dogs and cats 13 Flashcards

1
Q

diffusion barriers (sucralfate) when used, what are they, effect, indications and administration

A

chronic vomiting
- Sulphated sucrose and polyaluminium hydroxide
- In acidic environment cross polymerises to form viscous gel
○ Binds to necrotic tissue like a liquid band-aid
○ Also stimulates prostaglandin production, absorption bile salts and inactivation gastric pepsins
○ Stimulates mucosal defences
- Indications
○ Treatment of gastric ulceration (doesn’t prevent) and reflux oesophagitis
- Administration
○ Apart from food and other drugs (30 minutes except for digoxin, tetracyclines, fluroquinolones, its 2 hours)

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2
Q

histamine H2 receptors anatagnoists when used, action, indications, examples and how often need to give

A
  • Action
    ○ Competitively inhibits gastric acid secretion by 70-90% (by binding H2 receptors site on parietal cell)
  • Indications
    ○ Treatment of gastric ulceration due to NSAID, uraemia and other causes
    ○ Does not prevent NSAID-ulceration
  • Examples and how often need to give
    ○ Cimetidine (tagamet) q 6-8 hours
    ○ Ranitidine (zantac) q 12 hours
    ○ Famotidine (pepcid) q 24 hour
    ○ Nizatidine (tazac)
  • Reduce dose by 50% if impaired renal function
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3
Q

proton pump inhibitor action, 2 main examples, when used and indications

A
  • Inhibits gastric acid secretion by irreversibly binding proton-transporting enzyme at luminal surface of parietal cell
  • Complete inhibition of gastric acid secretion
    ○ More effective than H2 antagonists
    example
    1) omeprazole - mast cell tumours
    2) pantoprazole - suspected or confirm gastric ulceration
  • Indications -> ONLY WHEN STRONGLY SUSPECTED GI ULCERATION
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4
Q

prostalgandin E1 analogues main example, effect, wen used and efficacy

A

○ Misoprostol (cytotect)
○ Synthetic replcaement for PGE1 and therefore promotes gastric mucosal defence mechanisms
○ Used for prophylaxis against NSAID gastric mucosal injury (not effective as treatment)
○ Efficacy not proven in small animals

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5
Q

gastric acid suppression drugs for chronic vomiting what two drugs don’t need to give together and when should use

A

No need to give proton pump inhibitors AND histamine H2 receptor antagonists
So when should we use these drugs?
- WHEN HAVE - documented/strongly suspected GI ulceration
- NOT just cause vomiting and inappetant and primary have diarrhoea
○ Pancreatitis, cirrhosis, chronic kidney disease, gastritis, NSAID prophylaxis (only effective when 2 x dose and leads to side effects)
○ UNLESS-> these lead to GI ulceration

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6
Q

What are the 6 main GI causes of chronic vomiting and list the 3 main common first

A
  1. Inflammatory bowel disease/chronic enteropathy (diarrhoea (dogs), Vomiting (cats))
  2. Dietary intolerance/sensitivity
  3. Intestinal lymphoma (cats&raquo_space;dogs)
  4. Chronic pancreatitis
  5. Structural (pyloric stenosis)
  6. Other neoplasia
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7
Q

What are the 6 main non-GI differential diagnosis of chronic vomiting

A
  1. Hyperthyroidism (cats)
    1. Renal failure
    2. Liver disease
    3. Heart disease
    4. Hypercalcaemia
    5. Hypoadrenocorticism
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8
Q

Haematemesis what is it, is it significant and common cause

A
  • Digested blood = coffee grounds
    ○ Significant gastric ulceration or bleeding -> not always have melena (can be delayed)
  • Often concurrent melena but can be delayed
  • Significant haematemesis, especially if weight loss is also present, should ALWAYS be investigated
    ulcerated disease
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9
Q

what are the GI phyiological protections against ulceration

A

○ Gastric mucus and bicarbonate to form gel layer
○ High epithelial cell turnover (high energy requirements)
○ Tight junctions and lipoprotein layer of cells
○ Rich vascular supply
○ Protective prostaglandins (PEG and PGI2)

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10
Q

gastric ulceration what caused by and main consequences/clinical signs

A
  • Caused by anything that disrupts mucosal barrier or causes excessive acid secretion
  • Signs of melena, haematemesis, weight loss, pain and other associated disease
    Consequences of GI ulceration
  • Hypoproteinaemia
  • Anaemia
  • Electrolyte loss
  • Metabolic alkalosis
  • Pain -> due to reflux, oesophagitis, regurgitation
  • Anorexia
  • Decreased gastric motility -> GO reflux -> oesophagitis -> regurgitation
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11
Q

gastric ulceration what are the main causes

A

Primary GI disease
- gastritis, neoplasia (gastric carcinoma) - common in dogs, outflow obstruction
drugs - common - NSAIDS, corticosteroids
Systemic disease - liver disease, DIC, pancreatits (not as commo), hypoadrenocorticisim
gastric hyperacidity - gastrinomas, mast cell tumours

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12
Q

if suspect gastric ulceration for chronic vomiting what is the main approach

A
  • Rule out drugs
  • Rule out systemic disease
  • Rule out inflammatory intestinal disease
  • Rule out neoplastic disease (abdomen and elsewhere)
    ○ Any nodule find need to aspirate (mast cell tumour)
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13
Q

what inital tests to run in a chronic vomiting investigation

A
  • Haematology
  • Serum biochemistry and electrolytes
  • Urine analysis
  • T4 in cats
  • Survey abdominal radiographs (thorax if regurgitation)
    ○ Ultrasound instead for cats as wanting to rule out lymphoma
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14
Q

what is the main reasons cats vomiting and why is diagnosis more difficult in cats

