Intestinal Obstruction Due To Adhesion

INTESTINAL OBSTRUCTION DUE TO ADHESION By DR ADEKO OLUSEUN dept of family medicine olabisi onabanjo university teaching hospital, sagamu, nigeria.

OUTLINE

• STATISTICS AND CASE PRESENTATION • INTRODUCTION • EPIDEMIOLOGY • CLINICAL SIGNIFICANCE • PATHOGENESIS • CLINICAL PRESENTATION • MANAGEMENT • PROGNOSIS • CONCLUSION

ADHESIVE INTESTINAL OBSTRUCTION

• This refers to the blockage of the intestines, usually following surgery due to formation of adhesion as part of normal process of healing preventing the normal transit of products of digestion, intestinal secretions and gas. • It can occur at any level of GIT, but commonly in the small intestine.

• Adhesions are abnormal deposits of fibrous tissue which form within the peritoneal cavity.

• Adhesion formation after abdominal and pelvic operations remains extremely common and is a source of considerable morbidity.

• In clinical and autopsy studies of patients who had prior laparotomies, the incidence of intra-abdominal adhesions was 70-90%

CLASSIFICATION OF ADHESIONS • Congenital adhesions: these are present as embryological anomaly in the development of the peritoneal cavity. (vitello-intestinal bands, adhesions seen across the lesser sac). • Acquired adhesions: these may inflammatory and post-surgical.

• Inflammatory adhesions: arise after intraabdominal inflammatory processes e.g. appendicitis, acute cholecystitis, PID, TB abdomen. • Post-surgical adhesions: account for vast majority of adhesions. It occurs when injured tissue surface, following incision, cauterization or suturing fuse together to form scar tissue.

• Post-surgical adhesions form between the wound and omentum in over 80% of the pts. • The intestines are involved in 50% of the pts.

FACTORS ASSOCIATED WITH THE FORMATION OF POST-SURGICAL ADHESIONS

• These include: trauma, thermal injury, infection, ischaemia and foreign body. • Others are: tight suturing, abrasions, intestinal contents, blood, overheating by lamps and irrigation fluid.

CLINICAL SIGNIFICANCE • Intestinal obstruction: occurs commonly in the small bowel and results from kinking, angulation or creation of bands of tissue that compress the bowel. • Adhesions create a lifetime risk of IO. An operation 4 obstruction due to adhesions carries a higher likelihood of recurrence than a laparotomy 4 other indications • When obstruction recurs, the possibility of a cause other than adhesions is lower. • The no of prior episodes a pt has experienced is the strongest predictor of recurrence.

• Most of the pts with AIO have been found to have had surgery in the infracolic part of the abdomen, where loops of small intestine adhere and become obstructed. • Operations that frequently lead to AIO include: colon & rectal surgery, nonelective appendectomy, gynecological procedures, gastrectomy, abdominal vascular op, e.t.c.

• It should be noted that congenital and inflammatory adhesions rarely give rise to IO. • The problem of post-surgical adhesions +ses with the pt’s age, no of laparotomies and complexity of surgical procedures .

• Pts with a relatively low risk of adhesion formation are those who have undergone an elective appendectomy thru a small incision or a caesarian section thru a pfannestiel incision. • Prior lap thru a midline vertical incision has significantly increased the frequency of ant abd wall adhesion.

• Propensity to form adhesion appears to be patient specific. • Various individual factors e.g. nutritional status, disease like DM and the presence of concurrent infectious process, which alter leucocytes and fibroblast function affect adhesion formation.

• Other clinical conditions that may arise due to adhesions are: difficult re-operative surgery chronic abdominal pain chronic pelvic pain female infertility.

EPIDEMOLOGY OF AIO • AIO are responsible for a large proportion of general surgical admission. • Approx 1% of all surgical admission and 3% of laps are the results of AIO. • Over 20% of AIO occur within 1 month of surgery, and up to 40% occur within 1 year.

• Study done at ife revealed that out of 99 cases of IO seen btw 19851994, 44% were due to adhesion. (Lawal 2005). • Similar study done at ilesha revealed that out of 142 cases of IO seen during the same period, 41.5% were due to adhesion. (Adesunkanmi 1996). • Findings at OOUTH showed that 111 cases of IO were seen from 1997 till date, out of which 44 cases were reviewed. 15% were due to adhesion.

• Study done in Ghana btw 1998-2003 revealed 652 cases of IO and AIO was the 2nd commonest cause 27.2% with the M:F of 1.7:1 (Ohene-Yeboah 2006). • Findings at a UK hospital over a period of 12 months revealed 228 cases of IO, and AIO was the cause in 32%. (McEntee 1987).

