cats and dogs 14 Flashcards
What are the 13 steps in insertion of a oesophagostomy tube
- GA
- Right lateral recumbency - oesophagus access on left hand side
- Clip and prep cervical area left side
- Pre-measure tube to apex of heart and mark tube
- Push forceps through mouth and point up and out ½ way down the neck.
- Make a stab incision over the forceps tips
- Enlarge incision so forceps can push through hole
- Grab end of tube
- Pull back towards mouth-expand opening if wish
- Turn the tube around in mouth and push down the oesophagus
- Do a little wiggle/flip and ensure kink is gone and no tube in mouth
- Pull out to predesignated spot, quick skin prep
○ Ensure positioned in the right spot via endoscope (preferred) or radiograph - Secure with pursestring then a chinese-finger trap suture with non-absorbable suture material
Gastrostomy (G tubes) what used for, main consideration, biggest risk
type of enteral feeding BUT more for referral
- Long-term nutritional support
- Use 16-20 F tubes
- Must stay in place for 7-10 days
- Biggest risk is gastric wall necrosis, peritonitis
Gastrostomy (G tube) advantages and disadvantages
Advantages
- Long term (months to years) feeding
- Can be fed at home
- Good for oesophageal disease
- Big tubes
Disadvantages
- Need to wait until feed (up to 24 hours????)
- Must be in at least 2 weeks before stoma forms
- If stoma breaks down get septic peritonitis
- Need some specialised equipment
- Gastric wall necrosis possible
How to much to feed with nutritional management after abdominal surgery in cats and dogs (equations and illness factor)
Dogs
- Only multiply by an illness factor once they are tolerating RER amounts (1.2-1.4 dogs)
- RER = 70 (BW)0.75 or 70 + 30(BW)
Cats
- Only multiply by an illness factor once they are tolerating RER amounts (1.2-1.4 depending on activity)
- RER = 40 x BW (kcal)
What are the goals in nutritional management after abdominal surgery how many meals per day, what feed day1-4
- The goal is not to get to full RER quickly (or even at all)
○ Divide into 4-6 meals per day
○ Day 1: only feed 25% calculated requirements
○ Day 2: 50%
○ Day 3: 75%
○ Day 4: 100% - Stay at lower levels if not tolerating
what are some tips for nutritional management after abdominal surgery
- Bolus, intermittent much better
○ Walk around, keep in sternal during feeding
○ Walk around if possible afterward- • - LUKEWARM
- Push food in slowly
- Flush with bolus of water at start and at end
- Reduce IV fluid amount, especially in cat-
- If blocked-Coca Cola or pineapple juice
- First feeds should be < 10 mL/kg
- Don’t stop if one break-through vomit
what to feed for nutritional management after abdominal surgery
- No evidence one way or the other
- If lipaemic, avoid high fat foods
- Otherwise, completely balanced with reasonable fibre and protein
Immunomodulators what do they do, main example what it does and 2 other examples
- Added substances to improve gut health:
- Experimental models only
- Glutamine
○ Amino acid used by enterocytes as energy source
○ Reduces villus blunting and bacterial translocation
○ Variable outcomes in human studies, but safe except in renal or hepatic disease
○ Difficult to supplement in enteral formulations - Short chain fatty acids (acetate, butyrate, proportionate)
- Omega-3 fatty acids
When use with assisted enteral, partial parenteral, total parenteral, immunodulatory and probiotics
- Assisted enteral ○ As soon as possible, virtually all cases - Partial parenteral ○ Only until enteral is tolerated - Total parenteral ○ Only if enteral not tolerated - Immunodulatory ○ Don’t know yet - Prebiotics/Probiotics ○ Don’t know yet but not in pancreatitis or post-op
what are the 7 F’s for abdominal distention diagnosis
- Fluid
- Fat
- Faeces
- Flatus
- Feel a big mass
- Floppy
- Foetus
fluid causing abdominal distention presentation and clinical signs
- Fluid wave on ballotment
- Fluid elsewhere in the body
