Page 734 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Respir atory system: 3.4 Medical conditions of the lower respir atory tr act 709

VetBooks.ir 3.170 hypoxaemia, depression, disorientation and ataxia.
Tachypnoea, dyspnoea and respiratory stridor may
occur. Crackles, wheezes or decreased air movement
may be obvious on initial chest auscultation, but
may take up to 12–24 hours after the initial insult to
develop. Nasal discharge is common due to oedema
or inflammatory exudate in the upper airway.

Diagnosis
History and physical examination are usually diag-
nostic, but the presence of external thermal inju-
ries is confirmatory. Blood–gas analysis should be
performed if available. A venous concentration of
Fig. 3.170 External skin burns subsequent to a barn carboxyhaemoglobin above 10% is consistent with
fire. Smoke inhalation resulted in marked damage carbon monoxide toxicity. In horses without signs of
to the respiratory epithelium, causing respiratory significant respiratory distress, thoracic radiographs,
distress in this horse from excessive debris within bronchoscopy and cytological evaluation of tracheal
the trachea and bronchi. aspirate or BAL fluid are useful ancillary techniques
to confirm the diagnosis and determine the optimal
treatment.
Aetiology/pathophysiology
The insult to the respiratory tract occurs by direct Management
thermal injury (especially in the URT) and inhala- Tracheotomy may be required in cases of upper
tion of toxic chemicals, causing lung injury directly airway obstruction resulting from severe oedema
or indirectly through activation of an inflammatory and inflammation, or to remove pseudomembranes
response and low oxygen delivery to the lung due from the trachea to facilitate ventilation of the
to combustion processes. Pulmonary dysfunction lung. Humidified oxygen support by nasal insuffla-
first occurs through exposure to a high concentra- tion or via a transtracheal catheter is recommended
tion of carbon monoxide, which combines with hae- to displace carbon monoxide from haemoglobin.
moglobin to form carboxyhaemoglobin, resulting Bronchodilators may be indicated in cases of severe
in hypoxaemia. Hypoxaemia may be exacerbated if bronchoconstriction. Diuretics and NSAIDs are
concurrent bronchoconstriction in the lower air- usually required to control pulmonary oedema,
ways occurs in response to the irritating effects inflammation and pain. The use of corticosteroids is
of noxious gases. Pulmonary dysfunction may controversial and is usually avoided, as it can predis-
subsequently progress due to pulmonary oedema pose to infections. Some cases may require the use of
formation from lung inflammation, plus airway analgesics such as fentanyl, morphine or ketamine.
obstruction from the accumulation of inflammatory Supportive therapy is commonly indicated including
and necrotic cells in the airways. Extensive destruc- i/v fluids, plasma transfusion or parenteral nutrition
tion of airway epithelium also impairs host respira- supplementation. High-risk patients or those with
tory immune defences, predisposing to secondary confirmed bacterial infections should be treated
bronchopneumonia. with appropriate antimicrobials.

Clinical presentation Prognosis
Clinical signs will depend on the degree of exposure The prognosis is variable. Prolonged exposure to
and the types of gas inhaled. Animals may be mildly gases and extensive or severe thermal injuries carries
affected or clinically normal after smoke inhala- a poor prognosis. The onset of clinical signs may be
tion, with severe disease developing 12–24 hours delayed, therefore close monitoring is indicated in
later. Severely affected animals may show signs of any animal that has been exposed to smoke.