Intestinal Surgery: Reducing Morbidity and Mortality
World Small Animal Veterinary Association World Congress Proceedings, 2013
Theresa W. Fossum, DVM, MS, PhD, DACVS
Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, TX, USA

Diagnosis of small intestinal disease is based on the history, clinical signs, physical examination, radiographs, ultrasound scans, laboratory data, endoscopy, and/or biopsy. Diet, medications, stressful events, and response to prior therapy should be ascertained from owners. Clinical signs of small intestinal disease vary and are nonspecific, although weight loss, diarrhea, vomiting, anorexia and/or depression are the most common. Pain and shock may result from trauma, vascular occlusion, or complete intestinal obstruction. Severe vomiting, shock, or an acute abdomen suggests intestinal malposition, ischemia, perforation, or upper intestinal obstruction.

Hematologic and biochemical profiles should be performed on animals suspected of having small intestinal abnormalities to help identify concurrent systemic disease (e.g., renal disease, hepatic disease, hypoadrenocorticism, hypercalcemia, diabetes mellitus, pancreatitis) and to direct preoperative therapy. Dehydration, acid-base abnormalities, and electrolyte imbalances are common sequelae to vomiting, diarrhea, and fluid sequestration. These abnormalities should be corrected before induction of anesthesia if possible. Alleviating hypotension is important because it is associated with intense portal vasoconstriction that causes the breakdown of the intestinal mucosal barrier allowing increased endotoxin absorption. Profuse vomiting typically results in dehydration and may cause hypochloremia, hypokalemia, and/or hyponatremia. Duodenal vomitus may cause greater sodium, potassium, and water losses than gastric vomiting. Alkalosis generally occurs with loss of gastric fluid; however, metabolic acidosis may occur due to fluid depletion from vomiting, insensible water losses, lack of intake, and/or catabolism of body stores. Cross-matched whole blood or red cells should be administered when the packed cell volume (PCV) drops below 20% or if the dog is weak or clinically hypoxic. Chronically ill, anemic patients should be given whole blood if hypovolemic and packed red blood cells (RBCs) if normovolemic. Clotting factor deficiencies should be corrected with whole fresh blood or fresh or fresh-frozen plasma. Platelet-rich plasma or platelet transfusions should be used if the animal is severely thrombocytopenic. Administration of plasma (5 to 20 ml/kg), whole blood transfusions or hetastarch several hours before surgery should be considered if serum albumin concentrations are below 1.5 g/dl. If the patient has a severe protein-losing enteropathy, administration of plasma is seldom effective in raising the serum albumin concentration because most of the albumin is quickly lost into the GI tract. Therefore, hetastarch is usually preferred. There is some evidence that blood transfusions may impair intestinal healing and increase susceptibility to intraabdominal sepsis.

Plain radiographs may demonstrate abnormal gas-fluid patterns, masses, foreign bodies, abdominal fluid, or displaced viscera. Both lateral recumbent views and a ventrodorsal projection should be taken. A ratio of the maximum diameter of the small intestine to the height of the cranial end plate of the second lumbar vertebrae of > 3.0 was strongly associated (70%) with intestinal obstruction in cats, and a ratio of > 4.0 provided the 95% confidence interval for obstruction. Contrast studies are can demonstrate foreign bodies, obstructions, abnormal displacements, abnormal bowel wall thickness, irregular mucosal patterns, and distortion of the bowel wall. The positive contrast agent usually used for gastrointestinal radiology is micropulverized barium sulfate suspension; however, iodinated contrast or iohexol should be used when intestinal perforation is suspected but septic peritonitis cannot be demonstrated with abdominocentesis or diagnostic peritoneal lavage. Contrast studies are infrequently done now, due to the availability of ultrasound and endoscopy.

