Equine ophthalmology, renal, neuro Flashcards
Which lenses show which parts of the eye in a horse with close direct ophthalmology?
0 to -3D: fundus
+2D to +6D: vitreous
+7D to +8D: lens
+10D: cornea
What is a slit lamp used for?
To assess depth of lesions
What to assess on ophthalmic exam?
Symmetry, angle of eyelashes (normally horizontal/slightly down)
Ocular reflexes:
- PLR (direct and indirect)
- dazzle reflex
- menace response
- palpebral reflex
- corneal reflex
Check for cleft above upper eyelid (if not there may be swollen)
Third eyelid
Check tear duct opening is patent in nostril
Check eye from outside in
What nerve blocks can be used to help examine horse’s eye?
Auriculopalpebral nerve block (actually just palpebral)
- bundle near zygomatic arch above eye, inject S/C near nerve
- motor only
- won’t take away pain if suturing etc
Frontal nerve block
- feel over frontal orbit area
- S/C injection near supraorbital foramen
- sensory and motor?
How do ulcers appear with fluorescein?
Superficial ulceration - sharp edges, no epithelial under-run, no stain migration
Indolent ulcer - epithelial under-run
Deep stroll ulceration - very intense staining with stain migration (5-15 mins)
Descematocele - walls of ulcer stain intensely with stain migration (5-15 mins), central ulcer transparent and takes up no stain
What is the Seidal test?
Block eye so stays open
Fluorescein over whole eye
See aqueous draining through where a foreign body has penetrated
What is Rose Bengal used for?
Assesses tear film quality (stained areas haven’t got good tear film cover)
Assesses margins of conjunctival and corneal neoplasia (SCC)
Fungal ulcers
How to do cytology/C+S for the eye?
Sedate and block eye
Don’t put LA on eye if want to do culture
Cotton bud, brushes
What midriatic is used to dilate the pupil to examine the fundus?
Tropicamide
Not atropine as can leave dilated for 4 weeks
When is a CT useful for eyes?
Cases of exophthalmos
When is electroretinogram (ERG) useful?
To check retina working before cataracts surgery etc
Eyelid lacerations - When is management easier/prognosis better? How to manage?
Lower (easier to manage) and lateral better (medial tear duct can be affected)
Never cut tissue from eyelid - minimal debridement as most tissue likely to survive
Iodine povidone
Suture carefully to appose eyelid margins accurately
Use very thin suture material
Common eyelid masses?
Sarcoids
Melanomas - surgery easier as don’t need as wide margins
Lymphoma (third eyelid)
Hamangiosarcoma
Layers of the cornea?
Epithelium
Stroma
Descemet membrane
Endothelium
Ulcerative keratitis (corneal ulcers) - How common in horses? Clinical signs? Diagnosis? Depths? Treatment?
Very common
Pain, blepharospasm, epiphora, photophobia
Fluorescein (and rose bengal)
Superficial ulcer
- epithelium only
- painful (most nerve endings are in epithelium)
- well defined margins with fluorescein
- tend to heal with no complications if treated appropriately
- topical antimicrobial (e.g. chloramphenicol) +/- topical atropine (pre-emptive for uveitis but not generally necessary)
- healing rate approx 0.6mm/day
- no corneal scar
Deeper ulcer:
- epithelium and stroma
- same treatment as superficial but for longer period of time
- gentamicin
- EDTA and plasma?
- more likely to have uveitis so atropine may be more warranted
- scarring likely (collagen heals in different directions): if small = like chip in windscreen
- can get keratomalacia
What is keratomalacia? Why happens? Appearance? Treatment?
Complication of deep ulcers
= Melting ulcers (collagen being broken down)
Due to activation/production of proteolytic enzymes by corneal epithelial cells, leucocytes or microbial organisms (pseudomonas)
Can happen within hours
Gel like appearance and consistency on eye
Needs early aggressive therapy:
- topical serum
- topical EDTA (better in ambulatory setting, put saline in blood tube)
- topical tetracycline or doxycycline
- systemic NSAIDs (flunixin)
What is a descemetocele? Appearance? Presentation? Treatment?
Ulcer reached Descemet membrane (thickness of 4 cells)
Looks like a crater, black in centre
Fluorescein negative
Not necessarily very painful
Aggressive therapy necessary (same as for deep melting ulcers):
- topical serum q2h
- topical EDTA (better in ambulatory setting, put saline in blood tube) 2h
- topical tetracycline or doxycycline or gentamicin q 6h
- atropine? q4h
- systemic NSAIDs (flunixin)
Surgery therapy may be necessary:
- conjunctival flap
What can follow on from a descemetocele?
