Cats and Dogs Flashcards
What does a bitch pre-breeding exam consist of?
* Signalement, history
* General exam, hereditary disease
* Special reproductive exam
- digital palpation of vagina and vulva
- vaginoscopy
- cytology
- microbiology is a waste of time and money– always bacteria present
* B. canis test
In a bitch, when can you accurately diagnose a pregnancy by the different methods? What should you never use?
Ultrasonography > 20 days post LH surge
Abdominal palpation > 25 days post LH surge
Relaxin test > 28 days post LH surge
Radiography > 44 days post LH surge
** recall serum progesterone levels are NEVER to be used as an indicator of pregnancy in the bitch
How do you estimate the whelping date?
57+/- 1 day post D1 of dioestrus
* 65 +/- 1 day post LH surge
* 65 +/- 8 days post breeding (because there is such a long fertile period in the dog and the fertility of the sperm is so long, it gives a long window)
When is birth abnormal in a bitch?
* Whelping not observed after temperature drop
* Active labour > 4 hours and no pup produced
* green-coloured or malodorous vaginal discharge (before the first puppy comes out, it means the placenta separated)
* interval between pups > 30 minutes (with myometrial contractions)
* interval between pups > 2 hours (without myometrial contractions)
* signs of pain or diffuse vaginal bleeding
With elective caesarean section, how do you decide when it is time?
* Important to know d0 and D1
* progesterone drops 24 to 48 hours prepartum
* rectal temps drop 8 to 24 hours
* check fetal heart rates in last couple of days
If you suspect uterine inertia, what should you do?
* Assess hypocalcaemia clinically (do not just rely on blood Ca levels– they can be normal in a hypocalcaemic bitch)
* give 10% Ca solution IV
* Listen to heart while administering calcium
* Give calcium to effect
* oxytocin may be helpful but often not necessary
When might you see eclampsia in a bitch? What are the clinical signs? Treatment? Prevention?
Observed mainly in toy breed with large litters
* Clinical signs: tremors, nervousness, salivation; late stage: opisthotonus
* Treatment: Calcium IV to effect, oral calcium supplementation, wean puppies if > 4 weeks
* Prevention: adequate Ca: P ratio pre partum
When/ why might metritis occur in a bitch? Clinical signs? Diagnosis? Treatment?
* 0-7 days post partum due to retained foetal membranes/ fetuses, dystocia etc. and secondary infection
* Clinical signs: fever, anorexia, vaginal discharge, doughy enlarged uterus
* Diagnosis: cytology: neutrophils, bacteria (phagocytosed), membrane parts; WBC: leukogram can be normal initially
* Treatment: treat shock, AMs (broad spectrum), evacuate uterus
When might you see subinvolution of placental sites in a bitch? Clinical Signs? Treatment?
(delayed involution of placental sites)
* More often in bitches
* Clinical signs: sanguineous vaginal discharge > 6 weeks post partum
*Treatment: often self-limiting, OHE if necessary
What are the clinical signs and pathogenesis of false pregnancy in a bitch? Treatment?
* mammary development and galactorrhea
* Nesting and mothering behavior
* abdominal distension/ uterine enlargement
** Pathogenesis: decreased progesterone; increased prolactin
** Treatment: Prolactin antagonist (e.g. cabergoline)
What is the percentage of intact bitches that end up with pyometra?
24% of intact bitches before 10 years of age
What is the usual cause of canine pyometra? What percentage show clinical signs within 12 weeks of their last heat?
* E.coli is isolated in 96% of clinical cases
* 75-93% of affected bitches show clinical signs within 12 weeks of their last heat
Why does progesterone create the perfect environment for bacteria?
* Stimulates proliferation and secretion of endometrial glands (“uterine milk”)
* keep cervix functionally closed
* inhibits myometrial contractions
* Reduces immune response to pathogens
** effects are exacerbated if the uterus is previously primed with oestrogen– multiple oestrus cycles without pregnancy will have a “cumulative effect” (Cystic Endometrial Hyperplasia (CEH))
What is the classic canine pyometra case?
* Middle aged to old (mean age: 7.25 years)
* Intact
* In dioestrus
* Has not been pregnant
What is the atypical canine pyometra case?
* Breed predisposition e.g. Golden Retriever, Mini Schnauzer, Saint Bernard, Collie, Rottweiler etc.
* Anecdotal familial clustering
What are the two types of pyometra? What are the clinical signs?
Open and closed (referring to the patency of the cervix)
* Clinical signs: not definitive… pyometra should be suspected in any intact bitch presenting 4-12 weeks after having been in heat, with vaginal discharge, depressiong, PU/PD, vomiting and/or pyrexia
Treatment of canine pyometra
Ovariohysterectomy… if breeding the animal– evacuate the uterus:
- if you just gave AMs– likely uterine rupture and possible death due to endotoxaemia
- low dose prostaglandin F2alpha
- can be used in combination with aglepristone (given 24 hours prior to PGF2alpha
- treat bacterial infection with broad spectrum AM
- treat systemic signs if indicated
Prognosis for recurrence of canine pyometra?
* 10-80%
** if no response to treatment within 5 days:
- poor prognosis in regard to future fertility
- increased risk of recurrence of disease
Prognosis for future pregnancy?
* Dependent on uterine health
* prolonging anoestrus with androgens (e.g. mibolerone) recommended
* bitch should be bred on every heat until desire numbers of puppies are reached–> then spayed
What is the pregnancy rate of a bitch (fertile male and female)? When is a fertility exam justified? When is it ideally done?
* 75% chance to produce a litter
* only 6% of bitches miss twice in two consecutive cycles
* Therefore after two empty consecutive cycles, fertility exam justified- ideally done in anoestrus (few months before next expected heat)
Oestrus induction in a bitch?
* Deslorelin (GnRH agonist) implant or long acting injection
What can a prolonged cycle indicate?
* Follicular cysts (cytology can confirm cycle is prolonged, ultrasound can diagnose– follicles fail to luteinise)
* ovarian neoplasia
* iatrogenic
Treatment of follicular cysts?
GnRH or hcG
When does a dog typically get vaginitis? Clinical signs? Tx?
Puppy- prior to first oestrus
Adult- after first oestrus and in spayed females
* CS: discharge, may attract male dogs
* TX: puppy vaginitis spontaneously resolves often, check for brucellosis, phenylpropanolamine for adults
What is split heat?
* Physiological and behavioural signs of proestrous occur without progress to oestrus (common in young bitches)
* after 4 weeks “normal oestrous cycle” with ovulation occurs
Who is primarily impacted with shortened anoestrus? TX?
German Shepherds–
TX: delay oestrous with androgens (mibolerone; Cheque Drops)
What is ovarian remnant syndrome? Clinical signs? Tx?
* piece of ovarian tissue left behind at time of spaying
* bitches present with signs of prooestrous (+/- bleeding)
* can do hcG/GnRH stimulation test
* laparoscopy during oestrus or luteal phase
How can we tell if a bitch is spayed?
* look for midline incision
* measure LH and FSH–> would be high due to lack of negative feedback
How do you diagnose prostatic diseases?
* Sample of prostatic fluid–> collect ejaculate
What percentage of intact male dogs have benign prostatic hypertrophy/plasia (BPH)? TX?
> 90%
* TX: Castration
What are the major prostatic diseases? What are they often secondary to ? What’s the only one that is not treated by castration?
Benign Prostatic Hypertrophy/plasia (BPH)
* prostatitis- acute or chronic
* Prostatic abscesses- often secondary to prostatitis
* prostatic cysts
* Neoplasia: castration is not a cure!– grave prognosis by the time diagnosed it has almost always metastasized… almost always malignant adenocarcinoma
What can occur with Prostatomegaly?
* haematuria, haemospermia, tenesmus (flat faeces), dysuria, poor semen quality/ infertility, acute prostatitis: fever, anorexia, lethargy
Prostatomegaly diagnosis?
* Rectal palpation: size, symmetry, surface, pane
* RX
* Cytology and culture of prostatic fluid
* Urinalysis
* Retrograde cysturethrography
Treatment of prostatomegaly (except neoplasia)
Finasteride (5 alpha reductase inhibitor) or progesterone until breeding career is over… consider freezing semen
What is unique about feline repro?
mate multiple times to ovulate
How do you terminate pregnancy in a bitch?
* Ovariohysterectomy
* If not okay, then first confirm she is pregnant (if it too early, do not give anything):
- PGF2alpha (dogs are not as sensitive as other species- over a course of 5 days)
- dopamine agonists (prolactin, maintenance of pregnancy, antagonist)
- aglepristone (block progesterone receptors)
- corticosteroids
or a combination of the above
Speak through the stages of whelping (length too).
With a potential obstructive dystocia, what should be done?
* it is an emergency
*two procedures should always be done:
- vaginal exam (to feel or see stressed pup, check for contractions (hypocalcaemia if no contractions; obstructive if contractions)
- ultrasonography (if they are alive and how stressed they are)
What should you think about with an infertile bitch?
What should you think about in a bitch that fails to cycle?
* karotyping
What should you think about with an irregular oestrous cycle in a bitch?
Common repro related disease in cats
What are special considerations for neonate (first 6 weeks) and paediatric (first 12 weeks) anaesthesia?
* limited organ reserve
* exaggerated or prolonged effects of anaesthesia
* CV: low myocardial contractile mass, low ventricular compliance, SV and cardiac reserve are limited, CO is rate dependent, persistence of fetal circulation in foal up to 3 days (right to left shunt)
* Symp NS not full developed: minimal increase in HR and myocardial contractility–> further impairing ability to increase CO, poor vasomotor control and inadequate response to blood loss
*Resp: pulmonary reserve is minimal, more compliant chest–> greater work of breathing, higher minute volume
* Thermoregulation: immature thermoregulatory system, high body surface to mass ratio, prone to hypothermia
Major physiological differences affecting pharmacological properties of anaesthetics?
- Hypoalbuminemia–> more free drug
- Increased permeability of BBB
- Increased percentage of body water content–> greater apparent volume of distribution
- Fixed circulating fluid volume–> more susceptible to hypovolaemia
- Low body fat percentage– less drug redistribution in adipose tissue
- Immature hepatic metabolism- increased duration of action
- Immature GFR- increase duration of action
- higher metabolic rate– increase oxygen consumption and CO production
What should anaesthetic protocol include with drugs for neutering?
Sedative, muscle relaxant, analgesia, hypnotic
What might you use as premedication in a young adult for anaesthesia in a dog and cat?
* IM medetomidine & methadone- cats and dogs (or Ace & hydromorphone- dogs, or ketamine & midazolam & methadone- cats)
What might you use in IV anaesthetic induction in a young adult dog or cat?
* Propofol +/- diazepam (or Alfaxalone +/- diazepam, or diazepam & ketamine)
What might you use for maintenance in a young adult dog or cat?
Isoflurane in oxygen, balanced crystalloid solution (5 ml/kg/h)
What might you use for loco-regional analgesia in a young adult dog or cat?
* Line block with bupivacain or ropivacaine
* intra-testicular block with lignocaine (dogs)
What would you use in a young adult dog or cat for post op analgesia?
* NSAID (carprofen or meloxicam), +/- opioid
What might you use for neutering premed in paediatric dog or cat?
IM anaesthetic–> acepromazine (low dose) & methadone- dogs and cats (or hydromorphone (dogs), or ketamine (low dose) & midazolam & methadone-cats)
What might you use for neutering paediatric patient dog or cat IV anaesthetic induction?
* Propofol +/- diazepam
* Alfaxalone +/- diazepam
What might you use for maintenance in a paediatric patient in a dog or cat?
* isoflurane in oxygen, balanced crystalloid solution, +/- dextrose solution at 2 to 5 mL/kg/hr
What might you use for Loco-regional analgesia in a paediatric patient in a dog or cat?
Caution to total volume administered
* line block with bupivacaine or ropivacaine
* intra-testicular block with lignocaine (dogs)
What might you use for post op analgesia in a paediatric patient in a dog or cat?
NSAID (carprofen or meloxicam) +/- opioid
CV changes induced by pregnancy? CV changes during labor?
* estrogens decrease vascular resistance, combined with CO– BP unchanged, increased HR and SV
* Blood volume increased by 40%– plasma > RBCs = decreased PVC = decreased [Hb]
* Labor:
- Increased HR, CO, BP, and central venous pressure (CVP), increase oxytocin levels
- in dorsal recumbency, gravid uterus will compress caudal vena cava= decrease venous return which will decreased blood for to uterus
Respiratory physiological changes induced by pregnancy
* Progesterone increases CNS sensitivity to CO2– normal PaCO2 decreased to 30 mmHg, increased minute ventilation
* increased tissue oxygen demands (VO2)
* Decreased functional residual capacity (FRC)- gravid uterus pushes up on diaphragm= less space for lungs, more sensitive to hypoxemia and hypercapnia
* decreased FRC + increased minute ventilation = faster induction with inhalants
Physiological changes to the GIT during pregnancy
* Gravid uterus pushing on stomach
* Decreased gastric motility
* decreases oesophageal sphincter tone
* risk of regurgitation increased
Physiological changes to liver and kidneys during pregnancy
* Increased hepatic and renal blood flow– GFR increased by up to 60%, BUN and creatinine decreased
Physiological changes induced by pregnancy to uterus
* Uterine blood flow changes during pregnancy and labour
* Uterine contraction and oxytocin decrease uterine blood flow–> decreased foetal viability, effect worsen by anaesthesia
What are conditions that favour drugs crossing the placenta?
Drug: * Poor ionization in the dam- non-ionized can pass but becomes ionized and cannot pass back out
* Low molecular weight
* low protein binding
* high lipid solubility
(qualities of a good anaesthetic drug but bad for the foetus)
Placenta:
* thickness and surface area of placenta determine how much drug will transfer
* concentration gradient (dam to fetus) another determination
Patient:
* pH
*pK
General considerations when choosing drugs for Caesarean section
* Be prepared and quick
* Use smallest doses possible
* consider local anaesthetics
* Avoid long acting drugs
* Choose reversible drugs if possible
* Minimize inhalant concentration (reduced MAC in pregnancy)
* Dam is at increased risk for vomiting and regurgitation
* have warming devices, oxygen, intubation kits, dry gauze to wipe secretions from mouth and nose ready
* Emergency drugs ready: reversal agents (for dam and puppies), epinephrine, atropine, dextrose
Premedication for Caesarean section
* Opioids- minimal resp effects vs. analgesia–> methadone
* Avoid Acepromazine or alpha 2 agonists (NO XYLAZINE)
* May skip pre-med
* pre oxygenate the patient!!!
