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Misclassification of adverse drug effects as allergy is commonly encountered in clinical practice and can lead to use of suboptimal alternate medications which are often less effective.
- Nomenclature surrounding drug safety needs to be clear and unambiguous to avoid confusion.
- Adverse Drug Effect (ADE) = All drug induced disease. Majority are predictable based on drug's known pharmacology. Include harm related to medication errors and drug/food interactions.
- Adverse Drug Reaction (ADR) = Noxious or unintended reaction to a drug that is administered at therapeutic doses during normal use. Divided into predictable (majority 75-80%), related to pharmacologic actions of the drug in otherwise normal individuals) and unpredictable reactions (related to individual’s immunological response).
- "Drug allergies" are relatively uncommon with cited incidence of 10%. Immunologically mediated reactions (type I to IV) to a pharmaceutical and/or formulation (excipient) in a sensitized person. They are dose independent and unrelated to pharmacological action of the drug. Most commonly, IgE-mediated type I (immediate) reactions caused by rapid release of vasoactive mediators from mast cells and peripheral basophils causing generalized reaction including urticaria, angioedema, stridor, wheezing, and cardiovascular collapse.
- The skin is the most frequently and notably affected by drug induced allergic reactions.
- Antibiotics, particuarly Beta-Lactams, are the most important cause of immediate hypersensitivity reactions. Approximately 10% of patients report a history of penicillin allergy, however after complete evaluation, up to 90% of these individuals are able to tolerate penicillin and are designated as having “penicillin allergy” unnecessarily.
- Pseudoallergy can occur with opioids due to histamine release. Codeine and morphine are most commonly associated with pseudoallergy. Coadministration of an antihistamine or use of a semi or synthethic opioid (Fentanyl, hydromorphone) can prevent this reaction.
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Fall clean up = Poison Ivy, oak, sumac (Toxicodendron species) which is ubiquitous in North America but it can also be found in British Columbia, Mexico and in parts of Asia. These plants are truly the scourge of outdoor enthusiasts and agricultural workers responsible for up to 40 million cases of miserable often temporarily incapacitating rashes annually.
Fast Facts:
- Grows as plant, vine, or shrub with leaves ranging in color from light or glossy green to red and yellow in fall.
- Exposure by direct contact with plant, indirectly from oil resin on objects, clothes, pets, or airborne from burning plant.
- Urushiol toxin induced type IV hypersensitivity allergic contact dermatitis. This oily resin toxin is excreted from all parts of plant (stems, leaves, flowers, roots, vines). and is extremely stable staying active even after plant dies.
- Intensely itchy blistering rash starts 12-72 hours after contact and lasts up to 21 days. Characterized by red streaks or linear configuration where skin brushed up against plant sap. Inflammation (redness, swelling, hives, blistering) to thick leathery plagues depending on severity and vulnerability of skin location. Intense inflammation can mimic cellulitis.
- Rash is Not contagious but spread of oil on clothes, pets, tools, objects is!
- Delayed reaction accounts for seemingly "spread" of rash. Eruption rate depends on thickness of skin and dose of urushiol oil.
Treatment Tips:
- Prevention. Avoidance and universal precautions when gardening. Clusters of 3 leaves each trio growing on their own stem, hairy vines, no thorns, white berries.
- Cover skin to prevent exposure and if known contact immediately wash skin, clothes, objects.
- Hot water relieves itch as does cool compresses.
- Domeboro or witch hazel are astringents can reduce inflammation.
- External analgesics (e.g., benzocaine, lidocaine, benzyl alcohol) can help itching.
- Highly viscous or granular cream surfactant washes bind urushiol and can reduce exposure. Zanfel, Mean green, Gojo orange, various generic poison ivy removal scrubs now available. (Zanfel works wonders used every few hours and may alleviate need for steroids but is $$$ and several tubes are required).
- In severe cases, Steriod burst followed by 2-3 week taper to prevent relapse flare.