A

Why would cats vomit?
- Common with concurrent disease due to anatomy
○ Intestine, pancreas and biliary tree are very close leading to disease in one resulting in disease in others
Why is diagnosis more difficult in cats?
- All chronic inflammation in gut will lead to lymphocytic-plasmacytic inflammation
○ Difficult to differentiate inflammation from small cell lymphoma
- Often chronic history
- Diarrhoea not always observed
- Pruritis may be manifested as vomiting of hair balls
○ Owner may think that is normal however for some cats if just start vomiting hairballs when normally don’t then abnormal
- Only severe disease will cause weight loss

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15
Q

What are the 6 main differentials for chronic vomiting in cats

A
  1. Metabolic disease - thyroid and kidney - rule out first
  2. Dietary sensitivity/food intolerance/dietary responsive enteropathy
  3. Antibiotic responsive enteropathy
  4. Inflammatory bowel disease (steroid responsive enteropathy)
  5. Intestinal lymphoma
  6. Chronic pancreatitis
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16
Q

dietary sensitivity in cats types, other signs related how test and what generally occurs

A
  • True sensitivity is Type I mediated
  • Usually concurrent pruritis, young cats
  • Protein most antigenic
  • GI signs resolve within 1-2 weeks and should recur with rechallenge
  • HOWEVER only about 50% of dogs signs recur with rechallenge suggesting other reason for improvement on diet
    ○ Fibre may alter intestinal microflora -> soluble fibre also increases faecal water contents
    ○ Insoluble fibre increases faecal dry matter and highly fermentable fibre may increase methane production and worsen motility
    ○ High fat diets or poorly digestible starches may prolong gastric emptying and cause vomiting
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17
Q

inflammatory bowel disease in cats definition and the 3 types - EXAM

A
  • Definition
    ○ Chronic (>3 weeks) clinical signs with inflammation within the GI tract and no identifiable cause
    ○ Usually lymphocytic-plasmacytic
    ○ Loss of tolerance to antigens
  • Due to confusing nomenclature, now classified as:
    ○ Food responsive (not food allergy)
    ○ Antibiotic responsive (not speicific infection)
    ○ Immunosuppressive responsive (only true IBD)
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18
Q

Feline lymphoma what generally presents as, what are the 2 types, which good and which bad

A

present as chronic vomiting

a. Small cell lymphocytic -> one found in the gut, lymphocytes look normal
b. Large cell (lymphoblastic) -> large granular cells - BAD

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19
Q

Small cell lymphocytic lymphoma in cats general presentation, type of cell, diagnosis, predilection site

A

§ Well, older cat with chronic vomiting
§ Usually T lymphocytes extending up from bottom to top villus
§ Cells small, with minimal features of malignancy
§ Immunohistochemistry and PCR clonality testing to help distinguish from IBD
§ Predilection site: distal ileum

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20
Q

small cell lymphocytic lymphoma diagnostic difficulties and potential causes

A

§ Diagnostic difficulties
□ Not always changes on ultrasound and if so not pathognomonic (inflammation or neoplasia)
□ Where to biopsy and how
□ How to interpret the biopsy -> PARR testing useful
§ Potential causes
□ Genetic predisposition
□ Any chronic inflammation -> IBD, helicobacter
□ Cigarette smoke exposure
□ FIV

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21
Q

Large cell (lymphoblastic) lymphoma what cells, age, results in/character and prognosis

A

§ B and T lymphocytes, no effect on prognosis
§ Cats of any age
§ Rapidly progress, and form transmural masses and spreads to lymph nodes
□ Cats are sicker than with small lymphoma, signs of intestinal obstruction
§ Large granular lymphocytes highly malignant and metastasise to other sites
§ Poorer prognosis

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22
Q

Crhonic pancreatitis in cats, what generally reported with, clinical signs and diagnosis

A
  • Up to 100% reported with concurrent disease
    ○ Hepatomegaly, thickening intestines
  • Cause or consequence
  • Even more vague clinical signs
    ○ Anorexia, lethargy, vomiting, diarrhoea, weight loss, jaundice
  • Diagnosis
    ○ Little to no change bloods (no change lipase and amylase, TLI and PLI not helpful)
    ○ No real sensitivity in ultrasound
    ○ Pancreatic biopsy -> only way
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23
Q

What are the 5 main clinical priorities when presented with well but vomiting cat

A
  1. Examine to ensure no physical abnormalities
  2. Obtain full dietary history
  3. Rule out metabolic disease if indicated
    ○ Hyperthyroidism
    ○ Renal disease
    ○ Cholangiohepatitis/cholescystitis
    ○ Pancreatitis
  4. Treatment trial (work from top down)
    - diet
    - antibiotics
    - immune suppressive
  5. diagnosic investigation if treatment trial don’t work
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24
Q

treatment diet trail for well but vomiting cat which diet, when should see response and 3 possible outcomes and what to do

