Surgery of the stomach Flashcards
What are the four layers of the stomach wall?
Mucosa
Submucosa
Muscularis
Serosa
Position of the stomach
The greater curvature of the stomach is positioned caudally and the lesser curvature cranially
Anatomy of the greater omentum
Attached to the greater curvature of the stomach.
It extends caudally over the intestines to the level of the bladder.
It then folds back on itself to form a sac, the omental bursa.
Anatomy of the lesser curvature
Passes between the lesser curvature of the stomach and the porta of the liver.
Blood supply to the stomach
Provided by branches of the celiac artery.
The left and right gastroepioploic arteries run along the greater curvature of the stomach.
The left and right gastric arteries run along the lesser curvature of the stomach.
Lymphatic drainage of the stomach
Lymph from the stomach drains into the gastric lymph nodes, which are positioned within the lesser omentum, and the hepatic lymph nodes, which are positioned close to the hilus of the liver either side of the portal vein.
Pre-operative considerations for gastric surgery
Often present with vomiting and/or accumulation of air or gastric contents in the stomach.
This results in dehydration, hypovolaemia, acid-base imbalances and electrolyte disturbances, which should be corrected prior to surgery.
What acid-base imbalances can occur as a result of gastric vomiting?
Gastric vomiting often results in a metabolic alkalosis due to loss of gastric acid.
A metabolic acidosis can also be seen due to loss of duodenal bicarbonate and progressive dehydration leading to poor tissue perfusion and anaerobic metabolism.
Acid-base abnormalities can often be self-corrected by the kidneys following rehydration.
What electrolyte imbalances can occur secondary to gastric vomiting?
Gastric vomiting is often associated with hypochloraemia due to loss of gastric hydrochloric acid and hypokalaemia due to insufficient intake of potassium.
These abnormalities can be corrected with 0.9% saline with supplemental potassium.
Bacterial contamination in gastric surgery
Clean-contaminated procedure
Pack off the stomach with lap swabs
Use stay sutures to to minimise gastric spillage
Use bowel clamps
Abdomen should be lavaged with copious amounts of warm sterile saline prior to closure - should run completely clear
Separate set of instruments and clean gloves for closure
Should prophylactic antibiotics be used for gastric surgery?
No but peri-operative Abx may be needed in some patients
Surgical approach to gastric surgery
Ventral midline coeliotomy is most often indicated.
The normal stomach lies cranial to the costal arch and therefore the coeliotomy should be made as far cranially as possible.
This requires clipping and preparation for aseptic surgery as far cranially as the mid-sternum and caudally to the pubis.
The falciform fat overlies the cranioventral abdomen and should be removed for better exposure.
Abdominal retractors (Gossetts or Balfours) are useful to improve exposure of abdominal organs.
Gastrotomy indication
Most often indicated for full-thickness biopsy or foreign body removal
Gastrotomy method
Isolation of stomach and placement of stay sutures
Best made in body of stomach - midway between greater and lesser curvatures
Incision should be longitudinal
Stab incision (11 blade) and metzenbaum scissors
Usually closed with single layer appositional pattern
Submucosa is the suture holding layer
3-0/4-0 polydioxanone
If gastric ulceration they should be given H2 reecptor antagonists
Gastric foreign bodies
Gastric foreign bodies vary widely in nature: fur balls, toys, needles, string, knives and many more have been reported.
They result in clinical signs due to intermittent to persistent obstruction of the pylorus, gastric ulceration and/or gastric perforation.
Signalment of gastric foreign bodies
Any age, but young dogs are over-represented.
Animals that have previously ingested a foreign body.
Animals with pica e.g. pancreatic exocrine insufficiency, hepatic encephalopathy
Cats rarely.
History of animals with gastric foreign body
Known foreign body ingestion
Vomiting: mild to severe, intermittent to persistent
Lethargy, abdominal pain, depression and anorexia may be present especially in chronic cases.
