Varicella in Pregnancy

Varicella-zoster virus

Varicella (chickenpox) is a highly contagious disease caused by primary infection with varicella-zoster virus (VZV)2 and may cause maternal mortality or serious morbidity

> Reactivation of latent infection, usually many years after the primary infection, may result in herpes zoster (shingles), a painful vesicular eruption in the distribution of sensory nerve roots2

> Both varicella (chickenpox) and zoster (shingles) are notifiable diseases. Notification must be made to the Communicable Disease Control Branch of SA Health as soon as possible and at least within three days of suspicion of diagnosis, by telephone or post.


Route of transmission

> Infection with chickenpox is transmitted through airborne / respiratory droplets and direct contact with vesicle fluid


Incubation period

> 10 to 21 days (may be up to 35 days in contacts given high titre zoster immunoglobulin, ZIG)


 Period of infectivity

> 48 hours before the onset of rash until crusting of all lesions (usually day 6 of rash)

> Infectious period may be prolonged in people with impaired immunity


Infection Control

> Non-immune staff should not care for the woman / baby infected with chickenpox

> Varicella (and herpes zoster) vesicles contain large numbers of virus particles. Ensure appropriate transmission based (standard, contact and airborne) precautions including:

> A negative pressure room with door shut (chickenpox and disseminated shingles)

> Immune staff in attendance

> Gloves, gown

> All dressing materials should be treated as medical waste

> Chickenpox and disseminated shingles use standard, contact and airborne precautions

> Localized shingles use contact precautions (only immune staff in attendance, single room, gloves, gown)

> In herpes zoster (shingles), transmission of infection usually requires contact with vesicle fluid; however, there is also evidence of respiratory spread. Localized shingles requires standard and contact precautions (not airborne precautions)


Susceptibility to varicella

> Women and babies susceptible to infection with VZV (may be severe or life-threatening) include:

> No history of varicella (chickenpox or shingles)

> Seronegative for varicella antibodies (VZV-IgG negative)

> No documented evidence of varicella vaccination 


Significant Exposure

> For the purpose of infection control and prophylaxis, significant exposure of a susceptible woman who is pregnant to varicella includes:

> Living in the same household as a person with active varicella or herpes zoster

OR

> Direct face to face contact with a person with varicella or herpes zoster for at least 5 minutes

OR

> Being in the same room for at least 1 hour

> Chickenpox cases are infectious from 2 days before rash until lesions crusted


Management of maternal exposure to varicella-zoster virus

History of previous chickenpox

> No action required

No or uncertain history of chickenpox

> Obtain serology for antibody status (VZV-IgG) (if practicable)

> ZIG if required should be given within 96 hours. Testing should only be done if ZIG would still be able to be given, if required, within this window


Within 96 hours from exposure

> Zoster immunoglobulin (ZIG) should be given to all seronegative women within 96 hours (see adult dose under ZIG dosage below)

> However there may be some limited effect out to as late as 10 days post exposure

> Advise to seek medical care immediately if chickenpox develops


More than 96 hours following exposure

> Oral aciclovir or valaciclovir (see dosage below) should be considered for women:

> In the second half of pregnancy

> With a history of an underlying lung disease

> Who are immuno-compromised

> Who are smokers

Note: Advise women to seek medical care immediately if chickenpox develops


Management of varicella-zoster in pregnancy

Less than 24 hours since appearance of rash

> Oral aciclovir 800 mg 5 times a day for 7 days OR oral valaciclovir 1 g three times a day for 7 days]

> Monitor at home

More than 24 hours since onset of rash

> No oral aciclovir / valaciclovir and monitor at home if:

> No underlying lung disease

> Not immunocompromised

> Non-smoker

> Monitor in hospital if any of the above risk factors

> Offer appropriate fetal medicine counselling


Complications

> Advise to seek medical attention for the following complications:

> Respiratory symptoms

> Haemorrhagic rash or bleeding

> New pocks developing after 6 days

> Persistent fever

> 6 days

> Neurological symptoms

> Give aciclovir 10 mg / kg every 8 hours for 7 to 10 days (IV followed by oral [see dosage below]) and administer supportive therapy

Consider caesarean section if:

> Signs of significant fetal compromise

> Evidence of maternal respiratory failure exacerbated by advanced


Risk of fetal varicella syndrome (FVS) after maternal VZV

Timing of maternal infection:

>Less than 12 weeks gestation-  0.55%

>12-28 weeks gestation- 1.4%

>More than 28 weeks gestation- No cases of FVS reported


Refer to maternal fetal specialist for prenatal diagnosis and counselling

> Detailed fetal ultrasound for anomalies is recommended at least five weeks after primary infection

