Aspiration: Risk, Prophylaxis, and Treatment EPUB version of this bookEPUB version of this book

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 had administered water and brandy by mouth. Simpson 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. Among the 14 obstetric cases, 5 mothers died.

In a subsequent landmark paper, Mendelson reported a series of animal experiments that clearly described the clinical course and pathology of pulmonary acid aspiration. In the same paper, Mendelson 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 from aspirated liquid, but two mothers died from 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, meant to minimize the risk of pulmonary aspiration of gastric contents in parturients, has endured as a foundation of obstetric anesthesia practice.

INCIDENCE, MORBIDITY, AND MORTALITY

Maternal mortality from pulmonary aspiration of gastric contents has declined to almost negligible levels over the last several decades ( Fig. 28.1 ). This decline can likely be attributed to the following factors: (1) the greater use of neuraxial anesthesia; (2) the use of antacids, histamine-2 (H ₂) receptor antagonists, and/or proton-pump inhibitors (PPIs); (3) the use of rapid-sequence induction of general anesthesia; (4) improved training of anesthesia providers; and (5) the establishment and enforcement of nil per os (NPO) policies during labor and delivery. 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.

A bar graph shows maternal deaths due to anesthesia from 1952 to 2015, categorized by aspiration and other causes. — Fig. 28.1

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. 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 (a retrospective review of 172,334 consecutive patients undergoing general anesthesia and 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. 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.

Morbidity and mortality associated with aspiration vary according to (1) the physical status of the patient, (2) the contents and volume of aspirate, (3) the therapy administered, and (4) the criteria used for making the diagnosis. Since 1952, organizations in the United Kingdom have 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 rare (see Fig. 28.1 ). In the MBRRACE-UK reports from 2009 to 2015, there were no reported maternal deaths from aspiration. Prior reports from 2006 to 2008 identified 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 woman with a placenta previa who required an emergency cesarean delivery after eating a full meal and aspirated on emergence from general anesthesia. The UK Obstetric Surveillance System identified nine cases of aspiration in 1,496,720 maternities between September 2013 and August 2015, for an incidence of 6.0 per 1,000,000 maternities (95% confidence interval [CI] 2.18 to 11.4) and one mortality (case fatality 11%). Seven cases occurred in association with general anesthesia and two in women semiconscious for other reasons. Of the cases associated with anesthesia, one occurred during difficult tracheal intubation, one while intubated, one following tracheal extubation, two had a supraglottic (laryngeal mask) airway in place, and two had an oropharyngeal airway at the time of the event.

Data on pulmonary aspiration in obstetrics in the United States are less comprehensive. The Serious Complication Registry from the Society for Obstetric Anesthesia and Perinatology (SOAP) review of 307,000 deliveries from 30 US centers between 2004 and 2009 reported a failed tracheal intubation rate of 1 in 533, but no related cases of pulmonary aspiration. Prior to 1990, aspiration was the most common cause of anesthesia-related maternal death in the United States, with 17 deaths related to general anesthesia for every 1 death related to neuraxial anesthesia, although it is not clear from these data what proportion of deaths are attributable to aspiration. This ratio improved to 6:1 in the early 1990s and nearly equilibrated by 2002, likely due to both diminished use of general anesthesia and safer practices. However, mortality statistics are generally a poor predictor of maternal morbidity; several studies have indicated that perioperative aspiration is associated with important morbidity in obstetric patients. Furthermore, not all obstetric aspiration events occur in the context of general anesthesia. In a US closed claims analysis of 115 cases of pulmonary aspiration of gastric contents between 2000 and 2014, three identified obstetric patients were undergoing cesarean delivery with only one of the three receiving general anesthesia. A fourth identified obstetric patient aspirated during a cerclage procedure, prompting emergency cesarean delivery under general anesthesia.

A retrospective study of 48,619 patients undergoing cesarean delivery from 2007 to 2018 at two high-volume centers in Israel (general anesthesia rate 46.7%) reported three cases of suspected pulmonary aspiration. Two cases occurred during induction of general anesthesia for emergency cesarean delivery associated with a difficult airway, and one under deep sedation as an adjunct to spinal anesthesia. This represents an incidence of aspiration of 1 in 11,345 with general anesthesia and 1 in 25,929 with neuraxial anesthesia. There were no associated deaths. Taken together, these data reinforce that, while pulmonary aspiration in obstetric patients is rare, all possible measures must be taken to prevent it and vigilance must be maintained during both neuraxial and general anesthesia.

