UMEM Educational Pearls - By Hong Kim

Category: Toxicology

Title: Kratom: is it a safe herbal alternative to opioids?

Keywords: kratom, adverse effects, poison center data (PubMed Search)

Posted: 3/14/2019 by Hong Kim, MD, MPH
Click here to contact Hong Kim, MD, MPH

 

Kratom (Mitragyna speciosa) has been used for centuries in Southeast Asia to manage pain and opium withdrawal. It is increasingly being used in the U.S. for similar purpose. The U.S. DEA lists Kratom as a “drug of concern”.

Effects of Kratom leaves

  • 1 – 5 gm: mild stimulatory effects
  • 5 – 15 gm: opioid-like effects
  • >15 gm: sedative effects

A study reviewed National Poison Data System (2011 to 2017) to evaluate the clinical effects/outcomes of Kratom exposure.

Finding: (N=1807; single-substance: 1174; multiple-substance: 633])

  • 2/3 of all exposure occurred in 2016 – 2017 via oral route (83.0%)
  • 88.9% were adults (> 20 years old) 
  • 86.1% of the exposures occurred in private residence
  • Fatality: 11 (2 deaths occurred after an isolated exposure to Kratom)

Common symptoms

  • Agitation: 22.9%
  • Tachycardia: 21.4%
  • Drowsiness/lethargy: 14.3%
  • Nausea/vomiting: 13.2% - 14.6%
  • Confusion: 10.6%
  • Hypertension: 10.1%
  • Seizure (single/multiple): 9.6%
  • Respiratory depression: 3.6%

Disposition

  • Admitted to a health care facility: 31.8% (n=498)
    • Critical care unit: 14.0%
    • Non-critical care: 13.1%
    • Psychiatric facility: 4.7%

Bottom line:

  • Kratom use is associated with a wide spectrum of clinical signs/symptoms.
  • Death from isolated exposure to Kratom is rare. 

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Category: Toxicology

Title: Frequency of adverse effects after administration of physostigmine

Keywords: physostigmine, anticholinergic toxicity, adverse effects (PubMed Search)

Posted: 2/14/2019 by Hong Kim, MD, MPH
Click here to contact Hong Kim, MD, MPH

 

Physostigmine is a cholinergic agent that can be administered to reverse delirium associated with anticholinergic toxicity. However, it is infrequenly used since the reports of cardiac arrest in patients with TCA overdose.

A recently published study reviewed 161 articles – involving 2299 patients – to determine the adverse effects and their frequency after the administration of physostigmine. 

Findings

Adverse effects were observed in 415 patients (18.1%)

  • In patients with anticholinergic overdose: 7.7%
  • In patients with non-anticholinergic agent overdose: 20.6%

Specific adverse effects

  • Hypersalivation: 206 (9%) 
  • Nausea/vomiting: 96 (4.2%)
  • Seizure: 14 (0.61%)
  • Symptomatic bradycardia: 8 (0.35%) – including 3 with bradyasystolic arrest
  • Asymptomatic bradycardia: 4 (0.17%)
  • Ventricular fibrillation: 1 (0.04%) patient had a history of coronary artery disease
  • Cardiac arrest: 4 (0.17%)
  • Death: 5 (0.22%)

Of 394 TCA overdose, adverse effects occurred in 14 patients (3.6%)

Conclusion

  • Adverse effects from physostigmine occurs infrequently. 
  • However, inappropriate dosing or use of physostigmine can result in cholinergic toxicity.
  • For isolated anticholinergic toxicity (e.g. antihistamine overdose): physostigmine dosing: 0.5 mg (dilute in 5 – 10 mL normal saline) IV over 2 -5 minutes. May repeat every 5-10 minute to max dose total of 2 mg. (patient needs to be on cardiac monitor with atropine at bedside) 
  • Therapeutic goal: reversal of delirium
  • Avoid physostigmine in the presence of QRS widening (cardiac Na-channel blockade) and patients with history of underlying coronary artery disease.

