Dogs and Cats 22 Flashcards
1
Q
General history of a blocked cat and what need to differentiate
A
- Most have dysuria/stranguria ○ But sometimes owners haven’t noticed - Owners cannot differentiate between ○ Dysuria or dyschezia? ○ Stranguria vs. pollakiuria, polyuria, incontinence or behavioural? ○ NEED TO ASK QUESTIONS TO DETERMINE - Urethral obstruction or just cystitis?
2
Q
Talking to owners with a blocked cat what need to keep informed and their options
A
Three levels of care - keep informed - without highest level of care increase risk of recurrence
1) Unblock and home - (Ugh!)
2) Hospitalisation for one day
○ Catheterisation
○ Indwelling catheter
○ IV fluids
3) Hospitalisation as long as it takes
○ Catheterisation
○ Indwelling catheter until urine is clear
○ IV fluids
○ At least one day in hospital after catheter removal - majority are dysuric after this point - need to ensure inflammation NOT REBLOCKED
3
Q
Is azotaemia prognostic use for a blocked cat
A
- Magnitude of azotaemia is of no prognostic use - generally doesn’t have renal failure afterwards
○ Azotaemia takes days to resolve
4
Q
unblock the cat in treating a blocked cat preparation and equipment needed
A
- GA -> if sick - opioid and benzo, not sick - ketamine
- Equipment
○ Unblocking catheter
○ Sterile lube
○ Flush solution and syringe
○ Lidocaine
○ Indwelling catheter
○ Tape
○ Nylon on a straight needle
○ Adapter for urinary catheter
○ Empty fluid bag with IV tubing
○ Two people
5
Q
unblocking a blocked cat preference for unblocking and indwelling
A
- My preference for unblocking
○ Kendall Sovereign Sterile Tom Cat Catheter
○ 5 ½ inch
○ Open ended - My preference for indwelling
○ Kendall Sovereign Sterile Feeding Tube and Urethral Catheter - doesn’t kink
○ 5 French (3 ½ only if you are desperate)
6
Q
Unblokcing the cat technique up to draining the bladder
A
a. Dorsal or lateral recumbency with hip flexion -> dorsal best as can visualise
b. Get someone else to extrude penis
§ If cyanotic (chronic obstruction down into penis) -> squeeze and twist may just unblock
c. Massage penis and urethra
d. Pass lubricated urinary catheter 3-4 mm into tip of penis at first
e. Allow penis to return into prepuce then pull prepuce caudally and dorsally to straighten urethra - TO AVOID URETHRAL WALL
f. Twist and gently advance catheter
g. Attach extension set to catheter
h. Short, sharp flushes with 20ml syringe while twisting and advancing catheter - want to dilate the urethra
Cystocentesis? - NO -> some cats can get uroabdomen - RISK
7
Q
Unblocking the cat from draining the bladder
A
i. Fully drain bladder
j. Flush bladder repeatedly with isotonic electrolyte solution until urine is as clear as possible
k. Palpate bladder while flushing to evacuate sediment
l. Inject 0.5 ml lignocaine while withdrawing catheter (don’t overdo it!)
m. Fully drain bladder
n. Pass 5F flexible urinary catheter (indwelling catheter) (flush while advancing)
§ 2-4cm passed the pelvic brim
o. Secure with tape butterfly & mattress suture either side of prepuce
p. Secure catheter to tail (tape to catheter then tape to tail)
q. Attach to closed collection system or IV tubing and attach to empty IV fluid bag
r. E collar always
8
Q
Further treatment and monitoring after unblocking a cat
A
- Fluid therapy:
○ Initially 5-10 ml/kg/hr if euvolaemic & no contraindications
○ Then modify on the basis of urine output, PCV/TS, electrolytes and PE hydration status
○ Modify IV fluid rate to exceed urine output by maintenance and replacement requirements - MBS parameters q 2-12 hrs
- Urine output q 4-6 hrs
- PCV/TS/electrolytes q 2-12 hrs
- Consider need for analgesia and anti-inflammatory drugs
○ Personally I don’t want NSAIDs anywhere near possibly sick kidneys - Initially no antibiotics, prolonged corticosteroids or bethanechol - predispose to infection
9
Q
After unblocking the cat what to do with catheter and after removal what to do
A
- Leave urinary catheter in >24 hrs or until urine is clear (well kinda!)
