Cocaine overdose

Cocaine Overdose


Pathophysiology - Sympathomimetic toxidrome associated with following signs and symptoms:  

 

CNS: Cerebral ischemia/infarct, intraparenchymal or subarachnoid hemorrhage, cerebral artery vasospasm, cerebral vasculitis, cerebral atrophy, and cerebral vascular thrombosis.

 

Cardiac: Myocardial ischemia/infarct, cardiac arrhythmias, dilated cardiomyopathy, infective endocarditis (IVDA), aortic rupture/dissection, acceleration of coronary atherosclerosis.

Pulmonary: Nasal septal perforation, oropharyngeal ulceration, inhalational injuries (smoking crack cocaine), pneumomediastinum, pneumothorax, pulmonary infarct, hypersensitivity pneumonitis.

GI: Gastroduodenal ulceration/perforation, intestinal infarct/perforation, colitis.

Renal: ARF secondary to rhabdomyolysis, renal infarct.



OB: Placental abruption, low birth weight, microcephaly.


Psych: Paranoia, delirium, suicidal ideation


Initial approach and management:

Start with ABCs:

Airway and breathing — O2 as needed. 

If RSI intubation is needed  avoid succinylcholine - plasma cholinesterase (PChE) metabolizes both succinylcholine and cocaine, and coadministration of succinylcholine can prolong the effects of cocaine and the paralysis from succinylcholine 

In the setting of rhabdomyolysis and hyperthermia, succinylcholine may worsen hyperkalemia and cause life-threatening arrhythmias

Use rocuronium as paralytic and  benzodiazepines, etomidate, or propofol for induction

 

Cardiovascular complications result in 

Central cardiovascular stimulation responds well to benzodiazepines

Refractory or symptomatic cocaine-induced hypertension can use phentolamine (bolus of 5 to 10 mg intravenously (IV) every 5 to 15 min PRN) 

Alternatives nitroglycerin or nitroprusside

Avoid beta-blockers (unopposed α-adrenergic activity) 

Avoid calcium channel blockers (may potentiate seizures and death)

 

Massive cocaine toxicity may result in hypotension due to sodium-channel blockade, cardiac dysrhythmias, or cardiac ischemia

treat with 2 to 3 L of rapidly infused isotonic saline

if no improvement use direct-acting vasopressors such as norepinephrine or phenylephrine 

Obtain EKG to evaluate QRS for widening, if present use hypertonic sodium bicarbonate at a dose of 1 to 2 mEq/kg 

 

Psychomotor agitation can be treated with benzodiazepines like diazepam be given in an initial dose of 10 mg IV, then 5 to 10 mg IV every 3 to 5 minutes 

 

Hyperthermia -  cool rapidly, optimally in 30 minutes or less, to a goal core body temperature of <102°F. 

 

Gastrointestinal decontamination should be considered especially in cases of body packing but remember that the popular methods of cocaine use are nonenteral 

Activated charcoal reduces the lethality of oral cocaine - adminitter at 1 g per kg body weight (up to 50 g) Q4h. 

Cocaine abuse + abdominal pain => concern for aortic pathology or intestinal ischemia/infarct or colitis

 

Specific syndromes:

 

Chest pain — it causes vasoconstriction and enhances thrombus formation, increasing the risk of myocardial ischemia even in a very young patients. 

EKG changes and positive trops consider ASA +/- nitroglycerin, phentolamine (( IV bolus of 1 to 2.5 mg every 5 to 15 minutes PRN) to reverse cocaine-induced vasospasm, cardiology consult for cath

 

Crack lung — Crack lung is a syndrome of hemorrhagic alveolitis from inhalational cocaine use 

Ensure oxygenation, ventilation, and symptomatic care

Early intubation

 

Disposition:

Severe complications of cocaine abuse - admission

If acute findings from cocaine toxicity resolve - obs 6 to 8 hours and d/c if pt back to baseline. 

 

Pts with cocaine-associated chest pain (CACP) are observed for 8 to 12 hours while two sets of cardiac biomarkers and repeat electrocardiograms (ECGs) are obtained. 

