UMEM Educational Pearls

Sold under the name of K2, Spice. Patients exposed to this will present with dry mouth, paranoia, tachycardia, hallucinations but will resolved rather quickly over several hours. Observation in the ED and supportive care is usually all that is needed. A little history about synthetic marijuana:

• JWH-018 is a synthetic cannabinoid (SC) that acts at cannabinoid receptors.
• Synthetic cannabinoids were created s in the 1960’s and continued to be developed as appetite stimulants (e.g., dronabinol).
• The JWH series of SCs are named for the chemist who first synthesized them, John W. Huffman, Ph.D. (thus the JWH prefix).
• SCs recently appeared for sale in smoke shops and other outlets (such as gas stations) as herbal incense.
• These products contain plant material that mimics smell and appearance of marijuana but is adulterated with one or more SCs.

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• Procedural sedation consists of administering sedatives (i.e. midazolam, etomidate, propofol) or dissociative agents (i.e. ketamine) with or without opioid analgesics such as morphine and fentanyl.
• The widespread use of ketamine for procedural sedation may be limited by physician concern about unpleasant, vivid dreaming, hallucinations, and reactions after its administration known as recovery agitation.  This has been found to occur in 12 percent of cases and is seen less often in youth.
• In some instances, ketamine might be considered more ideal than other procedural sedation agents because it provides sedation, analgesia, and an amnestic-like dissociation between mind and body.
• Recent studies have shown that administering ketamine with a benzodiazepine such as midazolam significantly reduces the incidence of recovery agitation following procedural sedation; this alternative might therefore be considered when appropriate.
   

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Question

(Please note the prior version of this pearl was incorrect with respect to the images referenced. This version is corrected.)

Patient s/p blunt chest trauma. CXR (image 1) vs. lung ultrasound (image 2), do you see any inconsistencies?

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Is there a difference in the workup, etiologies, or prognosis between patients with syncope vs. near-syncope? Traditional teaching indicates that there is no difference, but that doesn't necessarily reflect common practice. Physicians sometimes are a bit less concerned about patients with near-syncope vs. patients with true, full-blown syncope; and many syncope studies exclude patients with near-syncope.

Grossman and colleagues recently published a useful reminder that patients with syncope and near-syncope have a similar 30-day rate of adverse outcome. However, they have a lower admission rate, reflecting the lower level of concern physicians have in their evaluation. Be wary of those patients with near-syncope. Don't be reassured just because they didn't hit the floor...yet!


 

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Many consider Paracelsus (1493–1541) as the father of modern toxicology.

• He was the first to emphasize the chemical nature of toxic agents.
• He stressed the need for proper observation and experimentation regarding the true response to chemicals.
• He underscored the need to differentiate between the therapeutic and toxic properties of chemicals when he stated in his Third Defense, "What is there that is not poison? All things are poison and nothing [is] without poison. Solely, the dose determines that a thing is not a poison."

The introduction of the dose–response concept might have been his most important contribution to toxicology, meaning that everything is toxic at the right dose (even oxygen and water).

• The benefit of IV alteplase (tPA) beyond the conventional window of 3 hours after onset of stroke symptoms was established by the randomized ECASS III Trial, which compared treating acute ischemic stroke with IV alteplase versus placebo, between 3 and 4.5 hours (median 4 hours).
• The study found a significantly more favorable outcome amongst participants who received alteplase (odds ratio 1.34, 95% CI 1.02 - 1.76).  The overall number needed to treat was 14.
• The standard exclusion criteria used in this study differed from those of others, and these characteristics must be taken into account when deciding which patients are eligible for treatment at up to 4.5 hours.
• Therefore, data from ECASS III can not be used to support treating at up to 4.5 hours in the following types of patients:

              -- Age > 80 years old

              -- NIH Stroke Scale > 25

              -- History of combination of previous stroke and diabetes

              -- On anticoagulation medication, regardless of INR

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Acute LV Dysfunction in the Critically Ill

• Approximately one-third of critically ill hospitalized patients develop acute LV dysfunction, most often due to a stress-induced cardiomyopathy.
• In these patients, up to 25% develop an acute dynamic LV outflow tract obstruction.
• Consider acute LV outflow tract obstruction in hypotensive patients with a new systolic ejection murmur in the left parasternal area.
• Aggressive IVFs is central to the management of these patients with LV outflow tract obstruction.

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Great resource for teaching in the emergency department....

Here is a great new app that you can use when teaching residents and students in the ED. It's the NEJM app. Great pics, videos, audio, procedures, and articles. And, it's FREE.

