Journal Feed Weekly Wrap-Up

We always work hard, but we may not have time to read through a bunch of journals. It’s time to learn smarter. 

Originally published at JournalFeed, a site that provides daily or weekly literature updates. 

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#1: Scheduled Acetaminophen and Febrile Seizure

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Patients given scheduled acetaminophen (APAP) after a febrile seizure had a lower rate of seizure recurrence during the same febrile illness as compared to the no-APAP group (9.1% vs 23.5% respectively).

Why does this matter?
Febrile seizures are the most common type of seizure in childhood and often end up in the ED. While the prognosis is great, it can be very distressing for patients and their families. Besides good return precautions, reassurance, and follow-up, there is not much more we can offer these patients. Previous trials have not shown a difference in seizure recurrence with acetaminophen vs placebo.

Tylenol is the new ‘tussin – good for what ails ya
This was a randomized controlled trial conducted at a single center in Japan. 438 patients who had a single febrile seizure were randomized to either APAP 10mg/kg PR q6h for 24h or no-APAP. 15 patients were ultimately excluded (10 for non-adherence, 5 lost to follow-up). They were well randomized, with similar baseline labs.

When they looked at all patients, the recurrence rate was 9.1% in the APAP group vs 23.5% in the no-APAP group (P<0.001). This effect was larger in the 22-60m age group when stratified by age (4.1% APAP vs 22.6% no-APAP, P<0.001). Ultimately, they did not report any serious complications from the febrile seizures or the APAP (hypotension, anaphylaxis, hypothermia).

You should take this with caution, as this is the first RCT to show that APAP has an effect on febrile seizure recurrence rate. However, if you are giving APAP for symptom control then you might as well schedule it. It could potentially save people from a bounce-back visit and has little downside.

Acetaminophen and Febrile Seizure Recurrences During the Same Fever Episode. Pediatrics. 2018 Oct 8. pii: e20181009. doi: 10.1542/peds.2018-1009. [Epub ahead of print]

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#2: Acute Flaccid Myelitis – Could You Make the Diagnosis?

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There has been a surge of acute flaccid myelitis (AFM) cases this year, similar to poliomyelitis. The etiology is unknown. Here is how to recognize and treat it based on what we know at this point.

Why does this matter?
If someone or their child has sudden onset weakness, where will they come? They will come to the ED. We need to be aware of this clinical presentation and know how to recognize and manage it.

Don’t be weak – learn about acute flaccid myelitis

Clinical Presentation

  • Here is the standard case definition.
  • It is similar to poliomyelitis.
  • There is rapid onset of flaccid weakness in one or more limbs over hours to days.
  • “Cranial nerve abnormalities, resulting in facial weakness, ophthalmoplegia, and bulbar signs such as dysarthria and dysphagia, may be variably present.”
  • This year, 99% of confirmed cases had a viral illness (respiratory or, less often, GI) or fever (81%) in the 4 weeks prior to onset of weakness.
  • MRI shows characteristic spinal cord gray matter edema, predominantly affecting the anterior horn or central cord; “also notable signal abnormality and enhancement of ventral nerve roots in some patients, as well as variable lesions noted in the brainstem, particularly the dorsal pons.”
  • CSF pleocytosis with >5 WBCs is often seen. But there is no, “cytoalbuminologic dissociation (elevated CSF protein in the absence of pleocytosis) as seen in Guillain Barré syndrome.”


“Report any illness to public health authorities that meets all of the following criteria:

  • A person with onset of acute flaccid limb weakness, AND
  • A magnetic resonance image showing a spinal cord lesion largely restricted to gray matter*†, and spanning one or more vertebral segments OR Cerebrospinal fluid (CSF) with pleocytosis (CSF white blood cell count >5 cells/mm3); CSF protein may or may not be elevated”

* Spinal cord lesions may not be present on initial MRI; a negative or normal MRI performed within the first 72 hours after onset of limb weakness does not rule out AFM. MRI studies performed 72 hours or more after onset should also be reviewed if available.

† Terms in the spinal cord MRI report such as “affecting mostly gray matter,” “affecting the anterior horn or anterior horn cells,” “affecting the central cord,” “anterior myelitis,” or “poliomyelitis” would all be consistent with this terminology.


  • See this for Interim Considerations for Clinical Management.
  • The cause is unknown and not confirmed to be related to enterovirus (EV-D68).
  • Consider other causes of weakness, such as herpes simplex virus neurologic infection, CNS bacterial infection, or Guillain-Barre syndrome.
  • Be alert for exacerbation of chronic medical conditions from the fever or weakness, such as asthma or diabetes mellitus.
  • Admit to the ICU if:
    • Respiratory muscle weakness on exam
    • Hypoxia/hypercarbia
    • Vital capacity < 15 mL/kg | negative inspiratory force (NIF) < 30 cmH2O
    • Impaired airway protection due to bulbar weakness, altered mental status, or autonomic instability
    • Cervical lesion on MRI
    • Rapidly progressive course
  • “Summary of Interim Considerations
    • a. General routine clinical management of children with AFM should adhere to basic standards of care for children with severe neurologic disease.
    • b. Physical and occupational therapy should be implemented as soon as the child is physically stable in order to optimize functional outcomes.
    • c. There are currently NO targeted therapies / interventions that are felt to have definitive efficacy in the treatment or management of AFM. Reviewing numerous possible targeted interventions, the experts found no concrete evidence for indication of corticosteroids, IVIG, plasmapheresis, interferon, antivirals, or other immunomodulatory agents in the treatment of AFM.
    • d. Plasmapheresis and immunosuppressive biologic modifiers, including corticosteroids, should be discouraged in the management of AFM.
    • e. The considerations for management described in this document will be revised as needed if more information becomes available.”