Induction drugs for Caesarean section
* Propofol, Alfaxalone
* Can consider Fentanyl + Midazolam if dam is exhausted after prolonged dystocia
Maintenance drugs in caesarean section
* propofol/isoflurane or sevoflurane
* will require IPPV due to dorsal recumbency
* Consider additional analgesics after removal or puppies
* don’t forget local analgesia
* Ephedrine maintains uterine blood flow while treating hypotension
Things to remember with puppy or kitten resuscitation
* Oxygen is the single most important thing you can provide
* Rub vigorously to stimulate breathing
* Doxapram under tongue if nothing
* provide warmth and oxygen rich environment
* reversal of the drugs given to the dam that could have transferred to the puppies through the placenta
Drugs for recovery after Caesaerean section
NSAIDs +/- Tramadol for dam for post-op pain
When should you desex female dogs?
6 months of age (in a shelter 8-12 weeks of age– claimed decreased stress and operative time, assurance de-sexed when rehomed)
What is the ovarian artery a direct branch of? What does it supply?
The aorta
* The ovarian a. supplies the ovary and the cranial aspect of the uterus
Where does the right ovarian vein drain into? Where does the left ovarian vein drain into?
* Right ovarian vein drains into the caudal vena cava
* Left ovarian vein drains into the left renal vein
Ovariohysterectomy in season
What is a major benefit of canine and feline spays?
What suspends the uterus and ovary from the abdominal cavity? What makes up x?
Broad ligament: mesovarium, mesosalpinx, mesometrium
What attaches the ovary to the uterine body? What does it continue on as?
Proper ligament (continused caudally as the round ligament that courses within the broad ligament, passing through the inguinal canal)
Indications for Caesarean Section
What is the uterine artery a branch of?
Internal pudendal artery
What lymphatic drainage exists from the canine and feline repro tract? Innervation?
* hypogastric and lumbar LNs
* Hypogastric plexus (symp), pelvic nerves (PS)
Why is ventral midline preferred over flank?
* Better access to peritoneal cavity if problems occur
* Can check haemostasis
* Access to right ovary can be difficult through flank approach
* Anecdotally increased incidence of seroma with flank procedures (3 x muscle layers)
Size of OVE incision in a dog? Cat? What should you always do first?
Canine: 1-2 cm caudal to the umbilicus extending 5 cm
Feline: 3-4 cm incision centred over the midpoint between the cranial rim of the pelvis and the umbilicus
* express the bladder
Clinical signs of pyometra and clinical pathology?
Diagnosis of pyometra
* abdominal palpation, radiographs, ultrasound (most sensitive– demonstrates presence of fluid and thickness of uterine wall)
Mean age of pyos?
6
Vaginal oedema– during oestrogenic phase, vaginal mucosa becomes swollen allowing a transverse fold to prolapse through vulva (esp Brachycephalic breeds)… regresses spontaneously, OVH permanent relief
Why do you avoid using chromic catgut in a continuous manner?
Less tensile strength and its loss of tensile strength relies on phagocytosis not hydrolysis and its rate is unpredictable
Neoplasia of the vulva/vagina dogs
Epesioplasty
Episoplasty is most commonly used in the treatment of chronic perivulvar dermatitis secondary to skin
folds and or infantile external genitalia. Cresenteric resection of redundant skin folds improves the
micro
environment, prevents vaginal hooding and allows improved air circulation and drying of
perivulvar skin.
Medical therapy with appropriate antimicrobial agents should be instituted prior to
surgery
Consequences of being entire
Indications for castration
Complications of OVH
* Haemorrhage, most common (76% of all complications)
* Wound healing complications e.g. suture reaction (esp cats), seroma, fistulous tracts
* Stump pyometra- progesterone produced by remnants of ovarian tissue or exogenous
* Ureteral ligation
* Ovarian remnant syndrome (mammary development, bleeding)
* Urinary incontinence (11-20%)
* Weight gain (26-38% gain reported)
When is scrotal ablation performed?
Signs and symptoms of a Sertoli cell tumour
Signs and symptoms, consequences of interstitial (Leydig) tumours
Size of incision in caesarean section ventral midline approach
2-3 cm cranial to and 5-6 cm caudal to the umbilicus
Clinical signs and diagnostic approach to testicular masses
* Also histo via excisional biopsy
* for high breeding value animals- testicular sampling (FNA and biopsy)
Why should you rub instead of swing a foetus?
Safer, swinging has been implicated in causing brain damage
What sutures and materials in a C-section?
* Cushing or Lembert pattern with synthetic absorbable monofilament suture
Why does pyo often occur during dioestrous?
* Cervix closed and progesterone increases secretions of uterine glands, inhibits myometrial contraction and closes the cervix, results in cystic endometrial hyperplasia, inhibits the leukocyte response facilitating bacterial colonisation
Treatment of pyometra
* PGF2alpha luteolysis (lowering progesterone) + Broad spectrum antibiotics (Clavulox or enrofloxacin)
* Surgical : OVH, care not to rupture distended uterus, lavage
Clinical signs and treatment of paraphimosis?
Urethral prolapse clinical signs and symptoms?
Treatment of urethral prolapse
Penile neoplasia tumour types in dogs and cats
Diagnosis and treatment of penile tumours?
How do you differentiate Vaginal Prolapse from Vaginal Oedema?
Circumferential prolapse of the vagina
Lump on a scrotum- what do you want to rule out first?
Mast Cell Tumour with FNA
Timing of castration
6-9 months as optimal age (no demonstrated negative effects in dogs and cats
Complications with castration
* Scrotal bruising/haematoma
* Haemorrhage
* Dermatitis
* Infection/abscess
* Persistent Priapism in cats
Fertility in cryptorchids
* Bilaterally affected animals- sterile; unilaterally affected animals- sub-fertile
Most common primary testicular neoplasms in dogs
Interstitial Cell Tumours (aka Leydig)
Sertoli Cell Tumours
Seminomas
In an abdominal cryptorchid, where do you look for the testicle(s)?
Underneath the bladder
What is a seminoma?
* Neoplastic change in cells responsible for spermatogenesis
Cryptorchid confirmation of location
* Abdominal or inguinal
* Palpation (fat, LNs)
* Ultrasound
Clinical signs of prostatic disease
* Dyschezia/ constipation
* Urethral bleeding/ discharge
* Pyrexia
* Hindlimb stiffness- weakness
Diagnosis of prostatic disease
* Radiography (mineralisation associated with neoplasia in castrated dogs, displacement of adjacent tissues- colon, bladder, osteolysis of vertebral bodies, positive contrast studies)
* U/S– enhances accuracy of FNA or biopsy
* Fluid samples for cytology and culture can be obtained by: sampling ejaculate, prostatic wash , U/S guided FNA
Indications of prostate surgery? Caution? Omentalisation?
* Biopsy, prostatic abscess, cystic disease, prostatic neoplasia
* avoid the dorsolateral aspects- neurovascular pedicle
*Omentum: vascular supply, lymphatic drainage, immuno-competent cells
Partial vs. Complete Prostatectomy
* Partial prostatectomy: potential for significant blood loss, temporary arterial occlusion, pre-place catheter to ID the urethra,
* Complete: Malignant neoplasia sole indication (uncommon due to late dx, early metastatic dx, lack of impact on distant disease, likely incontinence)
What is phimosis?
* Inability to extrude penise because preputial orifice is too small (congenital) or acquired due to trauma, infection, scarring, neoplasia…. from urine pooling and balanoposthitis, erectile pain
** Surgery- enlargement of a narrowed preputial os using a v-shaped incision on the dorsal surface and apposition of mucosa to skin
Paraphimosis
* INability to retract within the prepuce– congenital or acquired (trauma, infection, internal rolling and entanglement with hair)
What does a state of mild metabolic acidosis do to calcium?
Increases serum calcium level through increased tissue responsiveness to PTH
What do we need Ca most for parturtion?
Muscle contractions
Commercial Labrado breeding colon 7% rate of stillbirths in the last 2 years, uterine inertia- compared to GSD from colony with low SB/inertia rate
* high venous pH during whelping
* similar total Ca concentrations
* Lower ionised Ca concentrations
* higher PTH concentration
Likely Congenital– crossing with other breeds now
Changed food similar to what you’d do in dairy cows– which lowered the stillbirth rate
What tells you something: total Ca or ionized Ca?
** Ionized Ca
What are the local effects of MCT?
* Degranulation of MCT
- oedema
- ulceration
- swelling
Paraneoplastic effects of a MCT
Clinical presentation of MCT in dogs
Can be bad: rapid growht, local swelling, paraneoplastic signs, palpably enlarged spleen or draining LNs, anatomic location (mucocutaneous junctions and inguinal region)
What are the histological classifications of MCTs? What additional therapies might be used in different grades
* Grade 1- benign
* Grade 2- hasn’t decided
* Grade 3- aggressive with early metastases
How big are the margins for each histological classification?
What is meant by 3D surgical margins?
What would you do next?
A. FNA lump
B. FNA lump & spleen/liver
C. FNA lump, spleen, liver and get bone
D. Get incisional biopsy of mass
A. FNA lump BECAUSE your best chance to cure is your first cut
FNA cytology confirms MCT
A
Grade 1 MCT with incomplete margins
** a C- kit - if the tumour has a c- kit mutation known to be sensitive to tyrosine kinase inhibitor. Not quite Chemotherapy but similar idea. Wouldn’t choose C because it makes the dogs really sick and we aren’t even sure it will work– and we are not in Brisbane. It is not in an area that would have few side effects (e.g. a limb)
** B. probably
A. FNA lump
B. FNA lump and pre scapular lymph node
C. FNA lump, lymph node, and do further staging
D. Get incisional biopsy of mass
Rapid develop, so it is aggressive, so FNA lump and pre scapular lymph node (B)
FNA cytology = MCT
* FNA cytology LN poor cellular yield but occasional mast cell noted
A
A. Nothing- watch, wait, and see
B. Adjunctive chemotherapy
C. Revision surgery only
D. Refer for radiation
C. Revision Surgery (+ B is the optimal)
A. Limb amputation
B. Palliative chemotherapy only
C. Systemic chemotherapy
D. Refer
C or D gold standard
A. The prognosis for Billyis poor as he has multiple MCT
B. Adjunctive chemotherapy is necessary regardless of MCT grade
C. Staging is still necessary for each MCT
C. Staging is still necessary for each MCT
Important considerations for treatment of MCT?
When is a marginal incision acceptable?
What are the common MCT dermal tumours?
What are soft tissue sarcomas?
* Skin and S/C most common locations but can be anywhere
* Slow growing
* Locally invasive
* Low metastatic rate (grade dependent)
Soft Tissue Sarcoma (STS) presentation?
STS metastasis?
STS prognosis
STS Diagnosis
STS treatment?
* Pseudocapsule- tumour cells at capsule invade surrounding tissue
* Make STS appear easy to shell out– DO NOT shell out tumour
* Margin status predictive of local recurrence
* Local recurrence common after incomplete surgical resection
STS treatment depending on margins– complete or incomplete and grade?
What would you do next?
A. Incisional biopsy
B. Excisional biopsy
C. Amputate leg
D. Refer
A. Incisional biopsy
Incisional biopsy shows Grade 1 STS
C. Marginal excision and radiation
(Can do amputation, no indication for metronomic chemotherapy)
Incisional biopsy shows Grade III STS
A. amputate leg is the most curative but depends on owner…. otherwise B and C
** STS’ are not that responsive to chemotherapy
What are spot on products?
What are the active ingredients in Frontline? Mode of actions? How is it absorbed? Who can you NOT use it in?
Who can Fibronil spray be used in? Who can it NOT be used in?
What is the active ingredient in advantage? Mode of action? How is it absorbed? What does it treat?
What is advantix? Who can you NOT use it in? What is it for?
Imidacloprid + permethrin (fleas, ticks, and mossies)
What are the active ingredients in advocate? What is it for?
What is the active ingredient in Revolution? How is it absorbed? Who CAN it be used in safely (as opposed to ivermectin)?
What is the active ingredient in Activyl? What does it treat?
What are the four types of oral flea prevention?
General principles of diagnosing a MCT
* Cytology usually diagnostic & prognostic
* Can consider incisional biopsy– more $, great risk wound breakdown
* thorough planning is best
What are topical anti-inflammatories used in SA?
What are the types of topical medications used in animals?
What are the different schedules of drugs?
What are transdermal patches? Example?
What are the two times you might consider using antibiotics and gluctocorticoids together?
* Dogs with a normal HPA axis- the use of GC with antibiotics may be counter productive
* But short term use of combinations of corticosteroids and antibiotics with comparable pharmacokinectics on the skin like aminoglycoside antibiotics can be of clinical benefit
Why does infection triggered itch respond poorly to glucocorticoids?
* Protease pathway is not blocked
Common breeds associated with atopic dermatitis? Associated with demodex?
What do you need for dermatology in a SA clinic?
What bacterial infections commonly occur in domestic animal skin infections?
How does MRSP spread its resistance?
Properly set up microscope for unstained cytology
Why are dogs skin more susceptible to infection vs. humans?
DDX?
Alopecia
* Excess loss or failure to grow
* DDX:
- excess loss: self trauma or folliculitis
- failure to grow: endocrinopathy
Diagnostic approach to alopecia
Pyo traumatic dermatitis (aka hot spot)
* considered surface infection in most cases (usually staph)
* Treat with topical drugs
Treat topically
* oral antibiotics for 2-3 weeks
Short acting Dex (36 hours)– not steroids on going!!
* Topical antibiotic with steroid– e.g. He always uses fusiderm or neocort– (but does not penetrate, has lignocaine in it which is toxic to the skin so longer than a week causes a chemical burn– so never in thin skins– nowhere near scrotum in male dogs)
When would you perform a Trichogram?