- After catheter removal consider:
○ Wait 24 hours - cystocentesis, urine analysis (dipstick and sediment) - see if have signs of infection - THEN TREAT ANTIBIOTICS
○ +/- culture
§ Prazosin > phenoxybenzamine, ?dantrolene
§ Prob. not diazepam
10
Q
what are the basics in treatment for blocked cat
A
- Major body system assessment first
- ALWAYS stabilise before unblocking
- There is NO contraindication to rapid fluids
- Treat severe hyperkalaemia aggressively
○ Calcium gluconate is treatment of choice
○ Treat the patient not the number
11
Q
Blocked dogs how to diagnose and remove
A
Radiograph
- Ensure the legs are pulled forward to see the
- Fabella often sit where urethra is
Retrohydropulsion
- Anesthetise the dog
- Catheter in of penis, hold of end of penis
Someone else feel ventral area of urethra (through rectum) and compress and lift off -> moves calculi into bladder
12
Q
Uroliths do they cause obstruction, common and less common types, crystalluria what is it, is it normal, treatment needed
A
Uroliths
- Can cause urethral and rarely ureteral obstruction
- Multiple types
- Can be mixed / compound
- Common: Struvite, Calcium oxalate, ammonium urate (dogs)
- Less common : Cystine, calcium phosphate
Crystalluria
- Urolith vs. Crystals
- Can be normal
- Crystals ≠ Urolithiasis or stone forming tendency
- Alone does not justify treatment
- May be “in vitro”
13
Q
What are the 5 main factors affecting urolith formation
A
- Supersaturation of urine
- +/- Presence of an organic nidus - suture material within bladder urine -> crystals can precipitate out onto and come together
- Reduced solubility (urine pH)
- Presence of crystalization inhibitors or promoters
- Retention of crystals within urinary tract
14
Q
What are the main causes of uroliths and signs
A
- Genetics [breed]
- Diet
- Infectious agents (UTI)
- Life style
- Systemic disease
Signs
○ Subclinical (e.g. nephrolith)
○ Mild: LUT signs
○ Severe
○ Life threatening : obstruction
15
Q
What are the main ways to diagnose uroliths
A
- History
- Clinical signs (palpation) - can be small - may not be able to palpate
- Plain radiology +/- contrast
- Ultrasound
- Urinalysis
○ Fresh & non-refrigeration, in-house - Stone analysis
16
Q
What are some factors that help you guess urolith type and which types are common
A
- Age ○ young - urates (liver shunting, liver disease) ○ Older - Calcium oxalates - Breed - Gender ○ Female - struvite ○ Male - calcium oxalates - UTI - Crystals - pH ○ High - struvite ○ Low - calcium oxalate - Radiographic density ○ Calcium oxalate - show up well on radiographs - Size & number - Serum abnormalities
17
Q
Feline urethral plugs structure, what leads to and most common
A
- Typically > 50% matrix
- Mucoprotein gel ‘traps crystals’ -> rigid plug -> obstruction
- MOST COMMONLY STUVITE in LUT
18
Q
Treatment of uroliths
A
- Identify and treat any predisposing causes
○ Renal - nephroliths -> hard to treat, generally leave unless issue
○ Ureteral - harder due to stricture issues - stenting works well
○ Bladder -> multiple options, laparoscope,
Send stones / urethral plugs for quantitative analysis
19
Q
Key points of treatment of all uroliths
A
- Increased risk with bacterial UTI and in genetically predisposed individuals
- Therapy aims to reduce risk of recurrence
- Increased water intake, decrease USG
- Encourage urination - wet food diets, water fountains
- Avoid predisposing causes
- Treat all infections > 3 weeks and up to 3 months - may
- If UTI, re-culture urine 1 week post antibiotics (treat like complicated UTI)
20
Q
Dog struvite signalment, prediposing cause and what need to investigate
A
- Females > Males
- Tend to be small white fluffy dogs
- 3-8 years
- Most infected - main predisposing cause
○ Urease producing
○ Gold standard to culturing bladder wall, often just do urine or urolith - Radiodence, smooth
- Urine pH > 7
- Investigate for predisposing causes of infection
○ Underlying incontinence, prostatitis
21
Q
Struvite treatment
A
- Baseline plain radiographs ○ Number, size, location, density - Antibiotics ○ 3-4 weeks past dissolution - Diet (acidify the urine - C/D) ○ 3-4 weeks past clear radiographs - Urinalysis ○ Every 2 weeks - Monitor radiographs ○ Monthly - Time to dissolve - can be as quick as 2 weeks, 6 months within kidney ○ Within urethra or ureters CANNOT DISSOLVE
22
Q
Struvite prevention and when get recurrence
A
- Treat UTI
- (Feed preventative diet) -> don’t normally need - just treating underlying infection
- Monitoring: Aim pH 6 – 6.5, low USG, sediment
- Reoccurrence : - 40-55% without changing management (1% with C/D)
○ UTI
○ Poor monitoring
○ Poor owner compliance
○ Lack of removal of all stones surgically
23
Q
Calcium oxalate signalment, recurrence, predisposing, diagnosis and treatment options
A
- Male > Female
- Average 5 – 12 years old
- High reoccurrence rate as genetically driven generally
- May be metabolic / genetic factors
- Check for ↑[Ca]
- Treatment
○ Surgery
○ Voiding Uro-hydropropulsion
○ Lithotripsy
○ Cannot dissolve with diet once formed!
