Dog and Cat 8 Flashcards
Carpus arthrodesis how common, indications and what need to identify beforehand
- Most frequently arthrodesed joint • Indications: - Carpal hyperextension injury - high-rise syndrome - Joint luxation - Chronic, severe OA • Identify the LEVEL of injury - Palpation - Stress Radiography • Identify concurrent injury: - Collateral ligaments - Metacarpal fracture
Pancarpal arthrodesis what use
- plate fixation
- ESF
- Cross pinning (small animals only)
- THEN at least 8 weeks of a cast or splint
• Evolution of implant design: - DCP (dynamic compression plate) -> Hybrid -> Castless PCA
- Compression holes
Partial carpal arthrodesis what involved and why and the 2 main techniques used
- 80% of carpal motion at antebrachiocarpal joint
- Partial carpal arthrodesis – fusion of intercarpal and carpo- metacarpal joint
- Ensure no involvement of the antebrachiocarpal joint (difficult)
- Cats requirement for supination?
• Techniques: - Plate Fixation - T plate
- Pins (Very small animals only)
Stifle athrodesis indications and technique
• Indications: - Severe degenerative joint disease: - Intra-articular fractures - OCD - Instability from collateral or multiple ligament injury • Technique: - Plate fixation (pin techniques in small animals) - Maximise bone contact area by removal of intra-articular structures: ○ Cranial & Caudal Cruciates ○ Menisci - Long Lever arms – bone fracture - Compression
Stifle arhrodesis complications
1) Implant failure: ○ Insufficient bone contact ○ Cycling 2) Fracture: ○ Long Lever Arms ○ Plate Span 3) Infection: ○ Strict asepsis Consequences - implant removal
Hock arthrodesis how common, indications and what need to idetnfiy
• Indications: - Severe degenerative joint disease: - OCD - Joint Instability - Shearing Injury - Calcanean Tendinopathy - Hyperextension Injury • Identify LEVEL of injury: - Palpation - Stress Radiography • Identify concurrent injury
Hock arthrodesis technqiues and complications
Techniques: - Plate fixation (Cranial vs Medial) -> medial - ESF - Pin and Tension Band Wire - Pantarsal vs Partial Tarsal Arthrodesis: ○ Calcaneoquartal ○ Tarso-metatarsal • Complications - Plantar necrosis
Total hip replacement indications, outcome and complications
Indications:
- Severe degenerative joint disease (CHD) -> due to hip dysplasia
- Fractures of the femoral head/neck
- Salvage following acetabular fracture repair
- Avascular necrosis of the femoral head
- CONSIDERED - gold standard
Outcomes
- Good to excellent outcomes in 80-98% cases
Complications:
- Coxo-femoral Luxation - can revise the surgery and change the head size
- Sciatic neuropraxia
- Aseptic loosening
- Infection - require removal
Total hip replacement what are the 2 main techniques what provides stability
- Cemented:
- Polymethylmethacrylate - cohesive interface btn implant and bone
- Good early stability
- Aseptic loosening:
○ Enzymatic osteolysis
○ Cytokine induction of osteoclasts - > Bone Resorption - Uncemented:
- Press-fit or monocortical screws (early stability)
- Meticulous preparation
- Osseous integration with micro-interlock (Late stability)
Elbow total replacement indications, 2 techniques and 4 complications
Indications: - Severe bi-compartmental disease: - OCD - Coronoid process disease - Not luxation • Techniques - Lowa - TATE • Complications: - may result in amputation or arthrodesis 1. •Fracture 2. • Luxation 3. • Persistent lameness 4. • Infection
Stifle total replacement indications and complications
• Indications: - End-Stage OA: ○ OCD ○ Cruciate disease - Combination System: ○ Press-fit Femoral component ○ Cemented Tibial component • Complications: - Luxation - Infection - Aseptic loosening
Stifle total replacement outcomes
- Improved ROM - RANGE OF MOTION
- Improved objective functional data:
○ PVF 80% normal contralateral
○ Impulse 90% normal contralateral
Femoral head and neck excisional arthroplasty indications
- Fractures of the femoral neck or head
- Slipped capital physis (cats)
- Avascular necrosis of the femoral head (dogs)
- Chronic coxofemoral luxation
- Failed total hip arthroplasty
- Severe OA secondary to CHD & not palliated by medical management)
Femoral head and neck excisional arthroplasty technique and what equipment used and what done at the end
- Craniolateral approach to the hip joint
- Disarticulation if required
- External rotation of the femur
- Parallel to sagittal plane of neck:
○ Prevent caudal spur formation - limits the range of motion
1. • Oscilating Saw (preferred)
2. • Gigli Wire
3. • Osteotome & Mallet - Check cut surface of proximal femur before you close -> need to ensure take whole neck out
4. Rasp if spur present
5. Post-operative radiograph - to ensure you take enough
Femoral head and neck excisional arhtroplasty what are the 7 complications
- Infection
- Seroma
- Persistent lameness (leg shortening)
- Muscle atrophy
- Decreased ROM (extension and abduction)
- Patellar luxation
- Sciatic neuropathy
Femoral head and neck excisional biopsy outcome and how modified
- Never return to normal function based on PVF (PEAK VERTICAL FORCE) and impulse.
