Gastro 49 Small Intestine

• Lesion extrinsic to intestinal wall – adhesions, hernia, extraintestinal neoplasm, intraabdominal abscess
• Lesions intrinsic to intestinal wall – malrotation, crohns disease, TB, diverticulitis, neoplasm, trauma – hematoma, Intussuception
• Intraluminal – Gallstones, fecolith, foreign body

• Adhesions – 60%
• Neoplasms – 20%
• Hernia – 10%
• Crohns disease – 5%
• Miscellaneous – 5%

Increased peristalsis in bowel distal to obstruction – complete bowel obstruction cannot be ruled out on the basis of diarrhea

• ●The adhesions that form in the abdomen after abdominal or pelvic surgery result from tissue trauma and subsequent healing, and are a normal response of the peritoneal surfaces to surgical injury. Adhesion formation involves a complex interaction of many cell-secreted factors in areas of surgical trauma. The balance between fibrin deposition and degradation (ie, fibrinolysis) appears to be the critical factor in adhesion formation.
• ●Although adhesion formation is integral to the healing process, they can cause significant morbidity. Adhesions are the most common cause of bowel obstruction and should be suspected in any patient with a history of prior abdominal or pelvic surgery who presents with signs and symptoms of bowel obstruction. Other clinical consequences of adhesions include infertility and chronic abdominal pain.

• ●Indications of surgical lysis 
• - Postoperative bowel obstruction that persists after conservative management
• - For treatment of infertility and recurrent pregnancy loss

• ●The first line defense against adhesion formation is meticulous surgical technique. Although laparoscopy generally results in less tissue trauma than laparotomy, the incidence and severity of postoperative adhesions after laparoscopy is not necessarily lower than after laparotomy.
• ●For patients at high risk for developing adhesions having laparotomy (eg, gynecologic surgery, repeat laparotomy), we suggest using a solid physical barrier such as Interceed (oxidized regenerated cellulose) for adhesion prevention, rather than a liquid barrier agent, or no barrier (Grade 2B).
• ●For patients undergoing laparoscopic lysis of adhesions, we suggest the use of liquid barrier agents such as icodextrin (Grade 2C).
• ●We suggest avoiding the use of nonbarrier intraabdominal fluid solutions, antibiotics, and antithrombotic agents because they are ineffective and potentially harmful (Grade 2B).

• ●Technical measures limit or prevent the initial peritoneal injury
• - Meticulous hemostasis and gentle, minimal tissue handling 
• - Damage to the serosa can be prevented by minimizing trauma, bleeding, and ischemia, and by keeping the surgical field moist with frequent irrigation to prevent tissues from drying out.
• - Removing the talc or starch from gloves before entering the peritoneal cavity
• - Laparoscopy offers certain advantages over open abdominal surgery with respect to adhesion formation
• - Fine, nonreactive suture material should be used wherever possible; silk sutures, which are fibrogenic, should be avoided in the abdomen.
• - 

• ●Barrier agents
• - act primarily as a physical separation between the fibrin-coated peritoneal surfaces predisposed to adherence.
• - Solid - oxidized regenerated cellulose sheet or sodium hyaluronate-based carboxymethylcellulose sheet 
• - Liquid materials - Polyethylene glycol, Icodextrin solution, Hyaluronic acid solution, gel, and powder
•  

• ●Pharmacologic therapies
• -  glucocorticoids,  promethazine or ketorolac are effective only in animal model. No RCT in human.

• Indications of non-operative management in ASBO
• No signs of strangulation or peritonitis
• Surgery more than 6 weeks before ASBO
• Partial ASBO
• Signs of resolution on admission

Go for non operative management with NG decompression, IV fluid and observe patient closely. Water soluble contrast medium administration – Appearance of contrast in colon within 24 hours predicts resoulution of ASBO. If no contrast in the colon within 24-36 hours – Go for operative management.

