CHAPTER 70 Management of Pulmonary Edema
Pulmonary edema in horses is a serious and potentially fatal condition. It most commonly develops as a complication of general anesthesia and is noticed during the recovery period, although it may also develop at any time in association with severe respiratory distress. Pulmonary edema has also been reported uncommonly as a complication of accidental poisoning in horses, for example, in oleander poisoning and pine oil toxicosis. Congestive cardiac failure is uncommon in horses but can lead to development of pulmonary edema. Alveolar epithelial cells must be kept moist to maintain proper function, and there is constant replenishment of fluid in the lung to replace evaporative losses. Under normal circumstances, the supply of fluid is slightly in excess of loss, and excess fluid is removed by pulmonary lymphatics. The lymphatic system can cope with a massive increase in lymph flow with chronic disease, but this ability to upregulate flow is more limited in acute conditions. This explains why pulmonary edema is more commonly a feature of acute rather than chronic disease.
Pulmonary edema is defined as the abnormal accumulation of fluid and solutes in the extravascular tissues of the lung. Interstitial edema usually develops first because the pulmonary vascular endothelium contains many intercellular gap junctions that allow fluid to leak out of the blood vessels into the pulmonary interstitium. There are tight junctions between the alveolar epithelial cells that are relatively impermeable; therefore, alveolar edema is usually a later complication.
Edema fluid in the alveoli or interstitium reduces the effective lung volume, elasticity, and lung compliance, resulting in difficulty breathing. There is usually increased shunting of blood in the lungs through alveoli that are perfused but not ventilated, resulting in arterial hypoxemia.
Starling’s equation dictates that the two major causes of edema formation are increased transcapillary hydrostatic pressure gradients (high pressure pulmonary edema) or increased vascular permeability to fluid and protein (low-pressure pulmonary edema). In the clinical scenario, both these conditions may be present.
Possible causes of pulmonary edema include upper airway obstruction, increased pulmonary capillary permeability secondary to reperfusion injury or endotoxemia, and hypoxia-induced pulmonary vasoconstriction. Aspiration of gastric acid may also predispose to edema formation.
Upper airway obstruction resulting in extremely negative intrathoracic and intra-alveolar pressure during inspiratory attempts is implicated as a causative factor in many cases reported in the literature (negative-pressure pulmonary edema). There are many potential causes of upper airway obstruction in horses, including persistent dorsal displacement of the soft palate, laryngeal paralysis or edema, and obstructive airway masses. Nasal hyperemia and edema, caused by dependent pooling of blood in the nasal mucosa, develops to some degree in most horses that have been anesthetized and can result in substantial airway obstruction. Unilateral laryngeal paralysis is relatively common in horses and probably does not result in complete respiratory obstruction. Bilateral laryngeal paralysis, in horses with hepatic encephalopathy for example, is less common but more likely to cause complete respiratory obstruction. Overextension of the head and neck during anesthesia may result in stretching, excessive tension, and ischemia in the recurrent laryngeal nerves and postoperative bilateral laryngeal paralysis. Laryngotracheal trauma may occur during endotracheal intubation, resulting in postoperative laryngeal edema, swelling, and obstruction. Laryngospasm during intubation is uncommon in horses compared with other species.
Airway obstruction and increased inspiratory effort lower pulmonary interstitial pressure to a level where the pressure gradient between the pulmonary capillary and the alveolar interstitium is sufficient to promote edema formation. The pressure gradient created by the airway obstruction also alters cardiovascular dynamics: by augmenting venous return to the heart, pulmonary blood flow and pulmonary capillary hydrostatic pressure are increased, further promoting edema formation.
Sympathetic nervous system activation is common during anesthetic recovery, and high catecholamine concentrations may worsen pulmonary edema formation. Pulmonary arterial and venous pressures increase, and blood is shunted into the pulmonary vasculature from the systemic circulation, contributing to further increases in hydrostatic pressure.
Severe hypoxia and reperfusion injury may also be important causative factors in the development of pulmonary edema. Impaired arterial oxygenation is commonly encountered in anesthetized horses in dorsal recumbency and is associated with alveolar atelectasis and ventilation-perfusion mismatching. A period of hypoxia and ischemia during atelectasis, followed by reperfusion injury on lung reinflation, can lead to capillary endothelial damage caused by reactive oxygen species (free radicals) and inflammatory mediators secreted by activated neutrophils. This in turn can result in increased capillary permeability, transudation of fluid and protein, and eventually pulmonary edema.