24
Q
Treatment of calcium oxalate uroliths and monitoring
A
- Reduce crystal forming substances ○ Calcium ○ Oxalate ○ Increase pH ○ Lower USG - makes a large difference - Diet - Rx concurrent disease Monitoring ○ pH 7 – 7.5 (+/- K citrate) ○ USG < 1.020 to reduce risk of formation ○ Sediment ○ Radiographs every 3-6 months
25
Calcium oxalate recurrence and how to prevent
- High recurrence rate especially 6 months – 3 years
- Even with ideal prevention
- Consider Vitamin B6 supplementation
- Consider Hydrochlorothiazide diuretics
26
Urate uroliths what made of, form within, look, causes and dissolution
- Ammonium urate, uric acid, sodium urate
- Form in acid urine
- Radiolucent, smooth, round or oval
- Dalmatians
○ Genetic
○ Often male, 1-5 years old
- Others
○ Liver: shunts, dysplasia, failure
- Urate crystalluria in Dalmatians
- Dissolution: Low success rate
27
Urate uroliths treatment/prevention and monitoring in dalmatians
- Diet - reduce protein and purines -> U/D diet
- Allopurinol (xanthine oxidase inhibitor) - for dalmatians to block formation of uroliths
- Monitor
○ Rx UTI
○ pH 7 – 7.5
○ USG < 1.020
○ Ultrasound / contrast radiographs every 2-3 months as dissolving
○ [TP], [Alb] q 6 months -> should be coming down to ensure dietary therapy is successful
○ +/- Surgery
28
Urate uroliths treatment/prevention and recurrence with other breeds
- Liver disease – hepatic diets (e.g. L/D)
- No detectable liver pathology (e.g. hepatic / renal diets)
- Recurrence
○ 30-50% within one year of Sx
○ Lower risk if > 9 year (14%) vs. < 5 years (60%)
29
Cystine uroliths signalement, look like, forms in what urine and causes
- 100% males
- Relatively radiolucent, round, smooth
- Age 3 – 8 years
- Staffy, Australian cattle dogs, Rottweilers
- Formes in acid urine
- Inherited proximal tubule defect - RECURENCE NORMAL
- Abnormal transport of cystine by renal tubules
○ +/- other amino acids
30
Cystine uroliths treatment/prevention and recurrence
```
- Reduce protein (cysteine, methionine)
○ Diet – Hill’s u/d
- Increase pH ≥ 7.5 (K citrate - add this to get there)
- USG < 1.020
- Low Na diet
- (2-MPG if available)
- Penicillamine
○ Increased solubility of cystine
- Recurrence in 2-12 months unless take steps to prevent
○ Less recurrence if > 5 years old
```
31
cat uroliths what associated with most common, which form plugs and dietary aims for prevention
- 15 – 23% of FLUTD cases
- Uroliths: Struvite > Calcium oxalate
- Plugs : Most Struvite
- Dietary aims
○ Control urine pH
§ more important when comes to struvite - average 2 weeks for dissolution
○ Minimise building blocks of stone
§ Struvite dissolution / prevention: ↓Mg ,↓ P
§ Calcium oxalate prevention : ↓Ca, ↓Oxalate
○ Increase water intake -> ↓ USG
32
Define oliguria, anuria and polyuria
Oliguria - less than expected urine output, can be physiologic, pathologic or caused by partial urinary tract obstruction or rupture, various values have been used to define, in a hydrated, well-perfused patient, less than 1ml/kg/hr can be considered absolute and 1-2ml/kg/hr can be considered relative oliguria
Anuria - essentially no urine production, never physiologic and indicates the most severe form of renal disease or complete urinary obstruction
Polyuria - is generally defined as being above 2ml/kg/hr unless recieveing IV fluids above maintenance rates
33
Risk factors for developing acute kidney injury, what all lead to
- Shock
- Pre-existing renal insufficiency
- Concurrent cardiovascular disease
- Sepsis
- Use of diuretic and potentially nephrotoxic drugs
They all lead to hypotension and therefore hypoperfusion of the kidney
34
What are the 3 main life threatening problems from acute renal disease and how to treat
1) bradycardia, hyperkalaemia (and hypoperfusion) - calcium gluconate
2) presumptive hypocolaemia
3) metabolic acidosis
all acute resuscitative fluid therapy
35
What are the 3 main pathogenic changes in acute kidney injury and what clinical manifestations then occur
1. Vascular dysfunction
○ Decreased RBF, GFR, oligoanuria
§ Azotaemia, hyperphosphataemia, hyperkalemia
2. Glomerular dysfunction
○ Decreased GFR, oligoanuria
§ Azotaemia, hyperphosphataemia, hyperkalemia
3. Renal tubular epithelial injury
○ Casts, proteinuria, glucosuria, oliguria
§ Loss of regulation of water, lytes, acid-base
36
What are the principles of treatment of acute kidney injury
- Damage is done
- Support them through the complications associated with loss of renal functions
- Wait for recovery phase
- Potentially chronic kidney disease - is owner okay to manage this medically
37
What are the 8 steps in the treatment of acute renal injury
1. Correction of perfusion abnormalities and fluid deficit
2. Correction of acid-base and metabolic emergencies (hyperkalaemia and acidaemia)
3. Determination of pre-vs. renal vs. post-renal injury (or a combination thereof)
4. Determination of UOP, establishing urine production
5. Discontinue substances with nephrotoxic potential
6. Treating any treatable etiologies
7. Provide intensive supportive care and nutritional support and
8. Renal replacement therapies such as dialysis - not really available in Australia
38
Acute kidney injury correction of perfusion abnormalities, acid-base, metabolic emergencies (first 2 steps) how done
1) fluid therapy
- Goal is to stabilize animal and determine UOP, THEN to maintain a neutral fluid balance
- Acute resuscitative fluid therapy –your normal approach -> balanced isotonic crystalloids
- After resuscitation and rehydration, “maintenance” could be anything… depends on UOP:
Generally -> dehydration x body weight in kg = deficit to be replaced over 4-6 hours
2) Correction of metabolic derangements
- Main issue if blocked - hyperkalaemia
○ Indications include: measurement of serum potassium, detection of inappropriate bradycardia (or normal) in very sick Hypoperfused animal -> suggests this
39
How to avoid overhydration when giving fluid therapy for acute renal injury
```
- Recognize safety limits
○ Central venous pressure
○ Body weight
○ Respiratory effort
○ Oedema - mainly pulmonary oedema
- If occurs all fluid therapy must be stopped
```
40
Other metabolic derangements besides hyperkalaemia to correct for acute renal injury
- Metabolic acidosis… fluids will help A LOT… may need to consider sodium bicarbonate
○ Risks include: metabolic alkalosis, hypernatremia, paradoxic cerebral acidosis
- Sodium can be anywhere… rate of change is imp
- Phosphorus. Typically high. Can cause Hypocalcemia
- Magnesium. Typically high. Can cause hypokalaemia.