GASTROESOPHAGEAL ANATOMY AND FUNCTION DURING PREGNANCY

Esophagus

In adults, the esophagus is approximately 25 cm long and the esophagogastric junction is approximately 40 cm from the incisor teeth. In humans, the proximal one-third of the esophagus is composed of striated muscle, but the distal end contains only smooth muscle. Muscular sphincters at both ends are normally closed. The cricopharyngeal or upper esophageal sphincter prevents the entry of air into the esophagus during respiration, and the gastroesophageal or lower esophageal sphincter prevents the reflux of gastric contents. The lower esophageal sphincter is characterized anatomically and manometrically as a 3-cm zone of specialized muscle that maintains tonic activity. The end-expiratory pressure in the sphincter is 8 to 20 mm Hg above the end-expiratory gastric pressure. The lower esophageal sphincter is kept in place by the phrenoesophageal ligament, which inserts into the esophagus approximately 3 cm above the diaphragmatic opening ( Fig. 28.2 ). The lower esophageal sphincter is not always closed; transient relaxations occur that account for the gastroesophageal reflux that healthy people experience.

A paired anatomical view shows abdominal organs in nonpregnant and full-term pregnant states with labeled structures. — Fig. 28.2

Effects of Pregnancy on Gastric Function

Gastroesophageal reflux , resulting in heartburn, is a common complication of late pregnancy. Pregnancy compromises the integrity of the lower esophageal sphincter; it alters the anatomic relationship of the esophagus to the diaphragm and stomach, raises intragastric pressure, and in some women limits the ability of the lower esophageal sphincter to increase its tone (see Fig. 28.2 ). Progesterone, which relaxes smooth muscle, probably accounts for the inability of the lower esophageal sphincter to increase its tone. Lower esophageal pH monitoring has shown a higher incidence of reflux in pregnant women at term, even in those who are asymptomatic, than in nonpregnant controls. Therefore, at term gestation the pregnant woman who requires anesthesia should be regarded as having an incompetent lower esophageal sphincter . These physiologic changes return to their prepregnancy levels by 48 hours after delivery.

Serial studies assessing gastric acidity during pregnancy have proved difficult to perform because they require repeated placement of a nasogastric tube. However, in the most comprehensive study of gastric acid secretion during pregnancy, basal and histamine-augmented gastric acid secretion was measured in 10 controls and 30 pregnant women equally distributed throughout the three trimesters of pregnancy. No significant differences in basal gastric acid secretion were seen between the pregnant and nonpregnant women. The plasma concentration of the gastrointestinal hormone motilin is decreased during pregnancy. Studies have shown either no change or an increase in the plasma concentration of gastrin. A variety of techniques have been used to study gastric emptying during pregnancy and labor ( Table 28.1 ). Overall, the data suggest that pregnancy does not significantly alter the rate of gastric emptying. Moreover, gastric emptying has not been found to be delayed in either obese or nonobese term pregnant women who ingested 300 mL of water after an overnight fast. However, management of obese parturients should take into account the possible presence of other associated problems in this group of patients (e.g., hiatal hernia, difficult airway).

Table 28.1

Studies of Gastric Emptying During Pregnancy and Labor (1982–Present)