- Modified by:
○ Surgical technique (failure to remove all femoral neck)
○ Duration of clinical signs (muscle atrophy)
○ Age (immature vs mature)
○ Post-operative care (physiotherapy)
○ Body weight/condition
• Published outcomes: - Largely subjective
- Acceptable function
Excision arthroplasty of the glenoid when used, indications and outcomes
- Salvage for severe OA of the glenohumeral joint in small dogs
• Indications: - Glenoid dysplasia
- Chronic shoulder luxation
• Acceptable outcomes in limited numbers of cases in small dogs
Intraoesseous transcutaneous amputation prosthesis what are they, used for and complications
- Osseous and dermal integration of implants – robust prosthetic integration
- Partial amputation
• Complications: - Infection
- Epidermal ingrowth
- Marsupialisation
- Peri-prosthetic fracture
Oncologic limb sparing 2 main indications what is involved
• Indications: - Neoplasia of the extermities (OSA) - Distal radius • The affected bone is resected with appropriate margins (3cm) • Antebrachiocarpal disarticulation • Replacement of the missing segment: - Cortical allograft (bone bank) - Metal endoprosthesis - Ulnar rollover - Bone transport osteogenesis
Axial skeleton disease what commonly lead to and conditions involved
- Diseases that affect the axial skeleton frequently cause dysfunction of the bone or nervous system (brain and spinal cord)
- These conditions include congenital malformation, neoplasia, infection, and trauma resulting in fracture / luxation.
Congenital malformation and neoplasia of axial skeleton what involved
- Congenital malformation
- Atlantoaxial luxation/subluxation
- Cervical vertebral malformation (Wobbler) -
stenosis - Neoplasia
- Oral and skull neoplasia (MLOs)
- Primary and metastatic neoplasia of vertebral body
Infection of axial skeleton what called, common infection, how arrive, what leads to
Discospondylytis
- Infection in vertebral endplates
- Most commonly bacterial infection but can be fungal infection
- Haematogenous spread -> from urinary tract infection
- Lumbosacral disc space
- Loss of structural stability of the vertebrae and impingement of the spinal cord causing pain and neurological dysfunction
Instability/degeneration/trauma of oxial skeleton what are the 3 main diseases and what result in
1) Vertebral fracture / luxation
○ Severe trauma results in unstable vertebral column and varying degrees of spinal cord compromise
○ Can result in complete core transection -> BAD
2) Lumbosacral disease / instability
○ Can lead to budging of the disc - putting pressure on nerve
§ Lumbosacral pain and ataxia can result
3) Intervertebral disc disease
Musculoskeletal neoplasia what is the most common form and some other causes
- The most common form of primary bone cancer (85% of all cases) in dogs and cats is osteosarcoma (OSA).
- Other types of primary bone cancer
○ Chondrosarcoma
○ Fibrosarcoma
○ Haemangiosarcoma - Metastatic (secondary) neoplasia of the bone is less common in companion animals than it is in people.
Osteosarcoma distribution - common signs and signalment
Distribution
- OSA most commonly affects the appendicular (75%) vs. axial skeleton (25%)
○ ‘Away from the elbow, towards the knee’ - mainly in forelimb
○ FL 2.5 x HL - more common in forelimb
§ Proximal humerus
§ Distal radius ** - MOST COMMON SITE
§ Distal femur
§ Proximal / Distal tibia - hindlimb
§ Axial skeleton (skull, spine, ribs)
Signalment
- Typically affects large to giant breed dogs
- Middle to older aged (7-9 yrs)
- ? Males > females, neutered > non neutered
Osteosarcoma character and prognosis with different treatmetn options
- OSA is an aggressive tumour with local invasion and destruction and high metastatic potential - NOT GOOD
- Expected median survival time (MST):
○ Amputation and chemotherapy - curative intent treatment -> CANNOT CURE but best option
§ MST 250-350 days (8-11months) - quality of life is good
§ 2 year survival time of 20%
§ 3 year survival time of 10%
○ Amputation alone
§ MST 4-5 months
Osteosarcoma risk factors and poorer prognosis
- Negative prognostic factors for both mortality and metastasis
- Tumor location
○ Proximal humerus, distal femur, proximal tibia -> higher muscle mass so less likely to detect mass earlier
○ MST for prox. humerus is 132 days < other locations - High ALP levels
○ Dogs with ↑ ALP lived 156 days less than dogs with normal ALP - Increasing body weight
- Stage III disease (mets to lungs, bones, LNs)
○ Mets to bone (130d) longer MST than mets to lung (59d) or LN (59d)
Osteosarcoma diagnosis 6 options
- Signalment
- Clinical history - can present as lameness
- Clinical Pathology –ALP
- Radiographs
○ mixed lytic and proliferative pattern - sunburst affect - Cytology (ALP staining)
○ Fine needle aspirates -> medullary sample - Biopsy (Jamshidi needle core)
Want to get the central part of lesion -> don’t want to go through the bone
Osteosarcoma what are the 5 steps in staging
- 3 view thoracic radiographs - 2 laterals and ventrodorsal
