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attempted as diagnostic and therapeutic procedure. Needle thora- cocentesis should be performed immediately if there is a suspicion of a tension pneumothorax with signs of cardiovascular compromise. With a penetrating wound or deep stab wound, the first step of


treatment is preventing further entry of air into the pleural space. This can be achieved by suturing or packing of the wound. Covering the wound or wrapping the patient in cling film can work well as an emergency measure if transport to a tertiary care facility is required. An equine compression suit has also been used to reduce air aspira- tion with good success in the management of a deep axillary wound (Tallon et al., 2023 ). A mild pneumothorax might not require removal of the free air within the pleural space. However, if signs of respira- tory distress are present, emergency thoracocentesis is indicated. After clipping and aseptically preparing a 5 × 5 cm large square in


a dorsal aspect of the 11th through 15th intercostal space, ventral to the transverse processes, the area is infiltrated with a local anaes- thetic and a small stab incision is made cranial to the rib using a scal- pel blade. A small- bore tube (blunt- tipped teat cannula, 10–14- gauge intravenous catheter or 16- French or 24- French trocar catheter) is introduced into the skin incision and advanced into the pleural cav- ity. The catheter stylet or trocar is removed once the pleural cavity is accessed. It is helpful to connect the end of the catheter via an extension set to a 60 mL syringe that an assistant holds under nega- tive pressure. Once the plural cavity is entered, air can be aspirated confirming the correct location and presence of a pneumothorax. Air is then removed by repeated aspiration with a 3- way stopcock and large syringe or by attaching a suction unit, limiting the setting


to <−15 mmHg (<−20cmH 2 O) to minimise the risk of re- expansion pulmonary oedema (Khanoria et al., 2021 ). In people, oxygen ther- apy is used to combat hypoxaemia and in an attempt to increase the speed of air re- absorption from the pleural space. Free pleural air is gradually reabsorbed into pulmonary lymphatics and capillaries. Approximately 1.25–2.2% of the volume of a spontaneous pneumo- thorax can be reabsorbed over a 24- h period in people and resolution of a moderate to severe pneumothorax might take several weeks if there is no ongoing leak (MacDuff et al., 2010 ). The administration of oxygen leads to a partial replacement of nitrogen by oxygen in the arterial blood and alveolar space, thereby increasing the absorption gradient between blood and air in the pleural cavity and quicker air absorption (Grasmuk- Siegl & Valipour, 2023 ). The technique is effec- tive in animal models but its clinical usefulness has been questioned (Grasmuk- Siegl & Valipour, 2023 ; Zierold et al., 2000 ).


Pulmonary oedema


Pulmonary oedema can be caused by an increased hydrostatic pres- sure in the pulmonary vasculature, an increased permeability of the alveolar epi- and endothelium or a combination of both. Cardiogenic pulmonary oedema is the best described example of


hydrostatic pressure pulmonary oedema secondary to left- sided or generalised heart failure. While not occurring frequently in horses, any respiratory distress associated with an unexplained tachycardia,


DUNKEL


presence of a grade 3/6 or louder murmur or arrhythmia could in- dicate the presence of cardiogenic pulmonary oedema. Treatment with furosemide (1–2 mg/kg i.v. q 4–6 h) while monitoring hydration status might provide transient relief until a full cardiac assessment can be carried out. Anecdotally, hypertonic saline has been used in the treatment of pulmonary oedema either with or without addition of furosemide. There is limited evidence to suggest that hypertonic saline is beneficial for treatment of pulmonary oedema regardless of the underlying pathophysiology in any species. Early work in dogs with experimentally induced hydrostatic oedema showed no ben- efit when using hypertonic saline with or without furosemide over furosemide alone in the clearance of pulmonary oedema despite achieving greater diuresis (Wickerts et al., 1992 ). This highlights the fact that increased diuresis decreases the hydrostatic drive for the development of pulmonary oedema but does not increase clearance of already accumulated pulmonary fluid. If feasible, in- tranasal oxygen at 10–20 L/min is indicated in hypoxaemic patients


(PaO 2 < 65–60 mmHg). Negative pressure or post- obstructive pulmonary oedema is less


well described but not uncommon. It occurs secondary to a transient acute upper airway tract obstruction when the horse tries to inhale against the increased resistance of a partially or completely closed upper airway. The period of airway obstruction can be very short, only lasting minutes, for example with temporary occlusion of the nostrils or laryngospasm in horses recovering from anaesthesia or secondary to hepatic failure (Ball & Trim, 1996 ; Borer, 2005 ; Veres- Nyeki et al., 2011 ). Forceful inspiration against a closed epiglottis decreases intrathoracic pressure dramatically, thereby increasing the transpulmonary hydrostatic pressure and increasing venous re- turn to the right side of the heart and the lungs. Both mechanisms result in fluid extravasation from the capillaries into the intersti- tium and ultimately alveoli (Unger & Martin, 2023 ). Rarely, a sim- ilar situation might be encountered after sudden relief of chronic upper airway tract obstruction, but this has not yet been reported in horses (Unger & Martin, 2023 ). Treatment is focussed on estab- lishing a patent airway if upper airway tract obstruction persists. Furosemide and intranasal oxygen are frequently used; however, as the increase in hydrostatic pressure triggering pulmonary oedema resolves quickly once an airway is established, the need for diuretics has been questioned. Diuretics decrease the hydrostatic pressure, and therefore driving force, for development of pulmonary oedema but do not aid in clearing already existing pulmonary oedema. As the alveolar epithelium usually remains intact, inhaled or systemic beta- adrenergic drugs such as albuterol or clenbuterol might increase the speed of fluid clearance from the alveoli (Frank et al., 2000 ; Zanza et al., 2023 ). Providing the upper airway tract obstruction can be resolved, most horses improve rapidly over 12–48 h and recover completely. Other, rarer forms of pulmonary oedema include re- expansion


pulmonary oedema , neurogenic pulmonary oedema and ARDS . Re- expansion pulmonary oedema can occur when previously atelectic lung is rapidly re- inflated, for example with rapid drainage of pleu- ral fluid or evacuation of pleural air in a pneumothorax. The exact


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