Method of Assessment	Study	Study Period and Subjects	Gastric Emptying
Epigastric impedance	O’Sullivan et al. (1987)	Nonpregnant controls, third trimester, 60 min postpartum	No delay
Applied potential tomography	Sandhar et al. (1992)	Sequential study 10 mothers: 37–40 weeks’ gestation, 2–3 d postpartum, 6 w postpartum	No delay
Acetaminophen absorption	Simpson et al. (1988)	Nonpregnant controls, 8–11 weeks’ gestation, 12–14 weeks’ gestation	8–11 w: no delay 12–14 w: delay
	Macfie et al. (1991)	Nonpregnant controls, first, second, and third trimesters	No delay in any trimester
	Geddes et al. (1991)	Postcesarean delivery Epidural fentanyl 100 µg	Delay
	Gin et al. (1991)	Postpartum: day 1 and day 3, 6 w	No delay
	Wright et al. (1992)	Labor, epidural bolus: (1) bupivacaine 0.375%; (2) bupivacaine 0.375% + fentanyl 100 µg	Epidural opioids: delay
	Whitehead et al. (1993)	Nonpregnant controls, first, second, and third trimesters Postpartum: 2, 18–24, and 24–48 h	Pregnancy: No change Postpartum: • 2 h: delay • 18–24 h: no delay • 24–48 h: no delay
	Ewah et al. (1993)	Labor with epidural infusion: (1) bupivacaine 0.25%; (2) bupivacaine 0.25% + fentanyl 50 or 100 µg, or diamorphine 2.5 or 5 mg	Epidural opioids: delay
	Levy et al. (1994)	Nonpregnant controls, 8–12 weeks’ gestation	Delay
	Stanley et al. (1995)	Second and third trimesters and 8 w postpartum	No delay
	Zimmermann et al. (1996)	Labor with epidural infusion: (1) bupivacaine 0.125%; (2) bupivacaine 0.125% + fentanyl 2 µg/mL	No delay
	Porter et al. (1997)	Labor with epidural infusion: (1) bupivacaine 0.125%; (2) bupivacaine 0.125% + fentanyl 2.5 µg/mL	Epidural fentanyl total: • <100 µg: no delay • >100 µg: delay
	Kelly et al. (1997)	Labor with neuraxial bolus: (1) epidural bupivacaine 0.375%; (2) epidural bupivacaine 0.25% + fentanyl 50 µg; (3) intrathecal bupivacaine 2.5 mg + fentanyl 25 µg	Epidural fentanyl: no delay Intrathecal fentanyl: delay
Real-time ultrasonography	Carp et al. (1992)	Nonpregnant controls, third trimester	No delay
	Chiloiro et al. (2001)	Serial study in 11 women: first and third trimesters, 4–6 mo postpartum	No delay
	Fiszer et al. (2022)	80 low-risk nonfasted parturients in labor randomized to receive high dose versus low-dose epidural fentanyl	Epidural fentanyl > 100 µg versus < 100 µg: no difference
Real-time ultrasonography and acetaminophen absorption	Wong et al. (2002)	Third trimester crossover study	50- or 300-mL water: no delay Faster gastric emptying with 300 mL
Real-time ultrasonography and acetaminophen absorption	Wong et al. (2007)	10 obese parturients Third-trimester crossover study	50- or 300-mL water: no delay

Gastric emptying appears to be normal in early labor but becomes delayed as labor advances; the cause is uncertain. Parenteral opioids cause a significant delay in gastric emptying, as do bolus doses of epidural and intrathecal opioids. Gastric emptying measured by acetaminophen absorption in laboring parturients receiving an epidural infusion of bupivacaine/fentanyl demonstrated delay when the cumulative fentanyl dose exceeded 100 µg. However, in a randomized controlled trial of 80, nonfasted, laboring women comparing low-dose (cumulative fentanyl < 100 μg) and high-dose (cumulative fentanyl > 100 μg) epidural fentanyl, the ultrasonographically determined rate of gastric emptying (assessment of change in antral cross-sectional area [CSA]) was not different between groups. While previous studies evaluated gastric emptying by pharmacokinetic timing of paracetamol absorption in the duodenum, this study used direct ultrasonographic assessment of gastric contents and is likely more relevant for the real-time assessment of aspiration risk.

RISK FACTORS FOR ASPIRATION PNEUMONITIS

Mendelson categorized 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 resulted in more severe pathology and clinical severity when the liquid was highly acidic. His observations and other investigations 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 < 2.5 cause a granulocytic reaction that continues beyond the acute phase. Aspiration of particulate material can yield a clinical picture with severity on par or worse than that caused by the aspiration of acidic liquid. Aspiration of small volumes of neutral liquid results in a 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.”

Historically, anesthesia providers have considered a nonparticulate gastric fluid with a pH < 2.5 and a gastric volume > 25 mL (i.e., 0.4 mL/kg) as risk factors for aspiration pneumonitis. No human study has directly addressed the relationship between preoperative fasting, gastric acidity and volume, and the risk for pulmonary aspiration during anesthesia. There appears to be a reasonable scientific basis to use a gastric pH threshold 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 ( Fig. 28.3 ).

A line graph shows changes in partial pressure of arterial oxygen over time after tracheal instillation of fluids with different p H levels and saline. — Fig. 28.3

Animal studies have also demonstrated that an increase in the volume of tracheal aspirate is associated with a higher risk for aspiration pneumonitis. 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. The investigators made the assumption that this entire volume, if contained in the stomach, could be aspirated. However, Raidoo et al. 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 and 1.0 mL/kg but not with volumes of 0.4 and 0.6 mL/kg. Similarly, Plourde and Hardy refuted the assumption that all the gastric contents will 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 > 2.5 and a gastric volume as low as possible.