A

§ Which diet
□ Hydrolyzed or novel protein source
□ High soluble fibre content
□ Restrict access to other food
§ Should see response in 1-2 weeks
□ If do, continue diet for 6 months if completely balanced, and then can try other or previous diets
® Approx 50% won’t relapse
□ If partial response
® Can try alternative hydrolyzed or hypoallergenic diet -> may be variable individual response
□ If no/minimal response to diet
® Is cat still well, no loss in weight or dropping albumin
® Is there an increase in liver enzymes (cholangiohepatitis, but ruled out hyperthyroidism)
® OPTIONS -> Antibiotics, alternative diet or diagnostic pathway (if owner wants to know what is going on)

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25
Q

Treatment trail antibiotics for a well but vomiting cat which use, when respond and what if don’t

A

§ Amoxicillin 20 mg/kg bid for up to 6 weeks
§ Metronidazole 10mg/kg bid for maximum 3 weeks
§ Again should respond within 1-2 weeks and after 3-4 week course may only need dietary management
§ IF STILL NO RESPONSE TO DIET - need to ‘support’ the cat and happy with diagnosis move onto BELOW

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26
Q

Treatment trail with immune suppressive for well but vomiting cat what is the main thing to use, why and options for administration

A

§ Nutrition, micronutrient and fluids
§ Cobalamin
□ Supplementation improves clinical signs in cats with GI disease
□ This is regardless which diagnosis and treatments
□ Options
® Treat and measure response or
® Treat empirically (250ug injection once weekly for 4-6 weeks)

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27
Q

Diagnostic investigation if treatment trail don’t work or want to find out exactly what is happening on a well but vomiting cat what are the 3 main options, what good and bad about each

A
  1. Ultrasound
    ○ May be normal or show loss of layering with IBD, small cell lymphoma
    ○ May show masses, lymphadenopathy, focal intestinal thickening or effusion and can get samples
  2. Endoscopy
    ○ Limitation access to biopsy - good quality biopsy takes experience and training
    ○ Gastric good
    ○ Overlap with IBD in intestine
    ○ Tricky to get ILEUM -> access from the colon
  3. Exploratory laparotomy
    § Increased morbidity
    § Increase yield
    § Can assess disease outside of intestine
    § Can biopsy ileum easily
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28
Q

what are the 4 main options for treatment of IBD

A

1) prednisolone
2) other corticoteroids - not as effective - dexamethasone, budesonide
3) other immunosuppressives - chlorambucil
4) other therapies - not properly evaluted - mega-3 fatty acids, probiotics - don’t use

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29
Q

treatment for IBD prednisolone, when taper, what use with and side effects

A

○ Start to taper every 3-4 weeks until reach minimum effective dose
○ Continue diet and continue antibiotics for first 2 weeks of prednisolone
○ Side effects
§ PU/PD and alopecia (minimal)
§ Development of diabetes is a risk

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30
Q

treatment for IBD otehr corticosteroids what are the 2 main ones when give and main issue

A
  • not as effective as above
    ○ Dexamethasone
    § Only if cannot give oral medication and not eating well enough to place in food
    § 1/6th to 1/8th the oral pred dosage q 36-48
    § Profound immune suppression
    ○ Budesonide
    § Not evaluated in cats
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31
Q

Other immunosuppressives for treatment of IBD when use, what are the 2 options and which is better and why

A
○ Only if histologic diagnosis 
1. Chlorambucil 
§ Current choice as add on 
§ Generally well tolerated 
2. Ciclosporin 
§ Be careful with latent toxoplasmosis 
§ Not evaluated in feline IBD
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32
Q

treatment for IBD other therapies what are the 2 main options, when use or not

A

not properly evaluated
1) Omega-3 fatty acids
§ May interfere with palatability of diets, and cause diarrhoea
2) Probiotics - waste - DON’T USE
§ Lack of translational benefits in people
§ Well tolerated in cats
§ Recent abstracts suggests not effective in feline IBD

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33
Q

small cell lymphoma in cats, prognosis in terms of response to therapy and median remission

A
  • This is a ‘good’ tumour
  • Response to therapy 75-90%
  • Majority of cats alive and in remission at 2 years
    ○ Median remission 897 days
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34
Q

treatment of small cell lymphoma

A
  • Still support (cobalamin)
  • Still antibiotics and diet
  • Initial therapy
    ○ Prednisolone 3mg/kg once daily, reducing to 1-2mg/kg once daily when have clinical remission
    ○ Chlorambucil 2mg q 48 hours, 15mg/m^2 q 24 x 4 q 3 weeks, 20mg/m^2 q 2 weeks
    same as IBD
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35
Q

If treat IBD and small cell lymphoma the same do we need to differentiate?

A
  • DIFFERENTIATE VIA -> Immunohistochemistry and PAR sample

- Important due to prognosis -> IBD better prognosis than small cell lymphoma

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36
Q

what is a common concurrent disease to IBD in cats and treatment

A

Cholangiohepatitis/cholecystitis - most common
○ Antibiotics
○ Vitamin K if severe

