Midsemester 1 Flashcards
List some common diagnostic tests
Microbiology: infection presence (mostly G+, G- overgrowth= enteritis), resistance, antibiotic choice
Culture and sensitivity: ID organism and therapy
Haematology and biochemistries
What are the techniques used for haematology?
1% birds BDW in blood
25g
Blood smears immediately
Paedeatric lithium heparin or EDTA- centrifuge and decant plasma in another lithium heparin for lab biochem
insignificant:
- low bile acids
- high amylase (needs to be >15X)
- lipaemia: artifact, bad diet
- haemolysis- artifact
- high uric acid in periguin falcon (high protein)
- lower PCV and higher WBC in young
What are the characteristics of erythrocytes?
Erythrocytes: nucleated
- PCV (~40) lower in chickens compared to parrots (increased O2 capacity with flight)
- morphology: strongly regenerative if mitotic figures, reticulocytes regen, Non regenerative anaemia= chronic dx, overwhelming infection or nutritional
What are the characteristics of white blood cells?
WBC: manual count (nucleated RBC cause high counts)
- 40X: (no. WBC in 10 fields/10) X 2000
- heterophil- neutrophil without lysosyme->caseous pus
- eosinophils rare (tissue damage, parasite)
- monocytes- common
- lymphocytes- small or large
- basophils uncommon (tissue damage, inflam, hypersensitivity)
Leukocytosis:
- Normal: juvenille
- stress leukogram: 90% heterophil and 10% lymphocytes
- inflammation: similar and then monocytosis and basophilia
Leucopenia: (heteropaenia)
- chronic BM suppression
- overwhelming BM
- artifact
Lymphocytosis:
- leukaemia
- chronic inflammation
- normal
Lymphopaenia:
- overwhelming infection
- relative to heterophilia
Monocytosis:
- chronic granulomatous dx: abscess, TB
- no monocytopenia (values 0-1)
What are the characteristics of thrombocytes?
Thrombocytes:
- extrinsic clotting factor (no platelets)->release thromboplastin
- anti-inflammatory role
- phagocytic
List the biochemicals
Metabolites:
- uric acid (end product of protein digestion)
- protein
- cholesterol (liver from fat and carbohydrate)
- triglycerides
- urea (end product of protein digestion)
Enzymes:
- AST
- CK
- GLDH
- Amylase
Minerals:
- Calcium
- phosphorous
Electrolytes:
- Na, Cl, K
Bile acids
Liver disease biochem:
Hepatic necrosis: AST (+CK) and GLDH (mitochondria in hepatocytes)
Liver function: bile acids (rising levels= less entero-hepatic uptake) and cholesterole (energy source, significant if rising)
Cholestasis:
- GGT (bile occlusion, carcinomas)
Renal disease biochem
Decreased function: uric acid (produced in liver from protein->passed out through tubules-> elevate)
Hydration status: urea (over 1-2)
Reproductive disease biochem
Calcium: hypocalcaemia from eggs
Cholesterole: yolk
Triglycerides: yolk
Total protein: transport
GIT dx biochem
Na, Cl, K, amylase (broad)
Blood glucose biochem
Hyperglycaemia: DM (>33, persistent), stress, normal (artifact- RBC left in contact with plasma)
Lipids biochem
Cholesterol:
- hepatic lipidosis
- artherosclerosis
- diabetes mellitus
- hypothyroidism
Triglycerides:
- repro
How to interpret PCR:
High spec, sens detecting Ag not disease
- Ag can be intermittently shed, or at low []
False results:
- contamination of sample (feather from floor)
- inhibitors
- previous drugs- doxycycline for chlamydia->N- after 2 days
How to interpret serology:
Combine with PCR and do serial testing (accuracy), Detect Ab affected by: - host factors- ab levels - antigen factors- prepatient levels - assay factor- selection
Blood- low invasiveness, cheap
Use:
- flock outbreaks
- Specified Pathogen Free (poultry)
- immune status or individual
Interpreting cytology
FNAB, centesis, impression, washes
- cell type: haemic cells (blood and haematopoetic tissue)
- epithelial cells exfoliate easily- abundant in cytoplasm
- nervous tissue rare (basophilic, stellate)
Cell response:
- inflammation
- tissue hyperplasia
- benign neoplasm: mitotic figures, cytoplasm, unipopulation
- malignant
Interpreting radiology
Radiology:
- short exposure time, relatively powerful, high detail screens and films
