We studied the effects of hypophosphatemia on diaphragmatic function in eight patients with acute respiratory failure who were artificially ventilated. Their mean serum phosphorus level was 0.55 +/- 0.18 mmol per liter (normal value, 1.20 +/- 0.10). The contractile properties of the diaphragm were assessed by measuring the transdiaphragmatic pressure generated at functional residual capacity during bilateral supramaximal electrical stimulation of the phrenic nerves. Diaphragmatic function was evaluated in each patient before and after correction of hypophosphatemia, which was achieved by administration of 10 mmol of phosphorus (as KH2PO4) as a continuous infusion for four hours. After phosphate infusion, the mean serum phosphorus level increased significantly (1.33 +/- 0.21 mmol per liter, P less than 0.0001). The increase in serum phosphorus was accompanied by a marked increase in the transdiaphragmatic pressure after phrenic stimulation (17.25 +/- 6.5 cm H2O as compared with 9.75 +/- 3.8 before phosphate infusion, P less than 0.001). Changes in the serum phosphorus level and transdiaphragmatic pressure were well correlated (r = 0.73). These results strongly suggest that hypophosphatemia impairs the contractile properties of the diaphragm during acute respiratory failure, and they emphasize the importance of maintaining normal serum inorganic phosphate levels in such patients.

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Systemic air embolism has been frequently reported after penetrating thoracic trauma. In blunt thoracic trauma, systemic air embolism has been rarely diagnosed, and then only after an invasive procedure such as thoracotomy. Transesophageal echocardiography has been recently introduced for the early assessment of trauma patients and is considered a sensitive noninvasive procedure to diagnose air embolism. We report three cases of systemic air embolism in patients with pulmonary contusion secondary to a blunt thoracic trauma requiring controlled ventilation. Transesophageal echocardiography was performed for evaluation of hemodynamic instability, and it showed air bubbles in the left atrium and left ventricle during the insufflation phase, which disappeared during apnea. A decrease in airway pressure (release of PEEP, low tidal volume, high frequency jet ventilation) significantly reduced the systemic air embolism. We concluded that systemic air embolism can occur after blunt thoracic trauma, and transesophageal echocardiography enables a rapid and accurate diagnosis that may be useful for therapeutic management.