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Therapeutic use or overdose of tramadol has been associated with seizure.  However, it is unknown if there are any specific predisposing factor that increases a patient’s risk of seizure after tramadol use/overdose.

In a recently published study, eighty patient data with single ingestion of tramadol were reviewed.

  • 52.5% of the patient developed seizure
  • 11% developed serotonin syndrome

 

Risk of seizure

  • Higher risk of seizure were found in Asian patients (OR=7.1, 95% CI: 1.9 – 27.3) and patients with abuse/misuse of tramadol (OR=3.2, 95% CI: 1.2-8.3)
  • Patients who presented with opioid toxidrome were less likely to develop seizure (OR=0.12, 95% CI: 0.02 – 0.71) 
  • Acute overdose and age were not associated with increased risk of seizure.

 

Conclusion

In this small study, Asian patients and patients with abuse/misuse were at higher risk of developing seizure compared to patients who overdose tramadol.

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Take home naloxone (THN) programs have been expanded to help reduce the opioid overdose-related deaths. A study was done in Australia to characterize a cohort of heroin overdose deaths to examine if there was an opportunity for a bystander to intervene at the time of fatal overdose.

235 heroin-overdose deaths were investigated during a 2 year study period in Victoria, Australia.

  • 79% (n=186) of fatality occurred at a private residence
  • 83% (n=192) of the decedents were alone at the time of the fatal overdose
  • In 34 cases, decedent was with someone else.
    • Half of these witnesses were also significantly impaired at the time of the fatal overdose.
  • The opportunity for intervention by a bystander was present in only 19 cases.

Conclusion

  1. There was no witness or bystander in majority of overdose deaths.
  2. THN alone may only lead to modest reduction in fatal heroin overdose.

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Taking a double-dose of a single medication is presumed to be safe in most cases. However, there is limited data to support this assumption.

 

A retrospective study of the California Poison Control System was performed to assess adverse effects of taking double dose of a single medication. During a 10-year period, 876 cases of double-dose ingestion of single medication were identified.

 

Adverse effects were rare (12 cases). However, medication classes that were involved in severe adverse effects included: 

  1. Propafenone: ventricular tachycardia and syncope
  2. Beta blockers (BB): bradycardia and hypotension
  3. Calcium channel blockers (CCB): bradycardia and hypotension
  4. Bupropion: seizure 
  5. Tramadol: ventricular tachycardia

Conclusion:

  • Adverse effect from double dosing is rare.
  • Cardiovascular collapse can occur with BB and CCB
  • Seizure can occur with tramadol and bupropion.

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Category: Toxicology

Title: Bupropion overdose in adolescents

Keywords: Bupropion, TCAs, adolescents (PubMed Search)

Posted: 12/20/2018 by Hong Kim, MD, MPH
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Selective serotonin reuptake inhibitors are the most common anti-depressant used today. However, the use bupropion in adolescents is increasing due the belief that it has fewer side effects than TCAs.

Using the National Poison Data System (2013 – 2016), the adverse effects of bupropion were compared to TCA in adolescents (13 – 19 years old) with a history of overdose (self harm). 

Common clinical effects were:

TCA:  n=1496; Bupropion: n=2257

Clinical effects

TCAs

Bupropion

Tachycardia

59.9%

70.7%

Drowsiness/lethargy

51.5%

18.1%

Conduction disturbance 

22.2%

15.6%

Agitation

19.1%

16.4%

Hallucination/delusions

4.2%

23.9%

Seizure

3.9%

30.7%

Vomiting

2.7%

20.0%

Tremor

3.7%

18.1%

Hypotension

2.7%

8.0%

Death

0.3%

0.3%

 

Conclusion:

Bupropion overdose results in significant adverse effects in overdose; however, death is relatively rare.