- Other clinical signs
○ Temperature
○ Jugular vein -> distention suggests increase in hydrostatic pressure
○ Body condition
fluid causing abdominal distention what is the most important step and types within
DETERMINE TYPE OF FLUID
- exudate -blood, chyle, urine, neoplastic, infectious, inflammatory
- ascites - low protein, low cell fluid - MOST COMMON
- modified transudate
- pure transudate
exudate what is the most likely causes
§ Blood -> a little bit sometimes with bleeding tumours of liver and spleen § Chyle -> can be but rare § Neoplastic -> can be but rare § Infectious -> FIP can cause § Inflammatory -> can but rare
ascites fluid what are the 2 types and main causes
= low-protein, low-cell count fluid - MOST COMMON
○ Modified transudate
§ Increase vascular permeability OR increase hydrostatic pressure
□ Jugular distention and pleural effusion common clinical signs of increase hydrostatic pressure
□ EG -> portal hypertension, caudal to diaphragm -> abdominal effusion
□ EG -> cardiac or vena cava disease -> abdominal and pleural effusion
○ Pure transudate
§ Decrease in oncotic pressure, albumin <15g/L
□ EG -> hypalbuminaemia -> all cavities +/- dependent oedema
Physical exam -> fluid-filled abdomen (not painful), RR 60 breaths/min, HR 140bpm, Temperature 38 degrees, can’t hear lungs sounds ventrally, jugular vein distended, no cyanosis or pallor WHAT DOES THIS SUGGEST, causes and diagnostic plan
Ride-sided CHF
- Leads to increase in hydrostatic pressure
- Causes
○ Right atrial mass
○ Tricuspid valve disease
○ Pulmonic stenosis
○ RV cardiomyopathy
○ Pericardial effusion - cannot fill during diastole and increase pressure on right ventricular wall
§ Even after drainage of pleural effusion heart sounds still muffled as still fluid between you and heart
- Diagnostic plan
○ Radiograph - don’t want the animal to die!!!
○ Thoracocentesis - do this first
§ Then drain chest and ultrasound or radiograph
○ ONCE CONFIRM PERICARDIAL EFFUSION -> tap the pericardial sac -> will be bloody but blood WILL NOT CLOT
What are the 2 main mechanisms of low protein, disease leading to protein loss and 4 main causes
Causes of low protein - Decreased production - liver disease -> WILL ALSO SEE -> low urea, glucose, bile acid stimulation - Increased loss -> skin (can usually tell), urine (only albumin lost, confirm with urine via cystocentesis (urea:creantine protein ratio) , GI tract (albumin and globulin, can also have low lymphocytes or cholesterol) Protein-losing enteropathy 1. Severe IBD 2. Neoplasia 3. Lymphangiectasis 4. Intussusception
8 weeks old kitten, Brought in by breeder, distended and fluid filled abdomen, lethargy, dullness, pale mucous membranes
- No signs of pleural fluid and fluid is an exudate
WHAT IS IT, types and how expressed and greatest mortality in
Feline infectious peritonitis
- FIP is a virulence biotype of feline enteric coronavirus (FECoV)
- FECoV shed intermittently weeks to months and can be re-infected
- How host responds determines if no clinical signs or wet FIP (completely overwhelmed) or dry FIP (bi-modal, low grade inflammation and may hide in cells until older, present again at 10 years)
- FIP greatest mortality YOUNG cats
Feline infectious peritonitis what are the 2 main presentations and clinical signs associated - EXAM
FIP - wet
- Most common presentation is abdominal effusion
- Possible conjunctivitis
FIP - dry
- NOT ABDOMINAL DISTENTION - just inflammatory
- Higher involvement of central nervous system and eyes (conjunctivitis)
- Harder to diagnose
what are the 4 important diagnostic tools for the diagnoses of feline infectious peritonitis - EXAM
- History and signalment
- Haematology
○ Mild-moderate anaemia
○ Stress leukogram - Biochemistry
○ Hyperglobulinaemia
○ Organ-specific changes with dry FIP - Fluid analysis
○ May have green-yellow appearance
○ Often mucinous
○ Rivaltas test in clinic
