UMEM Educational Pearls - Toxicology

Category: Toxicology

Title: why is your patient blue? xenobiotic-induced methemoglobinemia

Keywords: methemoglobinemia, methylene blue (PubMed Search)

Posted: 5/20/2015 by Hong Kim, MD, MPH (Emailed: 5/21/2015) (Updated: 5/21/2015)
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Methemoglobin (MetHb) is produce when Fe+2 in heme is oxidized to Fe+3 under oxidative stress (caused by mediation and chemicals). MetHb does not bind to oxygen and thus decrease RBC’s O2 carrying capacity.

Among medication, overdose of local anesthesia - benzocaine, dapsone, and phenazopyridine are often implicated. (Table 1)

Think about methemoglobinemia in presence of low pulse oximetry (~85%) with lack of response to supplemental oxygen, cyanosis, dyspnea, etc. (see Table 2 – signs and symptoms of MetHb) in patients who are taking or overdosed on medication listed in Table 1.

Diagnosis: CO-oximetry detects toxin-induced hemoglobinopathies, including COHb and MetHb.

Treatment: Methylene blue (1 mg/kg over 5 min) in symptomatic patients or MetHb level > 25%. Resolution of methemoglobinemia should be noted in 30 – 60 min.

G6PD deficiency: Prevalence in the U.S. is 4-7% with highest prevalence in African American population (11%). Methylene blue causes hemolytic anemia in patients with G6PD deficiency within 24 hours of administration. However, G6PD status is often unknown in ED patients.  When caring for patients with known G6PD deficiency and methemoglobinemia, providers must carefully consider the risk and benefit of treating MetHb (including severity of poisoning/MetHb) with methylene blue.

Table 1. Causes of MetHb

Medication

 

Chemicals

Benzocaine, Lidocaine, Prilocaine

Aniline dye

Dapsone

Chlorobenzene

Phenazopyridine

Organic nitrites (e.g. isobutyl nitrite)

Nitroglycerin

Naphthalene

Nitroprusside

Nitrates (well water contamination)

Quinones (Primaquine & Chloroquine)

Nitrites (food preservatives)

Sulfonamides

Silver nitrate

Nitric oxide

Trinitrotoluene

Amyl nitrite

 

 

Table 2. Signs and symptoms

MetHb level (%)

Signs and symptoms

1-3% (normal)

 

·  None

3-15%

·  Low pulse oximetry (<90%)

·  Gray cutaneous coloration

15-20%

·  Chocolate brown blood

·  Cyanosis

20-50%

·  Dizziness, syncope

·  Dyspnea

·  Weakness

·  Headache

50-70%

·  CNS depression, coma, seizure

·  Dysrhythmias

·  Tachypnea

·  Metabolic acidosis

>70%

·  Death

·  Hypoxic injury

 


Category: Toxicology

Title: Dabigatran and Renal Replacement Therapy

Keywords: Dabigatran, Hemodialysis, Renal Replacement Therapy (PubMed Search)

Posted: 5/14/2015 by Kishan Kapadia, DO
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Dabigatran is an orally administered, potent, direct thrombin inhibitor approved for the prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation, and for the treatment and secondary prevention of venous thromboembolism.

Several pharmacokinectic studies have suggested that dabigatran possesses a number of ideal properties for expedited removal via extracorporeal methods.  Dabigatran has low oral bioavailability (3-7%) and is predominantly cleared (80%) by the kidneys.  It is not significantly protein bound, low-to-moderate steady state volume of distribution, and has a low molecular weight.  All of these attributes make it a candidate for extracorporeal removal.  Low protein binding may suggest redistribution into the plasma post extracorporeal removal.  

Dabigatran is a substrate for the multidrug efflux transporter P-glycoprotein.  Administration of the drug with potent P-glycoprotein inhibitors (ketoconazole, verapamil, amiodarone, quinidine) may significantly increase risk of toxicity, i.e. bleeding.

Most of the current evidence is based on case reports/case series where HD was the primary mode of removal.  

Caution: Redistribution effect in plasma dabigatran concentration was also observed in several cases within 20 min to 12 hours post cessation of renal replacement therapy.   Other limitations include:

1) Hemodynamic instability such as hypotension that may make initiation of extracoporeal removal difficult

2) Availability of indicators demonstrating effectiveness of extracorporeal removal 

3) Amount of time needed to prepare patient to receive extracorporeal therapy

4) Use of extracorporeal removal as a treatment modality has not been prospectively evaluated

Bottom line: Extracorporeal removal may be an option for patients in the setting of life-threatening bleeding but with consideration of several limitations and should not preclude or delay use of other supplemental hemostatic therapies.

