7.4 Upper & Lower GI Surgical Pathology & Postoperative Complications

Gastric Adenocarcinoma: Pathology, Staging & D2 Resection

Gastric cancer is a major cause of cancer-related mortality globally. Over 90% of malignant gastric neoplasms are adenocarcinomas arising from the gastric glandular epithelium.

The Lauren Histological Classification

• Intestinal Type (50% to 60%): Characterized by cohesive malignant cells forming distinct, recognizable glandular structures. Driven by environmental factors: chronic Helicobacter pylori gastritis progressing through the Correa cascade (superficial gastritis -> atrophic gastritis -> intestinal metaplasia -> dysplasia -> adenocarcinoma), high dietary salt and nitrates, and cigarette smoking. Predominantly affects older males and presents as an exophytic, polypoid, or ulcerated mass, most frequently in the distal stomach (antrum and incisura).
• Diffuse Type (30% to 40%): Characterized by poorly cohesive, discohesive sheets of infiltrative malignant cells containing intracellular mucin that displaces the nucleus to the periphery (signet-ring cells). Driven by genetic mutations, principally somatic or germline mutations in CDH1 (loss of the cell adhesion protein E-cadherin). Occurs equally in younger females and males, exhibits no geographic predilection, and carries a dismal prognosis. It infiltrates diffusely throughout the submucosa and muscularis propria without forming an intraluminal mass, producing rigid, leather-bottle thickening of the entire gastric wall (linitis plastica).

Clinical Presentation & Stigmata of Incurable Disease

• Early Symptoms: Insidious and non-specific: epigastric dyspepsia, early satiety, anorexia, unprovoked weight loss, and microcytic iron-deficiency anemia from chronic occult bleeding.
• Anatomical Site Manifestations: Distal/antral tumors cause gastric outlet obstruction (projectile vomiting of undigested food, epigastric distension, and a succussion splash); proximal/cardia tumors cause progressive dysphagia.
• Physical Stigmata of Advanced / Metastatic Spread:
  • Virchow's Node (Troisier's Sign): Metastatic enlargement of the left supraclavicular lymph node, seeded via retrograde flow from the thoracic duct.
  • Sister Mary Joseph Nodule: Palpable, firm subcutaneous nodule at the umbilicus, seeded via lymphatic remnants of the falciform ligament.
  • Krukenberg Tumor: Metastatic mucinous signet-ring adenocarcinoma to the ovaries, typically bilateral.
  • Blumer's Shelf: Hard, rigid peritoneal tumor shelf palpable in the rectovesical or rectouterine (Douglas) pouch on digital rectal examination.
  • Irish Node: Metastatic enlargement of the left anterior axillary lymph node.

Preoperative Staging & Principles of Resection

• Staging: High-resolution contrast CT of the chest, abdomen, and pelvis to detect visceral metastases and ascites. Endoscopic Ultrasound (EUS) provides accurate locoregional T (depth of invasion) and N (nodal) staging. Diagnostic Staging Laparoscopy with peritoneal washings is mandatory for locally advanced tumors (>= cT2) to detect subtle, radiologically occult peritoneal micrometastases (< 5 mm), which are present in 20% to 30% of patients and preclude futile open laparotomy.
• Oncological Resection:
  • Distal Tumors (Antrum / Lower Body): Subtotal Gastrectomy if an R0 resection is achievable. JGCA recommends gross proximal margins of 2 cm for T1, 3 cm for expansive T2+, and 5 cm for infiltrative T2+ tumors; use frozen-section assessment when adequate clearance is uncertain.
  • Proximal Tumors / Linitis Plastica: Total Gastrectomy with Roux-en-Y esophagojejunostomy.
  • D2 Lymphadenectomy: Standard for potentially curable cT2+ or cN+ disease; selected cT1N0 tumors need D1 or D1+. Stations depend on the gastrectomy: for total gastrectomy, D1 comprises stations 1–7, and D2 adds 8a, 9, 11p, 11d and 12a. For distal gastrectomy, D1 comprises 1, 3, 4sb, 4d, 5, 6 and 7, and D2 adds 8a, 9, 11p and 12a. These clear perigastric and specified arterial nodal basins. D2 reduces locoregional recurrence when performed in experienced centers. Retrieve at least 16 lymph nodes for accurate pathological staging; higher yields improve staging confidence.

