Angioedema and Dual Nurse Flight Crew Cricothyrotomy After Envenomation by a Severed Rattlesnake Head.

Crotalid envenomation may result in airway compromise from angioedema, anaphylaxis, or an anaphylactoid reaction. A 57-year-old man was transported by helicopter to the emergency department (ED) after a bite to his hand from a severed rattlesnake head. He rapidly developed facial and oropharyngeal edema that did not respond to standard treatment. After 2 unsuccessful attempts at intubation, the dual flight nurse team performed a cricothyrotomy. They notified the ED team en route, and antivenom was prepared before arrival. Angioedema was suspected because there was no concomitant urticaria, bronchoconstriction, or persistent hypotension. Edema and ecchymosis of the affected extremity were mild. Severe coagulopathy ensued, which was treated with bolus doses of antivenom and continuous infusion. This case report is significant for several reasons. It is the first detailing a prehospital cricothyrotomy performed by flight crew nurses for life-threatening airway edema caused by snakebite envenomation. In-flight notification enabled the ED staff to prepare and administer antivenom immediately after arrival. Despite the use of antivenom in bolus dosing, crotalid envenomation may be complicated by persistent or recurring coagulopathy, and continuous antivenom infusion may be useful. Finally, it highlights the danger of snakebite envenomation even after the death and decapitation of a snake.

Transaminase and Creatine Kinase Ratios for Differentiating Delayed Acetaminophen Overdose from Rhabdomyolysis.

INTRODUCTION: Rhabdomyolysis and delayed acetaminophen hepatotoxicity may be associated with elevated serum transaminase values. Establishing the cause of elevated transaminases may be especially difficult because of limited or inaccurate histories of acetaminophen ingestion. We hypothesized that the comparative ratios of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK) can differentiate acetaminophen hepatotoxicity from rhabdomyolysis. METHODS: A retrospective chart review of patients in four hospitals from 2006 to 2011 with a discharge diagnosis of acetaminophen toxicity or rhabdomyolysis was performed. Subjects were classified into three groups: rhabdomyolysis, acetaminophen overdose (all), and acetaminophen overdose with undetectable serum acetaminophen concentrations [acetaminophen(delayed)]. Ratios of AST, ALT, and CK were compared using non-parametric statistical methods. RESULTS: 1,353 subjects were identified and after applying our exclusion criteria there were 160 in the rhabdomyolysis group, 68 in the acetaminophen overdose (all) group, and 29 in the acetaminophen (delayed) group. The AST/ALT ratio for the rhabdomyolysis group was 1.66 (Interquartile range: 1.18-2.22), for the acetaminophen overdose (all) group was 1.38 (1.08-1.69, statistically lower than the rhabdomyolysis group, p = 0.018), and for the acetaminophen (delayed)group was 1.30 (1.06-1.63, p = 0.037). CK/AST ratios were 21.3 (12.8-42.2), 5.49 (2.52-15.1, p < 0.001), and 3.80 (1.43-13.8, p < 0.001) respectively. CK/ALT ratios were 37.1 (16.1-80.0), 5.77 (2.79-25.2, p < 0.001), and 5.03 (2.20-17.4, p < 0.001) respectively. Increasing CK to transaminase ratio cutoffs resulted in increasing test sensitivity but lower specificity. CONCLUSION: AST/ALT, CK/AST and CK/ALT ratios are significantly larger in rhabdomyolysis when compared to patients with acetaminophen toxicity. This result suggests that the ratios could be used to identify patients with rhabdomyolysis who otherwise might have been diagnosed as delayed acetaminophen toxicity. Such patients may not require treatment with N-acetylcysteine, resulting in cost savings and improved resource utilization.

Monitoring the corrected QT in the acute care setting: A comparison of the 12­lead ECG and bedside monitor.

