Images in emergency medicine. Skin damage following application of suction device for snakebite.
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Biomedical subjects
Publications and source records attributed to Christopher P Holstege.
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This article examines the role of common laboratory tests in the evaluation of a poisoned patient. Numerous laboratory tests maybe useful to clinicians caring for poisoned patients. Clinicians should not order a broad range of tests indiscriminately, but rather thoughtfully consider appropriate tests. The results of the tests should be reviewed in the context of the clinical scenario.
The diagnosis and subsequent prosecution of Munchausen by proxy (MBP) cases require the collaborative teamwork of health care teams, laboratory personnel, law enforcement, and social services. Poisoning occurs in a significant number of the MBP cases with a diverse variety of agents used. To aid laboratory professionals in determining the appropriate toxicology tests to perform in such criminal cases, health care professionals must focus their testing requests on substances that correspond to the victim's signs, symptoms, and ancillary test values. This article reviews MBP, with particular focus on poisoning agents that have been used in past reported cases.
A significant number of herbal products have been associated with hepatotoxicity. Attribution of liver injury to a specific herbal pro-duct may be difficult. There are few clinical or laboratory manifestations that specifically suggest that liver injury is the result of aspecific herbal. Compounding this difficulty is that the patient may have liver disease from another cause, may be consuming other potentially hepatotoxic products, or may be using a contaminated herbal product. The most important clue often is the temporal relationship between initiation of the herbal product and the appearance of liver injury; of equal importance is the resolution of the injury following withdrawal of the herbal product.
Despite that drugs have widely varying indications for therapeutic use, many unrelated drugs share a common cardiac pharmacologic effect if taken in overdose. The purpose of this article is to group together agents that cause similar electrocardiographic effects,review their pharmacologic actions, and discuss the electrocardiographic findings reported in the medical literature.
Hematoma blocks with lidocaine are routinely utilized in the Emergency Department to allow reduction of Colles' fractures. Lidocaine toxicity is a potential complication of this procedure. We present a case report of a patient who developed acute mental status changes and generalized seizure immediately following administration of lidocaine during a hematoma block. The rapid onset of seizure development following injection was most likely due to inadvertent intravascular administration.
The clinical syndrome of nerve agent toxicity varies widely, ranging from the classic cholinergic syndrome to flaccid paralysis and status epilepticus. All nerve agents are capable of producing marked neuropathology. Seizure control is strongly associated with protection against acute lethality and brain pathology. The mainstays of therapy of nerve agent poisoned patients are atropine, pralidoxime, and benzodiazepines. Fosphenytoin provides little therapeutic anticonvulsant effectiveness for nerve agent-induced status epilepticus. Tachycardia is not a contraindication to treatment with atropine in nerve agent toxicity. Atropine should be administered to alleviate respiratory distress, symptomatic bradycardia, and as an adjunct to benzodiazepines and pralidoxime to alleviate seizure activity. In significant nerve agent toxicity, a continuous pralidoxime infusion may be considered.
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The diagnoses and subsequent treatment of poisoned patients manifesting cardiovascular compromise challenges the most experienced emergency physician. Numerous drugs and chemicals cause cardiac and vascular disorders. Despite widely varying indications for therapeutic use, many agents share a common cardiovascular pharmacologic effect if taken in overdose. Standard advanced cardiac life support protocol care of these patients may not apply and may even result in harm if followed. This chapter discusses com-mon cardiovascular toxins and groups them into their common mechanisms of toxicity. Multiple agents exist that result in human cardiovascular toxicity. The management of the toxicity of each agent should follow a rationale approach. The first step in the care of all poisoned patients focuses on good supportive care.
Numerous types of envenomations may be encountered by health care workers depending on where in North America they work. Clinicians should be familiar with the animals in their region that may lead to envenomation.A rational approach with use of poison center or medical toxicology consultation services ensures that cases are managed appropriately.
Numerous diagnostic tests may be useful to clinicians caring for poisoned patients. Clinicians should not order a broad range of tests indiscriminately,but rather thoughtfully consider appropriate tests. The results'of the tests should be reviewed in the context of the clinical scenario.