 

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Alcohol withdrawal syndrome is frequently treated with benzodiazepines following CIWA-Ar (Clinical Institute Withdrawal Assessment of Alcohol scale). There are other medications that are used as either second line or as adjunctive agents along with benzodiazepines. A retrospective study compared the clinical outcomes between phenobarbital vs. benzodiazepines-based CIWA-Ar protocol to treat AWS. 

The primary was ICU length of stay (LOS); secondary outcome were hospital LOS, intubation, and use of adjunctive pharmacotherapy.

Study sample: 60 received phenobarbital and 60 received lorazepam per CIWA-Ar.

Phenobarbital protocol:

  • Active DT: 260 mg IV x 1 dose -> 97.2 mg PO TID x 6 doses -> 64.8 mg PO TID x 6 doses -> 32.4 mg PO TID x 6 doses
  • History of DT: 97.2 mg PO TID x 6 doses -> 64.8 mg PO TID x 6 doses -> 32.4 mg PO TID x 6 doses
  • No history of DT: 64.8 mg PO TID x 6 dose -> 32.4 mg PO TID x 6 doses.

Results

 

Phenobarbital

CIWA-Ar

ICU LOS

2.4 days

4.4 days

Hospital LOS

4.3 days

6.9 days

Intubation

1 (2%)

14 (23%)

Adjunctive agent use

4 (7%)

17 (27%)

 

Conclusion

Phenobarbital therapy appears to be a promising alternative therapy for AWS. However, additional studies are needed prior to adapting phenobarbital as first line agent for AWS management. 

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The management of pediatric hydrocarbon ingestion has not changed significantly over the past several decades. One of the earlier study that helped established the management approach is by Anas N et al. published in JAMA, 1981.


It was a retrospective study of 950 children who ingested household hydrocarbon containing products.

Discharged patients: n=800

  • They asymptomatic at their initial presentation and after 6-8 hours of observation.
  • All had normal CXR

 

Admitted patients: n=150

  • 79 symptomatic patients at the time of initial evaluation with abnormal CXR.
  • 71 patients were asymptomatic but CXR showed pulmonary involvement/pneumonitis or had pulmonary symptoms prior to hospital presentation
  • 7 symptomatic patients developed pneumonia

 

This study recommended that hospitalization is required in patients…

  1. Who are symptomatic at the time of initial evaluation
  2. Who become symptomatic during the 6-8 hour observation period.

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Category: Toxicology

Title: Anaphylatoid reaction to IV N-acetylcysteine

Keywords: anaphylactoid reaction, IV NAC (PubMed Search)

Posted: 9/13/2018 by Hong Kim, MD, MPH (Emailed: 9/14/2018)
Click here to contact Hong Kim, MD, MPH

Analphylatoid reaction is caused by non-IgE mediated histamine released. Intravenous N-acetylcysteine (NAC) infusion is well known to cause analphylatoid reaction. However, it’s incidence is unknown.

Recently, a large retrospective study of all patients who received 21-hour IV NAC in 34 Canadian hospitals (1980 to 2005) was performed. 

Anaphylactoid reaction was documented in 528 (8.2%) of 6455 treatment courses

  • Cutaneous reaction (urticarial, pruritus and angioedema) occurred in 398 (75.4%)
  • Systemic reaction (respiratory symptoms or hypotension): 34 (6.4%)
  • Both reactions: 96 (18.2%)

Over 90% patients developed analphylatoid reaction within 5 hours.

Onset of reaction: 

  • 1stNAC dosing (150 mg/kg over 1 hour): 133/528
  • 2ndNAC dosing (50 mg/kg over 4 hours): 371/528
  • 3rdNAC dosing (100 mg/kg over 16 hours): 24/528

Administered medication for treatment

  • Antihistamine: 371
  • Beta-2 agonist: 15
  • Epinephrine: 10
  • Corticosteroids: 7

Patient characteristics that were associated with higher incidence of Anaphylactoid reaction includes

  • Female
  • Single acute ingestion
  • Low serum acetaminophen level.