○ 10% dogs have macroscopic mets at Dx - Thorough orthopaedic exam - can they tolerate an amputation
○ Bone is 2nd most common site of metastasis - Nuclear Scintigraphy –Tc99-m - screen whole body for metastasis to other bones
- Evaluate regional lymph nodes
○ Axially and prescapular lymph nodes if forelimb - Whole body CT or MRI or radiographic survey
Osteosarcoma treatment goal and the 2 main types of treatment
- Effective treatment requires careful diagnostic workup and communication with the patient owner about expected outcome of treatment
- Goal of therapy is best QOL for patient
a. Curative Intent
b. Palliative therapy
1. Curative Intent
2. pallitative therapy
Curative intent treatment for osteosarcoma what is the goal, how achieve and the 2 main options and complications with this
- Goal is to provide best quality of life AND extend life for as long as possible
- Local tumour control can be achieved with either amputation or limb salvage
- Control of metastatic spread requires the use of adjuvant chemotherapy
○ Carboplatin
1. Amputation -> steps on previous lecture
2. Limb salvage - forelimb - Resect OSA affected bone
- Replace bone defect with metal endoprosthesis or cortical allograft
- Distal radius most successful
- Complications
○ Implant failure
○ Infection -↑ survival time
○ Local recurrence - 30% of cases - Equivalent MST with chemotherapy to amputation + chemotherapy
Osteosarcoma palliative therapy what is the goal and 5 options
- Goal is to provide best quality of life but not necessarily extend duration of life
1. Amputation –pain control
2. NSAIDs, Analgesics
3. Bisphosphonates –pamidronate, zoledronicacid -> inhibit osteolysis -> used for osteoporosis in people
○ Inhibits osteoblasts -> inhibits ongoing bone destruction
4. Radiation therapy
○ 75% good to excellent analgesic response for 3-4 months
○ Radiopharmaceuticals –Samarium-153
5. Combination therapy
○ XRT + Chemo + bisphosphonates
Palliative therapy osteosarcoma disease progression within
- Disease Progression
○ Development of metastatic disease
○ Pathologic fracture - generally leads to euthanasia decision -> cannot heal
○ MST > amputation alone but < curative intent
§ XRT + Chemo longest MST
Chondrosarcoma how common, common sites, character and median survival
○ Second most common primary bone
○ Nasal cavity = most common site
○ Flat bones (ribs, pelvis, scapula)
○ Slower progression, slower metastasis - chemotherapy not needed
○ *Grade may influence
○ Median survival = 979 days (2.7 yrs) surgery alone
Metastatic bone neoplasia how common in dogs, commonly from what cancers
- Rare in dogs compared to people
- Commonly from carcinomas
○ bladder, prostate, mammary
○ squamous cell carcinoma
○ diaphysis (nutrient foramen) - Sarcomas
○ especially following chemotherapy
Skull neoplasia what is the most common one, location, breed, radiographic findings, character, histological grade prognosis, prognosis and adjuvant therapy
MLO - Multilobular Osteochondrosarcoma (MLO)
- Affects flat bones of the skull
○ Maxilla, mandible, calvarium
- Older, medium-to large-breed dogs
- On radiographs, mass with nodular or stippled mineralized densities and lysis of bone
○ “Popcorn ball” appearance
- Slow-growing, locally invasive tumor with moderate metastatic potential
- Histological grade prognostic
○ Higher grade more aggressive biological behaviour
- Good Px if complete excision
- Adjuvant therapy no proven benefit
Oral neoplasia what are the 6 general appraoch to the diagnosis and management of oral massess
1. Biopsy the lesion THROUGH THE MOUTH (inside out) -malignant or benign ○ Bx from oral side not from skin side ○ Tumour type, grade 2. Radiology / CT of mouth / head / neck ○ Sx planning, staging, osteolysis 3. Assess regional lymph nodes ○ Palpation, FNA Cytology +/-biopsy 4. Tumour Staging ○ Thoracic radiographs or CT ○ Regional LN evaluation 5. Radical surgical excision ○ Maxillectomy or mandibulectomy 6. Adjunct therapy ○ Radiation (XRT), Cryotherapy, tumour vaccine
Oral neoplasia clinical signs and most common ones in dogs and cats
Clinical Signs - Mass in mouth - Halitosis - Dysphagia - Bloody discharge - Loose teeth (esp. SCC) - Drooling* - Poor grooming* -> * esp. cats Dogs - melanoma, then SCC, then fibrosarcoma Cats - SCC - can look like resorptive lesions
Malignant oral tumours list the 3 main ones and the 2 main benign ones
1) malignant melanoma
2) squamous cell carcinoma
3) fibrosarcoma
Benign
1) papillomas
2) fibromas
3) odontogenic tumours
4) epulides
Malignant melanoma what age generally occur in, location, character, types, treatment and prognosis
- Older animals
- Gingiva, mucosa, palate and tongue
- Locally invasive
- Met rapidly to the lungsand regional LNs
- Melanotic or amelanotic form - doesn’t have to have pigment
- Treatment: Wide excision, cryotherapy, immunotherapy (Oncoceptvaccine) - quite effective
- Prognosis: Guarded MST 8-9 months
Squamous cell carcinoma in oral cavity location, character, how common and treatment
- Tonsillar crypts or on the gingiva.
