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Biomedical subjects

John M Howell

Publications and source records attributed to John M Howell.

3 recordsLinked to original sources

Screening for inhalational anthrax due to bioterrorism: evaluating proposed screening protocols.

Eleven known cases of bioterrorism-related inhalational anthrax (IA) were treated in the United States during 2001. We retrospectively compared 2 methods that have been proposed to screen for IA. The 2 screening protocols for IA were applied to the emergency department charts of patients who presented with possible signs or symptoms of IA at Inova Fairfax Hospital (Falls Church, Virginia) from 20 October 2001 through 3 November 2001. The Mayer criteria would have screened 4 patients (0.4%; 95% CI, 0.1%-0.9%) and generated charges of 1900 dollars. If 29 patients (2.6%; 95% CI, 1.7%-3.7%) with >or=5 symptoms (but without fever and tachycardia) were screened, charges were 13,325 dollars. The Hupert criteria would have screened 273 patients (24%; 95% CI, 22%-27%) and generated charges of 126,025 dollars. In this outbreak of bioterrorism-related IA, applying the Mayer criteria would have identified both patients with IA and would have generated fewer charges than applying the Hupert criteria.

Adult↗

Are one or two dangerous? Clonidine and topical imidazolines exposure in toddlers.

Clonidine and the imidazolines, commonly found in topical ophthalmic and nasal decongestants, are chemically related drugs that have been responsible for many pediatric poisonings. These medications can cause significant morbidity in small doses. A review of the available literature reveals that young children have exhibited severe signs and symptoms after ingesting as little as one to two clonidine tablets or 2.5 ml of a topical imidazoline product. Central nervous system depression, respiratory depression, and cardiovascular instability are the most common features of poisoning. Signs and symptoms develop rapidly, within 4-6 h. Care is supportive. Death is rare, but many poisoned patients require monitoring in an intensive care setting.

Administration, Topical↗

Electrocardiographic changes associated with beta-blocker toxicity.

STUDY OBJECTIVE: We sought to characterize the ECG changes associated with symptomatic beta-blocker overdose. METHODS: The study population consisted of a prospective cohort of patients reporting to 2 regional poison centers with beta-blocker overdose. Each patient received an ECG on presentation and a structured follow-up. The inclusion criteria for symptomatic overdose included heart rate of less than 60 beats/min or systolic blood pressure of less than 90 mm Hg; symptoms consistent with decreased end-organ perfusion; therapeutic intervention with cardioactive medication; and corroboration by 2 of the authors that this was a clear-cut case of symptomatic beta-blocker overdose with cardiovascular toxicity. Exclusion criteria included cardioactive coingestants, age younger than 6 years, and no available ECG. RESULTS: Of 167 patients, 13 were determined to have symptomatic exposures. First-degree heart block (>200 ms) was the most common ECG finding (10/12) and also had the greatest likelihood ratio (5.31) when comparing those with symptomatic exposures with those with asymptomatic exposures. Comparing the asymptomatic with the symptomatic groups, the mean PR interval was 167 ms (95% confidence interval [CI] 162 to 171 ms) versus 216 ms (95% CI 193 to 238 ms), the mean QRS interval was 89 ms (95% CI 87 to 91 ms) versus 112 ms (95% CI 92 to 132 ms), the mean QTc interval was 422 ms (95% CI 417 to 428) versus 462 ms (95% CI 434 to 490 ms), and the mean heart rate was 72 beats/min (95% CI 69 to 74 beats/min) versus 66 beats/min (95% CI 59 to 73 beats/min). Two cases of symptomatic acebutolol exposure appeared unique by demonstrating disproportionate prolongation of the QTc interval, an RaVR height of 3 mm or greater, and associated ventricular tachydysrhythmia. CONCLUSION: The majority of clinically significant beta-blocker intoxications demonstrate negative dromotropic effects on ECG. Several ECG differences in acebutolol intoxication might reflect unique pathophysiologic processes relative to other beta-blockers.

Acebutolol↗