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37
Q

large cell lymphoma prognosis in terms of remission, median time, when good

A
  • Complete remission in 50-75%
  • Overal median remission 4-8 months, overall MST 6-8 months
  • Have longer survival if initial good response
  • Often unwell, so need nutritional support
  • Recent study shows bacteraemia in cats with LC lymphoma
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38
Q

large cell lymphoma in cats treatment basics and main options

A
Treatment basics 
- Cobalamin 
- Antibiotics 
- Nutritional support 
Treatment options 
- Palliative prednisolone 
- Palliative surgery 
- Multi-agent chemotherapy 
- Radiation therapy
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39
Q

patient preparation for GIT surgery what are the 4 main considerations

A

1) Common disturbances:
○ Dehydration
○ Electrolyte imbalances:
§ Hypochloraemia, Hyponatraemi, Hypokalaemia
○ Acid-base disturbances:
2) Treatment/correction of these pre-op problems important to:
○ Optimise outcomes
○ Prevent complications
3) Fasting for elective procedures can minimise risk of spillage but decreases gastric fluid pH
4) If gastro-oesophageal reflux anticipated –consider H2 antagonist or proton pump inhibitor
○ Rapid induction and airway control if vomiting reflux likely (prevent aspiration)

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40
Q

what are the 5 regions of the stomach and why important in surgery

A
  • Cardia - terminal part of oesophagus, gastro-oesophageal sphincter
  • Fundus - can be affected during GDV
  • Body - largest part
  • Pyloric Antrum - funnelling down into smaller cylinder -> WHERE DO GASTROPEXY
    Pylorus - outflow of stomach, muscular sphincter into proximal duodenum
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41
Q

what are the 7 main branches off the aorta

A
  1. Hepatic branch
    1. Splenic artery
    2. Celiac artery
    3. Cranial mesenteric artery - supplies all intestines
    4. Renal artery
    5. Testicular/ovarian
  2. Caudal mesenteric - colon
42
Q

drainiange of the GI tract, where go, why important in PSS

A

DRAINIAGE -> all to the portal vein -> liver -> recirculation of bile salts
- Important with porto-systemic shunts -> portal vein and caudal vena abnormal communication -> bile salts and other facts bypass liver -> hepatic encephalopathy

43
Q

what are halsteads principles for surgery

A
  • Gentle tissue handling
  • Accurate apposition of tissue layers
  • Preservation of vascular supply
  • Accurate haemostasis
  • Prevention of contamination
  • Recognition and appropriate treatment of contamination
44
Q

surgical appraoch to GI surgery what is needed, incision, equipment and approach

A
  • Adequate visualisation of the entire abdomen is important:
  • Ventral midline coeliotomy:
    ○ Xiphoid to pubis
    ○ Balfour Abdominal Retractors - self-retaining -> hold abdominal wall apart
    ○ Laparotomy Sponges
    ○ Suction - poole suction tip -> prevent contamination of GI content
  • Examine the ENTIRE gastro-intestinal tract:
    ○ Systematic -> cranial left first
    ○ Visual & Tactile –pulses, peristalsis, colour
  • Don’t miss the second lesion
45
Q

Antibiotic use in GIT surgery what used for what, is it continued post op

A

§ Agents present in tissues at time of incision (30 mins)
§ Selected for efficacy vs expected organisms
§ 1st generation Cephalosporins OK for gastric and small intestinal procedures
§ 2nd generation for colonic procedures (also mixed infections generally)
§ Not continued > 24 hrs post-operatively unless break in asepsis

46
Q

what is the bacterial load within stomach, small and large intestine therefore what antibiotics to use

A

§ Stomach 102/ gram - FIRST GENERATION
§ Small Intestine 104 / gram - FIRST GENERATION
§ Large Intestine 1010 / gram –also ^ No’s Anaerobes - SECOND GENERATION

47
Q

Spillage of GI contents within GI surgery what results in and 4 main ways to reduce contamination

A

○ Clean contaminated -> contaminated - DUE TO BREAK IN ASEPSIS
§ Without appropriate treatment -> peritonitis, death -> broad-spectrum antibiotics
- Techniques to reduce gross contamination / spillage:
a. Orogastric intubation -> help with feeding after surgery - PLACE PRE SURGERY
b. Isolation –moistened laparotomy sponges
c. Stay sutures –large full thickness bites
d. Suction

48
Q

What are the 4 steps that need to perform once gross contmaination of GI surgery has occurred

A
  1. Prophylactic antibiotic therapy becomes therapeutic antibiotic therapy
  2. Therapeutic therapy initiated with empirically selected agents based on expected organisms BUT MODIFIED based on microbial CULTURE & SENSITIVITY from sample taken AFTER LAVAGE
  3. Debridement of gross materials/contaminants
  4. Lavage 200-300ml/kg (Seim1995)
    ○ Reduction in bacterial load
    ○ Removal of adjuvant materials
    ○ Removal of inflammatory mediators
49
Q

peritoneal lavage when done, when change gloves and equipment, what use at what temp

A
  • Perform routinely prior to abdominal closure if hollow viscus entered
  • Change gloves prior to lavage
  • Use separate instruments to close post-lavage
  • Lavage fluids 37-39 degrees C:
    ○ Cooler fluid exacerbate hypothermia
    ○ Warmer fluids result in vasodilation →hypotension and increases adhesions
    ○ isotonic
  • All natural fluid and irrigation fluid is removed following lavage:
    ○ Residual fluid reduces immune clearance of debris and micro-organisms and is an adjuvant for peritonitis
    ○ Poole Suction tip
50
Q

Gastrotomy/gastrectomy what are the main indications and where cut stomach and why

A
- Indications:
○ Removal of Gastric Foreign bodies
○ Removal of neoplastic lesions
○ Removal of severe focal mucosal erosive lesions
○ Removal of necrotic stomach wall (GDV can occur) 
○ Obtain Biopsy samples
- Ventral Stomach Wall:
○ Relatively avascular area
○ Long axis vs short axis
○ Position influenced by indication
51
Q

