Airway, breathing, circulation, and disability (of neurological function) (ABCDs) defines a prioritized sequence of evaluation and treatment which provides a safe and effective method of managing any patient with a suspected air embolus in its early stage.
Speed of diagnosis and management is essential for all types of gas embolism. Failure of a patient to make a dramatic response to these first-line measures indicates the need to consider rapid institution of hyperbaric therapy.
All patients who have gas embolism have the potential to be hypoxemic. Thus immediate administration of 100 per cent oxygen is necessary. In an unconscious patient any obstruction in the oropharynx must be cleared under direct vision. If protective airway reflexes are intact, as demonstrated by a normal gag reflex, a tight-fitting oxygen mask with a reservoir should be used to provide flow rates of more than 12 l/min. If reflexes are depressed or absent, the airway must be secured at the earliest opportunity by intubation. Administration of 100 per cent oxygen optimizes tissue oxygen supply and attenuates bubble size by causing 'nitrogen washout'. It is essential to avoid exposure to nitrous oxide.
Circulatory arrest is a clinical diagnosis. Basic life support followed by advanced life support should be instituted. Any potentially lethal arrhythmias should be treated (Chamberlain.. eLaL 1994).
Closed chest compressions may have the additional benefit of dissipating any embolic gas into the pulmonary arterial tree. The circulation should be supported with warmed intravenous crystalloid solutions. Other therapeutic maneuvers that rapidly treat circulatory compromise include the prevention of further embolization (e.g. decompression of pneumothorax or occluding an open central venous catheter), attempted aspiration of air via indwelling central venous catheters, and placing the patient in the left lateral decubitus and/or Trendelenberg position. The last of these maneuvers prevents obstruction of the pulmonary outflow tract.
Patients requiring positive-pressure ventilation need strategies to keep their peak airway pressures below 50 cmH 2O. Lowering positive end-expiratory levels, reducing tidal volume, and permissive hypercarbia may significantly decrease systemic air embolism in the presence of barotrauma ( Sa.ada...eL,a/ 1995).
Delayed circulatory embarrassment may be negated by adminstration of 8 mg dexamethasone followed by a maintenance dose depending on the patient's clinical course.
An abnormal neurological status that does not respond rapidly to the above measures is an absolute indication for hyperbaric therapy. Seizure prophylaxis using standard anticonvulsant therapy should be considered in any patient with even the slightest alteration of the sensorium.
Hyperbaric centers in the United Kingdom and the Royal College of Physicians of London stress the significance of early compression in a hyperbaric chamber when first-aid measures fail to achieve complete resolution (James 1993).
Any acute symptoms or signs caused by air embolism can be ameliorated by hyperbaric oxygen therapy. Increased pressure has several effects on a fixed mass of gas. The volume of free gas is reduced (Boyle's law) and gas enters solution (Henry's law). Increasing the partial pressure of oxygen dissolved in the plasma permits supplemental oxygen delivery to the tissues. Increasing the partial pressure of oxygen in the alveoli favors nitrogen diffusion from bubbles in the pulmonary circulation and the alveoli, facilitating elimination.
The principles of hyperbaric therapy are rapid compression to several atmospheres followed by intermittent 100 per cent oxygen and 'air breaks' to prevent the symptoms of oxygen toxicity. Treatment periods are of the order of 4 to 6 h. The compression is carried out slowly to permit the gas dissolved in the plasma to equilibrate with the alveolar gas. It must be emphasized that rapid transfer of the patient to a hyperbaric chamber greatly improves the prognosis. Treatment instituted within 4 h is usually successful.
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