PATHOPHYSIOLOGY

Aspiration pneumonitis (Mendelson 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, 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. This effect leads to an increase in intra-alveolar 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. These inflammatory mediators lead to the chemotaxis, accumulation, and activation of neutrophils in the alveolar exudate, upregulation of adhesion molecules within the pulmonary vasculature, and activation of the complement pathways. The neutrophils subsequently release oxidants, proteases, leukotrienes, and other proinflammatory molecules. Amplification of these inflammatory processes may result in the development of acute lung injury or acute respiratory distress syndrome (ARDS) ( Fig. 28.4 ).

A pair of illustrations shows a normal alveolus and an alveolus with acute lung injury, with labeled cellular and structural components. — Fig. 28.4

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 (e.g., PPI or H ₂-receptor antagonist) or patients with gastroparesis or intestinal obstruction. The bacterial content adds to the inflammatory response of acid aspiration.

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.

After the acute period, the process resolves through the proliferation and differentiation of surviving type II pneumocytes in the alveolar epithelial cells. 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 fibrosing alveolitis—an accumulation of mesenchymal cells, their products, and new blood vessels.

Bronchospasm and disruption of surfactant likely account for the decrease in Pa o ₂ and increase in shunting that are observed. Aspiration of large solid particles may cause atelectasis by obstructing large airways. 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.

CLINICAL COURSE

In most cases of aspiration during anesthesia, the anesthesia provider witnesses regurgitation of gastric contents into the hypopharynx. Patients who aspirate while breathing spontaneously have a brief period of breath-holding followed by tachypnea, tachycardia, and a slight respiratory acidosis. Significant aspiration always results in hypoxemia caused by an increase in shunting and, frequently, bronchospasm.

An abnormality on a chest radiograph can be seen in 85% to 90% of patients who aspirate gastric contents. Because these chest radiographic findings may lag behind clinical signs by as much as 12 to 24 hours, the initial radiograph may appear normal. In mild cases, alveolar infiltrates are seen in the dependent portions of the lungs. Severe aspiration results in diffuse bilateral infiltrates without signs of heart failure (i.e., without engorged pulmonary vasculature and/or enlarged cardiac silhouette) ( Fig. 28.5 ).

A chest radiograph shows bilateral lung opacities following pulmonary aspiration in pregnancy. — Fig. 28.5

These symptoms and signs may progress to satisfy the Berlin Definition for ARDS. The criteria are as follows :

•
Clinical: within 1 week of known clinical insult
•
Chest imaging: bilateral opacities not explained by effusions
•
Biochemical: Pa o ₂/F io ₂ ratio ≤ 300 mm Hg with continuous positive airway pressure (CPAP) or positive end-expiratory pressure (PEEP) > 5 cm H ₂ O
•
Origin of pulmonary edema: not explained by cardiac failure or fluid overload

A new global definition of ARDS builds upon the Berlin Definition to include high-flow nasal oxygen with a minimum flow rate ≥ 30 L/min, Pa o ₂/F io ₂ ratio ≤ 300 mm Hg, or Sp o ₂/F io ₂ ≥ 315 to identify hypoxemia, the addition of lung ultrasonography as an imaging modality along with chest radiography, and not mandating specific respiratory support devices in low-resource settings.

TREATMENT

Management principles for the treatment of pulmonary aspiration include (1) tracheal suction; (2) rigid bronchoscopy in cases of aspiration of large, solid particles; and (3) management of hypoxemia with CPAP in nonintubated patients. Treatments that lack evidence to support their use are the administration of corticosteroids, routine use of prophylactic antibiotics, and lung lavage with saline and bicarbonate.

Initial Management

Pulmonary aspiration of gastric contents must be instantly recognized and trigger a rapid, systematic response. Critical management steps include positioning the patient in a head-down position and prompt suction of the upper airway followed by tracheal intubation and suction of the primary bronchi with a soft suction catheter. Fiberoptic bronchoscopy can be useful for evaluating the extent of aspiration and whether solid particles are present, and for the removal of liquid contents. Rigid bronchoscopy is useful for removing large food particles that cause airway obstruction. Lung lavage with saline or bicarbonate does not reduce the parenchymal damage caused by acid aspiration and can worsen hypoxemia.

Antibiotics

Prophylactic antibiotics are not efficacious for treatment of aspiration and may lead to the development of infection with resistant organisms. Infection is not a component of acute pulmonary aspiration of sterile gastric contents. Antibiotics should be administered only in the presence of clinical findings that suggest infection (e.g., fever, worsening infiltrates on chest radiographs, leukocytosis, positive result of Gram stain of sputum, clinical deterioration).

