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Y4 SA - Soft tissue surgery > Surgery of the GIT, liver and pancreas 1, 2 +3 > Flashcards

Surgery of the GIT, liver and pancreas 1, 2 +3 Flashcards

1
Q

What is a primary cleft palate?

A

Failure of fusion of the primary palate (lips and premaxilla)

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2
Q

What is a secondary cleft palate

A

Failure of fusion of the secondary palate (hard and soft palates)

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3
Q

What are the causes of a secondary cleft palate?

A

Attributed to inherited, nutritional, hormonal, mechanical and toxic factors
More common in brachycephalic breeds, also in Schnauzer, Labrador, Cocker Spaniel, Dachshund, GSD and cats (esp. Siamese)

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4
Q

What are the clinical signs of a cleft palate?

A

Drainage of milk from nares
Coughing, gagging or sneezing while eating
Poor growth
Chronic rhinitis
Cough

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5
Q

What is the importance of an early cleft palate diagnosis?

A

Early diagnosis allows tube feeding until animal is 8-12 weeks old, when tissues are better able to hold sutures, the cleft has often narrowed, the oral cavity is bigger (more room to work) and anaesthesia is better tolerated.

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6
Q

Describe medical treatment for a cleft palate

A

Medically treat patients with pneumonia and tube feed until they are better surgical candidates

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7
Q

Describe repair of a primary cleft palate

A

Surgical reconstruction of the medial and lateral components of the cleft and skin

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8
Q

Describe repair of a secondary cleft palate

A

Secondary clefts carry a high risk of complications (dehiscence) due to tension and several procedures may be required, esp. in young animals.
They are closed by various mucosal flaps with/without tension-relieving incisions

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9
Q

List the complications of cleft palate repair

A
  • Dehiscence is usually due to tension, motion or excessively tight sutures.
  • Persistent chronic rhinitis is common.
  • Young palates grow rapidly: reconstructed palates can become thin and develop oronasal fistulae that can be corrected at 8-10 months of age.
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10
Q

When is a maxillectomy/mandibulectomy indicated?

A

Used to remove sections of the maxilla and mandible of various sizes for wide excision of both benign and malignant masses.

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11
Q

Describe closure of a mandibulectomy/maxillectomy

A

Closed in 3 layers – buccal mucosa, muscular / subcutaneous tissue and skin

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12
Q

Describe post-operative treatment following a mandibulectomy/maxillectomy

A

Supportive treatment with antibacterials, anti-inflammatories and a pharyngostomy or gastrostomy tube for feeding are often required.
Dogs tolerate mandibulectomy / maxillectomy much better than cats

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13
Q

What is the most commonly diagnosed salivary gland disease in 1. cats and 2. dogs

A

Cats = neoplasia
Dogs = salivary mucocoele

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14
Q

What is salivary mucocoele

A

Subcutaneous or submucosal cavity containing saliva from a disrupted salivary gland or duct
In dogs the sublingual gland or duct is most often affected

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15
Q

Describe the aetiology and predisposition of salivary mucocoele

A

Trauma, neoplasia, sialoliths (mineralised “stones” forming in the salivary glands or ducts), foreign bodies or iatrogenic damage.
Most are idiopathic.
GSDs, Greyhounds, Poodles, Dachshunds and Australian Silky Terriers may be predisposed.

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16
Q

List the clinical signs of salivary mucocoele

A
  • Painless fluctuant swelling (may be acutely painful).
  • Sublingual mucocoeles = dysphagia, ptyalism, blood-tinged saliva.
  • Pharyngeal mucocoeles = inspiratory stridor, coughing or respiratory distress
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17
Q

List the DDx of salivary mucocoele

A
  • Salivary gland enlargement
  • Cervical lymphadenopathy
  • Haematoma or seroma
  • Oedema
  • Emphysema
  • Enlarged thyroid
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18
Q

How is salivary mucocoele diagnosed?

A
  • History and clinical signs.
  • Aspiration of mucoid, stringy fluid, often blood tinged with a low cellular content. Staining smears with PAS may confirm the presence of mucin.
  • Sialography with positive contrast material can lateralise the lesion (bilateral in up to 20% of dogs).
  • Ultrasonography can help to lateralise the lesion
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19
Q

How is salivary mucocoele treated?