- Trauma
- Dermatophytosis (ringworm)
- Parasites
- Anagen: Telogen ratio
Does not need oral antibiotics
Does not need oral antibiotics– topical will be faster, quicker, easier
Malassezia but could be bacteria so cytology
Cytology for surface infections
Treatment for surface infections
Maintenance and Prevention of Skin Infections
Diagnostics for pustules? Papules? Crusts? Annular scale (dry lesions)?
Eosinophil- does not mean allergy, just means skin infection
Degenerative neutrophil- toxic effects because of bacterial– just means bacterial infection
Systemic treatment for bacterial infections? Shampoos? What is the minimum course?
Treat for at least 7 days after clinical resolution, minimum of 3 weeks
Superficial bacterial infections take aways
Why do deep infections occur?
Deep infection diagnosis? Length of treatment? Likely microorganisms involved?
Choosing antibiotics for deep infections
Questions to ask for repeat derm infections
Common recurrent derm infections
Dermatophytosis- 3 common species?
Diagnosis of dermatophytosis
Treatment for dermaphytosis
When do you use a skin scraping?
How do you perform a skin scraping?
Deep skin scrapings, looking for?
Tips in deep skin scrape
Stained cytology microscope set up
When do you take an impression smear?
What is unique about cat MCTs?
* Staging more important
* Splenectomy more helpful
* No histological grading scheme but nasty appearance normally poor prognosis
* Surgery curative if possible
* Radiation poor results
* Chemotherapy if metastatic disease
* Tyrosine kinase inhibitors maybe
What are the early lesions in dry scaly or greasy skin? Chronic lesions?
Diagnostics for pustules, papules and crusts
Diagnostics for alopecia
Considations with Nodules
Diagnostics with nodules
What is meant by integrated flea control?
* Blood meal –> lay eggs (50/day)
* Eggs hatch faster when warmer
* Adults are less than 5% of population
* Flea dirt- digested blood and excrement from adult fleas
* Treat all animals in household with adulticide and IGR
* Environment? Flea bombs
* Wash bedding- hot water
* Vacuum, empty out vacuum bags
What are the common bacterial pathogens in pyoderma?
Do you need to use oral antibiotics?
Which antibiotics could you use?
What tests could you do to help make these decisions?
How are topically administered drugs absorbed?
Two ways:
* Drugs absorbed transdermally into the plasma e.g. fentanyl patch
* Long acting– topical administered and act locally e.g. fipronil
What are the benefits of topical drug administration? Challenges?
* Convenience, compliance, safety, maximize local drug concentrations
CHALLENGES:
* Penetration of stratum corneum- intercellular, transcellular, sweat glands/ hair follicles
* Absorption- lipids solubility, penetration enhancers (e.g. propylene glycol)
* skin is an organ, not just a barrier- some metabolism does occur in the skin
* Human safety (petting after application)- young children
* Metabolism phase I and phase II metabolic processes
* Species variation (wool on sheep vs. pigs)
Combined antibiotic and corticosteroid cream in treatment of moderate to severe eczema, friend or foe?
Rapid resolution but increase in fucidin resistant S. aureus
What are the presumed benefits of shampoo treatment? However, what is the other possibility?
* Removal of allergens, decrease antimicrobial load (chlorhex and miconazole), reduce itch (colloidal oatmeals)
* Surfactants are irritants– shampoo with 44 ingredients
Why is cytology so important in making good therapeutic choices with the skin?
Skin has limited ways it can react
What is a good antibiotic for Staph skin infections? If it doesn’t get better, what might be the problem?
Cephalexin
** Could be fungal, could be MRSP
MRSP risk factors
*Dog comes in with infection with a history of visits from multiple vet clinics, most common place to pick up is vet waiting rooms
* Dogs who have been hospitalized
* Dogs with a history of antibiotics AND drugs that affect the immune system (GCs, cyclosporin, etc.) ** immune system does not discriminate between staph and resistant staph
* High density living- contact with other dogs- grooming salons
* dogs who have had lots of ear infection– enough systemic absorption of antibiotics to change and skew staph bacteria towards resistance
Why do dogs get skin infections?
*Anatomical reasons– face folds like bull dogs
*Microclimate changes– left wet
*Decreased exfoliation/follicular obstruction
*Decreased immunity
*Self trauma (scratching)
*Atopic dermatitis
What is always true about Malassezia?
* Almost always surface infection, but bacteria can be surface, superficial or deep
If you see a rod shaped bacteria in a year, what is it likely to be?
Pseudomonas
How do you know if Malassezia is what is causing the problem?
Treat for it and see if it goes away
Surface infections, what kind of treatment?
Surface treatment
Other Causes of folliculitis? Pustules?
* Folliculitis: demodicosis, dermatophytosis
* Pustules: pemphigus foliaceous, contact allergy
Pustules/ papules and crusts general DDX
Infection, immune mediated, allergy
When would you use scapel blade cytology?
Dry papules for bacteria or cell types, acantholytic cells
When do you use FNA
Nodules, tumours, cysts
Equipment for opthamology
* Focal light– intense, bright light source with fibre optics
* Handheld magnification
* equipment to look at the fundus (interior surface of the eye retina, optic disc, macula, fovea, and posterior pole)– direct opthalmoscope or 20 D hand held lens
* Schirmer tear test strips
* topical local anaesthesia
* local anaesthetic for regional nerve blocks
* sterile spatula, MC and S swabs, glass microscope slides
* Tonometer
* Fluorescein stain
* Mydriatic NOT atropine
* Saline for irrigation
Diagnostic samples in an ophthalmic exam
Sherman Tear Test- evaluates tear production– at the beginning of the examination
Microbial Culture and Sensitivity
Dark room exam in ophthalmology
* Aniscoria- direct opthalmoscope set to zero– look at both eyes simultaneous– get the dogs or cats attention– retro illuminate the eyes– highlights the pupil size.
* Outside of eye - looking at eyelids, third eyelid, conjunctiva, and sclera (surface occular structures)
* anterior segment- cornea, AC, iris
* Dilate pupil (tropicamide): lens, vitreous, fundus exam
* Measure intraocular pressure (IOP)– concerned with inner structures of the eye
Light room exam
* Assess vision in light room
* Menace (care with cats as creating air currents can move whiskers)
* Moving object, visual placing
* Dazzle reflex
* Obstacle course exam
* Assess symmetry, size & position of the orbit, globes and eyelids
* Check for any discharge, redness or swelling around the eyes
* Palpate bony orbit, retropel globe
Retroillumination– ulcer, cyst, lens opacities determining if there is cataract or advanced aging change, if they do have cataract how much of the lens is affected– immature or mature where the whole lens is affected
What is used to dilate pupils?
Mydriacyl (Alcon) tropicamide opthalmic solution
This anticholinergic preparation blocks the responses of the sphincter muscle of the iris and the ciliary muscle to cholinergic stimulation, dilating the pupil (mydriasis). The stronger preparation (1%) also paralyzes accommodation. This preparation acts in 15-30 minutes, and the duration of activity is approximately 3-8 hours. Complete recovery from mydriasis in some individuals may require 24 hours. The weaker strength may be useful in producing mydriasis with only slight cycloplegia. Heavily pigmented irides may require more doses than lightly pigmented irides.
What is aqueous flare?
Checking for uveitis– characterising the degree of inflammation
* Frequently occurs with anterior segment disease in horses
* focal light essential to detect aqueous flare
** look for reflected light– opposite side
*left its reflecting off the iris, the right it is reflecting off the lens– we are looking in between looking at the aqeous humour hoping it is nice and black– if it is foggy there is flare such as RBCs or fibrin
What is the Schirmer Tear Test?
Corneal Cytology
* e.g. blunt end of scalpel scrape at the edge of the ulcer
** looking for bacteria, fungus, type of white cells
Tonometry
Does the dog have uveitis or glaucoma?
* pressure reading does not matter, looking at the difference
How do you perform fluorescein staining?
* Touch to bulbar conjunctiva– not too much stain- DO NOT touch the cornea with the Fluorsecein strip as it causes false positives
** fluorescein binds to mucous threads, granulation tissue, rough epithelium and it will sit in shallow facets (healed corneal ulcers with a shallow stromal deficit) – flush excess stain from the eye to avoid false positives
* Fluorescein can also determine patency of nasolacrimal ducts– apply dilute fluorescein liberally to the eye and fluorescein should be present in the nose within 5-10 minutes… this should be performed in all cases of conjunctivitis
Nerve blocks in a horse for the eye
Auriculopalpebral nerve provides motor supply to
orbicularis occuli muscle (branch of CN VII)
•
Frontal nerve provides sensation to the upper eyelid
and dorsal periocular skin (branch of CN V)
•
Blocking both nerves provides total akinesia and
analgesia to upper eyelid
Markers for the Auriculopalpebral N. block
Markers for the horse Frontal N. block
Fundus examination
Direct ophthalmoscopy
Highly magnified upright image of the fundus. Peripheral regions of the fundus are hard to examine.
* Turn the magnification setting to zero (real image allows for a better image of the fundus), brightest setting of light, resting against the examiner’s brow
* once a fundus reflection is viewed by retroillumination, slowly move forwards towards the eye– the fundus comes into focus when the direct ophthalmoscope is about 1-2 cm from the eye
Indirect ophthalmoscopy
* Better “scanning” view of the fundus but technically more difficult to perform
* different regions of the fundus can be simultaneously compared for disease
* 20 D lens is most common
* Inverted view of the fundus
Fundus
What is performed last in an ophthalmix exam
Fluorescein staining– performed last so it does not interfere with other tests like the Sherman Tear Test (STT)
Eye exam with discharge
What should you always perform in any discharging eye exam? When?
With magnification in a discharging eye exam, what are you checking for?
Exam for entropion, distichiasis, trichiasis, ectropic cilia, punctal atresia, under the eyelid for any foreign objects
What are you checking for with cytology in a discharging eye consult?
* any animal with inflamed eyelids or conjunctivitis
* Detecting infection, discerning between acute and chronic disease and will help determine antibiotic selection
What are you checking for with fluorescein in a discharging eye exam?
* Determining whether the NLD is working
NLD= nasolacrimal duct
Fluorescein
Flushing the NLDs
tap water, sterile saline, or artificial tears
Describe what you see:
* Epiphora (watery ocular discharge), overflow onto periocular skin, cornea clear, senile nuclear sclerosis
* Unpigmented eyelids
DDX:
* Block NLD, punctal atresia (absence of puncta)?
* Conjunctivitis- allergic, bacterial, viral, UV radiation (solar?)– common in unpigmented eyelids of dogs– eyelids also get sunburnt/ reddened
* Surface irritation- ectopic cilium, distichiasis, trichiasis
* FB?
** Further testing: STT, Conjunctival cytology, Fluorescein passage to nose, NLD flush or explore under GA
* 2 yo MN Labrador
* 3-4 week history of bilateral, eyelid swelling, mucopurulent discharge, swelling and redness in both eyes
Describe what you see:
* upper and lower eyelid erythema, oedema and alopecia. Mild watery discharge.
DDX:
* Bacterial, funal, viral, parasitic, immune- mediated blephartitis
* Neoplasia- MCT, Lymphosarcoma (LSA), sebaceous adenoma, lipoma
* Inflammatory conditions- nodular fasciitis, histiocytosis
TESTS:
* Skin scraping, sticky tape cytology, incisional biopsy, deep tissue microbial culture and sensitivity
TREATMENT:
* Bactericidal antibiotics which are effective against staph and strep
* Oral steroidal anti-inflammatory medications
* Review in 2 weeks… prolonged treatment may be required
Describe what you see:
* Narrow palpebral fissure, water discharge along lower eyelid margin, trichiasis, entropion
* Hair in contact with the tear duct (trichiasis- long hair gets in there OR eyelid conformation abnormal)
* Can’t see the lower eyelid margin either– eyelid is rolled in
* (Some cases also have concurrent ulceration)
DDX:
* Entropion- primary or secondary?
* Trauma
* Conjunctival FB
* Corneal ulceration
* Feline Herpes Virus infection
* (Distichiasis, ectopic cilium)
TESTS: apply topical anaestheisa- entropion may resolve indicating spastic entropion is present; fluorescein stain- is there concurrent ulceration?
* Diagosis: Entropion– Certain breeds predisposed: Rottweiler, Shar Pei, Great Dane, Weimaraner, Mastiff
- entropion is common in young and older dogs and cats
TREATMENT:
* young cats– secondary to FHV conjunctivitis & corneal ulceration
* older dogs and cats it occurs secondary to orbital fat atrophy and enophthalmos
* Treat primary cause if present e.g. FHV, trauma, FB
* Tackingi n young animals
* Surgical correction of eyelid position
Describe what you see:
* moderate to marked stick, mucopurulent ocular discharge, left eye
* Dull cornea, corneal vascularisation (keratitis)- well advanced
TEST:
STT, cytology (secondary bacterial conjunctivitis), fluorescein stain, MC& S unlikely to be necessary
Diagnosis:
Keratoconjunctivitis (KCS) or dry eye– common in dogs– certain breeds predisposed: Cavaliers, West Highlands, Bulldogs, Pugs, Cocker Spaniels, Schnauzers
- dogs with Degenerative Myelopathy (DM) and older dogs predisposed
- cats with FHV
TREAMTENT:
- clean eyes
- optimmune, cyclosporin or Tacrolimus eye drops/ ointments
- topical preservative free lubricants- applied regularly
- topical antibiotics
- canthoplasty or PDT (photodynamic therapy) surgery in refractory cases
Describe what you see:
* Epiphora, upper eyelid distichiasis
* Dull cornea with faint axial oedema and ulceration
DDX:
* Distichiasis (abnormal growth of lashes), ectopic cilium, trichiasis
* (Trauma)
* (Alkaline burn)
* (Chronic corneal epithelial defect)
TESTS
* Fluorescein staining to confirm ulceration
DIAGNOSIS
* Careful examination revealed distichiasis (bilateral) and secondary corneal ulceration
* Distichiasis common cause of epiphora (overflow of tears) in dogs
* Symptoms of disease more frequent in short- coated (bristly-haired) dog breeds e.g. Staffordshire Bull Terrier, Bull Dogs, Labrador, Boxers
* Less of an issue in Cavaliers and Poodles
TREATMENT:
*Transconjunctival excision in thick-eyelid breeds
* Cryosurgery in thin-eyelid breeds
Transconjunctival exicision
Describe what you see:
* swollen hyperaemic eyelids & periorbital region
* Conjunctival hyperaemia
* Third Eyelid (TE) protrusion
* Mild mucopurulent ocular discharge
* Mild exophthalmos (abnormal protrusion of eyeball)
DDX:
* Orbital trauma, orbital FB, Orbital infection: cellulitis & abscess, Orbital cyst, neoplasia, haemorrhage, severe uveitis, chronic glaucoma
TESTS:
* Physical palpation- open mouth! Check for abscesses- roof of the mouth
* Retropulsion
* Examination of the mouth
* Orbital ultrasound, CT, MRI
* Exploratory surgery
DIAGNOSIS:
* Ultrasound examination confirmed orbital abscess and probable FB
TREATMENT:
* Dental abscesses are a common cause for orbital cellulitis or abscess, so make sure you examine the mouth
* Neoplasia accounts for approx 50% of orbital diseases
* Many neoplasia is often primary and malignant
Special considerations when examining cats in an ophthalmic exam?
