Recurrent Airway Obstruction

Also known as: RAO, chronic obstructive pulmonary disease, COPD, heaves.

Do not confuse with: summer pasture associated obstructive pulmonary disease.

Description

Recurrent airway obstruction (RAO) is an inflammatory, obstructive respiratory disease of horses. Disease is induced by the exposure of susceptible animals to organic dust, which gives neutrophil influx to the airways, bronchospasm and mucus accumulation¹. This causes a cough, nasal discharge, and respiratory difficulty. When exposure to the allergen is eliminated, obstruction and clinical signs resolove or attenuate. However, animals are susceptible to reccurent episodes of airway obstruction throughout their lives, and so management is essential.

Since disease required exposure to organic dust, recurrent airway obstruction occurs in stabled horses that are, for example, bedded on straw and fed hay. The condition is therefore most prevalent in the northern hemisphere because horses tend to be stabled for large parts of their lives². Summer pasture-associated obstructive pulmonary disease (SPAOD) is a similar condition that occurs when horses kept on pasture are sensitive to environmental allergens, and may be considered the same disease as RAO but with different inciting factors¹.

Pathogenesis

When a horse with a history of RAO is moved from pasture to a stable, the hay it is fed and the straw it is bedded on harbour organic dusts. These dusts contain components which are capable of causing inflammation of the lungs, such as specific allergens, endotoxin, moulds and small particulate matter¹. Although small particles and endotoxin are known to cause pulmonary inflammation, there is evidence to suggest that there is an allergic component to recurrent airway obstruction. For example, bronchoalveolar lavage fluid in RAO has been shown to have increased levels of IgE specific for various moulds^haliwell, and the cytokine response appaears to be skewed towards TH2^lavoi: both of these facts are suggestive of an allergic mechanism.

On exposure to dust, neutrophils accumulate in the lung and quickly invade the lumen of the airway¹. Aiway obstruction then develops due to several mechanisms. Mucus becomes more viscous and accumulates in the luman, and bronchospasm is initiated by the actions of inflammatory mediators on airway smooth muscle and cholinergic nerves^Olszewski. Oedema of the airway wall also contributes to narrowing, and in horses suffering chronic disease, the wall remodels to give mucus metaplasia, smooth muscle hypertrophy and peribronchial fibrosis^{1, allen}.

Signalment

RAO usually becomes apparent in middle-aged and older horses, and persists for life^allen. There is some evidence that there may be a genetic component to the disease, as many horses do not suffer RAO when they are housed in environments that can provoke clinical disease in others^marti.

Diagnosis

A presumptive diagnosis may be made on the basis of the history and clinical examination.

Clinical Signs

Mildly affected horses generally present with a history of occasional coughing and exercise intolerance. Signs become more obvious as the disease progresses. Tachypnoea is often seen, and there may be a mucopurulent nasal discharge. Severely affected animals show signs of respiratory distress at rest. These can include flared nostrils, wheezing, paroxysmal bouts of coughing and a laboured abdominal component to expiration. Chronically, marked dyspnoea increases energy expenditure and the animal may lose condition, as well as developing a "heave line" due to hypertrophy of the external abdominal oblique muscle^{allen, merck, ivis}. Fever does not normally develop unless there are secondary bacterial complications.

On physical examination, thoracic auscultation typically reveals a prolonged expiratory phase of respiration and adventitious respiratory noises. Wheezes are most pronounced during expiration, and crackles are associated with the excessive mucus production^merck. However, the airways are so obstructed in some severely affected animals that there is insufficient air movement to generate audible breath sounds, and the lungs are very quiet on auscultation¹. In mildly affected horses, a rebreathing bag can be used to aid auscultation, but this should never be performed in dyspnoeic animals^{1, allen}. There may be an increased sensitivity of the cough reflex on tracheal compression.

Diagnostic Imaging

Endoscopy reveals excessive mucopurulent secretions in the trachea. Thoracic radiographs may be useful in cases that are not typical in their presentation or response to treatment, as they may help rule out other differentials such as including interstitial pneumonia, pulmonary fibrosis, or bacterial pneumonia^{1, allen}.

merck Radiographic findings in horses with RAO are peribronchial infiltration and overexpanded pulmonary fields (flattening of the diaphragm). Thoracic radiographs are of little benefit in confirming the diagnosis of RAO and may not be necessary in horses with characteristic clinical signs, unless there is no response to standard treatment after 14 days of therapy. However, they may be helpful in identifying the most important differential diagnoses, i

Laboratory Tests

Routine haematology and biochemistry are usually within normal limits, and there is little evidence to support the use of serum and intradermal allergy testing in the diagnosis of RAO^allen.

