SA neutering, urinary Flashcards
What neoplasia are a higher risk with neutering?
Osteosarcomas in Rottweilers (esp if spayed <1y)
Haemangiosarcoma and MCT in Viszlas (spayed any age)
TCC and cardiac tumours in spayed animals
What age to neuter animals?
Kittens from 4 months (pre-pubertal) - but GA risk with maturity of liver and kidneys, hypothermia risk (small glycogen reserves) etc
Puppies:
- benefits of prior to first season = reduced mamary neoplasia risk, uterine/ovarian vessels small, reduced inconvenience to owner
- disadvantages of prior to first season = anaesthetic considerations
- contraindications to prior to first season = juvenile vaginitis, juvenile urethral sphincter mechanism incompetence
- if after first season, always in anoestrus (>12 weeks after oestrus), >6-8 weeks postpartum (preferably >3 weeks post weaning)
- can do combined with caesarean
Medical options for neutering?
GnRH agonists
GnRH vaccine, antagonists - implant, injection
Pros and cons of surgical neutering?
Pros:
- permanent
- perioperative pain
- 100% effective
- eliminates neoplasia of repro tract
Cons:
- more expensive
- GA
Pros and cons of medical neutering?
Pros:
- quick
- cheaper in short run
- no anaesthetic
Cons:
- temporary
- pain on injection
- never 100% effective
- repro tract neoplasia still possible
- unknown effect on USMI etc
When not to neuter based on clinical exam?
Lactation False pregnancy (can make it permanent) In heat (uterus more engorged and friable) Skin pyoderma (post-op infection)
Open technique for dog castration?
Incise vaginal tunic and pop out testicle
Divide testicle and tunic - use clamp
Ligate vas deference and blood vessels individually, then together
Haemostat distal to ligatures, then divide
Check for haemorrhage
Close vaginal tunics, s/c tissue, skin
Closed castration technique for dog castration?
Keep testicle within tunic, ease out of incision
Place one encircling and one transfixing ligature around the entire spermatic cord and tunics
Haemostat distal to ligatures, then divide
Check for haemorrhage
Close vaginal tunics, s/c tissue and skin
Complications of dog castrations? How to avoid?
Urethra - vulnerable at first cut and when closing (make sure to push testicle forward)
Scrotum - dermatitis (care with clipping and scrubbing)
Scrotum - haematoma (care with haemostats)
Cryptorchids - Why are they a problem? How to find them? Where are they?
Vulnerable to torsion, higher risk of neoplasia (13.6x greater risk of seminoma or SCT), may or may not be functional
Often small/soft/misshapen
Palpation, US, exploratory laparotomy
Inguinal - may be able to ease down to normal incision or if not do separate inguinal incision
Abdominal - can be anywhere, exploratory laparotomy, follow ductus deferens
Bilateral castration recommended (sex linked autosomal recessive trait)
Keep the testicle!!
Bitch spay - How big an incision? How to locate ovaries? How to exteriorise the ovaries?
Incise from umbilicus to last pair of nipples (larger if deep chested, obese or large breed
Locate ovary by duodenal (right) and colonic (left) manoeuvres
Exteriorise ovary - stretch (pull ovary caudally, break with other hand) or cut suspensory ligament
How to ligate the ovarian pedicle?
3 clamp technique At least 2 ligatures Encircling and transfixing Or two encircling Or encircling and Miller's Ligate broad ligament as appropriate - ranges from barely existent to full of fat and blood vessels (make a window in an area without vessels)
How to ligate the cervix?
Traction everything cranially
Transfixing and encircling ligatures
Clamp and cut cranial to ligatures
Check for bleeding
How much blood is too much blood?
Check gutters and cervix Check broad ligament Use suction or swab to see Wait Muscle ooze?
Ovariectomy - Benefits?
Quicker Pyometra unlikely (exogenous progestins required) But no difference in pain score, surgical time, haemorrhage, short or long term complications
Bitch spay closure?
Simple continuous for muscle - less suture material, quicker, weakest point is knot
Skin - intradermal or cruciate/interrupted or staples
Flank cat spay technique?
Retriece uterus with finger or spay hook
Find an ovary on one end and bifurcation on other
Ligate pedicle - single ligature often fine
Traction on uterus to find other horn
Care clamping uterus - may tear, ligate caudal to tear
What drugs to use for neutering?
Antibiotics not indicated
Analgesia:
- LA - lidocaine (pedicles, midline, testicles, incision)
- full mu agonist in premed e.g. methadone
- NSAID if not contraindicated (renal/GI disease, receiving steroids)
- consider paracetamol
- 3-5d home pain relief
Comfortable animals don’t chew wounds or cry and settle at home = happy owner
Post op care for neutering?
Pain relief
Exercise - midline require strict rest policy, lead only walks for one month, avoid stairs, jumping, climbing
Owner to monitor wound for swelling, redness, discharge, pain
Deeding - reduced exercise so need less calories, reduced metabolism, so reduce ration by 20% when not exercising
What must all closing sutures of a bitch spay involve?
All bites must have strength holding layer = fascia of rectus abdominus
What late post op neutering complications are there?
Ovarian remnant: - signs of in heat - more common on right side - more common in dogs - check ovary in surgery to ensure completely excised Stump pyometra: - only if progestogen exposure and remaining uterine tissue Granulomas: - use of non absorbable suture material - poor tissue handling and aseptic technique - excessive devitalised tissue left Urethral sphincter mechanism incompetence: - multifactorial - exclude other causes (especially UTI) - 90% respond to phenylpropanolamine - second line ephedrine or estriol - surgical options
What innervation controls filling and emptying of the bladder?
Filling and storage
- mostly sympathetic via hypogastric nerve
- B receptors in detrusor muscle for relaxation
- A receptors in urethral smooth muscle and trigone for contraction
- also somatic via pudendal nerve - urethral striated muscle contraction and inhibition of detrusor reflex
Emptying:
- mostly parasympathetic via pelvic nerve
- stimulates stretch receptors in bladder wall
- contraction of detrusor muscle
- relaxation of urethral muscle
- = detrusor reflex
What allows urinary continence?
Brainstem micturition centre integrates urethral and detrusor function
Cerebral cortex gives voluntary control by over-riding the detrusor reflex
How to investigate urinary incontinence?
Detailed history - e.g. bed wetting, dribbling urine, constant or when excited etc, thirst (could just be PUPD)
Clinical exam (if puppy dripping urine every min etc likely ectopic ureter)
Biochemistry and haematology (check for UTIs etc)
FeLV test in cats
Urinalysis
Urine culture and sensitivity
Observe patient urinating
Plain abdominal radiographs - screen for calculi etc
IV urogram/CT angiography - to check for ectopic ureters
Retrograde (vagino) urethrogram
US exam of urinary tract
Urethroscopy/cytoscopy
Typical findings of abnormalities of the bladder filling phase?
Can urinate and empty bladder normally
Dribble urine between urinations
Often have reduced bladder capacity (likely due to the incontinence, not the cause)
Ddx of abnormalities of the bladder filling phase?
Ectopic ureter - congenital or acquired Reduced pressure at bladder neck: - congenital USMI - acquired USMI - intrapelvic/caudal bladder, short urethra, hypo plastic bladder (probably all part of USMI) - bladder neck mass (polyp, neoplasia, cystic calculus) - urethral dysplasia in female cats Involuntary contractions/urge incontinence: - bacterial infection - cystic calculus - drug induced - FeLV +ve cats - neoplasia of bladder neck
Typical findings of abnormalities of bladder emptying phase?