Place at the edge of table
* Looking down towards the ground, less likely to have their third eyelids prolapse (thinking they might jump off the table)
* Measure BP in all cats > 8 years of age because they are prone to primary or secondary hypertension which is a blinding condition– try to pick it up before they detatch their retinas
What is meant by Parallax in ophthalmology?
Using a light source to illuminate the deeper structures of the eye and looking at it from another direction
What are the three causes of discharging eyes? What should you always do?
- Increased ocular discharge
- Impaired drainage
- Both increased production and impaired drainage (rare)
** Always STT!! at the start of the exam (recall GA and sedation cause temporary reduction in STT in all species)
What makes up the fibrous tunic?
Cornea and sclera
The vascular tunic is made up of the choroid, the ciliary body and the?
iris
In some species, there is a highly reflective layer in the choroid that assists vision in dim light. Name the structure.
Tapetum (lucidum)
What are the two types of photoreceptors?
Rods and cones
Which photoreceptor is most sensitive in dim light?
Rods
The function of the lens is to focus light on the retina. What other part of the eye focuses light?
The cornea
What proportion of the focusing is achieved by the lens?
About one third
The lens becomes cloudy with age. What is this called?
Senile nuclear sclerosis
What is the semi-solid feature between the lens and the retina?
The vitreous
What part of the tear film do the meibomian glands produce? What are they also known as?
The outer fatty layer (contributes to the lacrimal fluid)
** Aka Tarsal glands
What is the function of the gland of the third eyelid?
It produces part of the tear film
The tear film is made up of three layers
Lipid, aqueous, mucous layer
What cells produce the mucous layer?
The goblet cells of the conjunctiva and the corneal epithelium
What cranial nerve supplies sensory innervation to the cornea?
CN V- trigeminal
Retroillumination vs. focal illumination
Conducted at the same time
Focal is just the surface
Retroillumination is where you use the same light source but use the back wall of the eye to reflect light back towards us
When do you conduct an STT?
Keys with cloudy eyes
Cloudy Cornea DDX
No retroillumination– it is not glowing
What is aqueous flare?
White cell infiltration into the aqueous humour – particulate matter in the air
what is this called? General information? Treatment?
*cats and horses rarely develop cataracts that is vision threatening, however different for dogs
Stages of xx?
Cataracts– insipiant (immature), moderate, mature (whole lens + causing vision loss)… hyper mature– lens shrinks like a raisin
Stages of Cataract Surgery?
Lens removal using an instrument like a pen to aspirate it out and then lens replacement
Cats and horses more variable- becomes noticeable when they are very old (cats 15-16; horses just becomes more yellow 20-25)
** See the pearl in the lens– middle eye have cataracts too– top, look like spoke wheels from a car
What is this? DDX?
semi set jelly and with age it becomes more liquified
Cholesterol like inclusions
How do you check IOP? Problem with increased IOP?
Tonometry
* Pressure build up in the eye causes endothelial disfunction = oedema
What would you do instead of a fundus exam in a cloudy eye?
Indirect ophthalmoscopy
Special considerations in a cloudy eye with fluorescein stain?
Causes of Ulcers and what you should do next
Treatment for ulcer
* iris when it gets inflamed, it is sticky– so can predispose to glaucoma and other things
* antibiotics to avoid vision and eye loss, serious consequences to infection
NSAIDs- pain relief and tx of underlying inflammation
Bandage Contact Lens for protection
Describe: watery discharge, brown, rectangular shaped corneal lesion, mild focal corneal oedema, fluorescein positive, miosis
DDX: Corneal FB, corneal fungal plaque, iris prolapse
Diagnosis: careful examination with magnification revealed corneal FB
TX: do not use forceps, 10 ml syringe with broken-off 25G needle. Removal with hydropulsion, alternative 2 x 25G needles to flick off… topical BS AB eye drop or ointment, oral NSAIDs, atropine? doxy? BCL? or TEF?
Other than BCL, what is another option?
Treatment for uncomplicated ulceration
* painful left eye
* moderate to severe conjunctival hyperaemia and chemosis
* Large, dorsal paraxial corneal epithelial erosion
* Fluorescein positive
DDX:
- Trauma
- Chronic epithelial erosion/indolent ulceration
- Alkaline ‘burn’ of the cornea
- Distichasis, trichiasis, ectopic cilia
- Other …
Diagnosis: •Slit lamp examination revealed upper central eyelid ectopic cilium
Treatment: Transconjunctival excision of hair
Describe
- Mild conjunctival hyperaemia
- Watery discharge
- Corneal ulceration with loose epithelial margins
- Mild focal corneal oedema
DDX
Trauma
Indolent ulceration
Alkaline ‘burn’ of the cornea
Distichasis, trichiasis, ectopic cilia
Other …
Treatment: Sterile Debridement & grid keratotomy, heavy sedation, topical anaesthesia (+GA), BCL/TEF/TT?, oral or injectable NSAIDs, topical AB eye drops, doxy
Test epithelium
* Is it stuck down? = healthy, easy to peel off in a sheet then we know we are dealing with chronic epithelial erosion or indolent ulceration, etc.
Describe: A complicated ulcer– stromal defect
- Blepharospasm
- Epiphora
- Conjunctival hyperaemia, chemosis
- Corneal ulceration, oedema, keratomalcia
- Aqueous flare
DDX:
- Bacterial ulcerative keratitis (commonly Pseudomonas)
- Corneal bullae
- Trauma, Alkaline injury
Tests: Cytology and MC&S
Treatment: topical fluoroquinalone antibiotics (saw rod shaped bacteria)… Ocuflox, topical atropine (sometimes in cats) we want to dilate the pupil so no complications from iris adhesions, oral doxy (vibravet), oral NSAIDs
** No bandage and no TEF because the eye is infected
Describe:
- 6 week old female kitten
- Sudden onset painful, closed & watery left eye
- Depression
- Sneezing & snuffly
- Mucopurulent discharge
- Blepharospasm
- Conjunctival hyperamemia, chemosis
- Corneal ulceration, keratomalacia
DDX:
- FHV, Calicivirus, Chlamydophila
- Bacterial, fungal keratitis
- Trauma, alkaline burn
- Eyelid abnormalities …entropion, trichiasis, distichiasis
TESTS:
- PCR for infections disease
- Corneal cytology?
- STT? Precorneal tear film deficiency?
- NONE??
Diagnosis: •Tentative diagnosis of acute lytic FHV keratoconjunctivitis was made
Treatment:
- Oral antivirals … Famvir
- Oral doycycline … Vibravet
- Oral Lysine
- Oral NSAIDs … Metacam
- Topical Antiviral … Idoxuridine, Cidofovir
- Topical lubricants
Describe:
- Diffuse, severe corneal oedema of endothelial origin (endothelium thin sheet on the cornea responsible for water balance)
- Moderate perilimbal hyperaemia
- Fluorescein negative
- Mild buphthalmos?
DDX
- Glaucoma (high intraocular pressure)
- Lens luxation
- Severe uveitis (low intraocular pressure)
- Corneal endothelial degeneration
- Keratitis
TESTS:
- Schirmer test test … 20 mm, both eyes
- Tonometry … IOP L 65 mmHg; R 12 mmHg– test for glaucoma and uveitis
- Gonioscopy, ocular ultrasound
Diagnosis: Primary glaucoma often associated with breeds/ inherited because the angle was normal (secondary glaucoma with an identifiable cause–e.g. trauma and full of blood or retinal detachment and now has glaucoma…. is treated differently)
Treatment:
- Trusopt, Azopt or Cosopt (Carbonic Anhydrase Inhibitor)reduce aqueous production
- Xalatan, Travatan (Prostaglandin analogues)- reduce outflow of aqueous out of the eye
- Topical corticosteroids anti inflammatory– all have some degree of inflammation (uveitis)– high pressure = inflammation
- Oral pain relief
- Laser glaucoma surgery??
- PROPHYLAXIS FOR FELLOW EYE!! CAI indefinitely once or twice a day to help delay onset of glaucoma
** Guarded prognosis longterm– unrecognized for days or weeks and already blind
Describe:
- Mild pain (third eyelid prolapse)
- Dilated pupil
- Anterior lens luxation
- Mild cloudiness
DDX
- Primary lens luxation
- Glaucoma & lens luxation
- Uveitis and secondary lens luxation
- Other lens abnormalities e.g. lens coloboma, microphakia
TESTS
- CONSENSUAL PLR, menace response
- Tonometry … IOP 24 mmHg
- Fluorescein stain … negative
Anterior Lens Luxation treatment
- Anterior lens lux = emergency
- Early lens removal surgery may help preserve vision
- Due to complications e.g. retinal detachment & glaucoma, complications higher than cataract surgery
- Medical management whilst awaiting surgery:
- Topical corticosteroids e.g. Prednefrin Forte or Maxidex
- Oral corticosteroids or NSAIDs
- Topical Atropine BID
- Topical Cosopt/Azopt/Trusopt
- Do not apply XALATAN
- Trap lens in posterior segment with Xalatan
- Long term prognosis if managed well is similar to surgery of anterior lens lux
- Enucleation or intraocular prosthesis best for chronic lens luxation & blindness
Vision loss in dogs DDX
Congenital
Developmental issue (cataracts, lens luxation, etc.)
Sudden (with a clear eye or cloudy eye) or progressive
Why is evaluation of vision loss challenging in animals?
What tests for assessing vision? Ancilliary vision tests?
Basic neurological exams… light response, dazzle, obstacle course
* Ancilliary vision test- like doing an ECG on the heart, it is a sequence of light flashes used to stimulate the retina and teh electrical response is recorded by a contact electrode on the cornea
* used predominantly to diagnose retinal disease e.g. SARDs and PRA, if normal in a blind animal it indicates central disease is present
Congenital/development causes of vision loss
Coloboma – if large vision loss as well
Tortuous vessels
Do not have in AUS
Sudden vision loss with a clear eye DDX
Syndrome– infectious disease viral and fungal especially cats– cryptococcus, aspergillosis
* German shepherds- aspergillosis
* Vislas or other long nose dogs- granulomas
** or immune mediated– small white fluffy dogs– Granulomatous Meningoencephalitis (GME)
Diagnosis? Treatment and Prognosis for optic neuritis?
Risk with corticosteroids especially for cats because they can end up with disseminated crypto
What is Sudden Acquired Retinal Degeneration Syndrome (SARDS)?
Thought to be immune mediated (may be associated with Immune Mediated Retinitis)
Sudden loss of vision in dogs (more common in females) which affects the retina– NOT CATS
* IN some dogs vision loss is over a period of weeks, some over night
* Any breed can be affected but small breeds may be predisposed
* DIAGNOSIS: Flat Electroretinogram (ERG)– no retinal function (absence of photoreceptor activity) even though they have a normal eye
DDX: causes of central (neurological) blindness and optic neuritis, both of which have a normal ERG
* most common in vet med are exudates or haemorrhage accumulation beneath the retina
DDX: hypertension, bullous retinal detachments (clear fluid under the retina), hypoproteinaemia, hyperviscosity, polycythemia, uveodermatologic syndrome and idiopathic
** Traction detachments: occur with organization and contraction of fibrous membranes (usually after inflammation and haemorrhage) which pull off the retina
* Rhegmatogenous retinal detachments: occur with tearing of the retina, which allows liquefied vitreous to enter the subretinal space, rare in animals
Causes? If bilateral?
Treatment of retinal detachment
Central blindness? Diagnosis?
By the time they lose vision due to neurological disease they often have other issues – e.g. seizures, ataxic, facial nerve paralysis
Ivermectin Toxicity
* generally on farms with dogs that have access to large animal anthelmintic preparations
Acute onset blindness (DDX SARD, optic neuritis, central lesion)
* negative menace response, dazzle response and PLR– blindness may be central without ocular lesions– but often see characteristic retinal oedema and folds with papilloedema
Sudden Vision Loss- Cloudy Eye DDX
What can cataracts be secondary to?
Cataracts
Diabetes- can develop rapidly (weeks)
Bilateral: think systemic disease
* unilateral- young dog– think trauma
…. in old dog– think neoplasia
** older cat– think hypertension (any cat)
Progressive Vision Loss DDX
•
ALWAYS Bilateral and symmetrical
•
Inherited in some breeds
•
Degenerative condition of photoreceptors
–
Rods then later cones
•
Night vision loss first
•
Fundic changes
–
Blood vessel thinning
–
Tapetal hyper-reflectivity
–
ONH becomes grey
•
May see secondary cataracts late in disease
Surface Ocular disease
•
Toy Poodle
•
Left eye
–
Reduced menace response
–
PLR reduced
•
Obstacle course
–
Tentative when right eye covered
•
You perform a fundus exam
Diagnosis: **optic nerve hypoplasia (OR optic nerve atrophy)
** problem if it was a breeding dog but not otherwise
Retinal haemorrhage secondary to hypertension
5 yo French Bulldog
Sudden vision loss
Tests?
Tests: PLR, vision test, fundus exam, CBC/Biochemistry, urinalysis, MRI +/- CSF tap, thoracic radiographs
** Findings: PLR absent, mydriasis, menace absent, bumping into obstacles, optic nerve head looks unusual
Medial lower eyelid entropion, large eyelid opening
STT:4 mm/ min right eye
6mm/min left eye
* Diffuse corneal melanosis- chronic corneal irritation
Diagnosis: Keratoconjunctivitis sicca (dry eye), oversized eyelid openings, medial lower eyelid entropion
Function of lacrimation? Three layers? How does it drain?