In patients who are intubated, a nonbronchoscopic bronchoalveolar lavage sample can be sent for laboratory analysis. Tracheal sputum samples may be insufficient to identify a bacterial pathogen, and some authorities recommend sampling of the lower respiratory tract with a protected specimen brush.

Empirical antibiotic therapy is appropriate in patients with suspected bacterial colonization of gastric contents. The “at-risk” group (see earlier discussion) includes patients who have gastroparesis or bowel obstruction and those who are receiving antacid therapy. The use of PPIs and H ₂-receptor antagonists is common in late pregnancy, given the prevalence of gastroesophageal reflux disease. Reduced gastric acidity from long-term antacid therapy increases the incidence of community-acquired and ventilation-associated pneumonia, but it is uncertain whether parturients on long-term acid-suppression therapy are at higher risk for developing bacterial pneumonia after aspiration. Nonetheless, empirical antibiotic therapy is also appropriate for parturients on long-term antacid therapy and for those with aspiration pneumonitis that fails to resolve within 48 hours. The choice of antibiotic depends on the observed local patterns of antibiotic resistance. The target pathogens are gram-positive organisms (e.g., Streptococcus pneumoniae , Staphylococcus aureus ) and some gram-negative organisms (e.g., Haemophilus influenzae , Escherichia coli , Enterobacteriaceae) when the diagnosis is made less than 48 hours after hospital admission (i.e., community-acquired pneumonia). Pseudomonas aeruginosa is a common pathogen in cases of nosocomial (hospital-acquired) aspiration pneumonia. Anaerobes are no longer believed to be present in the majority of cases. Pharmacologic therapy should be altered when specific pathogens and their antibiotic sensitivities are determined.

Treatment of Hypoxemia

Exudation of fluid into the alveoli, decreased surface activity of surfactant, and atelectasis all result in intrapulmonary shunting and hypoxemia. The administration of CPAP in patients breathing spontaneously or the administration of PEEP in patients undergoing mechanical ventilation restores functional residual capacity, reduces pulmonary shunting, and reverses hypoxemia. Supplemental oxygen should be given as required.

Corticosteroids

Despite decades-long use of corticosteroids in the management of aspiration pneumonitis, animal and human studies have failed to demonstrate a beneficial effect on pulmonary function, lung injury, alveolar-capillary permeability, or clinical outcomes after acid aspiration. Thus, the administration of corticosteroids for aspiration pneumonitis is not recommended. Further consideration of corticosteroids for aspiration complicated by ARDS is discussed below.

Management of Respiratory Failure

Aspiration of gastric contents can result in activation of inflammatory intrapulmonary pathways consistent with the pathophysiology observed in ARDS. The basic tenets of management of ARDS include the use of lung-protective ventilation strategies, the judicious management of fluids, and the application of basic critical care algorithms. The management of severe ARDS and hypoxemia resistant to conventional management involves the use of rescue therapies (e.g., prone positioning, high-frequency oscillatory ventilation, extracorporeal membrane oxygenation) usually used in the critical care setting (see Chapter 53 ).

Mechanical Ventilation

The key principles governing mechanical ventilation in ARDS involve limiting the inspiratory plateau pressure to 30 cm H ₂ O and providing the lowest effective tidal volume to prevent alveolar overdistention and tidal (cyclic) recruitment-derecruitment. Such lung-protective strategies correlated with improved outcomes in a prospective multicenter trial of the management of ARDS in which the use of low tidal volumes and plateau pressure (6 mL/kg and 30 cm H ₂ O or less) was compared with traditional ventilation strategy (12 mL/kg and 50 cm H ₂ O or less). Patients in the lower tidal volume group had a 22% reduction in mortality and an increase in ventilator-free days. Current recommendations for the treatment of ARDS include mechanical ventilation that minimizes ventilator-induced lung injury (low target tidal volume [6 mL/kg], plateau pressure < 30 cm H ₂ O, prone positioning for severe ARDS, and higher PEEP in moderate and severe ARDS). In addition, guidelines support the use of high-frequency oscillatory ventilation for those with severe hypoxemia and limiting extracorporeal membrane oxygenation to a subset of patients who have defined dead space and static lung compliance values.