Full thickness corneal laceration -> iris prolapse
Risk of infection getting into eye - need antibiotics
Risk of uveitis and recurrent ocular pain
So should fix:
- push back in, stitch cornea, reinflate
Stromal abscess - Appearance/clinical signs? Treatment?
Circular white-yellow lesion in cornea
Constricted pupil
Invading blood vessels
Fluorescein negative
Medical therapy - antibiotics (needs to penetrate through cornea so must be lipophilic e.g. chloramphenicol, NOT gentamicin)
Surgery if not improving/very painful- debridement or corneal grafting techniques
What causes viral keratitis? Appearance? Diagnosis?
EHV-2 (common in horses eyes without causing signs)
Multiple superficial, white, punctate or linear (dendritic) opacities
Fluorescein, rose bengal
Varying (normally high) degree of ocular pain
Difficult to diagnose - virus isolation and/or PCR
Treatment:
- topical Idoxuridine
- topical Trifluorothymidine
- topical Aciclovir (best)/Ganciclovir
- topical Interferon Y
Fungal keratitis - Risk factors? Presentation? Diagnosis? Treatment?
Rare in UK
USA risk factors:
- hot and humid
- previous administration of antibacterial and/or corticosteroids
May be fluorescein -ve initially (rose bengal +ve)
Poor vascularisation of lesions
Cytology essential +/- culture
Slow to resolve
Surgery usually necessary - keratectomy +/- conjunctival flap
Signs usually deteriorate 24h after starting anti fungal therapy due to massive fungus death with a dramatic PMN response and secondary uveitis
Topical:
- miconazole
- natamycin
- fluconazole
- itraconazole
- amphoteericin B
- voriconazole (best, use as many times per day as poss)
Still guarded prognosis
Immune mediated keratopathies - Presentation? Clinical signs? Treatment?
Insidious onset Usually unilateral Slight ocular discomfort (no uveitis) Vary from irregular corneal surface to deep bullae formation, vascularisation and oedema (yellow/green haze is pathognomonic for deep stromal) Medical: - topical corticosteroids - cyclosporin A - doxycycline Surgery: - keratectomy - cyclosporin A implant Characterised by WBCs, vascularisation and oedema
What is Equine recurrent uveitis (ERU)?
Uncommon in UK
Most referred cases are just an acute uveitis not treated sufficiently -> chronic uveitis
ERU - at least 2 separate episodes of uveitis (normal in between)
Active
Quiescent
Insidious - Appaloosas and Warmbloods
Causes of uveitis? Treatment for uveitis?
Primary or secondary to other eye disease (e.g. ulcer) or systemic disease (e.g. Rhodococcus)
Strong immune mediated component
Leptospira involved in many cases in Europe and USA (less in UK)
Recurrence episodes likely
Treatment:
- topical corticosteroids (if no ulcer present)
- topical NSAIDs? (if ulcer present, or better to treat ulcer first then use steroids)
- topical antimicrobials only needed if ulcer
- topical atropine (if responds quickly = mild, if needs lots to respond = severe case, danger of colic due to effect on gut motility, check other eye before each dose as if dilated then have systemic absorption)
- systemic NSAIDs (flunixin>bute)
Surgery:
- suprachoroidal cyclosporin A implant (works for mild cases)
- pars plana vitrectomy
- enucleation?
Clinical signs of anterior uveitis?
Pain - blephorospasm and epiphora
Chemosis - red eye
Constricted pupil
Aqueous flare - milky appearance of anterior chamber
Blood (hyphaema), pus (hypopyon) or fibrin in anterior chamber
Clinical signs of posterior uveitis?
Subtle Pain variable (often mild) Vitritis Retinal changes Typically diagnosed late in the course of the disease
Long term complications of uveitis?
Atrophy granula iridica Synechiae Cataracts Glaucoma Retinal pathology Blindness Phthisis bulbi
Types of cataracts in horses? Significance? Treatment?
Acquired or secondary cataracts (uveitis, trauma, tumour)
Developmental opacities, including congenital cataracts
Most are not progressive
Little effect on vision unless complete
Most do not require treatment
Treat primary cause if secondary
Surgery can be performed in foals (before 4mo)
Surgery in adults
- not if uveitis
- phacoemulsification
Lens anatomy?
Epithelium grows from centre to side of lens and becomes fibres - squeezes nucleus
Suture line at front looks like a Y (same at back but tilted)
Diagnosis of cataracts?
Retroillumination using light reflected from the tapetum - opacities appear dark
Transillumination (direct focal illumination) using direct beam light at 45 degrees angle into the lens - cataracts appear white
Types of cataract location/extent?
Photos
What is glaucoma? How common in horses? Significance? Signs? Diagnosis?
