UMEM Educational Pearls - Toxicology

Category: Toxicology

Title: Drug induced lactic acidosis.

Keywords: lactic acidosis (PubMed Search)

Posted: 4/20/2017 by Hong Kim, MD, MPH (Updated: 10/18/2021)
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Lactic acids are often elevated in critical care patients (e.g. septic shock). It can be also elevated in setting of drug overdose or less frequently in therapeutic use due to interference of oxidative phosphorylation. Some of the agents include:

 

  • Carbon monoxide
  • Cyanide
  • Propofol
  • Metformin
  • Propylene glycol
  • Salicylates
  • Beta-2 agonists
  • Thiamine deficiency/alcoholic ketoacidosis
  • Ethylene glycol/toxic alcohols
  • Nucleoside reverse-transcriptase inhibitors

 

Bottom line:

  • Although elevated lactic acid levels are often associated with underlying medical conditions, it is important to recognize drug-induced etiologies of lactic acidosis. 

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Category: Toxicology

Title: Sodium bicarbonate shortage Is there an alternate solution?

Keywords: sodium bicarbonate, sodium acetate (PubMed Search)

Posted: 4/6/2017 by Hong Kim, MD, MPH (Updated: 10/18/2021)
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FDA announced a shortage of sodium bicarbonate on 3/01/17.  Sodium bicarbonate is frequently used in acid-base disorder as well as in poisoning (cardiac toxicity from Na-channel blockade, e.g. TCA & bupropion, and salicylate poisoning).

 

Acetate is a conjugate base of acetic acid where acetate anion forms acetyl CoA and enters Kreb cycle after IV administration. Final metabolic products of acetate are CO2 and H2O, which are in equilibrium with bicarbonate via carbonic anhydrase activity.

 

Administration of sodium acetate increases the strong ion difference by net increase in cations, as acetate is metabolize, and leads to alkalemia.

 

Adverse events from sodium acetate infusion have been associated with its use as dialysate buffer: myocardial depression, hypotension, hypopnea leading to hypoxemia and hyperpyrexia. However, such adverse events have not been reported in toxicologic application.

 

 

Bottom line:

Sodium acetate can be administered safely in place of sodium bicarbonate if sodium bicarbonate is not available due to shortage.

Sodium acetate dose:

  • Bolus: 1 mEq/kg over 15 – 20 min
  • Infusion: 150 mEq in 1L D5%W @ twice maintenance rate   

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Category: Toxicology

Title: Pediatric poisoning trends

Keywords: Pediatric poisoning, household , fatalities (PubMed Search)

Posted: 3/30/2017 by Kathy Prybys, DO
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Children less than 5 years of age account for the majority of poisoning exposures in the United States. As expected, accessible household items are the most frequently reported exposures and include cosmetics and personal care products, household cleaning substances, medications, and foreign bodies. Opioids are responsible for the highest incidence of hospitalizations followed by benzodiazepines, sulfonylureas, and cardiovascular drugs (beta & calcium channel blockers, and centrally acting antiadrenergic agents).  Rise in buprenorphine use has led to significant increases in pediatric exposures. The most common sources of prescription medications were pills found on the ground, in a purse or bag, night stand, or pillbox. The 2015 American Association of Poison Centers Annual report lists 28 fatalities in children less than 5 year of age. Fatalities occurred from exposures to the following: narcotics (9), disc and button batteries (5), carbon monoxide (4), and other substances (10). 

Highlighted AAPC cases include:

  •  20 month old with ingestion of 20 mm Lithuim disc battery with several previous ED visits for abdominal pain who developed an aorto-esophageal fistula 
  • 13 month old with ingestion of unknown amount of salicylate pills 4 hours earlier with nausea and vomiting
  • 2 year old with ingestion of 5 tablets of 30mg Oxycodone ER seen in ED and discharged 7 hours later. EMS called next morning found patient unresponsive and apneic
  • 11 month old with ingestion of 1 unknown strength methadone pill found unresponsive and apneic at home

Poison prevention education of patients prescribed opioids or other highly toxic "one pill killers"  who have young children in their household is recommended and could be potentially life saving.

 

 

 

 

 

 

 

 

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Category: Toxicology

Title: How often do we encounter the signs and symptoms of clonidine overdose?

