ANESTHESIOLOGY

GISELE DE AZEVEDO PRAZERES, MD

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Pulmonary Aspiration

Introduction

Aspiration occurs when some kind of material -particulate (food, foreign body) or fluid (gastric contents, blood, or saliva)-enters from the pharynx into the trachea, usually in the course of a general anesthesia, when the patient’s airway reflexes are depressed.

Fortunatelly, aspiration and its consequences are serious but not common complications in modern anesthetic practice. Aspiration pneumonitis is potencially preventable and its incidence is aproximately 1-7 cases of significant importance in 10.000 anesthetics.The severity of pulmonary outcomes after an aspiration event is associated with the presence of comorbid diseases (ASA physical status III and higher) and procedures performed emergently.

Risk factors

Several risk factors can be identified in most cases of aspiration. Usually these factors are related to a patient condition predisposing to delayed gastric emptying or regurgitation, emergency status, difficulty in airway management, type of surgery, and specific patients populations (extremes of age, obstetric patients, ambulatory surgery patients).See Table 1.

Physiopatology

The consequences of pulmonary aspiration depend on the type of material aspirated, its volume and pH. It is now accepted that even a small volume of acidic material can cause severe pneumonitis. Aspiration can produce pulmonary embarassmant by severe mechanisms, but the classic “Mendelson Syndrome” (sequence of events following the aspiration of gastric contents) is caused by chemical injury due to acid material. Critical values for gastric pH and volume, (only a guideline in humans), are considered to be pH < 2,5 and volume >0,4 ml/Kg.

When an acidic fluid with these characteristics is aspirated, it immediately causes alveolar-capillary breakdown, resulting in interstitial edema, intraalveolar hemorrhage, atelectasis, increased airway resistance, and commonly hypoxia. These changes usually start within minutes of the initiating event, and may worsen over a period of hours. The first phase of the response is direct reaction of the lung to acid (chemical pneumonitis); the second phase is due to leucocyte or inflammatory response to the initial damage which occurs hours later, and may lead to respiratory failure.

Nonacidic fluid aspiration destroys surfactant, causes alveolar collapse, atelectasis and hypoxia. It also occurs destruction of lung architecture, and late inflammatory response (not as great as in acid aspiration ).

Aspiration of particulate food mattercauses both physical obstruction of the airway and a later inflammattory response due to the presence of a foreign body. It results in alternating areas of atelectasis and hyperexpansion, hypoxia and hypercapnia. When acid is mixed, damage is greater and prognostic is worse.

Signs and symptons

Aspiration may occur “silently”-without the anesthesiologist’s knowledge- during anesthesia. Patients should be monitored because changes like the appearence of tachypnea, rales, cough, cyanosis, wheezing and fever, may signal an aspiration event, during the course of an anesthetic procedure.

The patient who is suspected of aspiration should recover completely (with no pulmonary sequelae ) if, at the end of 2 hours, he shows none of the above signs and symptons, and has no increased oxygen requirement.

In contrast, aproximately 75% of patients with any of these signs and symptons within 2 hours, require supplemental oxygen to mantain Sp O2 >90%, ventilatory support or both. They also may develop pulmonary complications including radiographic evidence of adult distress syndrome (ADRS ), pneumonitis, or pneumonia (with or without positive viral or bacterial identification ).

Treatment

Treatment of aspiration pneumonitis is mainly supportive, consisting of oxygen and ventilatory support with positive end-expiratory pressure (PEEP ).Patients with particulate aspirate may need bronchoscopy to remove large obstructing pieces.

Antibiotics should be used only if infection is documented, its prophylatic use, steroid therapy and pulmonary lavage have not been shown to be useful.

Preventive measures

The first thing is to recognize patients at risk of aspiration. For these patients, associated to the fasting period (6-8 hours for solid food and 3-4 hours for clear liquids ), it may be used gastrokinetic medications like metoclopramide, which increase gastric emptiyng and esophageal sphincter tone; nonparticulate antacids such as sodium citrate, and H2 receptor antagonists like famotidine, ranitidine, and cimetidine (the last choice because of its nondesirable side effects ), which pH of gastric fluid.

Patients who are supposed to have easy intubations, may receive a rapid sequence induction, which consists of preoxygenating the patient and placing pressure over the cricoid cartilage Sellick maneuver. After doing this, general anesthesia is induced and a paralyzing dose of relaxant is administred.The patient’s trachea is intubated and the endotracheal ballon cuff is inflatted. Cricoid pressure should be released only after ensuring that endotracheal tube is correctly placed.

Awake intubation is an alternative to patients with difficult airways, because it allows spontaneous breathing and protects the airway from aspiration. It should be done with topical local anesthetic and the judicious use of sedation, before induction of general anesthesia.

Prognostic

The average hospital stay is 21 days, much of which is in intensive care unit. Complications range from bronchospasm and pneumonia, to ADRS, lung abscess, and empyema. The average mortality rate is 5%.

Bibliography

Buckley PP: Anesthesia and obesity and gastrointestinal disorders. In Barash PG, Cullen BF, Stoelting RK [eds]: Clinical Anesthesia, pp 1169-1183. Philadelphia, JB Lippincott, 1992.

Warner MA, Warner ME, Weber JG: Clinical significance of pulmonary aspiration during the perioperative period. Anesthesiology 78:56-62, 1993.

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