○ Immunohistochemistry of fluid confirms disease - most common
○ RT-PCR
what are some causes of fat or floppy causes for abdominal distention
FAT - Hypothyroidism - Hyperadrenocorticism - Obesity FLOPPY - Loss of dorsal muscle mass - Hyperadrenocorticism
chronic abdominal pain what are likely causes
- More insidious and more likely to be referred pain - pain could be elsewhere in the body
○ Chronic inflammation pancreas, urinary tract
○ Chronic gastric dilation
○ Gastric ulceration
○ Infiltrative neoplasia
○ Functional intestinal spasm
○ Musculoskeletal disease
Diagnosis for true chronic abdominal pain and are some differentials
1) any -itis - pancreatitis, gastritis etc
2) any ulceration
3) any distention, torison or compression - intestinal spasm main chronic one
4) Non GI -> intervertebral disc, fractured ribs, soft tissue injury, pleural disease
what is the approach to animals with chronic abdominal pain
- Full and thorough history
- Physical examination
- Radiographs
○ Lateral abdomen (+spine) + thorax - ANALGESIA -> important don’t want for full diagnostics
- Ultrasound if indicated
- Additional testing:
○ Urine analysis/culture
○ Pancreatic lipase
○ Endoscopy
Chronic pancreatitis breed, why difficult to diagnose and differentials
- Breed predisposition - cocker spaniels
- Difficulties in diagnosis
○ No specific clinical signs
○ No specific clinical pathology changes
○ No reliable change in PLI
○ Intermittent in nature - Differentials
○ Same as vomiting but include IBD
Chronic pancreatitis how to get diagnosis and treatment
- Definitive diagnosis - histopathology
○ then?, how?, why? - target treatment, possible effect on diabetes control or development of exocrine pancreatic insufficiency
○ Exploratory laparotomy - Treatment
○ Treat concurrent disease
○ Rule out (and treat) predisposing causes
§ Hyperlipidaemia
○ Analgesia when needed - gabapentin
○ Anti-inflammatory medication - prednisolone (0.5mg/kg - dog - at anti-inflammatory doses NOT immunosuppressive)
○ Anti-emetics when needed - not chronic
○ No evidence for diet except if hyperlipemia
what does the presence of detectable diarrhoea indicate
- The large intestine cannot cope with excess quantities of fluid entering from the small intestine
- Large intestinal function is in some way compromised, either by abnormalities of the wall or the contents of faeces
What are the 4 pathogenesis of diarrhoea
1) osmotic diarrhoea
2) secretory diarrhoea
3) increased permeability
4) deranged motility
OFTEN COMBINATION
what occurs with osmotic dairrhoea
○ Occurs when there are hyperosmolar solutes in the intestinal lumen
○ Water flows in to equal plasma osmolality
○ Sodium follows down the concentration gradient into the lumen (as the intestinal fluid is diluted) and brings more water
○ Large volume, watery diarrhoea generally doesn’t persist during fasting
what occurs with secretory diarrhoea
○ Characterised by an increase in the active ion transport mechanisms that are normally present
○ Net stimulation of secretion and inhibition of absorption
○ Lesion is biochemical
○ Associated with fluid overload of the large intestine
○ Typically, passage of large volumes of isotonic fluid and persists during fasting
what occurs with increased permeability diarrhoea
○ Permeability changes occur with diseases which there is disruption of the gut mucosa and/or an increase in the tissue pressure in lamina propria - generally more chronic
○ In both cases, the changes in permeability cause water and electrolytes to be secreted rather than absorbed
○ Retention of electrolytes then also creates an osmotic gradient
○ May also lose red cells and proteins
what occurs with deranged motility
○ Changes in intestinal motility rarely a primary cause of diarrhoea in animals
○ Increased motility contributes to diarrhoea in most diseases in some way
○ Increased motility may actually be protective mechanism