Clinical examination of gastric foreign body
Dehydration
Abdominal pain
Gastric distension
Melaena or haematemesis
Laboratory findings in gastric foreign body
Increased haematocrit due to dehydration or decreased haematocrit due to bleeding from sites of gastric ulceration
Increased urea and creatinine secondary to dehydration
Metabolic alkalosis or acidosis
Electrolyte abnormalities
Diagnosis of gastric foreign body
Radiography
Contrast gastrogram
Ultrasonography
Endoscopy
Gastrotomy.
Gastric foreign body on radiograph
gastric distension and radio-opaque foreign bodies may be evident.
Left and right lateral.
Gastric foreign bodies on contrast gastrogram
1-2ml barium sulphate liquid may coat a gastric foreign body, but cannot be followed by endoscopy until all contrast has left the stomach (approx. 24 hours).
Gastric foreign body on endoscopy
Endoscopy provides definitive diagnosis of a gastric foreign body and may permit retrieval
Treatment of gastric foreign body
Retrieval of the foreign body by endoscopy or by gastrotomy is indicated.
Prognosis for gastric foreign body
Good-excellent for complete recovery
Definition of gastric dilation and volvulus (GDV)
‘Gross gaseous distension of the stomach with rotation of the stomach around the long axis of the oesophagus.’
Rotation of the stomach is most often clockwise i.e. the gastric pylorus and duodenum move ventrally from right to left and may continue to move dorsal to the oesophagus and gastric fundus on the left side of the abdomen.
Pathogenesis of GDV
Uncertain.
It is not clear whether volvulus precedes dilatation or whether dilatation precedes volvulus.
The air that accumulates in the stomach is primarily atmospheric i.e. swallowed air, but also includes small amounts of gases produced by metabolism and bacterial fermentation.
What is required for air accumulation in the stomach?
Air accumulation requires one or both of the following:
Failure of eructation: dysfunction of the gastro-esophageal sphincter
Delayed or impaired gastric emptying: pyloric dysfunction
Risk factors for GDV
Large and giant breed dogs
Dogs with a first degree relative with a history of GDV
Deep chested dogs
Underweight dogs
Older dogs
Conditions or behaviours that promote aerophagia
Conditions or behaviours that promote aerophagia
Rapid gulping eating style
Exercise after eating
Dyspnoea
Pathophysiology of GDV
Gaseous distension of the stomach
-> alteration in normal stomach position
-> inhibition of eructation and aborad elimination of gas
-> secondary organ effects
Cardiovascular effects of GDV
Obstruction of intra-abdominal veins results in decreased venous return to the heart.
This results in decreased cardiac output, hypovolaemic shock and decreased organ perfusion.
Cardiac arrhythmias, especially ventricular premature complexes (VPC’s), are often seen (pre- or post-op).
Respiratory effects of GDV
Pressure of the stomach cranially on the diaphragm compromises the normal respiratory movements of the diaphragm, resulting in a decreased tidal volume.
Compensatory increases in respiratory rate and effort are ultimately insufficient resulting in an increase in arterial carbon dioxide and then a decrease in arterial oxygen.
Renal effects of GDV
Hypovolaemia and reduced cardiac output result in poor perfusion of the kidneys.
This in turn leads to oliguria/anuria, renal tubule damage which may be permanent and electrolyte /acid-base disturbances.
Gastric effects of GDV
An increase in intraluminal gastric pressure results in mucosal haemorrhage and necrosis and a decrease in gastric muscle activity exacerbating gastric dilatation.
Gastric rotation results in stretching and possible avulsion of the blood supply to the stomach.
The short gastric vessels supplying the greater curvature of the fundus of the stomach are most often avulsed.
Full-thickness gastric wall ischaemia and necrosis may result, especially at the level of the fundus, leading to gastric perforation and septic peritonitis.
Splenic effects of GDV
Stertching and avulsion of the splenic vessels or splenic torsion may result in splenic ischaemia and necrosis
Metabolic effects of GDV
Variable acid-base and electrolyte abnormalities can be seen.
§ Decreased tissue perfusion and oxygenation result in anaerobic metabolism and lactic acid production. This leads to a metabolic acidosis.