Fluids obtained from bronchoalveolar lavage or tracheal wash may be useful in the diagnosis of RAO. The presence of greater than 20% neutrophils in BALF confirms the presence of lower airway inflammation, thus and differentiates horses with RAO from those with eosinophilic pneumonitis, fungal pneumonia, or lungworm infestation. Normal horses have fewer than 10% neutrophils in BALF. Cytology of bronchoalveolar lavage fluid may also reveal Curschmann’s spirals , which represent inspissated mucus/cellular casts from obstructed small airways¹. BAL should not be performed in markedly dyspnoeic horses, and instead should be postponed until the dyspnoea is controlled. Aspiration of tracheal mucus or a tracheal lavage can also be used to evaluate lung inflammation but it is less reliable than BALF.

Other Tests

Reduction of respiratory distress after the administration of a bronchodilator confirms the presence of bronchospasm^{1, allen}. To test this, intravenous atropine can be administered at 0.02mg/kg. Horses with RAO (or SPAOD) should respond within 15 minutes¹. The dose of atropine should not be repeated as there is a risk of intestinal stasis.

Pathology

COPD (Image sourced from Bristol Biomed Image Archive with permission)

COPD scanning electron micrograph (Image sourced from Bristol Biomed Image Archive with permission)

Treatment

The mainstays of treatment

and prevention of RAO are environmental control, the use of bronchodilators to reduce respiratory distress and the administration of corticosteroids to reduce inflammation. Environmental control Environmental control is important in all stages of the disease and, as reported by many studies, may in itself result in clinical and functional improvement. Owners need to appreciate that environmental management is at least as important as medical treatment, and they should be made aware that even a brief exposure to dust is sufficient to induce inflammation in horses with RAO, which may take days or weeks to resolve. Bronchodilators Bronchodilators are used to counteract the broncho spasm and thereby relieve some of the respiratory distress experienced by horses with RAO. Although a large part of the airway obstruction may be due to bronchospasm, some obstruction of the airway may remain, despite maximal bronchodilation, due to the mucus accumulation and inflammatory changes in the airway wall. It is important to understand that bronchodilators do not treat the underlying inflammation. Corticosteroids Many horses benefit from corticosteroid administration early in the course of the disease in conjunction with bronchodilators, as this will address the underlying inflammation as well as bronchospasm. Corticosteroids can be administered systemically using intravenous or oral preparations, or by inhalation. (The association between cortico steroids and laminitis should be discussed with the owner.) The advantage of inhaled corticosteroids is that they are administered directly to the respiratory tract; therefore, the required therapeutic dose is lower, resulting in less systemic absorption and hence less risk of side effects. The pulmonary distribution of inhaled cortico steroids is poor during severe airway obstruction, so this method of administration should only be used after an improvement in lung function has been achieved with systemic corticosteroids and/or bronchodilators.

In mild to moderate cases, systemic corticosteroids may

not be required and inhaled corticosteroids may be used from the outset. Ideally, inhaled corticosteroids should be administered after inhaled bronchodilators to improve their penetration to the lower airways. In the majority of cases, medical treatment should be considered a short-term measure while environmental improvements are instituted.

References

1. Robinson, N E (2001) Recurrent Airway Obstruction. In Equine Respiratory Diseases, IVIS.
2. Robinson N E et al (1995) The pathogenesis of chronic obstructive pulmonary disease of horses. The British Veterinary Journal, 152, 283-306.
3. Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial.
4. Allen, K and Franklin, S (2007) RAO and IAD: respiratory disease in horses revisited. In Practice, 29(2), 76-82.
5. Halliwell R E W et al (1993) Local and systemic antibody production in horses affected with chronic obstructive pulmonary disease. Veterinary Immunology and Immunopathology, 38, 201-215.
6. Lavoie J P et al(2001) Neutrophilic Airway Inflammation in Horses with Heaves Is Characterized by a Th2-type Cytokine Profile. American Journal of Respiratory and Critical Care Medicine, 164, 1410-1413.
7. Marti, E et al (1991) The genetic basis of equine allergic diseases 1. Chronic hypersensitivity bronchitis. The Equine Veterinary Journal, 23, 457-460.
8. Olszewski M A et al (1999) Pre- and postjunctional effects of inflammatory mediators in horse airways. American Journal of Physiology, 277, 327-333.
9. McGorum, B et al (2007) Equine respiratory medicine and surgery, Elsevier Health Sciences.
10. Durham, A (2001) Update on therapeutics for obstructive pulmonary diseases in horses. In Practice, 23(8), 474-481.