Gastrectomy

(For malignancy)

Choice of procedure:

• See gastric adenocarcinoma topic

Operative goals:

• Adequate proximal and distal resection - R0 margin
• Adequate lymphadenectomy (generally D2)
  • D1: region of the cancer only
  • D2: removal of all of the stomach's draining lymph nodes
  • D3: removal of secondary nodal groups (pancreatectomy, coeliac nodes, etc)
• Adequate control of adjacent involved organs

Preparation

• Lithotomy, IV Abx, IDC

Common Initial approach for total/subtotal:

• Long midline incision to umbilicus (can excise xiphoid, or mobilise left lobe of liver if needed)
• Laparoscopic entry would be 3x 10mm ports across upper abdomen, 5mm LUQ, Nathanson
• Examine for metastatic disease
  • Start with pelvis to avoid dispersing malignant cells
  • Peritoneum
  • Greater omentum
  • Para-aortic nodes, root of mesentery
  • Run bowel
  • Upper abdominal organs

Subtotal:

• End up with proximal pouch supplied by only short gastrics
• Enter lesser sac/omental resection. Separate the entire gastrocolic omentum from the transverse colon, entering the lesser sac. Identify the right border of the lesser sac, divide the layer of thin peritoneum there, and thus separate the omentum from the transverse mesocolon completely.
• Control right gastroepiploic artery and gastrocolic vein. Follow the middle colic vessels down to the anterior surface of the neck of pancreas. Identify the gastrocolic trunk (of Henle) which will be running down from greater curvature towards pancreatic head. Control the gastrocolic vein at junction with SMV, including nodal tissue from the gastrocolic trunk (station 6). The gastroepiploic artery is 1cm cephalad to the vein, requiring a short distance of dissection through fat, and should be ligated at origin from the head of pancreas.
• Dissection of suprapyloric nodes. Divide the lesser omentum 1cm from its attachment at the liver, extending across to the left border of the hepatoduodenal ligament. Need to clear the common hepatic artery at this point.
• Identify the origin of right gastric artery and ligate. Dissect out suprapyloric tissue.
• Division of duodenum. Dissect posterior bulbar duodenum from anterior neck of pancreas for 3-5cm. Staple across - GIA 80 blue.
• Hepatic artery node dissection. Continue nodal dissection along CHA, still posterior to stomach. Need to dissect in the plane between nodal tissue and pancreatic parenchyma, identifying the small vessels penetrating that plane. Continue as far as right crus of diaphragm. Control left gastric vein - typically around CHA - can cause difficult bleeding.
• Coeliac axis dissection. Elevate and retract stomach towards patient's left.
  • Identify left gastric vessels at origin. Skeletonise and ligate. Continue dissection along splenic artery. Dissect stations 1, 3, 7 and 9 towards stomach. The left crus will be completely exposed.
• Identify origin of left gastroepiploic artery and vein and control. Leave short gastric vessels intact.
• Division of stomach. Completely free stomach from attachments, cleaning up remnant stomach to point of division. GIA 80 green.
• Reconstruction with Roux-en-Y
  • Divide jejunum 40cm distal to ligament of Treitz
  • Gastrojejunostomy
  • Enteroenterostomy
• Feeding jejunostomy?

Total:

• Mobilise/lymphadenectomy
  • As for subtotal, except also divide short gastrics and pars flaccida, then mobilise oesophagus by dividing phreno-oesophageal membrane
• Divide
  • D1 just distal to pylorus
  • Oesophagus just proximal to GOJ (depending margin required)
• Reconstruct - RYGB or Bilroth 2
  • Draw up the alimentary limb - 40cm distal to ligament of Treitz, since bile reflux is a big problem
  • Jejunojejunostomy
  • Oesophagojejunostomy (can be stapled with OrVil or sutured)

Post-op

• ERAS
  • No routine use of NGT decompression
  • No routine perianastomotic drain
  • Consider oral diet on D1 post-op (weak recommendation)

