Recurrent Airway Obstruction, Heaves, or “Broken Wind” in Horses

Filed Under: Horses

Is your horse suffering from repeated bouts of coughing, especially after being exercised? Have you heard your horse wheezing? Your horse may be suffering from chronic allergen-induced respiratory disease, termed recurrent airway obstruction (RAO). Much like asthma in humans, heaves, or “broken wind” as it is more commonly called, causes inflammation in the smaller airways of the lungs and constriction of the bronchioles (breathing tubes) in response to environmental allergen exposure.

RAO is typically induced by chronic exposure to hay and straw in a closed environment such as a poorly-ventilated stable. Dust from moldy grasses is believed to be the most common inciting cause for RAO development. The dust may contain mold particles, various endotoxins, and dust mites. Commonly implicated molds are Faenia rectivirgula, Aspergillus fumigatus, and Thermoactinomyces vulgaris. All of these irritants may cause an inflammatory response to occur within the airways of sensitive individuals.

Although RAO has typically been associated with the stabling of horses during bouts of cold weather, it can affect animals in warmer climates where experts speculate that conditions are such that mold levels are high enough, even when the horses are at pasture, to induce the inflammatory response. The similar disease syndrome associated with pastured horses in the southeastern United States is termed summer pasture-associated obstructive pulmonary disease (SPAOPD).

Although any horse may develop some inflammation of the air passages when exposed to enough irritating particles over a prolonged period of time, most researchers believe that there is a genetic susceptibility for disease development. Recently a possible gene has been implicated with the condition. Horses having two parents effected by heaves will have a 40% chance of being effected themselves. Horses having neither parent effected have approximately a 10% chance of heaves occurring. The prevalence of heaves is unknown but is believed to run from 12% to 80%, dependent on the geographical region, the weather, and how the horses are housed. The mechanical irritation of particles, endotoxins, and perhaps an allergic component may also play a role in the development of heaves.

Classical clinical signs of heaves include: flared nostrils, tachypnea (rapid respiration), wheezing, mucopurulent nasal discharge, and the delineation of a “heave line”. The typical breath seen with heaves is characterized by a prolonged and labored exhalation and a short inhalation. The inflamed and constricted smaller airways prevent the expulsion of air from the lower respiratory tract. A “heave line” develops because the abdominal muscles become thickened or hypertrophied because they are constantly worked during breathing, and therefore become enlarged and more apparent. Wheezing occurs due to narrowed airways that restrict air flow during expiration. Excessive mucus production may also lead to the development of crackles during the respiratory cycle. Coughing may be prevalent during exercise or eating. Clinical signs may range from mild to moderate. Clinical signs of heaves may be minimal when the horse is at rest but will become more clinically apparent when the animal is exercised. Heart failure may occur in chronic cases because the heart must pump harder due to the increase in pressure within the chest. The average age of onset in the horse is 9 years.

The diagnosis of heaves may be difficult and usually results from eliminating other causes of difficult breathing. A CBC, or complete blood count, is typically unremarkable on hematologic analysis. Horses with a secondary bacterial infection may exhibit a moderate elevation in the white blood cell count.

Horses with heaves will demonstrate neutrophilic inflammation on bronchoalveolar lavage. This may be helpful in differentiating heaves from an infection with lungworms or eosinophilic pneumonitis. Radiographs may be helpful in eliminating pneumonia as a possible differential diagnosis. With heaves, radiographs may demonstrate some peribronchial infiltration and some flattening of the diaphragm.

A diagnosis of heaves is typically based on pertinent history and the demonstration of classical clinical signs. Confirmation of a heaves diagnosis usually involves a referral center that may test pulmonary function following the aerosol administration of low doses of histamine which is compared to the responses of normal horses. Alternatively the change in pressure within a horse’s chest may be measured following a bronchodilator administration.

Most horses respond positively to environmental control which, in most cases, requires them to be housed outside and pastured. In some cases horses will respond to dietary changes in feedstuff to a cubed or pelleted ration, while some owners may find that dampening the hay before feeding may be of help. Reversely, if the horse has a reaction to a moldy pasture they will respond better when stabled. Bedding changes to shredded paper or peat moss may prove helpful.

Repeated bouts of RAO will result in permanent changes to the lungs. The goal of treatment is to slow down the progression of the disease. Corticosteroids are still the drug of choice for the management of RAO. Dexamethasone, a fast acting steroid, will provide fast relief by quickly reducing the resulting inflammation. Typically, within three days of corticosteroid use most horses will be breathing much better. When systemic corticosteroids are contraindicated the horse may be given an inhaled corticosteroid.

Corticosteroids available for inhalation are available in metered-dose inhalers that must be administered through a special inhalation device specifically designed with the equine patient in mind. Two such devices are the AeroMask®, manufactured by Trudell Medical International in London, or the Equine Haler®, which is available through Jorgensen Laboratories. Unfortunately, inhaled corticosteroids may be costly and may not be as fast or effective as the use of systemic corticosteroids.

Fast-acting rescue medications for those that are suffering severe distress include the use of bronchodilators. There is currently only one bronchodilator approved for use in the horse - clenbuterol, marketed under the trade name Ventipulmin® and is manufactured by Boehringer-Ingelheim. This drug is available in syrup form and relaxes the muscles located around air passages as well as remove mucus from the lungs. It may also reduce inflammation by a small degree. In addition, human rescue inhalers have been used in conjunction with the use of the AeroMask® or Equine Haler®.

Non-traditional products may be available in the near future for the treatment of ROA. VibraVM® is one such device, designed to generate sound waves that go through the airway to liquefy and dislodge mucus and other secretions contained therein. This product is also believed to relax constricted bronchial airways. A similar human device is currently being evaluated for the treatment of humans with cystic fibrosis.

Antibiotics should be given in cases involving a secondary infection. Severe bouts of heaves may require oxygen.

With recurrent airway obstruction the condition may be managed but it is never cured. The prognosis is dependent upon the stage of lung obstruction that has already occurred and the ability of an owner to provide long-term relief and prevention of the causative factors involved in the development of heaves.

Horses failing to respond after 14 days of treatment should be reevaluated with radiographs.

McAllister, Toni. “Helping Horses Breathe Easier”. Veterinary Practice News. March 2008. P. 30-31.

Orsini, James, and Thomas Divers. Equine Emergencies Treatment and Procedures. 3rd Edition. Saunders. 2008. Pp. 468-469.

Radostits, Otto, and Clive Gay et al. Veterinary Medicine. 10th Edition. 2007. Pp. 1928-1935.

Rush, Bonnie, and Jason Grady. “Recurrent Airway Obstruction (Heaves). Compendium for Continuing Education for Veterinarians”. Equine. Vol 3(4). May 2008. Pp. 198-205.

Smith, Bradford, ed. Large Animal Internal Medicine. Second Edition. 1996. Mosby. Pp. 594-597.

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