Another Spoonful
There was a new MMWR update on AFM last week. This new info is included above.


#3: Is Biphasic Anaphylaxis Real?

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Out of 83 patients with severe anaphylaxis, 1 had a probable biphasic allergic reaction, which was mild and consisted of rash only. No patients developed true biphasic anaphylaxis.

Why does this matter?
Ah, the infamous biphasic reaction. Is this real? The literature reports biphasic allergic reaction occurs anywhere from 1-23% of the time. This study looked at severe cases of anaphylaxis in the ICU to see if they could find answers.

Is there such a thing as biphasic anaphylaxis?
This was a retrospective review of 83 patients at a single center with severe anaphylaxis, requiring ICU admission. Of these, 99% received antihistamines, 90% steroids, and just 80% epinephrine. One patient out of 83 (1.2%) had probable biphasic allergic reaction, and this was merely skin changes, not life-threatening and not anaphylactic, according to the study definition. Of the 3 possible and 1 probable biphasic allergic reactions, they occurred at an average of 14 hours from the initial reaction. This study had some issues. The most important is that of patients with severe anaphylaxis, 20% didn’t receive the most important therapy – epinephrine. So, even with suboptimal treatment, the incidence of biphasic allergic reaction within 72 hours was very low and the single probable reaction was mild. Another issue is the retrospective nature was limited in determining what was and was not an allergic reaction, such as rash or hypotension for other reason, such as sepsis. My take home point is that true biphasic anaphylactic reaction is rare or non-existent. Most patients simply need to be observed a few hours to ensure they don’t have persistent anaphylaxis, especially those with ingestion of a food as the cause of the reaction.

Another Spoonful
The Skeptics Guide to EM did an in-depth, outstanding summary of biphasic anaphylaxis. Their bottom line: “Prolonged observation is likely unnecessary,” once symptoms resolve in the ED. Don’t miss this post.

Low Incidence of Biphasic Allergic Reactions in Patients Admitted to Intensive Care after Anaphylaxis. Anesthesiology. 2018 Nov 5. doi: 10.1097/ALN.0000000000002500. [Epub ahead of print]

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#4: Drip Lidocaine On Skin Before Injection to Reduce Pain

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When performing common bedside procedures, drip 1-2 mL of the lidocaine that you are getting ready to inject onto the skin prior to injection. This study suggests that it decreases the patient’s report of pain associated with the procedure.

Why does this matter?
Bedside procedures are common, and they hurt. Any tricks of the trade to decrease pain associated with these procedures are welcome!

It’s already there. It’s easy to do. It’s cheap. Why not?
Lidocaine dripped directly on the skin from a syringe is water soluble. It has no direct anesthetic effect. However, the authors of this study postulated that when the lidocaine is dripped onto the skin, the mere touch and the cooler temperature of the lidocaine (relative to the skin) can interfere with the transmission of acute pain signals through A-delta fibers and C fibers. In this study, the authors used 1-2 cc of 1% lidocaine from the syringe that was going to be used to perform local anesthesia. It was dripped right onto the skin just prior to locally anesthetizing that area subcutaneously in standard fashion. This was the intervention group. The control group proceeded with subcutaneous lidocaine injection for local anesthesia as we have typically performed it in the past.

481 patients were randomized to either the intervention or control group. The authors found that there was a statistically significant improvement in the primary outcome of procedural pain with the intervention group (dripped lidocaine) when assessed with the visual analog scale score. The control group rated their pain on the visual analog scale (VAS) at 16.6 +/- 24.8 mm, while the intervention group rated their pain on the same scale at 12.2 +/- 18.2 mm. These findings imply that this simple lidocaine dripping intervention led to a 26% relative reduction in procedural pain.

So here are my thoughts. The VAS goes from 0 to 100 mm. So, if you look at the pain ratings above, they are already starting out pretty low. In fact, the minimum clinically important difference in VAS score is approximately 10 mm, which was not met in the study. Also, the subgroup analysis shows that PICC insertion was the only procedure in which pain scores showed a statistically significant drop when lidocaine was dripped onto the skin pre-procedure. There wasn’t a statistically significant drop in pain scores with other procedures such as paracentesis or lumbar punctures. However, upon reviewing the data, this looks like it may have been the case due to under-powering. However, why not do it? It has very little to no downside. The lidocaine is already there in the syringe. You don’t have to cool it or prepare it in any different way. It is only a cc or two. Plus, this study shows that it may help. So, let’s all get out our syringes of lidocaine and drip a few drops out before these bedside procedures. It’s worth a try!

Comparison of Two Lidocaine Administration Techniques on Perceived Pain From Bedside Procedures: A Randomized Clinical Trial. Chest. 2018 Oct;154(4):773-780. doi: 10.1016/j.chest.2018.04.018. Epub 2018 Apr 24.

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