Distended bladder
Poss constant dribbling of urine
Often no normal urination
Ddx of abnormalities of bladder emptying phase?
Partial/complete urethral obstruction Chronic distension of bladder: - urethral obstruction - pelvic trauma - intervertebral disc protrusion - feline dysautonomia Dyssynergia
What is USMI in female dogs? Signs? Forms? Aetiology?
Urethral sphincter mechanism incompetence
Commonest cause of incontinence in bitch
Intermittent involuntary passage of urine
Incontinence usually whilst dog is relaxed (lying down/sleeping)
Do not constantly dribble urine, can urinate normally
Acquired:
- usually medium/large breeds (Dobermans, Boxers, Irish Setters, OESD)
- usually neutered females (but no proof spaying actually causes it)
Congenital:
- juvenile bitches (prior to first season
- 50% resolve after first season
- ectopic ureter in main ddx (both conditions can be present)
Aetiology:
- low urethral tone
- hormonal influence - spayed bitches, prior to first season
- obesity
Treatment for USMI in female dogs?
Medical: - increase muscle tone with phenylpropanolamine or ephedrine, or estriol - weight loss - treat secondary UTI Surgical: - colposuspension - urethropexy -hydraulic occluder
Presentation USMI in male dogs? Treatment?
Uncommon Usually older, castrated medium/large breeds Usually overweight Treatment: - phenylpropanolamine or ephedrine - oestrogen based drugs? - weight loss - surgery: vas deferensopexy, prostatopexy, hydraulic occluder
What are ectopic ureters? What may happen/be present at the same time? Which dogs is it more common in?
Congenital anomaly, ureter bypasses bladder to empty into urethra, vagina or rectum
Congenital USMI or hypo plastic bladder may co-exist
Secondary UTIs common (cystitis, hydroureter, pyelonephritis)
Most are unilateral
Intramural more common
Female:male 20:1
Golden/Lab retrievers, skye terriers, siberian huskies - greater incidence
Treatment for ectopic ureters?
Treatment of associated UTI
Early surgical management before irreversible secondary changes - referral
Exploratory coeliotomy
Cystotomy to assess trigone area
Uteronephrectomy - for unilateral ectopia, severe hydronephrosis
Ureteral transection and re-implantation - for extramural ectopia
Intravesical repair - for intramural ectopia
What is IV urography (IVU)? What is needed for a diagnostic study?
IV injection of iodine based contrast medium and documentation of its transition through the kidneys, ureters and into the bladder with multiple radiographs
Need:
- adequate renal function and hydration
- good patient prep (fasting, enema)
- GA/heavy sedation
- multiple VD and lateral radiographs at short intervals
What are the phases of IV urography (IVU)?
Start with a plain study (2 orthogonal views)
Rapid IV injection of contrast (iodine based)
Immediate radiograph (angiogram) - homogenous enhancement of kidneys and renal vessels
2 mins = nephrogram - enhancement of kidneys and renal pelvis
5 mins = pyelogram +/- ureters - enhancement of kidneys, renal pelvis and ureters
10 mins = ureters
20 mins - ureters +/- bladder - fading in the kidneys
40 mins = bladder
How to do cystography?
Catheterise and empty bladder
Instill/insufflate with contrast medium (air/gas or iodine based contrast) until reasonably distended
How to do retrograde urethrogram/vaginourethrogram?
Catheterise, empty bladder, inflate bladder moderately full with air/gas (creating back pressure)
Place catheter tip in tip of penis/just within vulva and clamp
Inject iodine based contrast and expose at end of injection
When would you use IVU, cystography and retrograde urehtrograms?
IVU:
- good for ureters and kidneys
- indicated for suspected ectopic ureter, uteroliths, ureteral stenosis, renomegaly, integrity
Cystography:
- good for bladder
- indicated for radiolucent calculi, bladder masses, bladder rupture
Retrograde urethrogram:
- good for urethra, (bladder)
- indicated for stranguria (urethrolith, stenosis, inflammation, neoplasia), integrity
Need GA for all
Need adequate renal function and hydration for IVU
Normal location, opacity, shape, margination and size of the kidneys on radiography?
Location:retroperitoneal space, left more caudal
Opacity: homogenous ST opacity +/- fat at hilus
Shape: bean shaped in dog, slightly more rounded in cat
Margination: sharp and smooth
Size:
- best assessed on VD
- dog: length = 2.5-3.5 x length of L2 vertebral body
- cat: length = 2-3 x length of L2
Normal appearance of the kidney cortex, medulla and pelvis on ultrasound?
Cortex - echoic, similar or hypoechoic to liver
Medulla - near anechoic, least echogenicity of all organs
Renal pelvis and diverticula (renal sinus) - hyperechoic (bright), should not contain any urine (anechoic)
Causes of unilateral and bilateral focal and generalised renomegaly?
Unilateral focal renomegaly: - neoplasia - cysts - abscess - haematoma Bilateral focal renomegaly: - neoplasia/metastasis - PKD - FIP Unilateral generalised renomegaly: - neoplasia - hydronephrosis - perinephric pseudocyst Bilateral generalised renomegaly: - AKI - pyelonephritis - lymphoma - FIP
Causes of microrenale?
CKD - uni or bilateral
Dysplasia - uni or bilateral
Atrophy (chronic obstruction) - unilateral
How do the kidneys look with CKD on radiography and US?
Non specific changes - poor correlation with function
Variable, may appear normal in early stages
Classic end stage - small and irregular, but may be smooth
US - poor corticomedullary definition, small, irregular
How do renal cysts appear on US?
May be solitary (can develop as part of CKD) If multiple indicate PKD Thin walled Mostly unicameral Distal acoustic enhancement May distort surface
Define pyelectasia and hydronephrosis?
Pyelectasia = mild to moderate dilation of the renal pelvis secondary to diuresis (IVFT, furosemide) or inflammation (pyelonephritis) Hydronephrosis = moderate to severe pelvic dilation often secondary to obstruction (ureteral calculi, masses) with overall enlargement of the kidney
Normal appearance of ureters on radiography, US and IVU?
Radiography and US - not usually visible
IVU:
- location: retroperitoneum, lateral the spine on VD
- size: 1-2mm, peristalsis
- ureterovesicular junction: J shaped, in the trigonal region, ureteral jets (US)
How do ureteroliths appear on radiography and US?
Radiography - mineral opacity structures in region of ureters
US - dilation of ureter lumen, hyperechoic (shadowing) structure within the lumen
Normal location, shape, margination, size and opacity of the bladder on radiography?
Location: caudoventral abdomen, just cranial to pelvic inlet, caudal extremity is retroperitoneal
Shape: divided into body and neck, pear-shaped in dogs, ellipsoid in cats, long thin bladder neck in cats
Margination: smooth and sharp
Size (and position): varies with volume of urine
Opacity: homogeneous ST opacity
Normal appearance of bladder on US?
Pear shaped organ in caudal abdomen with anechoic contents
Wall thickening depends on the filling status but should be thin and smooth
In trigonal region (neck), ureteral papillae sometimes visible (jets)
How does cystitis appear with imaging?