INTRODUCTION: Prolongation of the QT interval is a well-recognized complication associated with many commonly used medications. Emergency Department monitoring of the corrected QT (QTc) both before and after medication administration is typically performed using the 12­lead electrocardiogram (ECG). The purpose of this study is to compare the QTc reported on the 12­lead ECG to that reported by single brand of bedside monitor. METHODS: A convenience sample of emergency department patients over the age of 18 undergoing bedside monitoring and who had an ECG ordered by their treating physician were enrolled. These patients underwent simultaneous ECG and monitor QTc calculation. The primary outcome of interest was the correlation between the monitor and ECG QTc. Secondary outcomes included ability of each method to identify patients with a QTc >500ms and the ability of each method to identify patients with a QTc <450ms. RESULTS: A total of 125 patients had simultaneous ECG and monitor QTc measurements recorded. There was moderate correlation between the monitor and ECG QTc (Pearson's correlation coefficient=0.55). The median difference between the ECG QTc and the monitor QTc (ECG QTc minus monitor QTc) was -7ms (IQR -23 to 11ms). CONCLUSION: We found that there was moderate correlation between the QTc reported on the 12 lead ECG and that reported by the bedside monitor. This correlation is not strong enough to support the use of the bedside monitor as a substitute for the 12­lead ECG when evaluating a patient's QTc.

Massive diltiazem and metoprolol overdose rescued with extracorporeal life support.

The management of overdoses of cardioactive medications in the emergency department can be challenging. The reversal of severe toxicity from one or more types of cardioactive medication may fail maximal medical therapies and require extreme invasive measures such as transvenous cardiac pacing and extracorporeal life support. We present a case of massive diltiazem and metoprolol overdose refractory to maximal medical therapy, including intravenous calcium, glucagon, vasopressors, high dose insulin, and lipid emulsion. The patient experienced refractory bradydysrhythmia that responded only to transvenous pacing. Extracorporeal life support was initiated and resulted in successful organ perfusion and complete recovery of the patient. This case highlights the potential utility of extracorporeal life support in cases of severe toxicity due to multiple cardioactive medications.

Fatal Fentanyl: One Pill Can Kill.

OBJECTIVE: The current national opioid epidemic is a public health emergency. We have identified an outbreak of exaggerated opioid toxicity caused by fentanyl adulterated tablets purchased on the street as hydrocodone/acetaminophen. METHODS: Over an 8-day period in late March 2016, a total of 18 patients presented to our institution with exaggerated opioid toxicity. The patients provided a similar history: ingesting their "normal dose" of hydrocodone/acetaminophen tablets but with more pronounced symptoms. Toxicology testing and analysis was performed on serum, urine, and surrendered pills. RESULTS: One of the 18 patients died in hospital. Five patients underwent cardiopulmonary resuscitation, one required extracorporeal life support, three required intubation, and two received bag-valve-mask ventilation. One patient had recurrence of toxicity after 8 hours after naloxone discontinuation. Seventeen of 18 patients required boluses of naloxone, and four required prolonged naloxone infusions (26-39 hours). All 18 patients tested positive for fentanyl in the serum. Quantitative assays conducted in 13 of the sera revealed fentanyl concentrations of 7.9 to 162 ng/mL (mean = 52.9 ng/mL). Pill analysis revealed fentanyl amounts of 600-6,900 µg/pill. The pills are virtually indistinguishable from authentic hydrocodone/acetaminophen tablets and are similar in weight. To date, our county has reported 56 cases of fentanyl opioid toxicity, with 15 fatalities. In our institution, the outbreak has stressed the capabilities and resources of the emergency department and intensive care units. CONCLUSIONS: A serious outbreak of exaggerated opioid toxicity caused by fentanyl-adulterated tablets purchased on the street as hydrocodone/acetaminophen is under way in California. These patients required higher dosing and prolonged infusions of naloxone. Additionally, observation periods off naloxone were extended due to delayed, recurrent toxicity. The outbreak has serious ramifications for public health and safety, law enforcement, and healthcare facilities and resources.

The effects of opioids on the lung.

