VETM4450 - Equine Medicine and Surgery - Midterm #2

From Antonina Degroot set via quizlet

How far does the equine respiratory field reach to

The 16th intercostal space

How can horses modulate the upper airway resistance

- Dilation of external nares

- Vasoconstriction of nasal mucosa

- Dilation/stabilization of pharynx

- Increase area of rima glottidis

- Extension of head

How does inhalation modulate lower airway resistance

It dilates airways

How does exhalation modulate lower airway resistance

It narrows airways

What is the most important modulator of lower airway resistance

Airway smooth muscle

Horse normal RR (adults, foals, neonates)

Adults: 8-24 brpm

Foals: 20-40 brpm

Neonates: 60-80 brpm (this is 0-24 hours old)

Resting tidal volume

4-5 L

Exercising tidal volume

13 L

How much air can a horse breath in during maximal exercise

75 L O2/min

What is locomotor respiratory coupling

When a horse is running, their breathing is synchronized with their stride (during gathered phase, their gut contents move backwards to allow more room for inhalation, during the extended phase their gut contents move forward to push air out during expiration)

Clinical signs we see with abnormal respiratory patterns

- Heave lines

- Paradoxical respiration

- Synchronous diaphragmatic flutter

What is a stridor

High pitched inspiratory noise

What is a stertor

Low pitched, raspy inspiratory noise

Why do we hear a tracheal rattle?

Due to mucus in the trachea

What are normal airway/breath sounds created by

Airway turbulence

Where and when are normal airway/breath sounds loudest and quitest

Loudest: base of lung and on inspiration

Quietest: diaphragmatic lobes and on expiration

Describe crackles

- Short, popping sounds

- Sudden pressure equalization when collapsed airways open

- Can be from pneumonia

Describe wheezes

- High or low pitched musical sounds

- Oscillation of airways

- Caused by stenosis, compromise of lumen, thickening of airway wall

Describe pleural friction rubs

- Rubbing or creaking sound

- End of inspiration and beginning of expiration

Describe expiratory grunt

- Lound sound at end of expiration

- Indicates pain

Why may you hear no lung sounds or absent/diminished sounds

- Something like a abscess, tumour etc. could be stopping you

- Most common ventrally

Procedure for a rebreathing exam

- Place bag over both nostrils

- This causes inhalation of increasing levels of CO2

- This increases respiratory rate and depth as they try to get more oxygen

Utility of a re-breathing exam

- Enhances breath sounds

- Reveal abnormal sounds

Contradictions of a rebreathing exam

- Respiratory distress/unstable

- Severe or diffuse abnormalities

Thoracic ultrasound is useful for

- Pleural surface/superficial abnormalities

- Pleural space disease

- Some diaphragmatic hernias

Limitations of thoracic ultrasound

- Poor contact = poor image

- Aerated lung is not penetrated

Thoracic ultrasound is not useful/sensitive for

- Deep (axial) pulmonary disease

- Caudal mediastinal disease

- Axial diaphragmatic hernias

Which is more useful - U/S or rads in resp cases?

U/S typically more usefully due to size of horses

Indications of thoracic rads

- Thoracic trauma

- Unresponsive or recurrent trauma

- Extra pulmonary lung disease

- Deep lung disease

Limitations of thoracic rads

- Portable units are not capable in most ponies and horses (work for small ponies and foals)

- Summation

- Lack of orthogonal views

- Low sensitivity for small lesions

- Pleural fluid obsecures underlying structures

Indications for an endoscope

- Poor performance

- Abnormal respiratory noise

- Nasal discharge

- Epistaxis

- Coughing

- Facilitate sample collection

a dynamic endoscope can evaluate at a gallop

Limitations of endoscope?

