Death from ARDS and cardiovascular collapse following lidocaine administration.

نویسندگان

  • R A Promisloff
  • D C DuPont
چکیده

We read with interest the selected report of ARDS following administration of lidocaine by Howard and associates (Chest 1982; 81:644-45). A similar experience occurred at our institution and merits description. A 19-year-old woman had fiberoptic bronchoscopy performed to evaluate new, bilateral interstitial infiltrates. A diagnosis of histiocytosis X was made three years earlier when a pathologic, longbone fracture was noted. She had received cyclophosphamide and methotrexate in the past for this condition. At the time of bronchoscopy, she was receiving no chronic medications. The patient was pre-medicated with 1 mg ofhydromorphone and 0.5 mg of atropine intramuscularly. Less than 30 ml of 1% lidocaine solution was employed for topical anesthesia. Bronchoalveolar lavage ofthe right middle lobe and four transbronchial biopsies ofthe right middle and lower lobe were performed without incident. The patient tolerated the procedure well, and post bronchoscopy, the chest film was unchanged. Approximately 20 minutes after returning to her room, the patient was noted to develop hypotension and tachycardia and she became obtunded. An intravenous line was placed and saline solution and naloxone were administered without clear improvement. A respiratory arrest was observed, and she was promptly intubated. The vocal cords were widely patent and placement of an endotracheal tube yielded large amount offoamy pulmonary edema. She was placed on 100% oxygen with 5 cm PEEP and transferred to the Respiratory Intensive Care Unit. Corticosteroids, antihistamines and a vasopressor were started. Arterial blood gases on 100% oxygen with 5 cm PEEP revealed a PaO, of58 mm Hg. A chest roentgenogram demonstrated extensive bilateral alveolar infiltrates; the frothy pulmonary edema fluid continued to be suctioned out of the endotracheal tube. Hypotension and refractory bradycardia occurred. The patient subsequently died five hours after bronchoscopy. Autopsy revealed pathology consistent with the adult respiratory distress syndrome and changes consistent with histiocytosis. We feel our patient developed an anaphylactic, or delayed anaphylactoid, reaction tolidocaine with cardiovascular collapse and the adult respiratory distress syndrome. Although this case was similar to that of Howard and associates, the pulmonary deterioration in our patient was refractory to all forms of therapy. Since lidocaine is so frequently used in bronchoscopic procedures, this reaction should be looked for and an extensive history for lidocaine allergy should be sought before it is administered.

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عنوان ژورنال:
  • Chest

دوره 83 3  شماره 

صفحات  -

تاریخ انتشار 1983