoor case records of 35 patients who had undergone anastomosis at various levels in the gastrointestinal tract in a single surgical unit over a four year period from January, 1997 to December, 2000 were studied retrospectively. All anastomosis were performed by a single surgeon. Whether the patients were operated upon in a emergency or elective setting was noted. The various preoperative factors namely, bowel preparation, bowel rest, nutritional status, the presence of diabetes, whether the patient was taking any medications and whether the patient was suffering from any systemic disease such as HIV/AIDS were analyzed. Since all the 35 patients were operated upon by a single surgeon; uniformity of surgical skills was maintained for all the patients with respect to assessment of blood supply of the bowel ends and surgical technique of anastomosis. As far as the technique of anastomosis was concerned an analysis was made of a number of variables namely everting versus inverting anastomosis, single v/s double layer, stapled v/s sutured, the suture material used, omental wrapping of the anastomotic line and the usage of drains. The presence of bacterial contamination (spillage), abdominal sepsis, the presence of hypovolaemia (ionotropic support) and the number of units of blood transfused were the other significant intraoperative factors studied.


A retrospective analysis of the indoor case records of 35 patients who had undergone gastrointestinal anastomosis was done (Table 1). There were 26 male and nine female patients with a mean age of 42 years (29 to 65 years). Of the 35 patients 16 had undergone small bowel anastomosis, 17 had undergone large bowel anastomosis one patient had a gastrojejunostomy and one patient had choledochoduodenostomy. The mean haemoglobin level was 9.8 gm%. The mean serum albumin level was 3 gm%. Eighteen patients had undergone surgery on an emergency basis. No bowel preparation was done on these patients operated on an emergency basis. Three patients were diabetic, two patients were on antituberculous chemotherapy and one patient was tested positive for HIV. Uniformity of surgical technique was maintained by virtue of the fact that all patients were operated by the same surgeon. A double layered, inverting, handsewn anastomosis using 3.0 mersilk was performed after having confirmed adequacy of blood supply to the cut ends of the bowel. Omental wrapping was done in all except two patients namely in whom a gastrojejunostomy and choledochoduodenostomy was done. Intraabdominal drains kept in 25 patients. Bacterial contamination of the anastomotic site was a common accompaniment of the 18 patients who were operated on an emergency basis. Two patients were hypovolaemic (on ionotropic support).


Data of patients who underwent GI anastomosis
Levels of Anastomosis Small Bowel Large Bowel(n=17) Gastro
Choledocho Duodenostomy
  (n=16) Ileocolic(n=15) Colocolic (n=2) (n=1) (n=1)
Age (Mean) 38 yrs. 46 Yrs. 29 Yrs. 57 Yrs. 65 Yrs.
Sex (Male) 12 10 2 1 1
(Female) 4 5 — — —
Emergency 10 8 0 1 1
Elective 6 7 2 1 1
Bowel Preparation 6 7 2 1 1
Nutritional Status          
Hb. (Mean) 9.8 gm% 9.5 gm% 11.5 gm% 11 gm% 12 gm%
S. Albumin (mean) 3 gm% 3 gm% 3 gm% 3 gm% 3 gm%
Bowel Rest Post Operative Post op in All Preop. in 7 Preoperative and Post Operative Preoperative and Post Operative Preoperative and Post Operative
Diabetes 2 1 — — —
Medications 1 (Akt) 1 (Akt) — — —
Systemic Disease (HIV etc.) — 2 (HIV) — — —
Blood supply to cut ends Good Good Good Good Good
Bacterial contamination 10 8 Minimal — —
Abdominal Sepsis 10 8 Absent — —
Hypovolaemia — 2 (ionotropic support ) — — —
Anastomotic Technique
Everting vs. Inverting Inverting Inverting Inverting Inverting Inverting
Single vs Double Double Double Double Double Double
Stapled vs Sutured Sutured Sutured Sutured Sutured Sutured
Suture Material Mersilk 3.0 Mersilk 3.0 Mersilk 3.0 Mersilk 3.0 Mersilk 3.0
Omental Wrap Done Done Done Done Anteriorly Only
Drains 10 15 — 1 1
Leakage Nil 3 Nil Nil Nil

The mean volume of blood transfusions given was 1.4 units. Three patients developed anastomotic dehiscence as evidenced by leakage of intestinal contents through the drainage tubes. One of these patients was HIV positive, the other two were on ionotropic support at the time of surgery. All the three patients had undergone a colonic anastomosis without preparation on an emergency basis with extensive bacterial contamination and sepsis at the time of surgery.


The submucosa provides the GI tract with most of the tensile strength and is responsible for anchoring the sutures that hold the anastomosed bowel ends together. [38] The submucosa consists mainly of coarse, loosely interwoven, collagenous and elastic fibres together with a submucosal plexus of nerve fibres ganglia and many blood and lymphatic vessels.

The mucosal component of intestinal anastomosis is repaired by migration and hyperplasia of the epithelial cells which cover over the granulation tissue of the wound and thus seal the defect and create a barrier to the luminal contents.34 The sealing can be completed in a minimum of three days if the layers of the bowel wall are directly apposed.