 

 

 

 

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Category: Toxicology

Title: Ketamine for Alcohol Withdrawal?

Keywords: ketamine, alcohol withdrawal, ethanol (PubMed Search)

Posted: 4/10/2015 by Bryan Hayes, PharmD (Emailed: 5/7/2015) (Updated: 5/7/2015)
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Background

 

In addition to the down regulation of GABA receptors in chronic ethanol users, there is an upregulation in NMDA receptor subtypes. Although the pathophysiology is much more complex, when ethanol abstinence occurs, there is a shortage of GABA-mediated CNS inhibition and a surplus of glutamate-mediated CNS excitation. If GABA agonists are the mainstay of treatment, why not also target the NMDA receptor? Enter ketamine.

The Data

Only one study exists and was published recently.

  • Retrospective review of 23 adult patients administered ketamine specifically for management of AWS.
  • Mean time to initiation of ketamine from first treatment of AWS, and total duration of therapy were 33.6 and 55.8 hours, respectively.
  • Mean initial infusion dose and median total infusion rate were 0.21 and 0.20 mg/kg/h, respectively.
  • No change in sedation or alcohol withdrawal scores within 6 hours of ketamine initiation.
  • Median change in benzodiazepine requirements at 12 and 24 hours post-ketamine initiation were -40.0 and -13.3 mg, respectively.
  • One documented adverse reaction of oversedation, requiring dose reduction.
  • Authors concluded that ketamine appears to reduce benzodiazepine requirements and is well tolerated at low doses.

Application to Clinical Practice

While the dexmedetomidine studies should not be using reduction in benzodiazepine requirements as an endpoint, it may be acceptable for ketamine since it actually works on the underlying pathophysiology. More studies are needed but it's good to see we’re starting to look at it.

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There are some studies that have shown that NSTEMI patients have done worse when administered opioids. Most studies were not well controled and the exact mechanism was not clear. This study adds a biological mechanism to these fidnings.

Hobl et al. showed clopidogre concentrations delayt peak yhours, have overall decrease AUC and actually decrease active metabolites when morphine is administered IV. Morphine may not be the right choice in any ACS that receives clopidogrel.

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Category: Toxicology

Title: Clinical Predictors for Delirium Tremens in Patients with Alcohol Withdrawal Seizures

Keywords: Delirium tremens, DTs, alcohol withdrawal, seizures (PubMed Search)

Posted: 4/7/2015 by Bryan Hayes, PharmD (Emailed: 4/9/2015) (Updated: 4/9/2015)
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A new study from South Korea identified 3 potential clinical predictors of developing delirium tremens in patients presenting to the ED with alcohol withdrawal seizures.

  1. Low platelet count
  2. High blood level of homocysteine
  3. Low blood level of pyridoxine

If one or more is present, these findings may help assess alcohol withdrawal patients for the risk of developing DTs.

Application to Clinical Practice

  • The problem is that in the U.S., homocysteine and pyridoxine levels may not be readily available at all institutions.
  • Adjunctive treatment options including vitamin B12, folate, and pyridoxine may be considered if levels are available, but it is unknown if 'treating the numbers' actually prevents development of DTs.
  • At the very least, these clinical predictors may help risk assess patients for appropriate disposition.

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Category: Toxicology

Title: When should NAC be stopped after an acute acetaminophen poisoning?

Keywords: acetaminophen toxicity, NAC, hepatic toxicity (PubMed Search)

Posted: 3/19/2015 by Hong Kim, MD, MPH (Updated: 12/7/2021)
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Elevation of AST or ALT >1000 after acute ingestion of acetaminophen indicate hepatic toxicity. N-acetylcysteine (NAC) is an effective treatment for acute acetaminophen poisoning. However, in a setting a significant transaminitis, (> 1000s) NAC infusion is continued beyond the routine 21-hour protocol.

 

Currently, there is no specific guideline or “level” of AST or ALT where discontinuing NAC is deemed safe and appropriate.

 

A recent retrospective study (n = 37 patients with 343 pairs of AST/ALT) evaluated AST/ALT ratio as a possible indicator for discontinuing NAC infusion after an acute acetaminophen induced hepatic toxicity.