A
  • Drainage is only palliative and >95% recur.
  • Mandibular and sublingual sialadenectomy is more successful coupled with drainage of the sialocoele at the time of surgery ± drain placement.
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20
Q

List the possible complications of salivary mucocoele treatment

A

Haemorrhage, seroma, infection, recurrence and hypoglossal nerve paralysis

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21
Q

In which animals are nasal polyps most commonly seen?

A

Young cats

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22
Q

What are nasal polyps?

A

Pedunculated benign inflammatory lesions of the mucous membranes of the nasopharynx, auditory tube or middle ear

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23
Q

List the clinical signs of nasal polyps

A

Upper airway obstruction
Dysphagia
Dysphonia
Otitis externa if tympanic membrane disrupted
Horner’s Syndrome if tympanic bulla affected with pressure on sympathetic trunk

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24
Q

How are nasal polyps diagnosed?

A
  • Direct visualisation under GA in nasopharynx or ear canal.
  • Radiography may reveal a soft tissue density in the pharynx or bulla
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25
Q

How are nasal polyps treated?

A

Surgical excision
Medical treatment with oral prednisolone may reduce recurrence

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26
Q

What is the main complication with polyps?

A

Recurrence, esp. if underlying inflammation is not controlled or there is failure to completely excise the polyp

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27
Q

What are pharyngeal stick injury and/or abscess?

A

Occur in both dogs and cats due to penetration of the pharyngeal mucosa by a variety of objects

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28
Q

How do patients with a pharyngeal stick injury and/or abscess present?

A

Acute onset of marked pharyngeal discomfort with gagging, headshaking, pawing at mouth, opening mouth, hypersalivation, pain on opening mouth and painful retropharyngeal swelling with surrounding oedema.

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29
Q

How are pharyngeal stick injuries/abscesses diagnosed?

A

History, clinical signs, digital examination of pharynx, radiography, ultrasound

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30
Q

How are pharyngeal stick injuries/abscesses treated?

A
  • Remove FB (if present), arrest haemorrhage without compromising blood supply to the area and debride the wound
  • Endoscopy
  • Leave wounds open to drain and heal by second intention
  • Antibacterial therapy
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31
Q

When is a tonsillectomy performed?

A

For chronic, recurrent unresponsive tonsillitis or tonsillar neoplasia

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32
Q

Describe how to perform a tonsilectomy

A
  • Place a cuffed ET tube and pack the pharynx with swabs
  • Grasp the tonsil and retract from the tonsillar crypt
  • Then either sharply excise with scissors (controlling haemorrhaging vessels individually with ligatures or electrocautery) or clamp with a curved haemostat then ligate en masse and excise.
  • Close the tonsillar crypt with a continuous suture to help control haemorrhage
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33
Q

In which places do oesophageal foreign bodies most commonly lodge?

A

Where distension of the oesophagus is limited by surrounding structures:
- Thoracic inlet
- Heart base
- Caudal oesophagus just in front of the cardia

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34
Q

How does a patient with an oesophageal foreign body present?

A
  • History of FB ingestion
  • Regurgitation
  • Retching/gagging
  • Hypersalivation
  • Restlessness
  • Lethargy
  • Inappetence
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35
Q

What are the signs of a patient with an oesophageal FB that has lead to an oesophageal perforation?

A

Pneumothorax, mediastinitis, pyothorax or pleuritis may occur
- Pyrexia, depression and respiratory distress

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36
Q

How is an oesophageal FB diagnosed?

A

Thoracic radiographs
Oesophagoscopy

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37
Q

How is an oesophageal FB treated?

A
  • Endoscopic removal is possible in about 90% of cases. If you do not have access to an endoscope, consider referral
  • If the foreign body is firmly lodged, do not force it as this may cause perforation.
  • Push the FB into the stomach via endoscopy or fluoroscopy: bones can be allowed to digest unless they cause clinical signs, other objects can be retrieved via gastrotomy
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38
Q

Describe the procedure of oesophageal FB removal following extraction

A
  • Inspect the oesophageal lining for ulcers or tears
  • May need to use a feeding tube
  • Large perforations may require drainage/surgical repair
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39
Q

List the potential complications of oesophageal FB removal

A

Oesophagitis, ischaemic necrosis, dehiscence, leakage, infection, fistula, stricture formation, perforation of the aorta or pulmonary artery by the foreign body during removal (rapidly fatal!)