The serosa consists of a thin layer of connective tissue covering the muscularis externa. It is covered on its outer aspect by the mesothelial lining of the peritoneal cavity. Good serosal apposition is necessary to minimize the risk of leakage. [23] , [30] , [55] Extraperitoneal segments of the intestinal tract without a serosal covering lack this component of anastomotic protection and are at a higher risk of complications as seen in the oesophagus and lower third of the rectum.31

Incising the gut wall evokes an initial haemostatic vasoconstriction followed by a secondary vasodilatation and increased vascular permeability. This process results in oedema and swelling of the tissue end. The outcome must be borne in mind, while tying sutures because ischaemic necrosis may develop as the suture strangulates the swollen tissue. [56] The appearance of granulation tissue in the anastomosis marks the beginning of the proliferative phase of healing. The greater omentum plays a critical role in the intraperitoneal anastomosis by wrapping around the suture line and adding to the granulation tissue production. [2] During this proliferative phase of healing, wound collagen is undergone the lysis and synthesis, with a predominance of the latter in normal healing. Collagen plays an important role in determining anastomotic integrity and suture holding capacity in the few days of healing. [18] , [42] This protein is upregulated in tissues adjacent to the suture line as well as throughout the intestinal tract. Understanding these mechanisms provide means to manipulate the healing process. [44] , [76] , [96]


Although it is believed that all tissue types heal in an identical fashion, this does not hold true. Many of the components of the healing process are common to healing of tissues in various systems yet a variety of variations also exist between tissues and may alter the rate or the outcome of healing. These include the rapidity of gain in strength by intestinal wounds, manufacture of collagen by fibroblasts as well as smooth muscle cells and divergent regulatory effects of various substances on the process of healing namely vitamin A, steroids, lathyrogens etc. [29] , [58] , [40] , [86] (Table 2) Other physiological factors which influence the process of healing in the GI tract are its multilayered architecture, the large micro-organism content of the lumen, the influence of the serosa on sealing of the suture line and the unique vascular supply to the intestinal tract which slowly and selectively down regulates its own perfusion in states of hypo volaemic shock.

Table 2:
Components of the healing process
pH Variable throughout the GI tract in accordance with local exocrine secretions.
Microorganisms Aerobic and anaerobic, especially in the colon and rectum. Complications develop if they contaminate the peritoneal cavity.
Shear Stress Intraluminal bulk transit and peristalsis exert distracting forces on the anastomosis
Tissue Oxygenation Dependent on intact vascular supply and neocapillary formation.

Collagen Synthesis


Cell type

Firbroblast and smooth muscle cells.
Lathyrogens D-penicillamine has no effect on collagen cross-linking.
Steroids Contradictory evidence exists concerning their negative effect on intestinal healing.
Collagenase Activity Increased presence throughout the GI tract after transection and reanastomosis. During sepsis excess enzyme may promote dehiscence by decreasing suture holding capacity of tissues.
Wound Strength Rapid recovery to preoperative level


The analysis of results reveals that a number of factors both local and systemic significantly influence the healing of anastomosis in the gastrointestinal tract. These factors can be classified into preoperative, operative and postoperative for the ease of discussion (Table 3). The operative factors play a significant role in the healing of the anastomosis.

Blood Supply

In all the patients analyzed, the adequacy of blood supply to the anastomotic site was confirmed by the presence of bleeding from the cut bowel ends, the colour of the bowel and the pulsations of the adjacent mesenteric vessels prior to commencing the anastomosis. Blood supply to an anastomosis is of paramount importance and depends on the vasculature. Surgical mobilization of the intestine is a critical factor in determining subsequent perfusion at the anastomotic site. Excessive or rough mobilization may damage critical vessels as can tight suturing or stapling. [19] , [72] Conversely if mobilization is inadequate, tension on the anastomosis may also compromise anastomotic perfusion and in addition lead to increased inflammatory cell infiltrates. [46] Hence prior to the commencement of performing an anastomosis adequate pulsations of the mesenteric vessels vascularity and colour of the bowel ends to be anastomosed should be examined and confirmed. Another important factor which needs to be studied is the absence of any sort of distal obstruction.

Surgical Technique

Surgical technique is of significant importance to the successful outcome of the operation. Gentle handling of tissues, use of fine instruments for sharp dissection and ensuring adequate haemostasis without causing tissue damage are very important. The intestine should not be allowed to dry by using moist packs which can also help in isolation of the intestine from the peritoneal cavity. Sutures should be placed at an adequate distance from the margins. [45] , [91] The surgical knots must be tied securely without strangulating the intervening tissues. After the completion of anastomosis the adequacy of the lumen and viability of the tissue margins must be examined and the absence of tension, torsion and distal obstruction ensured. Finally a rigorous toilet of the peritoneal cavity should be done to prevent abscess formation which is extremely detrimental to anastomotic healing. All these precautions were taken in all the 35 patients studied.


Everting versus Inverting Anastomosis

Everting anastomosis are at a greater risk of leakage and cause more adhesion formation however the incidence of stenosis is lower. Various studies have compared the two methods with conflicting results. [1] , [6] , [30] , [41] Though results comparing the two methods are conflicting yet the inverted method is one which is widely practised all over the world. An inverting anastomosis was performed in all the patients in the present study. Out of the 35 patients, 3 developed anastomotic dehiscence (8.5%).