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Colorectal Carcinoma: Molecular Pathways & Surgical Principles

Colorectal cancer (CRC) is the third most common cancer worldwide. Most tumors originate within pre-existing benign adenomatous polyps.

Molecular Carcinogenesis

1. Chromosomal Instability (CIN) Pathway (Adenoma-Carcinoma Sequence, 85%): Described by Fearon and Vogelstein. Involves the sequential accumulation of genetic mutations:
   • Initiation: Loss or mutation of the APC tumor suppressor gene on chromosome 5q (seen in Familial Adenomatous Polyposis [FAP] and sporadic CRC), leading to intracellular beta-catenin accumulation and unregulated epithelial proliferation.
   • Progression: Activating proto-oncogene mutation in KRAS (chromosome 12p), promoting adenomatous polyp growth.
   • Malignant Transformation: Inactivation of tumor suppressor genes DCC / SMAD4 (chromosome 18q) and TP53 (chromosome 17p), culminating in invasive carcinoma.
2. Microsatellite Instability (MSI) Pathway (15%): Arises from defective DNA mismatch repair (dMMR) genes (MLH1, MSH2, MSH6, PMS2). Inherited in Lynch syndrome (HNPCC) via germline mutations, or acquired sporadically via epigenetic hypermethylation of the MLH1 promoter. Tumors are characteristically right-sided, mucinous, hypermutated, and carry a favorable prognosis with heightened responsiveness to immune checkpoint inhibitors (anti-PD-1 therapy).

Clinical Presentation: Right-Sided vs. Left-Sided CRC

Principles of Oncological Resection

• Vascular Ligation & Lymphadenectomy: Resect the affected bowel with its draining vascular pedicle and mesenteric lymphatic basin. For rectal cancer, low tie at the superior rectal artery origin with lymphatic clearance is usually appropriate; IMA high tie is selected for suspicious apical nodes or additional length. In colon resections, divide the appropriate feeding branches with their nodal drainage; a minimum of >= 12 regional lymph nodes must be pathologically examined to ensure accurate TNM staging.
• Standard Segmental Resections:
  • Cecum / Ascending Colon: Right hemicolectomy (ligating ileocolic and right colic arteries).
  • Hepatic Flexure / Proximal Transverse: Extended right hemicolectomy (ligating middle colic artery).
  • Splenic Flexure / Descending Colon: Left hemicolectomy (ligating left colic artery and inferior mesenteric vein).
  • Sigmoid Colon: Sigmoid colectomy (ligating sigmoid branches of inferior mesenteric artery).

Rectal Cancer & Total Mesorectal Excision (TME)

• The upper rectum has anterior and lateral peritoneal covering, the middle third has anterior covering only, and the lower third has none. Tumors can extend radially through non-peritonealized surfaces into the mesorectum.
• Total Mesorectal Excision (TME): Pioneered by Professor Bill Heald, TME is the international standard of care for middle and lower rectal carcinomas. The surgeon performs precise, sharp dissection under direct vision within the embryological avascular plane (the 'holy plane') between the visceral fascia of the mesorectum and the parietal endopelvic fascia. This excises the rectum and its surrounding fat, lymphatic vessels, and lymph nodes as an intact, unbroken package covered by a smooth mesorectal fascia.
• Circumferential Resection Margin (CRM): A clear CRM (> 1 mm) is the most powerful predictor of preventing local pelvic recurrence. TME reduces local recurrence rates from > 30% down to < 5% to 8% while preserving autonomic pelvic nerves (preventing erectile dysfunction and neurogenic bladder).
• Surgical Procedures:
  • Sphincter-Preserving Resection: Low Anterior Resection (LAR) with colorectal or coloanal anastomosis when negative margins and acceptable sphincter function are achievable, including selected low tumors. A protective loop ileostomy is considered for a low, high-risk anastomosis.
  • Sphincter/Levator Involvement or Inadequate Functional Clearance: Abdominoperineal Resection (APR / Miles Procedure) removes the rectum, anal canal and sphincter complex with a permanent end colostomy. Tumor distance below 5 cm alone does not require APR.