 

Pts with psychomotor agitation, hyperthermia, or other neurological complications consider admission unless pt is back to baseline and symptom free after  6 to 8 hours of observation.

Pearls:

The differential diagnosis of cocaine toxicity should include: methamphetamine abuse, ecstasy abuse, cathinone abuse, and LSD abuse

Smoking and IV injection offer rapid cocaine absorption (< 30 sec), as opposed to snorting (2.5 min) and ingestion (PO 2-5 mins).


Cocaine-induced MIs have been reported as late as 15 hours following substance abuse


References: Uptodate, EMDocs


What kind of mood elevator are you on?

SATS.jpg

Lithium toxicity

 

Background:

Uses: Lithium often prescribed for Bipolar disorder

Has a narrow therapeutic index: therapeutic dose close to a toxic dose

Mechanism of action is still incompletely understood. Lithium increases serotonin release and receptor sensitivity as well as inhibiting release of dopamine and norepinephrine. 

Elimination: Lithium is excreted exclusively by the kidneys. Any insult to kidneys can lead to impaired elimination 

 

Causes:

For acute overdose mainly intentional overdose

For chronic Li+ toxicity with present body stores any changes changes in absorption or elimination lead to lithium levels above the narrow therapeutic window like:

  • volume depletion

  • salt restriction

  • advanced age with resultant decrease in GFR, 

  • thiazide diuretics, NSAIDs, ACE inhibitors

  • heart failure

 

 

Workup at the ED:

  • Basic labs: CBC, BMP

  • Lithium level

  • Urinalysis

  • thyroid function panel 

  • Co-ingestants: acetaminophen, salicylates if intentional overdose is suspected 

 

Acute Lithium Toxicity presentation:

  • GI symptoms such as nausea, vomiting, and diarrhea, at times with significant volume loss. 

  • Dry mouth 

  • Lack of coordination

  • systemic and neurologic findings manifest late in acute lithium toxicity because  it takes time for lithium to distribute into tissues and the CNS

 

Chronic Lithium Toxicity presentation:

  • Potent neurotoxin,altered mental status, seizures, tremor, hyper-reflexia, clonus, fasciculations, and extra-pyramidal symptoms which can persist for month regardless of serum concentration 

  • serotonin syndrome, as well as neuroleptic malignant syndrome. 

  • nephrogenic diabetes insipidus (creates resistance to vasopressin)

  • abnormal ECG findings, including QT prolongation, T-wave inversions across the precordial leads, sinoatrial dysfunction, bradycardia, complete heart block, or unmasking of a Brugada pattern. 

  • Hypothyroidism 

  • hyperthyroidism and thyrotoxicosis

  • hyperparathyroidism and hypercalcemia

 

Treatment and Disposicion:

  • Supportive care and fluids at the ED

  • Consult Poison control center 

  • Renal service, for hemodialysis in severe intoxications

  • Psychiatric service, for patients with intentional overdose

  • Pt will most likely require admission for monitoring of electrolytes and renal function, hydration, medication adjustment

 

References:

https://www.acep.org/how-we-serve/sections/toxicology/news/august-2016/acute-and-chronic-lithium-toxicity/

Uptodate


POTD: Lithium Toxicity (Toxicology Thursday)

Lithium has been used to treat patients with bipolar disorder since the 1870s and is still widely used today, but has a very narrow therapeutic index! Toxicity can due to acute deliberate ingestions (18%) or, more commonly, chronic ingestions.

There are three categories of toxicity:

Acute: due to ingestion in a lithium naive patient, generally, an ingestion of > 7.5mg/kg of elemental lithium or 40 mg/kg of lithium carbonate. Prognosis tends to be better in acute poisoning because there is not sufficient time for distribution, which decreases the risk of neurotoxicity.

Acute-on-Chronic: an acute ingestion in a patient chronically on lithium

Chronic poisoning: occurs when chronic ingestion exceeds elimination. Highest risk of neurotoxicity because there is sufficient time to accumulate. Also the half life of lithium in chronic toxicity is prolonged due to underlying renal impairment.

