Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
555 Cards in this Set
- Front
- Back
|
Normal Anatomy of the Female Reproductive Tract |
-Vulva: external opening
-Vestibule: area between the vulva and vagina --proximal to the urethral tubercle -Vagina: between the vestibule and the cervix |
|
|
Congenital Abnormalities of the Vulva
|
-Vulvar Stenosis |
|
|
Vulvar Stenosis
|
-Small vulvar opening
-Congenital abnormality of the vulva -Results in difficulty breeding --common in collies and shelties -Animal may have recurrent UTIs --urine is trapped in the vestibule, causes irritation and infection |
|
|
Vulvar Stenosis Treatment
|
-Episiotomy |
|
|
Vulvar Clefts
|
-Vulvar opening is too large
-Congenital abnormality of the vulva -Generally extends dorsally towards the anus more than it should -Excise the edges of the defect and close in three layers --mucosa, submucosa, and skin closures |
|
|
Acquired abnormalities of the Vulva
|
-Vulvar hypertrophy
-Recessed vulva |
|
|
Vulvar Hypertrophy
|
-Acquired abnormality of the vulva
-Hypertrophy of the vulva is normal during estrus -If persistent, indicates ovarian cyst or tumor --Luteal phase and XXX exposure should shrink the vulva |
|
|
Recessed Vulva
|
-Acquired abnormality of the vulva
-Excessive skin folds cover the vulva --overweight dogs -Moist environment in the peri-vulvar folds allow accumulation of urine, feces, and debris -Predisposes skin to dermatitis, vaginitis, cystitis, and UTIs |
|
|
Peri-vulvar dermatitis
|
-Irritation of skin around vulva
-Can be due to a recessed vulva in overweight dogs -Treat by clipping hair, washing and drying frequently, topical treatments, and encouraging the dog to lose weight -If mild, can treat topically |
|
|
Vulvar fold excision
|
-Surgical treatment for recessed vulva
-Episioplasty or vulvoplasty -Definitive treatment involves excision of folds -Estimate the amount of skin to be removed, make half-moon incision --Remove skin and fat, suture skin back together |
|
|
Vulvar fold excision results
|
-Dermatitis is usually resolved
-UTI issues are usually resolved -Effective procedure with low morbidity |
|
|
Dog Vagina Anatomy
|
-Area from the vestibule to the cervix
-Proximal to the urethral tubercle -majority of the vagina lies dorsal to the pubis -LONG structure, long vestibule makes digital palpation difficult --Too cranial to evaluate on PE --Surrounded by bone -Can assess with contrast radiography, ultrasound, CT/MRI, exploratory laparotomy -Can assess via episiotomy also, but is rare |
|
|
Congenital anomalies of the vagina
|
-Segmental aplasia or hypoplasia
-Persistent hymen -Double vagina -Rectovaginal fistula |
|
|
Vaginal segmental aplasia or hypoplasia
|
-Congenital anomaly of the vagina
-Vagina is poorly developed or small -Lesion can be anywhere along the vagina and can range in severity |
|
|
Clinical signs of Vaginal segmental aplasia or hypoplasia
|
-Partial: non-clinical, but interferes with breeding and parturition
-Segmentation: complete occlusion can occur, results in retention or uterine fluids |
|
|
Treatment of Vaginal segmental aplasia/hypoplasia
|
-None
-Digital dilation -Vaginoplasty via episiotomy -Resection and anastomosis -OHE or vaginectomy -Usually case presents as a dystocia, perform OHE during dystocia |
|
|
Persistent Hymen
|
-Paramesonephric ducts fail to unite or fuse or cannulate with the urogenital sinus
-Can have a ventral septum or a medial partition -Common in animals that have additional congenital abnormalities |
|
|
Clinical signs of persistent hymen
|
-None, can be an incidental finding
-Breeding difficulties or whelping difficulties -Chronic vaginitis -Urine pooling, can look like urinary incontinence but actually is not -Cystitis -Chronic UTIs |
|
|
Persistent Hymen Treatment
|
-Breakdown digitally
-Surgical resection via episiotomy -Vaginoscopy with laser breakdown |
|
|
Double Vagina
|
-Congenital anomaly of the vagina
-Intact septum between vagini -One usually ends in a blind pouch --one is connected to the uterus and is functional --Functional side is usually stenotic |
|
|
Rectovaginal Fistula
|
-Abnormal communication between the vagina or vestibule and the rectum
-Commonly seen with atresia ani (no rectum) -Can present as “pooping out of the vagina” -Animal may have persistent UTIs and infections |
|
|
Rectovaginal Fistula Treatment
|
-Restore the lumen of the rectum and vagina, separate
-Close the fistula surgically -Reconstruct an anal opening if atresia ani is present --opening will not have a sphincter, animal will not be able to control defecation |
|
|
Acquired abnormalities of the Vagina
|
-Vaginal hyperplasia or edema
-Vaginal prolapse -Vaginal neoplasia |
|
|
Vaginal Hyperplasia/Edema
|
-Acquired abnormality of the vagina
-Exaggerated response of the vaginal mucosa to estrogen -Vaginal tissue protrudes out of the vulva -Only involves tissue cranial to the urethral tubercle --does NOT involve the urethral tubercle -Treatment depends on extent and the health of the exposed tissue -Will recur with each heat cycle and repeated exposure to estrogen |
|
|
Vaginal Hyperplasia/Edema treatment
|
-Depends on extent of exposure and health of tissue
-Healthy tissue will spontaneously regress with luteal phase -OHE will prevent recurrence -If not surgically corrected, will recur with next estrus cycle and exposure to estrogen -Unhealthy tissue needs to be resected --OHE is necessary to precent recurrence |
|
|
Vaginal Prolapse vs. Vaginal Hyperplasia
|
-Prolapse is less common than vaginal hyperplasia
-Can look very similar! -Vaginal prolapse involves the urethral tubercle, tubercle will also be extruded -Hypoplastic vagina does NOT involve the tubercle |
|
|
Vaginal prolapse Treatment
|
-Mild: spontaneously resolves during diestrus |
|
|
Vaginal Prolapse Excision
|
-Urinary catheter placement is helpful and important
-Staged circumferential incision -Mucosa is re-apposed with sutures |
|
|
Vaginal neoplasia |
-More common in dogs than in cats
-More commonly benign neoplasia -On average happens in animals around 10 years old -Clinical signs: --perianal swelling --vulvar discharge --stranguria --tenesmus |
|
|
Vaginal Leiomyoma
|
-Most common type of vaginal tumor
-Boxer dogs may be predisposed -Can be solitary or multiple |
|
|
Types of vaginal neoplasia
|
-Leiomyoma (most common)
-TVT -Lipomas -Leiomyosarcomas -Mast cell tumors -Carcinomas (scc) |
|
|
Diagnosis of Vaginal neoplasia
|
-Physical exam
-Cytology or biopsy is needed for definitive diagnosis -Treatment is driven by knowing the type of cells involved |
|
|
Vaginal Neoplasia Excision
|
-Perineal stand is helpful |
|
|
Vulvovaginectomy
|
-Removing the vulva and vagina |
|
|
History in horses with renal disease
|
-PU/PD
-Pigmenturia -Stranguria -Fever -Dental tarter -Weight loss -NSAID use -Aminoglycoside antibiotics --gentamicin or oxytetracycline |
|
|
Serum Biochemistry in Horses with Renal Disease
|
-Increase in creatinine indicates more than 75% loss of functional nephrons
--lots of damage and loss! -BUN is not very useful in large animal species -Electrolytes: --Na and Cl decreased with polyuria --K will be increased --Ca is increased with chronic renal failure -Metabolic Acidosis may be present -Decreased albumin indicates glomerular disease --may also indicate colitis -PCV is usually normal but decreased EPO from kidney can lead to anemia |
|
|
Normal Horse Urinalysis
|
-Usually horse urine is yellow/brown
--can be reddish, especially on snow -Mucus-like consistency -Specific gravity depends on hydration status -pH is alkaline, 7-9 -LOTS of CaCO3 crystals -Urine is usually cloudy -Protein should be negative, but may have a slightly false positive with high pH -Glucose should be negative -Some bacteria will be present in free-catch urine |
|
|
Isosthenuria in Horses
|
-1.008 to 1.012
-Indicates hydration OR loss of more than 66% of functional nephrons -Isosthenuria is when kidney filtrate is as concentrated as the plasma it is filtering -If animal is dehydrated AND isosthenuric, BIG DEAL!! Not normal!! |
|
|
“Blood” on dipstick
|
-Measures heme, not free blood
-Heme is in myoglobin, hemoglobin, and RBCs -Positive for “blood” on dipstick could be any of the three |
|
|
Urine Specific Gravity in Renal Failure
|
-Becomes isosthenuric, more than 66% loss of functional nephrons
-Kidney is unable to appropriately adjust and regulate osmolarity of kidney filtrate -Urine concentration is equal to the plasma concentration all of the time -Animal is continually isosthenuric, even when it is dehydrated or very well hydrated -Cannot adjust osmolarity |
|
|
Ultrasound for Horse with Renal Disease
|
-Can be very useful
-Transcutaneous image of the kidneys -Trans-rectal image of the ureters and bladder -Can sometimes see stones or hydronephrosis, nephroliths -Left kidney is visualized through the spleen -Right kidney is heart-shaped and closer to the body wall |
|
|
CaCO3 crystals in horse bladder
|
-Normal finding
-Horse urine has A LOT of CaCO3 crystals -Will settle ventrally, and can be shaken up with movement |
|
|
Fractional excretion of electrolytes in Horse urine
|
-Electrolytes are freely filtered through the glomerulus and re-absorbed in the tubules
-If tubules are damaged, electrolyte reabsorption decreases --fractional excretion of electrolytes gets larger -Kidney wants to save Na, should reabsorb most Na --excretion should be less than 1% -Can compare Na in urine and in plasma to creatinine in urine and plasma to find fractional excretion |
|
|
Fractional Excretion equation
|
Fe (Na) = 100 * (urinary Na * plasma creatinine)/ (plasma Na * urinary creatinine)
|
|
|
Urine GGT in Horses
|
-GGT is induction enzyme of tubules
--produced when a tubule cells is excited or stimulated -Over-produced when tubular interstitium is inflamed -Tubular cells in kidney or in liver can become inflamed and release GGT -Increases in renal GGT is shed into the URINE --not into blood! |
|
|
Azotemia in Horses
|
-ANY increase in creatinine is significant!
|
|
|
Hyponatremia in Horses
|
-Increased loss via kidneys or GI
-Decreased intake |
|
|
Pre-renal Azotemia
|
-USG will be above 1.025
-Animal will be DEHYDRATED -Urine creatinine will be higher than serum creatinine --50:1 ratio -Urine volume will be decreased -Most likely due to dehydration -Can also occur due to decreased renal perfusion secondary to severe hemorrhage, shock, decreased CO |
|
|
Renal Azotemia
|
-USG will be 1.008 to 1.012
-Animal will be dehydrated, but will have polyuria -Urine creatinine levels in comparison to plasma creatinine is dropping --less than 37:1 -Urine volume may be increased with CRF, decreased with ARF -Electrolyte changes will be present -Mild anemia with CRF |
|
|
Post-renal Azotemia
|
-USG is variable
-Animal will have normal hydration or will be dehydrated -Urine to serum creatinine ratio is variable -Urine volume will be decreased -Animal may also have dysuria, stranguria, ruptured bladder, or uroperitoneum |
|
|
Acute Renal Failure
|
-Recent renal insult
--disease, toxin, trauma -Large, swollen kidneys -Casts in urine -Enzymuria -Often responds well to treatment |
|
|
Chronic Renal Failure
|
-Can have a confusing history
-Longterm NSAID use -Small, irregular kidneys -Poor response to treatment -Animal will be hypercalcemic |
|
|
ARF vs. CRF in Horses
|
-Often not obvious!
-Response to treatment is key -Treat animal and see what happens |
|
|
Toxins in Acute Renal Failure
|
-Aminoglycoside antibiotics
--gentamicin, amikacin -Oxytetracycline -NSAIDs --phenylbutazone, flunixin meglumine, ketoprofen -Pigment nephropathy --myoglobin due to acute rhabdomyolysis |
|
|
Vasomotor Nephropathy
|
-Decreased blood flow to the kidneys
-Kidney starts to fail due to ischemia -Animal is usually sick due to another cause --diarrhea, sepsis |
|
|
Acute Tubular Necrosis
|
-Will see casts
-Enzymuria, high GGT in urine -Micro-hematuria |
|
|
Papillary necrosis
|
-Renal pyramids rot and fall off
-can occur after NSAID use, especially bute and water deprivation -Classic pathologic lesion from NSAID use -Microhematuria may be present --positive on dipstick, but not visible in urine itself -Pre-disposes animal to nephroliths |
|
|
Fixing Acute Renal Failure
|
-Cannot be fixed!
-No medication exists to make tubular epithelial cells grow faster or better -Renal tubular cells have to regenerate on their own -Can stop patient from getting worse while the cells heal -Can make patient feel better while cells heal --treat uremia (azotemia) |
|
|
Acute Renal Failure Treatment in Horses
|
-Maintain Euvolemia
--prevent further cell damage by maintaining renal perfusion -Extra fluids will not make cells heal faster, not helpful -Diuresis can only correct uremia --flush out toxins that make the animal feel sick --Does not make cells heal faster -Diuretics allows body to get rid of uremic toxins, does not help healing process -Maintain electrolyte and acid-base balance |
|
|
Fluid treatment for horses with Acute Renal Failure
|
-Appropriate fluids to maintain systemic BP
-Weigh animal every 6 hours to make sure they are not retaining fluids -Check electrolytes and acid-base balance -Convert oliguria into polyuria --furosemide, mannitol, dopamine -Prognosis is variable, depends on response to treatment |
|
|
DDx for horse with PU/PD
|
-Renal cause: CRF or ARF
-Endocrine issue --PPID (most common) --Diabetes insipidus (rare) --Diabetes mellitus (very rare) -Psychogenic, salt eater -Other causes are possible |
|
|
Testing for Renal disease in horses
|
-CBC/Chem
-Urinalysis |
|
|
Testing for PPID in horses
|
-Endogenous ACTH, ACTH stimulation test
-Dexamethasone suppression test |
|
|
Testing for Diabetes Insipidus in Horses
|
-Water deprivation test
--have to be careful! Do not do if horse has azotemia -ADH response test |
|
|
Testing for Diabetes Mellitus in Horses
|
-Blood glucose levels
--Hyperglycemia with glucosuria indicates diabetes mellitus -Urinalysis |
|
|
Contraindication for Water Deprivation Test
|
-AZOTEMIA!