- Locally invasive
○ Except for the tonsillar form, which are highly malignant, only 10% metastasise - Most common oral tumour in cats
- Treatment: Wide excision can be curative
○ Radiosensitive, cryosurgery
Fibrosarcoma of oral cavity location character, recurrence, treatment and type within goldern Ret
- Maxillary gingiva and hard palate and
- Aggressively locally invasive
- Recurrence following excision is common
- Treatment: Wide surgical incision, cryosurgery
○ They are not radiosensitive - Hi-Lo FSA in Golden Ret. Histologically benign appearance but biologically aggressive
Papillomas and fibromas of oral cavity character and common age
Papillomas
- Younger dogs and may be solitary or multiple
- These tumours will normally regress with age
Fibromas
- These are rare benign tumors of the oral cavity
Odontogenic tumours and epulides of the oral cavity, how common, main types and treatment
Odontogenic tumours
- Rare tumours which arise from the dental laminar epithelium
- Ameloblastomas being the most common
- They require radical excision or cryotherapy
Epulides
- The most common type of benign tumours
- 3 types described:
○ Fibromatous, ossifying, acanthomatous
- All arise from the periodontal ligament
- Treatment: excision, curetage, radation.
- Acanthomatous epulides, whilst benign, are regarded as very invasive and require wide excision with maxillectomyor mandibulectomy
What are the 5 main respiratory mechanisms
- Sneeze/ Reverse Sneeze
- Cough
- Nasal discharge
- Dyspnoea
- Stridor/Stertor
Sneezing what is it, why occurs, accompanied by and differential fr sneezing with and without discharge
- An explosive release of air from the lungs through the nose and mouth
- A protective mechanism to rapidly remove chemical and physical irritants from the nasal epithelial surface
- Often accompanied by nasal discharge
- Need to look at environment pollutants, stress (stocking density) etc.
Sneezing without discharge
1. Acute Foreign Body
2. Acute Allergic Process
Sneezing with discharge - Did it start serous and then become purulent?
- Cats- FHV,FCV
- Dogs -> rare to be just bacterial infection -> don’t just give antibacterial
Reverse sneezing why occurs, purpose and cause
- Usually nasopharyngeal irritation - generally quite benign
- Purpose is to move secretions and foreign material into the orophranyx so it can be swallowed
- Causes– excitement, epiglottic entrapment of the soft palate, nasal mite, viral infections, foreign bodies
Snuffling cause and when an issue
- Usually because the nasal passages are congested
- Not too much of a problem EXCEPT in nasal obligate breathers
○ Cats– respiratory viruses
○ Rabbits – bacterial infection often secondary to teeth problems
○ Obligate nose breathers such as horses and especially, rabbits and rodents can be greatly affected by nasal discharge that block the nasal passages
Cough define, stimulatedand types of cough
- Sudden noisy expulsion of air from the lungs against a closed glottis
- Stimulated by mechanical or chemical irritation of the pharynx, larynx, trachea, bronchi and smaller airways
- Categorise
○ Dry C⁺⁺– cough without expectoration
○ Productive C⁺⁺– material expectorated(maybe swallowed)
○ Goose honk C⁺⁺ -chronic , harsh dry cough characteristic of collapsed trachea
○ Nocturnal C⁺⁺- associated with the initial phase of cardiac disease, psychogenic coughing or collapsed trachea
Causes of cough
- Less common causes– pleural, pericardial, diaphragm, nasal, nasal sinuses and mediastinal disease
- If infection is it contagious?
○ Dogs- Kennel cough - give anti-inflammatories
○ Cats - Respiratory viruses FCV/FHV
○ Equine- influenza, strangles, herpes virus - Or opportunistic– eg. Pasteurella in rabbits - not contagious
Dyspnoea prolonged inspiratiory phase with and without noise what location is the problem most likely and same with prolonged expiratory phase
-Prolonged inspiratory phase with noise is likely to be an upper airway problem - stridor
-Prolonged inspiratory phase with no noise— think pleural space problem
§ Think pleural fluid, mass, abdominal organ through a hernia of the diaphragm
§ The respiratory rate is usually increased
-Prolonged expiratory phase why is it hard to get the air out?