Increased IOP (normal 15-30mm/Hg) Relatively uncommon in horses - conventional (60%) and unconventional (40%) aqueous humour drainage Pain not as common sign as in other species Horses relatively more tolerant of higher pressures Signs: - hydropthalmos or buphthalmos - corneal oedema - corneal striae - lens luxation - blindness Diagnosis: - signs - tonometry - US
Treatment for glaucoma in horses?
Medical:
- carbonic anhydrase inhibitors: topical (dorzolamide) and/or systemic (acetazolamide)
- B blockers: topical timolol
- NSAIDs and/or corticosteroids (topical and/or systemic)
- prostaglandin derivatives contraindicated in horses!
Surgery:
- laser destruction of ciliary body
- aqueous shunts
- enucleation
Chemical ciliary body destruction - intravitreal gentamicin injection
Fundus anatomy?
Photo Tapetal region - stars of Winslow Non tapetal region Retinal vessels Optic nerve - oval (roundish in foals), salmon pink, 3-5mm vertically and 5-8mm horizontally
What is the blood supply to the horse fundus?
Equine retina paurangiotic: 30-60 vessels radiate from optic nerve:
- 1-2 disc diameters
- less prominent dorsally and ventrally
- may be absent at 6 o’clock
Rest of retina avascular:
- stars of Winslow (from choroid vessels)
Layers of the retina? Colours? Why relevant?
Upper neurosensory retina = cling film (less shiny) Lower retinal pigment epithelium = black Tapetum behind retina in tapetal fundus = blue, green, amber Choroid = red Sclera = white Colours relevant as allows assessment of depth of lesions Pigment accumulation (clumping) indicates pathology
Most common pathology of the fundus in horses?
Bullet hole lesions
Butterfly wings of optic nerve - may be secondary to uveitis, herpes, may not be significant
Senile retinopathy - old horses, looks like cracks of non tapetal fundus, typically not a problem
How does forebrain disease present in horses?
Disorders of behaviour and personality - aggression, compulsive walking, loss of learnt behaviour, yawning
Seizures
Blindness
Altered states of consciousness: alert -> quiet -> depressed -> obtunded -> comatose
Head posture - head and neck turn, head pressing
Causes of forebrain disease in adult horses?
Trauma - most common
Abscess
Cholesterol granuloma (common to have but uncommon to have signs) - obstruct CSF flow -> hydrocephalus
Verminous
Infectious meningoencephalomyelitis - rare
Neoplasia - rare
Toxins - uncommon
Intracarotid injection
Sleep disorders - narcolepsy, sleep deprivation
Metabolic (common) - hepatic encephalopathy, intestinal hyperammoniaemia, electrolyte imbalances
(Trauma and metabolic most common)
What is cataplexy?
Sudden loss of muscle tone
Difference between narcolepsy and sleep deprivation?
Sleep deprivation - horses always need to eventually lie down for full cycle of sleep, happens if can’t lie down
Narcolepsy - sudden onset of sleep (diagnose by response to treatment), less common
Typical signs of hepatic encephalopathy?
Head pressing Yawning Saliva drooling Reduced consciousness state Blindness (central)
What causes neonatal seizures and epilepsy?
Low sezure threshold
Most common: perinatal asphyxia syndrome (NMS/HIE), sepsis, trauma
Also metabolic (hypoNa, hypoglycaemia), drug associated, idiopathic
Juvenile idiopathic Arab epilepsy - benign, up to 12mo
What do seizures look like?
Typically start at nose/mouth
May progress to leg thrashing
Signs of brainstem and cranial nerve disease
Vestibular disease - head tilt to affected side, nystagmus, loss of physiological nystagmus, ventral strabismus (check by raising head), ataxia
Facial nerve paralysis (VII and VIII frequently affected together)
Pharyngeal/laryngeal deficits - dysphagia
Other CN deficits
Severe brainstem lesions - gait abnormalities, coma (RAS)
What does vestibular ataxia look like?
Hypermetria (not flexing very much), wobbly, wide based stance, affected side weaker so go towards that side and forms circles
Can be compensated by vision - e.g. if treated and walking ok test with blindfold and only sign off if still walking ok
Worse up ramps
Causes of vestibular disease?
Trauma - central or peripheral
Idiopathic
Otitis media/interna (temporohyoid osteoarthropathy)
Causes and signs of facial nerve injuries? What prolonged/permanent deficits can be caused?
Commonly iatrogenic due to halters left on during field anaesthesia Trauma (+/- vestibular) THO (+/- vestibular) Signs: - dropped ear - ptosis - nostril deviation Possible deficits: - exposure keratitis - dysphagia (feed pouching) - poor performance: nostril collapse
What is Horner’s syndrome? Cause? Signs?
