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    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.


    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.


    Anaesthesia (general or local pharyngeal)
    Cerebrovascular accidents
    Gastroesophageal reflux
    Nasogastric tube feeding
    Neuromuscular diseases
    Seizures or post-ictal states


    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.


    Non-cardiogenic pulmonary oedema
    Pneumonia of infectious origin
    Pulmonary emboli
    Respiratory Distress Syndromes (e.g. ARDS)


    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



    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
         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)


          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).


    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


    Pulmonary recovery is usually complete in those patients surviving the
    acute phase.


    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.