Not visible on plain radiographs Cystography: - thickened (cranioventral) wall - irregular mucosa - blood clots Double contrast media - can see calculi and blood clots
How do bladder calculi appear on radiography and US?
Radiography:
- accumulate in most dependent part of bladder (ventrally)
- visibility dependent on radiopacity and size
- struvite, oxalate, calcium phosphate moderate to marked
- silicate moderate
- cystine and rate non opaque to faint
US:
- hyperechoic structures in dependent part of bladder
- strong distal shadowing (unless tiny)
How do bladder masses appear on radiography and US?
Radiography: - not visible on plain radiographs - will create a defect in contrast pool or as a ST opacity on pneumocystogram - predilection site: trigonum, dorsal bladder wall US: - most commonly TCC - sessile, polypoid echoic mass - trigonal region or bladder neck
Can bladder rupture be seen by radiography and US?
Not visible on plain radiographs, but may see loss of serosal detail (free fluid) and small bladder
If suspected, do positive contrast cystography - leakage of contrast
US rarely able to show defect, but will see free fluid
What is the only method of accurately assessing the urethra? How does it compare in males and females?
Retrograde (vagino)urethrogram
Males - prostatic urethra, membranous or pelvic urethra, penile urethra
Females - shorter and wider than males, entirely intrapelvic
Smoothly marginated
Can the uterus and ovaries normally be seen by radiography? US? Position?
Not unless greatly enlarged
Ovaries - in dorsal middle aspect of peritoneal space, caudal and ventral to each kidney
Uterus:
- width must be at least 2x width of small bowel to be detected
- US: identification of normal horns can be difficult, the body is located between the urinary bladder ventrally and the descending colon dorsally
How does canine cystic endometrial hyperplasia-pyometra complex appear on radiography and US?
Radiography:
- dilated, soft tissue opacity loops originating between bladder and colon
- mass effect displacing the intestines cranially and dorsally
Ultrasound:
- fluid dilation of uterine horns and body
- uterine wall appearance is variable and depends on degree of dilation and if hyperplasia is concurrently present
Normal location, size, shape and opacity of the prostate on radiography?
Location: caudal to the bladder, may be partly within the pelvic canal
Size: dependent on neutering status (rule of thumb <70% height of pelvic inlet)
Shape: symmetrical, ovoid to round, urethra centrally
Opacity: homogenous soft tissue opacity
Appearance of the prostate by US in neutered and intact dogs?
Neutered dogs:
- intrapelvic
- small and homogeneously hypoechoic
- round on transverse images and enveloping the urethra
- fusiform on sagittal images
Intact male dogs:
- ovoid, symmetrical and smoothly marginated
- significantly larger than in castrated dogs
- homogeneously to mildly heterogeneously hyperechoic
Causes of prostatomegaly? How do each appear?
Benign prostatic hyperplasia: - symmetrical enlargement - ST opacity - normal in entire older dogs Prostatitis (entire dogs): - regular or irregular shape - may see mineralisation - sometimes loss of serosal detail Prostatic neoplasia: - often irregular shape - often mineralisation (very specific for neoplasia in neutered dogs: carcinoma, TCC) - often loss of serosal detail - dorsal displacement of colon/rectum - may see metastatic disease to medial iliac lymph nodes and lumbar vertebrae (periosteal reaction, lysis)
What is AKI?
A spectrum of disease associated with a sudden onset of renal parenchymal injury
Results in:
- abnormal GFR, tubular function and urine production
- sudden inability to maintain fluid, acid-base and electrolyte balance
- possibly azotaemia
Causes of AKI?
Decreased renal blood flow: - hypovolaemia - dehydration - hypotension - renal vasoconstriction (PG inhibitors) - thrombi, DIC Toxins: - antibacterials e.g. aminoglycosides - chemotherapy drugs e.g. cisplatin - radiographic contrast media - NSAIDs - organic compounds e.g. ethylene glycol - lilies (cats) - grapes (dogs) Infectious: - Leptospirosis - FIP - Leishmania Pyelonephritis, septic emboli Glomerulonephritis Trauma Systemic diseases: - multiple organ failure - polycythaemia - lymphoma - hyercalcaemia
What are the 4 stages of AKI?
Initiation phase: - damage starts Extension phase: - ischaemia - hypoxia - inflammatory response - ongoing cellular injury - cell death Maintenance phase: - stabilisation of GFR - typically see azotaemia, uraemia - urine production variable Recovery phase: - azotaemia improves - tubules undergo repair - can be marked polyuria
Initiation and extension phases may be clinically silent
History/clinical signs of AKI?
Non specific!
Recent onset of anorexia, polydipsia, vomiting, diarrhoea
May get CNS signs in cases of ethylene glycol ingestion
Known toxin exposure?
Nephrotoxic drugs?
Signs of infection or previous UTI?
Ischaemic episode?
Check vaccination status - leptospirosis?
Physical exam of AKI?
Usually in good condition Dehydration Uraemic breath Hypothermia (unless infection) Ulceration of tongue/buccal mucosa Occasional neurological signs \+/- Kidney pain or enlargement Tachycardia if dehydrated Bradycardia if hyperkalaemia
Diagnosis of AKI?
Blood sample:
- azotaemia
- increased iP
- hyperkalaemia if oliguric (normal or hypo if polyuric)
- calcium variable (low with ethylene glycol, high with Vit D intoxication and neoplasia)
- metabolic acidosis
- increased PCV, TP (dehydration)
Urinalysis:
- isosthenuric (1.008-1.012)
- may be glucosuria, haematuria, proteinuria
- look at sediment for casts, WBCs, bacteriuria, crystals
Radiography - size, shape, opacity
Ultrasound - size, parenchyma, echogenicity
Differentiating between CKD and AKI?
CKD:
- weight loss
- previous history of PUPD/poor appetite/GI signs
- non regenerative anaemia
- kidneys typically small, firm and irregular
- often surprisingly well for degree of azotaemia
- normal or low K
- poor hair coat
AKI:
- good body condition
- acute onset of signs
- +/- history of toxin exposure
- kidneys may be enlarged or painful
- may be disproportionately sick for the degree of azotaemia
- +/- hyperkalaemia
- urine sediment may show casts
- good hair coat
Specific treatments for AKI?
Induce vomiting if recent toxin ingestion (antifreeze, lilies) - need early recognition Ethylene glycol: - 4 methylpyrazole (fomepizole) - ethanol (needs to be given within 8h) Leptospirosis or pyelonephritis: - antibiotics
What is seen in the urine with ethylene glycol toxicity? Prognosis?
Calcium oxalate monohydrate crystals
Poor prognosis if already azotaemic or oliguric
Fluids for AKI? How much? Monitoring?
Correct hydration status, acid-base status and electrolytes
Monitor hydration with MM, CRT, HR, RR, ABP, PCV and biochemistry
Don’t overload - no evidence that aggressive IVFT is better than restoration of normal perfusion
Give just enough but not too much
Measure BW accurately at least twice per day
What to do if rehydrated an animal with AKI but is oliguric? Define oliguric?
Oliguric = urine flow <1ml/kg/hr normally but <2ml/kg/hr if hydrated and well perfused
Give 3-5% BW in IVFT if not overhydrated
Reassess hydration, BP - reduce IVFT, place urinary catheter, start treatment to increase urine output
- furosemide (increases urine output but doesn’t improve GFR or outcome), initial 1-2mg/kg IV bolus, then 0.5-1mg/kg/hr CRI
- mannitol
How to correct hyperkalaemia with AKI?