§ Think small airway disease such as COPD (chronic obstructive pulmonary disease) in horses, asthma in cats
pleural space problem what is important with the examination
□ Auscultate the chest to see if chest sounds are increased, normal or decreased
□ Check ventrally and dorsally
® Loud/normal dorsally dull ventrally–pleural fluid highly likely
® Loud ventrally, dull dorsally – pneumothorax highly likely
® Loud all over lungs- harsh or crackles – diffuse disease often mixed respiratory pattern (insp and exp)
® Oedema – cardiogenic or non-cardiogenic
◊ Listen for murmurs, gallop rhythms
◊ Non cardiogenic – strangulation, head trauma, seizures, electrocution
® Dull in parts- aspiration pneumonia?, pulmonary contusions
Stridor define, what need to determine, what may need and common cause in old dogs
- Shrill harsh sound especially the respiratory sound heard during inspiration in laryngeal obstruction
- Does it only occur with exercise or at rest - rest brachycephalic
- May need tracheostomy or other form of oxygen delivery before diagnostics are performed
- Old dogs– laryngeal paralysis – usually chronic, worse in summer as unable to thermoregulate as efficiently, often there is a history of voice change (may be chronic -> history within the past year)
- May be at rest but often early in course of disease clinical signs seen with exercise or stress
Stertor what is it and due to
- Snoring, sonorous respiration
- Usually due to partial obstruction of the upper airway eg laryngeal stenosis, nasal obstruction, pharyngeal obstruction
what are the steps in normal inspiration
• contraction of diaphragm
⇓
• expansion of thorax
⇓
• drop in pressure in pleural cavity (754 mm Hg)
⇓
• expansion of lungs and drop in intra-alveolar pressure
⇓
• airflow down pressure gradient into lungs (until pressure equal to atmospheric pressure)
Paradoxical abdominal movement what occurs and causes
- The diaphragm is pulled inwards because the lungs are not expanding as they should
- Diffuse parenchymal lung disease causing poor lung compliance eg fibrosis, neoplasia
- Upper airway obstruction
- Diaphragm dysfunction
- Pleural space disease
Assessment of normal breathing what is the normal RR, respiratory pattern and effort
- Respiratory rate - 15-25bpm
- Normal respiratory pattern
○ Diaphragmatic contraction accounts for 70-80% of a resting inspiration
○ Diaphragmatic contraction results in passive abdominal movement
○ On inspiration, chest and abdomen move out - Normal respiratory effort
○ Inspiration is active, but effortless
○ Expiration is passive
Pulmonary auscultation what do harsh, crackles, wheezes indicate as well as absent lung sounds, what sounds hear of trachea, bronchoal tree and alveolar tree
- Harsh, crackles, wheezes
○ Crackles caused by fluid or alveoli opening and closing
○ Wheezes caused by narrow airways
Absent lung sounds = pleural space disease; no flow
Tracheal sounds -> soft no crackles
Bronchoal tree -> hear heart on background, increased sound due to turbulence
Alveolar sounds -> becoming softer again
What are some common clinical signs of dyspnoic patients
- Tachypnoea -> Increased abdominal movement
○ Paradoxical abdominal movement
○ Extended neck and abducted elbows (orthoponea) - indicated very severe dyspnoea
○ Open mouth breathing -> less resistance through mouth than nares
○ Cyanosis
○ Lateral recumbency
BEWARE -> of rapidly changing body position and pupillary dilation in cats
What are 6 anatomic origin of dysponea and location generally for increased inspiratory, expiratory and inspiratory and expiratory effort
- Upper airway
- Small airway
- Pulmonary parenchyma
- Pleural space
- Chest wall and diaphragm
- Look-alikes
Increased inspiratory effort
- Upper airway obstruction (stretor or stridor)
- Severe pleuritis (chronic pleural effusion)
Increased expiratory effort
- Small ariway disease
Increased inspiratory and expiratory effort
- Pulmonary parenchymal disease
List 4 main dog and 3 main cat upper airway diseases/conditions
- Dogs ○ Laryngeal paralysis ○ Brachycephalic airway disease ○ Tracheal collapse ○ Upper airway inflammatory polyps or neoplasia - Cats ○ Laryngeal neoplasia - LSA v SCC ○ Nasopharyngeal polyps ○ Laryngeal paralysis
What are the 3 main clinical signs of upper airway disease
- Dynamic v fixed obstruction
○ Dynamic = inspiratory dyspnoea -> due to pressure change inspiratory will be worse
○ Fixed = inspiratory AND expiratory dyspnoea - Long inspiratory phase - stretor or stridor
○ Stretor = nasopharyngeal - snoring sound
○ Stridor = laryngeal - Paradoxical abdominal movement - SEVERE DISEASE
small airway what are the 2 main diseases and clinical signs
- Lower airway disease (Asthma) in cats
- Chronic bronchitis in dogs
- Clinical signs
○ Increased airway resistance
○ Air trapping
○ Expiratory push
○ Cough
Pulmonary parenchyma disease what are the 6 main causes and clinical signs
Causes
1. Pulmonary oedema - cardiogenic vs non-cardiogenic
2. Pneumonia
○ Puppies with complicated bordatella infection
○ Old dogs with aspiration pneumonia