- Calcium. Can be anywhere. Use as little as possible (but use it prn)
- Hypertension. Treat but avoid precipitous decline.
41
In terms of prognosis is pre, renal, post or CKD, AKD worse
- Pre, renal or post-renal?
○ Pre and post renal causes have a better prognosis and are generally reversible
- CKD, AKD or both?
○ Acute or chronic kidney injury (acute worse prognosis)
42
In acute renal injury treatment determine urine output and how to initiate urine output
- COULD BE AT ANY OF THE BELOW POINTS AT ANY TIME
○ Anuria -> oliguria -> normal -> polyuria
○ Generally oliguria at the beginning and then progress to polyuria -> this is where the real issue is as if losing too much will be hypoperfusion of a sick kidney -> further damage
Initiating urine output
○ Furosemide -> need to get into the nephron to work (works at the luminal Na-K-2Cl symporter in thick ascending loop of Henle
§ Thus renal blood flow and filtration must be intact for it to work
§ Increase dose to establish urine output
○ Mannitol -> needs to get into glomerulus to work (therefore do not use if hypovolaemic)
§ Osmotic diuretic -> Increase intravascular space - possible for fluid overload if unable to perform glomerular filtration therefore if still no urine output with mannitol STOP THE TREATMENT
43
In the treatment of acute renal injury where is the decision making point and options
```
- Failure to induce UOP with repletion of fluid deficits indicates severe renal parenchymal injury
○ Euthanasia
○ Referral
○ Renal replacement therapy
§ Peritoneal dialysis
§ Intermittent haemodialysis
§ Continuous renal replacement therapy
○ (Ongoing medical management)
○ Regeneration
§ 4-12 weeks
```
44
in acute renal injury what things need to be monitored and managed
HR, ECG, blood pressure, respiratory rate, effort, auscultation, central venous pressure, measure urine output, calculate in and outs, body weight, electrolytes, acid base, pain management, nutrition, blood work
45
Prognosis for acute renal injury with the types
- Have the potential to recover partial or complete renal function
- Fair to good in patients with pre- and post- renal causes that are reversible and treated
- Mild non-oliguric intrinsic AKI carries a guarded prognosis with recovery possible after 3-6 weeks
- Oliguric AKI carries a guarded prognosis bit sudden onset of gradual return of function is possible over 4-12 weeks
- Anuric AKI carry grave prognosis for recover without dialysis
Can do renal transplantation for certain individuals in select centres mainly in north America
46
Chronic kidney disease how common, what occurs and at what percentage do you see PUPD and azotaemia and is it reversible
- More common than acute renal failure
- Gradual loss of nephrons over long time -> generally large reserve so don't see until advanced
○ 33% of remaining functional nephrons -> onset of PU/PD
○ 25% -> azotaemia
○ ONCE LOSE cannot replace nephrons > total GFR will never be as it once was
- Primary cause often not determined
- Generally irreversible
- Chronic reflects rate of loss of renal function (not abruptness of clinical signs)
47
What are the main causes of chronic kidney disease
```
- Inflammatory / infectious
○ Pyelonephritis, leptospirosis
- Glomerular disease
○ Glomernephritis
- Metabolic
○ Hypercalcaemia, hypertension
- Congenital
○ Persian - polycystic kidney disease
- Immune mediated
- Neoplasia
- Renal toxins & ischaemia
- Progression from acute renal failure
```
48
Chronic kidney disease staging why important, what stages on and what stages mean what
Important to stage as changes treatment
Main thing they are staged on is creatinine levels -> different from cats and dogs
Want to be diagnosing at stage 1 - reduce concentrating ability (won't see changes in BUN yet)
- Aim of stopping or slowly progression of disease
Stage 3 - patients that are systemically unwell
49
Clinical signs for chronic kidney disease
- Often vague & non specific
- Polyuria, Polydipsia
> 100 ml/kg/day dogs
> 50-60 ml/kg/day cats eating dry food
> 10 ml/kg/day cats eating tin food
- Dehydration
- Anorexia, Lethargy
- Weight loss
- Dull coat
- Nocturia
- Cervical ventroflexion
- Hypertension + complications
- GI ulcers, halitosis, oral necrosis, vomiting, diarrhoea
- Pallor
- Tachypnoea
- Hypothermia
- Small hard irregular kidneys (sometimes large)
- Tremor
- Osteodystrophy
- Arrhythmias
- Immunosuppression
- Blindness
- Seizures, coma, death
50
Chronic kidney disease diagnosis
- Via clinical & typical laboratory findings
- Haematology