Fluid therapy (0.9% NaCl or Hartmans)
Calcium gluconate 10% - antagonist of cardiac effects, monitor ECG
Dextrose - stimulates insulin secretion (glucose and potassium share a carrier)
Insulin
Sodium bicarbonate - K+ into intracellular space in exchange for H+
Treatment for vomiting and hypertension with AKI?
Vomiting: - H2 antagonists, PPIs - maropitant, metaclopramide Hypertension: - exacerbated by overdydration - reduce ICFT - diuretics - if persistent can use antihypertensives: nitroprusside, hydralazine, amlodipine
Dialysis for AKI?
If can’t induce diuresis consider euthanasia or dialysis
Removes toxic wastes
Allows time for kidneys to repair
Haemodialysis available at some referral centres
Peritoneal dialysis - expensive, time consuming, complications common, often poor response
Prognosis of AKI and how long to treat for?
If renal function returns to normal or improves and stabilises but not normal levels - taper fluids off
If renal function worsens or doesn’t improve sufficiently ro be managed at home - renal replacement therapy (dialysis) or euthanasia
Define UTI, bacteriuria and pyuria?
UTI = adherence, multiplication and persistence of an infectious agent within the urogenital system Bacteriuria = bacteria in the urine Pyuria = WBCs in the urine
Clinical findings and blood results with UTI?
Not always symptomatic
Upper UTIs may cause abdominal pain, renal failure or septicaemia
Lower UTIs may cause dysuria, pollakuria, haematuria or urinary incontinence (not PUPD)
Animals with pyelonephritis may also be PUPD
Blood results:
- lower UTIs likely none
- upper UTIs may be consistent with septicaemia or renal failure
Diagnosis of UTIs?
Urinalysis - WBCs and nitrate not reliable on dipstick
Urine sediment exam - significant numbers of WBCs (>5/HPF), bacteria
Urine culture
Treatment for UTIs? Difference for uncomplicated and complicated UTIs?
Treat underlying cause (e.g. DM, CKD, HAC, underlying LUT diseases)
Antibiotics based on:
- agar disk diffusion
- antimicrobial dilution technique (MIC)
- first line: amoxicillin, cephalexin, trimethoprim
Uncomplicated UTIs:
- no underlying structural, neurological or functional abnormality can be found
- usually successfully treated with a 10-14d course of antibiotics
- urine culture if possible 5-7d after cessation of therapy
Complicated UTIs:
- sexually intact dogs
- most cats
- animals with predisposing causes
- upper UTIs
- continue antibiotics for 4-6 weeks
- assume intact male dogs with UTI to have prostatic infection (consider blood-prostate barrier)
Complications of UTIs?
Polypoid crystals - caused by chronic bacterial infection, most common in bladder apex
Emphysematous cystitis - accumulation of gas in bladder wall and lumen secondary to infection with glucose fermenting bacteria, E.coli most common, most associated with DM
MAP crystals - usually caused by Staphs and Proteus producing urease (urea->ammonia)
Pyelonephritis - ascending infection from LUT
Prevention of UTIs
Avoid indiscriminate use of urinary catheters
Use a closed collection system
Avoid indwelling catheters in immunocompromised patients
(Risk of UTI increases with duration of catheterisation)
Do not use antibiotics as prevention - increases chance of resistance
Should antibiotics be used as a first line treatment for cats with dysuria?
No - bacterial cystitis is rare in cats
What is CKD?
Kidney damage/reduced function that has been there for 3 months or longer
Compensatory/adaptive changes have already occurred
= irreversible and slowly progressive
Causes of CKD in dogs and cats?
Congenital/familial: - renal dysplasia - polycystic kidney disease - amyloidosis - Fanconi-like syndrome Acquired - idiopathic tubulointerstitial nephritis - glomerular disease - amyloidosis - sequel to AKI - LUT obstruction - pyelonephritis - hypercalcaemia - renal neoplasia - nephrotoxic drugs - hypokalaemia in cats (controversial) - hypertension (debated)
Causes of CKD in dogs and cats?
Congenital/familial: - renal dysplasia - polycystic kidney disease - amyloidosis - Fanconi-like syndrome Acquired - idiopathic tubulointerstitial nephritis - glomerular disease - amyloidosis - sequel to AKI - LUT obstruction - pyelonephritis - hypercalcaemia - renal neoplasia - nephrotoxic drugs - hypokalaemia in cats (controversial) - hypertension (debated)
But cause is often not apparent at time of diagnosis
Why does CKD progress even in the absence of active kidney disease?
Due to adaptations in response to the loss of functioning renal mass
Intraglomerular hypertension - aims to maximise GFR
Increased single nephron GFR (SNGFR)
Systemic hypertension
Proteinuria
- dogs: tends to be caused by glomerular disease
- cats: tends to be caused by tubulointerstitial disease
- so may be why progresses more quickly in dogs
Precipitation of calcium phosphate in renal tubules
Clinical signs of CKD?
Weight loss/poor body condition Poor appetite Dullness, lethargy, sleeping more PUPD Dehydration Vomiting Constipation Poor hair coat Neurological signs Signs related to hypertension Oedema/ascites in severe protein losing CKD
Also on physical exam:
- pale mm
- hypothermia
- oral ulceration
- uraemia lesions
- retinal lesions (hypertension)
- osteodystrophy
- ascites or s/c oedema
What are the criteria for staging CKD?
Creatinine concentration (GFR estimate)
Proteinuria
BP
What are the IRIS I to IV CKD stages?
Stage 1:
- plasma creatinine <125mmol/L (<1.4mg/dl)
- some other renal abnormality present e.g. inadequate concentrating ability, abnormal renal palpation
Stage 2:
- plasma creatinine 125-180mmol/L (1.4-2mg/dl)
- clinical signs usually mild (e.g. PUPD) or may be absent
Stage 3:
- plasma creatinine 180-440mmol/L (2-5mg/dl)
- many systemic clinical signs may be present
Stage 4:
- plasma creatinine >440mmol/L (>5mg/dl)
- increasing risk of systemic clinical signs and uraemia crisis
What are the IRIS substages for CKD?
AP0: - non proteinuric (UP/C <0.2) - minimal risk (SBP<150mmHg) AP1: - borderline proteinuric (UP/C 0.2-0.5) - low risk (SBP 150-160mmHg) AP2: - borderline proteinuric (UP/C 0.2-0.5) - moderate risk risk (SBP 160-180mmHg) AP3: - proteinuric (UP/C >0.5) - high risk (SBP >180mmHg)
Overall IRIS staging?
Plasma creatinine stage I to IV
Proteinuric (P), borderline proteinuric (BP) or non proteinuric (NP)
Risk based on BP (AP0, AP1, AP2 or AP3)
nc = no complications
c = complications present (actual evidence of damage e.g. hypertensive retinal lesions, ventricular hypertrophy)
E.g. Stage 2 - BP - AP0nc
What is involved in the optimal minimum database for CKD?
History - including exposure to toxins or nephrotoxic drugs
Physical exam - eyes, palpate thyroid in cats
Haematology, biochemistry, urinalysis
BP
Abdominal radiographic survey
Abdominal US
What may be seen with haematology and biochemistry with CKD?
