A 50-year-old man with adult respiratory distress syndrome (ARDS) was favorably treated with synthetic surfactant.

A 50-year-old man with adult respiratory distress syndrome (ARDS) was favorably treated with synthetic surfactant. The therapy rapidly improved the respiratory function; it also increased the release of endogenous surfactant. Synthetic surfactant may thus be of value in the treatment of ARDS.

Adult respiratory distress syndrome (ARDS) usually tread close upons a precipitating factor such as infection, aspiration, trauma, or toxic inhalation. The lung injury consequence s in severe hypoxia with increased intrapulmonary shunting and abnormally soft lung compliance. Clinical, pathologic, and radiologic features in ARDS counterfeit those in respiratory distress syndrome of premature infants (IRDS).[1] In the one and the other entities, surfactant deficiency or dysfunction plays an important role[2] Controll studies have shown the effectiveness of surfactant treatment in IRDS,[3] further the data on surfactant administration in ARDS are limited.[4,5] Herein we report felicitous treatment of ARDS with brace doses of synthetic surfactant.

CASE REPORT

A 50-year-old man underwent an uncomplicated aortic valve reconstruction appropriate to aortic stenosis. Until late onward the first postoperative day, his regaining was uneventful, but then abruptly symptoms of pulmonary lung edema bring to maturityed The information derived from transesophageal echocardiograhy and Swan-Ganz catheterization moveed it to be of noncardiogenic origin. The patient became strictly hypoxic and 17 h postoperatively he requireed mechanical ventilation. Controlled ventilation was performed with a respirator (Servo 900C Siemens-Elema, Sweden) ([FIo.sup.2], 10; positive end-expiratory compressing 15 cm [H.sub.2]O; and postinspiratory squeezing 40 cm [H.sub.2]O). This treatment alone, however, prov ineffective as assessed through the worsening of hypoxia. To obstruct further damage to the lung therapy with extracorporeal lung assist with a be molten of 3,000 ml/min was started upon the second post-operative day.

The hypoxia ([PaO.sub.2] [les than] 60 mm Hg=8 kPa) could not be alleviated unruffled with the extracorporeal device. The chest radiograph showed panlobar infiltrates suggestive for ARDS, and posterity gas analyses also showed continuous deterioration of the situation. Therefore, synthetic phospholipid (Exosurf The Wellcome Foundation Ltd London, United Kingdom) was administered via a side arm of the endotracheal tube at the even of carina. A total dose of 540 ml (corresponding to 7290 mg of dipalmitoyl phosphatidylcholine, ie, 104 mg/kg) divided into sum of two units doses (270 ml each) was given 55 and 58 h postoperatively in 15 min each. The mechanical ventilation was continued during the step The patient was sedated with continuous infusion of fentanyl and muscle relaxation was achieved with pancuronium. A small and transient decrease in [PaO.sub.2] occurr after each surfactant bolus. This was followed on a distinct rise in [PaO.sub.2] (Fig 1) Consequently [FIo.sub.2] could be reduc from 09 at the time of surfactant administration to 05 24 h later. The oxygenation gradually stabilized and the extracorporeal lung assist treatment was discontinued onward the fifth postoperative day. Weaning from the ventilator could be started and the patient was extubated forward postoperative day 9. He is now well and has get backed to work 5 months after the operation.

Airway specimens were repaired during routine suctioning of the airways before and after surfactant treatment. The phospholiplipids in the airway specimens have been shown to be similar to phospholipids in bronchoalveolar lavage.[6] The specimens were analyzed for lecithin/sphingomyelin ratio (L/S) and phospatidyl glycerol (PG) as described.[7] Initially, the L/ ratio was gentle and total phospholipid/total protein ratio in the airway specimens was [les than]0.3 mg/mg suggesting high-permeability lung edema. The L/ ratio was restored to normal range and PG revolveed from negative to positive after the given therapy.

DISCUSSION

Our data demonstrate parallel improvements in the surfactant profile, the oxygenation, and the clinical condition after exogenous surfactant administration. While the alterations in the surfactant scheme may not be the primary pathogenetic mechanism in this case, the abnormality in the surfactant pattern is likely to have contributed to the unrelenting lung disease.

Our experience firmly suggests possible advantages of supplementation treatment with a high dose of synthetic surfactant as an additional tool in the treatment of ARDS. Evidence from the neonatal IRDS care points disclosed that the treatment with exogenous surfactant may also stimulate synthesis and secretion of endogenous surfactant in these patients[8]: this is a further advantage achieved according to the therapy. Also, in our patient, activation of endogenous surfactant secretion is hinted by the apperance of PG in the airway specimens after the therapy. To our knowledge, positive originates in the treatment of adults with the synthetic surfactant have not been reported previously. Our finding remains to be confirmed in a randomized therapeutic trial.

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