A 49-year-old man at handed with an atypical pneumonia entailing an adult respiratory distress syndrome (ARDS).

A 49-year-old man at handed with an atypical pneumonia entailing an adult respiratory distress syndrome (ARDS). The refractory hypoxemia caused a myocardial infarction, leading us to attempt pharmacologic treatments. Almitrine bismesilate (AB) infusion allowed improvement of arterial oxygenation during 115 h without adverse weight This case is, to our knowledge, the first reported put offed treatment using AB for hypoxemia proper to ARDS.

Almitrine bismesilate (AB) increases [PaO.sub.2] and decreases [PaCO.sub.2] in patients with COPD[1-3] The AB has also been assessed in patients with the adult respiratory distress syndrome (ARDS).[4-6] It entails a transient if it be not that significant improvement in [PaO.sub.2] and in the alveolar-arterial [POsub2] difference,[4] a reduction in ventilation/perfusion inequalities as measured at the multiple inert gas elimination technique,[5] and an increase in [PaO.sub.2] comparable with that of a issue of 10 cm [H.sub.2]O.[6] The major side imports of AB are an increase in pulmonary arterial pressure[7] and a peripheral neuropathy during long-term administration.[1]

We report upon a patient with ARDS, becoming to atypical pneumonia, presenting with sharp refractory hypoxemia having caused a myocardial infarction, in whom a treatment of AB allowed a continue lengthen in timeed and reproducible improvement of arterial oxygenation without any apparent adverse effects

CASE REPORT

A 49-year-old male teacher was admitted to the ICU for respiratory failure. His medical history revealed a coronary arterial bypass 5 years previously, without following symptoms. He was a heavy tobacco smoker and was treated for hyperlipemia. During the week preceding admission, the patient complained of agitation (38 [degrees] C), increasing dyspnea, and thirsty cough. On physical examination, he was febrile (382 [degrees] C) the pulsation rate was 120 beats for minute, and the blood press 90/45 mm Hg. Respiratory rate was 50 for minute. Dry rales were heard bilaterally. Laboratory examination originates follow: hematocrit was 38.6 percent; hemoglobin, 129 g/dl; WBC consider 7.7 [multiplied by] [10.sup.9]/L with 6 percent band cells; platelet deem 164 [multiplied by] [10.sup.9]/L; prothrombin time, 65 percent of rule and activated partial thromboplastin time, 304 s; bilirubin, 16 [mu]M/L; alkaline phosphatase, 35 U/L; aspartate aminotransferase and alanine aminotransferase, 450 and 537 U/L respectively; lactate dehydrogenase, 2103 U/L; chest x-ray, bilateral interstitial infiltrates; and arterial descendants gases ([FIO.sub.2] = 0.4), pH 72 [PaCO.sub.2] 25 kPa, [PaO.sub.2] 80 kPa, oxygen saturation ([SaO.sub.2]) 88 percent base excess--15 mmol/L

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Broad appearance antibiotic therapy with amoxicillin/clavulanic acid and erythromycin was started. The nearest day, because of worsening hypoxemia and clinical signs of respiratory muscle fatigue, the patient was intubated and mechanical ventilation initiated. Bronchoalveolar lavage showed 14x[10sup4] cells/ml 34 percent macrophages, 2 percent lymphocyte 62 percent polymorphonuclear, 1 percent eosinophils, and 1 percent basophils. progeny and lavage cultures remained sterile. While receiving 100 percent [Osub2] with a pule of 5 cm [H.sub.2]O, arterial children gases were pH 7.34, [PaCO.sub.2] 57 kPa, [PaO.sub.2] 988 kPa, and [SaO.sub.2] 91 percent Peak inspiratory squeezing (PIP) was 40 cm [Hsub2]O A mixed ventilatory method combining high frequency jet and conventional ventilations was started the same day, allowing one as well as the other a decrease in PIP (25 to 30 cm [Hsub2]O) and a transiently better oxygenation ([FIO.sub.2] 055 [SaO.sub.2] 90 percent) The situation worsened throughout the next 6 days, however, requiring a progressive increase in [FIO.sub.2] to 10 with [SaO.sub.2] between 80 and 90 percent As a complication of this bitter hypoxemia, the patient had an inferior myocardial infarction (creatine kinase/creatine kinase-MB=769/120 U/L) A trial of nitric oxide (35 to 50 ppm) delivered via the inspiratory line was luckless for increasing [PaO.sub.2]. As pulmonary arterial influence was in the normal range, sum of two units tests with AB, 1 mg/kg intravenously during 1 h were performed, 24 h apart (Table 1) As the one and the other tests were beneficial to [SaO.sub.2] and well tolerated, a continuous infusion was administered, the dosage being adjusted (01 to 05 mg/kg/h) to maintain a [SaO.sub.2] [greater than or equal to] 85 percent The AB was infused for a total of 115 h

Figure 1 displays calculated shunt (Qs/QT) while the patient was ventilated with 100 percent [Osub2] during the AB infusion at different dosages. The solitary significant complications of ARDS were returning pneumothoraces requiring chest tube drainage. Otherwise, the patient movement forwarded well and was extubated after 26 days. He currented a marked weakness for which a muscular biopsy and an electromyography were performed. The diagnosis was mild myogenic muscular atrophy without inflammation. There were no electrophysiologic signs of peripheral neuropathy. The patient improved and was discharged from the hospital after 42 days. Three month later, the patient walks freely without any paresthesia or dysesthesia.

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