Complications

Dumping syndrome

• • Combination of GIT and vasomotor symptoms due to rapid post-prandial gastric emptying
  • Can develop after any operation on the stomach, but is common after partial gastrectomy with Billroth II reconstruction, and RYGB
  • Symptoms
    • GIT - abdominal pain, early satiety, nausea/vomiting, diarrhoea, bloating
    • Vasomotor - diaphoresis, tachycardia, palpitations, headache, syncope
  • Early
    • Abrupt delivery of a hyperosmolar, high-carb load into small intestine causing vasomotor activation (light-headed, weak, diaphoretic, tachycardic)
    • Rapid shift of extracellular fluid occurs into the small intestine to achieve isotonicity
    • Luminal distension then occurs, with the resultant symptoms
    • Occurs within 30 minutes of a meal
    • Secondary to lack of pyloric sphincter
    • Symptoms sometimes ameliorated by recumbence or saline infusion
    • Dietary change is mainstay of treatment - avoid all high-sugar foods and drinks, and don't eat and drink at the same time. Octreotide can be considered.
  • Late (less common)
    • Occurs 1-3 hours after a meal
    • Related specifically to carbohydrates being delivered rapidly to the small intestine. They are quickly absorbed, resulting in hyperglycaemia. The large bolus of endogenous insulin then causes an overcompensation, resulting in profound hypoglycaemia, which activates the adrenal gland to release catecholamines, leading to the vasomotor symptoms.
    • Most patients improve after months or years of time, dietary modification and medication
    • Options for re-operation are varied, with varied results.
  • Management
    • Dietary measures are usually sufficient
      • Avoid foods with large amounts of sugar
      • Frequent small meals rich in protein, fat and fibre
      • Separate liquids from solids during a meal
    • Medical management
      • Loperamide for diarrhoea
      • Anticholinergics can slow gastric emptying and treat spasms
      • Octreotide - inhibit gastric emptying and prolong intestinal transit time -  effective but expensive
    • Surgery
      • Depends on initial operation
      • Pyloric reconstruction is an option
      • For patients with a gastrojejunostomy but no gastrectomy, takedown of the gastrojejunostomy can be done
      • For patients with a prior gastrectomy, convert a loop gastrojejunostomy to a Roux-en-Y reconstruction

Metabolic disturbances

• • Iron deficiency anaemia (30% of patient)
    • Combination of decreased iron intake, impaired iron absorption, and chronic blood loss
    • Generally corrected with oral supplements
  • B12 deficiency anaemia
    • Risk is dependent on the amount of stomach removed
    • Occurs secondary to lack of intrinsic factor meaning no B12 absorption
    • Subtotal gastrectomy patients should have lifelong B12 supplementation
  • Osteoporosis/osteomalacia
    • Appears to be caused by deficiencies in calcium
    • Risk increases with the extent of gastric resection, and is usually associated with a Billroth II
    • Typically develops 4-5 years post-op
    • Give calcium and vitamin D supplements
    • Patients with Billroth II that bypasses the duodenum should also have vitamin ADEK supplements

Afferent loop syndrome

• • This is the duodenojejunal loop proximal to the gastrojejunal anastomosis after either a Billroth II or gastrojejunostomy. Occurs as a result of partial obstruction of the afferent limb, which is then unable to empty its contents.
  • A long afferent limb is usually the underlying problem
  • Pancreatic and hepatobiliary secretions accumulate, resulting in distension and cramping
  • The intraluminal pressure eventually increases enough to empty the contents of the afferent loop forcefully into the stomach, resulting in projectile bilious vomiting that immediately relieves symptoms.
  • Can be aggravated by blind loop syndrome - bacterial overgrowth occurs in the static loop, and the bacteria bind with vitamin B12 - leading to megaloblastic anaemia, fat malabsorption and deficiency in fat-soluble vitamins.
  • Investigation
    • Failure to visualise the afferent limb on upper endoscopy is suggestive
    • Radionuclide studies imaging the hepatobiliary tree have also been used with some success - normally should pass into the stomach/distal small bowel after being excreted; if this does not happen, consider afferent loop obstruction.
  • Management
    • Surgical correction
      • Convert the Billroth II into a Billroth I
      • Enteroenterostomy below the afferent and efferent loops
      • Conversion to a Roux-en-Y reconstruction

Efferent loop obstruction

• • Rare
  • Mostly occurs within the first post-op month
  • Presentation
    • Colicky LUQ pain
    • Bilious vomiting
    • Abdominal distension
  • Diagnosis
    • Upper GI series
    • CT with oral contrast, with failure of contrast to enter the efferent limb
  • Management
    • Needs surgery
    • Reduce the retroanastomotic hernia (if this is the cause) and closing the retroanastomotic space to prevent recurrence

Alkaline reflux gastritis

• • Presentation
    • Tends to occur after Billroth II reconstructions
    • Severe epigastric abdominal pain
    • Bilious vomiting
    • Weight loss
  • Diagnosis
    • Technetium biliary scan demonstrating bile reflux into the stomach
    • Gastroscopy - friable, beefy red mucosa
  • Management
    • Medical
      • Aimed at relief of symptoms
      • Most medical therapies haven't shown much benefit
    • Surgical
      • Conversion of the Billroth II into a Roux-en-Y gastrojejunostomy, in which the Roux limb has been lengthened to >40cm

Gastric atony

• • Occurs after truncal and selective vagotomies, but not after highly selective vagotomies
  • Diagnosis
    • Confirm by scintigraphic assessment of gastric emptying
    • Consider other causes of delayed gastric emptying, and post-operative adhesions, afferent or efferent loop syndrome, and internal herniation
  • Management
    • Prokinetics - metoclopramide/erythromycin - see separate topic
    • Gastrectomy may be required in rare refractory cases