Gastric Adenocarcinoma

Gastric adenocarcinoma is the dominant gastric malignancy and arises from the glandular mucosa.

Lauren histology broadly separates intestinal and diffuse patterns. Diffuse cancers, including poorly cohesive and signet ring phenotypes, infiltrate the gastric wall and have a greater tendency toward peritoneal dissemination.

Linitis plastica represents diffuse infiltrative involvement producing a rigid poorly distensible stomach.

Curative management requires adequate local resection and treatment of micrometastatic disease.

Upper gastrointestinal endoscopy with multiple biopsies: establish histology and tumour location.

CT chest, abdomen and pelvis: determine regional and distant disease.

Staging laparoscopy with peritoneal cytology: important before perioperative treatment in resectable locally advanced disease and particularly with cT3 or cT4, node positive or poorly cohesive cancers.

Endoscopic ultrasound is most useful for early lesions when deciding between endoscopic resection and surgery.

Early gastric cancer

Selected superficial mucosal cancers with a very low risk of lymph node metastasis can undergo endoscopic submucosal dissection.

The resected specimen must be assessed for:

Depth of invasion
Differentiation
Ulceration
Lymphovascular invasion
Horizontal and vertical margins

Noncurative endoscopic pathology requires surgical gastrectomy with lymphadenectomy in a fit patient.

Resectable locally advanced disease

For most fit patients with T2 or greater or node positive resectable adenocarcinoma, perioperative systemic therapy is appropriate.

A standard FLOT regimen every 14 days is:

Docetaxel 50 mg/m² IV
Oxaliplatin 85 mg/m² IV
Leucovorin 200 mg/m² IV
Fluorouracil 2600 mg/m² continuous IV infusion over 24 hours

Four cycles are given before surgery and four after surgery when tolerated. Perioperative FLOT improved median overall survival compared with older epirubicin based regimens.

A current option for resectable gastric adenocarcinoma is the addition of:

Durvalumab 1500 mg IV every 4 weeks during perioperative FLOT, followed after surgery by 1500 mg IV every 4 weeks for up to ten additional cycles. This reduced recurrence and improved event free survival compared with FLOT alone.

Surgery

The operation is determined by tumour position.

Distal cancer: distal subtotal gastrectomy is preferred when an adequate oncological proximal margin can be achieved. It provides equivalent oncological control with less morbidity than total gastrectomy in appropriately selected distal disease.

Diffuse, proximal or extensive disease: total gastrectomy is usually required.

Perform appropriate regional lymphadenectomy. D2 lymphadenectomy is the standard oncological dissection in experienced centres.

Routine splenectomy is not required unless the tumour directly involves the spleen or splenic hilar clearance is specifically necessary.

After total gastrectomy, reconstruct with Roux en Y oesophagojejunostomy.

Postoperative nutritional consequences include weight loss, iron deficiency, vitamin B12 deficiency, calcium and vitamin D deficiency and dumping symptoms. Lifelong vitamin B12 replacement is required after total gastrectomy.

Metastatic disease

Test advanced adenocarcinoma for:

HER2
PD L1 combined positive score
MSI or mismatch repair deficiency
CLDN18.2 where available

These biomarkers determine whether treatment includes HER2 targeted therapy, immune checkpoint therapy or CLDN18.2 directed therapy.

A malignant outlet obstruction can be treated with endoscopic stenting, endoscopic gastroenterostomy or surgical gastrojejunostomy depending on performance status and expected survival.

Operate in metastatic disease only for a defined indication such as perforation, uncontrolled bleeding or obstruction not adequately controlled by less invasive measures.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Bowel Perforation

Bowel perforation is full thickness disruption of the gastrointestinal wall allowing enteric contents, bacteria and gas to escape into the peritoneal cavity or adjacent tissues.

It may result from peptic ulcer disease, appendicitis, diverticulitis, colorectal malignancy, bowel ischaemia, obstruction, inflammatory bowel disease, trauma, foreign body, iatrogenic injury or anastomotic failure.

Perforation may be free, producing diffuse contamination and peritonitis, or contained by adjacent bowel, mesentery or omentum, producing local inflammation or abscess.

The management question is not simply whether a perforation exists. It is whether contamination is controlled and whether the underlying defect requires immediate source control.

Free perforation commonly produces sudden severe pain followed by rapidly progressive peritonism. Tachycardia, fever, ileus and abdominal distension follow.

With severe contamination, patients develop hypotension, oliguria, altered mentation, metabolic acidosis and septic shock.

Contained perforation may produce localised pain, fever and tenderness without diffuse rigidity.

Steroids, immunosuppression and advanced age can blunt peritoneal findings despite major contamination.

Keep fasting, establish large bore IV access and resuscitate with balanced crystalloid according to perfusion response. Insert a urinary catheter in significant sepsis or shock and a nasogastric tube when vomiting, ileus or major distension is present.

Start antibiotics promptly.

For a stable community acquired perforation:

Ceftriaxone 2 g IV every 24 hours plus metronidazole 500 mg IV every 12 hours.

For severe sepsis, extensive contamination, healthcare associated infection or substantial resistant organism risk:

Piperacillin tazobactam 4.5 g IV every 8 hours by extended infusion, with renal adjustment.

Source control depends on location and pathology and may consist of primary repair, resection with primary anastomosis, resection with diversion, exteriorisation, drainage or definitive treatment of the diseased organ.

Free perforation with generalised peritonitis, uncontrolled sepsis, bowel ischaemia or haemodynamic deterioration requires urgent surgery.

A small contained perforation may occasionally be managed with antibiotics, bowel rest and selective percutaneous drainage when the patient is stable and there is no diffuse contamination. This strategy requires reliable serial assessment.

The choice between anastomosis and stoma is physiological, not ideological. Shock, vasopressor dependence, gross faecal contamination, severe bowel oedema, poor perfusion and major comorbidity increase anastomotic risk and may favour diversion or damage control surgery.

During source control, obtain intra abdominal cultures in complicated infection where results may change antimicrobial therapy.

After adequate source control, limit antibiotic treatment to approximately 4 days. Persistent fever, ileus, pain or organ dysfunction should trigger investigation for ongoing leakage, abscess or failed source control rather than automatic extension of therapy.

Gastric Adenocarcinoma

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management