PULMONARY ASPIRATION DEFINITION Entry of gastric contents or other foreign substances into the respiratory tract. This in turn may produce obstruction of the airways and/or chemical inflammation of the lung. TOXIC CAUSES Any agent causing loss of protective airway reflexes, in particular those resulting in central nervous system depression or seizures. Pulmonary aspiration of certain hydrocarbons can occur without significant depression of the level of consciousness and may result in hydrocarbon pneumonitis. NON-TOXIC CAUSES Anaesthesia (general or local pharyngeal) Cerebrovascular accidents Gastroesophageal reflux Nasogastric tube feeding Neuromuscular diseases Seizures or post-ictal states CLINICAL FEATURES The clinical signs and symptoms are typically those of a chemical pneumonitis and develop rapidly, usually within two hours, following the aspiration. These symptoms/signs include dyspnoea, cough, fever, wheeze and cyanosis. These signs and symptoms may be partially or completely obscured by the clinical features (especially CNS depression) of the precipitating intoxication. The diagnosis may be confirmed by the presence of an infiltrate on chest x-ray and/or relative hypoxaemia, or by bronchoscopy. Severe cases may progress to severe hypoxaemia (PaO2 < 50 mmHg), apnoea and shock. DIFFERENTIAL DIAGNOSIS Non-cardiogenic pulmonary oedema Pneumonia of infectious origin Pulmonary emboli Respiratory Distress Syndromes (e.g. ARDS) RELEVANT INVESTIGATIONS Chest x-ray: Typically shows diffuse bilateral infiltrates (massive aspiration) or densities in dependent lung segments (posterior segments of upper lobes, superior segments of lower lobes and basilar segments of lower lobes). However, any distribution of x-ray infiltrate in the clinical setting should suggest the diagnosis. Arterial blood gas analysis: Hypoxaemia and respiratory acidosis. Alveolar-arterial O2 gradient correlates with severity of pneumonitis. Bronchoscopy TREATMENT Initial management is supportive and includes: Establishment of airway patency Ensuring adequate ventilation Administration of supplemental oxygen Vigorous airway suctioning to remove any residual aspirated material Nebulised bronchodilators Fluid therapy to maintain normovolaemic state Prophylactic antibiotic therapy is not indicated. Antibiotics should only be given to treat bacterial superinfection (see below). Antibiotic selection is empiric in the first instance but may subsequently be modified on the basis of culture results. A suitable regimen covering the usual oral anaerobes is: Benzylpenicillin 600 mg intravenously every 4 to 6 hours for 1 to 2 days for a total of 10 days (may switch to amoxicillin-clavulinic acid when oral therapy appropriate) plus Metronidazole 500 mg intravenously every 12 hours for 1 to 2 days followed by 400 mg orally every 12 hours for a total of 10 days or as a single agent Clindamycin 600 mg intravenously slowly (over 30 minutes) every 8 hours for 1 to 2 days followed by 300mg orally every 6 hours for a total of 10 days. Aerobic gram-negative bacilli are likely in alcoholic or chronically hospitalised patients and is this situation, replace benzyl penicillin with Cefotaxime 1g intravenously every 8 hours or Ceftriaxone 1g intravenously daily. Corticosteroids are of no benefit and may be detrimental. Bronchoscopy is useful in those patients suspected to have aspirated large particles that might be retrieved from the airway (suggested by persistent atelectasis). CLINICAL COURSE AND MONITORING Mortality is dependent on the extent of the initial aspiration and correlates with both the extent of the radiologic infiltrate and the arterial-to-alveolar oxygen tension ratio. Most patients improve rapidly. The chest x-ray infiltrates usually resolve within two weeks. Clinical deterioration occurring at about 48 hours following the aspiration indicates likely bacterial superinfection. This deterioration is marked by recurrent fever, leucocytosis, development of purulent sputum and a new or extending pulmonary infiltrate on xray. LONG-TERM COMPLICATIONS Pulmonary recovery is usually complete in those patients surviving the acute phase. AUTHOR(S)/REVIEWERS Author: Lindsay Murray, Queen Elizabeth II Medical Centre, Perth, Australia. Peer Review: Rio de Janeiro 9/97: J.N. Bernstein, E. Birtanov, R. Fernando, H. Hentschel, T.J. Meredith, Y. Ostapenko, P. Pelclova, C.P. Snook, J. Szajewski London 3/98: T. Della Puppa, T.J. Meredith, L. Murray, A. Nantel.