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40
Q

What are vascular ring anomalies?

A

Developmental anomalies of the aortic arches in which the oesophagus and trachea are encircled and constricted by blood vessels

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41
Q

Most cases of vascular ring anomalies have which feature?

A

A persistent right aortic arch

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42
Q

A persistent right aortic arch is inherited in which breeds?

A

German shepherds
Irish setters

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43
Q

How are vascular ring anomalies treated?

A

Ligation and division of the least important vessel forming the ring (ligamentum arteriosum in PRAA).
Surgery should be done as soon as possible as medical management has poor results

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44
Q

What is a hiatal hernia?

A

Herniation of cardia of stomach through oesophageal hiatus

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45
Q

A hiatal hernia is associated with which condition?

A

Gastroesophageal reflux

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46
Q

How is a hiatal hernia treated?

A

In persistent herniation, combined suture reduction of oesophageal hiatus, oesophagopexy and left fundic gastopexy
Guarded prognosis

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47
Q

When is gastrotomy indicated?

A

Foreign body removal
Exploratory reasons

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48
Q

Describe the surgical approach of a gastrotomy

A
  • Ventral midline coeliotomy.
  • Pack off stomach and stabilise region of incision on the avascular area between the greater and lesser curvatures with 3-4 stay sutures.
  • Incise stomach (mucosa is quite tough) and explore.
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49
Q

Describe surgical closure following a gastrotomy

A

2 layers
Inverting pattern
Simple continuous
Then Cushing or Lembert sutures
Lavage abdomen before closure

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50
Q

What happens in gastric dilatation and volvulus?

A
  • The pylorus and proximal duodenum move ventrally then cranially, with the pylorus migrating from right to left and ending up dorsal to the oesophagus.
  • Gas and fluid rapidly accumulate in the stomach and cause gastric distension
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51
Q

What are the risk factors for GDV?

A
  • Pure breed large or giant breed
  • Increased thoracic depth to width ratio
  • Inherited
  • Feeding fewer meals per day
  • Eating rapidly
  • Aggressive or fearful temperament
  • Decreased food particle size
  • Exercise or stress following a meal
  • The Gordon setter, standard poodle, Weimaraner, Irish setter, great Dane, Bassett hound and St. Bernard are at greatest risk
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52
Q

Describe the haemodynamic effects of GDV

A

Increased intraabdominal pressure due to gastric distension reduces abdominal blood flow and venous return to the heart leading to cardiogenic shock.
Occlusion of splenic vessels frequently causes splenic enlargement and congestion

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53
Q

How does GDV cause respiratory dysfunction?

A

Pressure on the diaphragm from the distended stomach reduces diaphragmatic movement and causes dyspnoea

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54
Q

How does GDV cause cardiac dysfunction?

A

Reduced coronary blood flow and myocardial depressant factor from compromised abdominal organs cause myocardial ischaemia / necrosis and cardiac arrhythmias (premature ventricular contractions and ventricular tachycardia).

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55
Q

How does GDV cause gastric necrosis?

A

Increased intragastric pressure compresses gastric wall blood vessels and reduces perfusion

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56
Q

How does GDV potentially cause septic/endotoxic shock?

A

Mucosal ischaemia in the stomach and intestine compromises mucosal integrity and allows bacterial translocation

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57
Q

What may occur after correction of GDV due to free radical production etc?

A

Reperfusion injury

58
Q

How does GDV appear on radiography?

A
  • Right lateral abdominal radiograph shows gastric malposition with air entrapped in the pylorus separated from air in the gastric body by a soft tissue density, causing a typical “reverse C” or “Popeye” sign.
  • If the stomach has been decompressed before radiography the gas may be less obvious, but the soft tissue fold should still be visible.
59
Q

If … is visible on radiography of a GDV, it may indicate gastric necrosis and perforation

A

Pneumoperitoneum

60
Q

How can laboratory test results be used to diagnose GDV

A
  • Haematology = haemoconcentration, a stress leucogram and thrombocytopaenia.
  • Serum biochemistry = increased ALT and bilirubin due to hepatocellular damage, increased BUN and creatinine due to hypotension and various electrolyte abnormalities.
  • Plasma lactate = helpful in predicting prognosis and the presence of gastric necrosis
61
Q