3. Pulmonary haemorrhage
○ Pulmonary contusions, rodenticide, ITP
4. Pulmonary thromboembolism
5. Severe, diffuse, metastatic disease (neoplasia)
6. Interstitial disease
○ Interstitial fibrosis in west highland white terriers
Clinical signs
- Short, shallow breaths = can be subtle
- May hear crackles
Pleural space disease what are the 5 main causes and clinical signs
Cause 1. Pneumothorax ○ Traumatic v spontaneous v iatrogenic 2. Hydrothorax ○ Congestive heart failure 3. Pyothorax 4. Haemothorax ○ Trauma vs coagulopathy v neoplasia 5. Solid tissue Diaphragmatic hernia (organs), neoplasia Clinical signs - Paradoxical (asynchronous) abdominal movement during inspiration - Dull lung sounds ○ Ventrally dull - fluid ○ Dorsally dull - air ○ All over for severe fluid and air accumulations - Inspiratory dyspnoea with chronic pleural effusions/pleuritis
Chest wall and diaphragm what are the 4 main conditions within that lead to dyspoea
1. Thoracic muscle paralysis ○ Lower motor neuron disease ○ Cervical spinal disease ○ Fish mouth breathing 2. Diaphragmatic hernia ○ Congenial vs traumatic 3. Phrenic nerve transection 4. Flail chest ○ Flail segment in the chest - generally ribs fractured in multiple areas § Section of chest moves in opposite direction of what the chest should do
List 6 conditions that look like respiratory disease by leading to dyspnoea
- Metabolic acidosis
- Sepsis - cytokines can react with respiratory centre
- Hyperthermia
- Pain
- Anxiety/fear
- Drugs (opioids, steroids)
What are the 3 most common things dyspnoeic animals will have after trauma and others
○ Pulmonary contusions ○ Pneumothorax ○ Haemothorax 3 MOST COMMON ○ Diaphragmatic rupture ○ Flail segment ○ Upper airway rupture ○ Neurogenic pulmonary oedema ○ Spinal cord injury
What are the 3 main things that cause dyspnoeic cats, what most common in and general clinical signs
1) Cardiogenic pulmonary oedema § Skinny old cats, young cats § Gallop rhythm or heart murmur +/- thyroid slip § Hypothermic 2) Pleural effusion § CHF, Pyothorax in young cats § Muffles heart and lung sounds, hypothermic 3) Lower airway disease § Younger cats § History of COUGH § Hyperthermia
What are the 3 main things that causes dyspnoea in small breeds and 2 in brachycephalic breeds
- Old toy and small breed dogs ○ Cardiogenic pulmonary oedema ○ Collapsing trachea ○ Mitral valve disease - Brachycephalic breeds ○ Upper airway obstruction ○ Aspiration pneumonia
what are the 2 main causes of dyspnoea in large breeds and 3 in puppies
- Old large-breed dogs ○ Laryngeal paralysis ○ Cardiogenic pulmonary oedema § Dobies and giant breeds § Typically have an arrhythmia - Puppies ○ Neurogenic pulmonary oedema ○ Pulmonary haemorrhage - rodenticide toxicity ○ Pneumonia § Bacterial or viral
What are the 7 main diagnostics to run on dyspnoeic patient and when don’t perform
- Upper airway exam
- Thoracic ultrasound (TFAST)
- Thoracic radiographs
- Arterial blood gas analysis
- CT scan
- Tracheoscopy/bronchoscopy
- Airway cytology
Unstable patient -> DO NOT PERFORM ARTERIAL BLOOD GAS/RADIOGRPAHS
- No stress, supplemental oxygen needed
Quantifying hypoxaemia what are the 2 ways, when do and what is cyanosis
- No immediate need if dyspnoeic!
- If signs are subtle, or you are unsure
1. Pulse oximetry
2. Arterial blood gas - Cyanosis
○ Life-threatening hypoxaemia
○ PaO2 20-40mmHg, >5g/dL deoxyhaemoglobin
○ Difficult to see with severe anaemia
Arterial blood gas what are the 3 ways to get information and which are the best with normal ranges and what ranges have clinical significance
1. Arterial blood gas - GOOD ○ PaO2 normal = 80-100mmHg 2. Venous blood gas - NOT SO GOOD ○ PvO2 normal = 40mmHg 3. O2 saturation of Hb ○ SaO2/SpO2 > 90% at PaO2 of 60-70mmHg Sig - PaO2 values <75mmHg ○ Treated with oxygen supplementation - PaO2 values <55mmHg ○ Life-threatening and required immediate action
Pulse oximetry how done, location, normal and acceptable levels
- Optical transcutaneous non-invasive method
- Continuous measurement
- Sensory on
○ Pinna, lip, skin fold, toe, tongue
Normal = 95-99% Acceptable = 93-99%
SpO2 95% = PaO2 90mmHg
SpO2 93% = PaO2 80mmHg
SpO2 90% = PaO2 60mmHg - Curve starts to get step at this point
What are the 5 ways to supplement oxygen in dyspnoeic patient and how to assess if working
1) flow by oxygen
2) oxygen mask
3) nasal oxygen catheters
4) oxygen hood
5) oxygen cage
Assess
1. Assess for improvement of respiratory distress
2. Pulse oximetry: SpO2
Flow-by oxygen and oxygen mask what makes them good and bad, flow rate and when used
- Flow-by oxygen
○ Easy and well tolerated
○ Tubing help closely to animals nostril/mouth
○ 2-3 litres per minute of oxygen
○ FiO2 achieved: 0.25 to 0.4 (25-40% inspired oxygen)
○ Useful when performing initial evaluation, not for long-term
○ Able to analyse the head - mucous membranes etc. - Oxygen mask
○ Easy and cheap
○ Stressful for some patients, OK when sedated
○ May require restraint
○ Useful when performing initial evaluation
○ Relatively low inspired oxygen concentration
○ Flow depends on size of animal and of mask