- digital
- birds under 50g- dental machines (better exposure)
- birds over 50g- normal machine
Restraint:
- box- looking for egg
- anaesthesia- face mask, sedate with midazolam
- plexiglass
Positioning:
Lateral:
- wings dorsal and cranial (superimpose coracoids)
- legs: caudal and dorsal (superimpose acetabular)
- carina of keel parallel to plate
Ventro-dorsal:
- anaesthetised
- wedge head up on foam, won’t regurgitate
- wings: foam support underneath and sandbag on top
- legs: parallel to tail
- carina superimposed over spine
-
Interpreting ultrasound
Cheaper, less commonly used air sacs interfere USE: - yolk peritonitis - GIT dilated full of ingesta - nodules - abdominal distension
Interpreting computer tomography
Very useful, $$, need radiographer
Very detailed
Use:
- Ovary enlarged in breeding season->pressure on abdomen->herniate
- Jaw fractures in snakes- useful to show owner 3D
Interpretation of fluoroscopy
Real time - GIT motility studies
Place bird in dark box
Use:
- vomiting or dilated proventriculus on rads
- proventricular dilation disease: backflush from oesophagus back into crop
- obstruction: ingesta moving to proventriculus but not ventriculus
will burn bird if prolonged exposure
Interpreting endoscopy
Anaesthesia
Examine internal organs:
- pericardial effusion (can’t detect on rads), lungs, kidneys, ureters, spleen, adrenal glands, GIT, fungal granulomas on air sac- biopsy
External opening:
- mouth- trachea->syrinx
- Ear- pinnae small
- Cloaca- expand with saline to allow passage, opening of ureters, oviduct, urodeum, proctodeum, (papillomas)
Biopsy: 1.9mm, 2.7mm
Feather function and normal feather loss
Flight, communication, waterproofing, insulation
Feather loss:
Moulting: thyroid gland, diurnal cycle and photoperiod control
- spring and autumn (pre and post nuptial moult/breeding)
- few feathers at a time, bilaterally symmetrical
Describe stuck in moult
Canaries or high producing chickens
Inappropriate diurnal exposure
Malnutrition: no energy to moult. dull colour, feather damage, feather loss
Treatment:
- distinct diurnal cycle (dark room 8-12 hours) and correct diet->usually triggers moult
- desorelin implant last resort
Traumatic feather loss causes
Predator avoidance
social
self-inflicted
nesting- want chicks out
Infectious causes of feather loss: parasites
Parasites:
- over diagnosed
Mites:
->cnemidocoptes: scaly faced mite, scaly leg mite
- pinholes from proliferative reactions in keratin
- Ivermectin fortnightly X 3 via crop (28d WHP)
- > red mite: nocturnal, blood feeding, common
- > Fowl mite: very common,
- pyrethrin (2 week WHP)
Lice
Infectious causes of feather loss: bacterial and fungal
Secondary to trauma
- self trauma: Quaka mutilation syndrome
- cockatoo: axillary dermatitis
- Ringworm/favus (uncommon): biopsy, griseofulvin, itraconazole, wash with enilconazole shampoo
Psittacine beak and feather disease
All parrots susceptible, new world’s are resistant and rare in cockatiels
- basophilic cytoplasmic inclusion body
- juvenilles
- incubation: 21-25 days->years
- shed in faeces, crop secretion and feather dust
- incurable
CS:
acute:
- juvenilles
- lethargy, weakness suddenly
- regenerative anemia, pancytopaenia
- death 24-48hours
- severe hepatic necrosis
Chronic:
- cockatoos
- feather: loss of primaries (lorikkeets) and colour chanegs
- beak: overgrown, underrun, necrotic (constant pain)
Other parrots: colour change, feathers fall out if handled, untidy (feather dystrophies)
Diagnosis:
- histopathology
- dead- send cloaca
- feather- pluck
- serology; haemaglutination, haemaglutin inhibition test
- PCR: blood from blood feather- immune response
Treatment:
- avian interferon- experimental
- supportive care
Prognosis:
- some can effectively recover (lorikeets)
- some live 10-30 years despite CS
- mostly die ~2 years- immunocompromise
Avian polyomavirus
All parrots. mostly budgerigars, macaws, conures, eclectus parrots, caiques (rarely african grey parrots, cockatoos, cockatiels)
- Viraemic form: dead in 1 day, viral inclusion bodies