* Required to moisten and nourish cornea and flush away foreign objects, a waste product– stimulated by conjunctival, corneal, or nasal irritation
* Three layers: lipid layer ( spreads tear film evenly and reduces evaporation); aqueous layer (lacrimal gland and gland of the TE); inner mucous layer (from goblet cells in conjunctiva and corneal epithelium- binds tears to the cornea)
** Drains via lacrimal puncta and canaliculi to nasolacrimal ducts
Vascular supply to the eye?
* External ophthalmic artery- principal supply to the eye
branches from the Maxillary artery
* Internal ophthalmic artery supplies CNII and spreads over retina from optic disc
Ophthalmological exam
- Examine from distance: symmetry and eye position
- Examine more closely: menace response and globe retropulsion and digital orbital examination
- Focal light examination: pupillary light reflexes (direct and consensual), dazzle response, anterior chamber exam (depth, abnormal contents?), initial lens examination (pupillary dilation required for complete exam)
- Examination under magnification: eyelids, conjunctiva, sclera, corneal surface, anterior chamber, iris (colour and topography)
- Schirmer Tear Test (Normal dog 15 mm/60 sec; Normal cat 10 mm/ 60 sec)
- Collect diagnostic samples
- Perform tonometry and check beneath the third eyelid
- Fluorescein stain: check for corneal ulceration, passage to nares when nasolacrimal duct is patent (usually within 5-10 minutes)
- Mydriacyl (Alcon) application to dilate pupil: examin lens with focal light and magnification; examine the fundus
Normal range of duration for stage one of parturition of a bitch is? Is there evidence of straining in stage one?
6 to 12 hours
No evidence of straining in stage 1
What is the normal interval between pups in stage 2 or parturition in the bitch?
15 minutes to 2 hours
Is a green to black vulval discharge normal in a bitch during parturiton? Ewe?
Bitch- yes ; ewe- no
Average gestational length in a cat? Rabbit?
Cat- 65 days; Rabbit- 30 days
What does it mean for a newborn to be altricious? What is an example of a species that is?
Their skin is without pigment or hair at birth. Rabbit.
Where does the green-black discharge come from in the bitch?
Part of the chorion
What are the stimuli to the straining reflex in an animal during parturition?
* Stretching of the vagina, stretching of the cervix, suckling of the puppies already born.
Acepromazine is a sedative, it is not an analgesic. What is it likely to cause in a bitch?
* Hypotension with an associated reflex tachycardia
What is ventricular tachycardia?
* A rapid and irregular heart rate associated with premature contractions (VPC’s) identified on an ECG trace
Will morphine cross the placenta to enter the unborn puppy?
Yes
What is a possible consequence to puppies of morphine administration during whelping?
Depressed post natal respiratory drive
With a bitch during parturition with generalized skeletal muscle twitching, abscence of straining when vagina is distended with speculum, and failure to deliver a pup after two or more hours– what might you think is one of the problems?
Hypocalcaemic
What hormones deal with mobilizing stored calcium?
* Parathyroid hormone
* Cholecalciferol
What could the vet have done better in the case of two dead pups and dead mom?
* Correction of hypocalcaemia with IV calcium gluconate prior to surgery
*Aggressive fluid therapy piror to surgery for correction of fluid balance and any acid/ base anomalies was indicated
* if pre medication is required (though commonly not required) then a low dose or partial mixed opioid would be more appropriate (butorphanol or bprenorphine). Acepromazine provides excellent sedation but is profoundly hypotensive. Morphine provides excellent analgesia but causes marked cardiovascular depression
* clip prior to anathesia so she doesn’t have to be under as long
* pre-oxygenating the bitch is a good idea since all induction agents, and inhaled gaseous anaesthetics are cardio-respiratory depressive
* Isoflurane inhalation should be kept to a minimum to reduce cardio respiratory depression and resulting hypotension
* prior preparation is important- a warm dry area should already be prepared for the puppies
Normal readings for STT dog? cat? horse?
* Dogs 15-25 mm/ 60 sec (less than 10 diagnostic for dry eye)
* Cats 10 mm (less than 5mm is diagnostic for dry eye)
* Horses 20-30 mm (less than 10 mm is diagnostic for dry eye)
Normal IOP readings in a dog? Cat? Horse?
* Dog 12-25 mmHg
* Cats 12-25 mmHg
* Horses 15-30 mmHg
Punctal atresia
Absence of one or more puncta in eyelids– function to collect lacrimal fluid
Dacryocystitis
* Inflammation of the nasolacrimal sac/duct
Entropion
Turned in upper or lower eyelid
Distichiasis
Hair or cilia growing through meibomian (tarsal) glands
Ectopic cilia
Hair or cilia growthing through conjunctiva
Trichiasis
* Hair from the skin/ face touching the eyes
Corneal ulceration
Defect of the corneal epithelium with or without loss of the stroma (supportive tissue of the epithelium)
Blephartitis? Conjunctivitis?
Blepharitis- inflammation of the eyelids
Conjunctivitis- inflammation of the conjunctiva (the mucous membrane that covers the front of the eye and lines the inside of the eyelids)
Uveitis
Inflammation of the uvea– iris, ciliary body and/or choroid
Keratoconjunctivitis sicca
Inflammation of the cornea and conjunctiva in dry eyes
Corneal oedema
Increased water content in the cornea giving it a blue/white appearance
Keratomalacia (Melting corneal ulceration)
severe form of corneal ulceration associated stromal degeneration and loss
Corneal lipid dystrophy
Unusual bilateral and symmetrical opacity of the cornea, not associated with inflammation
Keratitis
Inflammation of the cornea
Pannus
aka Superficial Stromal Keratitis is an immune mediated disease of dog conjunctiva and cornea, exacerbated by UV radiation
Corneal sequestration
* Degenerative process of the cat cornea where by it becomes amber/black colour
Aqueous flare
Cells and protein observed in the anterior chamber when the eye is inflamed (uveitis)
Cataract
Opacity of the lens or lens capsule
Lens luxation
Disinsertion of the lens so that it luxates into the anterior or posterior chambers
Glaucoma
Increased intraocular pressure resulting in damage to the optic nerve
Vitreous degeneration
Degeneration of the vitreous. Usually associated with liquefaction
Optic nerve hypoplasia vs. optic nerve atrophy
Optic nerve hypoplasia- Congenitally small optic disc usually due to decreased numbers of retinal ganglion cells– fundoscopically the nerve appears small, round and grey– Toy and miniature poodles probably autosomal recessive (and other breeds)
* Optic nerve atrophy- acquired degernation of optic nerve
Collie eye anomaly
Congenital disorder of the retina, occasionally associated with retinal detachment or optic nerve head colobomas occur in some severe affected dogs which can also result in retinal detachment and therefore blindness
(Shetland Sheepdogs, Australian shepherds, Border Collies, and some other breeds)
* main lesion is choroid hypoplasia (pale area lateral to the optic disc with bizarre choroidal vessels)
Retinal dysplasia
Congenital disorder of the retina, occasionally associated with retinal detachment
Progressive Retinal Atrophy
An inherited disorder leading to vision loss
Optic neuritis
* Inflammation of the optic nerve– bilateral or unilateral– if the inflammation extends into the globe, the optic disc will appear swollen, elevated and hyperaemic. The margins of the optic nerve also become indistinct
* Can be caused by Distemper or other viral diseases, fungal disease (especially Cryptococcus in cats), neoplasia, granulomatous meningoencephalitis, or be idiopathic
* Diagnostics: CBC, chemistry panel, urinalysis, chest radiographs, and titers as indicated, MRI or CT scan possibly indicated, CSF taps have the highest diagnostic yield
** Treatment directed at the primary cause– vision can be preserved if treated early
Nyctalopia? Hemeralopia?
Nyctalopia- loss of night vision
Hemeralopia- loss of day vision
Episcleritis/ episclerokeratitis
Inflammation of the fibrous coat of the eye
What is stress? What is a stress response? What happens if the stress response is interupted?
Physiology of stress
HPA axis: neural responses, endocrine responses, immune responses
* Autonomic system- sympathetic stimulation– adrenal medulla releases adrenalin: increase HR and BP, hydrolysis of glycogen to glucose, focussed attention and responses
What are compulsive disorders? What are there causes?
* Stereotypies: repeated motor patterns
* Compulsions: fixation on a goal
* Repetitive, exaggerated, sustained
* Out of context behaviours
* Interferes with normal functioning
Examples of breed dispositions of compulsive disorders
What are displacement behaviours?
Unable to express stress, frustration, conflict (psychological causes of compulsive disorders) results in displacement or redirected behaviours
What is a major psychological stressor for pets? What is true of psychological stressors?
* Lack of control and predictability (e.g. inconsistent owner interactions, lack of training and inconsistent commands)
* Stressors are additive (threshold theory, one stressor may initiate compulsive response but other stressors maintain the behaviour)
LOOK for multiple causes
Pathophysiology of compulsive disorders
Examples of compulsive disorders in dogs
Examples of compulsive disorders in cats
Treatment of compulsive disorders
* Acute management of self harming- bandages, muzzle
* Reducing stress– Request-Response-Reward interactions (instead of punishment); Consistent routine; Daily walks- aerobic exercise, stimulation, social interaction; opportunity to control aspects of the environment e.g. meals from food dispensing toys
** Pharmacotherapy: SSRIs (fluoxetine, sertraline); TCAs (clomipramine, amitriptylline, doxepin), Do not use if NOT anxiety based skin condition, most effective in early stage!! So treat early!! Wean off after two months of complete clinical resolution– 75% for 2 weeks, then 50% for 2 weeks, then 25% for 2 weeks– recommence at lowest effective dose if reappears
DDX to compulsive disorders
* CNS lesions– circling (brain stem and forebrain, vestibular, lumbosacral stenosis, hydrocephalus, neuromas)
* Seizures
* Sensory neuropathies (reduced pain in distal extremities, trigeminal dysfunction (cats)
* Musculo-skeletal (response to pain may mimic or trigger CD)
* Dermatological (anything that causes licking)
* Conditioned behaviour (attention seeking)
* Acute conflict behaviour (occurs in response to a trigger)
Diagnosis of Compulsive disorders- characteristics that allow some certainty in diagnosis
Failure of compulsive disorder treatment due to?
Poor owner compliance, long problem duration, did not attempt treatment
* More common in large breeds
* Male 2X > females
* Differentials: Dermatological, neurological or displacement behaviour
Treatment: behavioural and dermatological
Causes of licking in dogs and cats
Treatment for acral lick dermatitis (lick granuloma)
Removal of stressors, response substitution (no punishment), acute management of self harming, medication
What should you do about flank sucking?
*Dobermans
* Damp ruffled skin to raw open sores
* If no physical damage with normal functioning then may be acceptable coping mechanism
* IN some cases constant sucking when not sleeping or engaged in other activity
Tail Chasing DDX? What should you do about it?
* DDX: conflict, frustration, reinforced, epileptic, episodic behaviour, neuropathological, psychotic/hallucinary, dermatitis
Treatment: other possibilities: Neuropathic pain: Gabapentin, Carbamazepine
Possible pathological reasons for aggression?
* Anal glands, otitis, dental disease
* Skin problems–association with pruritis or malodours skin disorders that received vet treatment and biting family members
Psychogenic Alopecia (Overgrooming)
* History: environmental or social change may be trigger, more common in indoor cats (confinement stress? social stress? social isolation?), excessive grooming, chewing, pulling out hair (away from owner is previously punished)
* Hair loss: focal, partial, bilateral, common in groin, ventrum, medial and caudal thighs, skin normal to erythematous and/or abraded
* Cats: licking can be conflict behaviour, becomes generalized, stress may affect the immune system, large percentage of cases have underlying medical problems: allergy, endocrine, infections: parasitic, fungal, bacterial, trichogram important to determine cause is grooming (but still multiple aetiologies)
** DIAGNOSIS OF EXCLUSION
Hyperaesthesia in cats clinical signs
DDX to Hyperaesthesia in cats
Treatment of Hyperaesthesia in cats
What is canine atopic dermatitis?
A genetically predisposed inflammatory and pruritic allergic skin disease with characteristic clinical features most commonly associated with IgE antibodies to environmental allergens
What is the difference between normal skin and skin with atopic dermatitis?
If we look closely at the EM of a normal dog SC we can see normal lamellar appearance to the intercellular spaces
However if we look at the skin from an AD dog this lamellar structure is gone.
There is significant evidence for both innate and acquired barrier defects in atopic humans and dogs.
- It is thought that in humans (and likely in dogs) that inherited innate barrier function defects are a (if not the) major primary risk factor for atopic dermatitis.
- Decreased ceramides in lesional and nonlesional skin
- Decreased expression of filaggrin in atopic Beagles and humans
- In huamn patients with a genetic predisposition toward AD, upregulation of the stratum corneum chymotryptic enzyme results in premature breakdown of the corneodesmosomes and thinning of the stratum corneum (and higher pH from dec FLG also encourages this).
Why does AD vary so much between dogs and breeds?
* Complex genotype that varies between breeds and gene pools. Breeding programs to eliminate AD are therefore unlikely to succeed but this complexity could explain variations in clinical phenotype and response to treatment.
increased risk for AD
* Urban life
* High human population density
* increased average annual rainfall
* Adoption at the age of 8 to 12 weeks
* Regular bathing of young healthy dogs
DDX atopic dermatitis
Diagnostic Plan- Step 1 in potential Atopic dermatitis
- Is it scabies/ flea/ demodex— give Bravecto/Nexgard to rule out
** Also resolve infection
What if the dog is still itchy when infection free from Bravecto or Nexgard?
Contact avoidance trial– booties, coat, avoid grass in the park, etc.
Classical atopic areas– food elimination trial
What is a skin prick test?
What is an elimination diet?
* Eliminate suspected allergy, symptoms disappear then reappear when you feed it again, then disappear when you take it away, and reappear when you give it one more time (REPEATABLE)
** MINIMUM 6 to 8 weeks, total compliance needed
* Reassess before rechallenge… if 14 days and no flare… sequential rechallenge
What is a restricted antigen diet?
