Definition

Two entirely separate clinical aspiration disorders exist. One occurs after the aspiration of solid food and produces a picture of laryngeal or bronchial obstruction, an the other results from direct acid injury to the lung and produces an “asthma-like” syndrome. Pulmonary aspiration occurs when the gastric contents escape from the stomach into the pharynx and then enter the lungs. This results from preexisting disease, airway manipulation, and the inevitable compromise in protective reflexes accompanying the anesthetized state. Aspirates are commonly categorized as contaminated, acidic, alkaline, particulate, and nonparticulate. Fewer than half of all aspirations lead to pneumonia. Pneumonia occurs most often in patients with aspiration of infected material or who are immunocompromised.

Incidence and prevalence

Although the incidence of regurgitation is estimated to be frequent (as high as 15%), pulmonary aspiration complicates only about one in 3000 anesthetics. This incidence is roughly doubled for cesarean section surgery and emergency surgery. Fortunately, the majority of aspiration incidents require little or no treatment.

Pathophysiology

Although vomiting and gastroesophageal reflux are common clinical events, aspiration usually occurs only when normal protective reflexes (swallowing, coughing, gagging) fail. Three broad categories of failure are (1) depression of reflex protection, (2) alteration in anatomic structures, and (3) iatrogenic disorder. Reflex responses to aspiration are automatically blunted with depression of consciousness. The most common setting for depression of reflex protection occurs during anesthesia induction and emergence.

Three aspiration syndromes have been identified: (1) chemical pneumonitis (Mendelson syndrome), (2) mechanical obstruction, and (3) bacterial infection. Because acute chemical pneumonitis poses the greatest difficulty to anesthesia providers, the pathophysiology, presentation, and anesthetic implications of Mendelson syndrome are discussed. The triphasic sequence of (1) immediate respiratory distress combined with bronchospasm, cyanosis, tachycardia, and dyspnea followed by (2) partial recovery and (3) a final phase of gradual return of function is characteristic of Mendelson syndrome. This acute chemical pneumonitis is caused by the irritative action of hydrochloric acid, alkaline aspirates, or particulate materials, which are damaging to the lungs.

The pathophysiology of aspiration pneumonitis is typically characterized by four stages: (1) The aspirated substance causes immediate damage to the lung parenchyma, resulting in tissue necrosis. (2) Atelectasis results within minutes caused by a parasympathetic response that leads to airway closure and a decrease in lung compliance. (3) One to two hours after the injury, there is an intense inflammatory reaction characterized by pulmonary edema and hemorrhage. Inflammatory cytokines play a central role in this, including interleukin-8 and tumor necrosis factor alpha (TNF-α) released by alveolar macrophages. Neutrophils also play a key role in this phase by releasing oxygen radicals and proteases. Fluid fills the alveolar capillary membrane, causing hypoxia and hypercarbia. (4) Later, secondary injuries result from fibrin deposits and necrosis of alveolar cells by 24 hours after the insult.

Clinical manifestations and diagnosis

Arterial hypoxemia, the hallmark sign of aspiration pneumonitis, is frequently the first sign of aspiration. Because the majority of aspiration incidents are asymptomatic or mildly symptomatic, unexplained hypoxemia occurring in otherwise healthy patients postoperatively may frequently be a vague sign of silent aspiration. Other signs to alert the anesthetist to the possibility of aspiration include tachypnea, dyspnea, tachycardia, hypertension, and cyanosis.