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pneumothorax. Endoscopy is invaluable for assessment of the upper respiratory tract, identifying the site and cause of obstruc- tion or detecting inhaled foreign bodies. This should be done after an airway has been established by tracheostomy to avoid collapse or death during the procedure. Thoracic ultrasonography is a rapid assessment tool to confirm the presence and characteristics of pleural effusion, pneumothorax and pulmonary consolidation or abscessation. Pulmonary oedema might be suspected if multiple coalescing comet tails are visualised. Thoracic radiographs are useful to rule out radiographically visible lesions or obtain a bet- ter impression of size and location of a lesion but are rarely nec- essary or indicated in the first emergency assessment. Thoracic ultrasonography is more sensitive than radiography in detecting pleural effusion, pulmonary consolidation and atelectasis (Reef et al., 1991 ) and it is often quicker in an emergency. Exceptions are cases where widespread subcutaneous emphysema makes ultra- sonography difficult and radiography becomes an important tool. A pneumothorax can be readily identified on thoracic radiographs focusing on the caudodorsal aspect of the lung and detection of diaphragmatic hernias, a rare cause of respiratory difficulties, is often easiest using this modality. However, obtaining good quality radiographs with a hand- held x- ray generator can be challenging in adult horses and access to a ceiling- mounted x- ray system is advantageous. In foals and miniature horses, use of computed tomography has been advocated for enhanced visualisation of intrathoracic structures including the lung parenchyma (Lascola et al., 2013 , 2016 ; Schliewert et al., 2015 ). The need for general anaesthesia in often severely compromised patients will
likely
limit its usefulness in emergency cases, even if the animal is of an appropriate size. Arterial blood gas analysis remains the most widely used tool to
assess respiratory function and acid base status in the clinical setting to determine the need for oxygen treatment and identify hypoventi- lation. Analysis should ideally be performed within 10 min of obtain- ing the sample and any free air must be expelled and syringes sealed airtight. Blood collected in glass syringes kept on ice or in propylene syringes designed for blood gas analysis kept at room temperature can be stored up to 2 h before without significantly altering results (Deane et al., 2004 ; Kennedy et al., 2012 ; Picandet et al., 2007 ). An arterial sample can usually be obtained from the transverse facial artery in a standing horse.
How urgent is it? Pathophysiology of respiratory distress
The most severe and rapidly fatal cause of respiratory distress is complete obstruction of the upper airways as this prevents any in- halation of air. The only treatment in these situations is an imme- diate emergency tracheotomy.
Intranasal oxygen is not effective
as the oxygen cannot be inhaled into the lungs. The situation can be compounded by the development of negative pressure pulmo- nary oedema and clinicians need to watch out for worsening of the
DUNKEL
condition once an airway has been established which could indicate progressive pulmonary oedema. A rapidly developing tension pneumothorax can also lead to
fast deterioration and death. The rising intrathoracic pressure results in collapse of the lungs, compression of the caudal vena cava with decreasing venous return to the heart and increased pulmonary vascular resistance, further worsening cardiac output and ultimately leading to cardiopulmonary collapse and death. Immediate decompression of the pneumothorax is, therefore, lifesaving. Oxygen therapy is useful but only in conjunction with decompression. Pulmonary oedema can cause acute, severe and potentially fatal
respiratory distress by sudden flooding of the alveoli and small air- ways. The flooding can be caused by either an increase in hydro- static pressure or increased vascular permeability, or both. In cases of hydrostatic pressure pulmonary oedema, the alveoli fill with a protein- poor transudate (cardiac failure, negative pressure pulmo- nary oedema) once the lymphatic drainage capacity is overwhelmed. Pulmonary epithelium and endothelium often remain intact and quick reversal is possible if the underlying cause is addressed. Increased permeability pulmonary oedema is caused by a sudden increase in endothelial and/or epithelial permeability, often due to damage or destruction of the endothelial and epithelial barrier (acute respiratory distress syndrome (ARDS), neurogenic pulmonary oedema). This results in filling of the alveoli with protein- rich inflam- matory exudate, blood and debris. Reversal is much more difficult and slower, due to the tissue destruction. Removal of the underlying cause (treating cardiac failure;
establishing an airway; treating underlying disease) and oxygen insufflation is the mainstem of treatment in either case of pulmo- nary oedema. Furosemide is indicated in cardiac failure to lower the vascular hydrostatic pressure but is not effective if hydrostatic pressure is already normal, which is often the case in negative pressure pulmonary oedema, or if increased permeability is the underlying cause. Acute asthma caused distress by bronchoconstriction and bron-
chodilatory therapy is, therefore, paramount. Although clinical distress can be severe, hypoxaemia is often only moderate and fatal- ities are extremely rare in horses. Additional oxygen therapy is very useful, if available, and recommended in people alongside broncho- dilation to avoid worsening of ventilation- perfusion mismatch (see below).
Pleural effusion secondary to pleuropneumonia or neoplasia
cause respiratory distress through a combination of systemic in- flammation and hypoxaemia, secondary to filling of alveoli and small airways with exudate in mild cases and destruction of pulmonary parenchyma in severe cases. Pleural effusion exerting pressure onto the lung tissue and causing alveolar collapse and atelectasis can ex- acerbate the situation. However, similar to asthma, sudden death due to hypoxia or cardiovascular collapse is rare with the exception of the most severe cases and even emergency treatment with oxy- gen and thoracic drainage would probably not have resulted in sur- vival in these horses.
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