* Avoid antigens found in their original diet… e.g. fed beef prior, change to venison though may have to home cook as many dog foods have undeclared types of protein, etc.
* but not clinically proven therefore– best is Home cooked NOVEL protein and NOVEL carbohydrate
Purified maize to remove all proteins, ;line cleaning , ELISA testing
The aim of this diet is to ensure all hydrolysed peptides are of very low molecular weight (< 1 kDa) in order to ensure they are non-immunogenic. This diet is essentially purified corn starch (protein removed) and hydrolysed chicken, turkey, duck feathers. To minimise risks of diet contamination there is complete cleaning of manufacturing lines before production, single diet production and post production quality control (PCR to check for poultry and beef proteins) and chromatography to ensure anallergenic molecular weight of the hydrolysis.
Independent studies showing usefulness of these diets for elimination diets are still lacking. There are two company sponsored trials involving a total of 34 dogs using a non-validated pruritus score and a validated CADESI 03 lesional score, that showed significant improvement in dog’s global score when this diet was fed to dogs with suspected cutaneous food reactions (many of which had previously failed on hypoallergenic diets). Palatability was reported to be high. These were low evidence studies based on design but warrants further evaluation.
What are hydrolysate diets?
Enzymatically modified to reduce the molecular weight of proteins to reduce the risk of immunogenic reaction. The aim is to overcome the difficulty in identifying a novel protein source.
** but not clinically proven therefore– best is Home cooked NOVEL protein and NOVEL carbohydrate
Purified maize to remove all proteins, ;line cleaning , ELISA testing
The aim of this diet is to ensure all hydrolysed peptides are of very low molecular weight (< 1 kDa) in order to ensure they are non-immunogenic. This diet is essentially purified corn starch (protein removed) and hydrolysed chicken, turkey, duck feathers. To minimise risks of diet contamination there is complete cleaning of manufacturing lines before production, single diet production and post production quality control (PCR to check for poultry and beef proteins) and chromatography to ensure anallergenic molecular weight of the hydrolysis.
Independent studies showing usefulness of these diets for elimination diets are still lacking. There are two company sponsored trials involving a total of 34 dogs using a non-validated pruritus score and a validated CADESI 03 lesional score, that showed significant improvement in dog’s global score when this diet was fed to dogs with suspected cutaneous food reactions (many of which had previously failed on hypoallergenic diets). Palatability was reported to be high. These were low evidence studies based on design but warrants further evaluation.
So what do I feed during a food trial?
- Croc and tapioca
- RC Anallergenic *
- Home cooked
What are some irritants for an AD dog?
* Environmental irritants, shampoos, exogenous environmental proteases– they can all activate kerationcytes to participate in and modulate the immunological response
So what can happen with a poor barrier?
Increased water loss–> dry skin–> itch
Increased allergen dose–> allergy flare–> itch
Irritants–> irratable skin–> itch
Treatment general rules AD
* Life long disease– cannot cure a Westie of being a Westie
* Not an allergy- failure to address all aspects of the disease, the barrier dysfunction, the allergic components and infections will lead to failure
* Continual maintenance required– not stopping and starting treatment
* Treatment needs to consider client’s life style, compliance, etc.– consider quality of life for the animal
- Infection control
- Flea control
- Mild shampoos
- Topical glucocorticoids
- Oral and injectable glucocorticoids
- Oclacitinib (Apoquel)
NO EVIDENCE FOR: Antihistamines, Fatty acids, Cyclosporine
Why is shampoo therapy often beneficial with AD?
Shampoo therapy is often useful in AD because (see above).
Some formulations have sustained-released microcapsules which break open once the coat dries to release contents
Ingredients in shampoos that may help moisturise are fatty acids, lipids, urea, glycerin, colloidal oatmeal and chitosanide
e.g. Epi-soothe Spherulites® (Virbac) oatmeal and chitosanide;
Allergroom S® (Virbac) contain glycerin, lactic acid, urea and chitosanide.
HOWEVER: not all dogs are improved by shampoo therapy. Can increase barrier dysfunction by drying due to their detergent action (stripping lipids), can increase pH which leads to increasing chymotryptic activity leading to premature breakdown of corneodesmosomes that hold the stratum corneum together to create the barrier. And can irritate dysfunctional skin.
Shampoos should not be relied upon as the sole moisturising treatment except in very mild cases.
It should also be remembered that even “non-irritant” shampoos may irritate skin with a dysfunctional epidermal barrier. Not all dogs are improved by shampooing!
What other treatment options aside from shampoo for AD?
* Fuciderm– topical ointments
* Settle inflammation with daily use at first then drop back to twice weekly and add in moisturizer.
* Wet wrap therapy- apply cream over affected area, wet T-shirt, write out and put on damp to improve penetration, repeat BID in severe cases 20 minutes BID. Lower limbs can use glad wrap occlusion and vet wrap
* Oclacitinib (Apoquel)- JAKs inactivate the intracellular proteins called STATs to induce gene transcription– induce JAK/STAT pathways– short term use but side effects of pyoderma, skin nodules, otitis externa, demodicosis
Maintenance of AD
- Identification and avoidance of flare factors (infections, shampoos, botanical contacts, fleas, foods, emotional stress)
- Allergen specific immunotherapy- suppression of DCs that support generation of effector T cells (Th1, Th2, Th17 cells), Ag specific IgE, mast cells, basophils, eosinophils, effector T cell migration into tissue and induction of IgG4. IL-10 from Treg cells has multiple effects on reduction of allergic inflammation.
- Cyclosporine- problm causes broad spectrum suppression of T cell functions (PE every 6 months- urine culture after 12 weeks on therapy and every year)
- Topical glucocortiocoids- problem longterm side effects
- Oral glucocorticoids- minimal effective dose if you have to e.g. topical steroids with low dose twice weekly GCs topical on the day prior to oral dosing
- Topical immunomodulators
- Recombinant interferon
- Antihistamines
- Fatty acids
- Barrier treatments- fixing the skin barrier- Omegaderm supplementation improved epidermal lipid levels in atopic dogs
DDX for white/ grey crusts?
DDX for yellow crust?
DDX for dark crusts?
Clinical features? Diagnosis? Treatment
?
Sebaceous adenitis: Immune destruction of sebaceous glands
* Breed related: Akita, Samoyed, Vizsla, Maltese, Gold Ret, Std Poodle, GSD, Cats, Rabbits
* Diagnosis: Histopathology (end stage or active inflammation)
* Treatment: Ciclosporin if active
End stage
Oil soaks
Cover baby oil/coconut oil 30 mins
Wash off and descale with Palmolive detergent
Phytosphingosine shampoo/mousse/conditioner
Repeat as needed eg monthly soaks to normalise skin and weekly phytosphingosine
Clinical signs? Diagnostics? Treatment?
Pemphigus foliaceous (PF)
* Auto-antibodies, desmosomal proteins, loss of cellular cohesion
* Clinical forms: breed related (Jack Russels, Akita, Alaskan Malamute, Keeshonds; cats: DSH, Siamese derivations), drug induced/ triggered, secondary to chronic skin disease
* Clinical signs: pustular disease: Papules, pustules, crusts, follicular pustules cause alopecia
* Diagnosis: Cytology– acantholytic cells (keratinocytes that have lost their adhesions– cell becomes a sphere– form rafts, a row stuck together– round, blue and bigger than a neutrophil)
* Therapeutic trials: Antimicrobials: Enrofloxacin, Clindamycin
Treatment: Cats sometimes responsive to low dose pred, not so much dogs. Dogs require steroid sparing immunosuppression azathioprine– bone marrow suppression, hepatopathy, pancreatitis (require close monitoring)
Pemphigus foliaceous
How big should you punch biopsy be for PF?
Deep recuts at 500 micron intervals
Pathogenesis?
Discoid lupus erythematosus
Pathogenesis: UV induced, basal cell cytotoxicity, Ab and Cell mediated injury
* Breeds: Scotch Collies, Border Collies, Shetland Sheep Dogs, Maremma, Weimeraner, Kelpie, any
* Clinical signs: depigmentation, loss of architecture, erosion/ ulceration/ crusting, nasal planum (BEWARE mucocutaneous pyoderma and nasal hyperkeratosis)
* Diagnosis: antibacterial trial, histopathology
* Treatment: sun avoidance, pimecrolimus 1% (ELIDEL); oral corticosteroids short duration, doxy and nicotinic acid
Lupoid onychodystrophy
Diagnosis: failure to respond to antibiotics or biopsy (dew claw amputation, referral for digit sparing biopsy of the germinal epithelium)
Treatment: Aggressive early Tx, CyA (Cyclosporin) + Glucocorticoids, Fatty acids
Cutaneous histiocytosis- dendritic cell proliferation
Diagnosis: FNA, histopath (culture, special stain)
* Treatment: Prednisolone, Doxy and B3, CyA (Ciclosporin)
Cutaneous vasculitis
* Pathophysiology: AbAg excess, endothelial injury, ischaemia
* Clinical signs: Purpura, erosions, ulcers, crusts, alopecia, extremities +/- multifocal
* Diagnostic approach: Drug history, systemic disease, histopath, imaging, blood culture, urine culture
* Treatment: Improve perfusion: pentoxifyline, immunomodulation: referral, prednisolone, dapsone, azathioprine
Erythema multiforme
Pathophysiology: Cytotoxic T cell attack on keratinocytes, drug, viral, neoplasia
Clinical signs: variable lesions, serpiginous, arciform, target lesions, multifocal ulceration
* Diagnostic approach: histopathology (ALONG THE EDGES), selection is critical to diagnosis, drug history, thoracic radiograph, PCR (feline herpes)
* Treatment: Cyclosporin
Packed with eosinophils.. bitten on lateral aspect
Keys to appropriate flea control
* Correct medication interval, correct application technique (may have to watch them), correct timing with shampoos/ swimming (avoid within 2 days before or after Frontline, avoid 2 hours after revolution, avoid 12 hours after advantage), correct dose for each pet, all pets in the house treated
** Efficacy drops at the end of the month
* Speed of kill is not instantaneous
* Environmental fleas can persist > 140 days
* Closed environment = easier to control
Speed of control for top flea treatments?
If dogs or cats live in a closed environment, what kind of flea treatment is needed?
If dogs and cats live in open environments, what kind of flea control?
DDX for pruritis in a dog or cat
AD, food allergy, scabies, bacterial pyoderma, Malassezia dermatitis
Likely problems with failing flea control
* Poor compliance, access to flea “nests”, untreated animals, resistance
If you suspect flea “nests”- what should you recommend?
* Determine if inside or outside the home
* Inside–> prolonged emergence
* Outside–> indefinite emergence–> requires ongoing adulticides
** can also use flea shampoos once weekly– & avoid daily swimming
How do you recognize flea bite hypersensitivity?
* Historical clues: spring/ summer exacerbation, inadequate flea control, fleas not always seen,
* Primary lesion: crusted papules
* Treatment/ Diagnosis (response to tx, trial): Nitenpyram or spinosad, nexgard, bravecto, activyl
** can give short term Pred/Apoquel if required… environmental flea treatment
* Long term: other pets in house. Dogs: IGR +/- adulticide; Cats: Selemectin/ Comfortis/ Activyl
Scabies- Sarcoptes scabei var canis (obligate parasite, foxes, cats, humans)
* Burrow through stratum corneum
* Can survive up to 3 weeks off host (longer at lower temps)
* Disease: Hypersensitivity to mite antigens, pruritis is low until seroconversion
Lesions: PRIMARY: papules and hyperkeratosis; Secondary- from pruritis
Distribution: sparsely haired regions
Zoonosis
Diagnosis: superficial skin scrapes: papules, elbows, pinnae
** only find mites 10% of the time
Therapeutic trials: Revolution, Nexgard, or Bravecto
Treatment: Antibiotics if secondary infection, Pred only if not infected, warn clients of possible worsening first week
What are the two kinds? Predisposing factors? Where are they?
Demodex canis (obligate parasite, transmitted at birth, present in all dogs, disease results from genetic/ immunological factors, concurrent disease, immunosuppressive drugs)
Predisposing factors: mean age onset 4.2-5.9 years, terriers juvenile < 18-36 months– breed, body condition, oestrus, fair-good prognosis… adult: hyperA, hypoTh, leishmaniasis, neoplasia, immunosuppressive drugs, 50% idiopathic… localized disease or generalised disease
** Aetiology: identified in follicles and sebaceous glands
* History: chronic disease (especially AD), prior decrease in immune drug use, young onset with no underlying causes)
Diagnosis: deep skin scrape, trichnograms- periocular, paws, exudative/pustular samples, tape preps (also:biopsy, otic swabs, LN aspirate)… look for concurrent bacterial infection (cytology, culture and sensitivty) OR look for underlying disease if adult onset– biochem and haematology, thyroid assessment, ACTH stim, radiographs and ultrasound
** Treatment: “benign neglect” desexing recommended, treat underlying condition.. do not treat with miticidal therapy because you want to see if it becomes generalized or can resolve on its own… spontaneous recovery rare. Concurrent infections common (S. pseudintermedius, Pseudomonas spp)– so Cephalexin, Clindamycin, Enrofloxacin
** If you have to treat: MLs
What are some signs of a sore eye?
* Blepharospasm (closing the eye)
* Weeping eye
* Rubbing the eye
* Sleeping more than usual
* Protects the eye
DDX? Tests? Treatment?
* Conjunctival cytology, skin scraping, FNA, biopsy
* With allergic conjunctivitis usually associated with other conditions- skin, ears, feet
* Tx: anti-inflammatory drugs- topical, systemic
* Antibiotics- Cephalexin 22 mg/kg BID, Clindamycin
Topical steroids
TX: Lysine powder
Initial DDX? Tests? Found inflammatory cells & epithelial cells, diagnosis? Treatment?
* DDX: infection, degeneration, ulceration
Tests: corneal cytology, MC&S, fluorescein stain
Diagnosis: Ulcerative Keratitis with stromal loss (deep corneal ulceration)
**Treatment: - debride and conjunctival graft (referral)
- temporary tarsorrhaphy (stitch the TE up)
- topical antibiotics- drops preferred- Ofloxacin, Chloramphenicol, fortified Cephalexins (750 mg in 15 ml artificial tears)
- topical atropine (if the iris is spasming, because it is painful)
- supportive therapy- pain relief, anti-inflammatory medication
DDX? Tests? Diagnosis? Treatment?