• Further indications for delayed operation
• Evolving peritoneal signs
• Persistent ileus >72h
• NG drain >500ml on 3rd day
• Pain lasting for 4 days or more
• CRP ≥75mg/dl
• WBC≥ 10000/mm3
• Free intraperitoneal fluid ≥ 500ml on CT
• Reduction of CT small bowel wall contrast enhancement

• Indications of surgical management for ASBO
• Signs of strangulation or peritonitis
• Surgery within 6 weeks before ASBO
• Carcinnomatosis or irreducible hernia
• Complete SBO (no evidence of air within the large bowel)
• No signs of resolution within 72 hours

Open surgery for several surgeons still remains the safestand most effective operative approach, although laparoscopic approach appears to be safe and feasible in the hands of experienced laparoscopic surgeons and in selected patients.

• Water-soluble contrast follow-through is valuable inpatients undergoing initial non operative conservativemanagement in order to rule out complete ASBO and predict the need for surgery.
• Water-soluble contrast administration has both diagnostic and therapeutic value

Gastrografin may be administered on the dosage of 50–150 ml, either orally or via NGT and can be given both at immediately admission or after an attempt of initial traditional conservative treatment of 48 hours.

Defined by the presence of particulate faeculent material mingled with gas bubbles in the lumen of the small intestine (as seen in the colon on CT), it is believed the result of delayed intestinal transit and to be caused by incompletely digested food, bacterial overgrowth, or increased water absorption of the distal small-bowel contents due to obstruction

• Avoiding unnecessary peritoneal dissection
• Avoiding spillage of intestinal contents or gallstones
• Use of starch-free gloves

Prevention with hyaluronic acid-carboxycellulose membrane or icodextrin, has actually gained a capital relevance.

The physiologic consequences of enterocutaneous fistulas depend upon the composition of the fistula drainage, which differs for proximal versus distal intestinal fistulas, and volume of the fistula. The physiologic classification of enterocutaneous is as follows

• ● Low output fistula - <200 mL/day
• ● Moderate output fistula  - 200- 500 mL/day
• ● High output fistula - >500 mL/day

• Factor // Likely to close // Unlikely to close
• Anatomical location // Oropharyngeal, Esophageal, Duodenal stump, Lateral duodenal, Pancreaticobiliary,
• Jejunal // Gastric, Ligament of Treitz, Ileal
• Tract length // >2 cm // <2 cm
• Defect size // <1 cm2 // >1 cm2
• Fistula output // Decreasing // Stable or increasing
• Surrounding bowel // Healthy // Distal obstruction or stricture, Abscess, Active inflammation, Bowel discontinuity
• Etiology // Appendicitis, Diverticulitis, Postoperative //
• Crohn disease, Malignancy, Radiation, Foreign body (mesh)
• Nutritional status // Well-nourished // Malnourished
• Sepsis // Absent // Present

• RESUSCITATION
• RESTITUTION (SNAP)
• - Sepsis, skin care
• - Nutrition
• - Anatomy - define intestinal anatomy
• - Plan
• RECONSTRUCTION
• REHABILITATION

• a. Management of Sepsis –
• The usual manifestations of sepsis (pyrexia, leukocytosis, tachycardia, and tachypnea) are often only very subtly present or may even be completely absent.
• Present instead with cachexia, jaundice, hyponatremia, and hypoalbuminemia.
• Despite the lack of classical signs of active infection in these patients, surgical intervention is frequently associated with sudden and catastrophic deterioration, with rapid progression to septic shock and death from multiple organ failure.
• All patients with enterocutaneous fistulas should be assumed to have active sepsis, until proved otherwise.
• Use broad spectrum antibiotics followed by antibiotics according to sensitivity pattern.
• o Radiological drainage
• o Surgical drainage
• b. Skin care –
• Digestive juices may be alkaline or acidic, the corrosive enzymes ay rapidly digest the abdominal wall. may result in skin destruction and severe pain or in severe cases, rapidly progressive destruction of the abdominal wall, resulting in spreading secondary infection and death.
• Use of devices and techniques to facilitate fistula site drainage.