-Do not do test if animal is azotemic |
|
|
Azotemia + Isosthenuria
|
-Indicates renal disease
|
|
|
Tubulointerstitial Chronic Renal Failure
|
-Chronic interstitial nephritis
--chronic renal failure with an old insult, tubules have not “bounced back” -Chronic obstruction -Chronic pyelonephritis |
|
|
Glomerular Chronic Renal Failure
|
-Proliferative glomerulonephritis
--immune complex deposition --secondary to streptococcus in humans -Amyloidosis |
|
|
Treatment for Chronic Renal Failure
|
-Prognosis is poor
-Usually a progressive disease -Can stabilize animal with diuresis, makes animal feel better -Avoid dehydration! -If glomerulonephritis, treat inciting cause |
|
|
Pigmenturia DDx
|
-Hematuria
-Hemoglobinuria -Myoglobinuria -Pyrocatechines -Porphyrins -Bladder stones are most common cause for pigmenturia |
|
|
Hematuria in Horses
|
-Can be due to trauma
-Papillary necrosis -Cystitis -Will see “blood” on dipstick -Whole RBCs in urine sediment, urine will be red |
|
|
Hemoglobinuria in Horses
|
-Hemolysis, hemolytic process
-Will see “blood” on dipstick -Serum will be cherry red, urine will be dark red |
|
|
Myoglobinuria
|
-Rhabdomyolysis, muscle wasting, trauma, or breakdown
-Will see “blood” on dipstick -Urine will be red, serum will be clear --myoglobin is small, cleared from system but still filtered into urine |
|
|
Diagnosis of Myoglobinuria
|
-High muscle enzymes
-Clear serum -Normal sediment in urine -Due to exertional rhabdomyolysis, breakdown of muscle after exercise |
|
|
Myoglobinuria Treatment
|
-Diuresis to prevent pigment nephropathy
-Rest -Anti-inflammatory drugs or analgesics |
|
|
DDx for incontinence in Horses
|
-Neurogenic is most common
--upper motor neuron vs. lower motor neuron disease -Idiopathic neurogenic incontinence: --polyneuritis equi --Sabulous cystitis -Infectious neurogenic incontinence: --Equine herpes Virus 1 --Equine protozoal myelitis -Bacterial cystitis -Trauma -Congenital issue |
|
|
Lower motor neuron vs. upper motor neuron incontinence
|
-Flaccid vs. spastic
-No micturition vs. dribbling -Lesion at S1-S4 vs. lesion more cranial |
|
|
Polyneuritis equi
|
-Idiopathic neurogenic incontinence
-Idiopathic inflammation of the nerves, especially in the distal spinal cord -paraesthesia or hyperalgesia may be present around the tailhead -Diagnose with biopsy of sacrocaudalis dorsalis lateralis muscle -No definitive treatment -Prognosis is poor -Chronic, progressive degeneration of nerves in bladder and other nerves |
|
|
Sabulous Cystitis
|
-Idiopathic neurologic incontinence
-“Sandy” cystitis -CaCO3 crystal buildup makes a sandy plaque in the blader -Most common cause -Idiopathic bladder paralysis -Only affects the bladder -No definitive treatment -Prognosis is poor |
|
|
Equine Herpes Virus 1
|
-infectious cause of neurogenic incontinence in horses
-Fever, abortion storms, Upper urinary tact disease -Usually animal will have some ataxia or incontinence -Highly contagious!! -Reportable disease |
|
|
Other causes of equine incontinence
|
-Bacterial cystitis: usually secondary to urolithiasis or bladder paralysis |
|
|
Work-up for equine incontinence
|
-Neurologic exam
-Rectal exam to feel for cystoliths or sabulous urolithiasis --causes inflammation -Cystoscopy -Ultrasound exam of the bladder |
|
|
Congenital renal diseases in Horses
|
-Usually are very rare, but exist and need to be aware of them
-Renal agenesis, kidney did not form -Renal hypoplasia or renal dysplasia -Polycystic kidney disease -Fetal glomeruli -Ectopic ureters -Can show up later in life! |
|
|
Rare causes of renal disease in Horses
|
-Leptospirosis |
|
|
Complication of lower Urinary tract disease
|
-Urethral obstruction
-Any cat that presents with lower urinary tact signs should be assessed! -Especially with male cats |
|
|
Feline Lower Urinary Tract Disease FLUTD
|
-Umbrella term for clinical signs
-Stanguria, pollakiuria, hematuria, periuria -Does not really indicate underlying cause |
|
|
Possible causes for FLUTD
|
-Behavioral
-Neurologic disease -Urolithiasis (30%) -Bacterial infection (uncommon, 10%) -Feline Urethral Obstruction -Feline idiopathic cystitis (most common) --can develop urethral obstruction as a complication of cystitis |
|
|
Interstitial cystitis
|
-Diagnosis of exclusion
--have to exclude stones, bacteria, and all other causes |
|
|
Signalment of cat with FLUTD
|
-Young to middle-aged cats, 2-6 years
--Older cats are more likely to have neoplasia, urolithiasis, or infection -Males and females are equally represented when there is a non-obstructive disease -Feline urethral obstructions are always in male cats |
|
|
Clinical signs of FLUTD
|
-Crying, howling during urination
-Stranguria, straining to urinate -Pollakiuria, frequent urination -Passing only small amounts of urine (obstruction) -Licking genital area -Hematuria (macroscopic or microscopic) -Periuria, inappropriate elimination -Straining to defecate, abdominal pain, vomiting, lethargy, depression, recumbency -PALPATE IMMEDIATELY! |
|
|
Straining to defecate as FLUTD sign
|
-Looks a lot like straining to urinate!
-Owner will bring in “constipated” cat who is actually straining to urinate |
|
|
Bladder Palpation
|
-Firm, hard bladder: emergency!
-Soft bladder: no big deal |
|
|
Feline interstitial Cystitis
|
-Can affect 50-60% of cats that present with FLUTS
-Small non-palpable bladder (if not obstructed -Resolves in generally 7 days -Unknown underlying cause -Bladder inflammation and pain --no infection -Decreased production of GAGs, decreased protection of the bladder? -Stress component? -High recurrence rate, 39% will present again within a year |
|
|
Feline urethral Obstruction clinical signs
|
-Firm, hard bladder
--size varies from moderate to large -Painful abdomen, cat may growl/hiss/vocalize during palpation -Look at perineum and tip of the penis --tip of penis can be red or purple --blood on perineum --obstruction at tip of penis -Proceed with a complete physical exam if the animal is stable --focus on cardiovascular system, obstruction can lead to hyperkalemia |
|
|
Feline urethral Obstruction as an Emergency
|
-Kidney is primary regulator of K
-Obstruction results in increasing intravesicular pressures, ureteral, renal pressure --reduces GFR, reduces urine production --decreased urine production results in increased K retention, decreased K excretion -Progressive decreases in renal blood flow lead to renal ischemia and nephron loss |
|
|
Effects of Hyperkalemia
|
-Increasing intracellular and extracellular K concentration results in change in resting membrane potential
--resting potential becomes less negative -Fast Na channels and Na/K ATPase becomes inactivated -Difficult to depolarize the cell -Cardiac atrial cells are affected, automaticity of the heart is affected --results in arrhythmia -Cats with obstructions do not follow normal ECG pattern changes --have other electrolyte abnormalities |
|
|
Causes of Feline Urethral Obstruction
|
-Male anatomy!
--urethra is long and opening is tiny -Urethral plugs are most common --aggregates of proteins, crystals, WBCs, RBCs, etc. -Infection -Strictures -Stones (can just be in bladder but cause infection and therefore cause obstruction) -Urethral spasms -Idiopathic |
|
|
Treatment of Feline Urinary Obstruction
|
-Severity of clinical signs varies depending on length of time of obstruction
1. Stabilize cardiovascular system 2. Relieve the obstruction 3. Post-obstructive treatment |
|
|
Stabilizing a cat with urethral Obstruction
|
-IV catheter
-Bloodwork (CBC/CHem) --check electrolytes and kidney values --PCV, TS, Glucose -ECG to look for arrhythmias -Doppler blood pressure (hypotension is rare) |
|
|
Treating Hyperkalemia in Obstructed cat
|
-Treat if there is an arrhythmia AND elevated K levels
-IV fluids to dilute the K -Ca gluconate to Stabilize the heart rate and rhythm -Shift K intracellularly --insulin with or without dextrose --bicarbonate -Enhance excretion of K, unblock the cat |
|
|
Ca gluconate for Heart stabilization
|
-Works very quickly
-Increases cell membrane threshold potential -Re-establishes difference in resting membrane potential and threshold potential -3ml/cat over 5 minutes while monitoring ECG -May be repeated if needed -Effects should be immediate! |
|
|
Dextrose/Insulin for Hyperkalemia
|
-Moves K intracellularly
-Stimulates Na/K ATPase pump -Insulin stimulates pump, dextrose causes natural endogenous insulin release -Takes about 30 min to see an effect --lasts 1-2 hours -0.5g/kg of 50% dextrose IV -1 unit regular insulin |
|
|
Bicarbonate for Hyperkalemia
|
-Rarely given
-Slow effect, takes 30 min or more -Pushes K intracellularly by taking H out of the cell -HCO3 needs to be buffered, cell gives up H --CO2 is exhaled in lungs |
|
|
“Unblocking” a cat
|
-Cat is sedated with IV anesthesia
--opioid, valium, ketamine are most commonly used --can do sacral-coccygeal epidural with lidocaine -Clip perineum and surgically prepare -Sterile procedure! Use sterile gloves and drape if possible -Flush and retropulse the obstruction |
|
|
Decompressive cystocentesis
|
-Externally remove urine from the bladder
-Considered in cats when urinary catheter cannot be placed -delay happens in “unblocking procedure” --buys time -Risk rupture of the bladder and leakage of urine into abdominal cavity! -Not a treatment, just buying time -Relieves some back-pressure in urethra, can make passing the catheter easier |
|
|
Monitoring Urethral Obstructions in Cats
|
-Check urine output every 2-4 hours
--Minimum output should be 1-2ml/kg/hour -If urine production drops, check catheter and hydration of the cat -Monitor for post-obstructive diuresis --maintain fluids! -Can flush the bladder every 4-6 hours to remove grit and cells -Leave catheter in place 24-48 hours or until the urine is clear --no not remove before electrolyte abnormalities are resolved |
|
|
Causes of Urethral Obstructions in Cats
|
-Feline interstitial cystitis
-Infection -Uroliths |
|
|
Diagnostic work-up of cat with Obstruction
|
-Urinalysis
-Urine culture -Abdominal radiographs -Abdominal ultrasound -Uroendoscopy (rare) |
|
|
Medical treatment for Urethral Obstruction in Cats
|
-Antibiotics: only indicated if bacteria is present on urinalysis or urine culture
-Pain management is very important! -Urethral relaxation medications --alpha-2 receptor antagonists, prazosin, phenoxybenzamine |
|
|
Other therapy for Feline Idiopathic Cystitis
|
-goal is to decrease the severity and recurrence rates
-Decrease clinical signs -Do not have a “cure” -Short-term therapy in non-obstructive cats: --SQ fluids to flush bladder, questionable benefit --Pain management: oral buprenorphine -Avoid NSAIDs! |
|
|
Other therapy for Feline Idiopathic Cystitis
|
-Environmental enrichment |
|
|
Summary of FLUTD
|
-Non-obstructive and obstructive idiopathic cystitis is most common etiology |
|
|
Dietary factors that influence formation of uroliths
|
-Water intake
--determines concentration of substances in urine -Na content -Fat content -Carbohydrate content -Diet digestibility -Content of calculogenic substances -Quantity consumed -Meal frequency -Diet influence on urine pH |
|
|
Water intake and urolith formation
|
-The more water the animal drinks, the more dilute the urine
-More dilute urine results in less chance of material precipitating -More saturated urine allows calculogenic substances to form a stone -Increasing Na content of diet increases water intake |
|
|
Fat and Carbohydrate in diet and urolith formation
|
-Influence the amount of metabolic water generated by body
-Water is produced when fat is combusted in the diet -Urolith prevention diets tend to be high-fat |
|
|
Diet digestibility and urolith formation
|
-If diet is not very digestible, more stool will be produced
--more water will go into stool instead of into urine -Lower digestibility increases water that is absorbed in the gut -higher digestibility increases water that is excreted in urine |
|
|
Impact of diet on urine pH and urolith formation
|
-Certain uroliths are soluble at certain pH
-diet can influence pH of urine -Meal frequency can impact urine pH |
|
|
Factors that prevent urolith dissolution
|
-Uroliths are not diet-induced disease
--diet does not have a huge impact on urolith formation --at best, uroliths are a diet-sensitive disease -IN most cases, effective diets are extreme and are not designed for long-term maintenance |
|
|
Hill’s Canine U/D
|
-Diet designed to decrease kidney disease or uremia
-Restricted in protein, Ca, P, Na, K, and Mg -High in fat, low in protein -Associated with protein depletion, dilated cardiomyopathy, and pancreatitis -Medullary washout, hypoalbuminemia, |
|
|
Dietary and medical management of Urolithiasis for Struvites
|
-Magnesium ammonium phosphate
-Associated with UTIs in dogs -Very soluble in acidic environment, low pH (6.7 or below) -Also need to treat infection, use antibiotics |
|
|
Struvite Dissolution diet
|
-Can be used with infection if infection has been treated appropriately
-No need to use a preventative diet if infection is under control -See patient regularly, do urinalysis regularly --can catch potential uroliths early -Stone will re-form if infection is not prevented -LOW protein diet, lowest protein diet there is --can only be used for a short period of time |
|
|
Sterile struvite diet
|
-CAN use a prevention therapeutic diet
-As long as urine pH stays acidic, should not have an issue |
|
|
Struvite prevention
|
-Prevent recurrence of UTIs
--most important -Promote an acidic urine pH, less than 6.7 --can be done if stone is sterile -Promote water intake |
|
|
Protein restriction and urolith formation
|
-MAP urolith has ammonium
-Ammonium is produced in urine from degradation of urea -Urease bacteria breaks down urea, causes high ammonium concentration -Restrict protein, less protein breakdown, less urea is formed --less urea, less opportunity for urease bacteria to break down urea and form ammonium |
|
|
Ammonium Urate uroliths
|
-Common in Dalmatians
-Liver disease, shunt -Often idiopathic -Metabolic abnormality -Formed from uric acid --purine precursor |
|
|
Protein restriction and urolith formation in a cat
|
-Cannot restrict protein intake in a cat! They will just break down tissues and get protein anyway
|
|
|
Treatment and prevention of Ammonium Urate Uroliths
|
-Allopurinol: reduces uric acid excretion
-Keep urine alkaline -Restrict or reduce purine intake in diet --alternative protein sources, not meat -Promote water intake |
|
|
Purines in the Diet
|
-Nucleotide, in DNA
-Want a food that does not have cell nuclei to avoid purines -Look for non-cellular protein sources --egg with albumin --Soy protein -Only purine-restricted diet is Royla Canin Urinary UC diet --low purine, egg and corn gluten |
|
|
Cystine Uroliths
|
-Relatively rare
-Common in newfoundlands, mastiffs, English bulldogs -Can be treated with 2-MPG -Alkalinizing diet can help dissolve uroliths -Promote water intake |
|
|
Calcium Oxalate Uroliths
|
-Common in dogs and cats
-Cannot be dissolved! Have to surgically remove or break up with laser -No proven methods for preventing recurrence -Solubility is the same regardless of pH |
|
|
Etiologic risk factors for Calcium Oxalate Uroliths
|
-Hypercalcinuria
-Hyperoxaluria -Decreased inhibitors of Calcium oxalate -Decreased urine volume |
|
|
Water intake and Calcium Oxalate uroliths
|
-Increased water intake causes increased urine volume
--dilutes calculogenic substances -May also increase the number of urinations per day --minimizes time available for urolith initiation and growth -USG in dog: below 1.025 -USG in cat: below 1.035 |
|
|
How to get an animal to drink more water
|
-Put salt in diet
--would need A LOT -Do things that make animal want to drink --running water fountain -Feed canned food -Add water to food -Add something to the water to make animal want to drink it -Make drinking a pleasurable experience for the animal, experiment with water sources -Make water easy access, put bowls all over the house |
|
|
Prevention or Calcium Oxalate urolith recurrence via Calcium intake
|
-Increased calcium excretion in the urine is a risk factor
-Not only Ca from diet is the issue -Can be due to renal calcinuria or resorptive calcinuria (released from bone) -Lots of conditions leads to Ca excretion -In diet, dietary acidification is key for increasing urinary excretion of Ca --Alkaline or neutral urine pH is best! |
|
|
pH and Calcium oxalate uroliths
|
-Acidifying diets will increase Ca resorption from bone
-Alkaline or neutral diets are best for animals at risk of Ca oxalate uroliths --NOT because of solubility, because of bone resorption |
|
|
Oxalate Intake and Calcium oxalate urolith formation
|
-Can be absorbed from diet or produced endogenously
-Endogenous oxalate can be an concern --by-product of glycine and vitamin C metabolism --DO not give vitamin C supplements to pets! -Vitamin V6: cofactor in glycine metabolism --deficiency can lead to increased oxalate production |
|
|
Calcium restriction in the diet
|
-May increase oxalate uptake in the gut
-Normally oxalate is not absorbed, complexes with dietary calcium -Without Ca present, oxalate is not complexed and excreted |
|
|
Inhibitors of Calcium Oxalate formation
|
-Mg and citrate
-Decreased Mg can result in increased CaOxalate urolithiasis in cats (not proven) -Potassium citrate alkalinizes urine --effect on urine citrate concentrations and efficacy in preventing CaOxalate uroliths is unknown |
|
|
Diets marketed for prevention of Calcium Oxalate urolith recurrence
|
-Hill’s C/D multicare (cats)
-Nestle-Purina UR st/ox (cats) -Iams Moderate pH/O (cats) -Royal canin Urinary S/O (feline and canine) |
|
|
Summary of Urolithiasis and Diets
|
-Urolithiasis is rarely the direct result of diet
--has underlying metabolic or infectious causes -In most cases effective diets are extreme and not designed for long-term maintenance -Determine urolith composition -Treat any underlying conditions -Promote water intake -Modify urine pH when appropriate |
|
|
Feline Lower Urinary Tract Disease FLUTD
|
-Idiopathic cystitis (79%
-Urolithiasis (13%) -Neoplasia (2%) -Congenital malformations (5%) -Infection (1%) |
|
|
Acidifying ingredients in Cat foods
|
-Animal source proteins
-Methionine -acidifying calcium salts (CaCl) -Palatability enhancers -Phosphoric acid |
|
|
Cat food formulation in 1990’s
|
-Produced urine pH 6-6.5
-Restricted Mg content -Saw decreased struvive uroliths, increase in calcium oxalate uroliths --no change in idiopathic cystitis |
|
|
Treatment of idiopathic cystitis
|
-Treat symptomatically, treat pain and inflammation |
|
|
Urinary Disease in Farm Animals
|
-Upper urinary tract is “quiet,” diseases look like all other internal medicine cases
--kidney (ARF, pyelonephritis, amyloidosis) -Lower urinary tract is “noisy” --ureter, bladder (cystitis), urethra (urolithiasis) |
|
|
Acute Renal Failure in Farm Animals (Hemodynamic)
|
-dehydration
-Endotoxemia --septic mastitis, metritis, diarrhea -Sickness from primary condition can lead to secondary renal failure |
|
|
Acute renal failure in farm animals (toxic)
|
-History of treatment or exposure is key!