Single Layer Versus Double Layer

This is another contentious issue. Both techniques have potential weaknesses that could threaten the anastomosis. [32] , [61] , [68] Though the two layers might provide adequate strength initially, they increase the inflammatory response in the early stages of healing owing to the extrasuture material and the ischaemia of the inverted tissues. The inflammatory reactions result in weaker anastomosis as more collagen is broken during the inflammatory phase of healing. Advocates of single layer argue the anastomosis results in a larger lumen with less damage to the tissue edge. In the present study a double layer anastomosis was performed in all the 35 patients.

Stapled Versus Sutured Anastomosis

Although stapled anastomosis make the procedure easier and faster yet they do not replace adherence to the principles of good surgical technique. [17] Stapled anastomosis produce a larger stomal diameter, are constructed with less trauma, cause fewer adhesions and produce less inflammatory response. Consideration of adequate blood supply, absence of sepsis and tension applied to use of staples as well as suture materials. As the diameter of each staple is less than that of a suture, staples are at a greater risk of pulling through the tissue edges in the presence of tension. The adverse effect is bleeding from the anastomotic line secondary to the B shaped staples which are designed to permit blood flow through to the tissue edges. It is important to keep in mind that stapling does not promote better healing in compromised situation such as sepsis or ischaemia and the same principles of good surgery always apply. Due to non availability of stapling devices all the anastomosis in the present study were handsewn.

Suture Materials

Both absorbable and non absorbable suture materials are used with variable success. The suture material should be strong enough to provide the necessary mechanical support of the anastomosis but fine enough to minimize trauma as it makes its way through the tissues. Similarly the needle should be chosen so as to limit the tissue damage because each passage through the gut wall results in further damage to the tissue edge. The ideal suture material should retain its strength until the anastomotic integrity is secured by the healing process and should cause minimal tissue reaction and discourage infection. It should also provide easy handling and knotting. [87] , [88]. In all the 35 patients studied, the suture material used was mersilk 3.0. Besides silk the other non absorbable sutures used are nylon and prolene. The quality that favours the use of non absorbable sutures is their prolonged retention of tensile strength. The absorbable sutures which are used are chromic catgut, polyglycolic acid (Dexon), polyglactin (Vicryl) and polydioxanone (PDS). Their use is justified by the rapid healing rate of intestinal tissues. Absorption eliminates the foreign body residue seen with non absorbable sutures. Synthetic absorbable sutures retain 50% of their original strength for two weeks and are degraded by hydrolysis which is unaffected by the enzymes present in an inflammatory or infected environment. Monofilament sutures have the advantage of not providing a nidus for organisms to proliferation. In the intestinal tract non absorbable monofilament sutures come closest to the ideal suture in achieving successful anastomotic healing. Sutureless anastomosis have been used since the Murply’s button in 1892. [65] The Boerema button used for transaction of the oesophagus in cases of oesophageal varices and the valtrac bio fragmentable anastomotic ring have also been used. [11] , [65] These devices work by compressing two inverted rings of bowel tissue with the device itself eventually sloughing and being passed anally. Glued anastomosis have been performed only in animals but appear unsafe. [14] , [83] , [84] Laser welded anastomosis although promising in initial studies remain to be proven effective. [62] , [64]

Omental Wrapping

All anastomosis excepting two (i.e. gastrojejunostomy and choledochoduodenostomy) in the present study were wrapped by omentum. A plain catgut stitch was taken in order to keep the anastomotic line covered by the omentum. The use of healthy omental tissue to wrap intestinal anastomosis can improve outcome. [2] , [31] , [39] , [63] Besides physically sealing the suture line, omental wrapping promotes neovascularization and granulation tissue formation, controls infection and provides lymphatic drainage in the peri-anastomotic region.

The wrapped omentum must be viable because free omental grafts have no protective effect. [16] , [38]

Anastomotic drains

Intraabdominal tube drains were kept in 25 patients. They were removed on 6th post operative day. The diagnosis of anastomotic dehiscence in the three patients was made out after finding intestinal contents coming out from the drains on fifth post operative day. Placement of drains at the anastomotic site has long been a contentions issue among surgeons. [24] , [25] , [52] , [71] The argument in favour of the claim that they drain fluid accumulations before infection can occur and also give the indication of an anastomotic leak. Those opposed to the use of drains claim that the drain provides a retrograde conduit for organisms, to enter the peritoneal cavity from outside, may erode the anastomosis, promote adhesion formation and cause discomfort to the patient. [9] , [57] The surgeon therefore has to use his or her discretion based on experiences. It is important to remember that the drain should be removed as soon as the drain stops functioning.