Suture material and patterns used in stomach

A
  • Synthetic monofilament absorbable materials are preferred: - swayed on
    ○ Reduced tissue trauma from tissue drag
    ○ Reduced wicking
  • Taper point needle–smaller holes vs cutting
  • 2-layer simple continuous appositional closure:
    ○ Mucosa/Submucosa - higher collagen content -> appositional simple continuous or interrupted
    ○ Serosa/muscularis
52
Q

what are the 3 main indications of using stapling in stomach, how works, advantages and 2 types

A
- Indications:
○ Gastrotomyclosure (rare)
○ Gastrectomy(reduces spillage)
○ Anastamosis
- Deploy 2 or more rows of titanium staples:
○ Rows of staples may be of same or different sizes
○ +/-integrated knife for tissue division
- Advantages:
○ Rapid
○ Consistent spacing and closure
- Types 
1. Linear Staplers
2. circular staplers
53
Q

What is the most important post-operative consideration with gastrotomy, what decreases this and therefore results in

A
  • Want to get them eating as soon as possible
  • Gastro-intestinal motility can be reduced by:
    ○ Handling
    ○ Desiccation
    ○ Incision –Disturbs myoelectricalconduction from pacemaker
    ○ Opioids AVOID
    ○ Pain
    ○ Recumbency/lack or early ambulation
    ○ Lack of enteral nutrition
  • Poor motility results in:
    ○ Pain
    ○ Anorexia
    ○ Vomiting
    ○ Gastric distension
54
Q

What are the 4 main post-operative therapies for gastrotomy

A
  1. Analgesia
  2. IVFT to:
    ○ Replace ongoing loss
    ○ Supply Maintenance
    ○ Maintain perfusion
  3. Prokinetic Therapy:
    ○ Cisapride, Ranitidine, Metoclopramide, Erythromycin
  4. Enteral (into staomch) or parenteral (into bloodstream (bypass stomach)) nutrition
55
Q

What are 4 main indications for immediate enteral or parenteral nutrition

A

○ Patients without adequate nutrition for 3 or more days
○ Evidence of more than 10% weight loss
○ Inadequate mm mass
○ Serum albumin < 2.5 g/dLin cats / <2.1 g/dLin dogs

56
Q

Enterotomy what is it, indications and technique

A

opening of the small intestines
- Indications: - determined via clinical signs, history, imaging
○ Foreign body removal
○ Access to the major duodenal papilla for common bile duct cannulation
○ Tissue biopsy
- Technique
1. Isolation of affected segment:
§ Moistened laparotomy sponges
§ Milk chyme away from incision
§ Assistant finger clamps or Doyen intestinal forceps
2. Anti-mesenteric incision through UNAFFECTED intestinal wall
3. Suction to remove luminal fluid

57
Q

Enterotomy closure pattern, what include, bites and size, what also used to closure commmonly

A
  • Closure
    ○ Single layer appositional (simple continuous, simple interrupted, staples) -> start above the incision site
    ○ Submucosa provides suture holding strength
    ○ Everted mucosa may be trimmed if required
    ○ Sutures must engage submucosa–full thickness passage easiest.
    ○ 3mm bites –Full thickness -3mm apart
    ○ 3/0 for larger dog, 4/0 for cat or smaller dog
  • Omentalisation:
    ○ Perform routinely
    ○ Vascular supply, seals leaks
58
Q

intestinal biopsy what needed, 2 techniques and complications

A
  • Full thickness samples for histopathology:
    ○ (if endoscopic bxfails or location unsuitable)
    ○ Multiple sites (Gastric, duodenum, jejunum, LN)
    ○ Colon generally not sampled routinely due to increased risk of more significant complications
  • Techniques:
    ○ Suture Lift Wedge
    ○ Dermal punch biopsy - full thickness of the wall
  • Not benign procedure –12% incidence of peritonitis and death (Shales 2005)
    ○ Attention to technique important
59
Q

Enterectomy what is it and 4 main indications

A
intestinal resection and anastomosis 
- Indications:
○ Severely damaged intestine
○ Damage to segmental vascular supply
○ Intestinal neoplasia
○ Segmental incarceration/strangulation
60
Q

enterectomy what is the 6 steps within

A
  1. Isolate segment and identify good mesenteric vessels
  2. Milk chyme from site
  3. Doyen intestinal forceps
  4. Ligate vasculature
  5. Excise tissue –ensure sufficient tissue extends from Doyen forceps to increase ease of closure
  6. closure - Suture onto mesenteric side, knot OUTSIDE OF LUMEN, second suture on antimesenteric side (simple interrupted)
61
Q

What are the 3 main closure techniques for enterectomy

A

1) end to end - most common
2) side to side - functional end to end
3) mucosal eversion

62
Q

end to end closure in enterectomy what is involved

A

□ Most commonly performed technique
□ Appositional patterns recommended:
® Inverting patterns narrow lumen
® Everting patterns increase adhesions
® Apposition -> Primary healing & rapid bridging of the mucosal defect
® Single layer appositional closure:
◊ Simple continuous –separate each side i.e.180 degrees then180 degrees
-> avoids purse-string effect
◊ Simple interrupted
} Correct tension produces apposition without crushing tissues.

