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. 

Follow Dr. Clay Smith at @spoonfedEM, and sign up for email updates here.

#1: Cauda Equina – How to Not Miss It

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Cauda equina is a disabling, potentially reversible, time-sensitive diagnosis. Here are pearls to keep you from missing it.

Why does this matter?
Cauda equina is a devastating disease that causes significant patient morbidity. It also requires significant resources to diagnose. This article is here to tell you that your history and physical exam findings may not be enough to rule this out, and you should be moving towards MRI when you are concerned.

Protect the horse tail

  1. History and physical exam in isolation had poor sensitivity for the identification of cauda equina syndrome (CES).

  2. Risk factors include: obesity, female gender, pre-existing spinal disease (e.g. spinal stenosis, thickened ligamentum flavum).

  3. One study found that 89% of patients with CES had acute worsening within the past 24h; however, it may present gradually over weeks as well.

  4. CES is most commonly caused by a large central disk herniation/prolapse at L4-5 or L5-S1.

  5. Exam findings consistent with CES included: bilateral sciatica, reduced perineal sensation, urinary retention, loss of anal tone, loss of sexual function, motor/sensory changes in lower extremities, and diminished patellar and Achilles reflexes.

  6. Post-void residual > 500ml had OR of 4.0, which increased to 48.0 when combined with two of the three following symptoms: bilateral sciatica, subjective urinary retention, or rectal incontinence.

  7. The gold standard for diagnosis is MRI. CT myelography may be used when MRI is contraindicated.

  8. Management requires emergent neurosurgical evaluation.

  9. High-risk features include bladder dysfunction and rapid onset.

Evaluation and management of cauda equina syndrome in the emergency department. Am J Emerg Med. 2019 Aug 20:158402. doi: 10.1016/j.ajem.2019.158402. [Epub ahead of print]

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See this EM@3AM post.

#2: FOCUS for Unstable PE

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Focused cardiac ultrasound (FOCUS) is sensitive for detecting the presence of PE in those with a HR > 100bpm or systolic blood pressure <90 and highly sensitive for detection of PE in patients with a HR  > 110bpm.

Why does this matter?
FOCUS in an insensitive test when looking for PE in the general population. However, when applied to a subset of patients with unstable vital signs, it’s thought that sensitivity is much higher. This may be a viable tool for PE detection in those too unstable or unable to go for CTA.

Getting to the heart of it
This was a prospective observational multicenter cohort study involving a convenience sample of patients from six urban academic EDs.  Providers ranging in skill from 3rd year medical student to fellowship trained EM faculty performed FOCUS on patients with suspected PE with a HR >100 or SBP <90 before CTA, the current gold standard for PE diagnosis. FOCUS assessment included right ventricular dilation, McConnell’s sign, septal flattening, tricuspid regurgitation, and tricuspid annular plane systolic excursion (TAPSE).  Findings were positive if any one of theses five measures were found. 136 patients were enrolled and FOCUS exam for PE in all patients was 92% sensitive (95%CI 78-98%) and 64% specific (95%CI 53-73%). In a subset of patients with HR >110 FOCUS was 100% sensitive (95%CI 88-100%) and 63% specific (95%CI 51-74%). The most sensitive measure was a TAPSE of less than 2.0cm (93% sensitive; 95%CI 75-95%). In all patients there was substantial interobserver agreement (κ= 1.0; 95%CI 0.31-1.0).  My takeaway, with the caveat that the provider is proficient in FOCUS, is that in a patient with contrast allergy, too unstable, too obese, or with too poor renal function for CTA, FOCUS can be used to quickly and reliably expedite disposition and management of those with unstable PEs.

Another Spoonful
What’s TAPSE? Check out this video to learn how to do it in minutes.

For more, see this emDocs post.

Increased Sensitivity of Focused Cardiac Ultrasound for Pulmonary Embolism in Emergency Department Patients With Abnormal Vital Signs. Acad Emerg Med. 2019 Sep 27. doi: 10.1111/acem.13774. [Epub ahead of print]

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#3: Cerebellar Bleed – Does Neurosurgery Help?

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Surgical decompression of a cerebellar intracerebral hemorrhage (ICH) may improve survival, but it does not seem to improve survival with favorable neurological outcome.

Why does this matter?
Classically, a large cerebellar ICH is considered a neurosurgical emergency. In fact, the AHA guidelines recommend, “surgical hematoma evacuation for cerebellar ICH with diameter greater than 3 cm [or 13.5cm3] to improve outcome.” But is this correct?