○ Non regenerative anaemia, stress leukogram, leukocytosis (infection)
- Biochemistry
○ Azotaemia, ↑P, ↓K, ↑Amylase, ↑Lipase
- Urinalysis
○ Impaired concentrating ability
○ +/- Proteinuria
○ C&S (consider in every case)
- +/- Prolonged BMBT (buccal mucosal bleeding time)
- +/- Renal biopsy in select cases
51
Measuring renal function what are the 3main ways and what results
- GFR is gold standard – yet cumbersome, $
- Creatinine – yet affected by muscle mass, age, breed, sex
○ Late biomarker
- SDMA – by product of protein arginine methylation - main one used now
○ Reflects GFR
○ More accurate, sensitive, earlier detection of CKD than creatinine levels
52
What are the 5 main chronic kidney disease treatment aims
1) Ameliorate the clinical signs of uraemia
2) Identify and treat underlying / primary processes
3) Minimise disturbances associated with water / electrolyte / vitamin / mineral loss
4) Support adequate nutrition
5) Modify progression of renal failure
53
Nutrition for chronic kidney disease what does it do when and how done
- “No other single therapeutic modification is more likely to enhance the long term outcome of patients with CKD than a renal diet”
- Delays clinical signs, reduced uraemic crisis, improved quality of life, delays progress, increased survival
- When and how done
○ Start early (stage 2 onwards)
○ Introduce slowly
§ Can take 4-6 weeks to transition with fussy cats
○ Start at home
○ Should be > 90 % diet
○ Renal diet ≠ Senior diet
54
What are the components of renal diets
```
○ Protein restriction - avoiding excessive protein workload for kidney
○ High caloric density - fat and carbohydrate
○ Phosphate restriction
○ Omega 3 supplementation
○ Antioxidants
○ Potassium supplementation
○ Alkalinisation
○ Sodium restriction
○ Water soluble vitamin supplementation
○ Water
```
55
Providing Hydration with chronic renal disease what is involved
- Ad. Lib water: fountains, bowls, encouragement, tin / wet foods, broths
- SC fluid therapy: small patients, stage 3 or 4, balanced electrolyte solutions, q 1-3 days
- IV fluid therapy
- O tube: medications, water, food, at home
56
What are the 4 main underling conditions that need to be treated for those with chronic renal disease
1) hypertension
2) proteinuria
3) anaemia
4) renal secondary hyperparathyroidism
57
hypertension in relation to chronic kidney disease, what occurs in, associated with, percentage and result
- Cause / consequence of CKD
- Loss of renal auto-regulation -> glomerulus exposed to hypertension -> further renal damage
- Associated with increased risk of uraemia & death
○ Important to monitor during check ups
- 30% dogs with CKD are hypertensive
- Results in end organ damage to :
○ Eye, Kidney, Cardiovascular system, Brain (common)
58
Measuring blood pressure where and how done, and what is normal
- Quite environment
- Owner present
- No sedation
- 5-10 min for patient to acclimatise
- Gentle restraint (cuff level with heart) - lateral recumbency
- Cuff width 40% of limb / tail circumference
- Record cuff size, limb
- Same operator each time
- Discard first result
- Average of 5 – 7 readings (each reading within 20%)
100-160 normal
Anything above 160 getting high, above 180 too high
59
Proteinuria in chronic kidney disease animals what does it do and how measured
- Reduces survival
○ Inflammation and damage to tubules
- Increased risk of uraemic crisis
- Quantitatively measured by a urine protein: creatinine ratio (UPC)
○ Single urine sample
Cut off different in cats and dogs
Interpret in light of serum creatinine levels
60
Treatment and monitoring for hypertension and proteinuria
- Rx / correct underlying process
- ACEi: Vasodilate efferent arteriole: lower intra-glomerular filtration pressure-> reduce drive for proteinuria
- Ensure not dehydrated - can be nephrotoxic
- Aim to half or normalise UPC
- Monitor serum creatinine after 1-2 weeks
○ Allow no more than < 30% increase
○ Stable [creatinine] + ↓ UPC = good response
○ ↑ [creatinine] +/- ↑ UPC = progressive disease
- Or Angiotensin receptor blockers
○ Telmisartan
61
Anaemia secondary due to chronic renal disease what due to, results in and treatment principles
- Due to ↓ EPO, ↓ RBC survival, ↑ RBC loss, plasma erythroid inhibitory substances, nutritional abnormalities
- Resultant hypertension and SNS activation and hypoxia promotes further renal injury
Treatment principles
○ Control GI bleeding
○ Transfusion (pRBC > whole blood)
○ Anabolic steroids NOT recommended
○ Erythropoietin
62
Anaemia secondary to chronic renal disease treatment and in cats