 

Bottom line

  1. Anaphylactoid reaction to NAC is uncommon
  2. Cutaneous symptoms are most common
  3. Female, single acute ingestion and low serum acetaminophen levels are associated with incidence of anaphylactoid reaction. 

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Various intial doses of naloxone (0.4 to 2 mg) are administered to reverse the signs and symptoms of opioid toxicity. However, there is limited data regarding the duration of action of naloxone is correlated to the administered dose.

A recently published retrospective study investigated whether initial naloxone doses (IV), low-dose (0.4 mg) vs. high-dose (1-2 mg), lead to different time to recurrence of opioid toxicity.

 

Study sample: 274 patient screened but 84 patients were included.

  1. Low-dose naloxone (0.4 mg IV): 42
    • Mean age: 50
    • History of opiod/heroin use: 33 (78.6%)
    • Positive opioid/opiate on drug screening: 27 (64%)
    • Median time to repeat naloxone dose: 72 min (IQR: 46 - 139)
    • 12 patients (29%) required continuous naloxone infusion

 

  1. High-dose naloxone (1 - 2 mg IV): 42
  • Mean age: 48
  • History of opiod/heron use: 32 (76.2%)
  • Positive opioid/opiate on drug screening: 26 (62%)
  • Median time to repeat naloxone dose: 77 min (IQR: 44 - 126)
  • 17 patients (41%) required continuous naloxone infusion

Higher rate of adverse effects (withdrawal symptoms - vomiting, agitation, tachycardia, etc.) were observed in high-dose group (41% vs. 31%) but this was not statistically signficant. 

Conclusion:

  1. High-dose naloxone (1 - 2 mg) does not result in longer duration of reversal of opioid toxicity.
  2. Duration of opioid toxicity reversal by naloxone administration were similar to previously reported duration of action of naloxone (30 to 90 min).
  3. Note: there are several lmitations to the study study including retrospective design - documentation issues, small sample size, patient selection - patients were included if positive response to naloxone was observed, unknown opioid exposure, variable dosing in high-dose group (1 to 2 mg vs. 0.4 mg) and naloxone was given via IV only.   

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Category: Toxicology

Title: Can transaminase and CK ratio help differentiate rhabdomyolysis vs. delayed acetaminophen overdose?

Keywords: transaminitis, delayed acetaminophen toxicity, rhabdomyolysis (PubMed Search)

Posted: 7/26/2018 by Hong Kim, MD, MPH (Updated: 10/18/2021)
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Elevated transaminases are found in both rhabdomyolysis and delayed acetaminophen (APAP) toxicity. Establishing the cause of elevated transaminase can be difficult when there is unclear history of acetaminophen ingestion.

A retrospective study of patients with delayed acetaminophen toxicity or rhabdomyolysis from 2006 to 2011 was recently published.

The authors compared AST/ALT, CK/AST and CK/ALT ratio of 

  • 160 in the rhabdomyolysis group
  • 68 in the acetaminophen overdose (all)
  • 29 in the delayed acetaminophen overdose group

Results

AST/ALT ratio

  • Rhabdomyolysis group: 1.66
  • APAP overdose (all): 1.38
  • Delayed APAP overdose: 1.3

CK/AST ratio

  • Rhabdomyolysis group: 21.3
  • APAP overdose (all): 5.49
  • Delayed APAP overdose: 3.8

CK/ALT ratio

  • Rhabdomyolysis group: 37.1
  • APAP overdose (all): 5.77
  • Delayed APAP overdose: 5.03

Conclusion

  • Significantly higher ratio of AST/ALT, CK/AST and CK/ALT were found in rhabdomyolysis patients than delayed APAP overdose patients.
  • These finding are based on small study population and need further validation/research before clinical application.

