History

In 1848, Sir James Simpson first suggested aspiration as a cause of death during anesthesia. Hannah Greener, a 15-year old given chloroform for a toenail extraction, became cyanotic and “sputtered” during the anesthetic. A “rattling in her throat” then developed, and she soon died. Her physician administered water and brandy by mouth. Simpson¹ contended that it was the aspiration of water and brandy, and not the adverse effects from the chloroform, that caused her death. In 1940, Hall published a report of 15 cases of aspiration, 14 of which occurred in mothers receiving inhalation anesthesia for a vaginal or cesarean delivery.² Among the 14 obstetric cases, 5 mothers died.

Subsequently, Curtis Mendelson, in a landmark paper, reported a series of animal experiments that clearly described the clinical course and pathology of pulmonary acid aspiration.³ In the same paper, Mendelson also audited 44,016 deliveries at the New York Lying-In Hospital between 1932 and 1945. He identified 66 (0.15%) cases of aspiration, of which the aspirated material was recorded in 45 cases; 40 mothers aspirated liquid, and 5 aspirated solid food. Importantly, no mothers died of acid aspiration, but 2 mothers died of asphyxiation caused by the aspiration of solid food. At this time general anesthesia usually involved the inhalation of ether, often as Mendelson observed, by “a new and inexperienced intern.” Mendelson therefore advocated (1) the withholding of food during labor, (2) the greater use of regional anesthesia, (3) the administration of antacids, (4) the emptying of the stomach before administration of general anesthesia, and (5) the competent administration of general anesthesia. This advice became the foundation of obstetric anesthesia practice during subsequent decades.

Incidence, Morbidity, and Mortality

Maternal mortality from pulmonary aspiration of gastric contents has declined to almost negligible levels in the past 3 decades (Figure 29-1).^4–6 This decline can probably be attributed to the following factors: (1) the greater use of neuraxial anesthesia; (2) the use of antacids, histamine-2 (H₂) receptor antagonists, and/or proton-pump inhibitors; (3) the use of rapid-sequence induction of general anesthesia; (4) an improvement in the training of anesthesia providers; and (5) the establishment and enforcement of nil per os (NPO) policies. Arguably, the common use of neuraxial analgesic/anesthetic techniques, both during labor and for cesarean delivery, is the single most important factor in this remarkable decline in maternal mortality from pulmonary aspiration.

The reported incidence of aspiration pneumonitis depends on the criteria used for making the diagnosis. The relative risk for aspiration in pregnant versus nonpregnant women can best be estimated from comparisons within single-study populations. Olsson et al.⁷ reported an overall incidence of aspiration of 1 in 2131 in the general population undergoing anesthesia and 1 in 661 in women undergoing cesarean delivery (i.e., a threefold higher aspiration risk). In two other surveys related to aspiration (one a retrospective review of 172,334 consecutive patients undergoing general anesthesia and the other a review of 133 cases of aspiration from the Australian Anaesthetic Incident Monitoring Study [AIMS]), there were no cases of pulmonary aspiration in women undergoing either elective or emergency cesarean delivery.^8,9 However, in the latter two studies, emergency surgery was a significant predisposing factor for aspiration; this finding may be relevant for the practice of obstetric anesthesia, given that many obstetric surgical procedures are performed on an urgent or emergency basis. The AIMS study also implicated obesity as a significant risk factor for aspiration; others have noted that obesity is associated with an increased risk for maternal mortality.^4,5

Morbidity and mortality associated with aspiration vary according to (1) the physical status of the patient, (2) the type and volume of aspirate, (3) the therapy administered, and (4) the criteria used for making the diagnosis. Since 1952, the Department of Health in the United Kingdom has published detailed triennial reports on all maternal deaths. Data from these reports, now administered by the body Mothers and Babies—Reducing Risk through Audits and Confidential Enquiries across the UK (MBRRACE-UK), indicate that death from pulmonary aspiration in obstetrics is vanishingly rare (see Figure 29-1).^4–6 In the last five reports, which cover the 15-year period from 1994 to 2008, there were three maternal deaths from aspiration; one was an obese parturient, the second was a mother anesthetized 3 days after delivery, and the third was a women with a placenta previa who required an emergency cesarean delivery after eating a full meal and aspirated on emergence from general anesthesia. Although the number of anesthetics, particularly general anesthetics, administered to parturients during this 15-year period is unknown, there were approximately 10.5 million deliveries, indicating that the mortality rate from aspiration was less than 1 in 3.5 million deliveries.