- Recombinant human EPO (rHuEPO)
○ For dogs with clinics signs and PCV < 20-22%
○ SC 1-3 times / week + Iron supplementation
○ Monitor PCV weekly
○ Expensive
○ Corrects anaemia, improves quality of life
○ Development of antibodies limits use
§ 50% dogs develop these, but only 33% have worsened anaemia
- Cats
○ 30-65% have anaemia
○ rHuEPO or Darbepoietin SC + Iron - generally respond within 1-5 weeks
○ Increased PCV, improves quality of life and survival in responders
63
Renal secondary hyperparathryoidism from chronic renal disease what seen treatment and what if low ca
- ↑ PTH
- +/- ↓ iCa / Tca
- Absorption from bone - rubber jaw
- Rx: Low P diet
- If ↓ Ca: Rx Calcitriol
○ Monitor iCa
○ Avoid ↑ Ca
○ Prolongs survival
○ Not used in cats
64
Prognosis of chronic renal disease, what depends on and prognostic factors in dogs and cats
- Variable, depends on
○ Clinical signs, severity and rate of progression, what can be reversed, age, quality of care (vet and owner)
- Establish prognosis after accurate staging and correcting reversible factors
- Cats > Dogs
- Progressive disease
- Prognostic factors
○ Cats: IRIS stage, proteinuria, anaemia, weight loss, phosphate, uroliths causing obstruction
○ Dogs (less known): IRIS stage, proteinuria, hypertension, weight loss, increasing age
65
With neurological cases what are you thinking it terms of remembering possible differentials
```
- DAMNIT-V
○ D - degenerative
○ A - auto-immune, anomies, allergic
○ M - metabolic
○ N - neoplasia and nutritional
○ I - idiopathic, infectious, inflammatory
○ T - toxic
○ V - vascular accident
```
66
Neurological cases what need to consider with signalment and history
- What conditions occur commonly in this species, breed, age group
- Acute vs chronic
- Intermittent or continuous
- Progressive, static, or improving
- Single animal affected vs multiple animals affected
- Toxins
○ Check vomit, faeces, urine and feed/pasture
○ Are other animals in the household or herd affected?
○ Toxicity screen
- Nutrition and husbandry
○ Feed, pasture, supplements
- Possible trauma
67
How to determine whether primary or secondary cause of neurological issues
2. use blood and urine tests to screen for secondary causes
- Electrolytes
- +/- BATT
3. localise and investigate causes of primary neurological disease
68
Primary neurological disease what are the 4 main areas that can be affected and areas wihin
1) Brain disease
- forebrain
- brain stem
- cerebellar
2) Spinal cord
3) peripheral - neuropathy, junctionpathy, myopathy
4) multifocal
69
What clinical signs seen with forebrain dysfunction and what is normal
```
® Altered mentation/consciousness
® Altered behaviour
® Seizures
® Wide circling
® Contralateral proprioceptive deficits
® Normal CNs
® Intact spinal reflexes
```
70
What clinical signs are seen with brain stem dysfunction and what is normal
® CN signs (tend to be multiple)
® Vestibular signs (can also be peripheral)
® Head tilt (can occur with diencephalon too)
® RAS (retriculo activating system) (alter ---> coma) - KEEPS YOU ALERT
® CV and respiratory signs
® UMN gait disturbances
◊ Most commonly bilateral
◊ Paresis, dysmetria, spasticity, recumbency
® Intact spinal reflexes but tendency for hyper-reflexivity
® Intact pain sensation
71
Cerebellar dysfunction clinical signs seen
® The cerebellum is the co-ordinator
◊ There is ataxia (incoordination) without weakness
◊ Exaggerated movements
} Intention tremors and hypermetria
◊ May be menace defects with normal vision
◊ May have concurrent vestibular deficits
72
Spinal cord neurological lesions how common clinical signs
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most commonly presented as small animals
§ UMN VS LMN signs
§ Spinal pain
§ Paresis
§ Altered spinal reflexes § Reduced
□ Proprioception
□ Motor function
□ Pain sensation
§ Normal mentation
```
73
Peripheral neurological lesions what present with and the main types
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§ Present with flaccid paralysis
§ Is it
□ Neuropathy
® LMN-like signs
® Peripheral conditions are more likely to be progressive and multi-limb than LMN spinal cord conditions
□ Junctionpathy
□ Myopathy
```
74
Clinical signs knucking single hindlimbs, kunckling both hindlimbs and hunched over splinting dog what else besides neurological disease
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1) Hunched over splinting dog
○ Back and abdominal pain possible
○ Vomit or off food?
○ Reluctant to move up and down stairs?