= interruption of sympathetic innervation to head (and neck)
Most commonly iatrogenic due to extravascular injection of irritant substance (PBZ, Buscopan)
Signs:
- mitosis, enophthalmos, ptosis, protruding third membrane
- hyperaemic membranes, sweating
What is Cauda Equina Syndrome? Signs?
Sacrococcygeal spinal cord segments, cauda equina, sacral plexus and peripheral nerves to bladder, rectum, anus, tail and perineum
May or may not involve lumbosacral nerve roots to lumbosacral plexus -> gait abnormalities
Signs:
- degrees of hypotonia, hyporeflexia and hypoalgesia of the tail, anus and perineal region
- urinary bladder paralysis
- rectal dilation
- penile prolapse
- may also see LMN weakness and paresis of pelvic limbs
Can be difficult to distinguish UMN disease with urinary retention and secondary contusion of tail and anus from recumbency
What causes Cauda Equine Syndrome?
Trauma - sacrococcygeal fracture and luxation, avulsion of cauda equina
Inflammatory - polyneuritis equi +/- CN signs
Viral/immune - EHV1 +/- ataxia, CN signs
Verminous - EPM
EHV1 myeloencephalopathy - Presentation in a herd? Pathophysiology? Signs? Diagnosis?
Uncommon Sporadic or outbreak Clinical signs occur due to vasculitis and thrombosis of arterioles in spinal cord -> viral endotheliotrophism Sudden onset and early stabilisation of signs: - ataxia - paresis - urinary incontinence Diagnosis: - lesion location - rule out other causes - history of respiratory and/or abortion - CSF sample: xanthochromic +/- EHV1 Abs - detection of virus from nasopharyngeal swabs or buffy coat - high Ab titres
Management of EHV1 myeloencephalopathy? Prognosis?
Isolate
Prognosis reasonable with good nursing care
- better if not recumbent
- recovery days-weeks
- poor prognosis if recumbent >24h
Vasculitis - NSAIDs, corticosteroids, aspirin
Antivirals - acyclovir, valacyclovir
What spinal cord diseases are seen in the UK?
Spinal cord trauma
Cervical vertebral malformation (CVM)/cervical vertebral stenotic myelopathy (CVSM)/Wobbler syndrome
Signs of spinal cord trauma? Sites of predilection?
History of sudden onset ataxia or recumbency - sometimes an observed incident
No progression, frequently improvement, but later progression due to callus formation may occur
Trauma may play a role in acute exacerbation of CVM
Sites of predilection:
- occipitoatlantoaxial region
- caudal cervical
- mid back: usually unstable fracture, paraplegia and recumbency (dog sitting)
Signs vary from ataxia and paresis to recumbency
Assessment for posible spinal cord trauma?
Complete physical exam Ensure no unstable fracture Neuro exam and lesion location Sedate fractious horses - xylazine Plain radiographs may reveal fracture in acute cases CSF analysis may rule out other causes
Treatment for spinal cord trauma?
Early aggressive anti-inflammatories - NSAIDs (flunixin), DMSO good if acute Box rest if standing Nursing care if recumbent Surgical therapy? Neck brace? Elevate food and water, not in hay nets
Prognosis of spinal cord trauma?
Always guarded but can be remarkable recoveries
Poor prognosis with luxations, unstable fractures, poor initial response to treatment in first 24-48h, continued recumbency
Intended use and value may be important
Delayed callus formation may lead to compression
What is cervical vertebral malformation? Aetiology?
Narrowing of the cervical vertebral canal causing compression of the spinal cord, often in combination with malalignment and malformation of the cervical vertebrae
Most common cause of ataxia is UK
Multifactorial aetiology - congenital, familial (TBs, Was), dietary (high CHO), management (including exercise)
Related to DOD
What are the 2 types of CVM?
Type 1: - young horses - compression as a result of developmental abnormalities - dynamic stenosis - any site Type 2: - older horses - OA of articular processes - static stenosis - C5-C6 and C6-C7 most common
How does CVM present? Diagnosis?
Ataxia of all 4 limbs
Hindlimbs more severely affected (by a maximum of 2 degrees of ataxia)
Neck pain rarely seen
Radiography:
- stenosis of vertebral canal: dynamic or static
- abnormal articular processes
- subluxation of vertebrae on flexion or extension of neck
- enlarged vertebral physical growth regions
- overriding of vertebral arch and next caudal vertebral body causing dynamic stenosis during flexion or extension
- proliferation of articular or periarticular soft tissues
No radiographic abnormalities doesn’t rule out CVM
Myelography:
- narrowing of spinal cord wall by >50%
- risks of anaesthesia
- iatrogenic damage to spine, diffusion of contrast material into brain
- not performed very often
What to look for when assessing spinal cord for CVM?