Ultrasonography can detect and define intestinal and other abdominal masses plus evaluate intestinal wall thickness (a normal small intestinal wall is 2 to 3 mm thick), the appearance and symmetry of the various wall layers, the number of peristaltic contractions, the pattern of intestinal contents (gas-hyperechoic, mucus-echogenic without acoustic shadowing, fluid-anechoic), the location of the lesion, and the extent of disease. Five layers are normally visible ultrasonographically in the intestinal wall: the hyperechoic mucosal surface, hypoechoic mucosa, hyperechoic submucosa, hypoechoic muscularis and hyperechoic serosa. Ultrasound is very in helping the clinician decide whether to perform endoscopic or surgical biopsy of the intestines. If the intestine generally looks the same throughout all or most of its length, then endoscopic biopsy is usually appropriate. If ultrasound reveals that the only sections of bowel that appear involved are out of reach of the endoscope, then surgical biopsy is often preferred.

Gastroduodenoscopy allows visualization and biopsy of the duodenum (and sometimes the upper jejunum) while colonoileoscopy allows visualization and biopsy of the ileum. Visualization of intestinal mucosa may detect ulcers, erosions, infiltrated mucosa, and/or lymphangiectasia that cannot be detected with radiographs or ultrasound. Endoscopy also allows multiple biopsies of the small intestine, and in particular allows one to direct the biopsy to obvious mucosal lesions.

The benefits of stabilizing the animal's condition before surgery must be weighed against the risk of ischemic necrosis. Explore the animal without delay if one or more of the following is true: 1) The animal has received a penetrating abdominal injury; 2) Large numbers of neutrophils (greater than 25,000/ul) or very toxic neutrophils are identified on cytology of the effusion; 3) Bacteria are found in abdominal effusion; 4) The blood-to-peritoneal fluid glucose difference is greater than 20 mg/dl; 5) The peritoneal fluid lactate concentration is greater than 2.5 to 5.5 mmol/l; 6) Extraluminal gas bubbles (i.e., spontaneous pneumoperitoneum) or volvulus are identified during imaging; 7) Esophageal or gastric intussusception is identified during imaging; or 8) Bacterial culture of the fluid is positive for pathogenic bacteria.

Consider exploring the animal without delay if the above factors are not identified but an emergency is suspected and one or more of the following is true: 1) The peritoneal fluid has greater than 13,000 nucleated cells/µl; 2) The peritoneal fluid pH is less than 7.2; 3) The peritoneal fluid pCO2 is greater than 55 mm Hg; 4) The peritoneal fluid pO2 is less than 50 mm Hg; 5) The peritoneal fluid glucose concentration is less than 50 mg/dl; 6) A negative blood-to-fluid lactate difference exists; or 7) The animal deteriorates clinically despite aggressive medical management and complete obstruction, perforation, strangulation, necrosis or sepsis is suspected.

Intestinal Resection and Anastomosis

Intestinal resection and anastomosis are recommended for removing ischemic, necrotic, neoplastic, or fungal-infected segments of intestine. Irreducible intussusceptions are also managed by resection and anastomosis. End-to-end anastomoses are recommended.

Make an abdominal incision which allows complete exploration of the abdomen. Perform a thorough examination of the abdomen and collect any non-intestinal specimens. Exteriorize and isolate the diseased intestine from the abdomen by packing with towels or laparotomy sponges. Assess intestinal viability and determine the amount of intestine needing resection. Double ligate and transect the arcadial mesenteric vessels from the cranial mesenteric artery that supplies this segment of intestine. Double ligate the terminal arcade vessels and vasa recta vessels within the mesenteric fat at the points of proposed intestinal transection. Gently milk chyme (intestinal contents) from the lumen of the identified intestinal segment. Occlude the lumen at both ends of the segment to minimize spillage of chyme. Place forceps across each end of the diseased bowel segment. Transect the intestine with either a scalpel blade or Metzenbaum scissors along the outside of the forceps. Make an oblique incision across the intestine if the luminal diameters are the same. When two pieces of intestine are being joined that are of unequal size, use a perpendicular incision across the intestine with the larger luminal diameter and an oblique incision (45- to 60-degree angle) across the intestine with the smaller luminal diameter to help correct size disparity). Make the oblique incision such that the antimesenteric border is shorter than the mesenteric border. Suction the intestinal ends and remove any debris clinging to the cut edges with a moistened gauze sponge. Trim everting mucosa with Metzenbaum scissors just before beginning the end-to-end anastomosis.

