Prehospital Agitation and Sedation Trial (PhAST): A Randomized Control Trial of Intramuscular Haloperidol versus Intramuscular Midazolam for the Sedation of the Agitated or Violent Patient in the Prehospital Environment.

INTRODUCTION: Violent patients in the prehospital environment pose a threat to health care workers tasked with managing their medical conditions. While research has focused on methods to control the agitated patient in the emergency department (ED), there is a paucity of data looking at the optimal approach to subdue these patients safely in the prehospital setting. Hypothesis This study evaluated the efficacy of two different intramuscular medications, midazolam and haloperidol, to determine their efficacy in sedating agitated patients in the prehospital setting. METHODS: This was a prospective, randomized, observational trial wherein agitated patients were administered intramuscular haloperidol or intramuscular midazolam to control agitation. Agitation was quantified by the Richmond Agitation and Sedation Scale (RASS). Paramedics recorded the RASS and vital signs every five minutes during transport and again upon arrival to the ED. The primary outcome was mean time to achieve a RASS less than +1. Secondary outcomes included mean time for patients to return to baseline mental status and adverse events. RESULTS: Five patients were enrolled in each study group. In the haloperidol group, the mean time to achieve a RASS score of less than +1 was 24.8 minutes (95% CI, 8-49 minutes), and the mean time for the return of a normal mental status was 84 minutes (95% CI, 0-202 minutes). Two patients required additional prehospital doses for adequate sedation. There were no adverse events recorded in the patients administered haloperidol. In the midazolam group, the mean time to achieve a RASS score of less than +1 was 13.5 minutes (95% CI, 8-19 minutes) and the mean time for the return of normal mental status was 105 minutes (95% CI, 0-178 minutes). One patient required additional sedation in the ED. There were no adverse events recorded among the patients administered midazolam. CONCLUSIONS: Midazolam and haloperidol administered intramuscularly appear equally effective for sedating an agitated patient in the prehospital setting. Midazolam appears to have a faster onset of action, as evidenced by the shorter time required to achieve a RASS score of less than +1 in the patients who received midazolam. Haloperidol offers an alternative option for the sedation of an agitated patient. Further studies should focus on continued investigation into appropriate sedation of agitated patients in the prehospital setting.

K2--not the spice of life; synthetic cannabinoids and ST elevation myocardial infarction: a case report.

INTRODUCTION: The adverse effects of synthetic cannabinoids are not well-described nor have they been thoroughly studied. CASE REPORT: A 16-year-old male with a past medical history of asthma and attention deficit hyperactivity disorder (ADHD) presented to the emergency department (ED) complaining of 24 h of substernal pressure associated with dyspnea, nausea, and vomiting. He reported smoking tobacco cigarettes daily and occasional marijuana use but denied recent use of marijuana. The initial electrocardiogram (EKG) revealed ST-segment elevations in leads II, III, AVF, and V4-V6. The initial troponin level was reported as 1.47 ng/mL, and the initial creatine kinase MB (CKMB) level was 17.5 ng/mL. The patient admitted to smoking "K2" 60-90 min prior to the onset of symptoms. The patient manifested persistent ST elevations with a peak troponin of 8.29 ng/mL. The urine drug immunoassay was positive for benzodiazepines and opiates. Cardiac catheterization revealed normal coronary arteries, no wall motion abnormalities, and normal systolic function. DISCUSSION: Synthetic cannabinoids may have significant potential adverse effects. Chest pain due to myocardial ischemia is rare in adolescents. When evaluating patients with chest pain, it is important to elicit a detailed drug history, specifically inquiring about synthetic cannabinoid use. Urine drug immunoassays may be unreliable and in this case did not detect synthetic cannabinoids.

Phenol Toxicity Following Cutaneous Exposure to Creolin®: A Case Report.

INTRODUCTION: Phenol is a caustic that may cause cutaneous or gastrointestinal burns depending on the route of exposure. Significant absorption may result in systemic toxicity. We present a case of topical phenol exposure resulting in cutaneous burns and systemic phenol toxicity. CASE REPORT: A 9-year-old girl was exposed to Creolin(®), a general-purpose disinfectant containing phenol, when her mother applied this product to her head and upper torso. The patient required endotracheal intubation due to depressed mental status; she had cutaneous erythema in the distribution of contact with the cleanser. An initial EKG revealed sinus tachycardia with brief runs of monomorphic ventricular tachycardia. On hospital day (HD) 1, the area of erythema extended to both upper extremities and hyperpigmentation developed over the affected areas, which continued to darken during the hospital course. The patient was extubated late on HD 1. On HD 2, the patient's urine was noted to be a dark green color that resolved later that day. On HD 3, areas of desquamation and decreased sensation developed in skin areas of maximal contact with the cleanser. The patient developed a mild transaminitis with peak AST and ALT levels of 84 units/l and 99 units/l, respectively. The patient was discharged to home on HD 4. DISCUSSION: Our patient presented with signs of cutaneous and systemic phenol toxicity characterized by dermal burns, depressed mental status, cardiac dysrhythmias, and elevated hepatic transaminases. Phenol exposure may cause systemic toxicity following limited dermal exposure.

Cocaine-induced agitated delirium: a case report and review.

Cocaine use continues to be a major public health problem in the United States. Although many of the initial signs and symptoms of cocaine intoxication result from increased stimulation of the sympathetic nervous system, this condition can present as a spectrum of acuity from hypertension and tachycardia to multiorgan system failure. Classic features of acute intoxication include tachycardia, arterial vasoconstriction, enhanced thrombus formation, mydriasis, psychomotor agitation, and altered level of consciousness. At the extreme end of this toxidrome is a rare condition known as cocaine-induced agitated delirium. This syndrome is characterized by severe cardiopulmonary dysfunction, hyperthermia, and acute neurologic changes frequently leading to death. We report a case of cocaine-induced agitated delirium in a man who presented to our institution in a paradoxical form of circulatory shock. Rapid evaluation, recognition, and proper management enabled our patient not only to survive but also to leave the hospital without neurologic sequelae.