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Acute Diverticulitis: Hinchey Classification & Management

Colonic diverticula are acquired pseudodiverticula (mucosa and submucosa herniating through weak points in the circular muscularis propria where nutrient vessels, the vasa recta, penetrate). Over 90% occur in the sigmoid and descending colon. Acute diverticulitis is initiated by inspissated fecaliths obstructing the neck of a diverticulum, causing mucosal abrasion, bacterial proliferation, ischemia, and micro- or macro-perforation.

Clinical Presentation

• Characterized as 'left-sided appendicitis': constant, severe, aching pain in the left lower quadrant (LLQ), low-grade fever, leukocytosis, anorexia, nausea, and altered bowel habits (constipation or diarrhea). In patients of Asian or African descent, right colonic diverticulitis is more prevalent, mimicking acute appendicitis.

Diagnostic Imaging Modality

• Contrast-Enhanced CT of the Abdomen and Pelvis: The investigation of choice (sensitivity and specificity > 95%). CT stigmata include sigmoid wall thickening (> 4 mm), pericolic mesenteric fat stranding, visualization of diverticula, extraluminal gas, and loculated pericolic or pelvic abscesses.
• Contraindications: Colonoscopy, flexible sigmoidoscopy, and barium enemas are strictly contraindicated during the acute episode due to high risks of converting a contained microperforation into a free, catastrophic fecal peritonitis. Diagnostic colonoscopy is routinely deferred for 6 to 8 weeks following complete clinical resolution to evaluate the colonic mucosa and rule out an underlying stenosing colorectal carcinoma.

The Modified Hinchey Classification & Management Algorithms

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Postoperative Complications: Chronological Evaluation of Postoperative Fever

Fever is among the most frequent postoperative clinical challenges. Evaluating postoperative fever requires a rigorous chronological approach and an evidence-based understanding of the distinction between benign physiological pyrexia and surgical site sepsis, traditionally organized around the mnemonic of the '5 Ws':

1. Wind (Postoperative Days 1 to 2): Early Postoperative Fever vs. Atelectasis

• Debunking the Atelectasis Myth: For decades, surgical dogma taught that pulmonary atelectasis is the primary cause of early postoperative fever (frequently claimed to account for > 90% of fevers within the first 48 hours). Primary clinical evidence has thoroughly disproved this causal link. Seminal prospective clinical studies (notably Engoren M. Lack of association between atelectasis and fever. Chest 1995;107:81-84, PubMed 7813318, and subsequent prospective surgical studies) demonstrated no statistically significant association between the presence or radiographic severity of atelectasis and the presence of postoperative fever. Alveolar collapse per se is mechanical and non-pyrogenic; it does not produce endopyrogens or trigger the hypothalamic thermal set point.
• Pathophysiology of Early Postoperative Fever (< 48 Hours): Early postoperative fever is predominantly a benign, sterile physiological neuroendocrine and inflammatory response to surgical tissue injury. Mechanical tissue trauma, operative dissection, and cell disruption activate local tissue macrophages, monocytes, and endothelial cells to release pyrogenic cytokines:
  • Interleukin-6 (IL-6): The principal systemic cytokine reflecting the magnitude of tissue trauma and driving hepatic acute-phase reactant synthesis.
  • Interleukin-1 (IL-1 [alpha and beta]): Primary endogenous pyrogens that stimulate the preoptic area of the anterior hypothalamus.
  • Tumor Necrosis Factor-alpha (TNF-alpha): Incites systemic inflammatory cascades and endothelial activation.
  • Interferon-gamma (IFN-gamma): Synergistically amplifies macrophage activation and pyrogen release.
  • These cytokines act upon the hypothalamic vascular endothelium at the organum vasculosum laminae terminalis (OVLT), inducing local cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) synthesis, which elevates the central hypothalamic thermoregulatory set point.
• Clinical Role & Management of Atelectasis: While atelectasis does NOT cause postoperative fever, it remains a frequent and clinically significant early pulmonary complication. General anesthesia, neuromuscular blockade, opioid-induced respiratory depression, and diaphragmatic splinting secondary to upper abdominal or thoracic incisions reduce functional residual capacity (FRC), leading to alveolar collapse in dependent lung bases.
  • Clinical Features of Atelectasis: Mild tachypnea, mild tachycardia, hypoxemia (decreased SpO2), diminished breath sounds, and fine end-expiratory bibasilar crackles.
  • Management Protocol: Therapy is directed strictly toward pulmonary re-expansion and oxygenation, NOT antipyresis. Interventions include vigorous chest physiotherapy, incentive spirometry, optimal multimodal patient-controlled analgesia (enabling deep inspiration and coughing), and early out-of-bed mobilization. Antibiotics are strictly contraindicated for simple atelectasis because it is an uninfected mechanical collapse. However, persistent atelectasis with retained secretions can progress over 72 to 96 hours to true hospital-acquired bacterial pneumonia.
• Dangerous Causes of Early Fever: Assess urgently for necrotizing soft-tissue infection (e.g. Clostridium perfringens or Group A streptococci), aspiration pneumonia and pre-existing peritonitis. Malignant hyperthermia is a separate, noninfectious anaesthetic emergency: rising end-tidal CO2, rigidity and acidosis after a trigger require immediate trigger cessation, oxygenation and dantrolene.

