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Transcript of Toxicology
By Douglas Stanglin, USA TODAY
CAPTIONBy Ashtabula Division of Fire/AP
One man died and six people were hurt, including two suspects, when a homemade methamphetamine lab exploded inside a nursing home in Ashtabula, Ohio, authorities say.
Update at 3:41 p.m. ET: WKYC-TV
reports that dead man has been i
dentified as Shaun Warrens, 31, of Ashtabula.
Police said he was neither a resident no
r employee of the Park Haven Nursing Home.
Two other suspects who
were burned are expected t
o be charged.
The Associated Press reports that police believe two visitors and one Park Haven resident knew about the meth lab, Police Chief Robert Stell told the Star Beacon of Ashtabula.
OP poisoning is a relatively common and major cause of death from poisoning in low-income countries. pesticide poisoning kills upwards of 300,000 patients a year. - It has been also used in chemical warfare.
SLUDGE BBB/ dumbbels
Quick Tox Update
COMMON & BRAND NAMES
Krokodil, Crocodile, Permonid
Opioid; Sedative; Stimulant
Desomorphine is an opioid that has gained attention because of low-quality black market synthesis in Russia, where it began being sold as "krokodil" in 2010. Synthesized from codeine (using iodine and red phosphorous, in a process similar to that used for street methamphetamine) the final street product is often contaminated with corrrosive, toxic chemicals. Heavy opioid users who inject street desomorphine can experience serious medical problems. News reports sometimes refer to desomorphine as "flesh eating" because of these problems.
“The surest poison is time.” —Ralph Waldo Emerson (1803-1882)
or Adam Berman or soon-to-be tox fellow
27 year old male called in as a notification for unresponsiveness. Mother found empty pill bottles by his side.
Essential Cases in Toxicology
You are working in a rural clinic in Burundi and family members carry in a 27 y/o male with no PMH. You examine the patient who is somnolent.
A drowsy 27 y/o M presents to the ED after taking a handfull of his grandmother's BP pills. On exam, you note a weak, thready radial pulse.
Consider Glucagon....(in refractory hypotension).. 2-5 mg IVP
Insulin (increases inotropy/chronotropy) 0.1 U /kg up to 1U/kg and Dextrose
-20-30 minutes before taking effect
Lipid Emuslion Therapy?
What antedote is most effective?
A- pralidoxime 1mg IV
B- atropine 2mg IV
C Diazepam 5 mg IV
D- Albuterol 0.5 mg neb
O2 98% on RA
The Case of the Sleeping Beauty
— Delirium/confusion/agitation, sedation, seizures, coma (often precedes cardiovascular signs)
— Restlessness, delirium, mydriasis (big pupil), dry, warm skin, tachycardia, ileus, urinary retention
— Sinus tachycardia, hypertension,
hypotension (due to alpha1-adrenoreceptor
blockade), broad complex tachycardia
(can develop bradycardia pre-arrest)
The ECG is one of the
most vital investigations
in this scenario
— Diagnostic features include prolongation of QRS, PR intervals, dominant R wave in aVR, and QT prolongation
— QRS widening reflects the degree of fast sodium channel blockade
Boehnert and Lovejoy (N Engl J Med): examined QRS duration and found that:
QRS <100ms no significant toxicity
QRS > 100ms is predictive of seizures,
QRS > 160ms is predictive of ventricular tachycardia
Niemann and Bessen study: RAD, QRS prolong., QTc prolong., and sinus tachy in setting of OD had a PPV of 66% and NPV of 100%
Liebelt (1995): large R wave (>3mm) in aVR had a PPV of 81%
If QRS >100ms:
sodium bicarbonate 100 mmol bolus every few minutes while monitoring the effect on ECG until HD stable (1-2mEq/kg)
the optimal total dose is “enough” (to reverse cardiotoxicity)
Once stable after resuscitation:
consider further sodium bicarbonate to maintain pH 7.5- 7.55/
QRS width (aim for <100 ms)
if there is ongoing arrhythmia, QRS >140 ms, or hypotension then options include:
sodium bicarbonate infusion(3 amps NaHCO3 in 1L D5W at 2x maintenance)
Consider hyperventiliation and/or hypertonic saline for pH 7.5-7.55
BREAK DOWN THE CASE
It is often prudent to consider a bolus of sodium bicarbonate prior to intubation to counter the effects of increased acidosis while ventilation is ceased.
Blackman K, Brown SG, Wilkes GJ. Emerg Med (Fremantle). Plasma alkalinization for tricyclic antidepressant toxicity: a systematic review. 2001 Jun;13(2):204-10. PMID: 11482860
Harvey M, Cave G. Intralipid outperforms sodium bicarbonate in a rabbit model of clomipramine toxicity. Ann Emerg Med. 2007 Feb;49(2):178-85, 185.e1-4. PMID: 17098328
Liebelt EL, et al. Serial electrocardiogram changes in acute tricyclic antidepressant overdoses. Crit Care Med. 1997 Oct;25(10):1721-6. PMID: 9377889
Liebelt EL, et al. ECG lead aVR versus QRS interval in predicting seizures and arrhythmias in acute tricyclic antidepressant toxicity. Ann Emerg Med. 1995 Aug;26(2):195-201. PMID: 7618783
McCabe JL, et al. Experimental tricyclic antidepressant toxicity: a randomized, controlled comparison of hypertonic saline solution, sodium bicarbonate, and hyperventilation. Ann Emerg Med. 1998 Sep;32(3 Pt 1):329-33. PMID: 9737495
Murray L, Daly FFS, Little M, and Cadogan M. Chapter 3.65 TCAs: Tricyclic Antidepressants; in Toxicology Handbook, Elsevier Australia, 2007. [Google Books Preview]
Murray L, Daly FFS, Little M, and Cadogan M. Chapter 4.24 Sodium bicarbonate; in Toxicology Handbook, Elsevier Australia, 2007. [Google Books Preview]
Eddleston et al Early management after self-poisoning with an organophosphorus or carbamate pesticide – a treatment protocol Critical Care 2004, 8:R391-R397 (DOI 10.1186/cc2953) Open Access
Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning.Lancet. 2007 Aug 14
Roberts DM, Aaron CK.Management of acute organophosphorus pesticide poisoning.BMJ. 2007 Mar 24;334(7594):629-34.