> Repeat ultrasounds until delivery. If abnormal may consider fetal MRI

> VZV fetal serology is unhelpful

> Amniocentesis not routinely advised if ultrasound normal, because risks of FVS low but negative VZV PCR may be reassuring


Management of infants exposed to maternal varicella zoster

Maternal chickenpox > 7 days before delivery

> No zoster immunoglobulin (ZIG) required

> No isolation required

> Encourage breastfeeding

> No other interventions even if baby has chickenpox at or very soon after birth unless preterm < 28 weeks gestation or low birth weight < 1,000 g > Very preterm infants (≤ 28 weeks gestation) born with chickenpox should receive intravenous aciclovir 20 mg / kg / dose every 8 hours as a slow infusion (1-2 hours)

 

Thank you to Christine DeFranco PGY-4 EM Resident for this review of VZV in pregnancy!

Managing Dislocations of the Hip in the ED

Source: EM Practice Podcast – Dec 2017
** There are no existing ACEP guidelines on this topic.


Pre-Hospital Management
  • Stabilizing and pain control
  • Neurovascular compromise
    • If suspected then d/w med control for considerate of immediate reduction and splinting vs. rapid transport to ED
    • If no suspicion the patient can be immobilized in current position
  • Don’t forget C-spine precautions as these injuries are often distracting

Overview

Etiology:

  • Typically traumatic in origin
  • Over 2/3 Hip dislocations occur in patients who present after MVCs without seat belts with the knee hitting the dashboard and the body moving forward over a fixed femur.
    • Often associated with posterior wall/lip fractures of the acetabulum

Definitions:

  • Simple vs. Complex
    • Simple Dislocation – does not involve fracture
    • Complex Dislocation – involves fracture

Pathophysiology:

  • Posterior & Inferior dislocations are most common – about 90% of dislocations
  • Fracture of >40% of the acetabular rim is considered an UNSTABLE FRACTURE (requires ORIF)
    • If there is a posterior acetabular fracture you must get a CT to eval for unstable fractures
  • Sciatic nerve injury
    • Seen in about 14% of traumatic hip dislocations
    • Check sensory along the posterior leg, ability to dorsiflex the ankle and ankle reflexes
  • 95% of traumatic hip dislocations will have another associated injury
    • Be sure to complete a full trauma survey on these patients per ATLS guidelines

Imaging
  • Initial image should be a bedside AP pelvic radiograph
  • Look for Shenton’s Line

  • Lateral film can seal the diagnosis if unsure based on initial bedside AP
  • CT if neeeded

Treatment for Native Hips (non-prosthetic)

Consultation

  • Ortho Consultation are required for the following:
    • Complex hip dislocations
    • Irreducible dislocations
    • Non-concentric reductions
    • Neurovascular deficits despite reduction

Reductions

Who:
– Simple dislocations can & should be reduced by the ED physician!

When:
– Reduction should be performed within 6 hours of injury to decrease risk of avascular necrosis
– No more than 3 attempts at reduction should be made by the ED provider

Transfers:
– If patient requires transfer to a different hospital, an attempt at reduction should be made by the ED provider.
– Patients transferred without reduction had a 4-fold risk of severe sciatic nerve compared to those transferred after reduction (16% vs 4%).

Analgesia:
– Be sure pain is controlled prior to attempting reduction

  • Ultrasound guided fascia iliaca compartmental block work great
    • Reduces need for systemic analgesics
    • Improves patient comfort
    • Increases likelihood of successful reduction
    • Reduce need for procedural sedation
    • Be sure to have completed a full neurological exam prior to blocking your patient
      LINK TO VIDEO
  • In many cases, procedural sedation and systemic analgesia may also be needed (in addition to nerve block) in order to adequate pain control and muscle relaxation.

Reduction Techniques

Old School:
Allis’s Maneuver

Newer techniques:
Captain Morgan
Over-Under/Whistler
East Baltimore Lift

No evidence exists to recommend one technique over the other.


Immobilization

After successful reduction the hip should be immobilized in extension and external rotation with slight abduction
– Use an abduction pillow to help hold this position
– Knee immobilizer can be used if no abduction pillow is available

Don’t forget to obtain a post reduction film to confirm alignment


Other Recommendations
– Early passive range of motion and rehab is usually recommended
– Patients should remain non-weight bearing until seen by an Orthopedist


Notes on Prosthetic Hip Dislocations
  • Quite common
    • Incidence of ~2% of patients who undergo THA
    • 60% occur within first 3 mo, 77% occur within the first year
  • