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: Prehospital Tourniquets Reduce PRBCs and Save Limbs

Spoon Feed
Prehospital use of tourniquets (TQ) for extremity trauma markedly reduced transfusion requirement and likely also reduced the need for fasciotomy or amputation.

Why does this matter?
Recent mass shootings and the Stop the Bleed campaign have increased awareness for TQ use. We know TQs save lives in a military setting. But does TQ use really make a clinically important difference in a civilian setting?

Tourniquets save limbs and red cells
This was a case-control study from a single center. They found 127 patients with compressible bleeding who had a commercial TQ applied in the prehospital setting due to penetrating extremity trauma and matched them to 77 otherwise similar patients who did not have a TQ applied at any point. Most had the TQ on for just over 20 minutes upon arrival to the ED. For the primary outcome of PRBC transfusion, the TQ group received just 2 units vs 9.3 in the non-TQ group. The TQ patients also arrived with a higher SBP and required fewer fasciotomies and amputations than the non-TQ patients. TQ was not associated with an increased risk of nerve palsies or greater infection risk. One of the main concerns about civilian TQ use has been nerve injury and ischemic limb complications. This study’s results are reassuring in that regard. There is a possibility for confounding given the retrospective design, but the results are consistent with prior military studies of TQ use.

Pre-hospital tourniquet use in penetrating extremity trauma: decreased blood transfusions and limb complications. J Trauma Acute Care Surg. 2018 Oct 23. doi: 10.1097/TA.0000000000002095. [Epub ahead of print]

Open in Read by QxMD

#2: New AHA Bradycardia Guidelines

Spoon Feed
The newest AHA guidelines address the evaluation and management of bradycardia and conduction disorders. This includes sinus node dysfunction, AV blocks, and bundle branch blocks.  Here’s what you need to know as an emergency physician.

Why does this matter?
We frequently see patients who present with bradycardia, either symptomatic or asymptomatic. We need to be experts in managing this.

Here’s what you need to know

Sinus node dysfunction (formerly called sick sinus syndrome) is a broad term that encompasses a variety of conditions:

  • Sinus bradycardia with HR < 50 bpm
  • Ectopic atrial bradycardia with HR < 50 bpm
  • Sinus pause > 3 seconds
  • Sinus arrest
  • Chronotropic incompetence: HR does not increase appropriately during physical exertion.
  • Tachy/brady syndrome: Atrial tachycardia (usually A fib) is most commonly followed by sinus pauses at the termination of the tachycardia. This transition often leads to syncope or near syncope.
  • Isorhythmic dissociation
  • Sinus node dysfunction must occur in the presence of symptoms. In other words, Lance Armstrong’s resting heart rate of 32 bpm is not sinus node dysfunction.

Workup and management

In all situations, first consider reversible causes of SND or blocks, especially hyperkalemia or hypokalemia. Those with reversible causes generally don’t need a permanent pacemaker. See Table 7 from the guideline.

Then consider atropine with a few words of caution:

  • Paradoxical bradycardia: You must give at least 0.5mg of atropine. Giving less may cause bradycardia.
  • Avoid in heart transplant patients: Atropine causes heart block or sinus arrest in up to 20% of patients. Bradycardia in heart transplant patients is often defined as < 70-80 bpm.
  • Is the QRS narrow or wide? AV block with a narrow QRS generally indicates the block is at the AV node and conducting through the His-Purkinje system normally. Therefore, atropine will help. If the AV block is infra-nodal, atropine does not help and has even been reported to worsen conduction delays. Try a catecholamine instead (or just pace them) unless there is concern for possible cardiac ischemia as a cause of the bradycardia.

If hemodynamically unstable or with severe symptoms, pace the patient either transcutaneously or transvenously.

Consider aminophylline, which inhibits the suppressive effects of adenosine on the SA node, in 3 situations:

  1. Acute inferior MI with 2nd or 3rd degree AV block: 250mg IV bolus
  2. Heart transplant: 6mg/kg in 100-200 mL of IV fluid over 20-30 minutes
  3. Spinal cord injury: Often refractory to atropine and catecholamines due to de-innervation. Use the same dose as for heart transplant.

Who gets a permanent pacemaker?

  1. Patients with irreversible, symptomatic sinus node dysfunction
  2. Patients with complete heart block or at risk for developing CHB (i.e. infra-nodal block):
  • Mobitz I (if infra-nodal)
  • Mobitz II
  • 2:1 AV block (if infra-nodal)
  • High grade AV block
  • ECG with alternating LBBB and RBBB
  • Syncope + BBB + HV interval > 70ms (HV interval is a measurement of His-Purkinje system to evaluate for conduction disease)

Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: Executive Summary, Journal of the American College of Cardiology (2018), doi: j.jacc.2018.10.043.

Open in Read by QxMD

#3: Migraine – A Better Steroid than Dexamethasone?

Spoon Feed
Methylprednisolone acetate (MPA) 160mg IM was not better than dexamethasone 10mg IM (both given with metoclopramide 10mg IM) for reducing headache days in the week following an ED visit in migraine patients.

Why does this matter?
Dexamethasone has been found to reduce headache recurrence in migraine patients, NNT = 9. Would a longer acting steroid be even better than dexamethasone, which has anti-inflammatory effects for roughly 72 hours?

Doc, I still have a headache
This was a RCT including 207 patients with moderate to severe migraine comparing metoclopramide 10mg IM in each group combined with either dexamethasone 10mg IM or MPA (Depo-Medrol) 160mg IM (which has effects lasting 14 days). They found no difference in the primary outcome of headache days the following week: 3 in the dex group and 3.3 in the MPA group, not statistically significantly different. None of the secondary outcomes were different either. More patients had injection site reactions in the MPA group. It was surprising how many patients in both groups had persistent headache in the week following an ED visit. Hundreds of patients were excluded as having possible secondary cause of headache or non-migraine cause. Also, patients in the MPA group had baseline headache a median 72h vs median 48h in the dex group. Maybe the MPA group was at a disadvantage due to chance imbalance in randomization. So, how does this help us? First, I am not going to use MPA for headache. It’s not better than dexamethasone and causes more pain at the injection site. Next, we can tell patients that most will not be headache free the following week and set realistic expectations.

A Randomized Trial of a Long-Acting Depot Corticosteroid Versus Dexamethasone to Prevent Headache Recurrence Among Patients With Acute Migraine Who Are Discharged From an Emergency Department. Ann Emerg Med. 2018 Nov 15. pii: S0196-0644(18)31288-5. doi: 10.1016/j.annemergmed.2018.09.028. [Epub ahead of print]

Open in Read by QxMD


Leave a Reply

Your email address will not be published. Required fields are marked *