Use 3-0 or 4-0 monofilament, absorbable suture (polydioxanone or polyglyconate) with a swaged-on taper or tapercut point needle. Place simple interrupted sutures through all layers of the intestinal wall. Angle the needle so the serosa is engaged slightly further from the edge than the mucosa. This helps reposition everting mucosa within the lumen. Tie each suture carefully so as to gently appose the edges of the intestine with the knots extraluminally. Appose intestinal ends by first placing a simple interrupted suture at the mesenteric border and then placing a second suture at the antimesenteric border approximately 180 degrees from the first (this divides the suture line into equal halves and allows determination of whether the ends are of approximately equal diameter). The mesenteric suture is the most difficult suture to place in the anastomosis because of mesenteric fat. It is also the most common site of leakage. If the ends are of equal diameter, space additional sutures between the first two sutures approximately 2 mm from the edge and 2 to 3 mm apart. If minor disparity still exists between lumen sizes, space the sutures around the larger lumen slightly further apart than the sutures in the intestine with the smaller lumen. To correct luminal disparity that cannot be accommodated by the angle of the incisions or by suture spacing, resect a small wedge (1 to 2 cm long and 1 to 3 mm wide) from the antimesenteric border of the intestine with the smaller lumen. After suture placement inspect the anastomosis and check for leakage.

While maintaining luminal occlusion adjacent to the anastomotic site, moderately distend the lumen with sterile saline, apply gentle digital pressure, and observe for leakage between sutures or through needle holes. Close the mesenteric defect with a simple continuous or interrupted suture pattern (4-0 polydioxanone or polyglyconate) being careful not to penetrate or traumatize arcadial vessels near the defect.

Serosal Patching

Serosal patching is placement of an antimesenteric border of the small intestine over a suture line or organ defect and securing it with sutures. Serosal patching serves to provide support, a fibrin seal, resistance to leakage, blood supply to the damaged area, and may prevent intussusception. Patches are commonly used following intestinal surgery when closure integrity is questioned or dehiscence is repaired. Patches which span visceral defects are covered with mucosal epithelium within 8 weeks. Most commonly, jejunum adjacent to the defect or area of questionable viability is used for the serosal patch, although other sources could include stomach, other intestinal segments, or urinary bladder.

Use one or more loops of intestine to form the patch. Use gentle loops to avoid stretching, twisting, or kinking the intestine and mesenteric vessels. If using more than one loop of intestine, suture these loops together before securing the patch to the damaged area. All sutures used to create or secure the patch engage the submucosa, muscularis, and serosa; they should not penetrate the intestinal lumen. Place interrupted or continuous sutures in healthy tissue to secure the patch and isolate the damaged area.

  

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Theresa W. Fossum, DVM, MS, PhD, DACVS
Veterinary Medicine & Biomedical Sciences
Texas A&M University
College Station, TX, USA


Friendly Reminder to Our Colleagues: Use of VIN content is limited to personal reference by VIN members. No portion of any VIN content may be copied or distributed without the expressed written permission of VIN.

Clinicians are reminded that you are ultimately responsible for the care of your patients. Any content that concerns treatment of your cases should be deemed recommendations by colleagues for you to consider in your case management decisions. Dosages should be confirmed prior to dispensing medications unfamiliar to you. To better understand the origins and logic behind these policies, and to discuss them with your colleagues, click here.

Images posted by VIN community members and displayed via VIN should not be considered of diagnostic quality and the ultimate interpretation of the images lies with the attending clinician. Suggestions, discussions and interpretation related to posted images are only that -- suggestions and recommendations which may be based upon less than diagnostic quality information.

CONTACT US

777 W. Covell Blvd., Davis, CA 95616

vingram@vin.com

PHONE

  • Toll Free: 800-700-4636
  • From UK: 01-45-222-6154
  • From anywhere: (1)-530-756-4881
  • From Australia: 02-6145-2357
SAID=27