In the present study, the 18 patients who underwent surgery on an emergency basis had an unprepared bowel. As a result there was contamination of the anastomotic site by the bowel contents. The three patients who developed anastomotic dehiscence belonged to this category of unprepared patients. In all three cases the anastomosis was colonic. Bacterial contamination of the anastomotic site is a significant factor which influences the outcome. An early and significant decrease in the suture holding ability of anastomotic tissue occurs in the oesophagus, stomach and ileum as well as in the colon. After 2 days the breaking strength in oesophageal anastomosis decreases by 37% from initial values. Gastroduodenostomies lose 64% of their strength and colonic anastomosis 72%. The loss in strength is a reflection of an imbalance between collagen synthesis and degradation and usually occurs in the first three days of healing. [20] , [41] , [50] This is a crucial time for the anastomosis because its integrity depends on the suture holding capacity of the tissue. Significant bacterial contamination causes increase in local concentration of leucocytes. Leucocytes are responsible for a significant degree of collegenolytic activity. Increased collagenolytic activity leads to higher incidence of anastomotic breakdown. Anastomotic healing is significantly affected by the bacterial population in the respective part of the bowel.


It is a time tested widely accepted fact among surgeons that efficient mechanical bowel clearance prevents anastomotic dehiscence. In the present study mechanical bowel preparation was achieved in 16 patients. In 15 patients this was achieved by administration of polyethylene glycol (peglec) on the day prior to surgery and in the single patient who underwent gastrojejunostomy it was achieved by ryles tube washes prior to surgery. None of these patients developed any leak. The use of low residue diets prior to surgery and of mechanical bowel preparation that clear the bowel by means of mucosal irritation or osmotic cattarhesis is commonly practised. The only drawback or rigorous bowel preparation is diarrhoea leading to fluid and electrolyte deficiency prior to surgery. However there are conflicting reports on this issue. Burke et al have provided further evidence that question the use of bowel preparation showing no difference in outcome after colonic surgery between prepared and unprepared patients. [13] In the present study the three anastomotic failures reported belonged to the group of unprepared patients who were operated on an emergency basis.


Out of the 15 patients who underwent elective surgery 2 patients had then large bowel cleared by low residue diet in addition to the peglec preparation prior to surgery. The purpose of administering low residue diet is to decrease the faecal content of the large bowel. Blumquist et al investigated the effect of preoperative low residue diet on anastomotic strength after surgery. [10] They concluded that low residue diet did not impair colonic healing. However long term (1 month) preoperative low residue diet lowered collagen synthesis with less strength gain during the phase of fibroplasias, a finding that suggests that intraluminal bulk acts as a stimulus for collagen synthesis. Surgical diversion undoubtedly reduces the bacterial load at the site of anastomosis. This promotes healing especially in the colon. However absence of intraluminal bulk reduces the long term accumulation of collagen at the anastomosis and decreases and delays the gain in strength. [82] All the patients in the present study were kept nil by mouth for 4 days postoperatively.


In the present study the 18 patients who underwent emergency surgery had abdominal sepsis. Three of these patients developed anastomotic dehiscence. The fibrinopurulent exudates filling the anastomotic space despite rigorous lavage in peritoneal sepsis prevents fibroplasia and angiogenesis from bridging the gap as in healing by primary intention and as a result the anastomosis heals by secondary intention. The local use of antibiotics reverses this process to primary healing. The septic process increases collagenolysis. The synthesis of collagen in the presence of sepsis is also decreased. [3]


The assessment of nutritional status was done based on two bio chemical parameters namely haemoglobin and serum albumin estimation. The mean value of serum albumin in these patients was 3.0 gm%. While the mean value of haemoglobin of 35 patients evaluated was 9.8 gm%. As the other criteria for evaluation of nutritional status were not studied, it was not possible to correlate these values to the outcome of the anastomosis. However many studies reveal that both prolonged and short term malnutrition diminish anastomotic healing. [50] , [51] , [91] The mechanism through which malnutrition affects anastomotic healing is not fully understood and may be due to lack of essential amino acids for collagen synthesis or deterioration in the patients immunocompetence. The majority of well nourished GI surgery patients do not require special nutritional regimens. Enteral nutrition is the first choice whenever possible. It has the advantage of augmenting host defenses by sustaining the gut barrier and so diminishing the problem of bacterial translocation, an important factor implicated in multiorgan failure. [4] Only if the patient exhibits intolerance to various enteral nutrients should TPN be considered. Vitamin C is an important vitamin in the process of intestinal healing. Vitamin C deficiency leads to an inability to secrete procollagen into the extracellular space. [36] Ketone bodies as a nutritional factor in GI surgery appear to be superior to glucose. They inhibit the intestinal mucosal atrophy associated with glucose based parenteral nutrition. [54] Growth hormone has been shown to increase the uptake of glutamine and several other aminoacids by the small intestine a process which explains the anabolic effect and nitrogen retention attributed to growth hormone. [49]


The mean volume of blood transfused in patients undergoing anastomosis of the small bowel was 1.2 units, in patients with large anastomosis it was 2 units, The mean value for 35 patients evaluated was 1.4 units. Blood transfusions are known to have an immunosuppressive effect. As a result tumour growth may be enhanced, the incidence of tumour recurrence may be high, [27] , 28 there can be prolonged allograft survival in transplantation procedures20 and increased susceptibility to infection. [79] , [94] In the peritoneal cavity there could be delayed healing of anastomosis and increased incidence of intraperitoneal sepsis. [37] , [73] , [77] , [95] Lymphocytes are believed to play a significant regulatory role in cutaneous healing. [8] , [10] , [69] Blood transfusion affects lymphocyte blastogenesis and lymphocyte interaction with other immune cells. [53] , [93]

Another effect of transfusion is to decrease lymphocyte interleukin (IL-2) production. Administration of IL-2 reverses the negative effects of blood transfusion on chronic healing. [78] In the present study all the three patients who developed anastomotic leak had been transfused a mean of 2 units of blood. However the use of blood transfusion is mandatory under certain circumstances such as shock or extensive resection etc.