Eddleston M. Buckley NA. Eyer P. Dawson AH. Management of acute organophosphorus pesticide poisoning. Lancet. 2008;371(9612):597-607.
Eddleston M, Singh S, Buckley N. Acute organophosphorus poisoning. ClinEvid 2003;9:1542–1553.
Eddleston M, Szinicz L, Eyer P, Buckley N. Oximes in acute organophosphorus pesticide poisoning: a systematic review of clinical trials. QJM. 2002;95:275-283.
Leading cause of poisoning deaths (50d/1mill pres)
TCAs are weak bases and fx as NE, dopamine, serotonin reuptake inhibitors and GABA-A receptor blockers.
The CASE of the Sloppy Winemaker and the boy who thought he could
Vitals: HR 55, BP 107/62 , RR 12, O2 91%
On exam you note, pupils are equal/reactive, rales on auscultation, secretions at his mouth, and muscle faciculations.
The CASE of the SAD Resident:
BUN/Cr 23/12, Na is 140. K is 3.8, Cl is 104 and bicarb is 19.
The Brady Bunch
surface and room sprays
baits for cockroaches
shampoos against head lice
crop protection and livestock dipping
nerve agents (sarin)
DUMBBELS: diarrhoea, urination, miosis, bronchorhea, bradycardia, emesis, lacrimation, salivation
SLUDGE: salivation, lacrimation, urination, defaecation, emesis
and mechanical ventilation
hemodynamic monitoring and management
remove contaminated clothes
Standard Therapy in the US
And the Bolus Approach
-> recurrent boluses q5min, treats bradycardia, hypotension and excess secretion production
pralidoxime chloride 30mg/kg IV -> 8mg/kg/hr: muscle weakness
benzodiazepines: midazolam 0.2mg/kg, seizures or agitation
activated charcoal if presents with 1-2 hours
Respiratory Issues secondary to Acute Cholinergic:
• A cause of delayed Respiratory Failure
– Proximal muscle weakness and cranial nerve lesions
– Typically 1-4 days after cholinergic crisis has resolved
• Prolonged effects on Nicotinic receptors – Pre synaptic post synaptic failure
-confusion, lethargy, coma, central
Dimethoate or fenthion had higher proportion of death and morbidity requiring ET.
Dimethoate-poisoned patients died sooner than those ingesting other pesticides and often from hypotensive shock.
Fenthion poisoning initially caused few symptoms but many patients subsequently required intubation.
Acetylcholinesterase inhibited by fenthion or dimethoate responded poorly to pralidoxime treatment compared with chlorpyrifos-inhibited acetylcholinesterase.
Not all OPs are created equal
Eddleston M et al Differences between organophosphorus insecticides in human self-poisoning: a prospective cohort study. Lancet. 2005
Glasgow Coma Score & Mortality
Normal GCS 5%
GCS <14 30%
GCS <10 60%
OP Type & Mortality
N Chlorpyrifos 7%
N Fenthion 14%
N Dimethoate 21%
Load quickly until atropinsed
– Doubling protocol
– If you are needing more than 60 mgs consider other additional diagnosis and complications
Role of 2-PAM??
Vitals : HR of 44, BP 71/45, RR 22, pulse ox of 97%.
SA node: bradycardia
AV node: 1/2/3rd degree block
QRS and Qtc prolongation
Hypotension (decreased CO or vasodilation)
CNS: in severe OD, lethargy, coma, ischemia/seizures
Acute lung injury
Activated Charcol (if not aspiration risk)
Calcium: (first line)
1g of calcium chloride (1-2 amps)
1g of calcium gluconate (3-6 amps)
then start infusion
60-120 mg/kg/hr Ca gluconate
What to try next?
Anticholinergic (antimuscarinic effects)
Sodium Channel Blockage
Cardiotoxic effects primarily result from blockade of inactivated fast sodium channels in a use-dependent manner (blockade is higher at faster heart rates).
Alpha-1 adrenergic receptor blockade
-Activated Charcoal 1gm/kg
Benzos for seizures
Fat Emulsion Therapy (20% Intralipid of 1.5 mL/kg and infusion of .25 mL/kg/min for 30-60min
-Nerve Gas developed in 1938-1944 in Germany as a war-fare agent.
-Death may follow in 1 to 10 minutes after direct inhalation of a lethal dose. Sarin is 26 times more deadly than cyanide.
-1995: Aum Shinrikyo sect released an impure form of sarin in the Tokyo Metro. Thirteen people died.
-21 August 2013: Sarin was used
in an attack in the Ghouta region
of the Rif Dimashq Governorate
of Syria during the Syrian civil
war. Varying sources gave a
death toll of 322 to 1,729.
Killer Bs: Bradycardia/Bronchorrhea/Bronchocontriction
Mar 06, 2012
One dead after meth lab explodes at Ohio nursing home
Starring Steven Bunch, MD
The process of AGING
Indications for sodium bicarbonate in tricyclic antidepressant overdose:
hypotension resistant to fluid challenge
Consider for prevention of severe cardiotoxicity resulting from:
seizure – leads to metabolic acidosis
prolonged intubation attempts – leads to respiratory acidosis