2. Water (Postoperative Days 3 to 5): Urinary Tract Infection (UTI)

• Etiology: Strongly associated with indwelling urinary (Foley) catheters. Ascending infection by enteric pathogens (Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Enterococcus faecalis).
• Clinical Features: Dysuria, suprapubic tenderness, cloudy or foul-smelling urine, and spiking fever.
• Management: Prompt removal of the urinary catheter, urine microscopy and culture, and targeted oral or IV antibiotics.

3. Wound (Postoperative Days 5 to 7): Surgical Site Infection (SSI)

• CDC Classification:
  • Superficial Incisional SSI: Involves only skin and subcutaneous tissue.
  • Deep Incisional SSI: Involves deep soft tissues (fascia and muscle layers).
  • Organ / Space SSI: Involves any anatomical space opened or manipulated during surgery (subphrenic abscess, pelvic collection, anastomotic leak).
• Clinical Signs: Spreading wound erythema, local warmth, edema, increasing unprovoked pain, and purulent drainage. Fever typically spikes around postoperative day 5.
• Management: Removal of skin sutures or surgical staples, gentle opening of the wound to evacuate purulent fluid, thorough saline washout, and loose packing with saline-soaked gauze. Systemic antibiotics are reserved for patients with spreading cellulitis (> 2 cm margin), systemic sepsis, or organ/space collections.

4. Walking (Postoperative Days 7 to 10+): Venous Thromboembolism (DVT / PE)

• Etiology: Virchow's triad (venous stasis from immobility, endothelial injury during pelvic/abdominal dissection, and surgical hypercoagulability).
• Clinical Features: Unilateral calf swelling, pain, warmth (Deep Vein Thrombosis); sudden-onset pleuritic chest pain, dyspnea, tachypnea, tachycardia, hypoxia, and hemoptysis (Pulmonary Embolism).
• Diagnosis & Management: Compression venous duplex ultrasonography for DVT; CT Pulmonary Angiography (CTPA) for PE. Immediate therapeutic anticoagulation (low-molecular-weight heparin or direct oral anticoagulants).

5. Wonder Drugs (Anytime): Adverse Drug Reactions

• Drug-induced fevers provoked by broad-spectrum antibiotics (beta-lactams, cephalosporins, vancomycin), heparin (including Heparin-Induced Thrombocytopenia [HIT]), anticonvulsants, or allopurinol. Characterized by fever with relative bradycardia and eosinophilia; resolves promptly upon drug discontinuation.

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Surgical Suture Classification & Abdominal Wall Closure Principles

Understanding suture material science and biomechanics is critical for secure wound reconstruction and preventing catastrophic incisional failure. Suture materials are classified by origin (natural vs. synthetic), filament structure (monofilament vs. braided/multifilament), and absorption kinetics (absorbable vs. non-absorbable).

