RESPIRATORY DISTRESS IN HORSES
pathophysiology is incompletely understood but increased capil- lary leakage due to trauma to the pulmonary capillaries, changes in hydrostatic forces and ischaemia- reperfusion injury have all been suggested. In horses, only a few cases have been reported. Two horses experienced pulmonary oedema in recovery after general anaesthesia and the authors suspected that re- inflation of the de- pendent, atelectic lung and intraoperative hypoxaemia might have contributed (Ball & Trim, 1996 ; Day et al., 1993 ). A third case de- veloped pulmonary oedema after tissue plasminogen activator in- stillation into the pleural space of a horse with pleuropneumonia to dissolve restrictive fibrinous pleural adhesions. This might have triggered rapid expansion of the previously collapsed and adhered lung (McGorum et al., 2018 ). Neurogenic pulmonary oedema is a syn- drome that shares many features with ARDS and both are examples of permeability pulmonary oedema. Neurogenic pulmonary oedema affects approximately 1% of human patients with traumatic brain in- jury and has been reported in small animals, but not horses. Again, the pathophysiology is incompletely understood: localised brain ischaemia is thought to activate trigger zones, leading to a massive increase in α- adrenergic discharge. Sudden pulmonary vasocon- striction and increased permeability then result in extravasation of protein- rich fluid and intra- alveolar haemorrhage. Acute respiratory distress syndrome is a syndrome of severe pulmonary dysfunction, caused by a widespread uncontrolled inflammatory reaction in the lungs triggered by intra- or extrapulmonary disease. In horses, it is best described in foals secondary to viral or bacterial pneumo- nia (Dunkel et al., 2005 ; Lakritz et al., 1993 ) while reports in adult horses remain sparse. It has been reported following near drown- ing, smoke inhalation, influenza and experimentally after injection of perilla mint ketones and gram- negative sepsis (Austin et al., 1988 ; Begg et al., 2011 ; Humber, 1988 ; Kemper et al., 1993 ; Schmidbauer et al., 2004 ; Sembrat et al., 1978 ). Cases require intensive treatment of the underlying cause and secondary respiratory failure including intranasal oxygen and possibly systemic corticosteroids.
Acute severe equine asthma
Equine asthma is characterised by the triad of pulmonary inflamma- tion, bronchoconstriction and increased mucus production. During an acute asthma attack, the clinical signs of respiratory distress are largely secondary to severe bronchoconstriction. Emergency treat- ment, therefore, aims to relieve the immediate bronchoconstric- tion while longer term management changes and anti- inflammatory therapy decrease pulmonary inflammation which in turn will de- crease the drive for bronchoconstriction and mucus accumulation. As immediate rescue medication, systemic or inhaled fast- acting bronchodilators in combination with corticosteroids and removal of offending antigens are indicated. Albuterol/salbutamol 540 mcg/6 puffs have a rapid onset of action within 5 min but the effect only lasts 30–60 min. Salmeterol has a slower onset of action of up to 60 min but remains effective for approximately 6 h. The expected clinical effect of both drugs is difficult to predict as many studies
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focus on improvement of pulmonary function, rather than clinical scores (Calzetta et al., 2020 ) and most study subjects are not in res- piratory distress. Salmeterol achieved a decrease in clinical score from 6 to 4 at 30 min (with 2 being normal and 8 the worst score with severe nostril flaring and abdominal breathing effort) (Henrikson & Rush, 2001 ), highlighting that a temporary partial improvement, but not return to normal limits, might be a realistic expectation. Atropine (0.02 mg/kg i.v.) has long been considered one of the most potent bronchodilators in horses. It has been used as rescue medi- cation and for diagnostic purposes but due to its systemic side ef- fects including tachycardia, arrhythmia, pupillary dilation and colic, its use is limited to these indications (de Lagarde et al., 2014 ). N- butylscopolammonium bromide (Buscopan®) 0.3 mg/kg i.v. causes an improvement of some measures of respiratory function within 2 min of administration comparable to atropine but this is short- lived (30–60 min). The improvement might be difficult to detect when re- lying on clinical parameters such as respiratory rate, effort and nos- tril flare alone to judge the response (Couetil et al., 2012 ; de Lagarde et al., 2014 ). Arterial hypoxaemia does not improve with either drug (de Lagarde et al., 2014 ). An underwhelming immediate response is likely due to persistent mucus accumulation, inflammation and air- way smooth muscle remodelling, highlighting the need for concur- rent anti- inflammatory treatment (de Lagarde et al., 2014 ). While a positive response to trial treatment with a bronchodilator confirms the presence of bronchoconstriction, a negative or equivocal imme- diate response does, therefore, not rule out asthma. Systemic corti- costeroids, particularly dexamethasone at 0.05–0.1 mg/kg q 24 h i.v. or i.m., are still the most effective drug in improving lung function, even if environmental management remains suboptimal. However, the effects are not immediate, and it takes 3–7 days until the full treatment impact can be appreciated (Leclere et al., 2010 ; Robinson et al., 2002 ). Inhaled fluticasone and ciclesonide are less effective than systemic dexamethasone in the treatment of acute asthma ex- acerbation (Lavoie et al., 2019 ; Robinson et al., 2009 ) and systemic corticosteroids are recommended in the initial treatment of acute severe asthma. In people, administration of intranasal oxygen is rec- ommended alongside bronchodilators. During bronchoconstriction, poorly ventilated areas of the lung undergo hypoxic vasoconstric-
tion. When administering inhaled β 2 agonists, systemic absorption via the bronchial tree, the oropharynx, and possibly, the upper gas- trointestinal tract can reverse this protective vasoconstriction, po- tentially worsening ventilation: perfusion mismatch and hypoxaemia (Bush & Griffiths, 2017 ). However, this is not a frequently recognised problem in horses and should not prevent veterinarians from using bronchodilators if no oxygen is available.
Pleural effusion
Pleural effusion is a less common cause of acute respiratory distress as accumulation of a significant volume is required before respira- tory compromise is noticed. However, horses with infectious pleu- ropneumonia induced by long- distance travelling often experience
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