Positive End-Expiratory Pressure

PEEP is a recommended component of the initial ventilatory support in the setting of ARDS. A randomized clinical trial of ARDS (n = 549) compared the effects of low and intermediate PEEP levels set according to predetermined combinations of PEEP and F io ₂ in the setting of a lung-protective mechanical ventilation strategy. There were no significant differences in hospital mortality (24.9% versus 27.5%, respectively) or days to unassisted breathing (14.5 versus 13.8 days, respectively) between the two groups. However, the role of comparatively higher levels of PEEP in protective ventilation strategies for ARDS is far from clear. An experimental model for acute lung injury from acid aspiration demonstrated that the titration of PEEP improved arterial oxygenation but was associated with lung inflammation, as evidenced by histopathologic evaluation. This study supports the concept of best PEEP as a compromise between alveolar recruitment, lung inflammation, and hyperinflation. Current PEEP strategies focus on degree of recruitability of the lungs, given the finding that higher PEEP benefits patients with high recruitability (severe lung injury), while the injurious effects of high PEEP outweigh the benefit in those with low recruitability (mild lung injury).

Fluid Management

In a 2 × 2 factorial trial design, the ARDS Clinical Trials Network Research Group evaluated the use of a conservative versus liberal intravenous fluid strategy and the value of guiding this intervention with central venous pressure or pulmonary artery occlusion pressure measurements. The group that received conservative fluid management, whether guided by central venous pressure and/or pulmonary capillary occlusion pressure measurements, had much lower net fluid balance, better lung function, and a shorter duration of mechanical ventilation and intensive care unit stay. Further, there appeared to be no increase in the incidence or duration of shock or need for dialysis in the conservative fluid management arm of the trial. A 2017 metaanalysis of studies comparing conservative and liberal fluid resuscitation strategies found increased ventilator-free days and decreased intensive care unit stay among patients managed with conservative fluid strategies. Thus, early management of ARDS (after initial resuscitation) focuses on limiting iatrogenic insult with conservative fluid management.

Basic Critical Care Algorithms

To minimize the risk for sepsis, central venous catheters and other invasive hemodynamic monitors should be discontinued as early as is clinically feasible. Aseptic precautions should be used during care, and infections should be treated with antibiotics specific to the bacterial pathogen. Whether tight and rigorous glycemic control should be employed is controversial. Occasional withdrawal of sedation and the use of prophylaxis for gastrointestinal bleeding and thromboembolic events are currently considered the standard of care in any critically ill patient (see Chapter 53 ).

Corticosteroids

Recovery from ARDS depends on the functional resolution of the underlying pulmonary disorder, which may follow one of two courses: (1) rapid improvement in lung function with an uncomplicated recovery or (2) slow improvements in lung function, oxygenation, and ventilation with prolonged weaning and recovery. The corticosteroid controversy in ARDS in the context of aspiration is still unresolved. Although a 2009 systematic review suggested potential benefit from corticosteroids, their use did not appear to improve lung function or recovery in patients with ARDS in two well-conducted randomized clinical trials and may be associated with long-term side effects. A 2007 randomized controlled trial reported shortened duration of mechanical ventilation but no impact on mortality in patients with ARDS randomized to receive a methylprednisolone infusion versus placebo. A 2014 metaanalysis of corticosteroid therapy among 1474 patients in 18 studies showed no impact on mortality. While there was no specific analysis of cases of ARDS from aspiration-related lung injury, corticosteroid therapy increased mortality in a subgroup of patients with influenza-related ARDS. At the current time, while data do not support the routine use of high-dose corticosteroids in ARDS for the attenuation of lung injury after pulmonary aspiration, management algorithms support consideration of their use for nonresolving ARDS early in the nonresolving phase (between days 4 and 14).

PROPHYLAXIS

The risk for aspiration is extremely low when gastric emptying is normal and patients, including parturients, are appropriately fasted. Factors predisposing to regurgitation, particularly in obstetrics, include emergency surgery, difficult/failed tracheal intubation, light anesthesia, and gastroesophageal reflux. The risk for failed intubation is 3 to 11 times greater in pregnant patients than in nonpregnant patients, reported as 1 in 250 at the end of a 17-year audit in the United Kingdom (1978 to 1994) and as 1 in 232 in an 8-year audit in the United States (2006 to 2013) (see Chapter 29 ). An analysis of the Multicenter Perioperative Outcomes Group Database of patients undergoing general anesthesia for cesarean delivery from 2004 to 2019 revealed a lower failed intubation rate of 1 in 808, which may reflect the integration of video laryngoscopy into obstetric anesthesia practice. Nonetheless, airway edema, breast enlargement, obesity, and the high rate of emergency surgery can all contribute to the risk for failed tracheal intubation in pregnant women. Aspiration pneumonitis is often associated with difficult or failed intubation during the induction of general anesthesia. In a survey conducted by SOAP, intubation was recorded as difficult in 14 of 19 cases of aspiration in which tracheal intubation was required. Moreover, Warner et al. reported that the risk for aspiration during emergence from anesthesia was almost as high as that during induction of anesthesia. Furthermore, the most recent US closed claims analysis and UK reports highlighted aspiration during cesarean delivery with both general and neuraxial anesthesia. Thus, prophylactic regimens must provide protection during both induction of, and emergence from, general anesthesia. A high degree of vigilance for universal pharmacologic aspiration prophylaxis and careful surveillance must be maintained for all patients undergoing cesarean delivery or other obstetric procedures with general or neuraxial anesthesia.