Haematology:
- may see normocytic, normochromic, non regenerative anaemia
Biochemistry:
- azotaemia
- hyperphosphataemia (initiates secondary hyperparathyroidism with metastatic calcification)
- increased or decreased total calcium (often increased total with normal or low iCa)
- hypokalaemia common in cats, uncommon in dogs
- hyperkalaemia in end stage CKD
- low albumin in PLN
- SDMA
Causes of increased blood urea and creatinine?
Urea - CKD, high protein diet, GI bleeding, dehydration
Creatinine - muscle mass, CKD
Urinalysis results for CKD?
Isosthenuria (1.008-1.012)
Or inadequate concentration (<1.030 in dogs, <1.035 in cats)
Inadequate concentration + azotemia = renal azotemia
Sediment - WBCs, RBCs, casts, crystals
Dipstick - check proteinuria
UPC - only id sediment is inactive
Culture
Treatment of a CKD uraemia crisis?
IVFT Hartmann’s or 0.9% NaCl Supply ongoing maintenance requirements Monitor electrolytes and azotaemia Reduce IVFT as animal starts eating and drinking
Treatment of stage 1 CKD?
Stop any nephrotoxic drugs
Treat any pre-renal or post-renal abnormalities
Reduce proteinuria if present:
- treat any concurrent associated disease process
- consider kidney biopsy
- ACEI (not if dehydrated or hypovolaemic) plus dietary protein reduction
- antiplatelet drugs (low dose aspirin or clopidogrel) if serum albumin <20g/L
Control hypertension:
- goal is to reduce SBP <160mmHg
- in dogs use, ACEI standard dose, then try double dose, then try or combining ACEI and Ca channel blocker (e.g. amlodipine)
- in cats use amlodipine OR telmisartan, then try increasing amlodipine dose, then try combining amlodipine and telmisartan
Combat dehydration:
- wet diet
- drinking fountains/dripping taps
- large bowls filled to top for cats
- chicken/fish flavoured water
Treatment for stage 2 CKD?
Everything as for stage 1 plus: Reduce protein with renal diet Control phosphate to <1.5 mmol/l - add phosphate binder if diet alone not enough (aluminium hydroxide, calcium acetate, pronefra) Supplement potassium if needed: - hypokalaemia quite common in cats - supplement IVFT with KCl - oral supplements (potassium gluconate, potassium citrate) - aim for >4mmol/l Semintra?
Why are renal diets beneficial? Which stages are they beneficial for?
Protein restriction - ameliorates clinical signs - reduced risk of uraemic crisis - reduces proteinuria - reduces PUPD - reduces acid load Phosphate restriction Omega 3 fatty acids Fibre Low sodium Water soluble vitamins
Beneficial to dogs in stage III and IV and cats in stage II, III and IV
Also for dogs in stage II when phosphate >1.5mmol/L and all dogs with proteinuric CKD
How slowly should renal diets be introduced?
Over 7-10 days for dogs
Over 2-3 weeks for cats
What are the phosphate targets fro CKD stages?
Stage 2: <1.5mmol/l
Stage 3: <1.6mmol/l
Stage 4: <1.9mmol/l
Treatment for stage 3 CKD?
Everything for stage 1 and 2 plus: Control phosphate to <1.6mmol/l Treat nausea and vomiting: - reduce gastric acid secretion with H2 antagonists (e.g. cimetidine) or omeprazole - sucralfate to treat ulcers - antiemetics (maropitant, metaclopramide) - appetite stimulants (mirtazapine, cyproheptadine) - consider feeding tube Control metabolic acidosis: - treat if HCO3- <15mmol/l - renal diet - sodium bicarbonate - potassium citrate Manage anaemia: - avoid excessive blood sampling - minimise GI blood loss - good nurtition - treat iron deficiency - blood transfusions - consider EPO (supplement iron if given, side effects are seizures, hypertension, local reactions, antibodies) Consider s/c fluids: - hartmanns or NaCl - 75-100ml up to daily - complications: hypernatraemia, fluid overload Control constipation: - correct dehydration - lactulose - may need enemas
Treatment of stage 4 CKD?
Everything for stages 1, 2 and 3 plus: Control phosphate to <1.9mmol/l Intensify efforts too provide nutrition More likely to require extra fluids (SC or via tube) Consider euthanasia
How to monitor CKD?
Initially monthly
Clinical exams - signs, appetite, BW, BP
Blood tests - urea, creatinine, phosphate, Na, K, albumin, PCV
Urine - measure UPC to monitor proteinuria, check sediment
Predisposing factors for urolithiasis?
Supersaturated urine
Urine pH:
- struvite and calcium phosphate form in alkaline urine
- cystine forms in acid urine
- calcium oxalate, rates and silicates form in neutral to acid urine
Presence of a nidus
Decreased frequency of voiding
Decreased inhibitors of crystallisation (e.g. decreased glycosaminoglycans, citrates and pyrophosphates)
UTI (struvites and urates)
Struvite uroliths - What are they? When do they form? Appearance on radiography? Shape? Predispositions? Which dogs? Which part of urianry tract?
Magnesium ammonium phosphate
Form in alkaline urine
Radiopaque
Multiple shapes - faceted or pyramidal when multiple present
UTIs predispose - Staph (urease converts urea to ammonia)
90% females
95% LUT
Calcium oxalate uroliths - When do they form? Appearance on radiography? Predispositions? Which dogs?
Neutral to acid urine Radiodense, often rough, round to oval Hypercalcaemia predisposes: - malignancy - hyperparathyroidism - vitamin D toxicosis Increased dietary oxalate predisposes - diet high in vegetables or Vitamin C Decreased citrate in urine predisposes - Ca citrate is more soluble than Ca oxalate 70% males More common in older dogs
Urate uroliths - What are most? When do they form? What do they look like on radiography? How do they form? Which dogs?
Most stones are ammonium acid urate
Form in acid urine
Radiolucent, smooth, round or oval
Dietary nucleic acids and endogenous purines
Oxidised by hepatic uricase to allantoin (soluble)
85% males
Dalmations and English Bulldogs (have impaired uric acid hepatic transport)
Dogs that get PSS (high ammonium rates in urine)
History and clinical signs of urolithiasis?
Variable - asymptomatic to complete urinary tract obstruction Pollakiuria Dysuria/urinary tenesmus Discomfort/vocalisation on urination Haematuria Renal pain
Physical exam:
- may feel stones in bladder
- poss abdominal pain (not usually)
- if blocked urethra: distended bladder, signs of azotaemia
Diagnosis of urolithiasis?
Palpation Radiography Pneumocystogram Double contrast cystogram US Voiding uroliths Urinalysis - large numbers of crystals in sediment like to be representative of the urolith
Medical management for urolithiasis?
Dissolution of the stone if can (can for struvite, urate, cystine):
- encourage water intake (ideally want USG<1.020)
- allow frequent voiding opportunities
- treat any concurrent UTI
Prevention of recurrence
How urgent is a blocked urethra?
Blocked urethra = emergency, can be fatal, within 24h will develop post-renal azotaemia and signs of renal failure, bladder may rupture
How to dissolve struvite uroliths? What if fails?
Antibiotics throughout Diet: - low in magnesium, ammonium and phosphate - reduced protein - maintain urine pH <6.4 - high Na for diuresis Check radiographs and urinalysis monthly Continue at least one month past radiographic resolution Clinical signs resolve after about 10d Rakes about 3 months on average to dissolve If fails: - not struvite? - poor owner compliance? - persistent infection?