Out of the three anastomotic dehiscence in the present study two of the patients were on ionotropic support at the time of operation. Hypovolaemia decreases tissue oxygen tension as measured with Clarke oxygen electrode in colonic anastomosis. [27] Values of 25 mm Hg or less are incompatible with healing [74] , [75] and a leak rate of 10% with a tissue oxygen tension of 55 mm Hg. Anastomotic blood flow may be significantly compromised by hypovolaemia because in this circumstance the GI tract shunts its own blood supply to support perfusion of other vital organs. Adequate oxygen delivery is a prerequisite to the hydroxylation of lysine and proline during collagen synthesis. [15] , [47] A close correlation also exists between tissue oxygen tension and anastomotic breaking strength and hydroxyproline content. However mild degree of hypovolaemia does not impair oxygen transport and has no significant effect on wound outcome. [43]


In the series of 35 patients analyzed only 3 patients had diabetes. But none of them developed anastomotic dehiscence. Little evidence indicates that diabetes affects GI healing. A direct effect of the diabetic state of the healing process is difficult to separate from an impairment caused by increased abscess formation. Insulin therapy reverses the impairment of healing in stomach and duodenal wounds. [33] , [85] , [89]


Non steroidal anti-inflammatory drugs (NSAIDs) decrease collagenolysis. [59] , [60] Others noted that NSAIDs have a favourable effect on anastomotic healing by increased collagen production. [12] In view of the conflicting reports the active use of NSAIDs is avoided. 5 FU decreases collagen synthesis and therefore compromises healing of both small and large bowel anastomosis. [22] In the present study 2 patients were on antituberculous chemotherapy, but none of them leaked.

Growth factors (transforming growth factor TGF-B) is a normal constituent of granules of platelets and released during the early events of the healing process. [6] It is chemotactic for fibroblasts and macrophages. [70] , [90] It also increases the production of collagen by both intestinal smooth muscle cells and fibroblasts and also macrophages. [70] , [90] It also increases the production of collagen by both intestinal smooth muscle cells and fibroblasts and also modulates the expression of collagenase. [48] , [26] Topical application has shown to accelerate intestinal wound healing in a pig model.66 The only drawback of TGF-B is increased formation of adhesions in the injured peritoneum. Recombinant GH improves intestinal wound healing by enhancing the aminoacid transport in the small bowel particularly of glutamine which is the main fuel of the small intestine.


Systemic conditions which are implicated in delayed GI healing are jaundice and uraemia. [35] , [67] These metabolic diseases are accompanied by malnutrition which may be the underlying cause for these observed effects. HIV infection leading to AIDS complex is another significant cause for impaired anastomotic healing and is associated with very high dehiscence rate. In the present study out of the three patients who developed anastomotic leak one of them tested HIV positive.


In conclusion greater understanding of the impact of local and systemic factors on anastomotic healing is essential nevertheless anastomotic leakage and dehiscence remain frequent and serious problem associated with high mortality. Patients most at risk are

1. those who perioperatively develop physiologic problems that lead to shock, hypoxia and therefore the resultant anastomotic ischaemia.

2. those with sepsis and unprepared bowel.

3. those with malnourishment, HIV and malignancy.

Bearing all these in mind, along with attention to technical details, it should be possible to limit complications associated with GI anastomosis to a bear minimum.


I thank the Superintendent of Rajawadi Municipal General Hospital, Mumbai for allowing me to publish this data.


1. Abramowitz HB, Butcher HJ. Everting and inverting anastomoses. An experimental study of comparative safety. Am J Surg 1971; 121 : 52.

2. Adams W, Ctercteko G, Bilous M. Effect on an omental wrap on the healing and vascularity of compromised intestinal anastomoses. Dis Colon Rectum 1992; 35 : 731.

3. Ahrendt GM, Tantry US, Barbul A. Intra-abdominal sepsis impairs colonic reparative collagen synthesis. Am J Surg 1996; 171 : 102.

4. Alverdy JC, Chi HS, Sheldon GF. The effect of parenteral nutrition on gastrointestinal immunity : The importance of enteral stimulation. Ann Surg 1985; 202 : 681.

5. Assoian RK, Komoriya A, Meyers CA, et al. Transforming growth factor-beta in human platelets. Identification of a major storage site, purification, and characterization. J Biol Chem 1983; 258 : 7155.

6. Ballantyne GH. The experimental basis of intestinal suturing. Effect of surgical technique, inflammation, and infection on enteric wound healing (review). Dis Colon Rectum 1984; 27 : 61.