§ The sequestration of gastric acid in the stomach can lead to a metabolic alkalosis.
§ Potassium abnormalities are often seen
§ Hypoglycaemia may result from the inefficient use of glucose during anaerobic metabolism, ineffective glucose homeostasis due to liver congestion or sepsis.
Inflammatory effects of GDV
Compromise to the stomach wall and intestinal hypoxia may result in the translocation of gastrointestinal bacteria and their toxins into the systemic circulation resulting in endotoxaemia.
This stimulates the release of inflammatory mediators, exacerbating hypovolaemic shock and promoting disseminated intravascular coagulation (DIC).
Therefore GDV can and will result in death if untreated.
Signalment of GDV
Large and giant breeds including GSDs, Irish setter, and Great Danes
No sex predisposition
Can occur at any age
History of GDV
Non-productive retching
Abdominal distension
Progressive weakness, recumbency, and rapid breathing
Clinical signs of GDV
Distended painful tympanic abdomen
Hypersalivation
Shock
- Compensatory
- Endotoxic
- Non-compensatory
Signs of compensatory shock
tachycardia, tachypnoea, slow capillary refill time, normal pulse strength, pale mucous membranes
Signs of endotoxic shock
tachycardia, tachypnoea, slow capillary refill time, normal pulse strength, injected mucous membranes, fever
Signs of non-compensated shock
bradycardia, weak pulses, slow capillary refill time, pale mucous membranes, hypothermia
Laboratory findings in GDV
Blood gas analysis: Acid-base abnormalities and an abnormal electrolyte balance especially abnormalities in potassium and sodium
Haematology: Increased packed cell volume, stress leukogram or decreased neutrophil count due to an exhausted inflammatory response and decreased platelets due to excess consumption
Biochemistry: Increased liver enzymes due to liver congestion, increased total bilirubin due to biliary stasis, azotaemia due to hypovolaemia and hypoglycaemia.
Clotting times: Increased prothrombin time and partial thromboplastin times due to DIC.
Diagnosis of GDV
Signalment, history and clinical signs are usually very suggestive of GDV.
Abdominal radiographs will confirm the diagnosis, but treatment should not be delayed by radiography.
GDV on radiographs
A gas-distended gastric silhouette
The ‘compartment sign’ – a soft tissue density divides the gas-filled stomach into two chambers or compartments
The pylorus (and connected duodenum) is dorsocranial to the fundus of the stomach
Small and large intestine loops are variably distended with gas
Gastric perforation may be associated with free peritoneal gas, often seen adjacent to the diaphragm dorsally or loss of serosal detail.
Treatment of GDV
Restoration of intravascular blood volume: treatment of hypovolaemic shock.
Gastric decompression
Surgery
Restoration of intravascular blood volume: treatment of hypovolaemic shock in GDV
Wide bore intravenous catheter in both cephalic veins
Shock doses (90ml/kg) of isotonic crystalloid fluids (Hartmanns)
Colloids for restoration of BP
Hypertonic saline for very large dogs - must be followed with isotonic fluids
ECG to monitor cardiac rhythm
Flow by oxygen
Initiate antibiotics
What antibiotics should be used for GDV surgery
A first or third generation cephalosporin or potentiated amoxycillin + metronidazole would be appropriate.
Gastric decompression with orogastric tube
Avoid sedation
Sternal recumbency or sitting position
Bucket on floor
Large bore orogastric tube
Bandage roll to hold mouth open
Can lavage with warm water or saline after emptied
Gastric decompression via percutaneous decompression
This should be conducted if an orogastric tube cannot be passed.
Clip and aseptically prepare an area of skin over the cranial left flank over the area of greatest tympany.
Palpate for the spleen and avoid if possible.
Insert a large gauge catheter or needle (14-18G). Gas should pass freely out of the catheter or needle.
Aims of surgery for GDV
derotation of the stomach, removal of necrotic tissue and gastropexy
Surgical approach to GDV surgery
Exploratory laparotomy via a ventral midline approach.