-Be sure to ask about specific drugs -Aminoglycosides -Oxytetracycline -NSAIDs -Heavy metals -Oxalate containing plants --improper mixing of feeds -Vitamin D |
|
|
Clinical signs of ARF in farm animals
|
-Non-specific signs, can look like anything
-Need lab tests to make diagnosis |
|
|
Diagnosis of ARF in farm animals
|
-Blood chemistry
--increased creatinine, magnesium, phosphorous, potassium --Decreased sodium, Cl, and calcium -Urinalysis is important --look for protein, blood, casts -Isosthenuria |
|
|
Treatment for ARF in farm animals
|
-Correct electrolyte abnormalities
-Give fluids to prevent renal ischemia --Monitor the fluid balance well -Treat primary underlying disease -Same treatment principles as ARF in all other animals |
|
|
Oak Toxicosis
|
-All parts of the oak is toxic!
-Buds and acorns are most often consumed and cause toxicity -Calves are predisposed -Cattle are more affected than sheep and goats, horses are least affected -Tannins are the toxin that causes issues --affects kidneys -Also has GI effect, can cause diarrhea and bloat -Often seen in multiple animals in a herd -Usually only eaten when there is nothing else to eat |
|
|
Chronic renal failure in farm animals
|
-Not very obvious
-No specific treatments -Economically treatment might not be worthwhile |
|
|
Pyelonephritis in farm animals
|
-Infection of the kidney and renal pelvis
-Usually ascending infection, rarely hematogenous --starts as cystitis that ascends up ureters to kidneys -E. coli and coliforms are most common -Corynebacterium renale is also very common -Sporadic disease, not contagious -Mostly affects adult cows after calving -Entire urinary tract is affected |
|
|
Risk factors for cows and Pyelonephritis
|
-Post-partum cows are most predisposed
-Obstetrical procedures -Urinary catheterization -Urine stasis -Stress due to pregnancy and parturition |
|
|
Clinical signs of Pyelonephritis in Cows
|
-Entire urinary tract is affected, clinical signs reflect infection
-Acute signs: --fever, hypogalactia, anorexia, colic, hematuria, dysuria --decreased milk production --Systemically ill animal --Colic is an uncommon sign in cattle, but common sign in pyelonephritis -Chronic signs: --weight loss, anorexia, may or may not have a fever |
|
|
Diagnosis of Pyelonephritis in Cows
|
-History and physical exam
-Rectal exam --if acute, left kidney will be big and painful with decreased lobulations --kidney may also be sensitive to touch --may be able to palpate the ureters if they are inflamed -increased fibrinogen -Increased WBC, leukpocytosis -May or may not have increased creatinine -Urinalysis may have RBCs, WBCs, protein, bacteria on culture -Can ultrasound the kidney |
|
|
DDx for pyelonephritis in cows
|
-Dysuria: cystitis or urolithiasis
-Colic: intussusception or other GI issue -Enlarged kidney: --amyloidosis --hydronephrosis --lymphosarcoma |
|
|
Pyelonephritis Treatment
|
-Antimicrobials based on culture and sensitivity
-Corynebacterium renale: Penicillin -Coliforms: Penicillin (penicillin concentrates in urine, is pretty effective) --can also use others after culture results and response to penicillin -Prolonged treatment may be needed -If unilateral, consider nephrectomy (expensive) |
|
|
Leptospirosis in Cattle
|
-Zoonotic
-Motile, gram- spirochete -Infection via exposure of mucus membranes to leptospirosis bacteria -Spread in urine, vaginal secretions, placenta, semen, or contaminated water (farm ponds) -2 types: host adapted and non-host adapted |
|
|
Host adapted Leptospirosis in cattle
|
-Leptospirosis interrogans Hardjo hardjoprajitno
-Leptospirosis borgpetersenii Hardjo hardjobovis -Rarely cause acute severe disease --more often chronic disease -Infertility, abortion, weak calves -Mastitis, agalactia -Chronic interstitial nephritis and chronic infection of genital tract aremost common manifestations |
|
|
Non-host adapted leptospirosis in cattle
|
-Causes disease! Nephritis, illness, and death
-Leptospirosis interrogans Ponoma -Leptospirosis interrogans grippotyphosa -Severe hemolytic disease -Interstitial nephritis -Tubular nephrosis -Fever, hemolytic anemia signs, hemoglobinuria, oliguria -Calves are more severely affected |
|
|
Leptospirosis in Cattle Diagnosis
|
-Serology: Microscopic agglutination Test
-Urine tests: culture is usually not helpful --can do FA or PCR -Renal tissue staining: --silver, immunoperoxidase |
|
|
Microscopic Agglutination test
|
-Test to look for leptospirosis
-For non-host adapted: rise in titer or high titer is suggestive -Vaccination status may confound results -For Hardjobovis: leptospiruria with low titers |
|
|
Treatment of leptospirosis in Cattle
|
-Antimicrobials
--oxytetracycline is nephrotoxic! Use carefully! --Penicillin has questionable efficacy -Supportive care --fluids --NSAIDs (again, nephrotoxic!) --blood transfusions can be used if anemia is severe |
|
|
Leptospirosis Prevention
|
-Reduce exposure
-Identify and treat carriers -Vaccinate --pentavalent --monovalent |
|
|
Renal Amyloidosis in cows
|
-Rare disease in cows
-Occurs after chronic inflammatory disease --mastitis --hardware disease --foot abscess --pneumnia -Amyloid protein is deposited in renal tissue -Causes protein losing nephropathy or protein losing enteritis -Clinical signs: non-specific --chronic diarrhea, edema, weight loss --looks like Johne’s disease! |
|
|
Diagnosis of Renal Amyloidosis in Cows
|
-Kidney will be large, non-painful, lobulated
-Proteinuria -Hypoproteinemia -High fibronigen -increased immunoglobulins |
|
|
Other kidney diseases in cows
|
-Glomerulonephritis
-Neoplasia (lymphoma) -Congenital diseases |
|
|
Cystitis in Farm animals
|
-Ascending infection
-Much more common in females than in males -Post-partum cows are most common --Post-partum bladder paralysis -Urachitis in calves can cause cystitis -Animal will not be systemically ill, unlike pyelonephritis -Will see dysuria and pollakiuria |
|
|
Omphalitis/Urachitis
|
-Infection of the umbilical stump
-Environmental contamination of umbilicus at or near birth -Many infections are internal, will not see external expression --external palpation may be normal -Diagnose with palpation and ultrasound -Will see increased fibrinogen, WBCs, urinalysis |
|
|
Sequelae of umbilical infections
|
-Septicemia
-Poor doer -Cystitis (via ascending infection from urachus) -Mechanical restriction of the bladder that can lead to a rupture -Dysuria and pollakiuria |
|
|
Pizzle Rot
|
-Ulcerative posthitis or vulvitis
-Seen most often in merino and angora goats -Contagious disease -Caused by corynebacterium renale --converts urea to ammonia, urease bacteria -High protein diet predisposes, increased protein gives more urea, more substrate -Ammonia is corrosive to epithelium -Wool and hair traps ammonia, causes necrosis of epithelium -Ulceration of prepuce, urethral mucosa, vulva, vagina -Treat with Penicillin -Prevent by trimming hair and low-protein diet |
|
|
Enzootic Hematuria in Farm animals
|
-Bracken fern toxicity |
|
|
Causes of Urinary Tract Trauma
|
-Abdominal trauma is most common
-Pelvic fractures -Penetrating wounds -Urinary calculi -Surgical complications -Iatrogenic -Anything that causes enough damage to traumatize the urinary tract will probably also cause other damage -Urinary issues are often overlooked when there are other issues going on |
|
|
Ureteral calculi and trauma
|
-Can cause major trauma to urinary tract!
-Can erode through the wall of the ureters -may cause abcessations in retroperitoneal space |
|
|
Surgical complications causing urinary tract trauma
|
-suture around ureter during a spay
|
|
|
Diagnosis of Urinary Trauma
|
-History
-PE -CBC/Chemistry -Evaluatio of peritoneal fluid -Abdominal radiographs -Abdominal ultrasound -Contrast studies |
|
|
History for patients with urinary trauma
|
-Often vague clinical signs
-Hematuria, dysuria, anuria -Abdominal swelling -Abdominal bruising indicates hemorrhage or urine leakage into peritoneal cavity -History of previous catheterization |
|
|
Physical Exam of a patient with Urinary trauma
|
-Abdominal distention
-Perineal bruising indicates distal/lower lower urinary tract leakage -Abdominal bruising -Pain on abdominal palpation -Hematuria, dysuria, anuria -Just because a patient can urinate does not rule out a bladder rupture --can still urinate with a ruptured bladder |
|
|
CBC/Chem and urinalysis for urinary trauma patient
|
-Hyperkalemia
-Azotemia -Increased phosphorous -Increased potassium -May present with normal bloodwork initially -Culture fluid to rule out infection |
|
|
Peritoneal Fluid
|
-Compare creatinine and potassium of abdominal fluid
-Compare to peripheral blood -If Creatinine is 2x in abdominal fluid as peripheral blood, urine in abdominal cavity! -Can also look at urea if trauma was very acute --diffuses quickly |
|
|
Serum creatinine ratio normal values
|
-Dog:
--serum: effusion should be 1:2 --potassium serum to effusion should be 1:1.4 -Cat: --serum: effusion should be 1:2 --potassium serum to effusion should be 1:1.9 |
|
|
Urinary trauma on abdominal radiographs
|
-Absence of a urinary bladder
-Loss of abdominal detail -Loss of retroperitoneal detail -Increased size of retroperitoneal space --kidney may be displaced from spine --whispy indicates leakage or hemorrhage |
|
|
Abdominal ultrasound for urinary trauma
|
-Evaluate kidney and retroperitoneal space
-Evaluate the bladder -not helpful for urethra and ureters, too small |
|
|
Contrast studies for urinary trauma
|
-Excretory urography
-Positive contrast urethrocystography --need to be sure to fill bladder with contrast to identify small leaks -CT angiography |
|
|
Initial stabilization of patient with urinary trauma
|
-IV fluids
-Correct electrolyte and acid/base abnormalities -Dialysis or urinary diversion may be needed --animal is not stable enough to undergo anesthesia -Evaluate for other traumatic injuries -Evaluate for cardiac arrhythmias and hemoperitoneum -Antibiotics are important for urine contamination and necrotic tissue |
|
|
Treatment for Hyperkalemia
|
-IV fluid therapy
-IV 10% Ca gluconate --50-100 mg/kg slowly over 5 minutes -Regular insulin and dextrose -Sodium bicarbonate (avoid unless patient is severely acidotic) |
|
|
Surgery of the Ureter
|
-Lacerations are common
-Most often end up doing a nephrectomy also, injuries tend to be very severe -Urine is not a good medium for ureter to heal --want to divert urine while ureter heals --nephrostomy tube |
|
|
Ureteral Implantation
|
-Can cut and re-attach ureter
|
|
|
Surgical treatment of the bladder
|
-Most common area for trauma
-Easiest to deal with surgically -Resect damaged or diseased tissue -Can lose 80% of the bladder and still be OK -Primary repair, single or double layer closure |
|
|
Surgical treatment of the Urethra
|
-Bladder can avulse off of the urethra, complete separation
-Can try to bring edges back together -Divert urine to give tissue a chance to heal -Blood supply and innervation is usually affected, poor prognosis -Distal urethral injury will have perianal bruising |
|
|
Cystostomy tube
|
-Diverts urine from urinary tract
-Gives damaged tissue time to heal outside of urine environment -Make stab incision in skin away from bladder (like lung) -Can use to assess healing, put contrast into urinary bladder -Can insert a wire through bladder, into urethra --can place urethral catheter |
|
|
Post-operative care for urinary tract trauma cases
|
-IV fluids
-Monitor azotemia and acid/base balance -Monitor animal for signs of a urinary obstruction -Monitor animal for signs of peritonitis -Monitor animal for signs of urine leakage |
|
|
Anatomy of the Penia
|
-Divided into 3 main portions
--root: connects penile body to the pelvis, ischiocavernosus muscle --body: corpus cavernosus, corpus spongiosus --glans: proximal part and distal part -Corpus cavernosum -Corpus spongiosum -Urethra -Os penis -4 paired muscles |
|
|
Glans of the penis
|
-Bulbus glandis: smaller proximal portion
-Pars longa glandis: larger distal portion -Separated by fibrous septum |
|
|
Corpus Cavenosum
|
-Tissue in the glans of the penis
-Arises from crura, comes together and forms part of body of the penis -2 portions that are separated by tunica albuginea -Extends just beyond the os penis -Runs dorsolateral to the body of the peins |
|
|
Corpus Spongiosus tissue
|
-Originates in the pelvic cavity as the bulb of the peins
--Bi-lobed expansion of the bulb of the penis -Surrounds penile urethra -Extends to the external urethral orifice |
|
|
Os penis
|
-Bone in the dog peins
-Begins caudal to the bulbus glandis -Extends almost to the tip of the glans penis -Tip is a fibrocartilagenous projection -Has distinct groove in ventral area that urethra runs through --stones can get caught in the groove, urethra cannot expand -Attaches to the bulbus glandis, pars longa glandis, and tunica albuginea |
|
|
Muscles of the penis
|
-Ischiocavernosus muscle
-Ishiourethralis muscle -Bulbospongiosus muscle: originaltes from external urethral sphincted, runs entire way down the body of the penis -Retractor penis muscle: originates from caudal vertebrae --fuses with external anal sphincter and runs along entire body of the penis |
|
|
Vasculature to the penis
|
-Internal pudendal artery and vein
-All branches eventually anastomose with each other -3 main branches: --artery and vein of the bulb of the penis --deep artery and vein of the penis --Dorsal artery and vein |
|
|
Nerve supply to the Penis
|
-Main innervation is from sacral and pelvic plexuses
-Main sensory nerve is a branch off of pudendal nerve --continues as dorsal nerve of the penis -Pelvic nerve is parasympathetic innervation -Hypogastric nerve is sympathetic innervation |
|
|
Prepuce
|
-Continuous with the skin of the ventral body wall
-Forms a complete tubular sheath -Parietal, visceral, and dermal layers -Preputial muscles arise from cutaneous trunci muscles -Dermal layer is fed by caudal superficial epigastric artery -Parietal and visceral layers are fed by external pudendal artery and vein, minor from dorsal artery of the penis |
|
|
Penis Physiology
|
-Os penis facilitates vaginal entry
-Internal pudendal artery allows for massive increase in blood supply --Canvernous tissues engorge -Venous drainage is obstructed during the “tie” |
|
|
Hypospadia
|
-Abnormal position of the urethral orifice
-Can be located at the gland, scrotum, perineum, anus -Failure of normal prepucial fusion, prepuce does not fuse -Rare condition -Most common in boston terriers -Will see dermatitis and staining of the hair in the area |
|
|
Scrotal Urethrostomy
|
-Neuter patient
-Retract retractor penis muscle, cut down to urethra -Make a new opening for urethra -Should not stricture when sutured to the skin --will contract down, but should not cause stricture |
|
|
Penile Wounds
|
-Hemorrhage is most common clinical sign
--may be intermittent, but profuse -Fights, fences, cars, gunshots, mating -Need to evaluate integrity of the urethra --subQ swelling is associated with urine extravasion -Urinary catheter may be necessary -Os Penis may be fractured -Amputation of the penis may be necessary |
|
|
Strangulation of the Penis
|
-Not common