Category: Toxicology

Title: Utility of physostigmine in antimuscarinic delirium

Keywords: antimuscarinic/anticholinergic toxicity, reversal of delirium (PubMed Search)

Posted: 7/12/2018 by Hong Kim, MD, MPH
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From 1960s to 1970s, physostigmine was routinely administered as part of the "coma cocktail." Since the publication of two cases by Pentel (1980) that resulted in asystole after administration of physostigmine in TCA poisoned patient, its use has declined significantly.

However, physostigmine still possess limited but clinically useful role in the management of patients with antimuscarinic/anticholinergic induced delirium.

Recently, a prospective observational study was performed in the use of physostigmine when recommended by a regional poison center.

In 1 year study period, physostigmine was recommended by a regional poison center in 125 of 154 patients with suspected antimuscarinic/anticholinergic toxicity. 

common exposures were

  1. antihistamines (68%)
  2. analgesics (19%)
  3. antipsychotics (19%)

57 of 125 patients received physostigmine per treating team.

  • median dose of physostigmine administered: 2 mg

Of the remaining patients,

  • 35 patients did not receive any sedative agents
  • 55 received benzodiazepines (56%)
  • others received propofol (n=10), haloperidol (n=8), olanzapine (n=4), dexmedetomidine (n=3), etc.

Delirium control

  • Physostigmine group 79% (45 of 57)
  • No-physostigmine group: 36% (35 of 97)

Adverse events (physostigmine group vs. non-physo group) - no statistically significant difference.

  • Intubation (n=7): 2 (3.5%) vs. 5 (5.2%)
  • physical restraints (n=10): 3 (5.3%) vs. 7 (7.2%)
  • vomiting (n=4): 3 (5.3%) vs. 1 (1.0%)

Conclusion:

Physostigmine can safely control antimuscarinic/anticholinergic-induced delirium.

 

 

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Category: Toxicology

Title: Midazolam for agitated patients

Keywords: acute agitation, midazolam, antipsychotics, (PubMed Search)

Posted: 6/14/2018 by Hong Kim, MD, MPH (Updated: 10/18/2021)
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Acutely agitated patients in the emegency room receive single or combination of benzodiazepine (lorazepam vs. midazolam) and antipsychotic (e.g. haloperidol) agents. Recently, use of ketamine has also been advocated to sedate agitated patients.

 

A recently published article compared IM administration several medications to treat acutely agitated patients in the ED. According to established protocol, each medication was administered in predetermined 3 week blocks:

  1. Haloperidol (5 mg)
  2. Ziprasidone (20 mg)
  3. Olanzapine (10 mg)
  4. Midazolam (5 mg)
  5. Haloperidol (10 mg)

Results

N=737 with median age of 40 years, 72% men.

Midazolam resulted in greater proportion of patients with "adequate" sedation (altered mentatl status scale <1) compared to antipsychotics at 15 min post administration. Among antipsychotics, olanzapine resulted in greater proportion of patient with sedation. 

  • Midazolam (71%)
  • Haloperidol - 5 mg (40%)
  • Haloperidol - 10 mg (42%)
  • Olanzapine (61%)
  • ziprasidone (52%)

Adverse effect were limited

  • extrapyramidal AE: 0.3%
  • hypotension 0.5%
  • hypoxemia 1%
  • intubation 0.5%

Conclusion:

Midazolam 5 mg IM achieve more effective sedation at 15 min in agitated ED patients than antipsychotics.

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Category: Toxicology

Title: Here comes the adexanet alfa!

Keywords: Factor Xa inhibitor, reversal agent, adexanet alfa, andexxa (PubMed Search)

Posted: 5/4/2018 by Hong Kim, MD, MPH (Emailed: 5/11/2018) (Updated: 5/11/2018)
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On May 3, the FDA approved adexanet alfa, the reversal agent for factor Xa inhibitors - apixaban and rivaroxaban. It received both U.S. Orphan Drug and FDA Breakthrough Therapy designations. 

Unlike indarucizumab (a monoclonal antibody fragment) to reverse dabigatran (direct thrombin inhibitor) associated bleeding, adexanet alfa is a recombinant modified human factor Xa decoy protein. 