63
Q

Side to side clousyre in enterectomy what equipment needed and how occurs

A

□ GIA staplers x2 or 1
□ Antimesenteric border -> puts row of staples down combining the two ends, cut in the middle of the 2 suture rows to create an opening between the two side, then staple up the top off and cut (creating pants)

64
Q

what are the 3 ways to manage luminal disparity within enterectomy

A

§ Vary spacing of sutures - mild sparsity only
§ Transect smaller segment a an angle (sort side is anti-mesenteric to preserve blood supply)
§ Spatulation of smaller segments -> linear incision along antimesenteric border to increase lumen diameter

65
Q

enteroplication/enteroenteropexy what is it, main indications and why controversial

A

stitch intestines together
- Indications:
○ Prevention of recurrence of intussusception (Oakes 1994)
○ Performed over small intestine from jejunum to ileum:
§ Recurrence at site distant from original site
§ Avoid kinking and sharp bends
§ Sutures must penetrate submucosa
- Controversial
○ Rate of complications > rate of recurrence (Applewhite2001)
○ High experimental morbidity in cats (Nash 1998)

66
Q

List the 5 main complications of enteroplication/enteroenteropexy

A

1) gastro-oesophageal reflux
2) septic peritonitis
3) adhesions
4) short bowel syndrome
5) ileus

67
Q

gastro-oesophageal reflux complication when generally occur and results in

A

○ May be silent
○ Reported in 57% of orthopaedic cases (Wilson 2006)
○ Likely higher in GIT surgical cases -manipulation
○ Results in oesophagitis and if severe potentially stricture
○ Shorter periods of fasting may increase gastric fluid pH

68
Q

septic peritonitis complication how common, when geatest risk and some risk factors

A

○ When occurring in the post-operative setting –most commonly assoc with enterotomyor anastamotic dehiscence
○ 7-16% incidence (Hosgood1988, Allen 1992, Ralphs 2003)
○ 12% incidence after full thickness biopsy (Shales 2005)
○ Risk Greatest in debridement phase 3-5 days post-op
§ Risk Factors:
□ Pre-operative peritonitis
□ Presence of a Foreign body
□ Hypoalbuminaemia
□ Delayed enteral Feeding

69
Q

adhesions as complication in GI surgery how common in what species, 3 main contributing factors and what may result in

A
○ Less common in dogs/cats than in humans and horses due to active fibrinolysis
○ Contributing factors:
§ Ischaemi- Haemorrhage
§ Foreign Bodies
§ Infection
○ May result in obstruction
70
Q

Short bowel syndrome what is it, due to, high risk and results in

A

○ Malabsorption from lack functional length of small intestine:
§ Reduced surface area
§ Gastric and intestinal hyper-secretion
§ Bacterial Overgrowth
§ Decreased transit time
○ Risk if > 50% length resected
○ Proximal resection better tolerated vs distal
○ Results in persistent diarrhoea, steatorrhea, weight loss, electrolyte disturbances

71
Q

short bowel syndrome treatment and prognosis

A

○ Appropriate treatment and time -> adaptation:
§ Increase in villus length and crypt depth (over 3 mths)
§ Fluid and electrolyte therapy
§ Early enteral nutrition:
□ Fibre is a key component:
® Stimulates adaptation, modulates motility, ^ water absorption, Binds bile salts -> reduces secretory diarrhoea
□ Glutamine –preferred energy source for enterocytes
§ If unsuccessful –loperamide/ antimicrobials
○ Prognosis –variable (length resection, presence ICV)

72
Q

Ileus when common, clinical signs, treatment/prevention

A
○ Common after GIT surgery -> Careful handling
○ High sympathetic tone
○ Clinical Signs:
§ Pain, Vomiting, Regurgitation, Abdominal Distention (NB similar to peritonitis)
○ Treatment/prevention
1. Correct underlying causes:
□ Sepsis
□ Electrolyte disturbance
□ Uraemia
□ Pain
2. Prokinetics
□ Metoclopramide, Ranitidine, Cisapride
3. Early Enteral Nutrition
73
Q

What are the 12 steps in the pathophysiology of septic peritonitis

A

1) peritoneal defecnce mechanisms compromised
2) intense inflammation reaction
3) pro-inflammatory mediations -> PG’s -> increase vascular permeability
4) third space of fluid, albumin, clotting factors
5) protein loss -> coagulopathy
6) systemic inflammation and microthrombi - SIRS
7) fluid loss and vasodilation -> decrease CO
8) reduced perfusion - anaerobic metabolism
9) acidosis secondary
10) catecholamine and cortisol response -> increase O2 demand
11) poor perfusion, disruption mucosal barriers -> bacterial translocation
12) endothelial damage and circulatory stasis promoter hypercoagulable state

74
Q

What are the 3 things acidosis forms secondary to with septic peritonitis

A

○ Poor perfusion of organs
○ Poor renal perfusion inhibits renal buffering mechanisms
○ Reflex rigidity inhibits ventilation

75
Q

what are 4 molecules that can act as a adjuvants for peritoneal inflammation

A

○ Gastric mucin –anti-complement effect
○ Bile salts –lower surface tension and lyse RBC’s releasing Hb
○ Haemoglobin –Hb interferes with phagocytic cell chemotaxis and phagocytosis and provided Fe for bacterial metabolism
○ Barium