Keywords: adult clonidine overdose (PubMed Search)

Posted: 3/16/2017 by Hong Kim, MD, MPH (Emailed: 3/24/2017) (Updated: 10/18/2021)
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Clinical signs and symptoms of clonidine overdose include CNS depression, bradycardia, and miosis. Other effects include early hypertension, followed by hypotension and respiratory depression, especially in children.

 

Although clonidine overdose in children is well described, frequency of clinical signs/symptoms in adults is not well characterized.

 

Recently, a retrospective study was performed in a hospital in Australia looking at clonidine overdose in adults.  

 

Among isolated clonidine overdose, patients experienced:

  • GCS < 15: 55%
  • GSS < 9: 5%
  • Miosis: 25%
  • Bradycardia (HR< 60): 68%
  • Median HR: 48 (IQR: 40-62)
  • Hypotension (SBP < 90 mmHg): 25%
  • Median LOS: 21 hr (IQR: 11 – 27 hr)
  • Intensive care: 23%
  • No deaths

Bottom line:

  1. The most common symtom of clonidicine overdose was bradycardia
  2. Clonidine overdose results in non-life threatening but prolonged clinical effect in adult.

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Category: Toxicology

Title: Acute Phenytoin Toxicity

Keywords: Dilantin, Ataxia (PubMed Search)

Posted: 3/16/2017 by Kathy Prybys, DO
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Phenytoin is a first line anticonvulsant agent for most seizure disorders with the exception of absence and toxin-induced seizures. It has erratic gastrointestinal absorption with peak serum levels occurring anywhere from 3-12 hours following a single oral dose. 90% of circulating phenytoin is bound to albumin but only the unbound free fraction is active to cross cell membranes and exert pharmacological effect. Measured serum phenytoin levels reflect the total serum concentration of both the free and protein bound portions. Therapeutic range is between 10-20 mg/L. Free phenytoin levels are not often measured but are normally between 1-2 mg/L. Individuals with decreased protein binding (elderly, malnourished, hypoalbuminemia, uremia, and competing drugs) may have clincial toxicity despite a normal total phenytoin level. Toxicity consists of predominantly ocular and neurologic manifestations involving the vestibular and cerebellar systems:

Plasma level, µg/mL    Clinical manifestations
<10     Usually none
10-20     Occasional mild nystagmus
20-30     Nystagmus
30-40     Ataxia, slurred speech, extrapyramindal effects 
40-50     Lethargy, confusion
>50     Coma, rare seizures

Treatment of overdose is primarily supportive with serial drug level testing and neurologic exams. There is no evidence that gastrointestinal decontamination improves outcome. Routine cardiac monitoring is not necessary for overdose following oral ingestions. Cardiac toxicity is rarely seen and only with parenteral administration. 

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Category: Toxicology

Title: Drug induced Excited Delirium

Keywords: EDS, Excited Delirium (PubMed Search)

Posted: 3/2/2017 by Kathy Prybys, DO
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Excited delirium syndrome (EDS) is a life-threatening condition caused by a variety of factors including drug intoxication.  EDS is defined as altered mental status, hyperadrenergic state, and combativeness or aggressiveness. It is characterized by tolerance to significant pain, tachypnea, diaphoresis, severe agitation, hyperthermia, non-compliance or poor awareness to direction from police or medical personnel, lack of fatigue, superhuman strength, and inappropriate clothing for the current environment. These patients are at high risk for sudden death. Toxins associated with this syndrome include:

  • Lysergic acid diethylamide (LSD)
  • Phencyclidine (PCP)
  • 3,4-methylenedioxymethamphetamine (Ecstasy)
  • Cocaine
  • Methamphetamine
  • Synthetic cathinones ("Bath salts")Mephedrone, Methylone,  Methylenedioxypyrovalerone (MDPV), designer drugs similar to amphetamine.
  • Synthetic cannbinoids

Ketamine at 4mg/kg dose can be given by intramuscular route and has been demonstrated to be safe and effective treatment for EDS.