Etiology 

Toxicity from chronic ingestions occur from impaired excretion due to:

  • Reduced GFR (NSAIDs, ACE inhibitors)

  • Increased renal tubular reabsorption (thiazides, spironolactone)

  • Calcium channel blockers (unknown mechanism)

 Renal processing is similar to that of sodium – meaning if the kidneys find any reason to retain sodium, it will also retain lithium! A major example is dehydration.

Serum lithium levels may be high, but the patient may be asymptomatic because effects only occur when moved intracellularly.

 

Manifestations:

Neurological:

  • Coarse tremor

  • Hyperreflexia

  • Nystagmus

  • Ataxia

  • Altered mental status

  • Seizures/non-convulsive status epilepticus

Renal:

  • Nephrogenic diabetes insipidus

  • Sodium losing nephritis

  • Nephrotic syndrome

Cardiovascular (usually mild)

  • Wandering atrial pacemaker

  • Sinus bradycardia

  • ST-segment elevation

  • Prolonged QT syndrome

  • T-wave flattening

Gastrointestinal

  • Nausea/vomiting

  • Diarrhea

  • Ileus

**this can worsen toxicity due to increased renal reabsorption of sodium and lithium

Endocrine

  • Hypothyroidism (inhibition of hormone synthesis)

    • Also worsens lithium toxicity

Evaluation:

Labs including TFTs, renal function, calcium, serum lithium level, EKG, cardiac monitoring. Make sure the tube was not treated with lithiated heparin. Remember, the serum level does not reflect the intracellular level, so a patient may be asymptomatic with high levels and normal levels do not exclude toxicity!!

However, generally:

  • Mild intoxication (1.5-2.5 mEq/L): nausea/vomiting, lethargy, tremor

  • Moderate intoxication (2.5-3.5 mEq/L): confusion, agitation, delirium, tachycardia, hypertonia

  • Severe intoxication (> 3.5 mEq/L): coma, seizures, hyperthermia, hypotension 

Treatment

Symptomatic treatment (e.g. benzos for seizures, magnesium for torsades).

IVF – the goal is to preserve GFR so that lithium does not get reabsorbed!

Activated charcoal does not work, but you may consider gastric lavage or whole-bowel irrigation for acute ingestions.

Hemodialysis for severe toxicity or renal failure

Patient should be admitted to a monitored setting. Admit to ICU for severe symptoms!! If patients are asymptomatic with a lithium level < 1.5 mEq/L, they may be discharged.

References:
https://emcrit.org/wp-content/uploads/2016/09/Lithium-Toxicity.pdf
https://www.ncbi.nlm.nih.gov/books/NBK499992/
https://www.uptodate.com/contents/lithium-poisoning


POTD: Alcoholic Ketoacidosis

Today’s topic will be for the people who used this 3-day weekend for a bender:

Alcohol Ketoacidosis (AKA)

Clinical Scenario:

Someone who has been on a bender and shows up to your ED after two days of vomiting, has a low bicarb, elevated anion gap, elevated lactate, urine ketones, and an elevated BHB level...probably has AKA. 

Background

  • Alcoholic ketoacidosis (AKA) is a starvation state in an alcoholic or binge drinker

  • Alcohol + No Food + Dehydration = AKA

  • Most often associated with acute cessation of alcohol consumption after chronic alcohol abuse

  • Can also be associated with first-time alcohol binge

  • one of the causes of anion-gap metabolic acidosis 

Clinical Features

  • episode of heavy drinking followed by vomiting and an acute decrease in alcohol consumption

  • N/V, nonspecific abdominal pain

  • can have associated gastritis or pancreatitis

  • normal mental status, but if patient is altered, look for toxic alcohol ingestion, postictal states from withdrawal seizures, or occult head injury

  • exam with acetone odor on breath

  • tachypnea (Kussmaul respiration), tachycardia, and signs of dehydration

Pathophysiology

ethanol metabolism.png

Nicotinamide adenine dinucleotide (NAD, or “Needs Additional Dextrose”) is depleted by ethanol metabolism, leading to inhibition of the Kreb’s cycle (or aerobic metabolism) in favor of ketone formation, depletion of glycogen stores, and suppression of insulin secretion  

Diagnosis

  • low, normal, or slightly elevated glucose

  • binge-drinking that ends in N/V and decreased intake

  • wide AG metabolic acidosis, especially one without an alternative diagnosis

  • (+) serum ketones

  • can have associated hypophosphatemia, hyponatremia, and hypokalemia

Treatment

  • Sugar and water!