PATHOGENESIS OF ADHESION

• Peritoneal healing differs from that of the skin. Skin re-epithelialization takes place thru proliferation of epithelial cells from the periphery toward the centre of the skin wound. • Peritoneum becomes mesothelialized simultaneously, and regardless of the injury, with new mesothelium developing from Islands of cells.

• The key site in adhesion formation is the surface lining of the peritoneum. • The delicacy of the peritoneal surface and its subsequent susceptibility to damage as well as the rapid rate of remesothelialization within 5-8 days are important factors in adhesion formation. • A wide variety of inflammatory stimuli (op, trauma, bacteria infection, irradiation, chemical) result in peritoneal injury.

• Peritoneal injury/inflammation triggers coagulative cascade which results in the formation of inflammatory exudate containing fibrin. • The fibrinous exudate is organized and fibroblast invasion is followed by the deposition of collagen and the formation of permanent fibrous tissue. • This process is not inevitable as the peritoneum possesses fibrinolytic activity which if not impaired, will lysed the fibrin within the exudate be4 organisation of the exudate can take place.

• This biological balance is illustrated below: Peritoneal injury Fibrinous adhesion Lysed

Organised

Resolution

Adhesion formation

• Studies have shown that injury to the peritoneum reduces its fibrinolytic capacity and the same injury also produces intra-abd adhesions. • Organisation of peritoneal exudate and collagen deposition commences within 5 days of peritoneal injury, suggesting that prolonged depression of mesothelial fibrinolysis may allow permanent fibrous adhesion formation

• Peritoneal injury results in a high conc peritoneal pro-inflammatory cytokines response esp TNFα, IL-1 and IL-6. • These cytokines inhibit fibrinolysis. • In conclusion, fibrous adhesion are formed within the peritoneal cavity when the normal fibrinolytic activity of the peritoneum is lost.

CLINICAL FEATURES • The symptoms and signs in AIO depend on nature of obstruction- simple, strangulation.

Simpl e Pain Colick y, inter Tende mitten absen rness tt Bowel Hyper sound

Stran gulate d contin uous prese nt Absen t

• Pain- earliest symptom • Vomiting- severity depends on whether high or low • Constipation – high/low • Distension- high/low • History of previous surgery/inflammatory conditions

• GPE- painful distress, dehydration, signs of shock • Vital signs- tachycardia, tachypnoea, hypotension, fever. • ABD- previous op scar, distension, tenderness, guarding and rebound tenderness in strangulation bowel sounds- hyper or absent DPR- empty rectum.

MANAGEMENT • Investigations • Treatment • Prevention • Prognosis • conclusion

INVESTIGATIONS • Laboratory-

FBC, E, U& Cr, Urinalysis, ABG

• Imaging studies- plain abd x- ray, CT-scan, Abd USS.

Imaging studies :Plain radiography Order plain radiographs first for patients in whom SBO• .is suspected Plain radiographs are diagnostically more accurate in• .cases of simple obstruction Plain radiography is of little assistance in• .differentiating strangulation from simple obstruction • .Dilated small bowel loops indicate SBO• .Absent or minimal colonic gas indicate SBO *

Radiograph for adhesive intestinal obstruction

:CT scanning CT is useful in making an early diagnosis of* strangulated obstruction and in delineating the myriad .other causes of a cute abdominal pain It also has proved useful in distinguishing the etiology of SBO (If it was extrinsic causes such as adhesions and hernia from intrinsic causes such as neoplasm or .Crohn's CT scanning is about 90% sensitive and specific in * .diagnosing CBO CT scanning enables the clinician to distinguish * between ileus and mechanical small bowel in .postoperative patients

.Bowel wall thickening indicates early strangulation * .Portal venous gas indicates early strangulation * CT scanning is useful in identifying abscess, hernias and * .tumors

Strangulated obstruction

:Ultrasonography Ultrasonography is less costly and less invasive than CT * . scanning It may reliably exclude SBO in as many as 89% of * .patients

Treatment • General principles • Conservative • Surgical

General principles

• Stabilize pt

• Replace ivf-diligent ivf resuscitation • NGtube –early bowel decompression • Urethral catheterization • Administer broad spectrum antibiotics-necrosis suspected

Conservative mgt

• History- Abd pain, Distention, Vomiting, Fever • Monitor vital signs

• Monitor NGTube effluent- Color, Volume • Monitor Abdomen- Abd girth, Tenderness, Guarding, Bowel sounds • Oral gastrograffin- Test

Surgical Mgt • Adhesiolysis • Bowel resection & anastomosis • Close follow up-non operative mgt

PREVENTION

• There are no of possible measures of preventing post-surgical adhesion formation. These are: 

Good surgical technique



pharmacological adjuvant therapy



Adjuvant barrier therapy

SURGICAL TECHNIQUES • Tissue injury- steps to avoid injury to tissue • Peritoneal suturing- sutures are foreign body, so may +se the risk of adhesion formation. Cover areas at higher risk of adhesion formation with omentum, peritoneal flap, falciform ligament, broad ligament.