The term opioid refers to a broad class of medications that are used most frequently for their analgesic effects. Along with this effect, they also produce euphoria, and it is for this reason that they have been used illicitly, as well as medicinally, for thousands of years. While the most well-known complications of opioid use and misuse include respiratory and central nervous system depression, there are many other toxicities that have been associated with these drugs. Many complications can occur with multiple different opioids, such as non-cardiogenic pulmonary edema, while many of the complications are unique to the opioid used as well as the route of administration. This review focuses on the pulmonary complications associated with opioid use and abuse, but opioids can affect nearly every organ system. Their effects on the pulmonary system can be direct, such as causing granulomatous change, but they can also work indirectly. For example, opioids cause respiratory depression by decreasing sensitivity of peripheral chemoreceptors to carbon dioxide and decreasing activity in the central respiratory centers. Opioids have also been reported to affect the immune system, and place users at increased risk for many different infectious complications. Patients can have a wide array of signs and symptoms, sometimes making it difficult to recognize opioids as a cause for a patient's clinical picture. Due to the sedative effects of opioids, patients are also often not able to provide a reliable history. Knowledge of the possible toxicities of opioids can help prepare a physician to recognize the many complications associated with opioid use.

Volatile substance misuse: an updated review of toxicity and treatment.

Educational campaigns and legislative actions may have led to an overall decrease in the prevalence of volatile substance misuse (VSM) in many countries; however, it is still a common practice throughout the world. Studies currently suggest that girls are misusing volatile substances more than before and at a prevalence rate equal to or exceeding that of boys in several countries. Products that may be misused are ubiquitous and relatively easy to acquire. The most commonly misused substances in recent studies are fuels such as butane or petrol and compressed gas dusters and deodorants that may contain fluorocarbons and/or butane. Detection of VSM is challenging, therefore physicians must maintain a high level of suspicion based on history and clinical presentation. Clues to misuse are often subtle and may include the patient's proximity to a volatile substance or paraphernalia when found intoxicated, dermal burns, blisters, pigments, or rashes, and chemical odors. The primary targets of toxicity are the brain and the heart. The leading cause of death from VSM is from ventricular dysrhythmias. Treatment of toxicity begins with support of airway, breathing, and circulation. Exogenous catecholamines should be avoided if possible due to the theoretical "sensitized" and irritable myocardium. In the case of ventricular dysrhythmias, direct current defibrillation and/or beta-adrenergic receptor antagonism should be used. New evidence demonstrates the addictive potential of VSM yet effective therapy remains uncertain. Further research is needed in developing methods for preventing, detecting, and treating the harmful effects of VSM.

Elimination kinetics of ethanol in a 5-week-old infant and a literature review of infant ethanol pharmacokinetics.

Primary ethanol metabolism occurs through alcohol dehydrogenase, but minor metabolic pathways such as the P450 enzymes CYP2E1 and CYP1A2 and the enzyme catalase exist. These enzymes have distinct developmental stages. Elimination kinetics of ethanol in the infant is limited. We report the elimination kinetics of ethanol in a 5-week-old African-American male who had a serum ethanol level of 270 mg/dL on admission. A previously healthy 5-week-old African-American male was brought to the ED with a decreased level of consciousness. His initial blood ethanol level was 270 mg/dL. Serial blood ethanol levels were obtained. The elimination rate of ethanol was calculated to be in a range from 17.1 to 21.2 mg/dL/hr and appeared to follow zero-order elimination kinetics with a R (2) = 0.9787. Elimination kinetics for ethanol in the young infant has been reported in only four previously published reports. After reviewing these reports, there appears to be variability in the elimination rates of ethanol in infants. Very young infants may not eliminate ethanol as quickly as previously described. Given that there are different stages of enzyme development in children, caution should be used when generalizing the elimination kinetics in young infants and children.

Effect of low-osmolality intravenous contrast on serum osmolal gap in adults.