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Drug-induced hypoglycemia is an often severe and symptomatic. It is a potentially preventable cause of significant morbidity. In one large study, it accounted for 23% for hospital admissions due to adverse drug events and 4.4% of overall admissions. The majority of hypoglycemic events occur with insulin and sulfonylureas. However, multiple drugs can affect glucose homeostasis and have been cited to cause hypoglycemia in therapeutic dose alone or in combination with other medications or illness. Factors that predispose to low blood sugar include reduced food intake, age, hepatic and renal disease, and severe infection. Beware of the possibility of inducing hypoglycemia in patients taking the following:
- Ethanol
- Insulin
- Pentamidine
- Quinine
- Quinolones (Gatifloxin others rare)
- Sulfonylureas
Agents with lesser quality evidence as predisposing medications or illnesses were present:
- Ace Inhibitors (with diabetic agents)
- Propanolol ( less likely in other beta blockers)
- Trimethoprim/sulfamethoxazole (in renal compromise)
- Salicylates (high dose or intoxication)
Drugs induced hypoglycemia should always be considered in the differential diagnosis of every patient presenting with low blood glucose. Octreotide antagonizes pancreatic insulin secretion and should be considered for first-line therapy in the treatment of sulfonylurea-induced hypoglycemia particularly when glucose levels cannot be maintained by dextrose infusions. Octreotide is administered 50 mcg subcutaneously (1-10 mcg in children) every 12 hours.
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Bupropion (Wellbutrin, Zyban) is one of the most frequently prescribed antidepressants and smoking cessation agents. A lesser incidence of undesirable side effects such as weight gain and sexual dysfunction when compared to other antidepressants lends to its popularity. Bupropion's mechanism of action is only partially understood but it is known to be a norepinephine dopamine reuptake inhibitor and anticholinergic receptor blocker at certain nicotinic receptors. Bupropion has a monocyclic structure similar to amphetamines. Seizures are a major concern in overdose. When first released, Bupropion was initially withdrawn from the market due to its narrow therapeutic window with seizures occurring at doses as low as 450 mg.
- Seizures are dose dependent and all types can occur. Incidence increases dramatically with higher doses. Benzodiazepines are first-line therapy.
- Most patients experience seizure within 8 hours however, seizures can occur up to 24 hours after ingestion even without preceding symptoms.
- Longer acting forms: SR, XL, ER cause prolonged toxicity and activated charcoal should be administered in the absence of contraindications (depressed mental status, lack of airway protection, seizure).
- Myocardial sodium channel blocking properties occur and sodium bicarbonate should be administered when this occurs.
- Cardiovascular effects including tachycardia, prolonged QT interval, QRS widening, arrhythmia, and cardiovasular collapse.
- Bupropion is extremely lipid soluble and intravenous lipids should be considered in severe poisonings. Intralipid has been successfully used in several cases of Bupropion poisoning with cardiovascular instability or severe CNS symptom with good outcomes.
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[CORRECTION]: Versed dose is 2-2.5 mg total not mg/kg
Patients with severe agitation present a unique challenge to the emergency department. Acute delirium is often due to psychostimulants such as cocaine, amphetamines, PCP, or synthetic cannabinoids, alcohol, or psychiatric illness. These patients require urgent evaluation necesssitating the use of physical and chemical restraints, not only for their own safety but also the hospital staff's. Fingerstick glucose, pulse oximetry, and vital signs must be expeditiously obtained. Severely agitated combative patients who are physically restrained are at high risk for morbidity from asphyxiation, hypermetabolic consequences (acidosis, hyperthermia, rhabdomyolysis), and death can occur.
Ketamine is phencyclidine derivative that causes dissociative state between the cortical and limbic systems which prevents the higher centers from preceiving visual, auditory, or painful stimuli. Ketamine has a wide safety profile and has been used worldwide for many years with few complications. It possesses ideal characteristics for rapid sedation of agitated patients:
- Rapid onset of action 1-3 minutes
- Preservation of airway reflexes
- Lack of respiratory or cardiac depression or QT prolongation
- Short half-life of 30-40 minutes
- Safe in situations with minimal to no monitoring
- Dose: Intravenous =1.5-2 mg/kg Intramuscular = 5-6 mg/kg (maximum 400 mg)
Experience with Ketamine in patients with excited delirium has shown good initial control of agitation however, patients often require additional medications for deeper or longer duration of sedation. Benzodiazepines are recommmended as second line agents particularly intravenous or intramuscular Midazolam 2-2.5 mg /kg.
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Pure opioid agonists such as Morphine, Hydromorphone, and Fentanyl stimulate opioid receptors and are the most potent analgesics. Fentanyl and fentanyl analogues are up to 100 times more powerful than morphine and 30-50 times more powerful than heroin.
- Fentanyl abuse is causing significant problems worldwide. In the U.S., age-adjusted rate of death involving Fentanyl has increased 80% in 2014.
