bubble_chart Overview

Aspiration pneumonitis refers to chemical pneumonia caused by the inhalation of acidic substances, animal fats such as food, gastric contents, and other irritating liquids and volatile hydrocarbons. In severe cases, respiratory failure or acute respiratory distress syndrome may occur.

bubble_chart Etiology

Clinically, aspiration of gastric contents with pneumonia caused by gastric acid is more common and significant than aspiration of hydrocarbon liquids. Kerosene, gasoline, dry lotion, furniture polish, etc., may occasionally be aspirated, particularly in children. In healthy individuals, due to the coordinated action of protective laryngeal reflexes and swallowing, food and foreign bodies generally do not enter the lower respiratory tract. Even if small amounts of liquid are accidentally aspirated, they can usually be expelled through coughing. However, in states of impaired consciousness—such as during general anesthesia, cerebrovascular accidents, epileptic seizures, alcohol intoxication, excessive anesthesia, or after taking sedatives—defensive mechanisms are weakened or lost, allowing foreign bodies to be inhaled into the trachea. Esophageal conditions, such as achalasia, upper esophageal cancer, Zenker's diverticulum, or incomplete esophageal emptying into the stomach, can lead to reflux into the trachea. Various causes of tracheoesophageal fistula may allow food to pass directly from the esophagus into the trachea. Iatrogenic factors, such as gastric tube stimulation of the pharynx inducing vomiting, or endotracheal intubation or tracheostomy impairing laryngeal function and suppressing normal pharyngeal movement, can result in aspiration of vomitus into the airways. Elderly individuals with reduced reflexes are more prone to aspiration pneumonia.

After aspiration of gastric contents, the acute pulmonary inflammatory response is triggered by gastric acid stimulation, with severity depending on the hydrochloric acid concentration in the gastric fluid, the volume aspirated, and its distribution in the lungs. When the pH of the aspirated gastric acid is ≤2.5, as little as 25 ml can cause severe lung tissue injury. Animal studies have confirmed that aspirating a liquid with a pH <1.5 at a volume of 3 ml/kg body weight can be fatal. The more widespread the distribution of the aspirated fluid, the more severe the damage.

bubble_chart Pathological Changes

When gastric contents are inhaled, gastric acid can immediately cause chemical burns to the airways and lungs. It irritates the bronchi, leading to intense spasms of the bronchial walls, followed by acute inflammatory reactions in the bronchial epithelium and peribronchial inflammatory infiltration. Gastric fluid entering the alveoli rapidly spreads to lung tissues, causing destruction and degeneration of alveolar epithelial cells, affecting capillary walls, increasing vascular permeability, and leading to fluid leakage from blood vessels, resulting in edema and hemorrhagic pneumonia. Simultaneously, due to damage to the alveolar capillary membrane, interstitial pulmonary edema forms. Within days, alveolar edema and hemorrhage gradually resolve and are replaced by hyaline membranes. Over time, pulmonary fibrosis may develop. If food or foreign objects are inhaled, bacteria residing in the pharynx can be carried into the lungs, leading to secondary bacterial infections dominated by anaerobic bacteria and the formation of lung abscesses. Pulmonary edema reduces lung tissue elasticity, decreases compliance, and reduces lung capacity. Additionally, the reduction in alveolar surfactant causes small airway closure and alveolar collapse, leading to microatelectasis. These factors collectively result in inadequate ventilation, ventilation/perfusion mismatch, and increased venous admixture, causing hypoxemia or metabolic acidosis. Massive vascular fluid leakage or reflex vasodilation can lead to hypotension. The pathological process of hydrocarbon inhalation is similar to that of gastric acid aspiration. Due to their low surface tension, hydrocarbons rapidly spread across large areas of the lungs upon inhalation and inactivate surfactant, making pulmonary atelectasis and edema more likely, leading to severe hypoxemia.

bubble_chart Clinical Manifestations

Patients often have a history of inhalation triggers and experience rapid onset, with symptoms typically appearing within 1 to 3 hours. The clinical manifestations are related to the underlying disease cause. For example, in cases of aspiration pneumonia caused by a tracheoesophageal fistula, symptoms such as spasmodic cough and shortness of breath often occur after eating. In cases of unconsciousness, inhalation may initially present with no obvious symptoms, but sudden dyspnea may develop 1 to 2 hours later, rapidly progressing to cyanosis and hypotension. Patients often cough up serous, frothy sputum, which may be blood-tinged. Moist rales can be heard in both lungs, sometimes accompanied by wheezing. Severe cases may develop acute respiratory distress syndrome.

Chest X-rays taken 1 to 2 hours after aspiration may reveal scattered, irregular, patchy shadows with blurred edges in both lungs. The distribution of pulmonary lesions is related to the patient's position during aspiration, commonly seen in the middle and lower lung fields, with the right lung more frequently affected. If pulmonary edema occurs, the patchy or cloud-like shadows in both lungs may merge into large areas, spreading outward from the hila, most prominently in the central and inner zones of both lungs. This appearance resembles that of cardiogenic acute pulmonary edema on X-ray, but the heart size and shape remain normal, and there are no signs of pulmonary venous hypertension.

bubble_chart Treatment Measures

In emergency situations, high-concentration oxygen should be administered immediately. Use a fiberoptic bronchoscope or endotracheal intubation to remove the foreign body, and apply positive end-expiratory pressure ventilation for the treatment of "acute respiratory distress syndrome." Correcting hypovolemia can be achieved with albumin or low-molecular-weight dextran. To avoid overloading the left ventricle and the leakage of colloidal fluid into the pulmonary interstitium, diuretics can be used. The use of adrenal corticosteroids remains controversial, with some advocating the administration of large doses of glucocorticoids within 12 hours of inhalation for 3–4 days to promote the absorption of pulmonary inflammation, while others hold opposing views. Antibiotics should only be used to control secondary infections and are not recommended for the prevention of bacterial infections, as their use neither reduces the incidence of secondary bacterial infections nor easily leads to the development of drug-resistant strains. The management principles after inhaling hydrocarbon liquids are the same as those mentioned above.

bubble_chart Prevention

The main measures to prevent aspiration pneumonia are to avoid the inhalation of food or stomach contents. For example, before surgical anesthesia, the stomach should be fully emptied. For unconscious patients, a head-down and lateral position can be adopted, and a gastric tube should be placed as early as possible. If necessary, tracheal intubation or tracheotomy should be performed. Strengthening nursing care is even more crucial.