Bronchopulmonary Aspiration

Thoracic Trauma

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Bronchopulmonary Aspiration Joseph LoCicero III, M.D. *

Since the classic description in 1946 by Mendelson of aspiration during obstetric anesthesia, bronchopulmonary aspiration has been studied extensively.s Although more is known of the mechanism of injury, therapeutic management and mortality rates have changed little. 2 Most of the effort today in clinical practice is to prevent aspiration of acidic gastric contents and, when aspiration does occur, to recognize the problem early and treat the patient aggressively. ETIOLOGY

Aspiration may be divided into two main categories: active and silent. Patients who vomit and aspirate gastric contents are considered to have active aspiration, whereas patients who aspirate during anesthesia or while intubated in an intensive care unit are considered to have silent aspiration. Adriani and Berson recognized that between 16 and 27 per cent of all anesthetized patients will have silent aspiration to some extent. l Such aspiration can be facilitated by a variety of mechanisms (Table 1). Insuffiation of air into the stomach during induction is a frequent cause of silent aspiration. Lower esophageal sphincter relaxation, secondary either to primary reflux or to medications, may enhance the potential for aspiration from an insuffiated stomach. During an intra-abdominal operation, bowel manipulation may cause reflux of bowel contents into the oropharynx, where silent aspiration may occur. Another less common cause for bronchopulmonary damage leading to the clinical picture of bronchopulmonary aspiration is the inhalation of oxidants such as hydrocarbons or phosgene. MECHANISM OF INJURY It is well recognized that aspiration of highly acidic materials (pH below 2.4) produces an intense bronchorrhea,5, 11 whereas aspirating mate*Assistant Professor, Department of Surgery, Northwestern University Medical School, Chicago, Illinois

Surgical Clinics of North America-Vol. 69, No.1, February 1989

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Table 1. Etiology of Silent Bronchopulmonary Aspiration Insuffiation during anesthetic induction Lower esophageal sphincter relaxation Bowel manipulation intraoperatively

rial of higher pH is no different from aspirating water. It has also been shown that highly acidic materials produce damage on contact with the trachea and bronchi. Hamelberg and Bosomworth showed that instillation into the trachea of acid at pH 1. 75 produced a pH change at the surface of the lung within 12 to 18 seconds. 5 Within 3 minutes, patchy infiltrates were present. This finding implies that neutralization of the acid will not result in clinical benefit because the changes are too rapid. It was also noted that the pH of the tracheal aspirate returned to normal within 15 minutes. Type I or membranous pneumocytes responsible for surfactant production are damaged by the acidic milieu. In addition, when an exudative response develops, surfactant levels decrease dramatically. Type II or granular pneumocytes proliferate whenever injury occurs and exclude the type I pneumocytes from the alveoli. This loss of surfactant produces alveolar-capillary block and a decrease in lung compliance. These changes will lead to bronchorrhea and a decrease in ventilation:perfusion ratios. This is expressed clinically as bronchospasm and dyspnea. As hypoxemia becomes worse, production of surfactant is further depressed. This interstitial edema will increase pulmonary vascular resistance. The resistance may also rise in part because of local hypoxemia. Additional insult to the lung comes from infection, which can develop either primarily or secondarily. Primary infection occurs when the aspirate is contaminated. Patients who have altered gastric pH, especially those patients who have gastric carcinoma, gastric outlet obstruction, or gastric ulcer, are at highest risk. 7 Also, patients who have been receiving H2 blockers are at risk. Laws and colleagues showed in a controlled study that these patients also develop bacterial overgrowth. 6 The gastric microHora proliferate and contaminate the lung directly. However, the usual situation is secondary colonization of the lung, as gastric contents with a low pH are usually sterile. In these cases, the exudative process produced by the acid within the lung allows opportunistic organisms, particularly oral microHora, to colonize the tracheobronchial tree. A more ominous situation is the colonization of the damaged lung by selected organisms not eradicated by the empiric antibiotics in general use in most hospitals today. Nearly all late-generation cephalosporins cover most bacteria with the exception of the enterococcus and Pseudorrwnas species, and these two organisms are emerging as the most common cause of secondary infections in bronchopulmonary aspiration. CLINICAL PICTURE Unrecognized bronchopulmonary aspiration carries a mortality rate of 40 to 80 per cent. 12 Patients who aspirate large food particles may asphyxiate