BACKGROUND: Contrast media used today is considered "low-osmolality." No study has evaluated the effect of intravenous contrast media on the measurement of the osmolal gap in adult patients. OBJECTIVE: To determine if "low-osmolality" intravenous contrast media administered to adult patients undergoing computed tomography (CT) of the abdomen and pelvis affects the osmolal gap. METHODS: We performed a prospective pilot study in the Emergency Department of a university-affiliated tertiary care center. Patients were enrolled if they were age ≥18 years and <60 years and the treatment team had ordered an abdomen and pelvis CT with intravenous (i.v.) contrast procedure and a serum basic metabolic panel (BMP) that included serum glucose, blood urea nitrogen, and sodium. Once enrolled, a serum osmolality and serum ethanol level was ordered and obtained on the same blood draw as the BMP before the CT. Patients were excluded if they had detectable ethanol on laboratory screen, if they were suspected to have ingested methanol, ethylene glycol, isopropanol, mannitol, or underwent CT with i.v. contrast within the prior 24 h. Paired samples were compared using the Wilcoxon signed-rank test. RESULTS: Of the 100 patients screened, 18 patients were lost due to withdrawal of consent or missing data. The median of the osmolal gap pre-CT was 8.18 with an interquartile range of 4.76-11.15. The median of the osmolal gap post-CT was 11.23 with an interquartile range of 7.29-14.83. The difference in the osmolal gap was a median of 2.34 (p = 0.0003) with an interquartile range of -1.32-5.97. CONCLUSION: Although the effect in our study was small, clinicians should be aware of the ability of contrast media to increase the osmolal gap.

Acute, sustained chorea in children after supratherapeutic dosing of amphetamine-derived medications.

Amphetamine-derived medications are being prescribed with increasing frequency to younger pediatric patients to treat attention deficit hyperactivity disorder. Although choreiform movements were reported in adults with amphetamine abuse and in those under therapeutic treatment for attention deficit hyperactivity disorder, previous literature concerning the pediatric population is spare. We describe two children who developed chorea after ingesting amphetamine-derived medications prescribed to treat attention deficit hyperactivity disorder. Patient 1, a 10-year-old boy, accidently received an extra dose of lisdexamfetamine dimesylate the night before the onset of acute chorea involving his arms, legs, and trunk. Patient 2, an 8-month-old boy, accidentally ingested his stepbrother's mixed amphetamine salts (Adderall XR) and developed acute chorea. Benzodiazepines, diphenhydramine, benztropine, and opioids did not suppress the chorea in either case. The 10-year-old received haloperidol, which significantly improved his abnormal findings, and he returned to baseline in approximately 48 hours. The 8-month-old was observed in the pediatric intensive care unit, and his signs resolved by 72 hours. Our cases demonstrate that choreiform movements of sustained duration can occur in children with acute supratherapeutic ingestions of amphetamine-derived medications.

Intracranial hemorrhage after prehospital administration of intramuscular epinephrine.

BACKGROUND: The administration of epinephrine by the intramuscular route can be life-saving in cases of anaphylaxis or severe allergic reactions. However, the use of this drug can lead to a rapid rise in blood pressure, which theoretically could lead to deleterious effects in patients of any age, with elderly patients at greatest risk. OBJECTIVES: To present a rare case of intracranial hemorrhage potentially resulting from the administration of intramuscular epinephrine in an elderly patient with an allergic reaction. CASE REPORT: We present a case report of a 65-year-old woman who developed an intracranial hemorrhage after a single, therapeutic, intramuscular dose of epinephrine for a wasp sting to the tongue. The patient underwent successful craniotomy with evacuation of the intracranial hematoma. CONCLUSIONS: In circumstances where the severity of the allergic reaction remains unclear (lack of airway compromise, cardiovascular collapse, or true anaphylaxis), careful consideration of the potential risks of intramuscular epinephrine, such as a rapid rise in blood pressure leading to intracranial hemorrhage, should be undertaken when using this medication in elderly patients.