 

This study found that post peak AST/ALT ratio of < 0.4 had sensitivity of 99% for identifying patients with resolving hepatic injury.

 

This finding requires validation prior to clinical application but this may be the first step to identifying a safe indicator to help guide clinician when NAC can be discontinued safely.

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Category: Toxicology

Title: How to Write for Prescription Naloxone

Keywords: naloxone, opioid overdose (PubMed Search)

Posted: 3/10/2015 by Bryan Hayes, PharmD (Emailed: 3/12/2015) (Updated: 3/14/2015)
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In the midst of an unprecedented opioid epidemic, there have been considerable efforts to expand access to naloxone (Doyon S, et al. J Med Toxicol 2014;10:431-4). If the situation arises when you need to write a prescription for it, here's how:

Option 1: Naloxone vial and needle traditional IM/SQ using 0.4 mg/mL injection vial and needles (least expensive $40, FDA approved)

Naloxone 0.4 mg/mL single dose vial and 3 cc, 23 g, 1 inch syringes, #2 each

SIG: Inject 1 mL intramuscularly upon signs of opioid overdose. May repeat X 1. Call 911.

Option 2: IMS/Amphastar 2 mg/2 mL prefilled syringe and mucosal atomization device ($95/kit, products FDA approved but intranasal administration is off-label)

Naloxone 2 mg/2 mL prefilled syringe and intranasal atomizer device, #2 each

SIG: Spray one-half of syringe (1 mL) into each nostril upon signs of opioid overdose. May repeat X 1. Call 911.

Option 3: Evzio Autoinjector ($200-700 per Rx though many insurances cover it and the company has vouchers available, FDA approved in 2014, evzio.com/hcp)

Evzio 0.4 mg, #1 two-pack

SIG: Use as directed upon signs of opioid overdose. May repeat X 1. Call 911.

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Category: Toxicology

Title: Patient has this CT Head - What is your diagnosis?

Keywords: cyanide, carbon monoxide, methanol, hypoglycemia (PubMed Search)

Posted: 2/26/2015 by Fermin Barrueto, MD
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Question

Patient has the following Head CT, what is your differential diagnosis? There are only a few characteristic toxins that can cause this type of finding on CT.

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Category: Toxicology

Title: Adverse Effects of Combined Lipid Emulsion + VA-ECMO in Poisoned Patients

Keywords: ECMO, fat emulsion, lipid, intralipid, poison, extracorporeal membrane oxygenation (PubMed Search)

Posted: 2/3/2015 by Bryan Hayes, PharmD (Emailed: 2/12/2015) (Updated: 2/12/2015)
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A new review summarized published adverse effects when IV lipid emulsion is used along with venous-arterial extracorporeal membrane oxygenation (VA-ECMO) in patients with cardiotoxic drug poisoning.

Not surprisingly, running fat through the ECMO circuit can cause some issues. Here's what's been published:

  • cracking of stopcocks
  • fat emulsion agglutination
  • clogging and associated malfunction of the membrane oxygenator
  • increased blood clot formation in the circuit

It's unclear how these findings should change management if using both treatment modalities, but at the very least, be aware that fat depostion in the VA-ECMO circuits and increased blood clot formation can occur.

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Category: Toxicology

Title: Drug Abuse Screens

Keywords: Drug Screens, Drug Intervals (PubMed Search)

Posted: 2/5/2015 by Kishan Kapadia, DO
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Performance Characteristics of Common Drug Abuse Screening Immunoassays

Drug/Class

Detection Interval (***)

Comments

Amphetamines

1-2 days (2-4 days)

Decongestants, ephedrine,l-methamphetamine, selegilene & bupropion metabolites may give False (+) results; MDA & MDMA are variably detected

Barbiturates

2-4 days

Phenobarbital may be detected for up to 4 weeks

Benzodiazepines

1-30 days

Benzos vary in reactivityand potency; False (+) results may be seen with oxaprozin

Cannabinoids

1-3 days (>1 month)

Screening assays detect inactive and active cannabinoids; Confirmatory assays detects inactive metabolite THCA (tetrahydrocannabinoic acid)

Cocaine                  

2 days (1 week)

Screening & confirmatory assays detect inactive metabolite BE (benzoylecgonine); False (+) results are unlikely

Opiates

1-2 days; 2-4 days (<1 week)

Semisynthetic opiates derived from morphine show variable cross-reactivity; Fully synthetic opioids (e.g., fentanyl, meperidine, methadone, propoxyphene, tramadol) have minimal cross reactivity; Quinolone may cross-react

Methadone

1-4 days

Doxylamine may cross-react

Phencyclidine

4-7 days (>1 month)

Dextromethorphan, diphenhydramine, ketamine, & venlafaxine may cross react

Propoxyphene

3-10 days

Duration of positivity depends on cross reactivity of metabolite norpropoxyphene

(***)Values are after typical use; values in parentheses are after heavy or prolonged use.