• b. Nutrition and Metabolic support –
• Administration of nutrients by whatever route, even in supraphysiological amounts, is unlikely to restore body composition or physiological function until sepsis is eradicated.
• Sepsis is associated with a significant increase in energy and nitrogen requirements, and it may not be possible to meet these except by parenteral nutrition
• Insulin resistance associated with sepsis may lead to hyperglycemia during glucose-based feeding, which in turn may be associated with increased infection rates and continued muscle wasting
• Enhanced nutrient-induced thermogenesis, associated with stimulation of the sympathetic nervous system – may lead to fever and respiratory failure.
• When spontaneous fistula closure is possible, parenteral nutrition allows oral fluids and diet to be withheld to ‘‘rest the gut’’ and promote fistula healing.
• Where there is obvious mucocutaneous continuity, o spontaneous fistula closure cannot occur and, provided skin care is not compromised, patients can be allowed to eat and drink.
• Daily TPN requirement – 30kcal/kg/day, for more septic patients, 40kcal/kg/day.
• Fistuloclysis – Infusion of feed directly through the fistula opening. If >75cm of distal bowel is present, then, patient can be safely fed. Advantages are – safer, less expensive, prevents distal small intestine atrophy.

d. Anatomy delination and Plan

Short bowel syndrome (SBS) is the result of surgical resection, congenital defect, or disease-associated loss of absorption.  It is characterized by an inability to maintain protein-energy, fluid, electrolyte, or micronutrient balances when on a normal diet.

• Infants
• - Necrotizing enterocolitis
• - Intestinal Atresia
• - Complicated gastroschisis
• - Long segment Hirshprung disease
• - Midgut volvulus

• Adults
• - Crohn’s disease
• - Traumatic injury
• - Mesenteric vascular diseases
• - Malignancy
• - Radiation

• Type 1
• small bowel resection with high-output jejunostomy (end jejunostomy)
• the most challenging to manage because of the high fluid replacement requirements. 

• Type 2
• small bowel resection with partial colon resection and resulting enterocolonic anastomosis (jejunocolic)
• most common subtype. 

• Type 3
• small intestine resection with small bowel anastomosis and intact colon (jejunoileal)
• best tolerated, the most adaptive potential

• 100cm in type 1
• 65 cm in type 2
• 30 cm in type 3

• Within 24-48 hours after resection, intestinal adaptation process begins.
• - Bowel dilates and thickens macroscopically and has increased villous height and surface area microscopically.
• - Intestinal transit time slows and enterocyte carrier capacity increases.
• - Long chain fatty acid enhance bowel adaptation
• - Strategies to increase bowel adaptation – administration of GLP-2 or glutamine.

• - Primary goal of medical therapy is to limit gastrointestinal loss of fluid, electrolytes and nutrients.
• - PPI to minimize hypersecretion.
• - Antimotility drugs to slow intestinal transit time
• - Bile acid binders to decrease steatorrhea and bile salt diarrhoea.
• - Elemental formula to minimize nutrition malabsorption.
• - Breast milk contains growth factors that potentially enhance bowel adaptation.

• - Profound dehydration
• - Malnutrition and weight loss 
• - Electrolyte disturbances
• - Vitamin and micronutrient deficiencies
• - With adaptation, small bowel progressively dilates, and have slow motility – gaseous distension – watery diarrhoea and crampy due to bacterial overgrowth.
• - Osteopenia due to vitamin D deficiency and calcium malabsorption.
• - Oxaluria – nephrolithiasis
• - Cholelithiasis, gastric hypersecretion and nephrolithiasis

• - Parenteral nutrition associated liver disease (PNALD) – contributing factors include
• o Liver immaturity in children
• o Disruption of enterohepatic circulation of bile acids
• o Recurrent sepsis

- Central venous catheter associated complications – sepsis, venous thrombosis

• When the terminal ileum is removed, bile salts cannot be reabsorbed. They are then excreted in the stool, thereby causing the unabsorbed fat to also be excreted (steatorrhea).    
• The fat in colon  binds with calcium in the stool, preventing the normal combining of calcium and oxalate. Oxalate, which would normally be excreted in stool, instead is absorbed through the colon and excreted in higher than normal amounts in urine. This can lead to oxalate kidney stones.