Health care providers are being increasingly confronted with the use of herbal medications by their patients. It is imperative that patients be questioned regarding herbal preparation use and that health care providers become familiar with these agents. Research into the active components and mechanisms of action of various herbals is ongoing [350]. Long-range studies need to be performed to follow patients for efficacy or toxicity in chronic use [351,352]. Adverse reactions to herbal remedies should be reported to the FDA MedWatch at http://www.fda.gov/medwatch. As withany therapeutic agent, risk of use must always be weighed against potential benefits.
OBJECTIVES: In the past, some moonshine products contained potentially toxic contaminants. Although moonshine production continues in the United States, no studies have analyzed the content of moonshine since the early 1960s. We hypothesize that moonshine continues to contain potentially toxic concentrations of contaminants. METHODS: Forty-eight samples of illicitly distilled moonshine were obtained from law enforcement agencies. An independent laboratory, blinded to both the moonshine source and a control sample of ethanol, conducted the analysis. Lead content was determined using atomic absorption spectrophotometry with a graphite tube atomizer. Alcohol content, including ethanol, acetone, isopropanol, methanol, and ethylene glycol, was determined using gas liquid chromatography with flame ionization detection. RESULTS: Ethanol content ranged from 10.5% to 66.0% with a mean value of 41.2%. Lead was found in measurable quantities in 43 of 48 samples with values ranging from 5 to 599 parts per billion (ppb) with a mean value of 80.7 ppb. A total of 29 of 48 (60%) of samples contained lead concentrations above or equal to the EPA water guideline of 15 ppb. Methanol was found in only one sample at a concentration of 0.11%. No samples contained detectable concentrations of acetone, isopropanol, or ethylene glycol. CONCLUSIONS: Many moonshine samples contain detectable concentrations of lead. Extrapolations based on the described moonshine lead content suggest that chronic consumers of moonshine may develop elevated lead concentrations. Physicians should consider lead toxicity in the differential diagnosis when evaluating patients consuming moonshine.
INTRODUCTION: Massive caffeine overdose is associated with life-threatening hemodynamic complications that present challenges for clinicians. We describe the highest-reported serum concentration of caffeine in a patient who survived and discuss the first-reported use of vasopressin and hemodialysis in a caffeine-poisoned patient. CASE REPORT: A 41-yr-old woman presented 3 h after ingesting approximately 50 g of caffeine. She subsequently underwent cardiopulmonary resuscitation and received multiple medications in an attempt to raise her blood pressure and control her heart rate without success. Vasopressin infusion increased her blood pressure to the point where hemodialysis could be performed. Despite ensuing multisystem organ failure, she survived and has made a complete recovery. CONCLUSION: Hemodialysis and vasopressin infusions may be of benefit in the management of caffeine-intoxicated patients who fail to respond to standard therapies.
Among the most popular and intriguing intoxicants of the Victorian Age, absinthe had all but disappeared after it was banned in nearly all developed countries in the early 1900s. A number of great artists and writers from the late 1800s used absinthe as a social drink, including Vincent van Gogh and Toulouse-Lautrec. A recent resurgence of absinthe use has occurred in Europe and is rapidly spreading to the United States. Despite its increasing popularity limited information exists on the mechanism of action and neurotoxicity of absinthe. This paper reviews some of the historical aspects of absinthe and aims to shed light on the mechanism of action and neurotoxicology of this the Green Fairy.
A 16-year-old boy presented to the emergency department with rapidly progressing extremity pain, edema, and ecchymosis after envenomation by a copperhead. Crotalidae polyvalent immune Fab (ovine) (CroFab; FabAV) was infused. Six vials were placed in 250 mL of normal saline solution, and the infusion was gradually increased. Fifty minutes after beginning, the infusion was increased to 640 mL/h. Within minutes of the rate increase, the patient experienced full-body urticaria, facial edema, voice change, and tachycardia. The infusion was stopped. Hydroxyzine pamoate, famotidine, methylprednisolone, and a 1-L bolus of normal saline solution were administered intravenously. The symptoms abated, and the remaining FabAV was infused at a slower rate without return of this reaction. This immediate hypersensitivity reaction was most likely a rate-related anaphylactoid reaction that has not been previously reported with FabAV.[Holstege CP, Wu J, Baer AB. Immediate hypersensitivity reaction associated with the rapid infusion of Crotalidae polyvalent immune Fab (ovine). Ann Emerg Med. June 2002;39:677-679.]