- necropsy: haemorrhage (pale carcass), liver destroyed, severe coagulopathy- easy bruising
Feather forms:
- drop primary wings and tail
Diagnosis:
- histopath
- PCR: blood (viraemic form in circulation) and cloaca (needs to be cleared in droppings)
Treatment: none
- most die, budgies can regrow feathers and live
- burn all nest boxes and stop breeding for 6 months
Feather damaging behaviour- disease of captivity
Causes:
- underlying pain: internal organ pain
- dermatitis
- underlying lesions
- malnutrition
- psychological problems: anxiety, boredom, fear, breeding
DX: - rule out physical - CBC, biochem, skin biopsy and culture - radiology - find out bird habits when physical ruled out; Antecedent (what preceds the behaviour) Behavioural Consequences
TX:
- only use collars if skin is broken, don’t sedate
enrichment plan:
- 80% foraging for food and 20% social and napping
- foraging, physical, sensory, social (indirect and direct), occupational
Describe the anatomy of the upper respiratory tract in birds
External nares->rhinal cavity
Nasal cavity (turbinates for smell)
Infraorbital sinus: ordour, humidify
- cervico-cephalic air sac: thermoregulation and buoyancy
Choana glottis-
Glottis- vertical slit opening laterally, arytenoid cartilage and no epiglottis. appose choanal slit (allow breathing)
Trachea: complete interlocking cartilage rings for strength and flexibility, longer and wider than other spp. Diameter decreases
Syrinx: diving two bronchi, voice production (site for obstruction of aspergillus granuloma)
Lungs: Dorsal (paleopulmonic) and ventral half, paired, fixed, recessed between ribs
air sacs:
- caudal to lungs: cranial thoracic and abdominal
- cranial to lungs: 2 cervical and intraclavicular sac
no diaphragm, push d sternum down, pivoting down on coracoid joint and ribs move out->air drawn into lungs and caudal sacs, sternum moves up and ribs come in->air through to cranial sacs (neopulmonic part) into lung and expired
Clinical signs of upper respiratory tract
Sneezing Staining of feathers above nares Sinus distension- infraorbital Occular discharge Matting of periorbital feathers Periocular alopecia Thickening eyelids SQ emphysema if cervicocephalic air sac is ruptured
Trachea: acute
- coughing
- open mouth breathing
- neck stretching
- resp noise (air over exudates)
- distress
Lung and air sacs: chronic
- increased resp effort
- mouth breathing
- tail bobbing (inspiration)
- sternal lift
- weight loss
Sinusitis
Causes: - hypovitaminosis A->hyperkeritinisation of MM of sinuses ->debris accumulates->infection - dust - chemical irritants - ammonia Infectious: - parasites (trichomonas) - virus - mycoplasma - chlamydia - fungal infection
Treatment:
- supportive: vitamin A parenteral
- nebulising: steam + emphaterycin B, enrofloxacin, DMSO
- nasal flushing:
- SX removal
Chlamydiosis
Chlamydiosis, psittacosis, ornithosis: - G- non-motile, obligate intracellular CS: - resp signs: conjunctivitis, loss/matting periocular feathers - dyspnea - sneezing - purulent nasal discharge - sinus distension
Gastrointestinal/hepatic signs:
- diarrhea
- biliverdinurea (green urates and urine)
- sick bird look- fluffed, anorexia, lethargic
- poor feathering
- neurological- torticollis (head tilt), tremors, convulsions, polyuria, infertility
Transmission:
- ingestion, inhalation and possibly egg
- carrier- stressed
- incubation: 4 days-2years
- shedding 72 hr after infection
- short immunity
Diagnosis: Three As
Antigen: PCR, biopsy and cytology
Antibody: immunocomb detects ab produced 2 weeks post infection
Ancillary: monocytosis, basophils high, AST, GLDH, ST, CK, enlarged spleen on rads
Treatment:
- tetracycline (inhibits protein synthesis) 45 days
- reduce Ca in diet (chelates)
- immunosuppressive, inhibit normal gut flora, hepatotoxic
other: oxytetracycline, chlortetracycline, doxycycline
Zoonotic
Non-infectious causes of upper resp disease
Functional: unlikely
External compression: fractured coracoid on trachea
Physical obstruction: pharyngeal dx, FB, millet seeds inhaled