Covering of the stomach with omentum confirms clockwise GDV
Fundus and pylorus should be palpated
Stomach tube advanced
Stomach and spleen assessed for ischaemia/necrosis
Gsatropext essential to prevent recurrence
Tube gastropexy advantages
Very simple technique
Quick to perform
Allows for postoperative gastric decompression
Allows parenteral feeding post-operatively
Tube gastropexy disadvantages
possible complications of wound infection, tube dislodgement and septic peritonitis (10% major complication, 45% minor complication).
Increased hospital stay
Adhesion known to lengthen with time
High recurrence rate than other techniques (0-29% in various studies)
Tube gastropexy
performed as for gastrostomy feeding tube placement, except that the tube is placed between the pyloric antrum and the right body wall.
Incisional gastropexy
Preferred option in most cases
A 5-6cm linear incision is made in the seromuscular layer of the pyloric antrum midway between the greater and lesser curvatures.
A similar linear incision is made through the peritoneum and transversus abdominus muscle in the right ventrolateral abdominal wall approximately 5cm caudal to and parallel to the costal arch.
The cranial edges of the abdominal wall and gastric incisions are apposed first, with a simple continuous suture of 2-0 or 3-0 polydioxanone and then the caudal edges of these incisions are apposed in a similar fashion.
Recurrence rate low
Post operative care - GDV
Fluid therapy
Electrolyte balance should be maintained
Analgesia
Broad spectrum antibiotics for 5-7 days
ECG monitoring
Water after 12hrs then food if no vomiting
GI motility drugs?
Oral nutrition should be encouraged as early as possible
Prognosis of GDV
Fair
Dependent on gastric viability
- gastric necrosis
- plasma lactate concentration
80% of surgically managed cases survive to discharge
Pathophysiology of gastric neoplasia
Adenocarcinoma is the most common canine gastric neoplasm
Lymphoma is the most common feline gastric neoplasm.
Others include mast cell tumour, leiomyoma, leiomyosarcoma and fibrosarcoma.
Mucosal ulceration associated with gastric neoplasms may result in significant bleeding and subsequent blood loss anaemia, iron deficiency and pan-hypoproteinaemia.
Gastric neoplasms obstructing the cardia will result in regurgitation, whereas neoplasms obstructing the pylorus will result in gastric retention and vomiting.
Diffuse gastric tumours may result in gastric motility disturbances.
Some gastric tumours may result in paraneoplastic syndromes
Signalment of gastric neoplasia
Older animals
Rough collies and Staffordshire bull terriers may be predisposed
History of gastric neoplasia
Vomiting or regurgitation of undigested or partially digested food
Haematemesis and melaena
Abdominal pain, anorexia, weight loss
Clinical examination of gastric neoplasia
Poor body condition, dehydration
Pale mucous membranes
Cranial abdominal pain or distension
Melaena
Laboratory findings in gastric neoplasia
Regenerative or iron-deficiency anaemia depending on chronicity of disease
Electrolyte and acid-base abnormalities
Radiography of gastric neoplasia
A soft tissue mass effect overlying the gastric shadow or gastric distension may be evident.
Barium meal for gastric neoplasia diagnosis
Barium may be retained within stomach for >15 hours.
The neoplasm may be outlined by barium.
Ultrasound of gastric neoplasia
Ultrasound can be used to identify gastric wall infiltration and gastric masses and can be used to assess spread of disease to local lymph nodes and other abdominal organs.
Gastroscopy of gastric neoplasia
Gastroscopy with biopsies can result in a definitive diagnosis.
However biopsy of the gastric mucosa alone may prevent definitive diagnosis of deeper lesions.
Surgical biopsy of gastric neoplasia
Histopathology of full thickness biopsies is usually required for definitive diagnosis.
Treatment of gastric neoplasia
Unfortunately most gastric neoplasms are not amenable to surgical resection due to their size or location within the stomach.
Occasionally tumours that have been identified early in the course of the disease or benign tumours can be removed via partial gastrectomy.