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Table 2. Clinical Picture of Bronchopulmonary Aspiration Symptoms Dyspnea, tachycardia, cyanosis Physical examination Rales, rhonchi

Laboratory findings Hypoxemia, hypercapnea Chest roentgenography Interstitial edema

early. If smaller food particles within the tracheobronchial tree go unrecognized, asphyxia may develop as late as 4 hours after aspiration. 4 Shortly after aspiration, the patient develops tachypnea, tachycardia, cyanosis, and dyspnea (Table 2). Physical examination of the patient shows widespread rales and wheezing, which are direct manifestations of the alveolar damage described above. Blood-gas determinations show a mixed pattern of both hypoxemia and hypercapnia. A chest roentgenogram will demonstrate a pattern of interstitial pulmonary edema very early in the course of this disease. This constellation of symptoms, originally enumerated by Mendelson, should alert one to the diagnosis of aspiration.

SURGICAL ASPIRATION Patients receiving general anesthesia, long-term sedation, or major regional blocks are at risk for bronchopulmonary aspiration (Table 3). Conditions that may contribute to aspiration in surgical patients include Zenker's diverticulum, esophageal obstruction, increased intracranial pressure, intestinal obstruction, or increased abdominal pressure secondary to ascites or obesity. Aspiration of gastrointestinal contents is the most significant problem, but blood produced during the trauma of intubation or copious oral or nasal secretions may also be aspirated during a surgical procedure. Aspiration may occur during almost any phase of a surgical patient's hospital stay. Following preoperative medication, some of the least trained personnel in the hospital transport patients to the staging area for surgery, where they may be unattended for some period of time. They have altered sensorium and, although they have received a drying agent, may still have retained gastric secretions. It is well known that aspiration may occur during induction of anesthesia or the conduct of the operation, but other critical times are important. One that is usually not considered is that of emergence from anesthesia. In the recovery room, although observed frequently, semiconscious patients may aspirate. In the early postoperative period, patients may have atelectasis and decreased functional residual capacity. They may not be able to cough and clear even the most minor aspiration. Aspiration has also occurred during the postoperative period Table 3. Predisposing Conditions for Bronchopulmonary Aspiration in Surgical Patients Gastrointestinal obstruction Obesity

Ascites or tumor Zenker's diverticulum

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Table 4. Common Misconceptions About Bronchopulmonary Aspiration Stomach is empty 4 hours after eating Preoperative starvation is desirable

Nasogastric tubes empty the stomach Regional anesthesia solves the problem

secondary to vomiting, acute gastric dilatation, myocardial infarction, or pulmonary embolism. There are several misconceptions about perioperative bronchopulmonary aspiration (Table 4). First, the stomach does not empty within 4 hours. It continues to secrete acid, and the volume actually may be increased by ingestion of saliva. Second, preoperative starvation, in general, is not helpful. Fasting stimulates release of hydrogen ion, and starvation may lead to a decrease in available energy stores, which may also stimulate gastric secretion. Third, although the stomach may be emptied by a nasogastric tube, it frequently is not completely drained. During removal of gastric contents, food particles or the stomach wall itself may block further removal of material. Finally, although regional anesthesia with an awake patient may be helpful in decreasing bronchopulmonary aspiration, supplemental sedation may negate this benefit. Moreover, older patients who become agitated during long procedures under regional anesthesia may require supplemental analgesia, which may place the patient at as much risk of aspiration as those receiving a general anesthetic.

BRONCHOPULMONARY ASPIRATION IN THE INTENSIVE CARE UNIT Active aspiration (vomiting) is the most common cause of aspiration in intensive care units. 12 However, intubated patients may easily develop silent aspiration around the endotracheal tube. In addition, as many as 10 per cent of patients who cannot clear their mouths of secretions may aspirate. Rarely, tracheoesophageal fistulas form in patients who have longterm intubation, leading to direct aspiration. The patients in an intensive care unit who are at greatest risk for the development of bronchopulmonary aspiration include those with neurologic deficits that do not allow for protection of the airway, those with altered sensorium from drug overdose, and those with severe myasthenia gravis.