-Constriction from preputial hairs or malicious acts -Dog will be painful, frequently licking prepuce -Dysuria may be noted -Minor trauma, give supportive treatment -Remove inciting cause -Can use topical antibiotics -More severe cases may need an indwelling catheter -Severe trauma may require partial or complete penile amputation |
|
|
Partial Penile Amputation
|
-More common than complete penile amputation
-If penis is shortened, may also need to shorten prepuce --do not want to urinate into preputial cavity -Preserve more urethra than bone, spatulate to preputial mucosa |
|
|
Os Penis issues
|
-Can have deformities or fractures
-Dysuria, hematuria, crepitus -Urethral obstruction -Some deformities may result in inability to retract some of the penis --tissue will dry out, dog will lick, becomes an issue -Usually can be treated conservatively --minimally displaced fractures do not need to be immobilized --displaced fractures can be splinted with urinary catheter --comminuted fractures can be stabilized with small plates -Severe cases of trauma may necessitate amputation |
|
|
Balanoposthitis
|
-Inflammation of the penis and prepuce
-LOTs of discharge from preputial cavity -Animal will be painful and inflamed -Adhesions can form between penile body and preputial cavity -can occur secondary to another cause, Need to treat underlying cause --penile injury --phimosis --preputial foreign body --neoplasia |
|
|
Phimosis
|
Cannot protrude the penis from the prepuce due to a problem with the prepuce
|
|
|
Balanoposthitis treatment
|
-Treat underlying cause
-Symptomatic treatment -May need general anesthesia -Lavage penis and preputial cavity -Cut adhesions between penis and prepuce -Antimicrobial infusion -Guarded prognosis, tends to recur |
|
|
Persistent penile frenulum
|
-Normal structure that should break down after birth but does not
-Band of tissue fuses glans portion of the penis to the prepuce -Causes ventral deviation of the glans -Painful! -Avascular tissue, can cut band and is fixed |
|
|
Penile tumors
|
-Melanoma, TVT, and SCC are most common
--papillomas, osteosarcoma of os penis -Important to get diagnosis of tumor type for treatment -Serosanguinous discharge -Can partially or completely amputate the penis -Radiation and chemotherapy are treatment options |
|
|
Complete penile amputation
|
-Pretty straight-forward procedure
-Elliptical incision is made along the base of the prepuce -Ligate blood supply from epigastric and pudendal vessels -Perform urethrostomy -Transect and remove penile body |
|
|
Paraphimosis
|
-Persistent protrusion of the penis, penis cannot be replaced into normal position or location without medical or surgical intervention
-Clinical signs depends on duration of protrusion -Glans become congested and discolored -Licking exacerbates the issue and can result in severe penile damage -Necrosis and urethral obstruction can occur |
|
|
Causes of paraphimosis
|
-Congenital:
--narrow preputial opening, hypoplastic prepuce -Acquired: --trauma, infection, priapism, foreign body, neoplasia, idiopathic -Conservative management is often successful! Need to replace the penis |
|
|
Medical Treatment for Paraphimosis
|
-Lubrication
-Hyperosmolar solutions -Local heat or cold -Reflect prepuce to improve circulation -Push penis caudally and pull prepuce cranially -Steroids or diuretics -Urethral catheter -Once peins gets back into the prepuce, condition resolves usually |
|
|
Surgical management of Paraphimosis
|
-Preputiotomy, remove part of prepuce
-Modification of the preputial orifice -Lengthen the preputial orifice -Penile amputation |
|
|
Conditions of the Prepuce
|
-Congenital
-Phimosis -Trauma -Neoplasia --benign: hemangioma, papilloma, histiocytoma --Malignant: Mast cell tumors, melanomas, hemangiosarcomas, SCC |
|
|
Phimosis
|
-Inability of the penis to protrude from the prepuce past the preputial orifice
-Urine stays in preputial cavity, cause inflammation and adhesions -Clinical signs depends on the size of the orifice and underlying cause -Rare -Usually the result of too small opening |
|
|
Preputial Neoplasia
|
-Not many benign tumors, most often malignant
-Mast cell is most common -SCC occurs also |
|
|
Neoplastic Conditions of the Prepuce
|
-Diagnosis is made by incisional, excisional, or cytological biopsy
-Treatment includes surgical removal and closure of the prepuce -Penis needs to stay covered by the prepuce -Urethral orifice needs to be maintained -Penile amputation and urethrostomy may be needed |
|
|
Priapism
|
-Persistent erection |
|
|
Urethral Prolapse in the penis
|
-Most common in English bulldogs |
|
|
Normal Micturition
|
-Depends on properly functioning anatomy and neurologic control
-Complex system -Parasympathetic, sympathetic, and somatic innervation |
|
|
Innervation to the bladder
|
-Hypogastric nerve: from L1-L4
--sympathetic innervation --releases norepi and relaxes the bladder and contracts sphincter -Pelvic nerve: from S1-S3 --parasympathetic innervation --ACh is released, causes contraction of muscles and urination -Pudendal nerve: S1-S3 --somatic innervation to external urethral sphincter --releases ACh -External urethral |
|
|
Parasympathetic innervation to the bladder
|
-Pelvic nerve from S1-S3
-Releases ACh -Stimulates detrusor contraction -Allows urination |
|
|
Sympathetic Innervation to the bladder
|
-Hypogastric nerve from L1-L4
-Releases Norepi -Causes relaxation of bladder muscles -Contracts sphincter, prevents urination |
|
|
Somatic innervation to the bladder
|
-Pudendal nerve from S1-S3
-Releases ACh -Causes contraction of sphincter, prevents urination |
|
|
Sensory nerves in the bladder
|
-Visceral afferents
-Pain afferents -Mechanoreceptors to sense stretching |
|
|
Patients with Micturition disorders
|
-Mostly urinary incontinence
-Also stranguria, polyuria, etc. -Need to differentiate pollakiuria from polyuria -May have behavioral issues -Need complete medication history |
|
|
PE findings for patient with micturition disorders
|
-may be completely normal
-recessed vulva -hypospadia -perineal dermatitis due to urine scald or excessive licking/grooming -Neurologic exam to look at reflexes, tone, etc. -Size and expressability of the urinary bladder |
|
|
Urinary incontinence
|
-Involuntary leakage of urine through the urethra
-Normal anatomy provides resistance, should not just leak -Resistance to flow is related to length of pathway, radius, viscosity -Female has less resistance to flow --shorter, bigger tube -Really mostly affects dogs |
|
|
Causes of Incontinence
|
-Anatomic abnormality
-Failure of bladder to distend and accommodate urine -Failure of the urethral sphincter |
|
|
Diagnosis of Incontinence
|
-Urinalysis and urine culture and sensitivity is important
-Radiographs -Ultrasound -Excretory contrast studies (rare, ultrasound is generally better) -Cystoscopy -Urethral pressure profiling |
|
|
Urethral Pressure profiling
|
-Way to definitively diagnose incontinence or micturition problems
-Catheterize the bladder, empty the bladder -Add saline into catheter and measure resistance and slowly withdraw catheter from urethra -Gives idea about compliance --less pressure, more resistance to flow, can add more slaine -Determines fill capacity of the bladder, urethral sphincter resistance, and urethral length -Gold standard |
|
|
Urethral Sphincter Mechanism Incompetence
|
-urethral Sphincter does not work
-Most commonly seen in spayed female dogs --OHE may be a risk factor, 5% prevalence -Rare in cats, but has been reported -Mostly in medium or large-breed dogs -Less resistance in female urethra, cannot rely on urethra when sphincter is not working -Usually occurs at night when animal relaxes |
|
|
Urethral sphincter Mechanism incompetence Pathogenesis
|
-Unknown!
-Estrogen deficiency? Estrogens increase sphincter tone --OHE removes estrogen source --spayed female dogs have similar estrogen levels as intact dogs during heat, dogs in heat do not dribble -Lack of feedback on FSH and LH results in increased FSH and LH --lead to decreased sphincter tone? -Concurrent anatomic abnormalities is common |
|
|
Anatomic abnormalities leading to Urethral Sphincter Mechanism Incompetence
|
-Usually concurrent with other etiologies
-INtrapelvic bladder --decreased filling capacity of the bladder, pelvis prevents complete expansion and filling of bladder --changes pressure on the sphincter, bladder is held up by the pelvis and urethra does not “kink” -Short urethral, less resistance |
|
|
Diagnosing Urethral Sphincter Mechanism incompetence
|
-Ideally use Urinary pressure, but don’t have it
-Rule out anything that could weaken sphincter --UTI, neoplasia, anatomic abnormalities -Assess response to medication and treatment |
|
|
Urethral Sphincter Mechanism Incompetence treatment
|
-Increase sphincter tone
-Estrogens: estriol and diethylstilbestrol --60-80% of dogs respond --may cause bone marrow suppression, rare -Alpha-agonist: phenylpropanolamine --stimulate alpha receptors on urethral sphincter --75-97% effective --can cause hypertension, tachycardia, restlessness, anxiety due to increased sympathetic tone -GnRH analogs: deslorelin --63% effective response --reduces FSH and LH level -If patient responds to treatment, assume they have USMI |
|
|
Urethral sphincter mechanism incompetence in male dogs
|
-Much less common
-Unknown cause -No clear association with castration -May respond to alpha-agonists (phenylpropanolamine) or testosterone --side effects of aggression, prostatic problems |
|
|
Urethral Bulking
|
-Treatment for urethral sphincter mechanism incompetence
-Bovine collagen or synthetic products -Inject into urethral submucosa, decrease luminal diameter -Response lasts about 8 months -- most animals respond but 50% still need medical therapy -Expensive products! |
|
|
Surgical treatment of Uretheral Sphincter Mechanism Incompetence
|
-Not widely used due to complications
-Colposuspension and urethropexy are main options -Repositions the bladder into the abdomen and anchors vagina to the body wall -Compresses sphincter and urethra, increases resistance -works in 70% of patients, 23% were improved but still need meds -10% have complications and dysuria, could become worse |
|
|
Hydraulic Occluder
|
-Mimics a sphincter
-Can use cuff increase resistance, device on own increases resistance -Applies pressure to the urethra -Successful in 36-92% of dogs -Urethral obstruction is possible if blown up too much! |
|
|
Ectopic ureters
|
-Congenital disorder where ureter enters somewhere else than the trigone of the bladder
-Most commonly ureter connects to urethra distal to the trigone -Can occur in any breed -Inheritable in English bulldogs, fox terriers, |
|
|
Clinical signs of ectopic ureters
|
-Causes constant dribbling
-Females have symptoms when less than 2 months old -Males have symptoms that show up around 8 months old -Delayed onset is possible, can mimic urethral sphincter mechanism incompetence --cannot use age as a main indicator -Does not cause incontinence, but increases risk or pyelonephritis -Constant dribbling of urine, not just at night |
|
|
Complications of Ectopic Ureters
|
-Urinary incontinence
-UTI -Pyelonephritis -Concurrent anatomic abnormalities --vestibulovaginal remnant --septal diverticuli --vaginal stenosis |
|
|
Diagnosing Ectopic Ureters
|
-History can be suggestive
-Ultrasound can be helpful, but not diagnostic --can still have urine jets at normal location, does not rule out ectopic ureter -Excretory urography may show pathway of urine -Cystoscopy is 96% sensitive |
|
|
Treatment of Ectopic ureters
|
-Extramural: surgical ligation and reimplantation
-Intramural: surgery or minimally invasive techniques --Laser ablation -Continence is restored in 50-70% of patients -Some patients may need PPA or urethral bulking therapy |
|
|
Urinary Bladder Dysfunction neurogenic cases
|
-UMN: spinal lesion from brain to L7
--increased sphincter tone --large bladder that is difficult to express -LMN: lesions caudal to S3 --decreased detrusor and sphincter tone, sphincter is wide open --large, easily expressible bladder |
|
|
Treating neurogenic causes of urinary bladder dysfunction
|
-Address underlying condition
-UMN: alpha antagonists: prazosin, phenoxybenzamine -LMN: parasympathomimetic |
|
|
Equine Castrations
|
-Most common surgical procedure for equine veterinarians
-Also one of the most common causes for malpractice claims -Technically easy procedure with lots of possible complications --20-38% complication rate -Try to prevent complications! |
|
|
Preventing complications in Equine castration
|
-Identify potential risk factors
-Have all equipment ready! -Use proper surgical technique -Recognize complications early -Use appropriate therapy -Try to improve outcome of the horse and decrease liability |
|
|
Horse scrotum anatomy
|
-Scrotum has separate compartments, split my median raphe
-Blood supply is from exernal pudendal vessels -Testes are oval, horizontal long axis -Epididymis is dorsolateral --head is cranial, tail caudal |
|
|
7 tissue layers of the scrotum
|
-Scrotal skin
-Tunica dartos -Spermatic fascia -Vaginal tunic (parietal and visceral) -Tunica albuginea -Testicular parenchyma |
|
|
Equine inguinal canal
|
-External inguinal ring, within external abdominal oblique muscle
-Internal inguinal ring, within internal abdominal oblique --rectus and prepubic tendons -Vaginal ring: outcropping of the peritoneum in the inguinal canal --size of vaginal ring determines if herniation occurs or not |
|
|
Equine vaginal ring
|
-Made of thickening of peritoneum
-Intra-abdominal -Size of vaginal ring determines if herniation will occur! |
|
|
Spermatic Cord
|
-Vaginal tunic
-Blood, nervous and lymph supply -Ductus deferens (in nesoductus deferens) |
|
|
Blood, nervous, and lymph supply to the testes
|
-Testicular artery
-Testicular veins, forms pampiniform plexus -Runs within mesorchium |
|
|
Cremaster muscle
|
-Outside of the parietal tunic
-Involved with thermoregulation -Source of hemorrhage during castration --especially in older horses |
|
|
Congenital Monorchidism in Horses
|
-Extremely rare
-Almost always chryptorchid |
|
|
Cryptorchidism in Horses
|
-Always need to remove both! Remove intra-abdominal testicle first
-Abdominal: testicle is in the abdomen -Inguinal: testicle is in inguinal canal -Complete: epididymis and testis have descended -Partial: epididymis has partially descended -Affected testis may not produce sperm, but will produce testosterone --stallion-like behavior -17% prevalence -Right and left side are equally retained, left retention is more often abdominal -Unknown heritability |
|
|
Testicular descent
|
-Gubernaculum shrinks, pulls testicle into the scrotum
-Gubernaculum becomes 3 parts --proper ligament: attaches testicle to epididymis --Ligament of the tail of the epididymis: attaches epididymis to scrotal fascia --Scrotal ligament: attaches scrotal fascia to scrotal skin |
|
|
Pre-operative history for Equine castration
|
-Duration of ownership
-Scrotal hernia as a foal --lots of foals will have scrotal hernia, manually reduce and eventually stays in abdomen --Largest risk factor for hernia after castration! |
|
|
Physical exam before equine castration
|
-Palpate BOTH testicles!