Tracheal diseases
Stricture (follow insult to trachea mucosa)
Infectious:
- ILT, diptheritic fowl pox (chicken), herpes virus
- aspergillus granuloma (grey parrots esp)
- air sac mites (gouldian finches and canaries)
Diagnosis and treatment of tracheal foreign body
Inhaled or aspergillus granuloma
DX: acute onset, endoscopy
TX:
- ET into cranial air sac (neopulmonic/gas exchange)
- catheter into trachea below millet seed and push gently-> blow air to dislodge
Diseases of lungs and air sacs
Lungs:
- parenchymatous disease
- fungal and bacterial
- hypersensitivity- mackaws+ african gray parrots/cockatoos-> feather powder
Air sac:
- saculitis: aspergillus, chlamydia
Extra-respiratory disease: fluid, fat, gas, enlarged organs, egg bound
Anaemic (increases RR)
DX:
- CS
- CBC
- Radiology
- endoscopy
Aspergillosis: aspergillus fumigatus
Predispose:
- African grays, ostriches, waterfowls most at risk
- immunosuppression: poor diet, overcrowding, concurrent infection
Exposure:
- needs high concentration (nest)
Pathogenesis:
- plaques and granulomas in sinuses, trachea, syrinx, lungs, air sacs, outside resp tract
DX:
- increased WBC
- Rads: air sac lines
- endoscopic
- PCR
- Serology- exposure
- PM mostly
TX:
- single, on lung- endoscopic debridement
- systemic itraconazole or voraconizole 3-12 months
- nebulising: emphaterycin B
Polydypsia
Water intake in excess of double daily maintenance requirement: 50-100ml/kg/day
- compare diet and species
Usually secondary to polyuria
Psychogenic
Osmoregulation in parrots
Plasma osmolality 300mOsm/L Balance between fluid intake and urine output - plasma osmolality and volume - osmoreceptors and baroreceptors - kidney - hypothalamus - pituitary gland
Avian kidneys
Avian mammalian nephrons:
Avian reptilian nephrons: no loop of Henle (does have glomerulus and collecting ducts)- doesn’t concentrate urine
- desert birds will have larger number
Uric acid: 10% goes through glomerulus and 90% goes through collecting ducts
Arginine vasotocin
avian equivalent to ADH
- produced in pituitary in response to increased osmolarity->kidney->reduce blood flow and increase urine reportion
- decreased urine output (cloacal resorption) and osmolality
Normal urine production: PU arise from affecting any of these factors
- normal plasma and urine osmolality
- sufficient function of nephron
- normal production and response to AVT
- efficient cloacal water resorption
PU/PD
Decreased plasma osmolality:
- dietary
- psychogenic polydyspsia
Increased urine osmolality:
- liver disease (biliverdinuria)
- diabetes mellitus (glucosuria)
- high renal phosphate
Decreased functional nephrons:
- nephritis
- toxins
nephrosis: no inflammation - > lead and zinc toxicosis and hypercalcaemia
Neoplasia (budgies and renal adenocarcinomas)
Renal gout: urate crystals in collecting tubules (white mottling appearance)
Immune mediated:
- amyloidosis
- membranous glomerulopathy
AVT response:
Diabetes insipidus:
- neurogenic (pituitary gland not producing enough)
- nephrogenic: not responding (pituitary adenomas)
- decreased cloacal resorption: fight or flight
- Enteritis: diarrhea taking water with it
Client advice:
- Quantify water intakes
- CBC and biochem: renal and liver function
- urinalysis- casts
- Heavy metal levels
- Radiology: kidney size, heavy metals and uroliths
- water deprivation tests
- kidney biopsy
Diabetes mellitus
Not common- budgerigars, cockatiels, galahs, larger parrots
Chronic hyperglycaemia + metabolic abnormalities
Lack of insulin or response
Glucose metabolism:
- insulin- anabolic hormone
- glucagon: catabolic- gluconeogenesis, lipolysis and glyconeogenesis
- somatostatin: modulates these two
Plasma glucagon: insulin ratio is 2-5 X higher than mammals
Type 1: selective destruction of pancreatic islets, toucans and parrots
Type 2: more common, obesity and iron storage
Non-specific: neoplasia and pancreatitis
Corticosteroid injections
DX:
- PU/PD
- polyphagia
- thin keel (burn protein first)
- > 38-44mmol/L glucose persistently elevated
- persistent glucosuria on dipstick
Management:
