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SA Alimentary > Surgery of the stomach > Flashcards

Surgery of the stomach Flashcards

1
Q

What are the four layers of the stomach wall?

A

Mucosa

Submucosa

Muscularis

Serosa

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2
Q

Position of the stomach

A

The greater curvature of the stomach is positioned caudally and the lesser curvature cranially

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3
Q

Anatomy of the greater omentum

A

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.

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4
Q

Anatomy of the lesser curvature

A

Passes between the lesser curvature of the stomach and the porta of the liver.

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5
Q

Blood supply to the stomach

A

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.

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6
Q

Lymphatic drainage of the stomach

A

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.

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7
Q

Pre-operative considerations for gastric surgery

A

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.

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8
Q

What acid-base imbalances can occur as a result of gastric vomiting?

A

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.

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9
Q

What electrolyte imbalances can occur secondary to gastric vomiting?

A

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.

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10
Q

Bacterial contamination in gastric surgery

A

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

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11
Q

Should prophylactic antibiotics be used for gastric surgery?

A

No but peri-operative Abx may be needed in some patients

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12
Q

Surgical approach to gastric surgery

A

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.

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13
Q

Gastrotomy indication

A

Most often indicated for full-thickness biopsy or foreign body removal

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14
Q

Gastrotomy method

A

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

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15
Q

Gastric foreign bodies

A

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.

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16
Q

Signalment of gastric foreign bodies

A

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.

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17
Q

History of animals with gastric foreign body

A

Known foreign body ingestion

Vomiting: mild to severe, intermittent to persistent

Lethargy, abdominal pain, depression and anorexia may be present especially in chronic cases.

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18
Q

Clinical examination of gastric foreign body

A

Dehydration

Abdominal pain

Gastric distension

Melaena or haematemesis

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19
Q

Laboratory findings in gastric foreign body

A

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

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20
Q

Diagnosis of gastric foreign body

A

Radiography

Contrast gastrogram

Ultrasonography

Endoscopy

Gastrotomy.

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21
Q

Gastric foreign body on radiograph

A

gastric distension and radio-opaque foreign bodies may be evident.

Left and right lateral.

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22
Q

Gastric foreign bodies on contrast gastrogram

A

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).

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23
Q

Gastric foreign body on endoscopy

A

Endoscopy provides definitive diagnosis of a gastric foreign body and may permit retrieval

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24
Q

Treatment of gastric foreign body

A

Retrieval of the foreign body by endoscopy or by gastrotomy is indicated.

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25
Q

Prognosis for gastric foreign body

A

Good-excellent for complete recovery

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26
Q

Definition of gastric dilation and volvulus (GDV)

A

‘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.

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27
Q

Pathogenesis of GDV

A

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.

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28
Q

What is required for air accumulation in the stomach?

A

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

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29
Q

Risk factors for GDV

A

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

30
Q

Conditions or behaviours that promote aerophagia

A

Rapid gulping eating style

Exercise after eating

Dyspnoea

31
Q

Pathophysiology of GDV

A

Gaseous distension of the stomach

-> alteration in normal stomach position

-> inhibition of eructation and aborad elimination of gas

-> secondary organ effects

32
Q

Cardiovascular effects of GDV

A

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).

33
Q

Respiratory effects of GDV

A

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.

34
Q

Renal effects of GDV

A

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.

35
Q

Gastric effects of GDV

A

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.

36
Q

Splenic effects of GDV

A

Stertching and avulsion of the splenic vessels or splenic torsion may result in splenic ischaemia and necrosis

37
Q

Metabolic effects of GDV

A

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.

38
Q

Inflammatory effects of GDV

A

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.

39
Q

Signalment of GDV

A

Large and giant breeds including GSDs, Irish setter, and Great Danes

No sex predisposition

Can occur at any age

40
Q

History of GDV

A

Non-productive retching

Abdominal distension

Progressive weakness, recumbency, and rapid breathing

41
Q

Clinical signs of GDV

A

Distended painful tympanic abdomen

Hypersalivation

Shock
- Compensatory
- Endotoxic
- Non-compensatory

42
Q

Signs of compensatory shock

A

tachycardia, tachypnoea, slow capillary refill time, normal pulse strength, pale mucous membranes

43
Q

Signs of endotoxic shock

A

tachycardia, tachypnoea, slow capillary refill time, normal pulse strength, injected mucous membranes, fever

44
Q

Signs of non-compensated shock

A

bradycardia, weak pulses, slow capillary refill time, pale mucous membranes, hypothermia

45
Q

Laboratory findings in GDV

A

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.

46
Q

Diagnosis of GDV

A

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.

47
Q

GDV on radiographs

A

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.

48
Q

Treatment of GDV

A

Restoration of intravascular blood volume: treatment of hypovolaemic shock.

Gastric decompression

Surgery

49
Q

Restoration of intravascular blood volume: treatment of hypovolaemic shock in GDV

A

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

50
Q

What antibiotics should be used for GDV surgery

A

A first or third generation cephalosporin or potentiated amoxycillin + metronidazole would be appropriate.

51
Q

Gastric decompression with orogastric tube

A

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

52
Q

Gastric decompression via percutaneous decompression

A

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.

53
Q

Aims of surgery for GDV

A

derotation of the stomach, removal of necrotic tissue and gastropexy

54
Q

Surgical approach to GDV surgery

A

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

55
Q

Tube gastropexy advantages

A

Very simple technique

Quick to perform

Allows for postoperative gastric decompression

Allows parenteral feeding post-operatively

56
Q

Tube gastropexy disadvantages

A

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)

57
Q

Tube gastropexy

A

performed as for gastrostomy feeding tube placement, except that the tube is placed between the pyloric antrum and the right body wall.

58
Q

Incisional gastropexy

A

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

59
Q

Post operative care - GDV

A

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

60
Q

Prognosis of GDV

A

Fair

Dependent on gastric viability
- gastric necrosis
- plasma lactate concentration

80% of surgically managed cases survive to discharge

61
Q

Pathophysiology of gastric neoplasia

A

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

62
Q

Signalment of gastric neoplasia

A

Older animals

Rough collies and Staffordshire bull terriers may be predisposed

63
Q

History of gastric neoplasia

A

Vomiting or regurgitation of undigested or partially digested food

Haematemesis and melaena

Abdominal pain, anorexia, weight loss

64
Q

Clinical examination of gastric neoplasia

A

Poor body condition, dehydration

Pale mucous membranes

Cranial abdominal pain or distension

Melaena

65
Q

Laboratory findings in gastric neoplasia

A

Regenerative or iron-deficiency anaemia depending on chronicity of disease

Electrolyte and acid-base abnormalities

66
Q

Radiography of gastric neoplasia

A

A soft tissue mass effect overlying the gastric shadow or gastric distension may be evident.

67
Q

Barium meal for gastric neoplasia diagnosis

A

Barium may be retained within stomach for >15 hours.

The neoplasm may be outlined by barium.

68
Q

Ultrasound of gastric neoplasia

A

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.

69
Q

Gastroscopy of gastric neoplasia

A

Gastroscopy with biopsies can result in a definitive diagnosis.

However biopsy of the gastric mucosa alone may prevent definitive diagnosis of deeper lesions.

70
Q

Surgical biopsy of gastric neoplasia

A

Histopathology of full thickness biopsies is usually required for definitive diagnosis.

71
Q

Treatment of gastric neoplasia

A

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.

SA Alimentary (37 decks)

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