○ Avoid risk of rebreathing (CO2 accumulation) - respiratory acidosis
Nasal oxygen catheters what need to give, how to apply and flow rate
○ Local analgesia (and wait)
○ Measure to medial canthus
○ Anchor as close to nose as possible - otherwise will shake off
○ Tape butterflies and suture or super glue
○ Variable inspired oxygen concentration
○ 100mL/kg/min will achieve FiO2 = 0.4
§ If use two can get up to 80%
○ Humidification of gas -> need to occur as otherwise dry and will result in dry airways
Oxygen hood and cage which preferred, what need to do, why good and bad
Oxygen hood - not preferred ○ Elizabethan collar (cone) ○ Clear plastic wrap over the top with a hole ○ No access to the patient - especially around the head ○ Moisture accumulation ○ Carbon dioxide accumulation ○ FiO2 = 0.3 to 0.4 Oxygen cage ○ HIGH inspired oxygen concentrations ○ LOW STRESS environment ○ Relatively EXPENSIVE ○ Limited ACCESS to patients ○ Temperature/humidity ○ Accumulation of CO2
What are the 3 main mechanisms of hypoxaemia and causes within
- Low inspired oxygen partial pressure
○ Low FiO2
○ Low barometric pressure (high altitude) - Hypoventilation
○ CO2 production > CO2 elimination
○ Higher PACO2 - respiratory acidosis
§ Normal PaCO2 = 35-45 mmHg
○ This increase results in a decrease in pressure of other gases including PaO2 in the alveoli - Pulmonary gas exchange abnormalities: venous admixture
○ Anatomic shunt (right to left)
○ Perfusion of poorly ventilated lung areas
○ Oxygen diffusion impairment
What are the 8 main causes of hypoventilation
- Airway obstruction
- Neuromuscular disease
- Anaesthesia
- Spinal cord dysfunction cranial to C4-C5
- Phrenic nerve dysfunction
- Chest wall injury
- Respiratory fatigue
- Excessive CO2 production (malignant hyperthermia)
Management of upper airway obstructive what are the 3 things that need to occur
- Oxygen supplementation
- Reduce Tissue metabolism to reduce CO2 production
And only if dyspnoea continues despite maximum oxygen supplementation - Increase Alveolar ventilation
Reduced CO2 production in tissues what are the 2 ways to do it
1) sedation - acepromazine, butorphanol, midazolam
2) reduction of body temperature - body surface wetting, ice packs, radiation, cool intravenous fluids NOT NSAIDS
In terms of sedation when trying to reduce CO2 production in dysponeic patient what are pros and precautions
○ Pros
§ Anxiolysis - reduced of oxygen consumption
§ Reduced metabolic heat production -> hyperthermia decrease
§ Less respiratory drive -> dynamic airway collapse decrease
○ Precautions
§ Cardiovascular collapse
§ Relaxation of pharyngeal dilator muscles -> airway collapse increase
§ Less respiratory drive -> respiratory arrest
What is the main way to increase alveolar ventilation for dyspnoeic patients when would you do it and goal
- Intubation - make airway patent again ○ Severe respiratory distress alone! § High grade upper airway obstruction or acute with high PvCO2 § Chronic upper airway obstruction with worsening pH § No improvement upon O2 and sedation ○ Goal § Preserve the patient's life § Safe diagnostics § Etiological treatment
Pulmonary gas exchange abnormalities leading to hypoxaemia what results from 3 main mechanisms and pathogenesis
- Degree of admixture of venous (non-oxygenated) blood with pulmonary end-capillary (oxygenated) blood
- Mechanisms
○ Anatomic shunt (right to left)
○ Diffusion impairment
○ V/Q mismatch: perfusion of poorly ventilated lung areas
Pathogenesis
○ Normal
§ Venous blood moves alongside alveoli where gas exchange occurs then moves into arterial blood system
○ Venous admixture
§ Flooded or collapsed alveolus without O2 HOWEVER venous blood still perfuse this area -> no arterialised blood from this section resulting in mixture of arterial and venous blood leaving the lungs -> low oxygen content
Wha are the main causes of pulmonary gas exchange abnormalities leading to hypoxaemia
○ Pulmonary parenchymal disease § Pulmonary oedema □ Cardiogenic or non-cardiogenic § Pneumonia § Pulmonary contusions § Atelectasis § Lung collapse: pneumothorax, pleural effusions § Pulmonary thromboembolism
What are the 5 steps in emergency management of dyspnoeic patient
- Oxygen supplementation and no stress
- Rule out or treat pleural effusion/pneumothorax
- Auscultation, US, thoracocentesis (Diagnostic and therapeutic) - Treat for the treatable in severely dyspnoeic cats
○ Empirical furosemide, terbutaline, corticosteroids - Give furosemide (diuretic), if CHF (cardiogenic heart failure) is likely
○ 2-4mg/kg, then 2mh/kg every hour until more comfortable
○ Not useful for cardiogenic pleural effusion - Sedation can be beneficial and humane
What to do if the 5 step emergency management of dyspnoea doesn’t work
INTUBATION/VENTILATION
- mechanical ventilation
- prssure-controlled ventilation
- volume controlled ventilation
Mechanical ventilation what for, what is good and bad about it
§ For ventilatory failure (hypoventilation)
§ For severe gas exchange abnormalities
Good
§ Allows 100% inspired oxygen concentrations