Alignment - straight line along middle (bit of step between C2-C3 ok)
Articular processes - round, smooth, regular
Growth regions (periarticular tissue) - check for spurs of bone
Intravertebral sagittal diameter (narrowest width of vertebral body/narrowest width of spinal canal = >50%)
Intervertebral sagittal diameter (caudal dorsal point of first vertebra to cranial point of other side of next vertebra)???
Management for CVM?
Surgery - expensive, may only improve by one grade (average)
Ataxic horse should not be ridden
Type 1: early detection in young foals and dietary restrictions have resulted in resolution of ataxia and successful careers, poor prognosis once advanced
Type 1 - intra-articular corticosteroids (US guided)
What is shivering (Shivers)? Signs? Which breeds? Cause?
Reflex hypertonia of flexor muscles of pelvic limbs
Initially horse snatches up the hindlimb when
being picked
Accentuated when turning or backing horse and if excited
Pelvic limbs are flexed and held in a spastic space for some time
Draft breeds
Always progressive
Cerebellar disease
What is stringhalt? Types?
Sudden involuntary exaggerated flexion of one or both hindlimb during attempted movement
2 types:
- Australian or plant associated: dandelion, flat weed? Treat by removing from pasture
- Sporadid stringhalt: aetiology not fully understood, treatment myotenectomy of lateral digital extensor
Radial nerve injuries - When mostly seen? Signs?
Most common from external blows or following recumbency in anaesthesia
Inability to flex shoulder, extend the limb and fix the elbow
Suprascapular nerve injury - When seen? Signs?
= Sweeny (shoulder slip)
Most commonly from external blows or poorly fitted collars in draft horses
Atrophy of supra and infraspinatus, abduction of limb and inability to advance shoulder
Treatment for peripheral nerve injuries (radial nerve, supra scapular nerve)?
Anti-inflammatories DMSO? Physiotherapy Vitamin E? Return of function may take days-months or may never return
Equine motor neurone disease - Cause? History? Signs? Diagnosis? Treatment? Prognosis?
Degeneration of motor neurons in spinal cord due to low vit E (and Se?)
Normally history of horse stabled with no access to pasture for a period of time
Signs:
- weight loss (muscle wasting)
- muscle fasciculations (esp when stood still)
- prolonged recumbency
- elephant on a barrel stance
- affects posture more than moving (move ok but affected when still)
- elevated tail
- ocular signs in 30-40% cases: brown pigment accumulation in retina
Diagnosis:
- vitamin E (and Se) levels - but if normal doesn’t rule out
- muscle biopsy (tail head)
Treatment: Vit E supplementation
Prognosis 40 (improve a bit)/40 (stabilise but not really improve)/20 (deteriorate)
Botulism in horses - Source of infection? Which types are bad?
Ingest preformed toxin (8 types - B, C, D)
- contaminated feed (big bales), grass/corn silage
- water (dead waterfowl)
- UK: associated with poultry litter and carcasses
Toxic-infectious route:
- type B grows in ingest of suckling foals
- infected wounds (gastric ulcers) - rare
Pathogenesis of botulism?
Blocks Act release at presynaptic membrane of neuromuscular junction
Failure of muscle contraction -> weak
Abrupt progressive onset flaccid paralysis of skeletal muscle
Signs of botulism?
Symmetrical weakness (muscle tremors)
Stumble, ataxia
Tongue weakness, dysphagia
Hang head, nose on ground
Eventually recumbent
Dyspnoea - intercostal and diaphragm paralysis
GI stasis, urine dribbling
Shaker foal syndrome (1-3mo, initial episodes of trembling)
Die in 10 days from respiratory muscle paralysis
Diagnosis and treatment of botulism? Prognosis?
Diagnosis: - identify toxin/spores (expensive) - stomach content (+/- faeces or feed) Treatment: - antitoxin - penicillin (not procaine!) - supportive, fluids Poor prognosis, especially if rapid onset tetraplegia Vaccine in USA (type B) - for mares twice in last month of gestation
Tetanus - Source of infection? Pathogenesis?
Soil, GI flora
Gram +, anaerobic, sporulates with right conditions (wounds) and releases toxins:
Tetanospasmin:
- neurotoxin
- migrates retrograde along motor neurone to spinal cord and brainstem
- inhibits release of glycine
- inhibits presynaptic inhibitory neurons in spinal cord
- muscles continuously contract
- tetany elicited by sound, light, touch
Tetanolysin:
- increases tissue necrosis at site
Signs of tetanus?
Elevated tail head Stiff gait Anxious - ears back, eyelids wide open, nostrils flared, head extended Lock jaw - drool, can't swallow Prolapsed third eyelid Recumbency, rigidity Secondary ulcers, trauma
Treatment for tetanus? outcome?