2) Older - degenerative spinal and joint disease
Knuckling in the hindlimbs
3) Knuckling in both hindlimbs - acute onset
- Intervertebral disc disease?
- Bilateral cruciate rupture
```
75
What are the 5 main diseases that look like neurological diseases but aren't
- Schiff-Sherrington - ascending inhibitory pathways destroyed
○ stiff forelimbs but can walk with
- Syncope may look like a seizure
○ Consider cardiac arrhythmias
- HL joint disease may not respond to placing, may appear to have los proprioception
- PSS (portosystemic shunt) - can look like pretty much anything
- Head bob syndrome - most common in staffy and bulldogs - NOT A SEIZURE - still coordinated
○ Unsure why they do it
76
Cats what 4 main disease that look like neurological but aren't
- Feline thromboembolism - can look neurological
- Localised tetanus - can look like thromboembolism
○ Generally confined to one leg as more resistant than dogs and horses
○ RARE
- Toxo, FIP, lymphoma
- Pendular nystagmus - due to congenital malformation in cat - NOT NEUROLOGICAL DISEASE
77
syncope what is it and the main cause
Syncope - transient loss of consciousness, spontaneous recovery
- Looks like seizures, episodic weakness
Cause
- Due to cerebral hypoxia or lack of other essential nutrients delivered to the brain
○ Cerebral blood flow mainly cerebral BP
= mean arterial pressure (MAP) - Intracranial pressure (ICP)
78
What are the 4 main steps in the clinical approach to syncope
1. Rule out respiratory problem - usually cough or tachypnoea - EASY TO RULE OUT
2. Rule out metabolic problem - usually weakness as well; blood glucose, electrolytes screening; PCV/TS - QUICK TO RULE OUT
3. Rule out cardiac problem - high index of suspicion if breed or heart murmur
4. Rule out neurological problem - at rest; will progress
79
important history about the even and background information to determine between syncope or seizure
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The event
- Consciousness
- Precipitating event
- Clonic-tonic movements of limbs
- Involuntary defaecation or urination
- Abnormal after event
- Pale mucous membranes
- Short duration
Background
- General activity levels - seizures generally occur at rest and syncope during exercise
- Coughing or respiratory signs
- Diarrhoea or vomiting
- Change in appetite or thirst
- Any medications
```
80
Physical exam for syncope cases what need to rule out
- cardiovascular - rule out cardiac problem
- respiratory tract - rule out respiratory problem
- left with neurological causes
81
ruling out cardiac causes with syncope how, when concerned about cardiac causes what need to do
Rule out cardiac problem
- Breed at risk (boxer, doberman)
- Young or old animal
- Did not lose consciousness
- Has a heart murmur or arrhythmia - not life threatening if cannot auscultate at the time BUT DOESN'T MEAN DOESN'T HAVE HEART CONDITION - can be
- Happened during exertion
When concerned about cardiac causes what next?
- Full CBC, biochemistry, UA, electrolytes
- Resting ECG - only gives you a point in time - not ideal
- Thoracic radiographs
- Echocardiogram
- Systolic BP
Further investigations
- ECG monitoring: event recorder, holter monitor
If normal echo and 24 hour ECG UNLKELY to have life-threatening disease so can wait a while until more specific signs develop
82
in syncpe investigation when to move onto ruling out neurological causes
- Normal in between times
- No trigger
- Neurological abnormalities
- Nothing on previous work-up
- No signs of anything extra-CNS wrong on physical exam
83
how does the rate of the heart travel
SA node -> intra-atrial fibres -> AV node (parasympathetic and sympathetic) -> right and left branches of conducting fibres in ventricle
84
anatomical pacemakers what occurs, why multiple, what are they and how often go off
- Depolarise spontaneously but with 'graded' automaticity
- Fail-safe mechanism
- Rate of depolarisation dog/cat
○ SA node: 60-180 times/minute
○ AV node: 40-60 times/minute - capable of polarisation without SA node but slower
§ Bradycardia if disease in primary pacemaker
○ Purkinje fibres: times/20-40minute
§ Final fail safe -> not very fast - if relying on purkinje fibres to be the pacemaker than can only sit there - not enough to remain consciousness
85
Assessing cardiac rhythm via an ECG what does it do, system used and changes due to
- Electrocardiogram (ECG) is recording of the cardia impulses by surface electrodes
- Two limb lead system most commonly used in companion animal
- Changes seen are as a result of net changes - parallel large deflection, perpendicular no deflection
○ Depolarisation parallel - additive - BIG CHANGE ON ECG
○ Depolarisation perpendicular
86
what is a atrial ectopic beat
- P wave abnormal
- QRS complex is normal - ventricular depolarisation is normal
- Supraventricular (above the AV node)
87
Arrhythmia what is it, do they all cause clinical signs and arise due to
- Arrhythmia = disturbance of heart rate, rhythm or conduction
○ Usually due to abnormalities of intrinsic system (automaticity)
- Not all arrhythmias cause clinical signs
- All arrhythmias tend to be exacerbated by hypoxaemia, ischemia, high SNS tone and electrolyte imbalances