- Size and maneuverability

- Sample collection

- May need sedation

- May induce respiratory distress

Ways to sample the upper airway

- Nasal swab

- Nasal-pharyngeal swab

- Guttural pouch fluid collection

- Biopsy of superficial lesions (cannot biopsy fungal plaques on large arteries)

Indications for a transtracheal wash

Infectious lower respiratory disease

Characteristics of percutaneous techniques for transtracheal washes

- Minimizes contamination

- More invasive

- Complications like subcutaneous emphysema and abscess or cellulitis

Indications for a tracheobronchial aspiate

Infectious lower respiratory disease

Characteristics of the endoscopic technique for the trachebronchial aspirae

- Minimally invasive

- Minimal complications

- Risk sample sample contamination - upper airway and endoscope

Indications for a bronchoalveolar lavage

Diffuse or chronic disease

Two different techniques for a bronchoalveolar lavage

- Blind (fine for diffuse disease)

- Endoscopic

Complications of bronchoalveolar lavage

- Coughing

- Trauma

- Bronchospasm

- Fever

Normal cell distribution for a tracheal aspirate

- 40-80% macrophages

- 1-50% epithelial cells

- < 20% neutrophils

- < 10% lymphocytes

- < 1% eosinophils

Normal cell distribution for a bronchoalveolar lavage

- < 530 cells/uL

- 40-70% macrophages

- 30-60% lymphocytes

- < 5% neutrophils

- < 2% mast cells

- < 0.5% eosinophils

Clinical signs of upper versus low airway disease

Upper:

- Nasal discharge

- Fever

- Lethargy

- Lymphadenopathy

- Cough

Lower:

- Cough +/- increase in respiratory effort

- Fever

- Lethargy

- Nasal discharge

- + History

What is considered a premature foal

- Generally < 320 days gestation

- +/- in utero distress

Why do premature foals have respiratory dysfunction

- Surfactant deficiency

- Decreased respiratory drive

- Weak muscles of respiration

- Highly compliant chest wall

- Poor lung compliance

Describe neonatal equine respiratory distress syndrome (NERDS)

- Non infectious

- Etiology is surfactant deficiency

- Will see hypoxemia (PaO2 < 60 mmHg), progressive hypercapnia and 1 or more risk factors (< 290 days gestation or < 88% of dam's previous gestation, induction of parturition, C-section)

Diagnosing NERDS

- Abnormal respiration (persistent tachypnea, paradoxical respiratory pattern)

- Thoracic radiographs will have a 'ground glass' pattern

- No congenital cardiac disease

- Response to O2 is minimal to absent (because they cannot open their alveoli due to lack of surfactant)

Pathophysiology of NERDS

- Surfactant production begins at around day 290 of gestation (88% into gestation)

- Type II alveolar cells make surfactant

- Surfactant prevents atelectasis at the end of expiration and increases pulmonary compliance

- Surfactant and lung maturation are not complete at birth

Therefore, premature foals have surfactant deficiency, leading to progressive atelectasis, decreased pulmonary compliance, ventilation/perfusion mismatching and increased work of breathing. A progressive disease occurs when there is progressive hypoxia and hypercapnia, resulting in respiratory failure.

Treatment of NERDS

- O2 supplementation (not always helpful)

- Corticosteroids

- Inhaled bronchodilators

- IV fluid therapy

- Nutritional support

- Systemic antibiotics

- Last line treatment is mechanical ventilation which is super expensive and not a cure

Guarded to poor prognosis

How do congenital respiratory abnormalities present

- Respiratory distress

- Dysphagia

Examples of respiratory congenital abnormalities

- Wry nose

- Choanal atresia

- Cleft palate

- Nasopharyngeal cyst

- Sub/aryepiglottic cyst

- Guttural pouch tympany

Acute lung injury and acute respiratory distress syndrome characteristics

- Foals less than 1 week of age

- Acute onset of respiratory distress

- Presence of known risk factor: pneumonia, sepsis, meconium or milk aspiration, thoracic trauma

- Absence of cardiogenic pulmonary edema

- Evidence of insufficient gas exchange

- Presence of diffuse pulmonary inflammation secondary to above risk factors

Treatment of acute lung injury and acute respiratory distress syndrome

- Treat underlying etiology

- Oxygen supplementation: intranasal, CPAP, mechanical ventilation

- Systemic anti-inflammatories: corticosteroids early and aggressively, taper before discontinuing