7. Barbul A. Immune aspects of wound repair (review). Clin Plast Surg 1990; 17 : 433.

8. Barbul A, Breslin RJ, Woodyard JP, et al. The effect of in vivo T helper and T suppressor lymphocyte depletion on wound healing. Ann Surg 1989; 209 : 479.

9. Berliner SD, Burson LC, Lear PE. Intraperitoneal drains in surgery of the colon. Clinical evaluation of 454 cases. Am J Surg 1967; 113 : 646.

10. Biomquist P, Jiborn H, Zederfeldt B. The effect of relative bowel rest on collagen in the colonic wall. Studies in the rat. Res Exp Med (Berl) 1984; 184 : 151.

11. Boerema J. The technique of our method of transabdominal total gastrectomy in cases of gastric cancer. Arch Chir Nerrl 1954; 6 : 95.

12. Brennan SS, Foster ME, Morgan A, et al. Prostaglandins in colonic anastomotic healing. Dis Colon Rectum 1984; 27 : 723.

13. Burke P, Mealy K, Gillen P, et al. Requirement for bowel preparation in colorectal surgery. Br J Surg 1994; 81 : 907.

14. Burkitt DS, Donovan IA. Intraluminal pressure adjacent to left colonic anastomoses. Br J Surg 1990; 77 : 1288.

15. Byrne DJ, Hardy J, Wood RA, et al. Adverse influence of fibrin sealant on the healing of high-risk sutured colonic anastomoses. J R Coll Surg Edinb 1992; 37 : 394.

16. Carrico TJ, Mehrhof AJ, Cohen IK. Biology of wound healing (review). Surg Clin North AM 1984; 64 : 721.

17. Cater DC, Jenkins DH, Whitfield HN. Omental reinforcement of intestinal anastomoses. An experimental study in the rabbit. Br J Surg 1972; 59 : 129.

18. Chassin JL, Rifkind KM, Turner JW. Errors and pitfalls in stapling gastrointestinal tract anastomoses. Surg Clin North Am 1984; 64 : 441.

19. Chowcat NL, Savage FJ, Hembry RM, et al. Role of collagenase in colonic anastomoses : A reappraisal. Br J Surg 1988; 75 : 330.

20. Chung RS. Blood flow in colonic anastomoses. Effect of stapling and suturing. Ann Surg 1987; 206 : 335.

21. Cochrum K, Hanes D, Potter D, et al. Improved graft survival following donor-specific blood transfusions. Transplant Proc 1981; 13 : 1657.

22. Cronin K, Jackson DS, Dunphy JE. Changing bursting strength and collagen content of the healing colon. Surg Gynecol Obstet 1968; 126 : 747.

23. de Waard JW, Wobbes T, de Man BM, et al. Post-operative levamisole may compromise early healing of experimental intestinal anastomoses. Br J Cancer 1995; 72 : 456.

24. diZerega GS. The peritoneum and its response to surgical injury. Prog Clin Biol Res 1990; 358 : 1.

25. Duthie HL. Drainage of the abdomen. N Engl J Med 1972; 287 : 1081.

26. Edwards DR, Murphy G, Reynolds JJ, et al. Transforming growth factor beta modulates the expression of collagenase and metalloproteinase inhibitor. EMBO J 1987; 6 : 1899.

27. Foster ME, Laycock JR, Silver IA, et al. Hypovolaemia and healing in colonic anastomoses. Br J Surg 1985; 72 : 831.

28. Foster RJ. Blood transfusions for surgical cancer patients : More harm than good? (editorial). Eur J Cancer Clin Oncol 1987; 23 : 1435.

29. Foster RJ, Costanza MC, Foster JC, et al. Adverse relationship between blood transfusions and survival after colectomy for colon cancer. Cancer 1985; 55 : 1195.

30. Foster MB, Stromberg BV, Blatchford GJ, et al. Colonic anastomoses : Bursting strength after corticosteroid treatment. Dis Colon Rectum 1994; 37 : 12.

31. Getzen LC. Clinical use of everted intestinal anastomoses. Surg Gynecol Obstet 1966; 123 : 1027.

32. Goligher JC, Graham NG, De Dombal FT. Anastomotic dehiscence after anterior resection of rectum and sigmoid. Br J Surg 1970; 57 : 109.

33. Goligher JC, Lee PW, Simpkins KC, et al. A Controlled comparison of one and two-layer techniques of suture for high and low colorectal anastomoses. Br J Surg 1977; 64 : 609.

34. Gottrup F, Andreassen TT. Healing of incisional wounds in stomach and duodenum : The influence of experimental diabetes. J Surg Res 1981; 31 : 61.

35. Graham MF, Blomquist P, Zederfeldt B. The alimentary canal. In Wound Healing : Biochemical and Clinical Aspects. Philadelphia, WB Saunders. 1992; 433.

36. Graham MF, Willey A, Adams J, et al. Role of ascorbic acid in procollagen expression and secretion by human intestinal smooth muscle cells. J Cell Physiol 1995; 162 : 225.

37. Greaney MG, Van NR, Smythe A, et al. Does obstructive jaundice adversely affect wound healing? Br J Surg 1979; 66 : 478.