- stabilise
- correct hyperglycaemia: insulin, oral hypoglycaemic agents (glucoside- weight loss)
- weight loss- diet
Kidney
Renal insult-> release of PG and thromboxane-> increased renal vascular resistance and decreased blood flow, recruit inflammatory cells-> decreased GFR, O2 and nutrients->further renal damage
Inflammatory causes: infectious: - pathogen and immune mediated Non-infectious: - trauma and yolk peritonitis
Non inflammatory causes:
Immune mediated: amyloidosis
Toxic: heavy metals, aflatoxins, iatrogenic
Other: nutritional, dehydration, metabolic, neoplasia
Clinical signs:
- fluffed, lethargic, weight loss
- increased thirst, anorectic
- dehydrated (increased urea)
- regurgitation or vomiting common- severely polydipsic
- persistent polyuria
- lameness or wing droop- articular gout
DX: PU/PD
- > 800umol/L blood uric acid and elevated in urine
- mild anaemia (PCV 30-37%
- Rad: renomegaly, mineralisation
TX:
- fluids SQ, IV, intra-osseous
- medications: allopurinol (stops uric acid production in liver), urate oxidase, colchicine (reduce uric acids and prevents fibrosis in kidney)
-
Gout
Uric acid precipitation out of blood when saturated levels are exceeded
Visceral gout: common, death in 3 days
CS: good BCS, extremely high uric acids
Articular gout: chronic renal failure - slower uric acid level rise - precipitates into cooler parts of body extremities TX: lower uric acid levels, analgesia PX: guarded
Heavy metal toxicosis
Excessive Zn excreted through kidneys and pancreas
Micronutrient, acute toxin, not cumulative, galvanised wire
Vomiting and diarrhea, PU/PD
Lead:
acute and cumulative toxin
Vomit and diarrhea, PU/PD, anaemia, seizures, ataxia, +- haematuria
DX: rads: cumulative CBC: lead- regenerative anaemia Biochem: Zn elevates uric acid Blood- lead test
TX:
Chelate: twice daily for 5 days and then twice weekly for 3 months
- Calcium EDTA: remove from soft tissue (then bone moves to soft tissue)
Remove metal: endoscopy
Supportive care: fluids and transfusion if weak
What is the sick bird look and how should you approach it?
- stringy saliva
- eyes half shut
- fluffed up
Decompensating:
- dehydrated
- hyperthermic
- catabolic state
- resp compromise
- pain
- blood loss
Masking phenomenon: will not appear very sick until late in the process
Approach:
- Unless flock medicine: tentative diagnosis>confirmed diagnosis in dead bird
- supportive care
Approach to dehydration
CS: - sunken eyes - mucoid saliva - decreased CPR on wing vein - tenting skin - decreased urine assume all sick birds are dehydrated
Fluid therapy:
- Hartmans for first 12 hours and then switch to saline
- volume: 10% BDW for first 3 days and then 5-7.5% daily
- if vomiting, diarrhea- 15% BDW
- can divide into 2-3 doses
Route:
SQ- difficult to overdose
Oral- gut damage
IV- jugular-> haematoma, basillic and median metatarsal vein possibly
Intra-osseous into ulna- budgies and cockatiels (~3 days use)
Approach to hypothermia
41 degrees normal- will compensate ambient temperature with metabolic process
- fluffed, lethargic, found on floor
- die within 24 hr
TX:
- heat lamp
- allow escape
- low flow O2 can cool down cage
- monitor signs
Approach to catabolism
CS:
- anorexia, melena (autodigestion), urates smell, weight loss - breast bone
TX:
- food and water easily accessible
- crop gavaging (2-3 X daily)
- oesophagostomy tube
Approach to respiratory compromise
CS:
- mouth breathing
- increased resp effort (sternal lift and tail bob)
- audible respiratory noise
- cyanosis
- collapse
TX:
Acute: tracheal obstruction
-> air sac catheter, anaesthetise, lay on right side, incise at last rib (if breathing now, confirm obstruction)
Chronic:
- low flow O2 therapy
- intranasal catheter
Approach to pain in birds
Acute: fight, flight or freeze
Chronic: withdrawal response
TX:
- remove source of pain (sling)
- calm bird: midazolam (IV, IM or intranasal)
- opioids: butorphanol, morphine and tramadol
- NSAIDs: meloxicam, careful if dehydrated
Approach to blood loss
Able to withstand larger blood loss than other spp.
- increased capillary surface area in muscles for rapid extravascular resorption to maintain vascular volume
- mobilise large numbers of immature erythrocytes
CS:
- HX and physical evidence of recent blood loss
- pale MM
- increased resp (compensate for RBC loss)
- weakness and lethargy
- PCV <20%
TX:
Mild: fluids, PCV normal ~7 days
Severe: homologous or heterologous transfusion
- reactions usually occur on 2nd or with heterologous (different spp)
- citrate in bag when collecting (cannot store)
Hospital care of sick birds
Security Warmth Biosecurity Feeding: preference, stomach tube Psychological care: may have to send bird home to eat
Surgical principles in practice
Condition the patient Anaesthetic and analgesic plan Planning Patient support Instruments, techniques minimise tissue damage, blood loss, inflammatory response
Prepping and draping
Pluck feathers (Minimal)
Chlorhexidine or povidone iodine (not alcohol)
drape with transparent drape if under 300g
towel clamps on large feathers
Surgery pearls
- Skin is closely attached
- Skin is thin
- Fatty SQ layer (don’t hold well, but post-op swelling not as severe)
- Extrinsic pathway- relies on tissue damage (clamp before incise to release thromboplastin)
- Blood loss- tolerate better (capillary SA absorbing EV fluid to avoid shock, mobilise immature erythrocytes, lack autonomic response to haemorrhage that leads to haemorrhagic shock)
- support with warmth, fluids and transfusion - avian heterophil lack lysozymes- drains won’t work
What should you do if you cannot get primary closure?
Skin grafts or flaps
Secondary intention: keep wet with hydrocolloid dressing (duoderm)
suture choice
Minimal reaction (avoid chromic gut) absorbable monofilament (nylon) - braided cuts good knot security Polydioxanone PDS Polyglactin 910 (Vicryl)
Crop surgery- ingluviotomy
Remove foreign bodies and access proventriculous (endoscope)
Approach:
- apterylae (between feathers) and avascular
- open skin and then crop
- two layer closure
- inverting in crop and then simple continuous in skin
Left flank coeliotomy
Salpingohysterectomy proventriulectomy liver and kidney biopsy Approach: - lie on RHS and abduct left leg - incise at second last leg (use radiosurgical unit to Cuarterise before incising through the abdominal muscles or will ligate - increase O2 as you enter the abdomen
Closure:
- two layers, simple interrupted or continuous
- quick- losing heat
- close skin with simple interrupted or continuous
Ventral midline coeliotomy
Ventricuolotomy
Salpingohysterectomy (bob prefers left flank as there is a lot of coelomic fat here)
intestinal SX
Cloacopexy
Approach:
- incise through linear alba (blunt dissection as muscles are thin)
- just in front of cloaca to sternum
Orthopaedics
Bones are light with thin, brittle cortices which will not hold screws
Fractures open and comminuted due to minimal soft tissue coverage
Joints:
contracture disease- reduce movement
fracture callus may impinge rang of motion, adhesions or ligament and tendons
width of bone X 1.5 fracture sits (must be outside this to release bird)
Muscles:
- pectoral muscles attached to humerous can cause rotational deformity
Bone healing
Primary healing: bone to bone, min callus, rigid fixation and perfect bone apposition
Endosteal callus formation: rapid when well aligned
Periosteal callus formation: fractures not aligned, movement
Soft tissue swelling->fibrous callus->bony callus->healed and remodeling
Rate of healing depends on:
- displacement of bone fragments
- damage to blood supply
- presence of infection
- movement at fracture site
External coaptation:
1 week: palpable callus, movement
3 weeks: endosteal callus, no movement
5-8 weeks: healed and beginning to remodel