  • Glucose stimulates insulin production, which stops lipolysis and halts further ketone formation. Glucose also increases oxidation of NADH to NAD, thereby further stopping ketone production. 

  • Start with 5% dextrose in NS. Once fluid and electrolyte losses are replaced, change fluids to 5% dextrose in 1/2 NS until oral intake is assured.

  • Give 100 mg thiamine (facilitates Krebs cycle)

  • Correct electrolytes

  • Repeat Chem7 to see if bicarb improving. If it’s not, consider ethylene glycol or methanol poisoning. This is the time for fomepizole and a call to your local toxicologist or poison center!

Disposition

Discharge if tolerating PO!

References

https://emcrit.org/toxhound/aka-aka/

https://lifeinthefastlane.com/ccc/alcoholic-ketoacidosis/

Tintanelli’s

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Cyanide Toxicity Distilled

Public service announcement: Don’t drink the Koolaid® (google Jonestown mass suicide)  Cyanide Toxicity

After a lecture today with our fantastic Maimo paramedics today, Dr. Lobel had insightful and nuanced feedback regarding treatment of cyanide toxicity and the current REMAC protocol.

Exposure: 

Typically, it is due to combustion of nitrogen containing polymers (think couches and kevlar)

Metallurgists, jewelers, and those working with electrolysis may have vats of liquid cyanide laying around; so, be wary. 

IV nitroprusside can also cause cyanide toxicity, even when administered in therapeutic doses. 

Also, apparently the hydrolysis of Amygdalin, which is present in cassava beans, peach pits, and apples seeds produces cyanide. So, depending on the quantity ingested, toxicity may become apparent. For the purposes of this POD, we will not go into the details of chronic CN toxicity. 

Mechanism: 

Cyanide inhibits: superoxide dismutase, carbonic anydrase, CYTOCHROME OXIDASE, succinic acid dehydrogenase.

Obviously, this causes inhibition of cellular metabolism, specifically the-critical-to-cellullar-survival Mitochondrion. 

Syptoms: 

Unfortunately they are non-specific, and overlap with CO toxicity. 

They can include:

Headache, anxiety, ams, lethargy

Cardiovascular collapse

Progressing to the seizure, coma, death pathway

Any unexplained lactic acidosis > 8 mmol/dL, CN toxicity should be considered. 

Treatment: 

As per Goldfrank’s Emergency Toxicology, 74% of confirmed cyanide cases did not receive an appropriate antidote. 

Past treatments included amyl nitrites (aka the “popper”), but this induces methemoglobinemia; therefore this should be avoided at all costs in a patient whose presumed exposure to cyanide gas could also be a concomitant carbon monoxide exposure. 

Hydroxycobalamin is probably the best go to if you only have one antidote available because when administered IV, it directly binds CN with high avidity. Therefore, when CN concentration in the plasma decreases, the CN inside the cells equilibrates down the gradient and shifts CN out of the cells, restoring the mitochondrial electron transport chain. 

This is where LOBEL’S ADVICE was really helpful:

Sodium thiosulfate is a useful adjunct because it recycles Cyano-met-Hgb to met-Hgb. It does not create more met-Hgb like the amyl-nitrites do. So, sodium thiosulfate can be safely administered along with cyanokit to create an additive effect. 

Of note, there are numerous case reports of patients being pulled from fires in cardiac arrest who achieve ROSC only after cyanokit has been administered. 