- Sources include production in illicit clandestine labs or diversion from legitimate pharmaceutical sales.
- 12 different analogues of Fentanyl have been identified in the U.S. drug traffic market.
- Commonly laced in heroin or cocaine or sold as fake Oxycodone or OxyContin tablets.
W-18 is a highly potent opioid agonist with a distinctive chemical structure which is not closely related to older established families of opioid drugs. While Fentanyl is approximately 100 times more powerful than Morphine, W-18 is about 100 times more powerful than Fentanyl.
- First discovered at the University of Alberta in 1982 in hopes of producing a non-addictive analgesic, 32 compound series named from W-1 to W-32, with W-18 being the most potent.
- Recently emerged on the streets of Canada when police in Calgary confiscated 110 green pills being sold as Fentanyl, known on the streets as "shady eighties" or "green beans pills" but chemical analysis revealed some pills containing W-18 instead.
- W-18 has never been used clinically as drug companies did not pick the patent, which lapsed by 1992 so little clinical experience.
- The effects of naloxone to reverse this synthetic opioid are unknown and higher doses are expected to to be required.
- Illicit drug manufacturers research pharmacological history in search of the more powerful, exotic, and new opioids to circumvent current legal regulations.
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Throughout medical history one of the basic tenets of poisoning therapy is to remove the poison from the patient. For hundreds of years, gastric decontamination has been the cornerstone treatment for acute poisonings by ingestion. This commonsense approach endeavors to remove as much of the the ingested toxin as possible before systemic absorption and organ toxicity occurs. Multiple GI decontamination methods have been utilized including gastric emptying by lavage and ipecac, toxin binding by activated charcoal, and increasing GI transit time with cathartics and bowel irrigation. Numerous studies have been conducted to assess the effectiveness of GI decontamination including measurement of amount of toxin removed by gastric retrieval, reduction of bioavailability by measuring blood levels, and finally comparison of clinical outcomes of patients treated with and without GI decontamination. Controlled studies have failed to show conclusive evidence of benefit and have even demonstrated resultant harm especially with use of gastric lavage. Activated charcoal has a tremendous surface area capable of binding many substances. Although viewed as relatively safe it does have risks in certain subsets of patients, pulmonary aspiration the most common, and is no longer routinely recommended.
Considerations for use of Activated charcoal (AC) use in acutely poisoned patients:
- AC does not bind alcohols, hydrocarbons, heavy metals
- Contraindications include diminished level of consciousness, seizure, emesis, unprotected airway, and intestinal obstruction
- Consider AC use in cases where there is potential for toxin to remain in the gut longer such as with delayed-release formulations or slowed gastric emptying
- Consider AC use in cases of expected severe toxicity with lack of effective antidote
The decision to use activated charcoal is no longer standard of care but should be individualized to each clinical situation weighing the risk versus clinical benefits.
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Caffeine is the most commonly used psychoactive substance in the world. It is widely available in coffee, tea, chocolate,soft drinks, OTC medicines, and energy drinks. The vast majority of people consuming caffeine appear to suffer no harm while enjoying it's stimulating effects. This has led to the widely held perspective that caffeine is a completely benign substance with no adverse health effects exists.
Although, children and adolescents are at particular risk, many caffeine containing products are specifically marketed at them. Alarmingly, statistics demonstrate that caffeine intake among children and adolescents has increased by 70% in the last 30 years. Energy drinks are of special concern as they represent the fastest growing component of the beverage industry, contain significant quantities of caffeine as well as high levels of sugar, and can place children at high risk for caffeine intoxication.
There are many negative health consequences documented with caffeine use which occur in a dose dependent manner with individuals differing in their susceptibility to caffeine-related adverse effects:
- Arrhythmias
- Anxiety
- Agitation
- Seizure
- Nausea,vomiting, diarrhea
- Diuresis
- Metabolic disturbances
- Hypotension
- Rare fatalities
Chronic Effects:
- Insomia
- Palpitations
- Headaches
- Diuresis
- Gastric acid secretion
- Urinary incontinence in women
- Adverse effect on wound healing process, the aging process of the human skin
- Low birth weight babies
- Withdrawal state
- Increased risk of cardiovascular events (heart attack,strokes, peripheral artery disease and kidney failure) in young adults with mild hypertension.
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Carbon monoxide (CO) is a colorless, odorless, tasteless toxic gas produced by incomplete combustion in fuel-burning devices and is a leading cause of poisoning morbidity and mortality.