Internal fixation:
2 weeks- union
3 weeks- remodelling begins
- min soft tissue damage
- alignment of bone
- rigid stabilisation and encourage early return to normal function
Types of fracture repair
External coaptation- splint Surgical: - IM pins - Plates - External skeletal fixation - Tie in fixator (IM tied in to ESF)
Aftercare of fractures
antibiotics analgesia physiotherapy 2-10d Radio assessment- 7-10 d Implant removal- 6-8 weeks
Signs of pain in birds
Acute: fight or flight
Chronic: withdrawal- conservation response
Effects of pain
Chronic pain will stimulate adrenals->corticosteroids (stress response)->slow healing-> lower recovery rates
Principles of analgesia
Pre-emptive analgesia: prevent pain transmission and reduce number of nerves involved
Multimodal therapy: remove source of pain (splints)
Reduce fear and stress
Several classes of drugs
Analgesia options
Opioids: mu-opiods need higher concentration (morphine, buprenorphine and fentynal) as there are more Kappa receptors in brain
NSAIDS:
- meloxicam 1 IM 1.5mg/kg PO BID
Local anaesthesia:
- lignocaine
- 1-4mg/kg
Anaesthesia in birds
GA for physical exam
Risk of dying mainly after sx (could be due to higher ASA score, small body size (heat loss) anatomy and small airway, catecholamine release when stressed, fluid overload, anaesthetist experience, inadequate monitoring, inadeuate post-op care, anaesthetic drugs
Solutions to anaesthesia complications
Better assessment and patient preparation
- PE: weight, temp, HR, RR, hydration, nutrition
- clin path: PCV, TP, blood glucose
- Address abnormalities: fluids, warmth, tube feed, analgesia, O2, reduce stress
- fasting depends on species, long enough to empty crop ~1-2hr, some 12-24 hours if good at gluconeogenesis
Better support and monitoring of patients while under
Better post- op care
Induction
Pre-medication: not needed if quick (rads)
- benzodiazepene and opioid (butorphanol + midazolam)
- 15 min prior (fast circ)
IM: medetomidine, ketamine
IV: median metatarsal vein in long legged: propofol and alfaxane (or medetomadine and ketamine in waterfowl as slow bolus)
Mask: difficult in water fowl (hold breathe), most birds good. Iso at 4-5% and then 1-2%, saturate tissue with O2- prevent cardiac arrest
Chamber: user risk, can cause agitation if bird sees you in tank
Intubation: complete rings (no cuff), stricture (uncommon), keep neck extended, use paedeatric tubes
Head elevated (fasted or not)
Maintenance
Depth:
- Increasing depth- decreases temp, cardiac output, tissue perfusion, causes resp compromise
Assess: visual RR and depth, HR, reflex (same as dogs)
Support:
- Thermal: warming before pre-med (radiant heater, heat pads, warmed air and fluids, warmed anaesthetic gas). monitor temp
- cardiovascular: decreased CO and systolic BP-> anaesthetic, patient positioning (back->CVC compressed), lack of movement, blood loss (SX)
- 10ml/kg/hr fluids IM, IO, SC
- respiratory: No diaphragm (rely on action of IC and sternal mm. which is lost in anaesthesia)
- ventilation: manual (bag), mechanically (small animal ventilator), via ET tube
- start before problems, initially same as pre-anaesthesia evaluation and then adjust
Monitoring:
- cloacal thermometer
- Stethescope, doppler, ECG
- Pulse oximeter (erroneously low ass. with nucleated erythrocytes), capnograph
Recovery
Discontinue anaesthetic Rising CO2->stimulate spontaneous breathing - face mask when extubated Watch for obstructive breathing pattern Slow fluids, continue other support Monitor cardiac function and body temp Recovery cage- close monitor
Post-procedural care and monitoring: - body temo, HR, RR and patient comfort Warm Food and water Hospitilisation duration: 1-2 days if SX