Because the incidence of aspiration pneumonitis is low, the efficacy of prophylactic regimens is measured by their ability to alter gastric pH and volume. In 30% to 43% of pregnant women, the fasting gastric volume is greater than 25 mL and the gastric fluid pH is less than 2.5. However, the percentage of term parturients at risk may not differ from that of patients undergoing elective abortion, postpartum sterilization, or gynecologic surgery ( Table 28.2 ). Gastric volume and acidity at term gestation are similar to gastric volume and acidity during early pregnancy and the postpartum period, and in nonpregnant patients. Decreased lower esophageal sphincter tone and a higher risk for difficult tracheal intubation are the primary factors that increase the risk for aspiration during pregnancy and the immediate postpartum period, and these are the factors that mandate the need for pharmacologic prophylaxis.

Table 28.2

Prevalence of Fasting Gastric Findings in Various Populations (%)

Population	pH < 2.5	Volume > 25 mL	pH < 2.5 and Volume > 25 mL
Pregnant	57–80	51–54	31–43
Nonpregnant	75–95	45–67	45–60
Postpartum	54–93	61	60
Children	93–100	64–78	64–77
Obese, nonpregnant	88	86	75

Preoperative Oral Fluid Administration

Multiple studies have described no increase in gastric volume or acidity after the oral administration of 150 mL of fluid (e.g., coffee, tea, water, other clear liquids, orange juice without pulp) in nonpregnant adults 2 hours before elective surgery. The patients in these studies all fasted overnight and were expected to have a low gastric volume when the test meal was given. Lewis and Crawford noted that allowing women undergoing elective cesarean delivery to consume a meal of both tea and toast 2 to 4 hours preoperatively increased gastric volume and decreased gastric pH compared with a fasted control group. Consumption of tea without toast resulted in an increase in gastric volume, but it did not alter gastric pH. Particulate material was aspirated from the stomachs of 2 of the 11 patients who consumed both tea and toast. The investigators did not state the volume of tea consumed by these patients.

When gastric emptying of both 50 and 300 mL of water was assessed in nonlaboring term parturients, the gastric emptying half-time for 300 mL was significantly shorter than that for 50 mL. When a similar study was conducted in obese nonlaboring term parturients (mean [± standard deviation] prepregnancy body mass index 41 ± 9 kg/m ²), the gastric emptying time for 300 mL was not longer than that for 50 mL. The latter finding suggests that the American Society of Anesthesiologists (ASA) Guidelines for Obstetric Anesthesia, which state that “the uncomplicated patient undergoing elective cesarean delivery may have modest amounts of clear liquids up to 2 h before induction of anesthesia,” could also be applied to healthy, obese pregnant women presenting for elective surgery. However, factors other than the rate of gastric emptying can influence the rate of pulmonary aspiration, particularly in obese subjects. Obesity is associated with a higher incidence of gastroesophageal reflux and difficult airway management (both intraoperatively and postoperatively; see Chapter 48 ). Moreover, the cesarean delivery rate is higher and the success rate of trial of labor after cesarean delivery is lower in obese parturients.