Describe the pre-operative management of a GDV pateint

A

Stabilise the patient with fluid resuscitation and gastric decompression

62
Q

Describe the appropriate fluid therapy for a GDV patient

A

Resuscitate the patient with high volume crystalloids, colloids and/or hypertonic saline
Place one or two short, large gauge catheters in either the jugular or cephalic veins to maximise fluid flow rates and delivery to the heart

63
Q

ALL GDV cases require … to prevent recurrence

A

Gastropexy

64
Q

Name the 3 ways of decompressing the stomach in a GDV patient

A
  • Stomach tubing
  • Needle paracentesis or trocharisation
  • Temporary flank gastrostomy under LA
65
Q

Describe the gastropexy procedure

A
  • Fixes the pylorus to the right abdominal wall
  • Prevents gastric volvulus but not dilation
66
Q

Name the two gastropexy procedures that can be performed to treat GDV

A

Incisional gastropexy
Tube gastropexy

67
Q

In cases of GDV describe when it is appropriate to remove the spleen

A
  • Spleen may appear very congested, but after the stomach has been repositioned this will generally improve.
  • If palpation of the splenic vessels detects thrombosis in the vessels, perform splenectomy.
  • If splenic torsion has occurred perform a splenectomy without correcting the torsion
68
Q

When is a partial gastrectomy indicated in GDV cases?

A

When there is gastric necrosis

69
Q

Which factors need to be assessed to determine viability of the gastric wall?

A
  • Active bleeding
  • Palpable pulses in the short gastric vessels
  • Reduced thickness of the gastric wall: indicates necrosis.
  • Increased pliability of the gastric wall: indicates necrosis
70
Q

How can serosal colour be used to determine viability of the gastric wall?

A

Dark reddish – purple areas are usually due to venous congestion and intra-mural haemorrhage and will usually recover.
Pale grey- green areas are usually necrotic and require resection

71
Q

Name the 3 techniques for a partial gastrectomy

A
  • Invagination.
  • Sharp excision with a scalpel blade or Metzenbaum scissors.
  • Stapling.
72
Q

Describe the appropriate post op care for patients that have undergone GDV surgery

A
  • IV fluids.
  • Monitoring for cardiac arrhythmias for 72h
  • Monitor electrolyte status.
  • Nil by mouth for 24-48hrs, then start with ice cubes, small amounts of fluids and small amounts of food.
  • Gastric mucosal protectants are indicated if gastric necrosis has occurred.
73
Q

List some possible causes of a gastric outflow obstruction

A

Pyloric stenosis
Pyloric muscular hypertrophy and dysfunction
Chronic hypertrophic pyloric gastropathy
Neoplasia

74
Q

Which two procedures allow resection of a substantial amount of the pylorus and distal stomach?

A

Gastroduodenostomy
Gastrojejunostomy
(Billroth type I and II)

75
Q

Describe a gastroduodenostomy (Billroth I) procedure

A

End-to-end anastomosis of the stomach and duodenum and is reasonably well tolerated

76
Q

Describe a gastrojejunostomy (Billroth II) procedure

A

Side-to-side anastomosis of the jejunum and stomach, often combined with a cholecystojejunostomy and a partial or total pancreatectomy

77
Q

Why does the gastrojejunostomy have a high mortality and morbidity rate?

A
  • Extent of surgery
  • non-physiological nature of the resulting digesta flow
  • risk of dehiscence
  • serious nature of the underlying disease
78
Q

What is an enterotomy?

A

Surgical incision into intestine

79
Q

Why are intestines resected at approximately 30° to the transverse?

A

Ensures adequate blood supply to the antimesenteric border and increases the luminal diameter at the anastomosis

79
Q

Describe the surgical approach to an enterectomy with end-to-end appositional anastomosis

A
  • Isolate and pack off affected area of gut and express contents, occlude lumen
  • Place crushing forceps on the section of intestine to be resected at approximately 30° to the transverse
  • Ligate jejunal branches of the cranial mesenteric artery supplying the terminal arcade of the section of gut to be removed.
  • Transect the intestine with a scalpel, using the line of the crushing clamps as a guide.
  • Transect mesentery with scissors
80
Q

Describe the main complications that can occur following an enterectomy with end-to-end appositional anastomosis?