-Larger testicular size in older animals -Some breeds have larger testicles -Larger testicles may need ligation during castration -If inguinal hernia is present, may have enlarged or painful testicles --may have large inguinal ring |
|
|
Risk of hemorrhage during equine castration
|
-Older horses
-Larger testicles -Donkeys -Hemostatic disorders --excessive bleeding after venipuncture |
|
|
Risk of evisceration during Castration
|
-Breed predilection
--standardbreeds, draft horses, mules -Pre-existing inguinal hernias -Inguinal hernia as a foal -Must use a ligature if you are worried about evisceration!! --only way to prevent evisceration is ligature in vaginal tunic |
|
|
Anesthetic technique for Equine castration
|
-Standing sedation:
--alpha-2 (xylazine, detomodine) -Local anesthesia (lidocaine) --testes and line along the scrotum --do not inject lidocaine into spermatic cord, just testicular parenchyma -Physical restraint is key --twitch --handler on the same side as the castrator! |
|
|
Benefits and drawbacks of standing castration
|
-Faster
-Less expensive -Standing under the horse and cutting his balls off!! -May increase incidence of infection, but unknown -Need very experienced handlers |
|
|
Recumbent castration in horses
|
-TIVA, short procedure
--12-15 minute surgical plane -Local anesthesia may extend the time needed -Can put animal dorsal or lateral --lateral, tie hind limb to neck |
|
|
Benefits and drawbacks of recumbent castration
|
-Better surgical view and access
-Safer for the surgeon -Takes longer for recovery time, increased risk -Increased risks of anesthesia |
|
|
Equipment needed for Equine castration
|
-Gloves
-Scalpel -Emasculator -Optional: --sponges --hemostats --scissors --allis tissue forceps --large absorbable suture |
|
|
Emasculators
|
-Serra: clamp, crush, cut
-Reimer: clamp, crush, cut -White’s: single crush only --small ruminants --less acceptable -ALWAYS GO NUT TO NUT --crushing side first, then cutting side 2nd |
|
|
Henderson Emasculators
|
-Originally designed for cattle
-Uses drill to spin testicle off --much faster than other emasculators -Can be done standing in cattle -Only used under anesthesia in horses, only for closed castrations -Low complication rate -MUCH faster |
|
|
Surgical preparation for castration
|
-“Aseptic” preparation
--quick! Not full sterile prep, leaving wound open -Infiltrate with local anesthetic --10ml per testicle -Grab testicle, push firmly into the scrotum --axial and caudal into scrotum --want to avoid abaxial muscles and vasculature -Make LONG incisions, do not want incision to heal too quickly --make incision in either side of raphe |
|
|
Closed castration
|
-Incision goes to, but not through the vaginal tunic
-Testicle stays in the vaginal tunic --strip testicle from the spermatic fascia, use gauze to sponge -Be aggressive! Need to tear fascia -Emasculate the entire vaginal tunic, spermatic cord, cremaster muscle -Leave emasculators in for 1.5-2 minutes plus 1 minute for every year older than 2 years -May or may not need transfixation ligature --adding transfixation ligature is the only way to prevent evisceration |
|
|
Pros and cons of closed castration
|
-Quick, easy
-Keeps peritoneal cavity “closed” -Less precise ligation -Large tissue wad in the crush, more material to crush |
|
|
Open castration
|
-Same initial approach as closed castration
-Incise the vaginal tunic --separate testis and spermatic cord from the tunic -Emasculate in 2 crushes --testicle --vasculature and ductus separately\-Leave emasculators on 1.5-2 minutes -May or may not need transfixation ligature |
|
|
Pros and cons of open castration
|
-Direct access to the spermatic cord
-Easy to grab the testicle -Not crushing the tunic or cremaster muscles --larger chance of bleeding -Possibility of evisceration, perceived risk? -Entering peritoneal cavity and leaving it open -Hydrocele? |
|
|
Modified open castration
|
-Open approach, bluntly separate mesorchium
-Crush vessels first -Crush vas deferens -Pull vaginal tunic back up to crush fascia and cremaster 2nd -Be sure to slide tunic out PAST emasculated cord pedicle -Make sure tunic emasculation is DISTAL to cord pedicle -May or may not need transfixation ligature |
|
|
Pros and cons of modified open castration
|
-Less risk of hemorrhage
-Less risk of evisceration with ligation -Increased surgical time, double crushing -Suture acts as foreign body and can cause reaction |
|
|
Scrotal Ablation
|
-removing all redundant scrotal tissue
-Castrate via any method -Close in 2 layers with absorbable suture -Less risk of infection because everything is closed -Less risk of hemorrhage -Cosmetic outcome -very expensive, has to be done under general anesthesia -Animal has to be under stall rest |
|
|
Castration Basic Rules
|
-Higher risk of hemorrhage or evisceration, use ligature!
-Long incisions -Stretch skin and SQ when finished -Lost of post-operative activity -Consider peri-operative antimicrobials |
|
|
Peri-operative care for Horse castrations
|
-tetanus toxoid
-NSAIDs -Antimicrobials: --not indicated for routine open/closed castrations --indicated if ligatures are placed, there is excessive hemorrhage, or contamination -Stall rest for 24 hours, then exercise daily --exercise is very important! -For scrotal ablations, 2 weeks stall rest |
|
|
Complications of Horse Castrations
|
-Excessive swelling: 30%
-Infection: 3-20% -Hemorrhage: 3-8% -Evisceration: 1-3% -Hydrocele: 0.3% -Peritonitis: 0.2% -Penile damage: 0.04% |
|
|
Excessive swelling after horse castration
|
-Some swelling is normal
--peak swelling in 3-4 days --should resolve in 10-12 days -Abnormal if swelling is present beyond 10-12 days -Stiff gait, reluctance to move -Fever -Dysuria -Can be due to small incisions or failure to stretch skin and SQ tissues -Inadequate post-operative exercise |
|
|
Treatment for excessive swelling post castration
|
-Rule out infection
--temperature, fibrinogen, smell -Re-establish drainage --sedate horse, aseptically prepare area and manually open incisions -Exercise animal 1-2x daily -Cold hose area -NSAIDs |
|
|
Untreated or excessive swelling after castration
|
-Paraphimosis, penis cannot retract
-Surgical site infection -Dysuria |
|
|
Infection after horse castration
|
-Increased risk with suture material
--foreign material in castration site -Can occur days to years after surgery -Fever, scrotal/preputial swelling, lameness, incisional discharge -Can be acute or chronic |
|
|
Acute infection after castration
|
-Resolves quickly with appropriate therapy
-Strep zooepidemicus, staphylococcus, pseudomonas, enterobaceriaceae -Open drainage is key! -Clostridial infection is life-treatening! --tetanus, botulism, necrotizing cellulitis or myositis --REFER! |
|
|
Chronic infection after castration
|
-“Champignon” mushroom infection
--streptococcus infection --usually from suture material --purulent discharge and mound of granulation tissue -“Scirrhous cord” --staphylococcus --Infection of the spermatic cord --draining tract develops |
|
|
Treatment of Infection after castration
|
-Swelling and fever = infection!
-Culture and sensitivity -manually open and stretch infection site -Lavage daily -Use targeted antimicrobial therapy -NSAIDs -Exercise animal daily to help with drainage |
|
|
Indications for referral of infection after castration
|
-Endotoxemia signs
--fever, anorexia, tachycardia, dehydration, toxic mucus membranes -Concern for necrotizing cellulitis or myositis -Tetanus or botulism suspicion -Non-responsive to initial treatment -Chronic infection |
|
|
Hemorrhage as complication of horse castration
|
-Some dripping is normal
--0-10 drips per minute, drip rate should decrease -Fast drip is abnormal, can’t count the drips -Steady stream of blood is abnormal -Can hear steady stream, bad news! -Address immediately! |
|
|
Sources and causes of hemorrhage after castration
|
-Testicular artery
-Cremaster muscle -Scrotal vessels -Skin bleeders -Improper application or malfunction of emasculator --skin within the emasculators --Emasculators that are too sharp, poor crush --Non-perpindicular placement on spermatic cord |
|
|
Treatment of hemorrhage due to castration
|
-Identify the source of the bleed
-Sedate animal -Re-emasculate or place transfixation suture if you can find the source of the bleed -Re-emasculate or place a crushing clamp --carmalt/Kelly forceps, leave on 24 hours -Transfixational or cruciate ligature |
|
|
Treatment of hemorrhage due to castration when you can’t find the bleed
|
-Pack scrotum full of gauze, tack to scrotal skin
-Close scrotum with heavy suture -Remove in 24-48 hours |
|
|
Aminocaproic Acid
|
-Can be used as adjunctive therapy for hemorrhage due to castration
-Inhibits fibrinolysis, clot stabilizer |
|
|
When to refer a hemorrhage from castration
|
-Hemorrhage despite packing of the wound
-Substantial blood loss -Hypovolemic shock -Suspect intra-abdominal hemorrhage --hypovolemia without external blood loss |
|
|
Eviceration due to castration
|
-Rare complication, but fatal!
-Usually occurs within 4 hours or surgery, can be up to 12 days -Most fatal complication -Omental is manageable in the field --ligate and transect, re-emasculate --consider antimicrobials if transfixation ligature is placed -Intestinal evisceration needs to be referred --triage before transport, have to support the bowel somehow --broad-spectrum antibiotics --Sedate or anesthetize --Banamine |
|
|
Triage for evisceration
|
-Prevent further trauma or contamination
-Clean with sterile saline -Replace into scrotum if possible --suture closed or use towel clamps -Do not replace into the abdomen, will get infected! -Support with moist towel sling |
|
|
Eviceration survival rates
|
-36-78% survival
-Decreased chance for survival if: --increased length of bowel --inguinal only surgical approach --resection and anastomosis is required |
|
|
Peritonitis as complication of castration
|
-Vaginal and peritoneal cavities communicate
-Septic peritonitis is rare after coastrations -non-septic peritonitis is common --hemoperitoneum --surgical manipulation --leykocytosis |
|
|
Clinical signs of Peritonitis
|
-Fever, depression, anorexia
-Tachycardia, dehydration, colic, diarrhea -increased fibrinogen -Abdominocentesis with culture and sensitivity |
|
|
Treatment for Peritonitis
|
-IV broad-spectrum antibiotics
-NSAIDs -Peritoneal lavage -Refer if animal has endotoxemia --abdominal drain and lavage --exploratory celiotomy |
|
|
Penile damage as complication of castration
|
-Mistaking a penis for a testicle can happen
-Excessive dissection --inflammation leads to swelling leads to paraphimosis -Can be inadvertently transected --REFER! Surgical repair or partial phallectomy |
|
|
Hydrocele as complication of Castration
|
-Accumulation of sterile serous fluid in vaginal cavity
-Can occur months to years after surgery -Mules are higher risk -Open castrations where vaginal tunic is left behind --fluid accumulates inside |
|
|
Clinical signs of Hydrocele
|
-Flocculent, non-painful scrotal swelling
-Can reduce fluid into the abdomen -Treat by just neglecting, typically is only a cosmetic issue -Surgically remove the vaginal tunic -Drainage can provide temporary relief |
|
|
Prevention of Castration Complications
|
-IN field: 22% complication rate |
|
|
Important points about Castrations
|
-Easy to do, but have a lot of issues |
|
|
Clinical Manifestations of Urolithiasis in small ruminants
|
-Acute urethral obstruction
-Urethral rupture -Ruptured bladder --uncommon, mostly in cattle -Ureterolithiasis or nephrolithiasis (rare) |
|
|
Small Ruminant Penis Anatomy
|
-Urinary Bladder
-Pelvic urethra -Perineal urethra -Sigmoid flexure (proximal and distal loops) -Penile urethra -Urethral process (Pizzle, common obstruction site) |
|
|
Urethral process
|
-In sheep and goats only
-Pizzle |
|
|
Urethral diverticulum
|
-“catches” retrograde catheter
-Most catheters in sheep and goats are not placed all the way into the pelvic urethra and bladder --stop at urethral diverticulum or distal urethra |
|
|
Common sites o urethral obstruction in small ruminants
|
-Distal loop of the sigmoid flexure
-Urethral process |
|
|
Common sites of urethral obstruction in cattle
|
-Just distal to the loop of the sigmoid flexure
--natural narrowing --site of insertion of the retractor penis |
|
|
History of sheep/goat with urethral obstruction
|
-Not much!
-Variable, depends on stage of disease -Usually very vague -Often unrelated to urinary system -Anorexia, depression -Abdominal distension -Colic signs -“animal is constipated” -Vocalization -Tenesmus, stranguria |
|
|
Clinical findings of Acute Urethral Obstruction in sheep and goats
|
-Depression
-Treading, tail flagging, kicking at belly -Bruxism (grinding teeth) -Repetetive stretching and straining -Tachycardia, bradycardia, tachypnea --usually TPR is pretty normal -Dehydration -Scleral injection from azotemia -Anuria, dripping urine -Crystals or dry blood on preputial hair |
|
|
Physical Exam of Acute Urethral Obstruction in sheep and goats
|
-Abdominal palpation
--may have distended bladder in small or young patients --difficult due to rumen -Rectal exam in small patients --pulsating urethra |
|
|
Urethral Rupture in Sheep and Goats
|
-Pressure necrosis and leakage of urine in SQ tissues of perineum and ventral abdomen
-Pitting edema --may be cool to the touch, indicates necrosis -Fistula may develop and allow urine to escape -Animal will smell like urine, urine is totally saturating the tissues |
|
|
Ruptured bladder in sheep and goats
|
-“Water belly”
-Prolonged bladder distension --can lead to pinpoint perforations, tears, necrosis --leads to uroperitoneum -Bilateral abdominal distension can result in a fluid wave -Depressed, weak, dehydrated animal -Scleral injection, bradyarrhythmias |
|
|
Ureterolithiasis or Nephrolithiasis in sheep and goats
|
-Very uncommon in ruminants and swine
-Acute ureteral obstruction may show signs of colic -Chronic ureteral obstruction or nephrolithiasis may present with vague signs of anorexia and weight loss --secondary to renal failure -On rectal exam will find ureteral enlargement, enlargement of the left kidney |
|
|
Diagnostic procedures for blocked goats
|
-Physical exam
-PCV, TS, CBC sometimes -Clinical pathology -Ultrasound (transabdominal) -Radiography -Endoscopy |
|
|
Ultrasound findings in blocked goats
|
-Transabdominal in small ruminants, camelids, swine
-IN a steer, may do trans-rectal -Marked bladder distention, should be right in the middle of the screen -Echogenic material within the bladder -Can image both kidneys from right paralumbar fossa --not done often, nephrolithiasis is rare -Perineal and distal urethra can be imaged |
|
|
Radiography for blocked goats
|
-Limited to small ruminants, pigs, small camelids, calves
-Caudal abdomen and ventral abdomen -Can see CaO2 or CaOx calculi (radiodense) -Absence of calculi on radiograps does not rule out urolithiasis --do contrast study for non-radiopaque stones |
|
|
Stones in small ruminants
|
-Caclium Carbonate
--radiodense -Struvite (Magnesium Ammonium Phosphate) --radiopaque |
|
|
Endoscopy for Urolithiasis in small ruminants
|
-Limited by the size of the urethra
--goat urethra is too narrow to image well -Can look at urethra, bladder, and ureteral openings in adult cattle -Need a small endoscope for small ruminants, camelids, and pigs -Can visualize the urethral calculi, strictures, or ruptures -Assist treatment by using laser lithotripsy |
|
|
Chemistry of small ruminants with urolithiasis
|
-Azotemia is most common finding
--post-renal azotemia -Hemoconcentration -IN severe cases may see ruptured bladder --hyperkalemia (causes cardiac signs, bradycardia) --hyponatremia, hypochloremia, hyperphosphatemia -Will see stress leukogram -Increased fibrinogen concentration |
|
|
Urinalysis of small ruminant with urolithiasis
|
-Proteinuria
-Hematuria -Crystalluria -Glucosuria |
|
|
Abdominocentesis for small ruminant with urolithiasis
|
-DO if uroperitoneum is expected
-Abdominal creatinine should be at least 2x creatinine in blood |
|
|
Treatment of urolithiasis in small ruminants
|
-Immediate salvage, send to slaughter
--only if animal is in good shape -Medical treatment: sedatives, muscle relaxants, banamine --not a good option -Surgical treatment -Euthanized |
|
|
Surgical treatment of urolithiasis in small ruminants
|
-Many options, depends on finances, comfort of surgeon, type of case, use of animal, etc.