How to prevent recurrence of struvite uroliths?
Encourage water intake
Prevent and control UTIs
Diet moderately restricted in Mg and phosphate that produces an acid urine?
How to prevent recurrence of calcium oxalate uroliths?
Encourage water intake
Identify and treat hypercalcaemia
Avoid excessive dietary intake of calcium, oxalate, vitamin C or vitamin D
Avoid excessive sodium in diet
Avoid high protein diets
Potassium citrate can be given to alkalinise the urine
How to dissolve urate uroliths?
Low protein, low purine diet that produces alkaline urine
Can supplement with sodium chloride to promote diuresis
Alkalinise urine if necessary with potassium citrate or sodium bicarbonate
Prevention of urate uroliths?
Encourage water intake
Allopurinol can be used for recurrent urates
Xanthine oxidase inhibitor - may predispose to insoluble xanthine stone formation (esp. if protein is not restricted in the diet)
Cystine uroliths - When seen? What do they look like on radiography? Which dogs?
Inherited disorder of renal tubular transport
Relatively radiolucent, smooth, usually round or oval, red-yellow brown, small, flat, colourless, hexagonal
90% males (90%)
Dachshunds
Also Basset Hound, English Bulldog
How to dissolve cystine uroliths?
Encourage water intake Diet - reduced in protein and methionine - alkaline urine Specific drugs - Thiols, MPG, D-penicillamine
Silicate uroliths - Which animals? Appearance on radiography and shape? When seen? Which breeds?
90% males
Radiodense, jack shape
Diets high in corn gluten, soya bean hulls, rice / ingestion of soil
GSD, OES, Golden and Labrador Retriever
Prevention of recurrence of silicate uroliths?
Encourage water intake
Avoid eating soil, soya, bean hulls, corn gluten
Calcium phosphate uroliths - When seen? How to prevent recurrence?
Usually present as part of mixed urolith
Encourage water intake
May be associated with metabolic diseases - hyperparathyroidism
Treatment for nephroliths and ureteroliths?
Less common than cystoliths
Dissolution of struvite stones may be possible, but takes long time
Surgical removal difficult
SUB
Unilateral nephrectomy may be required if hydronephrosis
Definition of FLUTD and feline idiopathic cystitis?
FLUTD = collective term for signs of LUT disease and abnormal voiding behaviour
Feline idiopathic cystitis = abnormal voiding behaviour after exclusion of other disorders with no obvious cause, chronic persistent or recurrent
What are the most common causes of FLUTD?
Non obstructive - idiopathic cystitis
Obstructive - urethral plug
Signalment of FLUTD?
Any age or sex - most common young-middle aged neutered cats (2-6yo)
Males more prone to obstruction
Persians appear predisposed
Predisposing factors for FLUTD?
Obesity
Indoor/sedentary cats
Dry diet
Multi cat household
History and clinical signs FLUTD? What to determine?
Dysuria (difficulty urinating)
Pollakiuria (increased frequency)
Haematuria
Inability to urinate (urethral obstruction)
Behavioural changes
Appear to lose litterbox training
Periuria (urinating in inappropriate places)
Determine if obstructed or not
Non obstructed cats - generally well, usually self limiting and resolves in 5-10d
Obstructed cats - emergency
Physical exam for FLUTD?
Assess bladder size/palpate
- obstructed cat: large, often painful
- non-obstructed cat: small, firm, may be painful
Check penis for signs of self trauma/crystals
Pathophysiology of feline idiopathic cystitis?
Alterations in neurotransmission to and from the bladder -> neurogenic inflammation
Reduced glycosaminoglycan layer (protects bladder lining)
FIC cats have reduced serum cortisol responses, adrenals are smaller
Urethral plugs - More common in males or females? What do they consist of?
More common in males
Most common cause of obstruction
Plug consists of mucus/glycoprotein matrix, often with other substances trapped in the matrix
What inherited and acquired anatomical defects can cause FLUTD?
Inherited: - vesico-urachal diverticulae - bladder hypoplasia - urethral strictures - phimosis Acquired: - strictures due to trauma - inflammation - iatrogenic damage
Investigations for FLUTD?
Blood samples very important in blocked cats
- hyperkalaemia
- hyperphosphataemia
- metabolic acidosis
- azotaemia
Urinalysis:
- highly concentrated USG predisposes to urolith formation
- dilute predisposes to bacterial infection
Radiography:
- plain: may see radio-opaque calculi/plugs
- contrast studies: retrograde urethrogram, double contrast cystogram to highlight uroliths, bladder masses, urethral narrowing
US:
- hyperechoic sedminent
- uroliths and acoustic shadowing
- bladder masses
- thickened bladder walls
Treatment for FLUTD?
Treat specific/underlying causes
- urethral plugs (emergency): cystocentesis to relieve pressure, fluid therapy, correct electrolyte and acid-base disturbances
- uroliths: dissolution, hydration, diet, surgical removal
If no obvious underlying cause then treat as idiopathic cystitis:
- most resolve spontaneously in 5-10d
- corticosteroids and antibiotics have no positive effect
- reduce stress
- pheromones (feliway)
- create dilute urine (wet diet, water fountains, fish or chicken stock)
- GAG supplements - attaches to bladder lining and decreases bladder permeability, analgesia and anti-inflammatory
- analgesia and anti-inflammatories (butorphanol, buprenorphine, NSAIDs if renal function ok)
- smooth muscle antispasmodics to relax urethra
- amitriptyline: tricyclic anti-depressant, reserve for chronic cases, need long term treatment, anticholinergic (increases bladder capacity), anti alpha adrenergic (relaxes urethral tone), anti-histaminic, anti0inflammatory, analgesic
How to treat urethral spasm? Why helpful?
May help reduce severity of FLUTD signs May help prevent urethra reblocking Smooth muscle antispasmodics: - ACP - prazosin - phenoxybenzamine
Side effects of amitriptyline?
May cause somnolence
May cause urinary retention
Raised liver enzymes, neutropenia and thrombocytopenia reported
What is the hallmark of glomerulopathies? Which breeds predisposed?
Proteinuria
Tends to be high magnitude proteinuria >2
Golden retrievers and labradors predisposed
Much less common in cats
Pathophysiology of glomerulopathies?
Deposition of immune complexes in glomeruli (Type III Hypersensitivity reaction) or Ab production against glomeruli (Type II Hypersensitivity reaction)
Activation of complement
Local damage by inflammation
Leakage of proteins
Varying from moderately increased albuminuria to severe proteinuria
Can also get amyloid plaque deposition (Siamese, Shar pei, Beagles)
What are the most important causes of glomerulopathies?
Borrelia burgdorferi Leptospirosis FIP Sepsis Pyelonephritis Pyometra
When to suspect a glomerulopathy?
Sick animal with proteinuria that does not resolve with treatment
Newly diagnosed azotaemia and/or high protein
Hypertension of unknown origin
Thrombo(embolic) event
At risk breeds
Diagnosis of glomerulopathies?
Biopsy is gold standard but logistically difficult so rarely performed in practice
Measure for moderately increased albuminuria to detect earlier
Can present with or without a protein losing nephropathy (60%)
Dipstick to check for proteinuria - if positive, quantify with UP/C ratio
Most easily confirmed by taking a cystocentesis sample and analysing haematology and biochemistry
Persistence should be confirmed by showing the presence of proteinuria in 3 samples, 2 weeks apart
When to start treatment for proteinuria with glomerulopathy?