○ Increased intestinal transit time decreases exposure to toxins - if slow gut down can increase exposure to toxin
What are 6 systemic diseases that effect small intestinal function
- Thyroid
- Exocrine pancreas
- Adrenal
- Vasoactive peptides - tumour of pancreas - RARE
- Increased hydrostatic pressure
- Liver disease
what are the 8 main differentials for diarrhoea
- Primary lymphangiectasis
- Dietary indiscretion
- Dietary sensitivity
- Lymphoma or other diffuse neoplasia
- IBD
- Neoplastic partial obstruction
- Viral, protozoal, bacterial, fungal, parasitic infection
- Partial FB obstruction
What is important with history for diarrhoea
1) history of diarrhoea - long, changed, continuous
2) SI vs LI
3) melena - indicates gastric or small intestinal bleeding
4) steatorrhea -> undigested fats in faeces (exocrine pancreatitis insufficency)
5) other signs - altered appetite, weight loss, abdominal distention/pain, vomiting, borborygmi (stomach noises)
6) background infor - vaccination, medications, prphylaxis (worming), diet, environemnt, scavenger
in terms of diarrhoea history/physical exam what is considered serious and not so serious
What is considered serious - Steatorrhea, polyphagia - Significant weight loss - Palpable abnormality - Geriatric animal (older) or paediatric (more likely infectious) - Evidence of hypoproteinaemia, anaemia - Unwell or dehydrated - When considered serious from owner When not serious so treat without investigation - Sick but likely self-limiting cause - Not sick - Owner constraints - When just diarrhoea
diarrhoea what are the basics of non-specific treatment essential and controvesial
- Essential ○ Fluid and electrolyte replacement ○ Diet ○ Fenbendazole - to ensure don't have giardia - Controversial ○ Motility modifiers ○ Antibiotics
diarrhoea investigation baseline data what are the main screenign tests
- Haematology
- Biochemistry (including electrolytes)
- Urine analysis
- T4 (Cats)
- Trypsin-like immunoreactivity (TLI) cats and dogs to test exocrine pancreatic function
○ Circulating trypsin
Screening tests for diarrhoea what can this tell you and what if you don’t find anything
What can this tell you -Low protein - Anaemia - Evidence of metabolic disease - Nothing If don't find anything - Animal is well ○ Can elect treatment trail ○ Can start diagnostics (less to more invasive) - Animal is sick or has lost body weight ○ Need to start diagnostics ○ Can start supportive treatment in meantime
What are 9 additional diagnostics for further investigations for diarrhoea
- Serum trypsin-like immunoreactivity (TLI)
- Serum folate (B9) and cobalamin (B12)
- Pancreatic lipase - NO DIFFERENCE
- Faecal analysis
- Other lab testing
- Imaging
- Biopsy
- Endoscopy
- Exploratory laparotomy
Serum trypsin-like immunoreactivity (TLI) what measures, when reduced, indication and when DON’T USE
○ Reduced in exocrine pancreatic insufficiency
○ Measures circulating trypsin and trypsinogen
○ Indication
§ Breed
§ Clinical signs - skinny, bright and happy, steatorrhoea, polyphagia
§ Previous history pancreatitis
§ Cats: not typical clinical signs as for dogs
○ This is not a test for a sick dog or cat
§ Generally dogs are WELL therefore don’t delay other diagnostics in SICK dog while waiting for TLI
Serum folate (B9) and cobalamin (B12) where abosrbed and therefore when low, what need to interpret with
○ Folate absorbed by specific carriers in proximal jejunum - produced by bacteria
○ Cobalamin absorbed by receptor-mediated endocytosis in ileum, required intrinsic factor (produced by pancreas)
§ Inherited defects of B12 absorption in giant schnauzers and border collies
○ Cats and dogs with chronic GI diseases often low serum cobalamin
§ Can’t interpret accurately in dogs without TLI
□ If normal TLI and decrease cobalamin then have small intestinal disease
§ Exocrine pancreatic insufficiency
□ Cobalamin decrease 74%, folate increase 32%
§ Bacterial overgrowth
□ Increase folate, decrease cobalamin