Choice of Anesthesia

The US Obstetric Anesthesia Work Force Survey demonstrated that general anesthesia was used for less than 5% of elective cesarean procedures by 2011. Two sequential analyses performed at a large tertiary care obstetric facility showed that the use of general anesthesia for cesarean delivery decreased from 7.2% to 3.6% from 1990 to 1995 with a further decline from 1% to 0.8% from 2000 to 2005. One maternal death resulted from a failed tracheal intubation in the first cohort, with no reported anesthesia-related mortality during the second study period. Hawkins et al. reported 67 maternal deaths resulting from complications of general anesthesia and 33 maternal deaths resulting from complications of neuraxial anesthesia in the United States during the years 1979 to 1990. Approximately 73% of general anesthesia–related maternal deaths were caused by airway difficulty, primarily failed intubation and/or aspiration. In contrast, data from the more recent period spanning the years 1997 to 2002 indicate that the mortality rates for cesarean delivery are similar for general and neuraxial anesthesia. Studies reviewing failed tracheal intubation during the periods 1993 to 1998, 1999 to 2003, and 2013 to 2015 in the United Kingdom showed that, while the rate of failed intubation during this period had not declined, there were no deaths from this potentially fatal complication. Although this relative change in maternal mortality from the complications of general anesthesia is very encouraging, other global factors such as obesity have increased the challenges presented to anesthesia providers, particularly with respect to emergency operative deliveries. Therefore, techniques for preventing pulmonary aspiration of gastric contents will remain or even become increasingly relevant to clinical practice.

Antacids

The ASA Practice Guidelines for Obstetric Anesthesia state: “Before surgical procedures (e.g., cesarean delivery and postpartum tubal ligation), consider timely administration of nonparticulate antacids, H ₂-receptor antagonist, and/or metoclopramide for aspiration prophylaxis.” Particulate antacids should not be used as prophylaxis because, when aspirated, they cause pulmonary shunting and hypoxemia of magnitude similar to that caused by acid aspiration and greater than that caused by saline, alkalinized saline, or sodium citrate. Therefore, nonparticulate antacids (e.g., 0.3 M sodium citrate, Bicitra, Alka-Seltzer effervescent) should be used. Efficacy of sodium citrate depends on the baseline gastric volume and acidity. A volume of 30 mL of sodium citrate neutralizes 255 mL of hydrochloric acid with a pH of 1.0. The duration of action of sodium citrate is variable and depends on the rate of gastric emptying. O’Sullivan and Bullingham assessed the efficacy of sodium citrate in pregnant women using noninvasive radiotelemetry pH pills. After the administration of 15 mL of sodium citrate to women in the third trimester of pregnancy, pH remained greater than 3.0 for less than 30 minutes. When the same study was repeated in laboring women, the mean time that gastric pH remained greater than 3.0 was 57 minutes in subjects who had received no analgesia and 166 minutes in those who had received meperidine. Nonparticulate antacids should be administered within 20 minutes of the induction of general anesthesia, particularly if the procedure is an emergency and there is insufficient time for a coadministered H ₂-receptor antagonist to be effective.

Histamine-2 Receptor Antagonists

The ASA Task Force on Obstetric Anesthesia concluded that H ₂-receptor antagonists are efficacious in reducing gastric acidity and volume. H ₂-receptor antagonists block histamine receptors on the oxyntic cell, diminishing gastric acid production and slightly reducing gastric volume in the fasting patient. When given intravenously, an H ₂-receptor antagonist begins to take effect in as little as 30 minutes, but 60 to 90 minutes are required for maximal effect. After oral administration, gastric pH is higher than 2.5 in approximately 60% of patients at 60 minutes and in 90% at 90 minutes. The duration of action is sufficiently long to cover emergence from general anesthesia for a cesarean delivery.

While cimetidine (200 to 400 mg intravenously or orally) reduces gastric acidity within 60 to 90 minutes with plasma concentrations sustained for approximately 4 hours, its side effect profile has limited its use in obstetric patients. Specifically, cimetidine may decrease the rate of plasma clearance of lidocaine by binding to the cytochrome P450 system in the hepatocyte and by reducing hepatic blood flow. Cimetidine crosses the placenta, but this does not appear to have harmful effects. Because arrhythmias and cardiac arrest have been reported with the rapid intravenous administration of cimetidine, a slow rate of intravenous administration or the oral route of administration is recommended. The use of cimetidine in obstetric anesthesia has largely been replaced by other H ₂-receptor antagonists.

Ranitidine , a chemically substituted amino-alkyl furan, has been evaluated after the administration of an intravenous or intramuscular dose of 50 to 100 mg or an oral dose of 150 mg. These studies demonstrated a gastric pH > 2.5 within 1 hour and sustained therapeutic concentrations for approximately 8 hours. Ranitidine does not have any major interaction with the cytochrome P450 system and does not alter plasma concentrations of lidocaine or bupivacaine after their epidural administration. Nizatidine (given in doses of 150 to 300 mg orally) and famotidine (given in doses of 20 to 40 mg orally or intravenously) are alternative H ₂-receptor antagonists. Both have a duration of action > 10 hours and do not interfere with the metabolism of other drugs by the cytochrome P450 system.

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