38. Greatorex G, Whitaker BL, Dixon RA. Anastomotic failure in relation to blood transfusion and blood loss. Proc R Soc Med 1970; 63 : 751.

39. Gulati SM, Thusoo TK, Kakar A, et al. Comparative study of free omental, peritoneal, Dacron velour, and Marlex mesh reinforcement of large-bowel anastomosis : An experimental study. Dis Colon Rectum 1982; 25 : 517.

40. Halsted WS. Circular suture of the intestine : An experimental study. Am J Med Sci 1887; 94 : 436.

41. Haney AF, Peacock EJ, Madden JW. The effect of multiple lathyrogenic agents upon wound healing in rats. Proc Soc Exp Biol Med 1973; 142 : 289.

42. Hargreaves AW, Keddie NC. Colonic anastomosis. A clinical and experimental study. Br J Surg 1968; 55 : 774.

43. Hawley PR. Collagenase activity and colonic anastomotic breakdown. Br J Surg 1970; 57.

44. Heughan C, Grislis G, Hunt TK. The effect of anemia on wound healing. Ann Surg 1974; 179 : 163.

45. Hogstrom H, Haglund U, Zederfeldt B. Beneficial effect of proteinase inhibitors on early breaking strength of intestinal anastomoses. Acta Chir Scand 1985; 151 : 529.

46. Hogstrom H, Haglund U, Zederfeldt B. Suture technique and early breaking strength of intestinal anastomoses and laparotomy wounds. Acta Chir Scand 1985; 151 : 441.

47. Hogstrom H, Haglund U, Zederfeldt B. Tension leads to increased neutrophil accumulation and decreased laparotomy wound strength. Surgery 1990; 107 : 215.

48. Hunt TK, Zederfeldt B, Goldstick TK. Oxygen and healing (review). Am J Surg 1969; 118 : 521.

49. Ignotz RA, Massague J. Transforming growth factor-beta stimulates the expression of fibronectin and collagen and their incorporation into the extracellular matrix. J Biol Chem 1986; 261 : 4337.

50. Inoue Y, Copeland EM, Souba WW. Growth hormone enhances amino acid uptake by the human small intestine. Ann Surg 1994; 219 : 715.

51. Irvin TT, Hunt TK. Effect of malnutrition on colonic healing. Ann Surg 1974; 180 : 765.

52. Irvin TT, Hunt TK. Pathogenesis and prevention of disruption of colonic anastomoses in traumatized rats. Br J Surg 1974; 61 : 437.

53. Johnson CD, Lamont PM, Orr N, et al. Is a drain necessary after colonic anastomosis? J R Soc Med 1989; 82 : 661.

54. Kaplan J, Sarnaik S, Gitlin J, et al. Diminished helper/suppressor lymphocyte ratios and natural killer activity in recipients of repeated blood transfusions. Blood 1984; 64 : 308.

55. Kripe SA, Fox AD, Berman JM, et al. Stimulation of intestinal mucosal growth with intracolonic infusion of short-chain fatty acids. JPEN J Parenter Enteral Nutr 1989; 13 : 109.

56. LaCalle JP, Sole JM, Pey GC, et al. Rotated intestinal anastomoses. Surg Gynecol Obstet 1982; 154 : 662.

57. Mall F. A study of intestinal contraction. Healing of intestinal sutures. Reversal of the intestine. Boston, U Holzer. 1887; 77.

58. Manz CW, LaTendresse C, Sako Y. The detrimental effects of drains on colonic anastomoses. An experimental study. Dis Colon Rectum 1970; 13 : 17.

59. Mastboom WJ, Hendriks T, de Man BM, et al. Influence of methylprednisolone on the healing of intestinal anastomoses in rats (see comments). Br J Surg 1991; 78 : 54.

60. Mastboom WJ, Hendriks T, van Elteren P, et al. The influjence of NSAIDs on experimental intestinal anastomoses. Dis Colon Rectum 1991; 34 : 236.

61. Mastboom WJ, Hendriks T, van Elteren P, et al. Piroxicam affects collagen changes around experimental intestinal anastomoses. Eur Surg Res 1989; 21 : 305.

62. McAdams AJ, Meikle AG, Taylor JO. One layer or two layer colonic anastomoses? Am J Surg 1970; 120 : 546.

63. McCue JL, Phillips RK. Sutureless intestinal anastomoses (review). Br J Surg 1991; 78 : 1291.

64. McLachin AD, Denton DW. Omental protection of intestinal anastomoses. Am J Surg 1973; 125 : 134.

65. Mercer CD, Minich P, Pauli B. Sutureless bowel anastomosis using Nd : YAG laser. Lasers Surg Med 1987; 7 : 503.

66. Murphy JB. Cholecysto-intestinal, gastro-intestinal, entero-intestinal anastomosis and approximation without sutures (original research). Med Rec 1892; 42 : 665.

67. Mustoe TA, Landes A, Cromack DT, et al. Differential acceleration of healing of surgical incisions in the rabbit gastrointestinal tract by platelet-derived growth factor and transforming growth factor, type beta. Surgery 1990; 108 : 324.

68. Nayman J, McDermott EW, et al. Effect of mechanical bowel preparation on anastomotic integrity following low anterior resection in dogs. Br J Surg 1989; 76 : 765.