76
Q

what are the 3 types of peritonitis and common causes

A

○ Primary Peritonitis:
§ Peritonitis without identified cause
§ FIP, monobacterial infections (Culp 2009)
○ Secondary:
§ Most common –leakage of intraluminal content from GIT or urogenital tracts.
§ Polymicrobial
§ Mortality rates up to 85% (Ralphs 2003)
○ Aseptic/Sterile Peritonitis:
§ Inflammation without infection (pancreatitis, desiccation, surgical biomaterials, gossypiboma (retained surgical sponge), Chemical –urine and non-septic bile)

77
Q

what are the 5 goals of surgical management of peritonitis

A

a. Identify and correct cause
b. Reduction bacterial load
c. Removal of gross contaminants and inflammatory mediators
d. Prevention of recurrence
e. Provide route for enteral nutrition

78
Q

identify and correct cause for peritonitis what is the most common cause, risk factors

A
  • GIT perforation/leakage most common cause (47-63%)
  • Previous abdominal surgery is a significant cause of Septic peritonitis (46% cases had surgery in 2 weeks prior to presentation)
  • Risk factors for peritonitis after surgery:
    ○ Pre-operative Peritonitis
    ○ Hypoalbuminaemia
    ○ Intestinal FB
  • Leakage rates from full thickness biopsy 12%
    ○ Increase total bacterial load and percentage of anaerobes aborad
79
Q

what are 7 other causes of leakage from GIT leading to peritonitis

A

1) necrosis from GDV
2) penetrating FB
3) trauma
4) ulceration with perfusion - NAIDS
5) feeding tube leakage
6) pancreatitic abscess
7) pyometra

80
Q

what are the 7 steps within diagnosis/treatment of peritonitis

A

1) midline laparotomy
2) debridement - removal of source
3) lavage
4) omentalisation
5) serosal patching
6) closure and drainge
7) post operative support

81
Q

Midline laparotomy to identify perionitis source where incise and what need to do

A

○ Xiphoid to pubis

○ Full and systematic examination of the peritoneal cavity (see previous lecture on laparotomy)

82
Q

debridement and lavage in treatment of peritonitis what is involved and what don’t need to use

A
  1. Debridement - remove the source
    ○ Removal / repair of source: (examples)
    § Cholecystectomy
    § GIT Resection and anastomosis
    § Liver lobectomy
    § Ovariohysterectomy (Pyometra)
    ○ Suture biomaterials with prolonged absorption profile
  2. Lavage
    ○ Reduction in bacterial load, removal of adjuvant materials and inflammatory mediators
    ○ 200-300ml/kg
    ○ Addition of AB or antiseptics has no reported benefit and may result in chemical peritonitis
    ○ Intraperitoneal iodine induces toxicity and chemical peritonitis in dogs
83
Q

Omentalisation when generally used and why does it help

A

○ Described for prostatic abscesses, pancreatic cyst and pseudocysts
○ Successfully used for plugging 20mm duodenal defects
§ Healing complete at 8 weeks
○ Omental wrapping:
§ Seal small leaks
§ Provide drainage & immunocompetent cells
§ Vascular supply and angiogenenic potential
§ Wrapping to prevent omentalisation resulted in leakage and septic peritonitis (McLaughlin 1973)

84
Q

serosal patching why used in peritonitis, what results in, where recommended and does it help

A

○ Peritonitis associated with increased risk of dehiscence (Crowe 1984)
○ Proteolytic activity results in collagen degradation
○ Serosal patching recommended for anastomoses and areas of hollow viscusorgans with potential for leakage (Crowe 1984):
§ Placement of serosa of healthy small intestine loops over focal regions of hollow viscous organs suspected of being unhealthy
○ Reduced mortality in a canine experimental model

85
Q

List the 4 options for closure and drainage of peritonitis surgery

A

1) primary closure without drainage
2) primary closure with drainage
3) open peritoneal drainage
4) VAC laparostomy

86
Q

Primary closure without drainage for peritonitis what are the 4 situations used in

A

® Primary problem identified and addressed
® Bacterial load reduced and residual contamination minimal
® Mortality rate 46%
® ICU care and plasma not available –preclude open abdominal drainage

87
Q

primary closure with drainage for peritonitis what drain most commonly used, potential problems but benefits

A
Jackson-Pratt drains most common - negative pressure resulting in fluid flow from abdomen 
□ Potential problems:
® Nosocomial infection
® Occlusion of drains with omentum
® Ineffective drainage
□ Benefits include:
® Reduced risk evisceration
® Reduced risk nosocomial infection
® No need for second sxprocedure to close abdomen –but cannot inspect viscera
88
Q

Open peritoneal drainage in peritonitis main benefits and technique

A

□ Benefits reported:
® Improved removal of bacteria, foreign material and inflammatory mediators
® Improved O2 tension –reduces anaerobe survival
® Affords early planned, serial re-exploration
□ Technique
a) Cranial 1/3-2/3 of the linea alba left partially open with a loose simple continuous monofilament suture pattern (1-6 cm gap)
b) Falciform ligament excision
c) Tack omentum to areas of leakage to prevent occlusion of opening
d) Sterile technique for bandage changes –in surgical suite under GA –allows serial re-inspection
e) Bandages weighed to assess fluid loss□ Mean open drainage duration 4 days in retrospective clinical studies (Greenfield 1987, Woolfson1986)

89
Q

open peritoneal drainage for peritonitis what criteria for closure, complication and is it done commonly