Symptoms can be easily misinterpreted (e.g., headache, nausea, dizziness, or confusion) thus victims may not realize they are being poisoned.
CO detectors use an audible alarm and are effective in alerting potential victims of presence of CO. Some versions offer a digital readout of the CO concentration. Detectors are not a simple alarm level (as in smoke detectors) but are a concentration-time function.
In the UL 2034 Standard, Underwriters Laboratories specifies response times for CO alarms:
- 70 ppm sounds alarm within 60-240 minutes
- 150 ppm sounds alarm within 10-50 minutes.
- 400 ppm: sounds alarm within 4-15 minutes.
Current Occupational Safety and Health Administration permissible exposure limit for CO is 50 parts per million as an 8-hour time-weighted average concentration.
CO detectors have a limited lifespan of up to 7 years.
Forty percent of residential detectors studied failed to alarm in hazardous concentrations, despite outward indications that they were operating as intended.
CO detectors 10 years and older had the highest failure rates.
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Designer drugs are structural or functional analogs of controlled substances produced to mimic pharmacological effects of the original compound while circumventing legal restrictions and detection on drug screens. Considered "legal highs" by the public, these highly potent drugs are produced in clandestine laboratories with no regulations for quality control or clinical testing for phamacological effects and thus present major threat to public health. Examples include synthetic hallucinogens (DOM: STP), opiates ( methylfentanyl:china white), stimulants (methamphetamine:crank, MDMA: ecstasy, cathinones:bath salts) and synthetic cannabinoids (spice).
The synthetic cannabinoids are the newest designer drugs and numerous cases of intoxication are being reported including some fatalties.Cannabinoids fall into 3 classes: endocannabinoids, phytocannabinoids, synthetic. Marijuana, the best known cannabinoid is plant derived and its psychoactive effects are mainly due to delta-9-tetrahydrocannabinol (THC) which binds with the endocannabinoid receptors CB1 and CB2 found throughout the central and peripheral nervous system and peripheral organs. The CB receptors interact with opiate receptors which is likely responsible for the analgesic effect.
Since 1984, the John Huffman research group at Clemenson University synthesized over 450 cannabinoid compounds for biomedical reseach known as "JWH compounds". These compounds hold great promise in the investigation of multiple diseases and development of new novel therapies. Over the last several years, these cannabinoid compounds began cropping up sprayed onto herbs marketed in colorful packets and sold on the internet, convienence stores, and head shops. Although clearly labeled as "not for human consumption" considered on the street as a legal alternative to marijuana.
Key Points:
- Common names: Spice, K2, Smoke, Skunk, Purple Haze, Scooby snax, Crazy Monkey.
- JWH 018 (4-5 fold greater affinity for CB receptor than THC), JWH 081,122, 210
- Exact composition of products unknown and ever changing to avoid legal restrictions.
- Cannabinoid dose can vary greatly between products and even within same package "hot spots" are found where the drug is more concentrated.
- Often shown to be contaminated with impurities like beta agonists clenbulterol
- No clinical human studies on effects or any routine detection assays available.
- Clinical effects can vary from commonly described anxiety agitation, tachycardia to sedation and somulence.
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Poison ivy, oak, and sumac (Toxicodendron sp) causes a highly puritic, allergic contact dermatitits (ACD) that affects between 10 and 50 million in the US every year. It is a significant occupational hazard as well a scourge for outdoor enthusiasts.
Toxicodendron species contain oleoresins, known as Urushiol compound, secreted by all parts of the plant. Contact with the oil usually occurs by brushing against or direct handling of the plant or contaminated items. This toxin triggers a type IV delayed hypersensitivity reaction in approximately 75% of the population. Within 12-24 hours an erythematous, often linear, vesicular rash develops but new lesions can occur up to 2 weeks later.
There is no ideal treatment for ACD induced by Toxicodendron species. Avoidance and barrier protection are the best strategies. Recommended medications include antihistamines, topical preparations, and systemic steroids. However, steroids require a 2-3 week course to prevent recrudescence of the rash and are not without undesirable side affects.
Zanfel, an OTC granular polyethlene paste, removes urushiol by binding with it to create an aggregate cluster that can be washed away with water. It is highly effective, providing rapid relief even as a sole agent but requires multiple initial applications and is expensive. Mean Green hand scrub has similar ingredients and is claimed to bond urushiol also. Excessive scrathing and abrasive scrubs can cause secondary cellulitis requiring antibiotics.