• - Longitudinal intestinal lengethening and tailoring (LILT) also called as Bianchi procedure.
• - Serial transverse enteroplasty (STEP)

• Lembert - Seromuscular 
• Albert - Full thickness [@ ALbert - ALl layers] 
• Connel - first stitch in angle

• A. Intestinal
• Ileocaecal region - Ulcerative (60%), Hyperplastic, Ulcero-hyperplastic.
• Ileal region, commonly - Stricture type.

• B. Peritoneal tuberculosis
• Acute.
• Chronic – Ascitic, Encysted (loculated), Plastic (Fibrous/adhesive), Purulent type.

C.Tuberculosis of mesentery and its lymph nodes.

D. Ano-recto-sigmoidal —Present as fistula, fissure, abscess, mass.

• Ulcerative type (60%) // Hyperplastic type (10%)
• 1. Secondary to pulmonary tuberculosis // 1. Primary GIT tuberculosis, could be due to bovine bacilli
• 2. Virulent organism // 2. Less virulent organism
• 3. Poor body resistance, old people // 3. Good body resistance, young individual
• 4. Multiple transverse ulcers commonly in the ileum, // 4. Chronic granulomatous lesion in the ileocaecal often in the caecum region
• 5. Clinically presents with diarrhoea, bleeding P/R, // 5. Presents as a mass in right iliac fossa loss of appetite and reduced weight
• 6. Complications: Stricture, intestinal obstruction // 6. Complication: Subacute intestinal obstruction
• 7. Chest X-ray shows primary lesion // 7. No primary lesion in chest X-ray
• 8. Barium study shows ileal strictures with hyper- // 8. Barium study—Pulled up caecum, obtuse ileomotility caecal angle

• • Stasis
• • Abundant Peyer’s patches - organisms get trapped in Peyer’s patches
• • Bacteria contact time with mucosa is more
• • M cells in Peyer’s patches phagocytose bacilli and transfer to host cells
• • Liquid content in the region
• • Increased rate of fluid and electrolyte absorption
• • Minimal digestive activity

• • Pulled up caecum
• • Obtuse ileocaecal angle
• • Hurrying of barium due to rapid flow and lack of barium in inflamed segment 
• • Narrow ileum with thickened ileocaecal valve

1. ATT

2. Supportive nutritional therapy. 

3. Surgery - 

• Indications for surgery
• • Intestinal obstruction.
• • Severe haemorrhage.
• • Acute abdominal presentation like perforation.
• • Intraabdominal abscess formation or fistula formation.
• • Uncertain diagnosis.

• Types of surgeries - 
• Limited ileocaecal resection (with 5 cm margin) is the surgical therapy of choice for ileocaecal tuberculosis.
• In single ileal stricture – stricturoplasty may be done.
• In multiple strictures resection of ileum and anastomosis  (ideal).
• In perforation of ileal bowel, resection and anastomosis

Superior mesenteric artery is commonly involved than inferior mesenteric artery. Often superior mesenteric vein can also get involved.

• • Embolism (50%)—Sources are from left auricle, as seen in atrial fibrillation, mural infarct, Atheroma from aorta or aneurysm, Endocarditis vegetations, Left atrial myxoma.
• • Thrombosis— may block the origin of the superior mesenteric artery and can cause ischaemia of full length of small bowel. It is life threatening.
• • Non-occlusive—due to hypotension/hypoperfusion

• • Pain initially around the umbilicus and later diffuse.
• • Persistent vomiting
• • Bloody diarrhoea, dehydration, shock and toxicity
• • Guarding and rigidity, rebound tenderness
• • On laparotomy – musty smell and dusky look of extensive gangrenous bowel is typical. When in doubt, ischaemia should be confirmed by oxygen support; warming; on table Doppler.