Suture Taxonomy & Biological Properties

1. Slowly Absorbable Synthetic Monofilament Sutures:

   • Polydioxanone (PDS / PDS II):
     • Composition: A synthetic monofilament polyester prepared from the polymer poly-p-dioxanone.
     • Absorption Timeline & Kinetics: Undergoes gradual non-enzymatic hydrolysis; completely absorbed by 182 to 238 days (roughly 6 to 8 months).
     • Tensile Strength Retention: Retains approximately 50% to 70% of initial tensile strength at 4 weeks, and 25% to 40% at 6 weeks.
     • Essential Classification Correction: Polydioxanone is a SLOWLY ABSORBABLE suture; it is NOT a non-absorbable suture. Describing PDS as non-absorbable is an obsolete factual error.
     • Clinical Advantages: Its monofilament profile eliminates bacterial capillary wicking and tissue drag. Its prolonged tensile strength retention perfectly matches the slow, 6- to 12-month collagen maturation trajectory of the linea alba and abdominal wall aponeurosis, making it the preferred standard for routine laparotomy closure and acute fascial repair.
   • Polyglecaprone 25 (Monocryl): Rapidly absorbable monofilament suture (hydrolyzed completely by 91-119 days; loses all tensile strength by 3 weeks); ideal for subcuticular skin closure, but strictly contraindicated for fascial load-bearing closures.

2. Truly Non-Absorbable Monofilament Sutures:

   • Polypropylene (Prolene / Surgipro):
     • Composition: Extruded monofilament strand of an isotactic stereoisomer of polypropylene.
     • Degradation Profile: Truly non-absorbable; unaffected by tissue enzymes, macrophage activity, or hydrolysis. Tensile strength is retained permanently (indefinite).
     • Clinical Properties: Exceptional biological inertness, minimal foreign body tissue reaction, extremely low bacterial adherence, and smooth tissue transit. Highly resistant to infection.
     • Indications: Vascular anastomoses (gold standard), permanent retention sutures, mesh fixation, and continuous abdominal wall mass closure where permanent non-absorbable tensile support is indicated.
   • Polyamide / Nylon (Ethilon / Dermalon): Monofilament synthetic polyamide. Hydrolyzes at an extremely slow rate (~15% to 20% loss per year) and functions clinically as a non-absorbable suture. High tensile strength, smooth passage, and low tissue reactivity; exhibits substantial knot memory requiring at least 4 to 5 secure throws. Ideal for percutaneous skin closure and microvascular surgery.

3. Rapidly Absorbable Braided Sutures:

   • Polyglactin 910 (Vicryl):
     • Composition: Braided synthetic copolymer composed of 90% glycolide and 10% L-lactide coated with polyglactin 370 and calcium stearate.
     • Absorption Kinetics: Rapid non-enzymatic hydrolysis, completely absorbed by 56 to 70 days (~8 to 10 weeks).
     • Tensile Strength Decline: Rapid degradation: retains ~75% at 2 weeks, ~50% at 3 weeks, ~25% at 4 weeks, and 0% tensile strength by 5 weeks.
     • Clinical Contraindication for Fascia: Braided multifilaments harbor bacteria within their interstitial spaces (capillary wicking) and generate tissue drag. Vicryl is strictly contraindicated for abdominal fascial closure or burst abdomen repair, because fascial aponeurosis requires months to heal; premature tensile failure leads to catastrophic incisional herniation and dehiscence. Indicated for intestinal anastomoses, peritoneal closure, and subcutaneous tissue approximation.
   • Polyglycolic Acid (Dexon): Braided synthetic absorbable suture with rapid hydrolytic absorption (60 to 90 days).

4. Natural Sutures (Historical & Specialized):

   • Surgical Catgut (Plain & Chromic): Collagen harvested from bovine intestinal serosa or ovine submucosa. Degraded by rapid enzymatic digestion (foreign-body phagocytosis); provokes intense tissue reaction and loses tensile strength unpredictably within 7 to 21 days. Obsolete for abdominal wall closure.
   • Surgical Silk: Braided natural protein filament spun by silkworm larvae (Bombyx mori). Degraded slowly over years, but exhibits high capillarity and tissue inflammation; prone to forming chronic suture sinuses.
   • Stainless Steel Wire: Permanent metallic monofilament; highest tensile strength, completely non-antigenic. Standard for median sternotomy closure, but difficult to handle with sharp ends that can lacerate surgical gloves.