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Category: Toxicology

Title: Tetrodotoxin Outbreak - in Minnesota!

Keywords: tetrodotoxin (PubMed Search)

Posted: 1/29/2015 by Fermin Barrueto, MD (Updated: 12/7/2021)
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Tetrodotoxin is lethal poison that blocks sodium channels. A famous sushi called "Fugu" is cut from a puffer fish that contains this poison. The idea is to get just enough of the toxin to cause peri-oral paresthesia but not too much to get seizures, paralysis and cardiac dysrrhythmias. A recent outbreak in Minneapolis, Minnesota was just reported in the MMWR so it can really happen anywhere, its a great read - dried puffer was bought from a market in NYC.

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6351a2.htm

2-3 mg of the toxin is lethal to an adult human. No antidote exists though I would try hypertonic sodium bicarbonate for the cardiac dysrrhythmias and appropraite supportive. If the patient survives 24 hrs, the patient will do well without sequelae if appropriately supported.

 


Category: Toxicology

Title: Can Hydroxocobalamin be administered via intraosseous access for acute cyanide toxicity?

Keywords: intraosseous, hydroxocobalamin, cyanide poisoning (PubMed Search)

Posted: 1/15/2015 by Hong Kim, MD, MPH (Updated: 12/7/2021)
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Hydroxocobalamin is an effective cyanide antidote when administered intravenously. Although intraosseous (IO) access is often used in critically ill patients with difficult or delayed IV access, the efficacy of IO administration has not been investigated until recently.

In a recent randomized animal study, acute cyanide toxicity was induced in two groups of swine where 150 mg/kg Hydroxocobalamin was administered via IV vs. IO. The survival rate, reversal of hypotension, and laboratory results were similar between the IV and IO group.

The finding of this study suggest that IO administration of Hydroxocobalamin is as efficacious as IV administration and its administration in acute cyanide toxicity should not be delayed due to lack of IV access when IO access is available.

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Category: Toxicology

Title: Whole Bowel Irrigation Position Paper Update... Well, Not Really

Keywords: whole bowel irrigation, WBI, GI decontamination (PubMed Search)

Posted: 1/6/2015 by Bryan Hayes, PharmD (Emailed: 1/8/2015) (Updated: 1/15/2015)
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The original position paper on the use of whole bowel irrigation (WBI) was first published in 1997 by the American Academy of Clinical Toxicology (AACT) and the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT) and updated in 2004.
 
The 2015 iteration concludes, "There is no new evidence that would require a major revision of the conclusions of the 2004 position statement."
 
Potential Indications
  1. Potentially toxic ingestions of sustained-release or enteric-coated drugs
  2. Substantial ingestions of iron, lithium, or potassium
  3. Removal of ingested packets of illicit drugs in "body packers"

Application to Clinical Practice

WBI can facilitate removal of select toxicants from the gastrointestinal tract in some patients, but there is no convincing evidence from clinical studies that it improves the outcome of poisoned patients.

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It is believed that administration of beta-blocker administration in patients with cocaine chest pain will produced increased vasoconstriction due to “unopposed alpha effect.”

 

Several retrospective studies on the use of beta-blocker in patients with cocaine-induced chest pain concluded the use of beta-blocker to be safe.

 

So is the unopposed alpha effect just a theory?

 

Lange RA et al. 1990 Ann Internal Med

Design: randomized, double-blind, placebo controlled trial.

 

30 (38- 68 years old) patients undergoing cardiac catherization for chest pain evaluation were studied.