§ Full control of ventilation and oxygenation
□ Rate, pressure, volume, inspiratory time § Positive pressure and PEEP (positive end-expiratory pressure) - to open up the alveoli for perfusion
BAD
§ Expensive and very labour intensive
§ Long term <24 hours: intensive care unit
Pressure-controled ventilation and volume control ventilation which is preferred and what is controlled and variable
Pressure-controlled ventilation -> preferable to protect against too high pressure
§ Present inspiratory pressure is delivered to patient - once pressure delivered then expiration
§ Pressure constant, volume variable
Volume-controlled ventilation
§ Present tidal volume is delivered to patient - once volume delivered then expiration
§ Volume constant, pressure variable
how to set up pressure and volume controlled ventilation
Start setting for volume controlled
§ Tidal volume = 8-10mL/kg
§ Respiratory rate = 15-20 breaths per minute
§ Inspiratory: expiratory ratio = 1:2 (or I=50% of E) (inspiratory phase shorter than expiratory phase)
§ 100% oxygen
§ PEEP (positive end-expiratory pressure) = 5cm H20
- Follow by adjusting volume and respiratory rate to patient needs
§ Oxygenation: PaO2 and/or SpO2
§ Ventilation: PaCO2 or PvCO2 or PetCO2
Start setting for pressure controlled
§ Inspiratory pressure = 10cm H2O above PEEP
§ REST AS ABOVE
List some common, less common and uncommon signs of nasal disease
Common
- Sneezing
- Stertor (snoring or snorting sounds)
- Nasal discharge
Less common
- Facial pain or deformity, epiphora
- Depigmentation or ulceration of the nasal planum(fungal)
Uncommon
- Systemic signs (lethargy, inappetence, weight loss) - generally stay localised to the nose
- Central nervous system signs -> through cribriform plate into brain
- Open-mouth breathing (with severe nasal obstruction)
What are the 3 main clinical signs of nasopharyngeal disease and possible causes
1) Stertor (also oropharyngeal)
2) Reverse sneezing - forceful inspiration -> clear nasopharyngeal area
○ Small breed terrier dogs more common -> acute don’t worry about
§ Trickle of water or syringe of water will stop the tickle in the throat
○ Nasal mites, irritation or more significant diseases
3) Gagging/retching
○ Also with post-nasal drip
What are the most common causes of uni and bilateral nasal discharge
- Unilateral ○ FB ○ Tooth root abscess/ oronasal fistula - Bilateral ○ Infectious disorders ○ Idiopathic inflammation ○ Systemic conditions - Either (may progress) ○ Neoplasia ○ Fungal ○ Polyps ○ Bilateral processes
what are the 7 main things need to do for a physical exam of nasal discharge
- Body condition
- Nasal or lacrimal discharge
- Facial symmetry and pain, oral cavity
- Gently retropulse eye -> should have some give and be symmetrical
- Palpate LNs
- Check nasal patency - if blocked and no air generally something solid
- Listen and watch breathing -> exaggerated or noise associated with breathing -> stridor or sterdor -> upper respiratory tract issues
When to investigate nasal discharge
- Acute paroxysmal sneezing in dogs ○ Dog -> foreign body generally easier to assess when early ○ Cat -> generally viral infection - Reverse sneezing if ○ Severe or progressive ○ Other respiratory signs ○ Atypical breed (nasal mites?) ○ Cats without URTI! - Facial pain or deformity - indicates destructive process - Nasal planum ulceration - Nasal obstruction - Epistaxis - Chronic nasal discharge and/or sneezing - Neurologic or systemic signs
sneezing what are the 4 main differentials and causes of serous and mucopurulent discharge
Sneezing - Nasal foreign body (esp. dogs) - Feline upper respiratory tract infection (URTI) - Canine nasal mites - Exposure to irritant aerosols Discharge - Serous ○ Normal (small amounts) ○ Viral infections ○ Irritants ○ Early stage of mucopurulent causes - Mucopurulent - not very specific -> don't learn them all ○ Viral, Bacterial, Fungal ○ Nasal parasites ○ Foreign body ○ Neoplasia ○ Nasopharyngeal polyps ○ Canine chronic L-P rhinitis ○ Feline chronic rhinosinusitis ○ Allergic rhinitis ○ Extension of oral disease
Epistaxis what are the 5 main nasal cause and some systemic causes
Nasal causes - Acute trauma - Acute foreign body - Neoplasia - common - Fungal infection - common - Other causes of MP discharge (uncommon) Systemic causes - less common -> want to rule out before biopsy - Coagulopathy - Systemic hypertension - Polycythaemia - Hyperviscosity syndrome - Vasculitis
Destructive lesions what are the clinical signs and differential diagnosis
signs - Stertor/obstruction - Facial pain - Epistaxis - Exopthalmos - Facial deformity - Naris/nasal planum depigmentation/ulceration Differential diagnosis - Tooth root abscess - Neoplasia - Fungal infection - most don't cause destruction but some can
What are the 5 things to diagnose epistaxis
1. Haematology, chemistry - is the patient anaemic ○ HCT, platelet count ○ TP, globulins 2. PT and aPTT - specific coagulopathy before do biopsy 3. Buccal mucosal bleeding time 4. vWF assay ○ affected pure breeds 5. Blood pressure