- Arises due to
○ Disorders of impulse formation OR
○ Disorders of impulse propagation and conduction
88
Disorders of impulse formation leading to arrhythmias what are the 3 mechanisms and what occurs
Disorders of impulse formation
1. Enhanced normal automaticity
2. Depressed normal automaticity
3. Abnormal automaticity
Blocks or delays in conduction system (slow) OR Re-entry (fast)
- May occur once or be repetitive like a 'circuit loop'
- May result from same set of causes as for impulse formation
89
What are the 5 questions that need to be answered with every arrhythmia
1. What is the arrhythmia
2. Could it indicate possible serious underlying cardiac disease
3. Could it indicate possible serious systemic disease
4. Is it a precursor of more 'malignant' arrhythmia
5. Is it compromising cardiac function
90
Causes of bradycardia milk and severe what ruling out
- Mild: rule out drugs, vagal mediation or electrolyte disturbances first
- Severe: rule out electrolyte disturbances first, then likely to be primary cardiac
91
Ventricular tachycardia and supraventricular tachycardia what always rule out first expect in what cases
Ventricular tachycardias
- Always rule out extra-cardiac first expect in boxers or Dobermans (predisposed to VT with dilated cardiomyopathy)
Supraventricular tachycardia
- Always rule out cardiac causes first unless obvious cause of physical examination
92
What are the 4 main arrthymias need to know for the exam and how to differentiate
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When given ECG only 4 options for EXAM
Is it a tachycardia or bradycardia
- Tachycardia
○ Atrial fibrillation - INVOLVES P WAVES
○ Ventricular premature complexes - INVOLVES QRS
- Bradycardia
○ Atrial standstill - NO P WAVES
○ A-V block - P and QRS not related or prolonged
```
93
Atrial fibrillation how does it occur and the 2 types
○ How works
§ Species differences
§ Numerous small re-entrant pathways creating rapid and disorganised depolarisation pattern in atria
§ Continually bombarded AV tissue and ventricular rate dependent on depolarisation and conduction characteristics of AV tissue
○ Types
§ Primary AF
□ Rare in dogs, IWH, rate 140-160 bpm
§ Secondary AF
More common in dogs, rare in cats, due to enlarged atria (DCM, MVD)
94
Atrial fibrillation how looks on ECG and how to diagnose
○ How looks on ECG
§ Irregular rhythm
§ Usually high SNS tone
□ V rate > 180-240bpm dogs, >240 bpm cats
§ Normal QRS complexes
§ Atrial rate > 500bpm - generally get F waves
§ AV junction refractor so irregular RR interval and R amplitude
○ How diagnose
§ Chaotic tachyarrhythmia with pulse deficits -> really chaotic
§ Signs of poor perfusion and clinical deterioration (possible congestive heart failure)
□ Secondary to DCM and mitral valve disease generally
95
Atrial fibrillation treatment aim and if serious underlying heart disease or if none
§ Aim to reduce ventricular rate to 140-160bpm - CANNOT REMOVE
If serious underlying heart disease
□ Digoxin first
□ If ineffective than add beta block OR diltizem (calcium channel blocker)
® Titrate dose up to avoid negative ionotropy
If no underling heart disease
® Treat at all? - don't treat
® Quinidine and DC conversion not great
96
Ventiruclar premature complexes how occur and what occurs
§ Originate below AV node (AV node still depolarising)
□ Abnormal depolarisation -> wide and weird QRS
§ Cannot access normal ventricular pathway system
□ RANDOM CELL WANTS TO BE PACEMAKER
§ Sinus rate unaffected so VPC followed by 'compensatory pulse'
§ Uniform or multiform
§ When have ventricular tachycardia can (develop into Ventricular fibrillation)
§ Accelerated idioventricular rhythm
§ Appears before next sinus beat (premature)
97
what is the common problem with ventricular premature complexes, what is unsure if treat
○ Common problem
§ Over-treated due to associated with MI and progression to ventricular fibrillation in PEOPLE
○ What if unsure?
§ Monitor and assess for signs of poor CVS function
§ Check electrolytes (especially magnesium)
§ Acid-base or pain from other things - treat these
98
Ventricular premature complexes when to treat
§ Not if HR < 170 bpm
□ = accelerated idioventricular rhythm (BENIGN)
□ Usually OK output unless concurrent myocardial depression
□ Treat underlying cause
§ YES if dog is:
□ A boxer
□ A doberman
□ Has SAS (Aortic stenosis) or DCM
□ GSD with inherited VT
□ Severely compromised cardiac output as a result
99
Bradycardia arrhythmias at what heart rate, are they pathological, how mediated and clinical signs
○ Dogs < 60bpm; cats < 90bpm
§ Individual variation - fit dogs can be normally under 60
○ May be much lower than this in healthy dogs and have no adverse effects
○ Not always pathological
○ Most vagally mediated arrhythmias are 'silent' and only discovered on PE
§ Concurrent wandering pacemaker on ECG
○ May have subtle clinical signs
100
Primary atrial standstill what need to do first
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Just know it exists and rule out hyperkalaemia first -
□ Most common cause
® Blocked urethra (male cats)
® Hypoadrenocorticism (addisions)
® Acute renal failure
```