 

Cocaine (intranasal administration) resulted in:

  • Increased myocardial oxygen demand
  • Increased coronary vascular resistance 22%
  • Decreased coronary sinus blood flow: 10%

 

Administration of propranolol (intracoronary infusion) resulted in additional:

  • Increase coronary vascular resistance 19%
  • Decrease coronary sinus blood flow by 15%
  • No additional change in myocardial oxygen demand

 

Complete coronary occlusion observed in 1 patient with ST elevation

Epicardial coronary arterial segment constriction >10% in 5 patients.

 

Bottom Line: Lange RA et al. 1990 demonstrates that the “unopposed alpha effect” does occur in coronary artery when beta-blocker is administered in a setting of acute cocaine exposure.  Overall, the use of beta-blocker in the ED management of cocaine-induce acute chest pain is not a prudent option.  It is unknown if the cocaine dose, last use of cocaine (days), or CAD history influence the “safety” of beta-blocker initiation/use during inpatient hospitalization.

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Category: Toxicology

Title: In-hospital outcomes for beta blocker use in cocaine-chest pain

Keywords: cocaine, chest pain, beta blocker (PubMed Search)

Posted: 12/1/2014 by Bryan Hayes, PharmD (Emailed: 12/11/2014) (Updated: 12/11/2014)
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Should beta blockers be withheld in cocaine-chest pain patients?

A new study retrospectively compared patients who received beta blockers as an inpatient to those who did not. Even though the beta blocker group had higher risk clinical characteristics, there was no difference in the composite primary end point of myocardial infarction, stroke, ventricular arrhythmia, or all-cause mortality within 24 hours of beta blocker use.

Important Limitations

The potentially dangerous interaction between beta blockers and cocaine is likely a much larger issue in patients with very recent cocaine use in the setting of a catecholamine surge. A retrospective analysis likely doesn't include those patients.

Application to Clinical Practice

While this study doesn't answer the question about beta blocker use in acute cocaine toxicity, it does provide some reassurance about the safety of beta blockers given for cocaine-related chest pain.

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Category: Toxicology

Title: Rhabdo Prevalence

Keywords: Sympathomimetic toxicity, Synthetic cathinones, Rhabdomyolysis (PubMed Search)

Posted: 12/4/2014 by Kishan Kapadia, DO
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Sympathomimetic toxicity is a known toxidrome that is complicated by the development of rhabdomyolysis.  There are multiple stimulant agents that induce sympathomimetic toxicity including, synthetic cathinones, cocaine, amphetamines, and methamphetamines.  

A recent retrospective, single-center, chart review in the age range of 14-65 years sought to determine the prevalence of rhabdomyolysis in patients with sympathomimetic toxicity and compare rates among patients using specific agents.  Rhabdomyolysis and severe rhabdomyolysis were defined as CK>1000 and 10,000 IU/L, respectively.

Rhabdomyolysis occurred in 42% of study subjects (43/102)

Prevalence in 89 subjects due to a single-stimulant exposure:

Rhabdomyolysis 

1) Synthetic cathinone (MDPV, alpha-PVP) 63% (12/19)

2) Methamphetamine 40% (22/55)

3) Cocaine 33% (3/9)

4) Other single agents (methylphenidate, pseudoephedrine, phentermine) 0% (0/6)

Severe Rhabdomyolysis

1) Synthetic cathinone 26% (5/19)

2) Methamphetamine 3.6% (2/55)

3) Cocaine 11% (1/9)

4) Other single agents (methylphenidate, pseudoephedrine, phentermine) 0% (0/6)

In this study, patients exposed to synthetic cathinones were more likely to develop rhabdomyolysis and severe rhabdomyolysis compared to the non-cathinone-exposed group.

Bottom Line:

Be aware of this increased risk from synthetic cathinones along with other stimulants.  Treat aggressively with IV fluids, rapid correction of hyperthermia, benzodiazepines to control manifestations of sympathomimetic toxicity to reduce muscle activity and metabolic demand.

 

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Category: Toxicology

Title: Identification of cyanide poisoning in smoke inhalation victims.

Keywords: Cyanide, smoke inhalation, lactate (PubMed Search)

Posted: 11/28/2014 by Hong Kim, MD, MPH (Updated: 12/7/2021)
Click here to contact Hong Kim, MD, MPH

Cyanide poisoning is rare but highly lethal. Cyanide exposure can occur during residential fire (most common source of exposure) where combustion of synthetic materials (i.e. plastic and polyurethane) releases cyanide gas as well as other toxic gases, including carbon monoxide. Although carbon monoxide poisoning can be readily identified by CO-Hb level using CO-oximetry, serum/blood cyanide level is not readily available for acute management.