Inflammation, degeneration, ulceration (does not always have fluoroscein uptake, also any area that is degenerate allowing the stain through the intracellular junctions, it will take up the stain… difference ulceration takes up the stain rapidly, degenerative cells takes up the stain slowly/ incompletely… check the other eye in the mean time…. use wood’s lamp)
* Fluoroscein stain, corneal cytology, MC & S
** Diagnosis: ulcerative keratitis- chronic corneal erosion (indolent ulcer, recurrent ulcer, Boxer ulcer)
** Treatment: surgery
- Debride with cotton bud/high speed ophthalmic burr (cut grooves in the cornea in the form of a ring, referral)
- Bandage contact lens
- Third eyelid flap/temporary tarsorrhaphy not usually necessary
- Topical antibiotic +/- topical atropine
- Supportive therapy - pain relief, anti-inflammatory medication
Fungal Keratitis (rare in a dog, more common in horses)
* Fluorescein stain, corneal cytology, MC&S
* Topical antifungal medication- voriconazole (Rolls Royce of antifungals), itraconazole
* anti-inflammatory medication
* Possible surgery
Cytology: eosinophils
Diagnosis: Eosinophilic Keratitis
Treatment: - topical anti-inflamm/ immunomodulating medication
- Dexamethasone (Maxidex) drops
- Cyclosporin (Optimmune) or compounded Tacrolimus
* DDX: FB, ulceration, neoplasia, perforation and iris prolapse
Tests: Fluorescein, MC&S, Corneal cytology, excisional biopsy
* Diagnosis: Feline Keratitis Nigrans– corneal sequestration, secondary to Feline Herpes Virus keratitis, lower eyelid entropion, exposure (especially Persians)
Treatment: - treat primary cause, artificial tears (for comfort), medical therapy unrewarding, surgery- keratectomy with “button” graft, pedicle graft or corneoconjunctival transposition
DDX: inflammation, immune- mediated disease, lipid aqueous, neoplasia
Tests: transillumination, examine using magnification, haematology, serum analysis, aqueocentesis
Diagnosis: anterior uveitis– Cat- neoplasia (lymphoma), FIP virus, Toxoplasmosis, FeLV, Cryptococcus, possibly FHV
– Dogs- neoplasia (lymphoma), uveodermatological syndrome
Lymphoma in cat
•Treat primary cause eg. Toxoplasmosis, Cryptococcosis
•
•Anti-inflammatory/immunomodulating medication - topical, systemic
•
•Secondary glaucoma or phthisis bulbi not uncommon
•
•Surgery - enucleation
DDX? Tests?
IOP= 50 mmHg
Diagnosis?
Inflammation, ulceration, glaucoma- increased intraocular pressure, neoplasia
Tests: PLR, menace, tonometry, ultrasound, gonioscopy on fellow eye
* Diagnosis: primary IOP > 40 mmHg; secondary- lens induced uveitis
* Treatment: treat primary cause e.g. uveitis and anti-inflammatory medication; reduce production of aqueous (CA inhibitors)– diode laser ablation, increased outflow (PG analogues), pain relief, surgery- enucleation
Functions of the hair coat
* Environmental protection
* Maintenance of skin microclimate
* psychosocial functions
Actinic keratosis
Hypotrichosis vs. alopecia
Hypotrichosis- reduction in the number of hairs in a normally haired region
Alopecia- lack of hair in a normally haired region
Scientific name for shedding? Hair growth? Hair rest phase? Short involution phase?
* Exogen
* Anagen (poodles have a longer growth phase which is why they need a haircut)
* Telogen
* Catagen
Follicular cycling is complex and not fully understood. Essentially the cycle can be broken up into anagen (growing phase), catagen (involution phase), telogen (resting phase) and exogen (shedding phases). Very few dogs need a hair-cut. Hairs grow, for a genetically predetermined period to reach the desired hair length and then remain in the resting phase, telogen. This conserves energy, protein and lipid. The telogen hair is NOT easily epilated. It is tightly anchored within the follicular shaft until the exogen phase. Control of cycling is largely by intrinsic factors such as growth factors, genetic factors, adhesion molecules and receptor expression within the follicle itself (epithelial-mesenchymal interactions) but can be modified by extrinsic factors like the environment (light, temperature and nutrition) and endocrine factors.
Anagen
Telogen (resting)
Examples of intrinsic and extrinsic factors of the hair growth cycle
Mechanisms of hair loss and examples
- Hair being lost prematurely (excessive loss)
A. Mechanical- pruritus, psychogenic, abnormal behaviours
B. Folliculitis- bacterial, fungal, parasitic
- Hair failing to be replaced (failure to grow)
A. disruption of follicular cycling without structural change to follicle- HyperA, HypoTh, Alopecia X…etc.
B. Distruption of follicular cycling WITH structural change to follicle- pattern baldness, colour associated follicular dysplasia, non- colour associated follicular dysplasia, follicular lipidosis
C. Folliculopathy- ischamic alopecia, traction alopecia, topical flea spot treatment alopecia, thermal injury
- Absence of follicles
A. Congenital alopecia- anhidrotic ectodermal dysplasia, hairless breeds
B. Cicatricial alopecia
Diagnostics of hair loss
* Age
- 0-4 weeks (congenital alopecias)
- 0-9 months (black haired follicular dysplasia, pattern baldness, follicular lipidosis)
- 6 months to 3 years (colour dilute follicular dysplasia)
- 2 to 4 years (non-colour linked follicular dysplasia)
- 3 to aged (endocrinopathy, alopecia X)
* Breed: e.g. Alopecia X (Pomeranians, Miniature Poodles, Alaskan Malamute); Follicular Lipidosis (Rottweiler)
* Sex/ entire or neutered:
- female (hypo or hyper oestrogenism, ventral pattern baldness)
- male (testicular neoplasia, hypogonadism, pinnal pattern baldness)
* History: systemic with cutaneous manifestations? Or just skin disease?
* Physical exam: e.g. temporal muscle wastage HyperA, neuromuscular disease +/- tragic facial expression (hypoTh)
** Dermatological exam: hair colour, dull hair? faded hair (colour change seen where follicular development is altered)> Changes in hair texture (mechanical hair loss and diseases with structural change to the follicle)? Area affected? Skin atrophy (hyperA or just senile change)? Increased skin thickness (hypoTh)? Comedones (follicular hyperkeratosis, rule out demodicosis and sebaceous adenitis)?
The optical appearance of the hair coat is determined by the uniformity of reflected light from the hair. A healthy coat with an even layer of sebum coating the outer cuticle of the hair shaft reflects light evenly and therefore looks shiny. When hairs stop growing for any reason (cycling disruption, folliculopathy) the “tiles” of the outer cuticle tend to open. This leads to uneven surface and altered light reflection creating an optically dull coat. A dull coat then usually represents prolongation in telogen and ALL the follicular cycling abnormality should be considered.
** Diagnostic tests
History suggestive of HyperA
lpolydipsia, polyuria 80-90%
lpolyphagia 80-90%
lmuscle weakness and lethargy 50-80%
lincreased panting 30%
lrecurrent skin infections
lurolithiasis
lanterior cruciate repair
History suggestive of hypothyroidism
lweight gain
lheat seeking behaviour
lmuscle weakness and lethargy
lrecurrent skin infections
ldecreased fertility (females)
lbehavioural changes
drug induced alopecia- flea spot on treatment
Canine Recurrent Flank Alopecia (CRFA)- indoor dogs that do not receive appropriate light affecting their pineal gland, etc.
Phlebectasia- HyperA
*pheomelanin resistant to oxidation–bronzing = sign something is wrong with the hair coat– it is not growing properly
** could mean the dog has a lot of sun exposure as well, but less likely
Cushingoid– skin problems due to lack of exfoliation
Cosmetic vs. Systemic disease using a trichogram
* looks normal- no pendulous abdomen
* Mechanical trauma- doesn’t have to be from scratching
Folliculitis– trichogram shows Demodex
Follicular dysplasia in a Doberman
Colour dilute follicular dysplasia
Follicular casting
- Vertically orientated scale (follicular casting) is where the scale extends into the follicle and aligned parallel to the longitudinal axis of the hair shaft (demodicosis, follicular cycling defects).
Common causes of canine otitis externa
Normal otitic flora in a dog
- Allergic dermatitis (41/100)
- Foreign body (12/100)
- Ear mites (7/100)
- Uknown (32/100)
Why canine otitis externa?
Microclimate change = inflammation and maceration therefore opportunistic infection
Allergies– atopic dermatitis or food allergy
** Microclimate changes: anything that causes inflammation of the ear canals– parasites, FBs, allergies, irritants, other diseases involving EAC such as PF, juvenile cellulitis…..anything that increases the moisture of the ear canals– swimming, over use of ear cleaners, high environmental humidity, breed factors, stenosis of proximal canal, etc…. anything that interferes with self cleaning– damage to the tympanic membrane, polyps, neoplasia or large FBs, hyperplasia of the canal lining secondary to otitis, congenital or acquired stenosis, etc.
Why treatment fails in canine otitis externa? What does otitis externa actually mean?
- Medication cannot penetrate to the bottom of the ear canal due to exudate, stenosis, polyps etc.
- The wrong dose of medication is applied
- The wrong choice of medication (must be active against target organisms, stable, safe e.g. if tympanic membrane is not intact)
- Poor owner compliance
- Failure to control inflammation
- Maceration. Your treatment also alters the microclimate of the ear. Long duration (longer than 2 to 3 weeks) or combination (aqueous cleaners with commercial ear drops with oily vehicles) leads to MACERATION of the ear canal. A macerated epithelium cannot form an effective epithelial barrier. The vehicles in the ear drops, plasticized gels, propylene glycol, mineral oil etc then become toxic to the epithelium and can promote ongoing inflammation.
* Otitis externa means inflammation of external auditory canal (not necessarily infection)– infectious otitis externa means otitis complicated by bacterial or fungal infection
Basic principles of treatment of canine otitis externa
- Resolve the current infection– remove all exudate, collect samples from all levels of the ear canal, ID the integrity of the tympanic membrane, assess the ear canal for glandular and epidermal hyperplasia, stenosis due to oedema or stenosis due to fibrosis, check for polyps and FBs and tumours… treat microbial overgrowth and address microclimate change by resolving inflammation (topical or systemic GCs), re-examine and repeat cytology is essential… treat for 7 days beyond cytological cure
- Control trigger disease– microclimate change– visualization for FBs (video otoscopy), systemic disease treatment
- Control secondary predisposing factors– sequelae that occure due to chronic inflammation of the EAC that will guaruntee relapse of the otitis externa irrespective of whether the trigger factor has been controlled– e.g. epidermal and or glandular hyperplasia, inflammatory polyps, fibrosis, stenosis, calcification of the EAC, cerumenoliths, otitis media, cholesteotomas and complete occlusion of the EAC
Keratosis obturans- ball of wax– automatic ear cleaning is disrupted for some reason– need to remove surgically
epithelial hyperplasia– reversible… have to get it back to normal in order to avoid recurrent otitis externa… these ears needs oral pred!
- Glandular hyperplasia. This is less amenable to treatment and glandular hyperplasia may persist post treatment and is often associated with rapid cerumen accumulation and recurrent otitis. Cerumenolytics and or drying agents are needed in such cases as long-term maintenance. These dogs are problematic. Currently I use AQUA EAR â for the drying agent and will commonly add dexamethasone 10mg/ 10mls to make a 0.1% concentration if irritancy is a problem. Where a cerumenolytic is required I will use PAWs EAR CLEANER â followed 5 minutes later by EPIOTIC. PAWs has a detergent like action that emulsifies the lipids in cerumen but if not flushed out can cause irritation..
Common reasons for treatment failure in otitis externa? How much ear meds in a cat? Large dog?
- Inadequate dose of aural medications. Making sure they know how much medication to put in and how to do it properly
- Failing to adequately clean the ear
- Failing to control inflammation
- Poor owner compliance
- Wrong choice of medication e.g. gentamicin not effective in the presence of pus, polymixin is a poor choice for Pseudomonas in AUS
- Failure to address trigger factors– e.g. atopic dermatitis
- Failure to re-assess patient, confirm cytological resolution and continue treatment for 7 days past clinical and cytological resolution
- Failure to address secondary changes e.g. epidermal or glandular hyperplasia
- Bacterial or fungal resistance
- Maceration due to diluted shampoos and overzealous use of ear cleaning agents
If the tympanic membrane is not intact, what drugs are safe to use aurally?
Squalene is middle ear safe… would have to rely on e.g. systemic antibiotics if bacterial though generally they are not as effective
How deep of a sample can you get when you are using a swab in a dog that is awake? Why is this a problem
* Different bugs in different parts of the ear canal
Tx?
** problem with gentamicin– won’t work with pus in the ear
Why does culture and sensitivity mean nothing for ear infections?
Heavy growth means nothing– not a quantitative culture
** qualitative
* In vitro
* same sampling limitations
* Sensitivity/ resistance can be misleading– e.g. Pseudomonas spp. 9 different strains, so they may all grow but may all have different sensitivity (different antibiograms)
* there will also be passenger bacteria e.g. Corynebacteria, Enterococcus that you can ignore
When to think about culture with ear infections?
What happens when you treat ears longterm?
When you treat ears for extended period, you get a lot of build up that causes the ear to remain wet and therefore makes it difficult to clean up the infection (toxic environment for the epithelium)…. so you have to get rid of the buildup.
* Squalene is as close as you can get to normal ear wax in terms of lipid concentration
* So ears with chronic treatment– get ears clean and then use Pred and Squalene to get ears clean
Young Cavalier with ear infections
Primary Secretory Otitis Media– must be treated early or permanent hearing loss… neurological signs, head, cervical pain…. end up with facial nerve paralysis but can be reversed if you recognize it early
** won’t allow mucous to drain through the eustachian tube
Take home messages ear disease? When do refer?
uVisualise everything
uA clean ear is half way there
uCytology, cytology, cytology, revisits
uCulture RESISTANT infections
uYou can not fix ears without ear drops
uDemonstrate administration
uDon’t neglect underlying disease/trigger
uDon’t neglect secondary changes
Eosinophilic Granuloma Complex– what is this?