-Always warn owner of potential complications -Big possibility of recurrence |
|
|
Pre-operative considerations for ruminants with urolithiasis
|
-Stabilize patient before surgery
--hypovolemia --electrolyte abnormalities --azotemia -Cystocentesis to evacuate the urine in the bladder --ultrasound guided --Bonnano self-retaining catheter -Fluid therapy: 0.9% saline --avoid K-containing fluids --if animal has severe hyperkalemia, give dextrose, sodium bicarbonate, or insulin -Perioperative antimicrobials --beta-lactam, ceftiofur, concentrate in urine -NSAIDs: use prudently! Avoid with azotemic patients |
|
|
Amputation of Urethral Process
|
-No option for referral or surgery, can amputate
-Sedation is needed in small ruminants and pigs --diazepam and ketamine, need full sedation -Animal is restrained on rump or in lateral recumbency, hind limbs flexed towards ventrum --straightens sigmoid flexure and extrudes penis -Remove ALL of the urethral process, do not want to leave any behind |
|
|
Cystostomy in small ruminants
|
-Allows clearance of cystic calculi and normograde flushing
-Preserves normal anatomy --good for breeding animals -Allows bypass of urine during post-operative period -Requires general anesthesia -Expensive! -May require a second surgery |
|
|
Cystostomy or Tube cystostomy in small ruminants procedure
|
-In dorsal recumbency under general anesthesia
-Start by amputating the urethral process -Place urinary catheter -Paramedian incision along the caudal abdomen, 1cm parallel to the penis -Isolate the bladder -Place stay sutures on each side of the bladder apex -Longitudinal cystotomy incision (try to avoid big vessels) -Suction of urine -Remove calculi, “hunt for stones” -Thorough lavage and flush via normograde catheter, make sure path is clear -Place foley catheter to divert urine post-operatively --separate stab incision on body wall, separate stab incision on bladder wall |
|
|
Tube Cystostomy post-operative care
|
-Antimicrobials until the foley catheter is removed |
|
|
Surgery of the Large Animal Female Urogenital Tract
|
-Common occurrence
-Most cases are done with local or regional anesthesia -Some procedures require general anesthesia |
|
|
Most common large animal female urogenital surgeries
|
-Caslick’s
-Perineal laceration repair -Cervical laceration repair -Cervicopexy for vaginal prolapse -Retention suture or bovine vulva -Urethroplasty -Hysterectomy/OHE -CEsarian section -Ovariectomy |
|
|
Anatomy of the female large animal urogenital tract
|
-Perineum:
--bound dorsally by base of the tail --laterally by semi-membranous muscles --ventrally by ventral commissure of the vulva -Constrictor vulvae muscle keeps vulva closed |
|
|
Vulva anatomy
|
-Vulvar labia
-Clitoris -Tubular tract from the labia to the level of the transverse fold (vulvovaginal fold) over the urethral orifice |
|
|
Caslisk’s Operation
|
-Surgery for pneumovagina in the mare
-Done to prevent involuntary aspiration of air into the vagina -With repeated foaling constrictor vulvae muscles become less able to make tight seal -Can be due to poor confirmation -Air enters the vagina -Causes chronic inflammation and can lead to chronic infections -Want to provide temporary closure of the vulva to minimize air that is sucked in -Close 2/3 of the vulva so urine can still come out but other stuff cannot get in --down to the brim of the pelvis |
|
|
Caslisk’s Procedure set-up
|
-Use stocks or lower half of barn door
--retraint, protect the surgeon -Tail bandage -Clean perineal region -Local anesthesia or sedation is needed --Xylazine and Butorphanol |
|
|
Caslisk’s etiology
|
-Ligamentous structure of the uterus breaks down with multiple parturitions
-Loss of structure causes uterus to sag -Uterus starts to pull the vagina and vulva cranially -As vagina is pulled, lips of the vulva open up -Allows air to be sucked in -Allows feces to fall into the vestibule and vagina |
|
|
Caslisk’s operation specifics
|
-Resect 3mm of mucosa from vulva labium at mucocutaneous junction but do not remove skin
-Length of incision is ½-2/3 of the vulvar length and ends at pelvis floor -Appose resected margins with suture --vertical mattress --simple continuous --continuous interlocking --staples |
|
|
Episioplasty
|
-Involves more reconstruction
-Resecting more mucosa |
|
|
Repetition of Caslisk’s operation
|
-Done repeatedly!
-Save skin -Need to make sure you only remove mucosa and not skin, other will not have enough skin to repeat -Want to create a biological seal, a scar bridge across vulva |
|
|
Breeder Stitch
|
-Extra suture placed at bottom of caslisk’s suture
-Allows mares to be bred early, on foal heat -Allows breeding without disrupting the caslisk’s suture |
|
|
Thoroughbreed Live Coverage
|
-Limits number of foals and breedings that can take place
-Maintains culture |
|
|
Perineal lacerations in Large Animals
|
-Occur during parturition
-Maiden mares are at greatest risk --foaling is variable, likely to be unattended -Occurs when foal’s limbs or head are forced caudally and dorsally -1st degree: mucosa, vagina, vulva --no consequence, no big deal -2nd degree: mucosa, muscularis of vulva, anal sphincter, and perineal body are involved --usually anus and perineal body are still separated -3rd degree: teating through recto-vaginal septum, muscularis of the rectum and vagina, and the perineal body --big deal!! Needs immediate repair! |
|
|
Perineal laceration repair
|
-Wait 4-6 weeks after parturition
--wait for some scar tissue and healing --too much swelling right after parturition -Withhold feed 24 hours pre-operatively --reduce bulk in the rectum, decreases tension on repaired suture line -Epidural anesthesia -2 stage repair --reconstruct shelf between the vagina and rectum --reconstruct perineal body itself |
|
|
Post-operative care for perineal lacerations
|
-Antibiotics for 5-7 days
-No feed for 48 hours post-operatively -Suture removal in 10-14 days -Should gave good healing by 5-7 days |
|
|
Perineal laceration repair failure
|
-Too much tension on the suture
-Need to make sure that suture and tissues are under as little tension as possible -Lack of tissue tension is really critical |
|
|
Important points of Pernieal laceration repair
|
-Lack of tissue tension is really critical!
-Maintain a loose diet, feed grass (5-7 days) -Pair with caslisk’s -Most common with maiden mares and heifers |
|
|
Cervical lacerations in Large animals
|
-Occur due to excessive stretching of the cervix during parturition
-Involves portiovaginalis -Tear is usually wedge-shaped in appearance -May have multiple tears or one large tear -Endometritis can result from incomplete closure of cervix due to laceration -More common in horses than in cows -Best way to diagnose is via palpation -Most occur ventrally, along bottom portion of cervix |
|
|
Perineal lacerations in cattle
|
-Less common than in mares
-Stage II parturition is slower, not as explosive --Not as traumatic to tissues |
|
|
Surgical treatment of cervical lacerations
|
-Best done during estrus cycle when cervix is relaxed
-Performed in standing mare -Epidural anesthesia is best -Closes in 2-3 days -Work from point furthest away to closest -Need to make cervix competent -Should be able to fit a finger into the cervix when finished |
|
|
Post-operative
|
-Cervix is edematous and hyperemic for 10-14 days
-Adhesions are generally not an issue --can occur between the cervix and vagina --prevent adhesions by placing 1-2 stay sutures on either side of the cervix |
|
|
Cervicopexy for Vaginal Prolapse
|
-Retains prolapsed vagina in the cow
-External os of the cervix is sutured to the prepubic tendon -Prevents vaginal prolapse, ties it back |
|
|
Cervicopexy surgical procedure
|
-Performed with epidural anesthesia
-Vaginal tissues are cleaned and replaced in pelvic canal -Use non-absorbable suture material -Go through 1.8cm of prepubic tendon and 3.4-5cm of vaginal floor -Avoid the bladder and urethra! |
|
|
Buhner’s suture for Vaginal prolapse
|
-Simple, effective vaginal or uterine prolapse retention suture
-Deeply placed circumferential suture -Replaces action of the constrictor vestibular muscle -Stock restraint is preferred with caudal epidural anesthesia |
|
|
Procedure for Buhner Suture
|
-Transverse skin incision 1cm long
--between anus and dorsal commissure of the vulva -2nd incision of 3cm below the ventral commissure of the vulva -Put needle in from top to bottom, pull sterile umbilical tape from top to bottom -Repeat on other side of the vulva and tie sutures together -Do not tie suture too tightly, need to be able to get fingers between suture |
|
|
Take-home points of Buhner Procedure
|
-Done with Buhner needle
-Replaces vaginal prolapse -Should be tight enough to prevent vaginal prolapse, but still allow urination -Only in food animals |
|
|
Alternate procedure for uterine prolapse
|
-Place suture in cervix, like a Buhner procedure
-Create purse-string around the cervix -Needs to be removed before parturition |
|
|
Indications for Urethroplasty in large animals
|
-Urine pooling in vagina (urovagina)
-Most commonly in older, thin, multiparous mares -Urogenital tract slopes cranioventrally, urine can fall into vagina -Characteristic external perineal conformation --anus and dorsal vulva have sunken appearance |
|
|
Urethroplasty Procedure
|
-Create a urethral “extension”
-Relocate the external opening of the urethra caudally so it does not deposit urine into an area where it can pool -Correction requires careful planning --do complete exam of the reproductive tract --rule out chronic cervicitis and endometritis -Prevent urine from refluxing back into the vagina --make urine come out more caudally |
|
|
Take-home points of Urethroplasty
|
-Used for treatment of urovagina or urine pooling
-Create urethral extension -Minimize tissue tension, otherwise will get breakdown of the tissue |
|
|
Monin’s Procedure
|
-Moves transverse fold that separates vagina and vestibule caudally
-“Elongates” urethra -creates a longer transverse fold |
|
|
Pouret’s Technique for Urethroplasty
|
-Section of the ligamentus and muscular attachments between the rectum/anus and caudal vagina/vulva
|
|
|
Post-operative care for Urethroplasty
|
-Antibiotics for 3-5 days
-NSAIDs for 3-5 days -Observe difficulty in urinating (Dysuria) -If any breeding is planned for 3-4 weeks post-surgery, AI is recommended |
|
|
OHE in large animals
|
-Main indication is uterine prolapse with complications that make replacement impossible or impractical
--Freezing, severe laceration, necrosis of uterine tissues -in mare is associated with chronic non-responsive endometritis |
|
|
OHE in the cow
|
-Standing procedure
-Epidural anesthesia, local anesthesia -Flank procedure --Go in on the left, do not have to deal with the intestines -Uterus is flushed with appropriate bacteriocidal medication before induction |
|
|
OHE in the mare
|
-General anesthesia
-Ventral midline laparotomy -Uterus is flushed with appropriate bacteriocidal medication before induction |
|
|
Ovariectomy in Large Animals
|
-Remove ovary with some sort of pathology
-Granulosa cell tumor is most common, other tumor types can also occur -Abscess may be present -Prevention of estrus -Bilateral ovariectomy is more commonly done to alter normal physiological cycles than to remove a pathological ovary |
|
|
Post-operative care of OHE in large animals
|
-Prophylactic antibiotics for 36-72 hours
-Monitor for post-operative bleeding or shock -Restrict exercise for 10-14 days -Monitor any post-operative infections or peritonitis |
|
|
C-section indications for large animals
|
-Dystocia
-Transverse presentation of the fetus -Uterine torsion -Uterine rupture -General anesthesia for the mare, ventral midline approach -Regional/local anesthesia for the cow, left flank laparotomy |
|
|
C-section technique
|
-Uterus is located and brought to incision site
-Make incision over a limb of the fetus (palpated through uterine wall) -Exteriorize hysterectomy site to minimize contamination of peritoneal cavity -Incise uterus and remove fetus -Separate allantochorion 2-5cm from margin of incision before closing -Close uterus with a double inverting layer with absorbable suture |
|
|
Post-operative care for C-section
|
-Tetanus prophylaxis
-Antibiotics -Oxytocin -Systemic support and fluid therapy -Monitor membranes for retention -Monitor for adhesions via rectal exam |
|
|
Most common reason for ovariectomy
|
-Granulosa cell tumor
-Can secrete hormones and cause aggressive behavior --testosterone and estrogens are secreted -Usually unilateral, can be bilateral -Affected ovary will be HUGE, contralateral will be small |
|
|
Surgical approach for Ovariectomy
|
-Colpotomy: remove ovary via vagina |
|
|
Chain of Craiser for Ovariectomy
|
-Twitch-like device that twists around ovarian pedicles
-Crushes pedicle, causes tissue damage -Results in clotting -Can be done “blindly,” by palpation -Tighten slowly and tightly to get proper clotting -Can be painful, use local block |
|
|
Ovariectomy post-operative care
|
-Perioperative antibiotics for 36-72 hours
NSAIDs for one or several days, depending on patient’s comfort -Monitor for secondary GI problems --Ileus/colitis -Adhesion and hematoma around pedicle are potential complications --minimize by good surgical technique -Peritonitis |
|
|
C-section in the Mare
|
-Pregnancy should be 330 days or greater
-Colostrum should be present in udder -Electrolyte levels in colostrum should have more K than Na -Small pelvic canal can require C-section -Repeat cervical lacerations -Twinning |
|
|
Twinning in Mares
|
-Bad news!
-Try to abort one -Bicornual pregnany, 50% foal survival -Unicornual pregnancy: 0% foal survival |
|
|
Critera for Emergency C-section in Mares
|
-Fetal problems
--malposition/dystocia -Consider health of mare, viability of fetus -Financial considerations -Facilities and clinical expertise are important factors |
|
|
Hysterotomy
|
-Terminal condition for the mare
-Sick mare -Severe injury with few alternatives -Immature foals or systemic response |
|
|
C-section in Mare Procedure
|
-General anesthesia
-Midline or flank approach -Rapid delivery is the goal! -Prepare surgical site ahead to time to decrease time for induction to delivery of the foal -Intubate the foal ASAP -Exteriorize as much of the uterus as possible -Peel back placenta from hysterotomy incision --use hemostatic suture along edge of the incision, placenta bleeds a lot -Inverting pattern to close the uterus -Oxytocin will cause involution of the uterus |
|
|
Post-operative care for a C-section in a mare
|
-Pain management
-Watch for excessive bleeding, prevent anemia -Retained placenta is a possibility -Fertility is usually fine after a C-section -Breeding soundness exam to assess injury caudal to the reproductive tract or cervical laceration from dystocia |
|
|
Sequelae of retained placenta
|
-Laminitis and metritis
|
|
|
Prognosis for C-section in mares
|
-90% survival
-Foal survival depends on when mare and foal go into C-section and rapid delivery --25-30% -Rapid delivery can result in placental separation and place foal at risk -Mare may need up to 1 year before next breeding for recovery |
|
|
Mare uterine torsion
|
-9-10 months of gestation
-Can look like a colic -Usually twists cranial to the cervix --on vaginal palpation, cervix will be in normal position -Diagnose via rectal exam |
|
|
Treatment for Mare uterine torsion
|
-Depends on the health of the uterus and the foal
-Rolling --a little more precarious in the horse -Standing flank laparotomy is ideal -Recumbent/general anesthesia laparotomy -Worry with ventral midline incision that it will not heal properly |
|
|
Prognosis for Mare uterine Torsion
|
-75% survival rate
-Uterine rupture can lead to hypovolemic flock -foal survival is 50% -Complications include asphyxia, abortion, stillbirth |
|
|
Take-home points for Mare uterine torsion
|
-Uterine torsion is cranial to the cervix
-Diagnose via rectal palpation -Usually 9-10 months of gestation -Corrected via flank laparotomy |
|
|
Uterine Prolapse in the Mare
|
-Very uncommon
-May involve a uterine artery bleed --can lead to hypovolemic shock -Relieve tension on the uterus so it can be replaced -Instill fluids to evert the uterine horns -Will need epidural or general anesthesia to correct |
|
|
OHE in the mare
|
-Very rare
-Indications: --chronic pyometra --uterine tumors -Clinical presentation: --abdominal pain, looks like colic --toxic --vaginal bleeding --infertility -Post-operative concerns: --peritonitis and bleeding |
|
|
Uterine Tumors in the Mare
|
-Myoxomyoma
-Leiomyosarcoma -Botryoid rhabdomyosarcoma -Hematoma -Abscess -Cervical hyperplasia -Metastatic Lymphosarcoma -Metastatic ovarian adenocarcinoma |
|
|
Treatment for Uterine tumors in mares
|
-Unicornual OHE
-Vaginal approach -Excisional biopsy of uterine mass |
|
|
Uterine Rupture in Mares
|
-Occurs during foaling
-Secondary to uterine torsion or hydroamnion |
|
|
Indications for Cow C-section
|
-Large fetus
-Poor cervical relaxation -Small pelvic canal -Uterine rupture or torsion -Hydrops amnion, hydrops allantois -Fetal malposition -Emphysematous fetus -Fetal monster |
|
|
Cow C-section
|
-Much more common than the mare C-section
-Done on-farm -Better prognosis |
|
|
Surgical approach for C-section in the cow
|
-Ventral midline
-Paralumbar fossa (left) -Paramedian -Local line block or paravertebral block -Epidural for vaginal manipulation -Exteriorize the uterus as much as possible --minimize contamination of the peritoneal cavity -Be sure to check for twins or additional fetuses |
|
|
Tissue planes to cut through in C-section
|
1. Skin
2. Cutaneous tissue 3. External abdominal oblique 4. Internal abdominal oblique (more muscular) 5. Transverse abdominal oblique |
|
|
Cow Uterine Torsion
|
-Occurs at term
-Causes Dystocia -Usually caudal to the cervix --can make diagnosis on vaginal examination -Treat by rolling (vaginal delivery) or laparotomy (C-section) |
|
|
Cow Uterine Prolapse
|
-More common in the cow than in the horse, but still uncommon
-Accident of parturition -Can be life threatening! -Occurs after parturition, usually with 24 hours -Can be managed on the farm -Elevate hind limb to reduce prolapse -If there is a uterine artery rupture there can be big issues -If caught early cow usually does quite well |
|
|
Cow uterine Prolapse complications
|
-Death due to uterine artery bleed
-Fertility will not be affected if there is fast replacement --minimize contamination -Correct hypocalcemia -If the animal does well in first 48 hours, outcome is improved |
|
|
Treatment for Cow Uterine Prolapse
|
-Replace when cow is standing!