It doesn’t take a brain surgeon to…
This was a meta-analysis of 4 observational studies to compare surgical evacuation of cerebellar ICH with non-surgical management. There were a total of 6,580 patients, 578 of which had cerebellar bleeds. Of these, they used propensity score matching to come up with two groups of 152 matched on age, anticoagulation status, and size of bleed. There was no difference in the primary outcome of favorable neurological status at 3 months – mRS 0-3 vs mRS 4-6: 30.9% vs 35.5%, respectively; aOR 0.94 (95%CI 0.81 – 1.09). They found, as secondary outcomes, that overall survival was better at 3 and 12 months. And they found a threshold hematoma size of 12 cm3, below which surgery significantly worsened neurological outcome. Yet, above 15 cm3, surgery improved survival but not neurological outcome. This study is retrospective, and even propensity matching cannot compensate for all potential confounders. We have taught that for large cerebellar bleeds, surgery is the way to go. This study informs us that it may improve survival, but likely not survival without significant disability. And performing surgery on smaller bleeds may actually make matters worse. The only definitive answer to this would be with a RCT.

Association of Surgical Hematoma Evacuation vs Conservative Treatment With Functional Outcome in Patients With Cerebellar Intracerebral Hemorrhage. JAMA. 2019 Oct 8;322(14):1392-1403. doi: 10.1001/jama.2019.13014.

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#4: Adrenal Crisis

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Adrenal crisis is increasing in frequency and can masquerade as something as seemingly benign as gastroenteritis. Read this summary to update your knowledge on the diagnosis and management of acute adrenal insufficiency.

Why does this matter?
Adrenal insufficiency is something you are going to see. Spot it; treat it; and save a life.

Crisis Averted

What defines adrenal crisis?
Adrenal crisis is an acute deterioration in health associated with either hypotension (SBP < 100) or relative hypotension (drop in SBP > 20mmHg from baseline) with symptoms and blood pressure that resolve within 1-2 hours of parenteral glucocorticoid administration. If symptoms do not resolve with steroids, a coexisting illness should be considered (e.g. sepsis).
If there is no hemodynamic compromise, this is called “symptomatic adrenal insufficiency” or “incipient adrenal crisis.” Don’t ignore these patients either.

What is the physiology of adrenal crisis?
Cortisol has a 90-minute half-life. Therefore, symptoms can start abruptly. Without the suppressive effects of cortisol, cytokines exert their influence unchecked. They cause an inflammatory surge leading to fever, vomiting, bodily pains, postural dizziness, and ultimately hypotension and mental status changes.

What precipitates adrenal crisis?

  • Infection

  • Surgery or other physical stress

  • Immune checkpoint inhibitors (e.g. melanoma treatment)

  • Medicines

    • CYP3A4 inducers (e.g. phenytoin, carbamazepine) increase risk of adrenal crisis on initiation of medication because they increase hydrocortisone metabolism. More steroids are needed to compensate for the faster metabolism.

    • CYPA3A4 inhibitors (e.g. HIV medicines, -azoles, clarithyromycin) increase risk of adrenal crisis on discontinuation of medicine. While on the medicine, metabolism slows down. On discontinuation, metabolism is sped up.

How is adrenal crisis treated?

  • Steroids:

  • Give hydrocortisone 100mg IV bolus. Then 50mg q6hrs. Once the patient responds, taper down to the patient’s normal oral dose in 2-3 days.

    1. Hydrocortisone is the preferred drug. But if not available, other steroids (dexamethasone, methylprednisolone, prednisone) can be given.

    2. Fludrocortisone is not necessary if giving more than 50mg of hydrocortisone every 24 hrs.

  • IV fluids

  • Give normal saline or D5NS. Remember, these patients have a tendency towards hyponatremia so this is one of the few times you should avoid lactated Ringer’s.


  • 3×3: During a mild febrile illness, patients should take an oral stress dose of steroids (e.g. triple dose of home steroids for 3 days).

  • Home injections: Self-injecting hydrocortisone 100mg IM (or SQ if not obese) is recommended for vomiting and/or diarrhea.

How are children different?

  • In children, adrenal crisis is defined by either:

    • Hemodynamic compromise (hypotension or sinus tachycardia)

      1. Marked electrolyte abnormality not explained by another illness (e.g. hyponatremia, hyperkalemia, hypoglycemia)

    • Hypoglycemia is more common in children than in adults.

Adrenal Crisis. N Engl J Med. 2019 Aug 29;381(9):852-861. doi: 10.1056/NEJMra1807486.

For more, see this emDocs post. 

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