Bruce Cload

Drug-induced rash with eosinophilia and systemic symptoms syndrome with bupropion administration

BACKGROUND Sustained-release bupropion is commonly used for the symptomatic relief of depressive illness and as an adjuvant in smoking cessation therapy. OBJECTIVE To report a case of bupropion-induced drug rash with eosinophilia and systemic symptoms syndrome, including acute hepatitis, obstructive lung disease, and myositis. METHODS After the patient discontinued use of bupropion, serologic tests, muscle biopsies, pulmonary function tests, a chest x-ray examination, venous Doppler ultrasounds, and an electrocardiogram were performed. RESULTS On discontinuation of bupropion and prolonged systemic corticosteroid therapy, there was complete resolution of symptoms. CONCLUSIONS To our knowledge, this is the first reported case of drug rash with eosinophilia and systemic symptoms syndrome induced by bupropion therapy. We report this case to notify clinicians of the potential serious multisystem complications that can occur with sustained-release bupropion therapy.

Potential impact of N-terminal pro-BNP testing on the emergency department evaluation of acute dyspnea

OBJECTIVES Measurement of the serum B-type natriuretic peptide (BNP) level and more recently its precursor, N-terminal proBNP (NT-proBNP), has been advocated to facilitate the diagnosis of heart failure in the emergency department (ED). We sought to determine the potential impact of adding NT-proBNP testing to the routine evaluation of emergency patients with acute dyspnea. METHODS This prospective cohort study enrolled a convenience sample of acutely dyspneic patients at a tertiary care ED. We excluded trauma patients and those under 30 years of age. Patients underwent standard evaluation, including radiography when indicated. At the point of final diagnosis and blinded to the NT-proBNP result, physicians documented the likelihood that heart failure accounted for the patients acute dyspnea on a 7-point Likert scale, the data from which was subsequently collapsed to 3 categories for analysis purposes. The primary outcome was the agreement between clinical impression and the NT-proBNP assay classified using manufacturer-recommended, age-specific cut-offs. Newly proposed cut-offs from a recent study were also evaluated. RESULTS One hundred and twenty-nine patients making 139 ED visits were enrolled (median age 76 years; 59% admitted). The serum NT-proBNP assay was positive in 119 (86%, 95% confidence interval [CI] 80%-91%) cases, including 75% (43/57, 95% CI 62%-86%) of the cases that the treating physician felt were not caused by heart failure, and 86% (25/29, 95% CI 68%-96%) where the treating physician was unsure. The median NT-proBNP concentration was higher in patients clinically believed to have heart failure rather than pneumonia or chronic obstructive pulmonary disease; however, the ranges of these values overlapped extensively (median 4361 pg/mL; interquartile range [IQR] 2386-10877 v. 1651 pg/mL; IQR 370-4745, respectively). CONCLUSIONS There is high discordance between the clinical impression of treating physicians and NT-proBNP concentrations, notably in patients who are believed not to have heart failure. Although the reference standard of ED diagnosis is imperfect, the broad overlap in NT-proBNP concentrations suggests poor specificity in this target patient population. The introduction of routine ED NT-proBNP testing using the current cut-offs would be expected to result in substantial indirect costs from further diagnostic testing. It remains unclear whether the introduction of this diagnostic test would have a positive impact on clinically relevant patient outcomes.

Where is the ET tube

A 79-year-old man developed acute onset of tongue and neck swelling while camping. Diphenhydramine was administered at the scene, and he was taken by car to the emergency department (ED) at a tertiary care hospital. His medical history included hypertension, asthma and chronic back pain. He was taking the following medications: lisinopril, salbutamol, ipratropium bromide, esomeprazole and ibuprofen. There was no change in diet or medications, and no insect bite. The patient had no known drug or food allergies. On admission to the ED, he was alert and stable, with a pulse of 78 beats/min, blood pressure of 199/87 mm Hg, respiratory rate of 18 breaths/min, temperature of 36.9°C, and room air oxygen saturation of 97%. His tongue, soft palate and anterior neck were edematous down to the supraclavicular notch, and his (Mallampati) airway patency score was 4. Despite this, he was able to talk and swallow saliva. His chest was clear to auscultation, and there were no wheals on the skin. Emergency treatment included the administration of 1:1000 epinephrine (0.5 mg intramuscularly), diphenhydramine (50 mg intravenously [IV]), ranitidine (50 mg IV), and hydrocortisone (100 mg IV) in rapid succession. The anesthetist and intensivist on call were notified. We anticipated a difficult airway and so we used the “triple set-up,” which included a difficult airway cart and percutaneous crycothyrotomy and tracheostomy sets. The anterior neck was infiltrated from the supraclavicular notch to the level of crycothyroid membrane with 10 mL of 2% lidocaine, plus 1:100 000 epinephrine. A midline vertical incision was made through the subcutaneous tissues in preparation for a tracheostomy. After sedating with ketamine (50 mg IV) and anesthetizing the hypopharynx with lidocaine spray, direct orotracheal intubation was attempted using a GlideScope® video intubation laryngoscope (Saturn Biomedical Systems Inc., Burnaby, BC). A 7.5 endotracheal (ET) tube containing a stylet was inserted to a depth of 23 cm beyond the teeth, but only the epiglottis was visualized during intubation. A colorimetric end-tidal CO2 detector (Portex® CO2 ClipTM, Smiths Medical ASD, Keene, NH) was connected to the ET tube and it demonstrated synchronous fluctuation in CO2 with the respiratory cycle. Oxygen saturation remained above 90%, but there was no humidification of the tube during expiration. Furthermore, the patient began to phonate and bubbles appeared at the corner of his mouth. We attempted to determine the position of the ET tube with direct laryngoscopy, however this was unsuccessful. A fibreoptic bronchoscope could not be advanced through the distal portion of the ET tube. The next step in emergency airway management should have been to: a) perform a chest x-ray to confirm ET tube placement; b) change end-tidal CO2 monitors; c) aggressively ventilate the patient through the ET tube with bag–valve unit; d) attempt video laryngoscopy again; or e) proceed directly to tracheostomy.