Data on pulmonary aspiration in obstetrics in the United States are more difficult to evaluate. Despite the establishment of an ongoing National Pregnancy Mortality Surveillance System by the Centers for Disease Control and Prevention (CDC), it is often difficult to obtain adequate and detailed information about every maternal death. Prior to 1990, aspiration was the most common cause of anesthesia-related maternal death in the United States; it has been calculated that at that time there were 17 deaths related to general anesthesia for every one death related to regional anesthesia.¹⁰ By the early 1990s, this ratio had improved to 6 to 1. By 2002, death rates for both general and regional anesthesia were similar.¹¹ However, mortality statistics are generally a poor predictor of maternal morbidity; several studies have indicated that perioperative aspiration can be associated with important morbidity in obstetric patients,^12,13 and thus all possible measures still must be taken to prevent pulmonary aspiration in obstetric patients.

Gastroesophageal Anatomy and Physiology

Risk Factors for Aspiration Pneumonitis

Mendelson³ divided aspiration pneumonitis into two types: liquid and solid. Whereas the aspiration of solids could result in asphyxiation, Mendelson demonstrated that the sequelae from the aspiration of liquids were more severe clinically and pathologically when the liquid was highly acidic (Figure 29-5). His observations, together with the results from other investigations,^64–72 suggest that the morbidity and mortality of aspiration depend on the following three variables: (1) the chemical nature of the aspirate, (2) the physical nature of the aspirate, and (3) the volume of the aspirate. Aspirates with a pH less than 2.5 cause a granulocytic reaction that continues beyond the acute phase.⁷² Aspiration of particulate material can engender a clinical picture with severity equal to or greater than that caused by the aspiration of acidic liquid.⁷¹ Aspiration of small volumes of neutral liquid results in a very low rate of mortality. However, aspiration of large volumes of neutral liquid results in a high mortality rate, presumably as a result of the disruption of surfactant by the large volume of liquid or from a mechanism similar to that seen in “near drowning.”⁶⁷

Historically, anesthesia providers have considered a nonparticulate gastric fluid with a pH less than 2.5 and a gastric volume greater than 25 mL (i.e., 0.4 mL/kg) as risk factors for aspiration pneumonitis.^64,69,70 No human study has directly addressed the relationship between preoperative fasting, gastric acidity and volume, and the risk for pulmonary aspiration during anesthesia.^73,74 There appears to be a reasonable scientific basis using a gastric pH cut-off value of less than 2.5 as a risk factor. In animal experiments, the risk for aspiration pneumonitis clearly increased with decreasing pH of the tracheal aspirate.^64,67 Awe et al.⁶⁴ illustrated this concept in a graph of PaO₂ versus time for aspirates of varying pH (see Figure 29-5).

Animal studies have also demonstrated that an increase in the volume of tracheal aspirate is associated with a higher risk for aspiration pneumonitis.⁶⁷ However, the volume of aspirated material associated with risk has been disputed. The commonly accepted volume of 0.4 mL/kg (approximately 25 mL in a 70-kg adult) originated from an experiment in a single rhesus monkey in which 0.4 mL/kg of an acidic liquid was administered into the right mainstem bronchus and resulted in the animal’s death.⁷⁰ The investigators made the assumption that this entire volume, if contained in the stomach, could be aspirated. However, Raidoo et al.⁷⁵ demonstrated variability in the response of juvenile monkeys to different volumes of an acidic tracheal aspirate. Death was seen with aspirate volumes of 0.8 mL/kg and 1.0 mL/kg but not with volumes of 0.4 mL/kg and 0.6 mL/kg. Similarly, Plourde and Hardy⁷⁶ refuted the assumption that all the gastric contents would be aspirated and demonstrated that gastric volumes of 0.4 mL/kg did not increase the risk for aspiration. Hence the gastric volume that puts a patient at risk for aspiration pneumonitis has not been determined. However, a reasonable goal of prophylactic therapy would be a gastric pH greater than 2.5 and a gastric volume as low as possible.

