2), particularly those requiring a rapid intervention (fluid maldistribution, anaphylaxis, and cardiogenic pulmonary edema), must be considered. Using a predefined cutoff of 0.65, the edema fluid to plasma protein ratio had a sensitivity of 81% and a specificity of 81% for the diagnosis of acute lung injury.īefore making the diagnosis of NPPE, other causes of pulmonary edema ( table 2 fig. 2compared protein concentration (Biuret method) in the pulmonary edema fluid (taken via a suction catheter inserted into the endotracheal tube) and blood. The edema fluid to plasma protein ratio is an additional method to discriminate between cardiogenic pulmonary edema and acute lung injury. The severity of hypoxic respiratory failure, chest radiographic findings, and the time course to recovery are key elements that need to be considered for making diagnosis of acute lung injury or acute respiratory distress syndrome. Diagnosis is made by exclusion of other causes, as outlined in figure 2. Activation of and damage to the pulmonary endothelium are the hallmark of acute lung injury or acute respiratory distress syndrome, 16which is caused by a variety of inciting events such as sepsis, systemic inflammatory response syndrome, aspiration, caustic inhalation, blood transfusions, or trauma. He was discharged later that morning without signs or symptoms of respiratory compromise on oral analgesics and usual surgical follow-up in 1–2 weeks.Īcute respiratory distress syndrome and acute lung injury represent a heterogeneous group of severe hypoxic lung diseases. Examination on the morning of the first postoperative day revealed clear lungs bilaterally and peripheral oxygen saturation of 95–97% on ambient air. With supplemental oxygen, diuretic treatment, and bronchodilator inhalation, his respiratory status continued to improve with peripheral oxygen saturations greater than 94% on ambient air 10 h after surgery. A diagnosis of NPPE was made, and the patient was admitted to the inpatient postoperative recovery room for overnight observation. Physical examination revealed crackles bilaterally at the lung bases, and a chest radiograph was performed, showing diffuse, bilateral, hazy, and interstitial opacity throughout both lungs, with normal lung volumes, normal heart size, and no pleural effusions ( fig. The patient coughed pink, frothy sputum during the course of the first postoperative hour. In the postanesthesia care unit, the patient's oxygen saturation was maintained with 100% oxygen administered via a nonrebreather facemask. Nondepolarizing motor blockade was not reversed because train-of-four monitoring of the ulnar nerve showed a train-of-four ratio of greater than 90%, demonstrating adequate spontaneous recovery. The patient was returned to the supine position for emergence and extubation. A total of 500 ml lactated Ringer's solution was administered during the 65-min surgical procedure. The patient was hemodynamically stable with minimal blood loss and was easily ventilated and oxygenated. The intraoperative course was unremarkable. A total of 0.5 mg hydromorphone was administered for analgesia. The patient was turned prone, bilateral breath sounds were reconfirmed, and schwannoma excisions were performed on the left thigh and the left flank. 3 Macintosh laryngoscope (Teleflex Medical, Research Triangle Park, NC) on the first attempt with direct visualization of the vocal cords. He was atraumatically intubated with a 7-mm ID endotracheal tube using a no. The patient was premedicated with 2 mg midazolam, and anesthesia was induced with 250 mg fentanyl, 500 mg thiopental, and 8 mg vecuronium given for facilitation of tracheal intubation.
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