Support - quiet, dark, low stimulation room, hydration, deep bedding
Eliminate source - open and flush wound, metronidazole
Antitoxin - neutralise unbound toxin, use if unvaccinated
Muscle relaxation - ACP, diazepam
Toxoid - as treatment use at separate site to antitoxin and always use if vaccinated or not, for prevention it is very effective, 2, 3, 6 months and booster at 1yo
If some response in 24-48h then encouraging
Survive 7d = fair-good prognosis
May need treatment for 14d
Mortality 50-80%
Pathway of vision for menace response?
Retina (PLR would also be negative) Optic nerve (PLR would also be negative) Visual cortex (contralateral) - expect other cerebral signs Cerebellum Facial nerve
Horse with negative left menace response (normal PLR), ataxia with hypermetria of all 4 limbs (worse on left) - where is the lesion?
Left cerebellum
Can’t be retina or optic nerve as PLR would be negative
Not visual cortex or would be other cerebral signs
Not facial nerve as also have ataxia
Why do horses have sweating with Horner’’s sundae?
2 mechanisms control sweating: autonomic B2-adrenergic nerves and humoral (adrenerfic agonist secreted from adrenal medulla)
Humoral is main cause of sweating in horses
So in Horner’s no adrenergic supply but local vasodilation -> increased local temperature -> add from cases
Why can ammonia cause forebrain disease?
Ammonia -> glutamate -> glutamine = add from cases
Signs of intestinal hyperammonaemia?
Brain oedema:
Diffuse
Add from cases
Definition of acute renal failure?
An abrupt and sustained decrease in GFR resulting in azotaemia and disturbances in fluid, electrolyte and acid-base homeostasis
More common than CRF in horses
Reversible in early stages
Is acute renal failure usually caused be a renal, pre-renal or post renal problem?
Usually pre-renal (haemodynamic) or renal
Post-renal less common (e.g. neonates with bladder rupture, rarely obstruction)
Haemodynamic (pre-renal) causes of acute renal failure in horses?
Hypovolaemia (colitis, sweat, blood loss)
Volume redistribution (e.g. effusions)
Decreased CO
Altered vascular resistance (e.g. sepsis and endotoxaemia)
Renal causes of acute renal failure?
Primarily acute tubular necrosis secondary to:
- ischaemia:
- or nephrotoxin exposure:
Less commonly glomerulonephritis (e.g. EIA or post infection e.g. Strep equi) or interstitial nephritis e.g. pyelonephritis
How can ischaemia cause acute renal failure (acute tubular necrosis)?
Prolonged haemodynamic changes
Renal infarction
NSAIDs
20% CO to kidneys but medulla more susceptible to ischaemia as only gets 10-20% of blood flow
What nephrotoxins can cause acute renal failure (acute tubular necrosis)?
Antibiotics - ahminoglycosides, polymyxin B, tetracyclines
Endogenous substances - haemoglobin, myoglobin (oxidative damage to tubules)
NSAIDs
Heavy metals
Why do nephrotoxins cause acute renal failure (acute tubular necrosis)?
90% of blood flow filtered by the cortex - susceptible to toxins
Kidney responsible for excretion of most drugs
Most drug toxicities are exacerbated by concurrent dehydration
Concurrent use of nephrotoxic drugs can potentiate toxicity
How to avoid acute renal failure with nephrotoxic drugs?
Monitor serum creatinine in horses on potentially nephrotoxic drug therapy - particularly if evidence of concurrent hypovolaemia, endotoxaemia or renal insufficiency
Treat aggressively if creatinine rises significantly
Reabsorption of aminoglycosides is time dependent so single dose will reduce toxicity and accumulation (use one high dose)
Pre treatment with calcium before aminoglycosides may reduce nephrotoxicity
Filtration and absorption of aminoglycosides? Which is most nephrotoxic? Are the effects time or dose dependent?
Neomycin is the most nephrotoxic - gentamicin & amikacin similar
Filtered by glomerulus (no metabolism ‐ all excreted by the kidneys)
Reabsorbed by proximal tubular epithelial cells
Accumulation in proximal tubular cells interferes with cells’ function
Time dependent
Why do NSAIDs cause nephrotoxicity? Are the effects time or dose dependent?
Toxicity due to renal medullary crest and papillary necrosis and sloughing of the tubular epithelial cells
Dose dependent effects
Secondary to ischaemia secondary to prostaglandin inhibition
Dose dependent
Clinical signs of acute renal failure?
Usually referable to the primary problem - e.g. acute colic or colitis
Anorexia and depression - uraemia, fluid, electrolyte and acid-base disturbances
May be just a worsening of the primary problem, or an apparent lack of response to therapy
Diagnosis of ARF?