With that being said, I have a attached a case report from 1970 he gave me. It is a fantastic read and quite hilarious regarding the description of the patient’s tragic tattoos, so definitely give it 2 minutes. 

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Local Anesthetic Toxicity

LOCAL ANESTHETIC TOXICITY, as available in our ED (4% cocaine and street cocaine will be addressed in a different post; tetracaine omitted). There are definitely more “caines”, but I want to address the “caines” that we use on a daily basis.

Toxic doses by drug (there are other “caines”, but these are most commonly used in our ED):

Lidocaine 1%: 4.5 mg/kg, max off-the-cuff dose is 300 mg. 1 vial is 50 mL and 500 mg, so try not to give a full vial, please.

Lidocaine 1% w/ epi: 7 mg/kg. Max dose is 500 mg or 50 mL.

Lidocaine 2% Viscous: special note that in children, as little as 5 mL can cause seizure

#paindosing Lidocaine IV dosing is 1.5 mg/kg, with a max of 200 mg, please note this is significantly below toxic dosing for local infiltration. The literature suggests 800 mg is the lower end of IV toxic dosing in adults.

Benzocaine 20% (aka hurricane spray), indicated doses are two 1 second sprays into the oropharynx (methemoglobinemia has been induced with these indicated doseages).

Bupivacaine 0.25%: 2 mg/kg, max total dose is 175 mg, or 70 mL.

Bupivacaine 0.25% w/ epi is 3 mg/kg, max total dose is 225 mg or 90 mL.

Mechanism of toxicity:

Na+ channel blockade, causing cardiac and central nervous system effects.

Methemoglobinemia is a risk for both ester and amide anesthetics, but it is more commonly associated with benzocaine and lidocaine.

Clinical effects of toxicity:

***first effects classically involve peri-oral paresthesias

Hypotension

Motor Paralysis

QRS prolongation

Tachydysrhythmia

Bradycardia -> asystole

Respiratory paralysis

Seizures

Prilocaine and Benzocaine are associated with methemoglobinemia (neither of which are used in our ED, but may be encountered OTC), so get a cooximetry.

Treatment of local anesthetic toxicity:

*Hypotension: give fluids, pressors, avoid calcium channel blockers, avoid beta blockers, avoid lidocaine.

**If systemic effects with cardiac involvement: give Intralipid 20%: This is available in room 22 (nerve block cart) and Resus 4; Dosing is 1.5 mL/kg as an IV bolus; Then make a drip of 0.25 mL/kg/min. (max 10 mL/kg/min)

***Treat seizures with Benzodiazepenes.

****If you cause methemoglobinemia, give methylene blue 1 mg/kg over 30 minutes with a repeat dose if MetHGb is >30% after 1 hour, or symptoms persist (eg, end organ damage), BUT PLEASE DRAW LABS PRIOR TO ADMINISTRATION because the dye may affect future laboratory tests that depend on photometric assay.

#intralipidspecialnote: if QRS acutely widens to greater than 120 ms, this is an indication of impending clinical decompensation and intralipid should be administered.

Final Side Note:

If a patient is allergic to any of the “caines” (cocaine included), you can always put together a 1% diphenhydramine solution, which has been shown to be non-inferior to lidocaine when infiltrated locally for anesthetic purposes. One caveat is that the time to onset of anesthesia is slightly longer.

Final, final aside: how to make 1% diphenhydramine solution

1 Get 50 mg vial of diphenhydramine, which comes in a 1 mL at our shop.

2 Get 4 mL NS in a sterile syringe, put 1 mL of 50 mg /mL and draw diphenhydramine solution into the syringe.

3 This will bring your total solution volume to 5 mL.

4 Thats 50 mg in 5 mL, or 10 mg/mL

5 Remember 1 mL weighs 1 gram, or 1000 mg.

6 Therefore 10 mg diphenhydramine to 1000 mg NS, which is a 1% solution.

7 Keep in mind some of this will eventually redistribute to the vascular compartment and eventually other tissues (eg CNS), so I would not dose more than 50 mg total for an adult-sized human.

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