Suture Comparison Matrix

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Acute Wound Dehiscence & Burst Abdomen

Acute abdominal wound dehiscence refers to separation of the closed fascial layers of an abdominal laparotomy incision. If full-thickness disruption permits intra-abdominal viscera (greater omentum and small bowel) to protrude through the skin, it is termed wound evisceration (burst abdomen). It occurs in 1% to 3% of midline laparotomies, typically between postoperative days 5 and 8.

Pathognomonic Herald Sign

• The sudden, dramatic appearance of copious, profuse, 'salmon-pink' serosanguinous fluid soaking through the abdominal dressings. This serosanguinous fluid represents peritoneal exudate escaping through the disrupted fascial edges. Any sudden soakage of dressings with pink fluid must be treated as wound dehiscence until proven otherwise!

Major Risk Factors

• Patient Factors: Advanced age (> 65 years), severe malnutrition (serum albumin < 30 g/L), morbid obesity, chronic steroid use, uncontrolled diabetes, jaundice, malignant cachexia, and heavy tobacco use.
• Operative & Technical Factors: Poor tissue purchase, insufficient suture length and excessive tension can cause fascial failure. For primary elective midline closure, EHS/AHS suggests small aponeurotic bites (5–9 mm), slowly absorbable suture, low tension and a suture:wound ratio >=4:1. Repair of damaged burst-abdomen edges requires a separate operative assessment. Postoperative surgical site infection (SSI) is present in over 50% of dehiscence cases. Elevated intra-abdominal pressure from violent coughing, retching, severe paralytic ileus, or acute urinary retention precipitates fascial tearing.

Emergency Management Protocol

1. Immediate Bedside Stabilization:
   • Calm and reassure the patient.
   • Position the patient immediately in low Fowler's position (head elevated 15-30 degrees) with hips and knees flexed to relax the abdominal wall musculature and reduce tension on the wound.
   • Cover the exposed eviscerated viscera immediately with sterile towels or gauze soaked in warm normal saline. This prevents desiccation of the bowel serosa, hypothermia, and atmospheric bacterial contamination.
   • DO NOT ATTEMPT TO FORCEFULLY PUSH THE BOWEL BACK INTO THE ABDOMEN AT THE BEDSIDE. Manual reduction can tear the edematous bowel wall or cause mesenteric avulsion.
2. Resuscitation: Keep strictly NPO, insert a nasogastric tube to decompress the stomach, establish large-bore IV access, administer balanced IV crystalloids, provide adequate intravenous analgesia, and administer broad-spectrum IV antibiotics.
3. Definitive Operative Intervention (Abdominal Wall Mass Closure): Transfer immediately to the operating theater for emergency re-exploration under general anesthesia:
   • Inspect the eviscerated bowel and omentum for ischemia, gangrene, or perforations.
   • Debride necrotic, devitalized fascial edges.
   • Continuous Mass Closure Protocol: Perform definitive mass closure of the abdominal wall including all layers (peritoneum, transversalis fascia, and rectus sheaths) except skin:
     • Suture Selection: Continuous suture using heavy gauge monofilament: either slowly absorbable (No. 1 or 2 Polydioxanone [PDS]) OR non-absorbable (No. 1 or 2 Polypropylene [Prolene]). Rapidly absorbable braided sutures (such as polyglactin 910 [Vicryl]) or braided silk are strictly contraindicated for fascial mass closure.
     • Suture-to-Wound Length Ratio (Jenkins / Israelsson Rule): The ratio of the length of suture placed to the total length of the wound must be at least 4:1. A 4:1 ratio prevents excessive tension, distributes intra-abdominal bursting pressures evenly, and accommodates postoperative abdominal distension.
     • Tissue Bite Size & Travel Distance: Take generous fascial tissue bites of at least 1.0 to 1.5 cm from the cut fascial margin, with an advancing travel distance (stitch interval) of roughly 1.0 cm.
     • Tension Control: Approximate the edges gently without strangulation. Excessive tension produces localized microvascular ischemia, fascial necrosis, and suture cut-through.
   • In the presence of severe intra-abdominal hypertension or massive bowel edema where primary closure would provoke abdominal compartment syndrome, leave the abdomen open as a temporary laparostomy utilizing a Bogota bag or commercial negative-pressure wound therapy (NPWT) system.