A phase 3 study showed that adexanet alfa decreased the anti-factor Xa activity of rivaroxaban by 92% from baseline and by 94% in apixaban treated participants.

ANNEXA-4 study involving participants with acute major bleeding (GI and intracranial) showed a significant decrease in the anti-factor Xa activity after the bolus dose of adexanet alfa and "effective" hemostasis was noted in 79% of the participants at 12 hours post infusion.

Andexanet alfa is expected to become available in June 2018.

 


Non-pharmaceutical fentanyl (NPF) is a major contributor to opioid overdoses and overdose fatality. In certain urban areas such as Vancouver, over 80% of heroin samples contain NPF.  For isolated heroin overdose ED patients, they can be safely discharged after brief observation period (~2 hours). However,  “safe” observation time for fentanyl is unknown.

Recently, a retrospective study evaluating the safe observation period in 1009 suspected (uncomplicated) fentanyl overdose ED visits (827 unique patients).

Results:

 In the field:

  • 476 (47.1%) received bystander naloxone
    • 422 (44.1%) had field GCS of 15
    • 547 (57.2%) had pulse oximetry of >= 95%.
  •  EMS administered naloxone to 546 (57.1%) patients (mean dose 0.4 mg IV)

In the ED:

  • 16 patients received additional naloxone in the ED
  • Mean length of stay: 173 minutes (IQR: 101 to 267 minutes)
  • 90% of the patients were discharged within 380 minute.
  • One patient was admitted and one patient died after discharge within 24 hours.

Conclusion:

  • Majority of the patients were safely discharged after 3 - 4 hours after receiving naloxone and if able to maintain GCS 15 with oxygen level 95% while able to ambulate normally.
  • However, some patient may require up to 6 hours of observation.  

Show References


Category: Toxicology

Title: Sometimes more is better: naloxone and clonidine toxicity.

Keywords: clonidine toxicity, high-dose naloxone (PubMed Search)

Posted: 3/18/2018 by Hong Kim, MD, MPH (Emailed: 4/12/2018) (Updated: 10/18/2021)
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Clonidine, (central alpha-2 receptor agonist) can produce opioid-like toxidrome in addition to its cardiac effects (bradycardia and hypotension). Previous studies have shown that naloxone has variable (~40%) success in reversing CNS/respiratory depression and cardiac effect.

A recent retrospective study (n=51) of pediatric poisoning showed that administration of 5 to 10 mg had improved reversal of clonidine toxicity.

Total of 51 somnolent patients: 5- 10 mg of naloxone reversed 40 patients

  • 22 patients awoke with 6 mg or less
  • Bradycardia reversed in 17 of 44 patients
  • Hypotension reversed in 7 of 11 patients

There was no adverse effect from naloxone administration.

Repeat administration of naloxone was required in some patients.

Bottom line

  • For pediatric clonidine toxicity, consider initial naloxone dose of 5 mg IV. 

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Category: Toxicology

Title: Why is the synthetic cannabinoid use making my patient bleed? - submitted by James Leonard

Keywords: adulterated synthetic cannabinoid, elevated INR, brodifacoum (PubMed Search)

Posted: 4/4/2018 by Hong Kim, MD, MPH
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Takeaways

In the past couple of weeks, there have been reports from Illinois about patients using adulterated synthetic cannabinoids, resulting in elevated INR and bleeding. To date, there are approximately 70 cases including 3 fatalities. Brodifacoum, a long-acting vitamin K mediated anticoagulant (similar to warfarin) has been identified in 10 cases. Brodifacoum is frequently used as rodenticide.

This week, Maryland Poison Center received our first notification of a patient with bleeding and elevated INR due to suspected adulterated synthetic cannabinoid use.

When evaluating our patient population:

  • Ask about synthetic cannabinoid use in patients with unexplained bleeding and elevated INR
  • Carefully examine patients with synthetic cannabinoid intoxication for any signs of bleeding, bruising or petechiae.  
     

