Neuroleptic Malignant Syndrome/Serotonin Syndrome

Let's talk about hyperthemia today, the weird kind. NMS and SS - I often get confused between the two, so this is as much as I can remember:

NMS is SLOW, it happens slowly and takes forever to resolve. Fever + rigidity.

SS is FAST, hyper reflexive and agitated, quick on and relatively quick off. Fever + clonus.

Both have fever/elevated temp. Treat both with benzos. For NMS, add on bromocriptine (SLOW down BRO). For SS, just use the other weird-sounding drug (cyproheptadine).

I think it's also important to learn to recognize potential offending agents when you are doing med recs on patients.

Definitely not a comprehensive list but here are some our patients might be taking (or you are giving them):

NMS

typical antipsychotics > atypicals. Classically, haldol, droperidol, thorazine, pheneragan. Metoclopramide. Less rare but atypicals like clozapine, olanzapine, risperidone, quetiapine, ziprasidone.

SS

sertraline, fluoxetine, citalopram, paroxetine, trazadone, buspirone, venlafaxine, valproate, tramadol, fentanyl, meperidine, ondansetron, metoclopramide, sumatriptan, linezolid, dextromethorphan, MDMA, LSD, St. John’s wort, ginseng.

Check this out for more details and some of the more nitty gritty:

http://www.emdocs.net/toxcard-differentiating-serotonin-syndrome-neuroleptic-malignant-syndrome/

A common missed ED diagnosis

Q for all of You.

If i were to tell you that there is a disease entity that has-

• an estimated prevalence of 2% in the US 

• significant morbidity

• is easily treatable

• and that many of us have likely missed it in the ED

Would you know what it is?

Well. You're about to.

Wernicke Encepahalopathy. 

What is it?

• An encephalopathy that occurs secondary to thiamine (B1) deficiency

It's a disease only seen in alcoholics, right?

• ehhh, not quite.

• Wernicke most commonly is found in alcoholics (an estimated 12.5% of them), but has also been found in people who have bariatric surgery, hyperemesis gravidarum, and AIDS (one study found evidence of wernicke in 10% of autopsies in AIDS patients)

Well how does it present.

• Classically has a triad of ataxia ophthalmoplegia, and AMS

• though the full triad is only seen in <10% of patients

Is there a diagnostic tool available?

• Sure is, diagnosis is made with 2/4 of the following criteria

  • Dietary deficiencies

  • Oculomotor deficiencies

  • Cerebellar Dysfunction (ataxia)

  • AMS/mild memory impairment

Why is it important that I treat it?

• An estimated 60% of patients will have residual defecits

How do I treat it

• pretty simple.

• THIAMINE. 

• 500mg IV thiamine three times a day for 3 days, followed by 250mg IV for 2-3 days

  • there is conflicting evidence about the amount of thiamine to give. Yet all agree that thiamine is relatively harmless- basically just give a lot of thiamine

  • IV administration is important here. chronically malnourished patients (especially those with ethanol usage) do not absorb thiamine well in the GI tract.

  • co-administer magnesium IV - hypomagnesemia promotes thiamine resistance

• the 100mg we give in our bannana bags is preventative, and can provide sufficient thiamine for 1 week

So you're saying every confused alcoholic that's stumbling in the ED requires hospital admission for IV thiamine? That'll do great for our boarding issues in the ED

• Not quite.

• But if your drink patient is clinically sober and is then witnessed to have a wide based gait on their way out the ED. take a minute. have a conversation. do a brief ocular neuro exam. look for weird eyeball movements. 

• often times patients will have rapid improvement from an IV thiamine dose (within 30 minutes). While not specific, if this happens the patient should definitely be admitted for IV thiamine. 

How about that thiamine before glucose thing. Do i need to withhold glucose from a hypoglycemic alcoholic.

• Meh. NO!

• in theory, a glucose load increases thiamine requirements. The though was that giving a dextrose load can push the at risk patient into Wernicke. But studies have not shown this to be the case. 

• give your hypoglycemic patient glucose. just do it. Swoosh style. 

What's the pathophysiology behind it?

• Never thought you'd ask!

• Every ED docs favorite cycle - the Krebs cycle

• Thiamine is a co-factor for pyruvate dehydrogenase, which converts pyruvate --> Acetyl-CoA, which then enters the Krebs cycle and results in ATP production

• So no thiamine = no ATP

• no ATP = bad. 

That's all.

-Elly

POTD: Less Commonly Abused Hallucinogens

We’ve reviewed the most commonly abused hallucinogens in previous POTD, but how do you recognize and treat a patient that has “licked a toad”? And how would you treat a college student who got high off nutmeg?  Here we discuss several less commonly abused hallucinogens:

Salvia
    ▪    Salvia divinorum
    ▪    a.k.a, “Salvia” “Sally” “Magic Mint”
    ▪    Smoked or chewed
    ▪    Not currently regulated under the U.S. Controlled Substances Act
    ▪    Symptoms/Effects: Visual hallucinations, object and body distortions, dysphoria, incoordination, dizziness, slurred speech
    ▪    Duration: Up to 30 minutes
    ▪    Treatment: Supportive

Bufotoxins
    ▪    bufotenine and 5-methoxy-dimethyltryptamine from venomous toads
    ▪    also contains cardioactive steroids, and catecholamines
    ▪    a.k.a., “love stone” “rock hard”
    ▪    Obtained from extract or “licking a toad”
    ▪    Symptoms/effects: Powerful psychedelic, GI irritation, salivation, n/v, cardiac toxicity similar to acute digoxin poisoning, hyperkalemia, bradycardia, AV block, Vtach, Vfib, cardiac arrest
    ▪    Serum digoxin immunoassay often positive
    ▪    Treatment: Atropine for bradyarrhythmias, may require pacemaker; antiarrhythmics for ventricular arrhythmia; dig-Fab Ab treatment has been effective

Morning Glory Seeds
    ▪    Ipomoea violacea, Ipomoea tricolor, etc
    ▪    Contain compounds similar to LSD
    ▪    Seeds ingested for their hallucinogenic effects
    ▪    Symptoms/effects: Similar to LSD
    ▪    Treatment: Reassurance, benzodiazepines in severe cases

Nutmeg
    ▪    Myristica fragrans
    ▪    Active compound: myristicin
    ▪    Large amounts of nutmeg (1-3 nutmeg seeds) can cause delirium with hallucinations
    ▪    Symptoms/effects: Hallucinations, tachycardia, flushing, dry mouth, nausea, abdominal pain
    ▪    May resemble anticholinergic poisoning, but pupils are small or normal
    ▪    Duration: 6 to 24 hours
    ▪    Treatment: Supportive

Jimson weed and Angel’s Trumpet
    ▪    Datura stramonium and Datura candida, respectively
    ▪    Contain atropine, scopolamine, and hyoscyamine
    ▪    Seeds/other parts of plant ingested or smoked
    ▪    Symptoms/effects: Delirium, hallucinations, seizures, anticholinergic effects
    ▪    GI emptying delayed and small seeds can become trapped in GI folds after ingestion
    ▪    Treatment: Consider GI decontamination in select cases with whole bowel irrigation for large ingestions, avoid anticholinergic medications, may try physostigmine

Source: Tintinalli’s Emergency Medicine, 9th Edition, Chapter 188: Hallucinogens pp 1247-1248