Small Bowel Adenocarcinoma

Small bowel adenocarcinoma is a rare epithelial malignancy arising most commonly in the duodenum, followed by jejunum and ileum. Predisposing conditions include Crohn disease, coeliac disease, Lynch syndrome, familial adenomatous polyposis and Peutz Jeghers syndrome.

Curative treatment depends on complete surgical resection with adequate regional lymph node assessment. Node positive disease has a substantially worse prognosis and generally requires adjuvant chemotherapy.

Symptoms depend on site.

Jejunal and ileal disease commonly presents with intermittent obstruction, abdominal pain, anaemia, occult bleeding or weight loss.

Duodenal disease may produce vomiting, jaundice or gastric outlet symptoms depending on location.

An adult with unexplained recurrent small bowel obstruction without previous surgery should be investigated for a structural lesion, including malignancy.

CT enterography or contrast CT: define the primary lesion, regional lymphadenopathy and distant metastases.

Upper endoscopy or enteroscopy: obtain tissue when the lesion is endoscopically accessible.

Mismatch repair or microsatellite instability testing should be performed because it has prognostic and therapeutic implications.

Regional nodal staging is important. N1 disease means one or two positive regional nodes and N2 disease means three or more.

Surgery

Resectable jejunal or ileal adenocarcinoma requires segmental small bowel resection with en bloc regional mesenteric lymphadenectomy.

A tumour involving the terminal ileum or ileocaecal valve usually requires ileocaecal resection or right hemicolectomy with appropriate nodal clearance.

Duodenal cancers involving the second portion or ampullary region commonly require pancreaticoduodenectomy. Selected proximal first portion or distal third and fourth portion tumours may undergo segmental duodenal resection when an oncologically adequate margin and nodal dissection can be achieved.

Adjuvant treatment

Stage I disease is generally observed after complete resection.

Node positive stage III disease should receive approximately 6 months of adjuvant fluoropyrimidine based chemotherapy, preferably an oxaliplatin containing doublet in a fit patient. High risk stage II disease may also justify adjuvant treatment, particularly with T4 disease, perforation, inadequate nodal harvest, poor differentiation, lymphovascular invasion or positive or close margins.

A standard modified FOLFOX6 regimen every 14 days is:

Oxaliplatin 85 mg/m² IV day 1
Leucovorin 400 mg/m² IV day 1
Fluorouracil 400 mg/m² IV bolus day 1
Fluorouracil 2400 mg/m² continuous IV infusion over 46 hours

An alternative CAPOX regimen every 21 days is:

Oxaliplatin 130 mg/m² IV day 1
Capecitabine 1000 mg/m² orally twice daily on days 1 to 14

Dose reduction is required for clinically significant renal impairment with capecitabine and for relevant treatment toxicity.

Metastatic disease

FOLFOX or CAPOX is a common first line approach for fit patients.

Test metastatic disease for mismatch repair deficiency or microsatellite instability. For MSI high or mismatch repair deficient advanced disease, immune checkpoint therapy is an important option.

A commonly used pembrolizumab regimen is:

Pembrolizumab 200 mg IV every 3 weeks or 400 mg IV every 6 weeks.

Obstruction from unresectable disease may require bypass or palliative resection when systemic therapy cannot restore gastrointestinal continuity quickly enough.

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 Infarction

Bowel infarction is irreversible transmural intestinal necrosis caused by sustained ischaemia.

It represents the end stage of several processes, including acute mesenteric arterial occlusion, mesenteric venous thrombosis, strangulated obstruction, volvulus, internal hernia and severe nonocclusive mesenteric ischaemia.

Once infarction is established, restoring perfusion alone is insufficient. Necrotic bowel must be removed while every possible centimetre of viable intestine is preserved.

Pain may initially be severe with limited physical findings if infarction follows vascular occlusion. As transmural necrosis progresses, the abdomen becomes tender with guarding and eventually generalised peritonitis.

Late manifestations include ileus, abdominal distension, gastrointestinal bleeding, fever, hypotension, metabolic acidosis, oliguria and septic shock.

In strangulated obstruction, a transition from intermittent colic to persistent focal pain should raise concern for evolving infarction.

Peritonitis in mesenteric ischaemia strongly predicts irreversible bowel injury.

CT angiography or contrast enhanced CT according to suspected cause: establishes the vascular or mechanical process and assesses bowel viability. Reduced or absent bowel enhancement, pneumatosis, portal venous gas or perforation support advanced irreversible injury, although operative assessment ultimately determines viability.

Check blood gas, lactate, full blood count, renal function, electrolytes and coagulation. Crossmatch blood.

Hyperkalaemia and worsening metabolic acidosis may become pronounced after extensive necrosis or reperfusion.

Bowel infarction is an emergency.

Begin balanced crystalloid resuscitation, correct major electrolyte and acid base disturbances and start broad spectrum antibiotics because mucosal barrier failure and necrosis cause bacterial translocation.

A practical adult regimen is:

Piperacillin tazobactam 4.5 g IV every 8 hours by extended infusion, adjusted for renal function.

If the mechanism is mesenteric vascular occlusion, administer full dose unfractionated heparin unless contraindicated and pursue revascularisation urgently.

Peritonitis, perforation or established necrotic bowel requires emergency exploration.

At surgery, first correct the reversible cause where feasible. Release strangulation, detorse volvulus or restore mesenteric arterial flow before deciding the final resection length.

Resect frankly necrotic bowel only. Marginal bowel may recover after restoration of blood flow, warming and physiological correction. Massive unnecessary resection can convert a survivable vascular catastrophe into permanent intestinal failure.

Primary anastomosis is appropriate only when bowel perfusion is clearly satisfactory and the patient is physiologically stable.

In severe shock, major contamination, bowel oedema or uncertain viability, use damage control principles. Leave stapled bowel ends in discontinuity if necessary, apply temporary abdominal closure and return for a second look operation in 24 to 48 hours.

Document residual small bowel length, presence of ileum, ileocaecal valve and remaining colon. These determine the subsequent risk and severity of short bowel syndrome.

When adequate source control has been achieved for associated intra abdominal infection, prolonged antibiotics are unnecessary. Current Surgical Infection Society guidance recommends no more than approximately 4 days after effective source control unless infection remains uncontrolled.

Small Bowel Adenocarcinoma

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management