A

□ Criteria for closure unclear but recommendations: (Woolfson1986)
® Improvement in colour and clarity of drainage fluid
® Reduction in volume drainage fluid
® Absence bacteria on cytology
® Repeat culture at closure –40% patients had different MC&S results (Greenfield 1987) and positive results increased mortality (Woolfson1986)
□ Nosocomial infection recognised complication
□ Superiority of open drainage not established in any trials in clinical reports in either humans or animals
→ Not done very commonly

90
Q

VAC laparostomy for periontitis how different from open, time to closure and why consider

A
® Visceral protective layer (?)
® Open cell foam
® Suction catheter
® Circumferential Occlusive film seal
® Continuous Negpressure -75-125mmHg via Suction unit
® Changed q 48 hrs
□ Time to closure: 2 days
□ Reduced morbidity &amp; Mortality in Humans vs Open Drainage - CHOOSE THIS OVER OPEN DRAINAGE
91
Q

What are the 4 main post-operative support factors needed for peritonitis cases

A

a. Analgesia
b. Enteral nutrition –maintain protein, glutamine maintains enterocyte health
c. Maintenance fluid, electrolyte, acid-base balance
§ Protein energy imbalance major contributor to mortality (Tennant 1993)
d. Feeding tube placement as proximal as possible to maximise physiology unless a contraindication for proximal GIT use exists
○ Jejunostomy has the highest rate complications 17-42% (Orton 1986)

92
Q

prognosis for peritonitis treatment mortality rate and survival rate for open drainage, primary closure, closed suction drainage and vaccum

A
  • Mortality rates remain high 20-70% (Hosgood1988) 85% Ralphs
  • Published survival rates:
    ○ Open drainage 52-80%
    ○ Primary closure 54%
    ○ Closed suction drainage 70%
    ○ Vacuum 50%
93
Q

what are the 4 things that fasting leads to, why important and which is best for intestinal mucosal health

A

Fasting leads to:
- Intestinal mucosal atrophy
- Increased enterocyte apoptosis
- Change in mucin composition
- Decreased glutamine and arginine transport
Role of nutrition
- Prognosis is poorer if negative nitrogen balance
ENTERAL NUTRITION is best for intestinal mucosal health
- Decrease cytokine production
- Increase mucosal blood supply and stimulate local growth factors

94
Q

what are the 3 main interventional nutrition for GI diseases and which most common

A
  1. Partial parenteral nutrition - only supplies part of nutrition and energy - not common
  2. Total parenteral nutrition
  3. Assisted enteral nutrition - most common
95
Q

total parenteral nutrition what does it require, how fast, what need to add

A
  • Requires central venous catheter
    ○ Strict asepsis required - longer length of time - gloves, aseptic technique needed
  • Gradual introduction to full RER
    ○ At least 40 mEq/L potassium to prevent refeeding syndrome
  • Also amino acids (not taurine), dextrose and lipids
    ○ Not calcium or fat soluble vitamins
    ○ Lipid reduced if high serum triglycerides
    ○ Protein content reduced if hepatic/renal disease
96
Q

what are the main complications of parenteral nutrition and the most common one

A
  • Mechanical
    • Phlebitis
    • Thrombosis
    • Septic
    • Metabolic
    • Gut atrophy - most common
97
Q

enteral feeding what is so good about it and what need to consider post intestinal surgery

A
  • BEST ONE TO USE
    ○ Reduction inflammatory markers
    ○ Reduction intestinal permeability
    ○ Improved survival
    ○ Improved morbidity
    What about post intestinal surgery?
    Balancing act
  • Concern about healing intestinal incision
    -Best way for intestine to heal is to be healthy
  • Best way for intestine to be healthy is to be fed
98
Q

enteral feeding what are the principles and how long for in certain situations, what if able to eat, vomit or doesn’t want to

A

Principles
- Ensure all other treatments adequate
○ Fluid/electrolyte
○ Analgesia
○ Anti-emetic
- Ensure no coagulopathy
- Assess anaesthetic risk
How long for?
○ Short-term if end-end anastomosis or post GDV (max 24 hours)
○ Short-term fine (< 48 hours) in mild-moderate cases pancreatitis
○ Majority of mild-moderate cases will resolve
- If able to eat, and wants to eat then feed a low-fat food
- Don’t stop feeding if one break-through vomit
- Avoid food aversion in hospital by force feeding

99
Q

Assisted nutrition what are the 2 options positives and negatives

A

1) NO - nasooesophageal tube
- needs to be long enough to sit in distal 1/3 oesophagus
- Oxygen catheters or soft infant feeding tubes - very small so small amount of food
- Will need to feed Ensure or equivalent in Aust/NZ supplemented with whey protein after first 24-48 hours
2 )Oesophagostomy tubes
- My technique of choice with ≥ 3 days no food including pre-hospital)
- Technically easy to place
- Allows for thicker liquid and blended foods
- Well tolerated
- Can commence feeding immediately
- Requires general anaesthesia for placement - PLACE IN DURING SURGERY
- Can lead to SEVERE gastric reflux if placed into the stomach
○ Don’t feed when animal recumbent and feed slowly

100
Q

Oesophageal tube what size for cat and dog and what is important in the management

A
  • 12-14 F cats
  • 16-18 F larger dogs
    Management
  • Clean and change bandage daily for 3 days then q 2-3 days
  • Can use as soon as awake
  • Check position before feeding and flush before and after feeding
  • Can remove easily -> just remove sutures and remove