NOT a diagnosis– reaction pattern of the skin
Eosinophil recruitment– simply by cytokines…
Allergies ** often is an allergy– flea allergy, atopic dermatitis, etc.
Viral infection
Fungal infection
Furunculosis
Tissue necrosis
Neoplasia
Miliary dermatitis
* DDX:
lFolliculitis (dermatophytosis, bacterial)
lAllergy (flea, atopy, food, mosquito)
lEctoparasites (Otodectes, Cheyletiella)
lImmune mediate (Pemphigus)
lNutritional (EFAs, biotin def)
** Historical clues
lNutritional (diet)
lFleas, Cheyletiella, Otodectes (current flea control)
lFood allergy (if seasonal)
lAtopy/Fleas (seasonal)
lPersians (dermatophytosis)
lCattery (dermatophytes, Cheyletiella)
** Clinical clues
lHead (atopy, food allergy, Otodectes)
lNeck (fleas, atopy, food allergy)
lPre-auricular (atopy, food)
lLimbs/paws (atopy, food)
lTail base, caudal thighs (fleas)
Persian cats with miliary disease
Always ring worm until proven otherwise
Feline Herpes Virus
Diagnostic recipe for miliary dermatitis
* Wood’s lamp (M. canis glows 80% of the time)
* Fungassay (hairs on the fungal assay, check everyday– colonies starting to grow and red change at the same time)
* Cytology/antimicrobial trial
lBiopsy ( if nasal planum/pads)
lInsect elimination trial
lFood trial
lIntradermal skin testing/Allercept serum testing
Acantholytic cells– PF
Problem
Cut into the crust for biopsy (nasal planum/pads)
Flea trial– what to use?
Food trial?
** If trials are not diagnostic … then what??
** Food trial and flea trial at the same time
lNovel protein (6-8weeks) (add EPO and B1)
lControl concurrent infection
lDo concurrently with flea elimination diet
lIndoor housing
**So you don’t have to keep the cat on steroids long term…. Intradermal skin testing/ Allercept serum testing is another option
Indolent ulcer- 98% of the time they are infected
DDX: SCC, feline sarcoid (papilloma virus)
* Causes: flea allergy, atopy, food allergy, over-grooming, idiopathic
* Diagnosis: cytology/antimicrobial trial, biopsy, insect elimination trial, food trial, intradermal skin testing
** Convenia! Because of anaerobic activity or clindamycin (not Cephalexin as no activity against anaerobes)
Eosinophilic plaque (really itchy!= e-collar)- pockets of degenerative neutrophils, full of bacteria
* Clinical clues: lick accessible areas ONLY (can help differentiate), erythematous/yellow foci, moist surface, extremely pruritic
* DDX: infectious granulomas, neoplasia, xanthoma (in diabetic cats– but are not itchy so you can tell them apart)
* Causes: flea bite hypersensitivity, atopy, food allergy, Idiopathic, reaction to their own saliva??
* Diagnostic recipe: Cytology (surface and FNA), AM trial (oral and topical), biopsy (if poorly responsive), insect elimination trial, food trial, intradermal skin testing/ Allercept serum testing
Oral granuloma/ ulcer (clinical clues: yellow foci)
** in the mouth– rare to have infections therefore won’t respond to AMs
* Causes: flea bite hypersensitivity, atopy, food allergy, idiopathic
* DDX: neoplasia, infectious granulomas
** TX: Ciclosporin
** Can be anaemic without owner noticing because swallowing blood
Specific v. non-specific Eosinophilic Granulomatous Complex Management– e.g. if you can’t get an answer
Why would you avoid Dex in cats if you could?
Diabetes
** Dex dose/ 7 = pred equivalent
** Steroid sparing strategies – minimal effective dose
* Feline herpetic dermatitis
Eosinophilic inflammation
Intra-nuclear inclusion bodies
IHC
Re-activation of latent infection
Mosquito allergy
lNose, pinnae and LATERAL pads
lOutside exposure
lSeasonal
** Tx: avoidance, vitamin B1 in humans
Mastocytosis
Why does grooming help?
Trichogram with broken hairs– know it is mechanical– but don’t know if psychogenic or otherwise
Self trauma in lick areas means eosinophilic dermatitis on DDx
Work up
lFlea trial
lFood trial (less likely if no involvement of the head)
lIntradermal skin testing?, biopsy?, behavioural consult?
How does the direct cutaneous arteries and vein supply in the subdermal plexus- apnniculus muscle help us in surgery?
Arterial supply that spreads out over a large area of the skin– allows us to rotate and transpose large areas of the skin to different parts of the body
helps us with ** tension issues or large dead spaces
How do we make incisions and close wounds?
What does perpendicular closure in relation to tension lines result in? What does diagonal closure result in?
Stage I of wound healing? How long?
What is the second phase of wound healing? How long?
What is the third phase of skin healing? How long?
How does wound healing impact treatment/ surgery in practice?
Recognize there are different stages and adapt treatment accordingly
What are Halsted’s Principles?
When would you place a surgical drain?
* area of high movement e.g. axilla
* bite wound- drain before definitive closure
* drains AROUND the drain– not through the lumen– so if you are expecting a lot of exudate produced, then use a larger drain= larger surface area
** ascending infection can be a problem…
** need for sterile gauze bandage for infection but also so exudate doesn’t get everywhere
** fenestration internal
How would you make your own active drain?
Routine surgery closure
* Subcutaneous, intradermal, and skin sutures
Closure of a laceration
* Deep superficial, superficial deep
Then simple interupted
** in limbs assess ligament and tendon damage
How do you handle a seroma? Where is it more likely to occur?
** if you drain it will likely just reform, but also potential for bacterial infection because of the protein enriched serum as an excellent medium to grow bacteria
Closure of an abscess?
Skin closure
- Abscess
•
Causes:
–
Penetration (e.g.
FB like grass
awns or
plant
material or
bite wound)
–
Infection
(e.g. anal gland
abscess)
•
Clip liberally and sterile surgery
•
Sample (centesis
or swab) for C&S
•
Lance and drain abscess
•
Lavage with 0.9% NaCl
•
Passive or active drain
•
Start empirical antimicrobial
How do cat and dog bite wounds differ?
Cat bites- cellulitis
* All will be contaminated, mixed bacterial population, aerobic, anaerobic
Bite wounds management
* Assess the whole patient and stabilize, external may be tip of the iceberg
* IV fluids, oxygen, imaging
* minimize further contamination– sterile gauze sponges, sterile gel, liberally clip hair around puncture wound, cleanse skin around the wound with warm saline and surgical preparation solution
** Explore wound– be prepared for bigger surgery (thoracotomy or laparotomy)
* IV antibiotics (cephalosporins)
** Explore, debride, lavage (0.9% NaCl), collect samples C&S– close dead space, primary closure of skin if possible but nothing wrong with leaving wound open if contamination present (follow with delayed primary or secondary closure) and use drains…
Open wound management
** through the phases of healing and repair– granulation tissue (resistant to infection due to excellent blood supply)
** Lavage– pulsatile lavage, gravity flow, or manual (8 psi) delivery via 35-60 ml syringe with 18-29 gauge needle
* Debridement– surgical, mechanical… daily or twice daily dressing changes
Dealing with tension
* Undermining
* Walking sutures
* tension releasing incisions
* tension suture patterns
* plasty techniques
Undermining
* does predispose to more dead space formation– so only use in a small area (2 cm laterally)
Tension releasing incisions
on the leg for example as limited amount of tissue
Tension sutures
* horizontal mattress can compromise blood supply if you’re cranking up on it tight– so vertical preferred
* stents- IV tubing cut into small lengths, spreads tension out
Plasty procedures
** flank
Examples of local flaps used in closure
Indications for ear surgery
Parts that make up the external ear, middle ear, inner ear?
Vascular supply of the ear? Motor and sensory?
Difference in anatomy of middle ear in cats vs. dogs
What clinical signs with otitis externa/media? Why document pre surgically?
Pre surgical assessment, what tests?
What is it? Tx?
* remove blood clot, reduce the dead space, prevention of further trauma (immobilizing the ear and treating the primary disease)
* Linear or S-shaped or punch biopsy on inner surface of the ear to drain the haematoma (stent tubing for drainage)… close the dead space– full thickness sutures through the pinna. PARALLEL incisions to the LONG axis ofthe pinna00 to prevent damage to the vascular supply of the pinna
** SUTURES PLACED WITH A STRAIGHT NEEDLE
Laceration of the ear treatment
Common SA neoplasia of the ear
SCC (chronic non-healing wounds)
* White cats have 13.4 x greater risk than coloured
* pinnectomy +/- vertical canal resection
Lateral wall resection indications
Indications:
–
Facilitate management of otitis externa that is
controlled with medication
–
Removal of benign neoplasia of external canal
–
NOT
indicated if stenosis of canal is
present or
Cocker Spaniels
–
Success rate 35- 50%
Total ear canal ablation and LBO? Potential Complications?
Indicated for end stage otitis externa/ media
* Hyperplastic, stenotic vert and horizontal canals
* removal of entire ear canal and lateral bulla osteotomy to drain bulla
Indications for an anal sacculectomy
(4 o’clock and 8 o’clock)
Open vs. Closed Anal Sacculectomy
* open- open up anal sac– non-neoplastic– advantage– you can see you have removed everything (internal is grey and glistening surface, easy to ID)….disadvantage- have to cut across the external anal sphincter therefore more trauma and more potential for infections
* closed approach- parianal approach- dissect down until the stalk… indicated for neoplasia. Do not need to transect. Can leave tissue behind
* results: FNA- hepatoid cells
* Thoracic radiographs- WNL
* Rectal palpation- no palpable sublumbar node enlargement
* Palpation of mass- freely moveable
Perianal Adenoma (most common perianal tumor in intact male dogs: hepatoid gland tumors, cicumanal gland tumors… androgen dependent– often have a concurrent testicular tumor as well (interstitial cell tumor)
** slow growing, non-painful, freely moveable, may occur on tail head, prepuce or scrotum, +/- ulcerated, diffuse form
TX: Resection and castration, castration alone if diffuse form, castration + cryosurgery for small lesions ** Always submit for histopathology!
** Good prognosis > 90% cured with castration and mass removal… recurrences may be adenocarcinoma
hint: castrated!
Perineal Adenocarcinoma
Next step: biopsy!
* Adenoma are androgen dependent… castrated male dog– think adenocarcinoma
**work up: caudal radiographs or ultrasound, rectal exam, chest radiographs for metastasis, +/0 adanced imaging to assess degree of invasiveness
** Treatment: aggressive surgical removal with margins if possible– radiation if margins are incomplete… does not respond to castration
Anal Sac Adenocarcinoma
* Large, invasive subcutaneous mass
* Hypercalcaemia- paraneoplastic syndrome (Lymphoma is most common, Anal Sac Adenocarcinoma is the next most common)
* Female
* Tx: surgery on primary mass +/- lymph nodes depending on if they are involved
** Correct hypercalcaemia prior to anaesthesia or surgery
Basics of canine breeding… puberty?
Dogs are non-seasonal breeders and ovulate spontaneously.
The onset of puberty in the bitch corresponds with the first oestrus and will occur anytime between 3.5 and 24 months (average: 10-12 months). In general, small breeds experience their first oestrus earlier and large breeds later. For some breeds it can be physiologic to not show heat up to the age of 24 or even 30 months of age, e.g. Afghan hound, Greyhound, Whippet, Saluki.
What is progesterone in ng/ml at the LH surge? Ovulation?
Plasma progesterone levels begin to increase slowly in late prooestrus but suddenly double (between 1.5 – 2.5 ng/ml) at the time of the LH surge, making measuring progesterone plasma levels a valuable tool to indirectly determine the LH surge.
Ovulation occurs approximately 2 days after the LH peak and is not dependent upon breeding. Canine oocytes are ovulated as primary oocytes and need to go through a phase of maturation before they can be fertilized. It takes 48 to 72 hours for them to undergo meiotic division to become secondary oocytes.
** 5 ng/ml at OVULATION
What is d0? d1-7? D1?
Difference in the progesterone curve in a pregnant v. non-pregnant bitch? What is true of dogs and progesterone?
Less sensitive to progesterone… no intrinsic mechanism of luteolysis
What does the pre-breeding exam consist of?
When does ovulation occur in a bitch? When are oocytes mature? Where do you inseminate with fresh semen and how? Where do you inseminate with frozen semen and how?
* fresh semen- vagina- natural or AI with catheter
* Frozen- uterus- AI with transcervical insemination (TCI) or surgically (because of limited lifespan)
How can you tell when you should breed?
* At the first sign of prooestrus (vulvar swelling/ bleeding), take the first vaginal smear for cytology and a serum sample for progesterone determination.
Keep doing this every other day until the serum progesterone indicates it is the time of the LH surge (doubling of serum progesterone level, most commonly ~ 1.5 – 2.5 ng/ml). Stop cytology at the first day of dioestrus (D1).
** Breeding reflexes– flagging, lordosis, standing for the male, reduced vaginal discharge (light coloured serosanguineous in the beginning, darker in the end)
** exfoliative cytology– keratinized and cornified cells in prooestrus and oestrous… becoming less in Dioestrous where leukoctyes can then come through and you will also get the intermediate cells and parabasal cells since the keratinized and cornified layer has now sloughed
* Vaginoscopy– vaginal folds swollen, moist, hyperaemic, gradually starting to shrink– folds becoming increasingly shrunken/angular (crenulated), pale in color, dry
Breeding reflexes in a bitch
How vaginoscopy can show pro-oestrous, oestrous, and dioestrous? How else does it help with determining breeding dates?
What can vaginal cytology help you determine?
List the cells you will see in vaginal cytology including all of the phases
Because the neutrophils can’t get through the keratinized/ cornified layer
When do you start sampling exfoliative cytology? What days? What else should you assess?
Serum progesterone at LH surge? Ovulation? Fertile period?
Pros and cons of vaginal semen deposition in natural mating? AI?
Pros and cons of TCI intrauterine semen deposition? Norwegian catheter? Surgical?
Time of breeding– natural or frozen?
What is a roll prep? What would you use it for?
* ear infection cytology