Only once confirmed (except no time to wait if systemically unwell/protein losing nephropathy/nephrotic syndrome)
1. persistent (3 measurements, 2 weeks apart)
2. renal (rule out pre and post causes)
3. quantified (UP:C)
Treat:
dogs >0.5
Cats >0.4
How to know if proteinuria is due to glomerulopathy or tubulointerstitial disease?
No accurate cut off but rule of thumb
>2 suggests glomerulopathy
<2 suggests tubulointerstitial
Treatment of proteinuria?
Mainstay of treatment is ACEI (benazapril)
- reduces efferent arteriole pressure leading to reduction in GFR and pressure within the glomerulus
- has mild effects on blood pressure
- but reducing GFR tleads to some increase in azotaemia, phosphate, and potassium (monitor!)
Angiotesnin II receptor blocker (telmisartan) - licensed in cats (not dogs), poss better than ACEI
More side effects with combined and not proven to improve outcome
Treatment of hypercoagulability with glomerulopathies? Why a problem? Why happens
Common consequence of glomerulopathies
Increases risk of thromboembolic events such as cerebro-vascular accidents or PTE
Due to loss of anti-thrombin III
Treatment options:
- low dose aspirin: cheap, reduces fibrosis
- clopidogrel: expensive, shown to be more efficacious in cats with other processes
- dalteparin: have to give frequently
Hypertension with glomerulopathies - Why a problem? Measuring? Treatment? Target?
Can have severe hypertension despite being non-azotaemic
Leads to end-organ damage (eyes, liver, heart, CNS, kidneys)
Measure accurately (best of five)
Standard treatment is amlodipine
Can increase proteinuria if uncontrolled
Target <150mmHg systolic
What diet to use for glomerulopathies?
Moderate protein restriction using a highly-digestible protein - reduces proteinuria and azotaemic events
Omega-3 supplementation reduces glomerular inflammation
If azotaemic, and indicated, place on renal diet
Pre/non-azotaemic….most likely beneficial to be on renal diet
Overall treatment for glomerulopathies?
ACEI or angiotensin receptor blockers to reduce proteinuria
Anti-hypertensive medication
Anti-thrombotic medication
Diet- moderate Protein Restriction/Omega 3 supplementation/renal diet
Treat based on IRIS recommendations if azotaemic
Prognosis of glomerulopathies?
Huge variation and difficult to easily quantify
Degree of azotaemia, presence of nephrotic syndrome, amyloidosis, and other co-morbidities affect survival
As a very general rule of thumb: otherwise healthy dogs with no-mild azotaemia roughly 6m-1y
Renal amyloidosis - Which breeds predisposed? What happens? Signs? Treatment?
Genetic predisposition in Shar-pei, Beagle, Siamese, Abyssinian
Deposition of amyloid plaques in glomeruli
Commonly results in high level of proteinuria (UP:C often up to 32, but on average is around 9)
Shar-peis commonly preceded by episodes of ‘Shar-pei fever’ = self-limiting swollen hocks/pyrexia
Rapidly progressive and commonly leads to nephrotic syndrome
Typical treatment + Colchicine and/or DMSO (no evidence that either are of any benefit)
Polycystic kidney disease (PKD) - Breeds? What is it? Age affected? Why is it a problem? Treatment?
Generally autosomal dominant (depends on breed
Persian (D), Ragdoll (D), British Short Hair (D), Bull terrier (D), WHWT (R)
Characterised by progressive cyst formation in kidney (also liver)
Cyst can present at a very young age but are generally slowly progressive
Clinically apparent when cystic lesions destroy 75% of functional nephrons and animal becomes azotaemic
Treat as per IRIS recommendations
Poor prognosis
Nephrotic syndrome - What is it? When seen? Characterised by?
Severe loss of protein from the glomerulus
Often seen in severe or end-stage glomerulopathies and common in amyloidosis
Characterised by:
- hypoalbuminaemia
- peripheral oedema
- hypercholesterolaemia
- +/- azotaemia
Very grave prognosis
Colloids should not be used although human albumin can be
Immunosuppression may be of benefit
Why do dogs get pyometra?
Cystic endometrial hyperplasia-pyometra
CEH develops during luteal phase (ovarian progesterone production) or with exogenous progestin therapy
Progesterone stimulates growth and activity of the endometrial glands and reduces myometrial activity
Colonisation of abnormal uterus with bacteria results in pyometra
Clinical signs of pyometra?
Signs tend to be more severe with closed pyometra Purulent vulval discharge (open pyometra) Inappetence Lethargy PUPD Vomiting Pyrexia Dehydration Palpably enlarged uterus?
Diagnosis and treatment of pyometra?
Diagnosis: - histroy - biochem, haem, urinalysis - vaginal cytology - radiography - ultrasound Treatment: - prompt and aggressive - IVFT - antibiotics (broad spectrum, bactericidal) - ovariohysterectomy - medical not recommended, may try if breeding animal with open pyometra (if successful, breed next cycle) - common adverse reactions to medical treatment and recurrence common
What causes uterine stump pyometra? Treatment?
Must have progesterone source:
- endogenous (incomplete removal of ovaries and uterine body)
- exogenous
Inspect ovarian pedicle scars, remove obvious abnormal tissue
When to suspect ovarian remnant syndrome? What to do?
Suspect incomplete removal of ovarian tissue if recurrent oestrus post OVH
Confirm with stimulation tests
Exploratory coeliotomy - exist scar tissue of ovarian pedicles and submit for histology
What causes uterine stump granuloma? Treatment?
Causes:
- poor aseptic technique
- excessive remaining uterine body
- ligatures on non absorbable suture material
Treatment - resect remaining uterine body and cervix
Fistulae associated with inappropriate suture material - Signs? Treatment?
Tracts discharging on flank, inguinal or medial thigh region
Temporary resolution with antibiotic therapy
Require exploratory coeliotomy, resection of ligatures and reactive tissue
Can be associated with multiple adhesions
What is vaginal hyperplasia/prolapse? When seen? How does it present? Treatment?
Oedematous enlargement of vaginal tissue during pro/oestrus
Mass may be seen protruding from vulval lips
Prolapsed tissue promotes straining
Mass may be traumatised by licking etc
Oedema spontaneously resolves after follicular phase but recurrence likely at next pro/oestrus
Mild cases can be treated conservative:
- prevent self trauma (collar)
- lubricate masss to prevent dessication
- reduction od prolapse and purse string suture around vulva?
Large masses may require resection (poss via episiotomy)
Indications for episiotomy?
Surgical exploration of the vagina
Excision of vaginal masses
Repair of vaginal lacerations post-mating
Treatment of strictures or congenital defects
Exposure of the urethral papilla
Facilitation of manual foetal extraction
What are episiotomies and episioplasties?
Episiotomy = an incision of the vulval orifice to allow access to the vagina/vestibule Episioplasty = reconstructive procedure to remove excess skin folds around the vulva
When is peri-vulval dermatitis due to excess skin folds seen?
Rare consequence of spying prior to first season
Clinical signs of ovarian tumours?
