Midsemester 1 Flashcards

1
Q

List some common diagnostic tests

A

Microbiology: infection presence (mostly G+, G- overgrowth= enteritis), resistance, antibiotic choice

Culture and sensitivity: ID organism and therapy

Haematology and biochemistries

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2
Q

What are the techniques used for haematology?

A

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

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3
Q

What are the characteristics of erythrocytes?

A

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
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4
Q

What are the characteristics of white blood cells?

A

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)
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5
Q

What are the characteristics of thrombocytes?

A

Thrombocytes:

  • extrinsic clotting factor (no platelets)->release thromboplastin
  • anti-inflammatory role
  • phagocytic
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6
Q

List the biochemicals

A

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

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7
Q

Liver disease biochem:

A

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)

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8
Q

Renal disease biochem

A

Decreased function: uric acid (produced in liver from protein->passed out through tubules-> elevate)

Hydration status: urea (over 1-2)

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9
Q

Reproductive disease biochem

A

Calcium: hypocalcaemia from eggs
Cholesterole: yolk
Triglycerides: yolk
Total protein: transport

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10
Q

GIT dx biochem

A

Na, Cl, K, amylase (broad)

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11
Q

Blood glucose biochem

A

Hyperglycaemia: DM (>33, persistent), stress, normal (artifact- RBC left in contact with plasma)

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12
Q

Lipids biochem

A

Cholesterol:

  • hepatic lipidosis
  • artherosclerosis
  • diabetes mellitus
  • hypothyroidism

Triglycerides:
- repro

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13
Q

How to interpret PCR:

A

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

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14
Q

How to interpret serology:

A
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
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15
Q

Interpreting cytology

A

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
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16
Q

Interpreting radiology

A

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
-

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17
Q

Interpreting ultrasound

A
Cheaper, less commonly used 
air sacs interfere 
USE: 
- yolk peritonitis 
- GIT dilated full of ingesta 
- nodules 
- abdominal distension
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18
Q

Interpreting computer tomography

A

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

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19
Q

Interpretation of fluoroscopy

A

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

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20
Q

Interpreting endoscopy

A

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

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21
Q

Feather function and normal feather loss

A

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
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22
Q

Describe stuck in moult

A

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
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23
Q

Traumatic feather loss causes

A

Predator avoidance
social
self-inflicted
nesting- want chicks out

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24
Q

Infectious causes of feather loss: parasites

A

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

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25
Q

Infectious causes of feather loss: bacterial and fungal

A

Secondary to trauma

  • self trauma: Quaka mutilation syndrome
  • cockatoo: axillary dermatitis
  • Ringworm/favus (uncommon): biopsy, griseofulvin, itraconazole, wash with enilconazole shampoo
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26
Q

Psittacine beak and feather disease

A

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
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27
Q

Avian polyomavirus

A

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
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28
Q

Feather damaging behaviour- disease of captivity

A

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

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29
Q

Describe the anatomy of the upper respiratory tract in birds

A

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

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30
Q

Clinical signs of upper respiratory tract

A
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
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31
Q

Sinusitis

A
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
32
Q

Chlamydiosis

A
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

33
Q

Non-infectious causes of upper resp disease

A

Functional: unlikely
External compression: fractured coracoid on trachea
Physical obstruction: pharyngeal dx, FB, millet seeds inhaled

34
Q

Tracheal diseases

A

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)

35
Q

Diagnosis and treatment of tracheal foreign body

A

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
36
Q

Diseases of lungs and air sacs

A

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
37
Q

Aspergillosis: aspergillus fumigatus

A

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
38
Q

Polydypsia

A

Water intake in excess of double daily maintenance requirement: 50-100ml/kg/day
- compare diet and species

Usually secondary to polyuria
Psychogenic

39
Q

Osmoregulation in parrots

A
Plasma osmolality 300mOsm/L 
Balance between fluid intake and urine output 
- plasma osmolality and volume 
- osmoreceptors and baroreceptors 
- kidney 
- hypothalamus 
- pituitary gland
40
Q

Avian kidneys

A

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

41
Q

Arginine vasotocin

A

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
42
Q

PU/PD

A

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:

  1. Quantify water intakes
  2. CBC and biochem: renal and liver function
  3. urinalysis- casts
  4. Heavy metal levels
  5. Radiology: kidney size, heavy metals and uroliths
  6. water deprivation tests
  7. kidney biopsy
43
Q

Diabetes mellitus

A

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
44
Q

Kidney

A

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)
-

45
Q

Gout

A

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
46
Q

Heavy metal toxicosis

A

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

47
Q

What is the sick bird look and how should you approach it?

A
  • 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
48
Q

Approach to dehydration

A
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)

49
Q

Approach to hypothermia

A

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
50
Q

Approach to catabolism

A

CS:
- anorexia, melena (autodigestion), urates smell, weight loss - breast bone

TX:

  • food and water easily accessible
  • crop gavaging (2-3 X daily)
  • oesophagostomy tube
51
Q

Approach to respiratory compromise

A

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
52
Q

Approach to pain in birds

A

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
53
Q

Approach to blood loss

A

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)

54
Q

Hospital care of sick birds

A
Security 
Warmth 
Biosecurity 
Feeding: preference, stomach tube 
Psychological care: may have to send bird home to eat
55
Q

Surgical principles in practice

A
Condition the patient 
Anaesthetic and analgesic plan 
Planning 
Patient support 
Instruments, techniques minimise tissue damage, blood loss, inflammatory response
56
Q

Prepping and draping

A

Pluck feathers (Minimal)
Chlorhexidine or povidone iodine (not alcohol)
drape with transparent drape if under 300g
towel clamps on large feathers

57
Q

Surgery pearls

A
  1. Skin is closely attached
  2. Skin is thin
  3. Fatty SQ layer (don’t hold well, but post-op swelling not as severe)
  4. Extrinsic pathway- relies on tissue damage (clamp before incise to release thromboplastin)
  5. 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
  6. avian heterophil lack lysozymes- drains won’t work
58
Q

What should you do if you cannot get primary closure?

A

Skin grafts or flaps

Secondary intention: keep wet with hydrocolloid dressing (duoderm)

59
Q

suture choice

A
Minimal reaction (avoid chromic gut) 
absorbable 
monofilament (nylon) - braided cuts 
good knot security 
Polydioxanone PDS
Polyglactin 910 (Vicryl)
60
Q

Crop surgery- ingluviotomy

A

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

61
Q

Left flank coeliotomy

A
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
62
Q

Ventral midline coeliotomy

A

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

63
Q

Orthopaedics

A

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

64
Q

Bone healing

A

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
65
Q

Types of fracture repair

A
External coaptation- splint 
Surgical: 
- IM pins 
- Plates 
- External skeletal fixation
- Tie in fixator (IM tied in to ESF)
66
Q

Aftercare of fractures

A
antibiotics 
analgesia 
physiotherapy 2-10d 
Radio assessment- 7-10 d 
Implant removal- 6-8 weeks
67
Q

Signs of pain in birds

A

Acute: fight or flight
Chronic: withdrawal- conservation response

68
Q

Effects of pain

A

Chronic pain will stimulate adrenals->corticosteroids (stress response)->slow healing-> lower recovery rates

69
Q

Principles of analgesia

A

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

70
Q

Analgesia options

A

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
71
Q

Anaesthesia in birds

A

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

72
Q

Solutions to anaesthesia complications

A

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

73
Q

Induction

A

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)

74
Q

Maintenance

A

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
75
Q

Recovery

A
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