-Replace as quickly as possible -Use epidural anesthesia -Make sure uterus is lavaged/washed -Reduce all intussusceptions, no telescoping! |
|
|
Mule
|
-Sterile
-Mating between a donkey and a horse -Mare donkey and stallion horse breeding |
|
|
Most common conditions relating to Equine male genitalia
|
-Generally related to trauma
-Hematomas -Lacerations -Contusions -Can be acquired or developmental --neoplasia -Infections -Inflammation -Nerve or vascular problems --phimosis --paraphimosis --priapism |
|
|
Phimosis
|
-Inability to extend the penis
-Stricture in the prepuce --can be congenital or acquired stricture -Space-occupying lesion --neoplasia, granulomas, abscess, fibrosis |
|
|
Paraphimosis
|
-Inability to retract the penis
-Injury to the penis itself and vasculature -Most commonly due to hematoma, laceration, purpura hemorrhagica -Treat by reducing edema and inflammation -Surgical approach also exists --reefing, phallectomy, phallopexy |
|
|
Priapism
|
-Prolonged erection without sexual stimulation
-Unknown etiology -Can be tranquilizer associated, phenothiazine tranquilizers --Acepromazine -Treat with supportive care -Flush corpus cavernosum penis -Form a vascular shunt between corpus cavernosum penis and corpus spongiosum penis |
|
|
Penile Hematomas
|
-Generally due to blunt trauma
--occurs during breeding with a mare that is not in heat --mare kicks or injures stallion -Corpus cavernosum rupture (rare in horse, more common in bull) |
|
|
Clinical signs of Penile Hematoma in Horses
|
-cool, non-painful swelling
-Prepuce may prolapse -Can result in penis being extended and unable to be retracted (paraphimosis) |
|
|
Treatment for Penile Hematoma in Horses
|
-Minimize the bleeding
-Reduce the edema and inflammatory response --“jockstrap” -Surgical intervention if there is an increasing hematoma or urethral obstruction |
|
|
Lacerations of the penis or prepuce in the horse
|
-Edema and inflammation are most common
-Manage with gentle cleaning -Topical antimicrobials -Sling support -Debride laceration and close -Treat penile lacerations the same as prepucial injury -Penile lacerations can penetrate into the corpus cavernosum penis --results in a lot of bleeding |
|
|
Reefing
|
-Resection of part of the prepuce
-treatment for Paraphimosis -Preputial resection and anstomosis |
|
|
Phallectomy
|
-Removing a portion of the penis
-Penile amputation -William’s technique -Scott’s technique -Vinsot’s technique |
|
|
Phallopexy
|
-Tacking part of the penis to the prepuce
-Prevents penis from extending too far out of prepuce -Prevents paraphimosis or priapism -Horse must be castrated, cannot have sexual stimulation --might tear sutures -MUST be able to retract the penis into the sheath |
|
|
Reefing as treatment for Paraphimosis
|
-AKA circumcision
-Post-phetotomy -resecting a portion of the prepuce |
|
|
Penile Neoplasia in the horse
|
-Squamous cell carcinoma is most common
-Squamous papilloma -Melanoma -Sarcoid -Granulomas (not neoplastic) --cutaneous habronemiasis due to fly strike --phycomycosis |
|
|
Treatment for Penile Neoplasia
|
-Cryotherapy
-Hyperthermia -Surgical resection -Intralesional cisplatin and topical 5-fluorouracil (SCC) -Radiation therapy |
|
|
William’s technique for Phallectomy
|
-Place a catheter in the urethra
-Extend penis -Make triangular incision with point facing towards the body and resect skin down to the urethra -Make incision into urethra -Suture urethral mucosa into the skin -Amputate the distal penis section at an angle -Suture remaining mucosa back to the penis, ligating all big vessels -Take off penrose train tourniquet and check for bleeding -Left with a triangular opening for urethra |
|
|
Take home points for Phallectomy
|
-Several procedures for phallectomy
-William’s procedure is preferred --less chance for urethral stricture -Procedure for penile neoplasia and paraphimosis |
|
|
Bull Penis
|
-Fibrous connective tissue penis
--Fibroelastic -Can have a penile fracture -Testicles are more vertical -Seminal vesicles, prostate, and bulbourethral glands all present -Prostate gland is more diffuse -Sigmoid flexure |
|
|
Stallion penis
|
-Musculocavernous penis
-Cannot have a penile fracture -Testicles are more horizontal -Seminal vesicles, prostate, and bulbourethral glands all present |
|
|
Penile Hair Ring in Bulls
|
-Common in young bulls
-Ring of hair around the prepuce -Etiology is unknown -Can result in nerve damage to the penis and pressure necrosis |
|
|
Penile Fibropapilloma in Bulls
|
-“Warts”
-Common in young bulls -Treat by excising -May be viral induced, viral papilloma |
|
|
Penile Hematoma in Bulls
|
-Due to traumatic event
-Rupture of the tunica albuginea “broken penis” -Seen in young breeding bulls during natural coverage --no experience and poor aim -Usually occurs on dorsal surface of the distal sigmoid flexure -Pressure causes rupture (75,000 mmHg) |
|
|
Treatment for Penile Hematoma in Bulls
|
-Conservative approach: 50% success in restoring breeding soundness
-Surgical approach: 80% success --use “bootlaced” suture pattern |
|
|
Complications of Penile Hematoma in Bulls
|
-Loss of nerve sensation to the penis
-Adhesions of penile elastic tissues -Abscesses -Recurrence of injury -Vascular shunts -Injury to the prepuce |
|
|
Boot-lace suture pattern
|
-Very strong
-Use 2 needles and strands -Create a figure 8 -Will look like a cruciate when pulled tight --“continuous cruciate” pattern |
|
|
Tunica Albuginea Rupture in Bulls
|
-Usually in breeding bulls and young bulls
-Hematoma resection and evacuation and repair of tunica albuginea |
|
|
Penile deviations in Bulls
|
-Affects the ability of the bull to successfully breed
-Can be spiral, ventral, s-shaped -Repair surgically --fascia lata graft -Resect tissue that is causing deviation and replace with tissue |
|
|
Prepucial lacerations in Bulls
|
-Very common, prepuce is loose
-Injury occurs due to breeding accident or prolapsed prepuce -Preputial resection is best treatment --resect redundant tissue -Can also put in sling |
|
|
Prolapse of the prepuce in bulls
|
-Treat by removing redundant tissue |
|
|
Prepucial Stricture |
-Causes phimosis, inability to extend the penis |
|
|
Hematuria
|
-Bloody urine
-Red urine -Need to differentiate between hematuria, hemoglobinuria, and myoglobinuria -Hematuria will have RBC in sediment -If hematuria is present, is there a urologic disease or a bleeding disorder? --intravascular hemolysis |
|
|
Hemoglobinuria
|
-Red supernatant in plasma and red urine
|
|
|
Myoglobinuria
|
-Clear plasma and red urine
-Myoglobin in plasma does not have a red color |
|
|
Blood in urine stream
|
-At beginning: coming from vagina or prepuce
-Late: coming from prostate, trigone, or bladder --end of contraction, squeeze of urination -Throughout: from kidney or bladder -If dripping from the penis, check prostate gland, prepuce, and penis --can happen in normal intact male dogs when they are sexually excited --can treat with finasteride |
|
|
Lower Urinary Tract Signs
|
-Pollakiuria
-Stranguria (straining to urinate) -Dysuria (difficulty urinating) -Incontinence (problem with the sphincter) -Associated with UTI, calculi, or tumor -Could be benign prostatic bleeding |
|
|
Finasteride
|
-Can treat dripping blood from the penis in intact dogs
|
|
|
Benign Prostatic Bleeding
|
-Treat for benign prostatic hyperplasia
-Castrate -If castration is not an option, treat with finasteride transiently |
|
|
Upper Urinary Tract bleeding
|
-Associated with UTI, calculi, or tumor
-Benign renal bleeding -RBC casts or large clots are possible in the urine -Animal may be anemic -Need to do ultrasound or radiographs, MRI, CT, Scintigraphy -Scoping procedures -Excretory urogram (contrast study) -Exploratory cystotomy, check bladder when inside out for vascular anomalies secondary to granulation tissue -Ureteral cannulation -Check sediments |
|
|
Benign renal bleeding
|
-Hard to find
|
|
|
Proteinuria
|
-Protein can be coming from anywhere in urinary tract
-Protein on dipstick: usually albumin -Urine protein Creatinine ratio: all proteins assessed -Bumin: all proteins -Early Renal Damage test, MA: microalbuminuria -Protein electrophoresis (SDS-PAGE) --differentiates high molecular weight proteins from low molecular weight proteins --Albumin= high molecular weight -Bence-Jones proteins (multiple myeloma) -Tamm-Horsfall proteins |
|
|
Proteinuria and Molecular Weight
|
-High molecular weight proteinuria:
--glomerular issue --albumin -Low molecular weight proteinuria: --tubular disease, tubular leakage |
|
|
Urine Dipstick for Protein
|
-Picks up more than 30 mg/dl of protein
-Mostly looks for albumin -Lots of false positives --Protein losing nephropathy, high pH, semen, pigments in the urine, high urine specific gravity --UTI or inflammation -Check microscopic sediment for UTI or inflammation -Dilute urine may make dipstick look negative or low even if proteins are present -Less than +1 with USG more than 1.013 is probably an insignificant finding -With dilute samples (USG less than 1.012, look further --UPC ratio -If protein is more than 2+ look further regardless of USG |
|
|
USG and Protein on dipstick
|
-Less than +1 with high USG (more than 1.013), probably OK
-Dilute sample (USG less than 1.012) with protein on dipstick, should look further -If protein is more than 2, always look further |
|
|
Early Renal Damage Test
|
-Looks for microalbuminuria
-Very sensitive test, not specific for the kidneys as a cause -1-30mg/dl -Picks up smaller amounts of protein in urine than the dipstick -Mild positive may correlate with “gray zone” --UPC 0.2-1 -Watch trend over time --some older dogs and cats have consistent microalbuminuria --25% of all dogs and cats are positive -Blood in sample will not cause positive microalbuminuria test until sample is grossly red or pink -Helpful in young animals that have genetic predisposition for protein-losing nephropathy |
|
|
Causes for protein in the urine
|
-Protein losing nephropathy
-Hypertension -Vasculitis -Phenylpropanolamine -Steroids -Neoplasia |
|
|
Urine Protein Creatinine Ratio (UPC)
|
-Not specific for albumin
- -Spot test on one urine sample can be used -Daily variation in protein in urine may cause changes in UPC --0.5 UPC can have 80% daily variation -Mix samples to average UPC and save money, pay for one test but get an average of 3 |
|
|
Normal UPC values
|
-Dogs and cats: less than 0.2
-0.2-0.5: borderline proteinuric -more than 0.4 or 0.5: proteinuric -Non-azotemic animals: --More than 0.5, monitor --More than 1.0, investigate --More than 2.0, intervene |
|
|
UPC levels in azotemic dogs and cats
|
-Intervene when UPC is greater than 0.5 in dogs
-0.4 in cats |
|
|
Protein in urine and kidneus
|
-Progressively damages tubular cells
-Decrease protein in urine --decrease protein in diet --ACE inhibitor decreases glomerular pressure, dilates afferent and efferent arterioles -Decreases glomerular pressure and amount of protein that leaks out of glomerulus |
|
|
Pre-renal proteinuria
|
-Hypertension, protein is pushed through the glomerulus
-Hyperproteinemia, lots of protein in the plasma |
|
|
Renal Proteinuria
|
-Normally proteins are not filtered through glomerulus, due to size and charge
-Protein losing Nephropathy can occur due to glomerular disease -Animal will lose a lot of albumin, check serum for decreased albumin -Can be due to tubular disease, UTI, calculi, tumors, renal bleeding, or inflammation --usually no hypoalbuminemia |
|
|
Post-renal proteinuria
|
-Lower urinary tract problem
-UTI, calculi, tumors, bleeding, inflammation in lower urinary tract |
|
|
Slit Diaphragm Molecules
|
-Hook up to complicated system that is connected to actin cytoskeleton in foot podocyte
-Changes shape of foot process and size of slit diaphragm -When podocytes are deformed, slit diaphragm size increases --Allows protein to leak from glomerulus into tubules |
|
|
Protein Losing Nephropathy as Glomerular disease
|
-Not necessarily renal failure to begin with
-Predisposed to high BP -Glomerulonephritis -Glomerulosclerosis -Periglomerular fibrosis -Amyloidosis -Minimal change disease (changes of foot process effacement, only visible on electron microscope) |
|
|
Glomerulonephritis
|
-Can be membranous, proliferative, or membranoproliferative
-Can be focal or generalized among glomeruli -IN glomerulus can be diffuse, global, segmental |
|
|
Glomerulosclerosis
|
-Podocytopathies
-Proteins in slit diaphragm is not working properly |
|
|
Genetic causes of Protein Losing Nephropathy
|
-Glomerular basement membrane abnormalities
--alport syndrome -Podocytopathies -Amyloidosis -Fibrillary deposits |
|
|
Immune-mediated glomerular nephritis
|
-Cause for protein-losing nephropathy
-Glomerular nephropathy with endothelial deposits --common in dogs -Membranous nephropathy with subepithelial depositis --common in cats -Proliferative glomerulonephropathy |
|
|
Renal Biopsies
|
-Wedge biopsy if renal dysplasia is suspected
-Tru-cut renal cortical core biopsies for other diseases --Need ultrasound guidance -Use thin section kit |
|
|
Progression of Protein Losing nephropathy
|
-Can be acute or chronic
-Can be mild, moderate, or severe -Can be stable or progressive -Proteinuria occurs first, early warning -Serum albumin decreases -Serum cholesterol increases -Azotemia is present (increased BUN and creatinine) -Tubular changes decrease Urine specific gravity --last thing to change with protein-losing nephropathy --opposite of kidney disease |
|
|
Cholesterol in Protein losing nephropathy dogs
|
-Cholesterol is HIGH
|
|
|
Complications and signs of Protein Losing nephropathy
|
-Nephrotic syndrome
-Thromboembolism -Hypertension -Chronic or acute renal failure -Sickness due to underlying cause of protein-losing nephropathy -Hypertension -Hypercoagulability |
|
|
Nephrotic syndrome
|
-Low albumin with high proteinuria
-Ascites, edema, or effusion -High cholesterol -Does NOT include azotemia and animal does not have to be PU/PD |
|
|
Causes of Protein Losing Nephropathy
|
-Gentic causes
-Tick-borne diseases -Immune-mediated diseases -Heartworm disease -Neoplasia |
|
|
Hypertension and Protein-losing nephropathy
|
-Can be silent
-May see signs associated with other target organ damage --eyes --cardiovascular system --kidney --CNS |
|
|
Thromboembolism and Protein losing nephropathy
|
-Can occur anywhere
-Pulmonary bed (dyspnea) -Saddle thrombus (hind leg weakness and poor femoral pulses) -Portal vein (may present like acute pancreatitis) -Sudden death due to thromboembolism in brain, heart, or lung |
|
|
Hypercoagulable state and Protein Losing Nephropathy
|
-Due to urinary loss of anti-thrombin III
-Platelet hypersensitivity --associated with hypoalbuminemia -Vasculitis due to underlying disease process -Vascular damage due to hypertension -Can do thromboelastography to determine if animal is hypercoagulable |
|
|
Acute or chronic renal failure and Protein Losing nephropathy
|
-Protein in the glomerular filtrate is toxic to renal tubular cells
-Tubular cells are lost, patient goes into renal failure -Azotemia can occur before PU/PD -May not show PU/PD even when very sick! |
|
|
Immune-mediated glomerular nephritis
|
-Idiopathic
-Infectious --lyme, ehrlichia, anaplasma, mycoplasma --heartworm --babesia, bartonella, leishmania --FeLV, FIP -Systemic lupus erythematosus |
|
|
Causes for Immune-mediated glomerular nephritis
|
-Antigen-antibody complexes are deposited in tubules
-Usually in lumpy-bumpy pattern on immunofluorescence -Antibodies can be against known or unknown antigens -Rarely to self-antigens -Can be due to neoplasia -Drugs: trimethoprim sulfa -Vaccines? -Food allergies? |
|
|