Abdominal pain after eating that occurs in individuals with ongoing poor blood supply to their small intestines known as chronic mesenteric ischemia

• • Gas bubble in the mesenteric vein is pathognomonic sign of irreversible mesenteric ischaemia.
• • CT / CT angiogram - occlusion at the ostium of SMA signifies thrombosis, Embolic occlusion is smooth filling defect, usually distal to origin of middle colic artery sparing proximal small bowel, right side colon and transverse colon. Emboli can be fragments causing multiple patchy necrosis of bowel at different sites.

• • Emergency laparotomy is done. With the help of Doppler the block is identified and the vessel is
• opened. The block is removed and the bowel is reperfused.
• • If patient has presented after 24-48 hours, gangrene might have already occurred, then resection and
• anastomosis is done.
• • If patient presents within 6 hours, it is possible to prevent gangrene and to salvage the bowel. Emergency SMA angiography is done. Heparin or thrombolytics are injected. Immediate laparotomy is done. SMA is opened (arteriotomy) over the obstruction and thrombus/embolus is removed using Fogarty catheter. Perfusion is maintained. Close monitoring is essential for possibility of formation of bowel gangrene and if it is so relaparotomy should be done for bowel resection.
• • Steroids are given to reduce lysosomal membrane destruction and effects of endotoxins; to maintain
• arterial resistance and complement activity. High dose hydrocortisone is used.
• • Higher generation antibiotics; critical care; ventilator, fluid, electrolytes and nutritional support (TPN) are essential

Intra-abdominal Pressure (IAP): Intrinsic pressure within the abdominal cavity. Normal IAP - 5-7 mmHg. 

• Intra-abdominal Hypertension (IAH): An IAP > 12 mm Hg (often causing occult ischemia) without obvious organ failure. 
• Grade I - 12-15 
• Grade II - 16-20 
• Grade III - 21-25
• Grade IV - >25

Abdominal Compartment Syndrome (ACS): IAH with at least one overt organ failing

Abdominal perfusion pressure - MAP - IAP

• Primary – Injury/disease of abdomino-pelvic region, “surgical”

• Secondary – Sepsis, capillary leak, burns, “medical”

• Recurrent – ACS develops despite surgical intervention

• Diminished abdominal wall compliance
• • Abdominal surgery
• • Major trauma
• • Major burns
• • Prone positioning

• Increased intra-luminal contents
• • Gastroparesis/gastric distention/ileus
• • Ileus
• • Colonic pseudo-obstruction
• • Volvulus

• Increased intra-abdominal contents
• • Acute pancreatitis
• • Distended abdomen
• • Hemoperitoneum/pneumoperitoneum or intra-peritoneal fluid collections
• • Intra-abdominal infection/abscess
• • Intra-abdominal or retroperitoneal tumors 
• • Liver dysfunction/cirrhosis with ascites 

• Capillary leak/fluid resuscitation
• • Acidosis
• • Damage control laparotomy
• • Hypothermia
• • Massive fluid resuscitation or positive fluid balance

• Others/miscellaneous
• • Increased head of bed angle
• • Massive incisional hernia repair
• • Mechanical ventilation
• • Obesity or increased body mass index
• • PEEP > 10
• • Peritonitis
• • Pneumonia
• • Sepsis
• • Shock or hypotension

1. Cardiac - compress IVC, decrease venous return, decrease CO, decrease tissue perfusion. 

2. Pulmonary - elevation of diaphragm, increased intrathoracic pressure, decreased tidal volume/ARDS 

3. GI - Gut perfusion decreased, gut edema increases. 

4. Renal - Decreased GFR, Oliguria, ATN

5. Neurological - increased ICP, decreased cerebral perfusion, brain anoxia

• Treatment of cause. 
• Fluid - double edge sword, no over resuscitation, benefit if the patient has inadequate right ventricle filling. 
• Abdominal perfusion pressure - >60mmHg, Optimize fluid first and add vasopressors. 
• Catheter, Enema, NG 
• Hemodyalysis, hemofiltration, Paracentesis 
• Decompressive laparotomy, followed by temporary closure techniques (Bogata bag closure, towel clip closure, mesh closure)