A
  • Dehiscence and peritonitis: usually within 3-5d of surgery.
  • Stricture formation (uncommon with single layer closure): correct by resection and anastomosis
81
Q

When you’re clamping off the intestinal lumen to do an enterectomy, which set of clamps (crushing or non-crushing) should you put on first? Why?

A

Put on the crushing clamps first, then place the non-crushing:
- Sets the boundaries for resection
- Ensures that where you are cutting is inviable tissue
- Minimises time that intestine you’re not resecting is clamped for

82
Q

Which technique should be used when biopsying the gut wall?

A

Small, full-thickness wedge biopsy

83
Q

When biopsying the intestine one of two techniques can be used, describe them

A
  • Longitudinal wedge, longitudinal closure: good general-purpose technique.
  • Longitudinal wedge, transverse closure: maintains luminal diameter very well, useful in small patients
84
Q

When are linear foreign bodies mostly seen?

A

In cats due to their tendency to play with and eat string, thread, tinsel etc

85
Q

Describe how linear foreign bodies affect the GIT

A
  • A linear piece of material becomes fixed proximally (usually under the tongue or at the pylorus) with the remainder extending down the GIT.
  • Peristalsis causes the intestine to bunch up along the material in accordion-like folds.
  • Partial intestinal obstruction occurs and may progress to erosion of the material through the mesenteric border of the gut, perforation and peritonitis.
86
Q

What should you NOT do to treat a linear foreign body?

A

Don’t just pull the material out unless you want the gut to perforate!

87
Q

Describe conservative treatment for a linear foreign body

A

If there are no signs of peritonitis and the material is looped around the tongue. Cut material and monitor patient until it is passed in the faeces – usually about 3 days

88
Q

Describe conservative treatment for a linear foreign body

A

If there are no signs of peritonitis and the material is looped around the tongue. Cut material and monitor patient until it is passed in the faeces – usually about 3 days

89
Q

Describe surgical treatment for a linear foreign body

A
  • If the material isn’t caught around the tongue (or if there is evidence of perforation) perform a ventral midline coeliotomy to remove the entire length of material.
  • Start with gentle traction at the distal end of the bunched area and work proximally.
  • Multiple enterotomies may be required, cutting the material and removing the section distal to the current enterotomy site.
  • Carefully evaluate the mesenteric border for gross evidence of perforation – if present, perform an enterectomy.
90
Q

What is intussusception?

A

Invagination of one bowel segment into another, usually secondary to small intestinal hypermotility

91
Q

What are the 3 consequences of intussusception?

A
  • Small intestinal obstruction.
  • Disruption of the vascular supply to the intussusceptum.
  • Adhesion formation between the two sections of bowel.
92
Q

How can intussusception be differentiated from a rectal prolapse?

A

By the ability to pass a probe between the prolapse and the anal ring (you can’t if it is a prolapse).

93
Q

How is intussusception diagnosed?

A
  • Signs of SI obstruction
  • Sausage-shaped mass may be palpable in the abdomen
  • Often difficult to visualise by radiography.
  • Contrast studies (barium enema) and ultrasonography
94
Q

How is intussusception treated?

A

Manual reduction by putting gentle traction on the intussusceptum while tenderly milking the intussuscipiens.
If reduction is not possible or the reduced tissue appears traumatised, perform an enterectomy.

95
Q

What is intestinal torsion?

A

Twisting of the small intestine on its mesenteric axis -> strangulation

96
Q

What are the consequences of intestinal torsion?

A

The cranial mesenteric artery and vein become compromised, with initial venous thrombosis followed by arterial thrombosis and necrosis of the gut.
Mucosal necrosis is followed by endotoxaemia, bacteraemia and peritonitis.

97
Q

What are the clinical signs of intestinal torsion and strangulation?

A
  • Sudden onset, rapid progression.
  • Abdominal pain and distension.
  • Severe depression and shock. May resemble GDV
98
Q

How is intestinal torsion and strangulation treated?

A
  • Intensive fluid therapy.
  • Antibacterials.
  • Reduction of torsion, resection of necrotic bowel.
    Prognosis very poor – those who survive surgery often develop short bowel syndrome.
99
Q

List the 3 indications for large intestinal surgery

A
  • Strictures due to chronic inflammatory disease
  • Neoplasia
  • Colectomy for intractable feline idiopathic megacolon and canine megacolon
100
Q

When is a colopexy performed?