- Prognosis is poor/guarded (due to lung disease that follows underlying cause)

Pathogenesis of neonatal bacterial pneumonia

- Hematogenous

- In utero

- Meconium or milk aspiration

Risk factors for sepsis following bacterial pneumonia

- Prematurity or dysmaturity

- Failure of passive transfer

- Maternal illness (placentitis)

- Poor environmental conditions

Most common etiology of bacterial pneumonia

Streptococcus equi supsp zooepidemicus

Diagnosis of bacterial pneumonia

- Physical exam

- Presence of a risk factor

- Thoracic U/S or rads

Treatment of bacterial pneumonia

- O2 supplementation

- Antimicrobials

- Supportive care

- Treatment of co-morbidities (joint sepsis, umbilical problems)

Risk factors of meconium aspiration syndrome

Fetal stress/hypoxia

Pathogenesis of meconium aspiration syndrome

- Premature passage of meconium

- Pulmonary dysfunction

- Mechanical obstruction of bronchi

- Surfactant inactivation/displacement

- Chemical pneumonitis

- Persistent pulmonary hypertension

Diagnosis of meconium aspiration syndrome

- Meconium staining (can see easily on hooves)

- Tachypnea and lung consolidation

- +/- respiratory distress

Treatment of meconium aspiration syndrome

- Aspiration of nasal passage/pharynx

- O2 supplementation

- Anti-inflammatories

- Broad-spectrum antimicrobials

- Supportive care

Milk aspiration is secondary to

- Generalized weakness

- Poor suckle reflex

- Functional abnormality

- Congenital abnormality

- Botulism

- Hyperkalemic periodic paralysis

- Bottle feeding (most bottles are not made for foals)

- Incorrect NG feeding tube placement

Diagnosis of milk aspiration

- History

- Physical exam

- Upper airway endoscope

- Thoracic rads

Treatment of milk aspiration

- Correct underlying cause

- NG feeding tube

- Broad-spectrum antimicrobials

Characteristics of equine herpes virus 1 viral pneumonia

- Severe and typically fatal

- Farm outbreaks may occur

- Premature or sudden parturition in late gestation mares

Clinical signs:

- CV and resp distress

- Congested and icteric MM

- Severe leukopenia and neutropenia

Diagnosis: PCR of nasal secretions or whole blood

Treatment: Acyclovir/valacyclovir and supportive care

Characteristics of equine influenza virus viral pneumonia

- Uncommon

- Outbreaks can occur in naive populations

- Disease will present as severe bronchointerstitial pneumonia

Characteristics of equine arteritis virus viral pneumonia

- Uniformly fatal

- Presents as severe interstitial pneumonia, edema, weakness, depression, leukopenia, and thrombocytopenia

Characteristics of rib fractures in foals

- 3-5% of foals

- 30% of foals presenting to NICU

- Most common in costochondral junction

- Multiple fractures are common

- Complications include: pulmonary contusions/lacerations, pneumothorax, hemothorax, diaphragmatic hernias, flail chest

Diagnosis of rib fractures

- Physical exam - crepitus or step on palpation

- U/S

Treatment of rib fractures

- Minimally displaced - stall rest

- Comminuted, open or complicated - surgical repair

- Pneumothorax - drain

- Hemothorax - ligate source if possible

Risk factors for pneumonia in foals

- Weaning

- Transport

- Heat stress

- Viral infection

- Other bacterial pneumonia

Strep equi zoo epidemicus clinical signs

- Nasal discharge

- Cough

- Tachypnea

- Abnormal respiratory auscultation (crackles and wheezes)

- Increased respiratory effort

Disease syndromes that strep equi zoo epidemicus causes

- Pharyngitis/tracheitits

- Guttural pouch empyema

- Pulmonary abscesses

- Bronchopneumonia

- Interstitial pneumonia

Diagnosing strep equi zooepidemicus

- Culture

- PCR

Tretment for strep equi zooepidemicus

- Supportive care

- Anti-inflammatories

- Antimicrobials (sensitivity is important)