Often asymptomatic until develop signs referable to an abdominal mass Hormonal dysfunction (depending on tumour type) Malignant effusion
What are the 3 categories of ovarian tumours?
Epithelial
Sex-cord stromal cell
Germ cell
Diagnosis and treatment of ovarian tumours?
Palpable mid abdominal mass? Haematology and biochemistry Radiography US Abdominocentesis Exploratory laparotomy Treatment: - ovariohysterectomy - poss chemotherapy depending on histology
What are most canine uterine neoplasias? Signs? Diagnosis? Treatment? Prognosis?
Majority are mesenchymal origin - most are leiomyomas
Often incidental finding at OVH
May compress adjacent viscera causing associated signs
May rarely cause secondary vaginal discharge/pyometra
Diagnosis: radiography and US
Treatment = OVH
Prognosis:
- excellent for benign tumours
- reasonable for leiomyosarcoma if no metastatic disease evident at time of surgery
- poor if metastasis present
What are most feline uterine neoplasias? Clinical signs? Prognosis?
Mainly adenocarcinomas
May compress adjacent viscera causing associated signs
May rarely cause secondary vaginal discharge
Prognosis must be guarded because of their metastatic potential
Rarely seen as majority of female cats in UK are neutered
Differentials to a mammary mass?
Mammary neoplasia Other neoplasia - lipoma, MCT Mammary hypertrophy Mastitis Foreign body Cyst Granuloma
When does the prostate move to the pelvic position and why? Which animals affected by prostatic disease?
Moves from abdominal to pelvic position at around 2mo due to gradual hypertrophy
Prostatic disease common in mid-older male entire dogs (rare in cats)
Clinical signs of prostatic disease?
Dysuria Tenesmus Flattened faeces Constipation Hindlimb pain/stiffness
Investigation of prostatic disease?
Rectal/abdominal palpation
Urinalysis, culture and sensitivity
Radiography - plain caudal abdomen, retrograde urethrogram
Prostatic massage - cytology, culture and sensitivity
Prostatic biopsy
Abdominal US
What diseases of the prostate are there?
Benign prostatic hypertrophy (BPH) Prostatitis Prostatic abscessation Prostatic cysts - retention cysts, paraprostatic cysts Prostatic neoplasia
Benign prostatic hypertrophy - Which dogs? Clinical findings? Treatment? Prognosis?
Common finding in entire male dogs >5yo
Rectal palpation - symmetrically enlarged, non painful
Treatment - castration, poss anti-androgens
Excellent prognosis
Prostatisis/prostatic abscessation - When seen? Clinical findings? Treatment?
Often associated with BPH
Rectal palpation - asymmetrical enlargement, painful
Usually febrile, depressed
Often stiff hind limb gait
Caudal abdominal pain
Rupture of abscess will result in peritonitis
Treatment = drainage of abscess at exploratory laparotomy (castrate at same time), follow up with 4-6 weeks antibiotics
Prostatic cysts - Clinical signs? Types? Treatment?
Can cause defaecatory and urinary signs, and/or abdominal distension/mass
Types:
- retention cysts (accompany other prostatic disease, usually BPH, within the prostate gland)
- paraprostatic cysts (unknown aetiology, “outside” the prostate gland)
Treatment:
- excision for paraprostatic
- surgical drainage and omentalisation for paraprostatic
- US guided drainage for small cysts, may need repeated drainage
- castration
- treat concurrent infection if present
Prostatic neoplasia - Is it common? Which dogs affected? Most common type and their behaviour? Clinical signs?
Uncommon Older male dogs (entire and neutered) Adenocarcinomas are most common - highly malignant - 80% metastasised by time of diagnosis - spread via lymphatics to lymph nodes, lungs and skeletal system, especially lumbar vertebrae - direct extension to colon, bladder Clinical signs: - weight loss - hindlimb weakness/pain - defecatory tenesmus - lumbar pain - dysuria, stranguria, haematuria - PUPD
Diagnosis and treatment of prostatic neoplasia?
Diagnosis:
- radiography: wispy/pallisading new bone on pelvis/lumbar vertebrae, mineralisation within prostatic parenchyma
- US
- biopsy
Treatment:
- symptomatic treatment: analgesia, stool softeners etc
- poss castration
- poss urethral stenting: palliative for dysuria due to urethral obstruction
- prostatectomy not generally recommened (possibly if early diagnosis)
Why is prostatectomy not recommended for prostatic neoplasia?
Often spread to trigone area by time of diagnosis
Preservation of blood supply and innervation difficult so incontinence very likely
Re-anastomosis of urethra/bladder is difficult
wound dehiscence early possible complication
Stricture formation later possible complication
Indications for scrotal ablation?
Scrotal disease
In conjunction with scrotal urethrostomy
PU in entire cats
Poss cosmetic - castration of older dog with pendulous scrotum
Differentials for testicular swelling?
Testicular neoplasia Scrotal hernia Orchitis Trauma Scrotal dermatitis Testicular torsion
Types of testicular neoplasia?
Sertoli cell tumour (SCT)
Seminoma
Interstitial cell tumour
All have equal frequency
Testicular tumours:
Sertoli cell tumour - When seen? Behaviour? Clinical signs?
Seminoma?
Intersitital cell tumours?
Sertoli cell tumour 50% occur in retained testicles Important because of their ability to metastasise (2-15%) and ability to produce oestrogen Clinical signs: - abdominal distension (abdominally retained testicle) - feminisation - haematological abnormalities - prostatic enlargement
Seminoma:
Metastatic rate 5-10%
Rarely produce oestrogen
Interstitial cell tumour
Don’t metastasis
Often incidental finding
May be associated with increased testosterone levels thought to increase incidence of peri-anal adenoma and perineal hernia
Investigation and treatment of testicular tumours?
Haematology (assess oestrogen associated myelotoxicity) especially if:
- tumour is large
- abdominally retained
- feminisation
Cost effectiveness of thoracic radiographs due to low metastatic potential
Evaluate local lymph nodes:
- radiography
- US
- at coeliotomy (abdominally retained testicles)
Treatment:
- castration
- fresh whole blood transfusion pre-op if severely anaemic
- fresh whole blood/platelet rich plasma if thrombocytopenic
- good haemostasis
Prognosis for testicular tumours?
Excellent if no metastasis/myelotoxicity
Improvement of haematological parameters may take months
But myelotoxicity may be fatal despite aggressive supportive care
Causes of phimosis? Problems caused? Treatment?
Rare
Preputial opening too small due to:
- trauma
- neoplasia
- infection
Infection/irritation occurs due to urine pooling in prepuce
Treatment if infectious/inflammatory disease:
- conservative treatment
- antibiotics if associated infection
- urinary diversion via catheter
- preputial lavage
Treatment if congenital anomaly/stricture:
- reconstructive surgery of preputial orifice
Aetiology of paraphimosis? Problem caused? Treatment?
Mating Trauma Penile haematoma, neoplasia Preputial foreign body Posterior paralysis Failure of preputial muscles
Penis may become traumatised and circulation impaired
Treatment:
- identify cause
- relieve constriction
- reduce oedema (massage, diuretics, corticosteroids)
- flush prepuce with saline and lubricant
- preputial reconstruction, partial penile amputation, castration
Treatment of preputial/penile lacerations?
Conservative management (e.g. most haematomas)
Surgical treatment
Fracture of os penis - conservative, urethral catheter as stent, stabilise with plate/penile amputation
