To the Editor: Naloxone is an opioid antagonist, used for rapid reversal of opioid effects. Naloxone has been known to cause adverse effects such as hypotension, arrhythmias, seizures, and rarely… Click to show full abstract
To the Editor: Naloxone is an opioid antagonist, used for rapid reversal of opioid effects. Naloxone has been known to cause adverse effects such as hypotension, arrhythmias, seizures, and rarely flash noncardiogenic pulmonary edema. A 29-year-old man with unknown medical history was brought to the emergency department by the emergency medical technician after they found him unresponsive on the streets. On initial encounter, the paramedics noticed that the patient was having agonal breathing and pin point pupils on examination. Paramedics immediately gave a push of 1 mg of naloxone intravenously, and the patient regained consciousness. On initial presentation to the emergency department, patient was profusely diaphoretic and had an episode of vomiting. Vital signs were significant for blood pressure of 90/55 mm Hg. Patient was started on intravenous crystalloids and was intubated to mechanical ventilation for airway protection. He was placed on pressure-regulated volume control mode of ventilation with settings of fraction of inspired oxygen 100%, respiratory rate 15 breaths per minute, positive end expiratory pressure of 5 cm H2O, and tidal volume of 450 mL. A stat chest radiograph confirmed the accurate positioning of the endotracheal tube but also showed increased bilateral pulmonary vascular congestion and haziness over the left lung as shown in Figure 1, highly suspicious of flash pulmonary edema. An arterial blood gas showed partial pressure of oxygen of 75 mm Hg making a P/F ratio of 75 indicating severe acute respiratory distress syndrome. Positive end expiratory pressure was increased to 20 cm H2O to correct the hypoxemia. Diuresis with 40 mg of intravenous furosemide was given, and the patient was immediately transferred to medical intensive care unit. A repeat arterial blood gas performed 2 hours later showed an improved P/F ratio of 219. Initial electrocardiogram revealed normal sinus rhythm, and transthoracic echocardiogram was unremarkable. A computed tomographic scan of the chest without intravenous contrast showed opacification in bilateral lung fields and dense consolidation in the dependent segment of the left lung as shown in Figure 2, suggestive of classical flash pulmonary edema. Serial arterial FIGURE 1. Chest radiograph showing bilateral pulmonary vascular congestion concerning for pulmonary edema. Arrows show increased pulmonary vascular congestion.
               
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