NEAR DROWNING In the United States, 7000 people die from drowning each year. Although many of the deaths are secondary to aspiration of water, approximately 10 per cent may be attributable to acute asphyxia and laryngospasm. Near-drowning syndromes can be caused by aspiration of as little as 2.2 ml per kg.9 Although victims of both fresh and sea water aspiration develop hypoxemia, the mechanism of this event is different. After sea water aspiration, the hypertonic fluid draws plasma into the lungs, producing

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fluid-filled but perfused alveoli, leading to ventilation-perfusion mismatches. After fresh water aspiration, the hypotonic fluid is absorbed rapidly into the circulation. However, the water changes the surface tension characteristics of pulmonary surfactant, leading to alveolar collapse and massive intrapulmonary shunting. Aspiration of a large enough quantity of fresh or salt water will likely cause significant serum electrolyte abnormalities. . Survival correlates best with a normal chest roentgenogram on admission following a near-drowning episode.lO Regardless of the initial arterial oxygen, a clear chest film is the best prognostic sign.

THERAPY

Little has changed in the initial therapy in patients with aspiration since the description by Mendelson. At that time, patients received oxygen; aminophylline; atropine, epinephrine, or both; and antibiotics. Today, the major additional therapeutic maneuver is early intubation and mechanical ventilatory support. This therapy, combined with positive end expiratory pressure, has led to the greatest success in the treatment of significant bronchopulmonary aspiration. If the aspiration is noted immediately, bronchoscopy may be of some benefit to clean the airway and remove particles. Lavage does not appear to be of any benefit because the acid is so readily absorbed. Corticosteroids may be given but probably are of no benefit. Indeed, in a controlled randomized trial in septic patients, Bone and associates showed that steroids may even be detrimental to some patients. 3 A roentgenogram of the chest should be obtained to determine if there is any significant atelectasis. The treatment for bronchospasm remains'the same. In patients who aspirated more than 2 hours previously, bronchoscopy is indicated only if there are areas of collapse visible on the chest film. Other treatments remain the same. In all patients, prevention of further aspiration is paramount. Increase in stomach pH may be maintained by H2 blockers. Nasogastric decompression of the stomach may also be helpful. Antibiotics should be instituted. Because most of the organisms that colonize the airway after aspiration are oral microflora, high-dose penicillin is the best presumptive empiric antibiotic until cultures demonstrate resistant organisms. All patients should maintain a high caloric intake. Intravenous hyperalimentation may be superior to attempted enteral feeding in these patients.

SUMMARY Bronchopulmonary aspiration rema~ns a significant threat to the surgical and intensive care unit patient, and mortality rates for this condition remain high. The key to improvement is prevention. However, if aspiration does occur, early recognition and aggressive treatment will produce the best results. Expeditious intubation, ventilation, removal of particulate matter,

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prevention of atelectasis, institution of antibiotics, and nutritional support are standards of care.

REFERENCES 1. Adriani J, Berson W: Aspiration during anesthesia and surgery. Am Surg 20:568-574,

1954 2. Blitt CD, Gutman HL, Cohen DD, et al: "Silent" regurgitation and aspiration during general anesthesia. Anesth Analg 49:707-713, 1970 3. Bone RC, Fisher CJ, Clemmer TP, et al: A controlled clinical trial of high-dose methylprednisolone in the treatment of severe sepsis and septic shock. N Engl J Med 317:653-658, 1987 4. Gardner AMN: Aspiration offood and vomit. Q J Med 27:227-242, 1958 5. Hamelberg W, Bosomworth PP: Aspiration pneumonitis: experimental and clinical observations. Anesth Analg 43:669-677, 1964 6. Laws HL, Bryant JW, Palmer MD, et al: Effects of preoperative medications on gastric pH, volume and Hora. Ann Surg 203:61~19, 1986 7. LoCicero J, Nichols RL: Sepsis after gastroduodenal operations: relationship to gastric acid, motility, and endogenous microHora. South Med J 73:878-880, 1980 8. Mendelson CL: The aspiration of stomach contents into the lungs dUring obstetric anesthesia. Am J Obstet Gynecol 52:191-205, 1946 9. Modell JH, Graves EA, Ketover A: Clinical course of 91 consecutive near-drowning victims. Chest 70:231-238, 1976 10. Pearn J: The management of near drowning (reView). Br Med J 291:1447-1452, 1985 11. Teabeaut JR: Aspiration of gastric contents: experimental study. Am J Pathol 28:51-67, 1952 12. Roberts RB: Pulmonary Aspiration. Boston, Little, Brown, 1977, p 4 Joseph LoCicero III, M.D. 303 East Chicago Avenue Ward Building 9-105 Chicago, Illinois 60611