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.