A

Usually done to prevent recurrence of rectal prolapse. Similar to an incisional gastropexy but between the colon and the abdominal wall.

101
Q

Define where the areas of the rectum and anus are

A

Rectum = the terminal portion of the intestine from the pelvic brim to the anal sphincter
Anus = the area between the anal sphincter and the skin

102
Q

What is atresia ani?

A

The rectoanal junction and/or distal rectum fail to form properly, resulting in obstruction to passage of faeces

103
Q

What are the clinical signs of atresia ani?

A
  • Present in neonates.
  • Abdominal distension and pain.
  • Lack of defaecation and/or faecal tenesmus
104
Q

How is atresia ani treated?

A

Surgical creation of a patent rectum/rectoanal junction.
The more severe the abnormality the more complex the surgery, the higher the complication risk and the poorer the prognosis.

105
Q

What is a recto-vaginal fistula?

A

Communication between rectum and vagina

106
Q

What are the clinical signs of a recto-vaginal fistula?

A

Incontinence
Faecal material passed through vulva

107
Q

What is a rectal prolapse?

A

Protrusion of rectal tissue (mucosa or all layers) from the anus

108
Q

Describe the aetiology of a rectal prolapse

A
  • Any condition causing persistent faecal tenesmus (need to pass stool)
  • Defects in supporting structures of the rectum or anus
  • Damage to innervation of the anal sphincter
109
Q

Which drug can be used to shrink oedematous tissue in a rectal prolapse

A

50% dextrose

110
Q

How are rectal prolapses treated surgically?

A

Surgical correction – non-absorbable purse-string suture for 1-5 days, colopexy or resection and anastomosis of prolapsed tissue if necrotic

111
Q

Describe the post operative care of a patient treated for a rectal prolapse

A

Stool softeners, low bulk diet, possibly sedation in the immediate postoperative period if tenesmus persists

112
Q

What is anal furunculosis?

A

Chronic, ulcerative, fistulous tracts involving a variable amount of the skin up to 360° around the anus

113
Q

Describe the aetiology/predispositions for anal furunculosis

A

GSDs predisposed, occasionally seen in Setters, collies and Labradors.
Aetiology - Many theories, but autoimmune disease linked to colitis is most likely theory

114
Q

List the clinical signs of anal furunculosis

A
  • Tenesmus
  • Perianal pruritis
  • Multiple, ulcerated fistulae/sinuses around anus ± purulent discharge
115
Q

How is anal furunculosis treated medically?

A

Best method of treatment
- Ciclosporin until lesions resolve
- Monitor serum biochemistry every two to four weeks through treatment in case of ciclosporine toxicity (liver/kidneys)

116
Q

How is anal furunculosis treated surgically?

A

Surgical excision is messy, difficult and requires extensive postoperative care with daily lavage.
Lengthy convalescence.
Extensive 360° lesions may require rectal pull through with attendant risk of incontinence etc. Up to 50% recurrence.

117
Q

Describe the aetiology of impaction or abscessation of the anal sacs

A

Possibly poor anal sphincter tone, narrow anal sac ducts or hypersecretion

118
Q

List the clinical signs of anal sac disease

A

Pain on defaecation, pruritus, rubbing anus on ground

119
Q

How is anal sac impaction treated?

A

Express anal sacs, teach client to express sacs themselves, excise if chronic problem

120
Q

How is anal sac abscessation treated?

A

Drainage (expression) and topical / systemic antibacterials. If recurrent, resect after treating infection.

121
Q

Describe the open anal sacculectomy procedure

A

Insert a probe into the anal sac duct with its tip pointed towards the skin surface and incise the anal sac over the probe, starting at the duct orifice (dotted line)

Alternatively, insert a fine pair of scissors into the duct and pull them towards the skin as they are closed to cut into the duct and sac, then dissect the sac free.
The anal sphincter is incised in this technique: appose it with fine monofilament absorbable suture.

122
Q

Describe the closed anal sacculectomy procedure

A

Fill the anal sac with saline, wax or resin then dissect it out without penetrating the mucosa:
Ligate and divide the duct when dissection is complete.
The anal sphincter is not incised with this technique.

123
Q

What are the potential complications of anal sac surgery?