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Category: Toxicology

Title: Suboxone for managing opioid addiction

Keywords: Buprenorphine, Suboxone (PubMed Search)

Posted: 2/16/2017 by Kathy Prybys, DO
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Takeaways

The current opioid epidemic is considered the worst drug crisis in American history responsible for 50,000 deaths per year in the US from overdose of heroin and opioid prescription drugs. A 200% increase in the rate of overdose deaths involving opioids occurred between 2000 and 2014. The continued rise in opioid related deaths calls for an urgent need for treatment. Three types of medication-assisted therapies (MATs) are available for treating patients with opioid addiction:methadone, buprenorphine, and naltrexone. Suboxone a combination of buprenorphine and naloxone, is emerging as one of the best choices for the following reasons:

  • Buprenorphine is a partial agonist that suppresses opioid withdrawal and cravings.
  • Binds opioid receptors with high affinity but low intrinsic activity.
  • Lasts 24 hours. Binds opioid receptors to prevent full opioid agonists such as heroin or prescription opioids from binding.
  • Less risk for dependency as increasing doses does not result in full opioid effect.
  • Less respiratory depression in overdose due to partial effect.
  • Naloxone, an opioid antagonist is poorly absorbed by oral route and is added to discourage injecting or snorting of suboxone as it can precipitate severe withdrawal.
  • Precipitated withdrawal can occur if other opioids are present with administration of Suboxone. This is particularly important with long acting opioids such as methadone.
  • Can be prescribed in the primary care setting and does not require a specialized clinic.
  • Comes in 2 or 8 mg tablet or sublingual film.

 

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Takeaways

Methadone overdose produces classic signs and symptoms of opioid intoxication - CNS and respiratory depression with pinpoint pupils. However, methadone overdose has also been associated with hypoglycemia – a relatively uncommon adverse effect.

Bottom line:

  • Methadone-induced hypoglycemia can occur, although rare, in an acute overdose.

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Category: Toxicology

Title: Urine drug testing

Keywords: Urine Drug Sreen (PubMed Search)

Posted: 1/19/2017 by Kathy Prybys, DO (Emailed: 1/20/2017) (Updated: 1/20/2017)
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Urine drug screens are most commonly performed by immunoassay technology utilizing monoclonal antibodies that recognizes a structural feature of a drug or its metabolites.  They are simple to perform. provide rapid screening, and qualitative results on up to 10 distinct drug classes with good sensitivity but imperfect specificity. This can lead to false positive results and the need for confirmatory testing. UDS  does not detect synthetic opiates or cannabinoids, bath salts (synthetic cathinones), and  gamma-hydroybutyrate. Most common drug classes detected are the following:

  • Opiates
  • Methadone
  • Benzodiazepines (not all)
  • Amphetamines 
  • Cocaine
  • THC metabolites
  • Barbituates
  • LSD
  • PCP
  • MDMA (Ecstasy)

 

 

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Category: Toxicology

Title: Risk factors of severe outcome in acute salicylate poisoning

Keywords: salicylate poisoning (PubMed Search)

Posted: 1/13/2017 by Hong Kim, MD, MPH (Updated: 10/18/2021)
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A small retrospective study of an acute poisoning cohort attempted to identify risk factors for severe outcome in salicylate poisoning.

Severe outcomes were defined as

  1. Acidemia pH < 7.3 or bicarbonate < 16 mEq/L
  2. Hemodialysis
  3. Death

A multivariate analysis of 48 patients showed that older age and increased respiratory rate were independent predictors of severe outcomes when adjusted for salicylate level.

Initial salicylate acid level was not predictive of severe outcome.  

Elevated lactic acid level was also a good predictor of severe outcome in univariate analysis but not in multivariate analysis.

Limitations

  1. Small sample size with single center study
  2. Retrospective study design
  3. Validation study of these predictors is needed.

 

Bottom line

  1. Older age and increases respiratory rate is associated with severe outcome (acidemia, hemodialysis or/and death) in this study.
  2. Data must be interpreted with caution due to small sample and retrospective study design.