 

However, elevated lactate level (> 10 mmol/L ) has shown to be highly correlated with toxic level of cyanide (40 micromol/L or 1 mg/L) in smoke inhalation victims (Baude FJ et al. N Engl J Med 1991;325:1761-6).

  • Sensitivity: 87%
  • Specificity: 94%
  • Positive predictive value: 95%

 

Bottom line: when managing smoke inhalation victims, think about cyanide poisoning in addition to carbon monoxide poisoning and check the lactate level. Lactate > 10 mmol/L is suggestive of cyanide poisoning and should be treated with hydroxocobalamin. 

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Category: Toxicology

Title: Opioid Prescription Drug Abuse - The Pattern of Abuse

Keywords: opioids, toxicology (PubMed Search)

Posted: 11/20/2014 by Fermin Barrueto, MD (Updated: 12/7/2021)
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The pattern of prescription drug abuse continues to center around semisynthetic opioids like oxycodone and hydrocodone. Federal regulations have now raised hydrocodone to a schedule II drug like oxycodone. Despite efforts, the slope for natural and semisynthetic opioids remains steep.  The ED measures of education, limit prescriptions for acute pain, minimize number of days/pills prescribed and utlize the prescription drug monitoring program are some basics that can assist you in better prescribing habits.

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Category: Toxicology

Title: Bactrim + ACE-Inhibitor/ARB + Older Adult = Increased Sudden Death

Keywords: Bactrim, trimethoprim-sulfamethoxazole, ACE-inhibitor, angiotensin receptor blocker, ARB (PubMed Search)

Posted: 11/5/2014 by Bryan Hayes, PharmD (Emailed: 11/13/2014) (Updated: 11/13/2014)
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A new population-based case-control study in older adults has linked the administration of trimethoprim-sulfamethoxazole (Bactrim, TMP-SMX) to increased risk of sudden death in patients also receiving angiotensin converting enzyme inhibitors (ACE-I) or angiotensin receptor blockers (ARB). [1]

Hyperkalemia is the suspected cause. [2] Compared to amoxicillin, TMP-SMX was associated with an increased risk of sudden death (adjusted odds ratio 1.38, 95% confidence interval 1.09 to 1.76) within 7 days of exposure to the antibiotic.

Practice Change

In older patients receiving ACE-Is or ARBs, TMP-SMX is associated with an increased risk of sudden death. When appropriate, alternative antibiotics should be considered.

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Category: Toxicology

Title: Lily of the Valley, Part 2

Keywords: Digoxin, Cardioactive Steroids, Digitoxin, Digoxin-specific Fab Fragments (PubMed Search)

Posted: 11/7/2014 by Kishan Kapadia, DO
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Digoxin-specific antibodies are produced in immunized sheep and have high binding affinity for digoxin and, to a lesser extent, digitoxin and other cardiac glycosides. The Fab fragment binds free digoxin and once the digoxin-Fab complex is formed, the digoxin molecule is no longer pharmacologically active.  The complex is renally eliminated and has a half-life of 14-20 hours (may increase 10-fold with renal impairment).  Reversal of signs of digoxin/digitalis intoxication usually occurs within 30-60 minutes, with complete reversal varying up to 24 hours.

Contraindication: None known.  Caution is warranted in patients with known sensitivity ot ovine (sheep) products.  Product may contain traces of papain and caution advised in patients with allergies to papain, papaya extracts, chymopapain.

Adverse effects

1) Monitor for potential hypersensitivity reactions and serum sickness

2) In patients with renal insufficiency and impaired renal clearance of dig-Fab complex, a delayed rebound of free serum digoxin levels may occur

3) Removal of the effect of digoxin/digitalis may exacerbate preexisting heart failure

4) Removal of digoxin/digitalis effect may cause hypokalemia

Laboratory interaction: Digoxin-Fab complex cross-reacts with the antibody commonly utilized in quantitative immunoassay techniques.  This results in falsely high serum concentrations of digoxin due to measurement of the inactive Fab complex.  Therefore, measure free digoxin levels, which may be useful for patients with renal impairment.

Dosing: Each vial of Fab product binds 0.5 mg of digoxin.

Digoxin-specific Fab (round up vial calculation)

# of vials = Digoxin concentration (ng/mL) x Pt Wt (kg)

                                               100