Patient management of suspected cases:

  • ACTIVELY bleeding:
    • Fresh frozen plasma
    • Activated prothrombin complex concentrate (KCentra®) in life threatening bleeding.
    • Vitamin K 10 mg IV
    • *** Start oral vitamin K at 50 mg TID and titrate to goal INR < 2 ***
  • NOT bleeding and INR < 10: vitamin K 50 mg PO BID with titration if needed.
  • NOT bleeding and INR > 10: vitamin K 50 mg PO TID with titration if needed.

Patient can be discharged when INR < 2 is achieved with oral vitamine K regimen only (without recent FFP infusion).

Review of published cases highlights that most patients are started on a median doses of 100 mg/day (range: 15 - 600 mg) and stabilize on a PO regimen of 50-100 mg/day. Prolonged PO vitamin K course of 2 – 3 months or longer should be anticipated.

Pease call the Maryland Poison Center at 1-800-222-1222 as we are working with the Maryland Department of Health and CDC to track these cases. 

 

 

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Category: Toxicology

Title: The Russian connection 2.0 -- Sergei Skripal

Keywords: nerve agents, organophosphate compounds (PubMed Search)

Posted: 3/18/2018 by Hong Kim, MD, MPH (Emailed: 3/21/2018) (Updated: 3/21/2018)
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Recently, an ex-Russian spy and his daughter were poisoned in Salisbury, England using a Soviet nerve agent called Novichok. He joins a list of defectors and ex-spies who's poisoning have been connected to Russia.

Nerve agents are organophosphate compounds, similar to the commercially available pesticides, but significantly more potent. Nerve agents such as VX take seconds to minutes to irreversibly inhibit acetylcholinesterase by “aging” and result in clinical toxicity. 

Signs and symptoms

  • Muscarinic: DUMBELS or SLUDGE and Killer B's
  • Nicotinic: muscle weakness & paralysis

Treatment

  • Decontamination
  • Atropine – 2 mg IV and double the dose every 3 – 5 minutes until clearing of bronchorrhea, bronchospasm and bradycardia
  • Pralidoxime – reverses inhibition of acetylcholinesterases that are not aged

Signs and symptoms of acute cyanide poisoning are not well characterized due to its rare occurrence.  Commonly mentioned characteristics of bitter almond odor and cherry red skin have poor clinical utility.

Recently published review of 65 articles (102 patients) showed that most patients experienced following signs and symptoms:

  1. Unresponsive: 78%
  2. Respiratory failure: 73%
  3. Hypotension: 54%
  4. Cardiac arrest: 20%
  5. Seizure: 20%
  6. Cyanosis: 15%
  7. Odor: 15%
  8. Cherry red skin: 11%

There is no clear toxidrome for cyanide poisoning.

In a poisoned patient, health care providers should consider cyanide in their differential diagnosis in the presence of severe metabolic and lactic acidosis (lactic acid > 8 in isolated cyanide poisoning or > 10 in smoke/fire victim).

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Category: Toxicology

Title: Toxin-induced nystagmus

Keywords: nystagmus, toxic (PubMed Search)

Posted: 2/22/2018 by Hong Kim, MD, MPH
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Abnormal ocular movement (e.g. nystagmus) can often be observed in select CNS pathology.

Certain drugs/toxin overdose can also induce nystagmus.

  • Anti-epileptics: carbamazepine, lamotrigine, topiramate, phenytoin
  • Ethanol
  • Ketamine, phencyclidine (PCP), dextromethorphan – vertical or rotary nystagmus
  • Serotonergic syndrome/5-HT agonists – opsoclonus
  • Monoamine oxidase inhibitors – ping-pong nystagmus
  • Lithium
  • Scorpion envenomation 

In an "unknown" intoxication, physical exam findings such as nystagmus may help narrow the identity of the suspected ingestion/overdose.