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Category: Toxicology

Title: Unexplained Lactic Acidosis, a clue to poisoning

Keywords: Lactic acidosis (PubMed Search)

Posted: 1/5/2017 by Kathy Prybys, DO (Emailed: 1/6/2017) (Updated: 1/6/2017)
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Lactic acidosis is the most common cause of anion gap metabolic acidosis in all hospitalized patients. An elevated lactate level is an important marker of inadequate tissue perfusion causing subsequent shift to anaerobic metabolism and occuring in a variety of disease states such as sepsis. In patients with unexplained lactic acidosis without systemic hyoperfusion or seizure suspect  the following toxins:

  • Acetaminophen: Early on in massive ingestion usually associated with coma.
  • Cyanide
  • Metformin
  • HIV Drugs: Nucleotide reverse transcriptase inhibitors = Didanosine, stavudine, zidovudine due to mitochondrial toxicity.
  • Ethylene Glycol: Spuriously elevated lactate may occur with ethylene glycol toxicity due to the structural similarity between glycolic acid and lactate.Check for osmolar gap.
  • Kombucha ``mushroom'' tea 
 

 

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Category: Toxicology

Title: Utility of lactic acid level for diagnosis of cyanide poisoning in smoke inhalation victims

Keywords: cyanide toxicity, lactic acid (PubMed Search)

Posted: 12/29/2016 by Hong Kim, MD, MPH (Emailed: 12/30/2016) (Updated: 12/30/2016)
Click here to contact Hong Kim, MD, MPH

Takeaways

Smoke inhalation victims (house fires) are at risk of carbon monoxide (CO) and cyanide poisoning (CN). CO exposure/poisoning can be readily evaluated by CO - Oximetry but CN level can be obtained in majority of the hospital.

Lactic acid level is often sent to evaluate for CN poisoning.

 

Bottom line:

  1. Lactatic acid levels should be sent in all smoke inhalation victims.
  2. Elevate lactate > 10 mmol/L is highly suggestive of CN poisoning
    .

 

 

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Category: Toxicology

Title: Acetaminophen induced liver failure

Keywords: Acetaminophen, Liver Failure (PubMed Search)

Posted: 12/16/2016 by Kathy Prybys, DO
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Acetaminophen is one of the most common pharmaceutical ingestions in overdose and a leading cause of acute of liver failure in the U.S.  Early recognition and treatment is critical for prevention of morbidity.

  • Vigilance and screening is required for this "silent poison", available in hundreds of OTC products and in combination with numerous prescription medications. Symptoms may not be present early in course (for up to 24 hours) in poisoning.
  • Maximal benefit with antidote treatment, n-acetylcysteine (NAC) is time dependent within 8 hours of ingestion. Fulminant hepatotoxicity is unusual in acute overdoses treated with NAC within 10 hours of ingestion.
  • Early prediction of poor prognosis is essential to identify patients who may require life-saving liver transplantation.  Kings College Criteria: Arterial pH less than 7.30, INR greater than 6.5, Creatinine greater than 3.4, Grade III or IV encephalopathy combined with Lactate greater than 3.5 and Phosphate greater than 3.75 may increase sensitivity.

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Takeaways

Recent study evaluated whether an acetaminophen (APAP) level obtained less than 4-hour post acute ingestion can predict which patient would not require n-acetylcysteine (NAC).  APAP cutoff level of 100 ug/mL was used for analysis. This was a secondary analysis of the Canadian Acetaminophen Overdose Study database (retrospective study). 

 

Bottom line:

  1. If initial APAP level of 100 ug/mL was applied as a cutoff point, it missed 27 patients (N= 1821) who had toxic APAP level at > 4-hour post ingestion that require NAC.  
  2. Only a very low (< 15 ug/mL) or undetectable initial APAP reliably identify (sensitivity 100%) patients who do not require NAC.
  3. Absorption of APAP can be delayed by coingestion of opioids or antimuscarinics.

 

 

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Category: Toxicology

Title: My patient really has all these drug allergies?

Keywords: Drug Allergy, ADR, ADE (PubMed Search)

Posted: 12/1/2016 by Kathy Prybys, DO (Emailed: 12/2/2016) (Updated: 12/2/2016)
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Takeaways

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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Category: Toxicology

Title: Management of heroin overdose patients in prehospital and ED setting: How long do they need to be observed?

Keywords: heroin overdose, observation period, bystander naloxone (PubMed Search)

Posted: 11/16/2016 by Hong Kim, MD, MPH (Emailed: 11/17/2016) (Updated: 11/17/2016)
Click here to contact Hong Kim, MD, MPH

Takeaways

Recently a review paper was published regarding the duration of observation in heroin overdose patients who received naloxone.