Just go to the App store and search "NEJM"

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For those that listen to EmedHome's EM Cast, you may have already heard this but I thought it's worth sharing with everyone else:

Many of us learned in our training that you should never give calcium to a hyperkalemic patient that is on digoxin or has digoxin toxicity. However, there's a paucity of data to support this contention. Here's one more article suggesting that calcium in the presence of digoxin or dig-toxicity may, in fact, be okay.

Levine and colleagues retrospectively evaluated 161 patients with digoxin toxicity, of whom 23 patients received calcium for hyperkalemia. None of the patients developed significant dysrhythmias in the first hour after calcium, and there was no increase in mortality rate.

Though not definitive, this is further support for treating hyperkalemia with calcium even in the presence of digoxin toxicity.

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Many patients report an allergy to iodinated RCM, sometimes adding to the complexity of diagnostic decision making.  Here are a few pearls to help:

• Seafood or shellfish allergy is NOT a risk factor for IHR to RCM
• Iodine and iodide are small molecules that do NOT cause anaphylactic or anaphylactoid reactions
• Life-threatening reactions occur in only 0.004 to 0.04 percent of nonionic low osmolality RCM infusions
  • Our radiology department uses primarily iohexol (Omnipaque) for IV contrast with a low osmolality of 844
  • Iodixanol (Visipaque) is the iso-osmotic alternative with an osmolality of 290

Bottom line: Despite the lack of cross reactivity with shellfish/iodine allergies AND the very low risk associated with today’s low osmolality agents, premedication is still indicated in patient’s with a history of IHR to RCM.

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Head injuries in children under 2yo are stress provoking, particularly with regard to when you should be getting a head CT.  Luckily, a large (42,412 children, 10,718 <2yo) multi-center trial exists to guide your behavior.

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• Seizure is very rarely associated with true ischemic stroke; the presence of seizure is, in fact, a  contraindication for administering t-PA in patients thought to have had a stroke.

• Thus, when patients present with an alleged stroke in the setting of seizure, be skeptical as to whether there truly was an ischemic stroke and do more investigating to ascertain a satisfactory conclusion.  In these cases, perhaps the patient suffered a hemorrhagic stroke, which is associated with seizure more often than is ischemic stroke.

• Post-seizure sequelae can present as focal neurologic deficit that mimics stroke (i.e. Todd's Paralysis), but note that these are generally associated with partial, not generalized, seizures.

• Finally, remember that patients who have had strokes in the past are at increased risk for having future strokes AND for developing a seizure disorder secondary to the focal area of brain tissue damaged by their prior stroke.  These patients, therefore, may present with a combination of true, new OR exacerbated, old stroke symptoms, with or without seizure.

The optimal hemoglobin concentration during critical illness is unknown. Although a liberal transfusion strategy (Hb 10-12 g/dL) was once believed to be beneficial for hemodynamics, evidence suggests targeting a conservative strategy (Hb 7-9 g/dL) does not increase mortality, while the unnecessary transfusion of blood products can cause harm (transfusion associated lung injury, infection, etc.) in the non-hemorrhaging patient. 

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Question

44 y/o female restrained driver s/p motor vehicle crash complaining of chest pain and shortness of breath. 

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Dabigatran (Pradaxa), an antithrombin medication, was discussed in an earlier pearl and thought I would play devil's advocate and explain the possible concerns:

• Yes you don't need INRs to evaluate therapeutic levels but the problem is also don't know if its subtherapeutic or supratherapeutic. This can be an issue during times of transition fromLWMH or coumadin. There are specific protocols to follow for "bridging".
• Though not clinically significant, there was an increase in myocardial infarction in thedabigatran (Pradaxa) group when compared to coumadin - remember vioxx?
• FDA approved dabigatran for stroke prevention, embolism, in AF patients. Though people will automatically translate all of the indications coumadin has that cannot be done yet.
• No reversal agent so in an acute (ED) setting, you are in trouble and are depending on the relatively short half-life to get you out of trouble.

Toxicology Mantra: You never want to be the first person or the last person to use a drug

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Valproic Acid in Status Epilepticus

• In previous pearls, we have discussed the treatment of status epilepticus (SE) with first-line (benzodiazepines) and second-line agents (phenytoin/fosphenytoin).
• Refractory SE is defined as the failure to respond to both first- or second-line antiepileptic medications.
• Valproic acid is listed in many algorithms as a third-line agent for treating SE.
• Avoid valproic acid in refractory SE patients who have hepatic disease or dysfunction.
• Although rare, valproic acid can cause a fatal hepatotoxicity in these patients. 

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