Pathophysiology

Aspiration pneumonitis (Mendelson’s syndrome) describes a chemical injury to the tracheobronchial tree and alveoli caused by the inhalation of sterile acidic gastric contents, whereas aspiration pneumonia may be regarded as an infectious process of the respiratory tract caused by the inhalation of oropharyngeal secretions that are colonized by pathogenic bacteria. Aspiration of gastric contents could therefore result in acid injury to the lung with or without bacterial and particulate matter–related effects.

Aspiration of acidic liquid injures the alveolar epithelium and results in an alveolar exudate composed of edema, albumin, fibrin, cellular debris, and red blood cells,^3,69,71,72 whereas the aspiration of neutral, nonparticulate liquid leads to an alveolar exudate with minimal damage to the alveoli. The phospholipid and apoprotein composition of surfactant changes, exerting a negative effect on its surface-active properties.⁷⁷ This effect leads to an increase in intraalveolar water and protein content and a loss of lung volume, resulting in a decrease in pulmonary compliance and intrapulmonary shunting of blood. The cellular debris and bronchial denuding cause bronchial obstruction. The exudative pulmonary edema, bronchial obstruction, reduced lung compliance, and shunting result in hypoxemia, increased pulmonary vascular resistance, and increased work of breathing. After the direct acid-mediated injury of the respiratory tract, an intense inflammatory response ensues from macrophage activation and secretion of cytokines, interleukins (IL) IL-1, IL-6, IL-8, and IL-10, and tumor necrosis factor-alpha (TNF-α).⁷⁸ These inflammatory mediators lead to the chemotaxis, accumulation, and activation of neutrophils in the alveolar exudate, up-regulation of adhesion molecules within the pulmonary vasculature, and activation of the complement pathways. The neutrophils subsequently release oxidants, proteases, leukotrienes, and other proinflammatory molecules.⁷⁸ Amplification of these inflammatory processes may result in the development of acute lung injury or acute respiratory distress syndrome (ARDS) (Figure 29-6).^77–79

The acidic contents of the stomach prevent the growth of bacteria under normal conditions. However, gastric contents may become colonized with pathogenic gram-negative bacteria in patients receiving antacid therapy or with enteral feeding tubes, gastroparesis, or intestinal obstruction. The bacterial content adds to the inflammatory response to acid aspiration.⁸⁰

Aspiration of particulate matter in the supine position most commonly involves injury to the posterior segments of the upper lobes and the apical segments of the lower lobes, whereas aspiration in the semirecumbent or upright position typically leads to injury to the lower lobes. The right lower lobe is the most common site of aspiration injury because the right mainstem bronchus has larger and more vertical architecture compared with the left mainstem bronchus. Obstruction of the bronchus or bronchioles results in bronchial denudation and collapse of the bronchopulmonary segments. Persistent or unresolved collapse can lead to lung abscesses and cavitation.⁸⁰

After the acute period, the process resolves through the proliferation and differentiation of surviving type II pneumocytes in the alveolar epithelial cells.^78,79 The type II pneumocytes actively transport sodium out of the alveolus, and water follows passively. Soluble proteins are removed by paracellular diffusion and endocytosis, and insoluble proteins are removed by macrophages. Neutrophils are removed by programmed cell death and subsequent phagocytosis by macrophages. Type II pneumocytes gradually restore the normal composition of the surfactant. In a subset of patients with ARDS, the injury progresses to a fibrosing alveolitis—an accumulation of mesenchymal cells, their products, and new blood vessels.

Bronchospasm and disruption of surfactant likely account for the slight decrease in PaO₂ and increase in shunting that are observed.⁷² Aspiration of large solid particles may cause atelectasis by obstructing large airways.³ Aspiration of smaller particulate matter causes an exudative neutrophilic response at the level of the bronchioles and alveolar ducts; the clinical picture is similar after the aspiration of acidic liquid.^66,71,72

Clinical Course

In most cases of aspiration during anesthesia, the anesthesia provider witnesses regurgitation of gastric contents into the hypopharynx.³

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