• Foreign materials- glove powder (talc, starch), fluff from surgical packs, materials extruded from GIT all provoke inflammatory rxn which potentiate adhesion formation • Sponges- strong association btw adhesion formation and use of sponges. When bowel need to be packed use atraumatic bag to reduce injury to the serosa.

• Intra-peritoneal blood deposithaemostasis is essential. Blood should be aspirated in irrigation solution • Minimally invasive surgery- use of MIS and laparoscopy technique

PHARMACOLOGICAL ADJUVANT THERAPY

• Involve use of agent against various causes & component of inflammatory process (infection, endotoxin, exudation) and/or of adhesion formation (coagulation, fibrin deposition, fibroblastic activity and proliferation) • Obstacle to overcome are: Ischaemic site are cut off from systemic drug delivery

Peritoneal membrane has an extremely rapid absorption mechanism Agent to be used should not affect normal wound healing process. The process of adhesion formation uses the same pathway as normal wound healing. • Some of the agent used are:

• NSAID- inhibits PG& TXA2 formation thereby modulate a no of aspect of inflammation. been found to reduce peritoneal adhesion in some animal models. • Glucocorticoid & Antihistamines- these agents attenuate inflammatory response mixed results from sutdies so far. side-effect of steroid: immunosuppression & delayed wound healing.

• Progesterone/Estrogen- In animal models progesterone was found to reduce adhesion formation while estrogen +ses adhesion. No confirmatory study in human yet. • Anticoagulant- crystalloid isotonic irrigation containing heparin reduces adhesion formation by inhibiting fibrin coagulation. Note that heparin may be associated with bleeding & delayed wound healing.

• Fibrinolytic- use of rtPA locally to enhance fibrinolysis has recorded limited success. There is risk of bleeding. • Antibiotic- broad spectrum antibiotic are used commonly 4 prophylaxis against post-op infections & adhesion formation. Antibiotic in intra-abdominal irrigation fluid actually causes adhesion formation.

ADJUVANT BARRIER THERAPY • Anti-adhesion barriers fall into 2 groups  Macromolecular solution barrier  Mechanical devices • Barrier solutions- These are:  Crystalloids- Intra-peritoneal instillation of normal saline or ringer’s lactate is thought to dilute the fibrin & also separate raw areas of peritoneum thereby preventing adhesion.

 32% DEXTRAN 70- by hydroflotation of intra-abd structures with dextran solution, a physiological separation occurs btw peritoneal surfaces. Thru dilution, dextran reduces local fibrin conc & preserve local plasminogen activators. Results in preventing adhesion has been inconsistent.  Hyaluronic acid (HA)- naturally occurring, biocompatible & non-immunogenic. It coats serosal surfaces & provides a certain degree of protection from desiccation and other types of injury.

HA Combined with phosphatebuffered solution (seprarcoat)- this is applied intra-op prior to dissection to protect peritoneal surfaces from indirect surgical trauma (abrasion, desiccation). Carboxymethylcellulose- a derivative of cellulose. It works by separating raw surfaces and allows independent healing of traumatized peritoneal surfaces.

• Solid barriers are:  Autologous peritoneal transplant- covering lesions of parietal peritoneum with microsurgically applied autologous transplant can completely prevent severe adhesion formation  PTFE (Gore-tex)- a non-reactive, antithrombogenic, non-toxic synthetic fabric with small pores that inhibit cellular transmigration & tissue adherence. It is strictly reserved 4 non- contamination ops. It prevents adhesion regardless of the type of injury or whether hemostasis is achieved.

Oxidized regenerated cellulose (Interceed): The only adjuvant approved 4 specific purpose of post-surgical adhesion prevention. It works by forming a barrier and physically separate raw peritoneal surfaces. It works well only when hemostasis is perfect as blood interferes with its fxn. HA-CMC-(Seprafilm)- non toxic, non immunogenic and biocompatible material.

PROGNOSIS • Difficult operation results in increased morbidity, e.g. enterocutaneous fistula may occur. • Risk of recurrence- previous hx of AIO is a strong predictor of recurrence. Operation 4 recurrence may further generate adhesion.

CONCLUSION

Adhesion formation is a complex process involving biochemical and biomechanical factors. The cascade leading to adhesion is the result of body response to an injury. Current knowledge about these steps have been discussed. A multifactorial approach including minimizing tissue injury with meticulous surgical technique, appropriate antibiotic use and biochemical agents and barriers will reduce amount and severity of adhesion. However, it is unlikely that the problem of adhesion with the resultant morbidity and economic cost will be resolved in the near