69. Orr NW. A single-layer intestinal anastomosis. Br J Surg 1969; 56 : 771.

70. Peterson JM, Barbul A, Breslin RJ, et al. Significance of T-lymphocytes in wound healing. Surgery 1987; 102 : 300.

71. Postlethwaite AE, Keski OJ, Moses HL, et al. Stimulation of the chemotactic migration of human fibroblasts by transforming growth factor beta. J Exp Med 1987; 165 : 251.

72. Sagar PM, Couse N, Kerin M, et al. Randomized trial of drainage of colorectal anastomosis (see comments). Br J Surg 1993; 80 : 769.

73. Schrock T, Cerra F, Hawley PR, et al. Wounds and wound healing (Clinical conference). Dis Colon Rectum 1982; 25 : 1.

74. Schrock TR, Deveney CW, Dunphy JE. Factors contributing to leakage of colonic anastomoses. Ann Surg 1973; 177 : 513.

75. Shandall A, Lowndes R, Young HL. Colonic anastomotic healing and oxygen tension. Br J Surg1985; 72 : 606.

76. Sheridan WG, Lowndes RH, Young HL. Tissue oxygen tension as a predictor of colonic anastomotic healing. Dis Colon Rectum 1987; 30 : 867.

77. Sheridan WG, Shandall AA, Alexander WJ, et al. A multicenter trial of the use of the proteolytic enzyme inhibitor aprotinin in colorectal surgery. Dis Colon Rectum 1989; 32 : 505.

78. Tadros T, Wobbes T, Hendriks T. Blood transfusion impairs the healing of experimental intestinal anastomoses. Ann Surg 1992; 215 : 276.

79. Tadros T, Wobbes T, Hendriks T. Opposite effects of interleukin-2 on normal and transfusion-suppressed healing of experimental intestinal anastomoses. Ann Surg 1993; 218 : 800.

80. Tartter PI, Quintero S, Barron DM. Perioperative blood transfusion associated with infectious complications after colorectal cancer operations. Am J Surg 1986; 152 : 479.

81. Uden P, Blomquist P, Jiborn H, et al. Impact of long-term relative bowel rest on conditions for colonic surgery. Am J Surg 1988; 156 : 381.

82. Uden P, Blomquist P, Jiborn H, et al. Influence of proximal colostomy on the healing of a left colon anastomosis : An experimental study in the fat. Br J Surg 1988; 75 : 325.

83. Undenfriend S. Formation of hydroxyproline in collagen (review). Science 1966; 152 : 1335.

84. Van der Ham AC, Kort WJ, Weijma IM, et al. Effect of antibiotics in fibrin sealant on healing colonic anastomoses in the rat. Br J Surg 1992; 79 : 525.

85. Van der Ham AC, Kort WJ, Weijma IM, et al. Healing of ischemic colonic anastomosis : Fibrin sealant does not improve wound healing. Dis Colon Rectum 1992; 35 : 884.

86. Van der Hem LG, Verhofstad MH, Bocken CF, et al. Pancreatic islet transplantation prevents impaired healing of intestinal anastomoses in diabetes. Transplant Proc 1994; 26 : 660.

87. Van Doorn K, de Man B, Hendriks T. The effect of lathyrogens on intestinal anastomoses in the rat. Exp Mol Pathol 1990; 52 : 37.

88. Van Winkel W Jr, Hastings JC. Considerations in the choice of suture material for various tissue (review). Surg Gynecol Obstet 1972; 135 : 112.

89. Varma S, Ferguson HL, Breen H, et al. Comparison of seven suture materials in infected wounds an experimental study. J Surg Res 1974; 17 : 165.

90. Verhofstad MHJ, van der Hem LG, Adam Van der Vliet J, Hendriks T. Pancreatic islet transplantation prevents the impaired healing of intestinal anastomoses in Lewis rats with streptozotocin-induced diabetes. Wound Repair and Regeneration 1995; 3 : 221.

91. Wahl SM, Hunt DA, Wakefield LM, et al. Transforming growth factor type beta induces monocyte chemotaxis and growth factor production. Proc Natl Aca Sci USA 1987; 84 : 5788.

92. Waninger J, Kauffmann GW, Shah IA, et al. Influence of the distance between interrupted sutures and the tension of sutures on the healing of experimental colonic anastomoses. Am J Surg 1992; 163 : 319.

93. Ward MW, Danzi M, Lewin MR, et al. The effect of subclinical malnutrition and refeeding on the healing of experimental colonic anastomoses. Br J Surg 1982; 69 : 308.

94. Waymack JP, Balakrishnan K, McNeal N, et al. Effect of blood transfusions on macrophage-lymphocyte interaction in an animal model. An Surg 1986; 204 : 681.

95. Wobbes T, Bemelmans BL, Kuypers JH, et al. Risk of postoperative septic complications after abdominal surgical treatment in relation to perioperative blood transfusion. Surg Gynecol Obstet 1990; 171 : 59.

96. Young HL, Wheeler MH. Collagenase inhibition in the healing colon. J R Soc Med 1983; 76 : 32.


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