Characteristics of rhodococcus equi

- Facultative, intracellular gram + coccobaccilus

- Pathogenic isolates

- Plasmid encoding virulence-associated protein

- Isolated from soil

- Virulent and avirulent shed in feces

- Endemic farms may have up to 33% of foals clinically affected and up to 50% mortality rate

Pathogenesis of rhodococcus equi

- Median age of diagnosis is 35-50 days old

- Inhaled

- Enter alveolar macrophages

- Disrupts endolysosome function

- Intracellular replication

- Pyogranulomatous inflammation occurs

Clinical syndromes caused by rhodococcus equi

- Pulmonary disease

- Chronic suppurative bronchopneumonia

- Extensive abscessation

Clinical signs of rhodococcus equi in mild disease, moderate disease and subacute disease

Mild disease:

- Mild fever

- Cough and increased resp. rate when handling/exercising

Moderate disease:

- Cough

- Fever

- Lethargy

- Increased resp. rate

- Decreased appetite

- Tachypnea

Subacute form:

- Acute death

- Acute respiratory distress

- High fever

Extra pulmonary disease caused by rhodococcus equi

- GI signs - enterotyphlocolitis, abdominal abscess

- Polysynovitis

- Uveitis

- Septic arthritis or osteomyelitis - moderate severe lameness, +/- effusion

Diagnosis of rhodococcus equi

- History and physical exam

- CBC

- U/S - look for abscesses

- Thoracic radiographs - alveolar pattern, nodular cavitary lesions

- Tracheal fluid - culture, PCR

When do you treat rhodococcus equi

- If they have clinical resp. disease

- They have extra pulmonary disease

- They have a minimum abscess score

What antibiotics you use to treat rhodococcus equi? What are the ADRs of treatment?

- Macrolides (azithromycin, clarithromycin)

- +/- rifampin

ADRs: diarrhea, hyperthermia, tachypnea

Other treatments for rhodococcus equi?

- Supportive care

- Supplemental oxygen

- Nebulization

- Analgesics

- Local therapy for septic arthritis

How to screen for rhodococcus equi on endemic farms?

- Thoracic U/S

- Rectal temp.

- CBC

How to decrease rhodococcus equi risk?

- Give R. equi hyperimmune plasma

- Decreases risk, does not treat

- 1 litre given within 48 hours of birth, 1 litre given between 2-4 weeks of age

What are the four equine picornaviruses

Apthovirus:

- Equine rhinitis virus A

Erbovirus:

- Equine rhinitis virus B1

- Equine rhinitis virus B2

- Equine rhinitis virus B3

Differences between equine rhinitis virus A and B

A:

- Endemic worldwide

- Shed in respiratory secretions and urine

B:

- 1 and 2 are endemic worldwide

- 3 is in Australia, UK and Japan

- Shed in respiratory secretions

Clinical signs of equine rhinitis virus

Clinical signs not often seen, but...

- Fever

- Serous mucous nasal discharge

- Coughing

- Anorexia

- Pharyngitis

- Submandibular lymphadenopathy

Co infections with other pathogens are very common

Diagnosing equine rhinitis virus

- Nasopharyngeal swab for PCR

- Serology (need paired serology if you are looking for an active infection)

Treatment for equine rhinitis virus

Supportive care

Prevention for equine rhinitis virus

- Isolation of new, young horses

- Vaccine is currently not fully licensed, and since the virus is low impact it probably won't take off

Transmission of equine influenza virus

- Aerosol (1-2 km)

- Droplets

- Fomites (3 days)

Incubation period of equine influenza virus

1-3 days, viral shedding for 10 days

What age does equine influenza typically impact

1-9 years old

When is equine influenza most prevalent in the year

Winter and spring (like most flu viruses)

Clinical signs of equine influenza

- Inappetence

- Fever

- Nasal discharge

- Cough

Uncommonly:

- Tachypnea

- Limb edema

- General weakness

Diagnosis of equine influenza

- Nasopharyngeal wash is the ideal sample

- Nasopharyngeal swab

- Nasal swab

- Paired serum titres

Treatment for equine influenza virus

Supportive care