A

Incontinence if caudal rectal nerve damaged.
Abscessation and fistulation if excision incomplete.
Anal stricture (rare).

124
Q

What considerations need to be made when approaching surgery of the liver and biliary tract?

A
  • The liver has both a large functional reserve (70-80%) and a powerful regenerative ability that mean that large amounts of liver can be resected without lasting consequences.
  • The canine liver has a resident clostridial population, which will proliferate in any avascular liver tissue left behind after surgery.
125
Q

Describe the advantages and methods of surgical liver biopsy

A
  • Allows inspection of the whole liver, better control of haemorrhage and obtains larger, better-quality biopsies than percutaneous biopsy
  • Biopsy the hepatic margin by the guillotine method
126
Q

When is a partial/complete lobectomy of liver indicated?

A

Hepatic neoplasia, abscess or trauma

127
Q

Describe the pathophysiology of portosystemic vascular anomalies (portosystemic shunts)

A
  • Anomalous vessels allow blood from the portal circulation to enter the systemic circulation.
  • Ammonia and various other toxins bypass hepatic metabolism and reach the brain leading to hepatic encephalopathy.
  • The liver is deprived of hepatotrophic factors and fails to develop normally.
  • The shunting vessels may be intra or extrahepatic, congenital or acquired
128
Q

Describe the predispositions for portosystemic shunts

A
  • Purebred dogs, with extrahepatic commoner in small breeds (e.g. Yorkshire terriers, poodles, Lhasa apso, Pekingese, miniature Schnauzer)
  • Intrahepatic commoner in large breeds (e.g. GSD, Labrador, Golden Retriever, Dobermann, Irish Setter, Samoyed, Irish Wolfhound).
  • DSH cats are most often affected by congenital shunts.
  • Congenital shunts present in young animals (<1yr), acquired in older animals (1-7yr).
129
Q

List the clinical signs of portosystemic shunts

A

Poor growth, anorexia, depression, vomiting, PUPD, ptyalism (esp. in cats), behavioural changes
Some animals develop urinary tract signs due to urate urolithiasis

130
Q

What are the clinical signs of hepatic encephalopathy? (due to portosystemic shunts)

A

Ataxia
Weakness
Head pressing
Circling
Depression
Seizures
Coma

131
Q

Physical exam of an animal with portosystemic shunts may reveal?

A

microhepatica and enlarged kidneys

132
Q

Describe the results seen on routine haematology and biochemistry screening in an animal with portosystemic shunts

A

Microcytosis, mild nonregenerative anaemia, poikilocytosis (increase in abnormal RBCs), low BUN, hypoalbuminaemia, occasionally increased ALT/AST/ALKP.

133
Q

How can portosystemic shunts be medically mamaged?

A
  • Highly-digestible, moderately restricted protein diet (soy protein best).
  • Antibiotics e.g. metronidazole or ampicillin to reduce gut flora and hence toxin production.
  • Lactulose – synthetic disaccharide that traps ammonia in the colon, reduces gut transit time and thus lowers ammonia production
    Worse prognosis than surgical treatment
134
Q

Describe surgical treatment of portosystemic shunts

A

Aims to identify and gradually occlude or attenuate the shunting vessel using a variety of implants, thus redirecting blood into the portal vasculature and the liver.

135
Q

Why can surgical management of portosystemic shunts only be used in congenital not acquired shunts?

A

Attenuation of acquired shunts will cause portal hypertension

136
Q

Why do animals with portosystemic shunts get urate urolithiasis?

A
  • Poor liver function leads to decreased urea production and increased urate in serum (and thus in urine).
  • Portal blood bypassing the liver allows ammonia levels in the peripheral blood (and urine) to increase.
  • Urate plus ammonia = ammonium urate uroliths.
137
Q

What is a cholecystotomy? When is it indicated?

A

Removal of the gall bladder: performed for cholelithiasis, cholecystitis, rupture or neoplasia of the gall bladder

138
Q

When is bile flow diversion indicated?

A

For obstruction or sever trauma of the common bile duct

139
Q

What are the indications for partial pancreatectomy?

A
  • Pancreatic abscess
  • Pancreatic neoplasia: adenocarcinoma, gastrinoma, insulinoma

Y4 SA - Soft tissue surgery (8 decks)

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