Causes of Vasculitis and Protein Losing Nephropathy
|
-Ehrilichia
-Rocky Mountain Spotted Fever -Infectious Canine Herpes virus -Hemolytic uremic syndrome -Hypertension leading to arteriosclerosis -Glomerulosclerosis |
|
|
Hemolytic uremic Syndrome
|
-Shiga-toxin from e. coli in improperly cooked meats
-Raw food diets or raw wildlife |
|
|
Glomerulosclerosis
|
-End-stage glomeruli
-Fibrotic glomeruli -Can be caused by Cushing’s disease, but will only cause mild glomerulosclerosis --mildly increased urine protein creatinine ratio --does not cause chronic renal failure or hypoalbuminemia |
|
|
Inherited Predispositions to Protein-Losing nephropathy
|
-Laboradors, golden retrievers, shelties
--higher risk for lyme nephritis -Wheaten terrier: protein losing nephropathy --have DNA test to screen for podocytopathy |
|
|
Wheaten terrier Protein-losing nephropathy
|
-Genetic Podocytopathy
-Looks like focal segmental glomerulosclerosis more than immune-mediated glomerular nephritis -Also predisposed to genetic irritable bowel, addison’s disease, and renal dysplasia -If UPC is high (Protein-losing nephropathy) and albumin and globulins are low but animal is not anemic, and cholesterol is normal, indicates Protein Losing enteropathy also |
|
|
Alport
|
-Glomerular basement membrane collagen IV Protein losing nephropathy
-Mimics membrano-proliferative glomerulonephritis -Need electron microscopy -Samoyeds, Navasota dogs, English cocker spaniels, English springer spaniel, dalmation, bull terrier -Different mutations cause same phenotype -Breeders use UPC ratio as diagnostic |
|
|
Basenji PLN
|
-Secondary to SIIPD
-Low albumin -Normal or high globulin |
|
|
Bernese Mountain Dog
|
-Autosomal recessive
-Mostly occurs in females, sex-linked -Thought it was a lyme nephritis, but is actually Protein losing nephropathy |
|
|
Greyhound PLN
|
-“Alabama rot”
-Affects skin and kidneys |
|
|
Newfoundlands PLN
|
-Glomerulosclerosis
|
|
|
Beagles
|
-Primary glomerulopathy
|
|
|
Shar pei PLN
|
-Predisposed to amyloidosis
|
|
|
Abyssinian and Siamese PLN
|
-Amyloidosis
-More often tubular than glomerular |
|
|
Protein Losing Nephropathy work-up
|
-History, PE, Eye exam
-CBC, chem, Urinalysis -UPC or MA -Urine culture to rule out UTI -Chest radiographs and abdominal ultrasound -Blood pressure -TEG for coagulability -Serology test for tick-borne diseases and lepto -Testing for immune-mediated diseases -Renal biopsy -Pedigree analysis if possible -DNA test if available |
|
|
Treatment for Protein-Losing nephropathy
|
-Treat underlying disease
-ACE inhibitor is standard --enalapril or benazepril -Renin inhibitors, anti-aldosterone -Antihypertensives -Antithrombotics -Colcicine to reduce future amyloid pigment deposition -Modified protein restricted diet -Omega-3 Fatty Acid supplement -Careful fluid therapy, may decrease albumin even more --changes oncotic pressure of plasma -Hypoallergenic diet? -Immunosuppressants -Thromboxane synthetase inhibitors -Other CRF or ARF treatment as needed -Dialysis, plasmapheresis, transplant |
|
|
ACE inhibitor for Protein Losing Nephropathy
|
-Changes glomerular hemodynamics
-Dilates efferent arteriole and afferent arteriole -Decreases glomerular filtration pressure, decreases the amount of proteins that are forced through the glomerulus -NEED ACE inhibitor to act on both afferent and efferent arteriole |
|
|
Anti-hypertensives for Protein Losing Nephropathy
|
-If necessary
-Give in addition to ACE inhibitors -Amlodipine |
|
|
Antithrombotics for Protein-Losing Nephropathy
|
-Low-dose aspirin, Coumadin, or vitamin E
-Prevent thrombotic events -In emergency, give IV streptokinase or heparin |
|
|
Omega-3 fatty acids
|
-Anti-inflammatory for the kidney
-Very helpful for protein-losing nephropathy -needs to be fish oil |
|
|
Steroids for Immune-mediated protein losing nephropathy
|
-Not recommended
-increase chance for hypertension and thromboembolic events --animals are already predisposed to these conditions -Only give in pulses -Helpful for increasing appetite -Mycophenolate is choice steroid at the moment |
|
|
Congenital Lower Urinary Tract issues
|
-Ectopic ureters
-Intrapelvic bladder -Urachal diverticulum -Patent urachus -Congenital hydronephrosis |
|
|
Congenital Ectopic Ureters
|
-Can be bilateral or unilateral
-Usually occult in males, do not show up -May be associated with other urinary tract issues or abnormalities -Many breeds predisposed -Siberian husky is at risk |
|
|
Intrapelvic Bladder
|
-“Short urethral syndrome”
-All or part of baldder is in pelvic canal -Get stagnation -predisposed to UTI and urinary incontinence -May present when animal is spayed and loses estrogen support -Weimaraner -Dobermans |
|
|
Inherited Kidney Abnormalities
|
-Renal agenesis (beagle)
-Renal dysplasia (many breeds) -Renal amyloidosis -Polycystic kidney disease (Persian cats) -Polycystic renal and hepatic disease -Multiple cystadenocarcinomas -Renal telangiectasia -Inherited glomerulopathoes -Inherited tubular abnormalities |
|
|
Inherited tubular abnormalities
|
-Glycosuria (Norwegian elkhound, scottie)
-Fanconi syndrome (Basenji) --glucose, AA, and bicarbonate get into tubules -Cystinuria (Irish terrier, newfoundland, dachshund, bassets, bull dogs) |
|
|
Familial Renal Disease
|
-Renal dysplasia/renal hypoplasia/ cortical hypoplasia/familial renal disease/juvenile renal disease
-Juvenile renal disease is best term |
|
|
Juvenile renal disease
|
-Abnormal renal development
-Renal biopsy shows fetal glomeruli and fetal mesenchyme -Inherited, occurs in clusters or test breedings -Can be environmental cause -Occurs in young dogs -Dog presents with chronic renal failure within 3 years of life --often less than 18 months -Do a biopsy after 16 weeks of age |
|
|
Juvenile Renal Disease History and PE
|
-PU/PD
-Chronic renal failure signs --weight loss, vomiting -Rubber jaw, mandible has not calcified -Stunted -Small kidneys -Hypertension |
|
|
Juvenile Renal Disease Diagnostics
|
-Looks like renal failure
-Urine is isosthenuric -May have a UTI or be predisposed to UTI -Radiographs and ultrasound show small kidneys -Diagnose with wedge biopsy after 16 weeks |
|
|
Juvenile Renal Disease Treatment
|
-Same treatment as chronic renal failure
-Pedigree analysis |
|
|
Juvenile Renal Disease Breeds
|
-Doberman
-Golden Retriever -Lhasa Apso -Shih Tzu -Soft-Coated Wheaten Terrier -Standard Poodle |
|
|
Renal Agenesis
|
-Congenital Kidney disease
-In Beagle -Bilateral animals do not live -If unilateral can be incidental finding |
|
|
Renal Amyloidosis
|
-Shar Pei (glomeruli)
-Beagle (glomeruli) -Abyssinian cat (tubules) |
|
|
Polycystic Kidneys
|
-Congenital kidney disease
-Persian Cats -Autosomal dominant -Chronic renal failure by middle age -Animal will have large kidneys -Diagnose via ultrasound |
|
|
Polycystic renal and hepatic disease
|
-Carin terrier
-West Highland White Terriers -Cysts in kidneys |
|
|
Breeds predisposed for Protein-Losing nephropathy
|
-Labrador
-Golden Retriever -Sheltie -Wheaten terriers -Samoyed -English cocker spaniels |
|
|
Samoyed
|
-Inherited predisposition for protein losing nephropathy
-X-linked recessive -Males die witihin 2-15 months -Female carriers can live longer |
|
|
Nacasota dog
|
-X-linked protein losing nephropathy
|
|
|
English Cocker Spaniel
|
-Autosomal recessive protein-losing nephropathy
-Shows up at 10-24 months |
|
|
English springer spaniel
|
-Alport
-Autosomal recessive protein losing nephropathy |
|
|
Dalmation
|
-Autosomal dominant protein losing nephropathy
|
|
|
Bull terrier
|
-Autosomal dominant protein losing nephropathy
|
|
|
Glycosuria and inherited tubular abnormalities
|
-Tubular transport for glucose is deficient |
|
|
Fanconi Syndrome
|
-Inherited tubular abnormality
-Tubular transport is deficient for multiple solutes --AA, glucose, Na, phosphate, uric acid, bicarbonate -Can be congenital or acquired -20% of Basenjis are affected -Some border terrier dogs |
|
|
Cystinuria
|
-Inherited Tubular Abnormality
-Auosomal recessive -Tubular transport deficiency for cysteine -Results in cysteine urinary calculi -Newfoundland, 30% are carriers -Irish terrier, bull dogs, lots more |
|
|
Spontaneous Hypertension in Dogs
|
-Secondary to renal disease, hyperadrenocorticism, or hyperthyroidism
|
|
|
Defining Hypertension in dogs and cats
|
-When there is associated target organ damage
-Normal: 160/95 -White coat syndrome: 180/100 -2 standard deviations from the mean? --would include dogs with renal disease, hyperadrenocorticism, glomerular disease, hyperthyroidism -Mostly clinically insignificant --not associated with increased morbidity and mortality -Certain breeds have higher BP than others normally |
|
|
Hypertension
|
-In people, usually primary
-In dogs and cats, due to underlying disease --renal disease --hyperadrenocorticism --hyperthyroidism |
|
|
IRIS Blood Pressure Guidelines
|
-Minimal risk: less than 150/ less than 95
-Low risk: 150-159/95-99 -Moderate risk: 160-179/100-119 -High Risk: more than 180/ more than 120 -Risk: likelihood that high blood pressure will further damage the kidney and other organs |
|
|
Direct Blood Pressure measurement
|
-Femoral arterial stick and catheter in artery
|
|
|
Indirect Blood Pressure Measurement
|
-Can do on a limb or on the tail
-Use cuff that is 30-40% of limb circumference --small cuff increases blood pressure measurement artificially -Dinamapp -Doppler (ultrasound, only systolic, but can be used on any leg) -PetMap -Finapress |
|
|
Calculating Hypertension
|
BP=COxSVR
-CO= HRxSV -SVR= arteriolar elasticity, circulating and local vasoactive agents, arteriolar sensitivity |
|
|
Factors affecting Blood Pressure
|
-Related to Heart Rate:
--Beta-adrenergic stimulation --Hyperthyroidism (more beta receptors near heart) --hyper kinetic --Pheochromocytoma (adrenal medulla tumor, releases catecholamine) -Related to Stroke Volume: --Fluid or salt overload --Renin-angiotensin-aldosterone system --Hyper-aldosterone, increases na retention and water retention --Cushing’s disease -Related to SVR: --caecholamines --high Na or Ca --Renin-angiotensin-Aldosterone --Antiogensin II --Cushing’s disease --Atherosclerosis (rare in dogs and cats) |
|
|
Secondary Causes of Hypertension
|
-Renal
-Adrenal -Thyroid -Diabetes -Hyperkinetic heart syndrome -Hypercalcemia -High salt intake (not all animals are salt-sensitive) -Alpha agonists (phenylpropanolamine) -Black licorice, has mineralocorticoid activity -Vitamin D toxicity |
|
|
Renal cause of hypertension
|
-increased CO or increased SVR
-Glomerular disease in particular -Normal renal disease -Pyelonephritis -Polycystic kidney disease -Renal dysplasia -Renovascular disease --thromboembolic event, infarct, renal arterial stenosis |
|
|
Adrenal cause of Hypertension
|
-Mostly in dogs, can also occur in cats
-Cushing’s disease: hyperadrenocorticism -Increases CO and SVR -Pituitary dependent production of steroids -Adrenal dependent production of steroids -Exogenous steroids -Hyperaldosteronism increases CO and SVR -Pheochromocytoma: tumor releases catecholamines --increases HR and SVR |
|
|
Thyroid causes of Hypertension
|
-Mostly in cats, increases HR and SVR
-In dogs usually iatrogenic, increases SVR |
|
|
Hyperkinetic heart Syndrome
|
-Due to anemia, hyperviscosity, polycythemia
-Increases CO and SVR |
|
|
Rare causes of secondary hypertension
|
-Hyperestrogenism
-Pregnancy toxemia -Coarctation of the Aorta -Intracranial disease (brain tumor) |
|
|
Target organ damage due to hypertension
|
-Due to damage of arteriolar and capillary beds
-Muscles detect BP is too high and vasoconstrict to protect capillary bed from high blood flow -Results in hypertrophy of myoepithelial cells in arterioles --Permiability of capillary bed changes -If there is no autoregulation, will have direct blow-outs and hemorrhage --retina or in nose |
|
|
4 Main end-organs for damage due to hypertension
|
-Eye
-Cardiovascular system -Kidney -CNS |
|
|
Eye damage due to hypertension
|
-Retinal hemorrhage
-Retinal detachment -Animal presents with blindness -May see intraocular exudation, closed angle glaucoma, corneal ulcer -Increased retinal tortuosity, tortuous vessels -Chronic situation will have retinal atrophy or hyper-reflective scarring |
|
|
Cardiovascular system damage due to hypertension
|
-Left ventricular hypertrophy
-Blood is pushing against a high systemic vascular resistance -Mild mitral murmur -Cardiomegaly (hypertrophic cardiomegaly) on radiographs -Arteriosclerosis -May present with nose bleeds |
|
|
Kidney damage due to hypertension
|
-Glomerulosclerosis
-Proteinuria -PU/PD due to pressure diuresis -Hard to know which came first, hypertension or kidney issues -If albumin is low, indicates that kidney problem started first |
|
|
CNS damage due to hypertension
|
-Stroke (cerebrovascular accidents)
-Will see neurologic signs --seizures, paresis or paralysis -not permanent change, animals either die or get better |
|
|
Hypertension is self-perpetuating
|
1. Hypertension leads to arterial damage, which leads to decreased arteriolar elasticity
-leads to increased systemic vascular resistance, leads to hypertension 2. Hypertension causes renal damage, leads to decreased arterial elasticity, decreased Na/Water handling, increased RAAs, increased sensitivity to angiotensin II, decreased renal vasodilators -Causes increase in CO and SVR, leads to hypertension |
|
|
Dogs and Cats with Hypertension
|
-Older, overweight, and male
-Blindness is most common presenting complaint -Nosebleeds, Chronic Renal Failure, Cushing’s disease, Neurologic signs -Breeds that come in with hypertension are predisposed to kidney disease or Cushing’s disease --Animal presents due to underlying disease -PU/PD is common, part of whole picture --renal disease, cushing’s, hyperthyroidism, pressure diuresis -Vomiting, anorexia, weight loss, ascites/edema, thromboembolic signs |
|
|
PE for animals with Hypertension
|
-Small kidneys
--hard to know if they are the cause, effect, or coincidence due to age -Low-grade mitral murmur due to left ventricular hypertrophy or dilated cardiac skeleton -Hyperthyroid cats: tachycardia, gallop rhythm, thyroid mass present -Cushing’s disease: hair loss, pot-belly, etc. |
|
|
Diagnostic tests for Hypertension
|
-Blood pressure measurements, repeat!
-Eye exams -CBC/Chem -Urinalysis and urine culture -Coagulation tests -Chest radiographs -Abdominal ultrasound -Cardiac workup (ECG, echocardiogram) -Cushing’s workup (ACTH stim) -Thyroid workup (thyroid panel, T3 suppression) -Renal workup (biopsy, tick titers) -Pheochromocytoma (regitine test, umentanephrines) -Brain scan |
|
|
Anti-hypertensive treatment
|
-ACE inhibitors
-Beta blockers -Ca Channel blockers -Angiotensin receptor blockers, Renin inhibitors, anti-aldosterone -Other vasodilators can be used in-house to regulate -Low salt diet: not all animals are salt sensitive --try not to give extra salt, but don’t restrict -Diuretics: animals usually need something stronger |
|
|
ACE inhibitors for Hypertension
|
-Often used, especially in dogs
-Helps decrease proteinuria -Azotemia can be an issue if animal already has cardiac issues, need to be careful with dose -Enalapril, benazepril |
|
|
Beta blockers for Hypertension
|
-Hyperthyroid cats with hyperkinetic syndrome
-Want to lower the HR -Atenolol |
|
|
Ca channel blockers for Hypertension
|
-First line anti-hypertensive drug in cats that are not proteinuric but are hypertensive
-Amlodipine -Can be added to dogs as 2nd agent |
|
|
Emergency Hypertensive Episodes
|
-Not common in pets |
|
|
Prognosis for Pets with Hypertension
|
-Good prognosis for vision if blindness was acute and only lasted a short time |