History and clinical signs
Minimum tests = urinalysis and serum biochemistry
- BUN and creatinine increased
- if pre-renal, urine will be maximally concentrated (>1.035) and is quickly reversible with fluids (try fluids and monitor creatinine)
- if renal, urine will be less concentrated (1.008-1.014 = isosthenuric) and won’t be quickly reversible with fluids
Fractional excretion of electrolytes (if excessive Na excretion then more serious)
GGT/creatinine ratio of urine
Proteinuria, glycosuria (trace protein is normal)
Sediment exam - casts, leucocytes, erythrocytes, bacteria
Electroyte changes - hyponatraemia and hypochloraemia, may see hypocalcaemia and hyperphosphataemia (opposite when chronic)
Metabolic acidosis
May see hyperkalaemia if oliguric but usually don’t esp if anorexic
What does it mean if urine is dilute (hypothenuric)?
Kidneys are working - actively diluting the urine
What can affect diagnostics of ARF when horse has been treated for colic etc?
IV fluids - make urine more isosthenuric
Sedatives - cause diuresis
What is special about normal equine urine?
Bubbles because of protein
Silty (crystals) - they excrete calcium carbonate
Treatment for ARF?
IVFT
- to improve renal perfusion
- correct metabolic disturbances
- induce diuresis
- aim to prevent pre-renal failure developing into intrinsic renal failure
- Hartmans
- replace fluid deficits and maintain on 2xM provided polyuric
Discontinue nephrotoxic drugs where possible
Nutritional support
Furosemide if oliguric (1-2mg/kg IV qid) - must be filtered at the glomerulus to work, care with exacerbating volume depletion and potentiating drug effects
Dopamine - potent renal vasodilator that acts directly on specific receptors on arterioles (care with arrhythmias)
Dopamine and furosemide are synergistic
Mannitol - not used often in adult horses, don’t use if volume overload
DMSO - osmotic diuretic
How much is maintenance fluids for a horse?
60ml/kg/day
What to monitor while treating ARF?
Monitor body weight, PCV and serum protein - estimate dehydration, if increase above expected baseline may be overhydrating or use CVP
Monitor biochemistry - creatinine should be reducing
Prognosis poor if poor initial response in azotaemia to fluid therapy
Clinical signs of CRF?
Chronic weight loss
Lethargy
Poor hair coat
PUPD
Poor performance
May see oral ulceration, gastroenteritis, excessive tartar and halitosis
Ventral oedema inconsistent - hypoalbuminaemia relatively mild and offset by increase in globulins, except for glomerulonephritis
Diagnosis of CRF?
Persistent isosthenuria (1.008-1.014) with azotaemia and clinical signs
Mild anaemia, mild hypoalbuminaemia
Electrolyte abnormalities - hypercalcaemia and hypophosphataemia (different to small animals), hyponatraemia, hypochloraemia, low bicarbonate
Ultrasonography
Endoscopy collection of ureter samples - culture, biopsy
Treatment for CRF?
Palliative only
Ensure water and salt always available
Improve nutrition with lower protein (<10% if poss) to manage BUN
Decrease Ca if high Ca diet (alfalfa)
Care with excessive fat supplementation due to risk of hyperlipaemia
Prognosis of CRF?
If mild to moderate elevations in creatinine (<200U/L) may survive long time
Poor long term prognosis and shorter time if creatinine is higher
>800U/L prognosis is grave
What is dysuria? How can it present? Signs? Causes?
= abnormal urination Pollakuria - increased frequency of urination Stranguria - straining to urinate Haematuria Pyuria May see urine dribbling or scalding Must differentiate from normal oestrus behaviour in mares Less commonly may see colic or tenesmus
Urethritis - Which horses? Causes? Signs? Diagnosis? Treatment?
Usually older gelding with preputial or distal urethral conditions (often obese horses)
Look for underlying conditions - trauma, neoplasia, habronemiasis, foreign body, urethral concretion (“the bean”)
Malodourous sheath, swelling
May present for red discharge on legs
Examine penis and prepuce, including urethral fossa
Clean +/- apply very mild topical antibacterial agents
How common is cystitis in horses? Diagnosis?
Primary bacterial cystitis is extremely rare
Look for initiating problem - e.g. urolithiasis, neoplasia, paralysis
Diagnosed on urine sediment exam (>10leucocytes/HPF+, >20organisms/HPF)
Factors contributing to formation of uroliths?