It made several conclusions regarding heroin overdose:

  1. Treat (naloxone) and release in a prehospital setting may be safe.
  2. Short observation period (minimum of 1 hour) for heroin OD patients who were treated in the ED may be safe.
  3. Bystander and first responder naloxone administration is effective and safe.

It should be pointed out that this is a review paper of limited number of articles with variable quality. Additionally, the clinical history of “heroin use” may be unreliable as fentanyl and novel synthetic opioids are also sold as “heroin.” Providers should exercise appropriate clinical judgement when caring for these patients. 

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Category: Toxicology

Title: Buprenorphine/naloxone (Suboxone) exposure in pediatric population

Keywords: buprenorphine exposure, pediatrics, retrospective study (PubMed Search)

Posted: 10/26/2016 by Hong Kim, MD, MPH (Emailed: 10/27/2016)
Click here to contact Hong Kim, MD, MPH

Takeaways

Recently, a retrospective study of unintentional buprenorphine/naloxone exposure among pediatric population was published. All patients were evaluated by toxicologists at the time of initial hospital presentation (or transfer) at the study center.

 

Bottom line

  • 83% and 80% of the patients experienced respiratory and CNS depression, respectively.
  • Majority of the patients became symptomatic within 8 hours of exposure (range not available).
  • Naloxone reversed respiratory depression. Median dose for single naloxone dose: 0.09 mg/kg; median dose for multiple naloxone doses: 0.19 mg/kg.
  • The reported “ceiling effect” on respiratory depression in adult does not exist in pediatric population.
  • The optimal time of observation is unclear but it is prudent to observe pediatric buprenorphine exposure for up to 24 hours.

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Takeaways

US, Canadian and European critical care and toxicology societies recently published a consensus recommendation is the management of CCB poisoning.

Bottom line:

1. First line therapy remains unchanged: IV calcium, atropin, high-dose insulin (HIE) therapy, vasopressor support (norepinephrine and/or epinephrine).

2. Refractory to first line therapy: increase HIE, lipid-emulsion, transvenous pacemaker

3. Refractory shock, periarrest or cardiac arrest: Above (#1 & #2) plus ECMO if available.

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Category: Toxicology

Title: "Leaves of 3 let them be"

Keywords: Poison Ivy, Toxicodendron, Urushiol (PubMed Search)

Posted: 10/6/2016 by Kathy Prybys, DO (Emailed: 10/7/2016) (Updated: 10/7/2016)
Click here to contact Kathy Prybys, DO

Takeaways

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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Naloxone has been used to reverse opioid-induced respiratory depression for decades. The “standard” dose of opioid intoxication has been 0.4 mg.  However, over the past decade, initial naloxone dose for opioid intoxication has evolved to recommend a lower initial dose (0.04 – 0.05 mg).

 

A recent article by Connors et al. reviewed 25 medical resources (internet, medical texts and study guides) of different medical specialties (internal medicine, medical toxicology, emergency medicine, pediatrics, anesthesiology, pain medicine and general medicine)

 

Findings:

  • 12 medical resources (48%) recommend using 0.05 mg or less IV as an initial dose.
  • 9 medical resources (36%) recommend using 0.4 – 0.5 mg or higher as an initial dose.
  • Maximum dose also ranged widely from 2 to 20 mg.

 

Recent editions of emergency medicine text (Rosen’s and Tinitinalli) recommend using 0.04 – 0.05 mg IV in ED patients with history of opioid dependence. Higher doses of naloxone are recommended for non-opioid dependent/apneic patients.

 

However, history of opioid dependence is difficult to obtain in patients with opioid induced CNS/respiratory depression.

 

Administering 0.4 mg or higher dose may/can acute agitation or opioid withdrawal symptoms that can utilize more ED resources to calm agitated patient/management of withdrawal. Thus it may be prudent to use low-dose strategy (0.04 mg IV with titration) to minimize the risk of precipitating naloxone-induced opioid withdrawal/agitation.

 

Bottom line:

In opioid-induced respiratory depression/apneic patients:

  1. Ventilate with bag-valve mask for apnea/hypoxia
  2. Administer naloxone: 0.04 mg IV every 2 – 3 min until reversal of respiratory depression/hypoxia is achieved.

To make 0.04 mg naloxone solution:

  • Dilute 1 mL of 0.4 mg naloxone with 9 mL normal saline in 10 mL syringe. 

 

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