- Tissue damage e.g. see uroliths secondary to renal damage
- Prolonged transit time e.g. neurological conditions
- Nidus formation e.g. area of necrotic tissue, leucocytes or desquamated epithelial cells
- Reduced inhibition of crystal growt - mucous natural inhibitor
When are nephroliths and ureteroliths usually seen? What are the consequences? Diagnosis? Treatment?
Usually secondary to other problem e.g. pyelonephritis, tubular necrosis, or papillary necrosis (NSAIDs)
Obstruction causes dilation of the renal pelvis to hydronephrosis
Renal failure if both affected, otherwise may only be non specific signs
Bacterial infection frequently accompanies the calculi
Diagnosis by palpation and/or ultrasonography
Removal of affected kidney or nephrectomy have been described
Cystic and urethral calculi - signs? Diagnosis? Treatment?
More common than nephroliths and uteroliths
Present with dysuria - haematuria, stranguria, pollakuria, pyuria
May see posturing to urinate - differentiate from oestrus in mares
May see colic, urine scalding, loss of condition
Diagnose by palpation or endoscopy
Calculi can be removed surgically - laparotomy, perineal urethrotomy in males, in females retrieve by forceps or hand after epidural
Antibiotics post removal
Recurrence common
Urinary acidifiers extremely difficult to administer in useful amounts
Decrease in calcium excretion should be aimed for - don’t feed alfalfa
Salt to increase water consumption and diuresis
How much do horses normally drink?
Around 20L per day
Increases with exercise, hot conditions - up to 90L per day e.g. endurance horse
What are the 3 main causes for PUPD in horses?
Renal failure/disease
Cushings
Psychogenic water consumption
Why does Cushing cause PUPD?
Glucosuria and osmotic diuresis
Antagonism of ADH by cortisol (most likely cause)
Impingement on the posterior pituitary decreasing ADH
Unlikely to be just one of these - not all glycosuric, not all impinge on the posterior pituitary and some can concentrate their urine with water deprivation
Work up for PUPD?
- Check if isosthenuria and azotaemia - if is, confirms renal disease
- If not azotaemic, do water deprivation test:
- contraindicated in azotaemic horses
- measure SG, PCV, TPP and BW
- withheld water and monitor min 12h
- stop test after 24-48h if urine SG>1.025, if >12-15% loss BW or 12g/L increase in TPP, or azotaemia
- if concentrates normally, then psychogenic or Cushings
- if doesn’t then need modified water deprivation test - Rule out Cushings on history, signalment, clinical signs or endocrine testing (also rules out DM)
- Modified water deprivation:
- modified 40ml/kg/day for 3-4 days
- expect SG >1.025 in horses with medullary washout - Response to ADH:
- response to ADH with central diabetes insipidus
- if no response then may be nephrogenic diabetes insipidus
Differential diagnoses for red urine? What must be determined from the owner?
Haematuria - whole RBCs on sediment exam
Pigmenturia
Haemoglobinuria
Important to determine if red urine throughout urination, at beginning (distal urethra) or end of urination (proximal urethra)
Or is there just a red discolouration on the hindlimbs or a haemorrhagic discharge
Causes of haematuria?
Cystitis, pyelonephritis, urolithiasis
Urinary tract neoplasia
Drug toxicity - esp NSAIDs, glomerular disease
Urethral defects - e.g. ischial arch or terminal urethra (stallions, geldings)
Exercise induced haematuria (usually microscopic due to increased filtration of RBCs across glomerular barrier)
Idiopathic renal haematuria and renal vascular anomalies:
- haemorrhage, often with blood clots in an otherwise well animal
- can be severe and life threatening
- pathogenesis not clear
- if unilateral, nephrectomy may be indicated
Causes of pigementuria (red urine)?
Myoglobinuria
Myopathy - exercise associated, other signs, elevated muscle enzymes
Pasture associated (atypical myopathy) - sycamore and other Acer app:
- hypoglycin A
- very ill horse, unable to metabolise fatty acids
- very high CK, may have VPCs
- treat aggressively - poor prognosis
Causes of haemoglobinuria?
IMHA:
- usually secondary in horses (e.g. penicillin, Strep equi abscesses, lymphoma)
- often large proportion of extravascular haemolysis so may be mild haemoglobinuria
Neonatal isoerythrolysis
Oxidative injury to RBCs - e.g. methaemoglobinaemia and haemolysis with red maple leaf toxicity, onions
EIA
Piroplasmosis
Iatrogenic > 20% DMSO
Snake venom
DIC, end stage liver failure
Treatment required for a cyst at margin of pupil, if rest of clinical exam normal?
No treatment needed
What to do if thorn penetrated eye? Painful, blood discharge, reduced pressure?
Emergency referral for second opinion
Treatment for cobble stone appearance of third eyelid? What if fails?
2 weeks dex, neomycin, polymyxin B
Elective referral if no change
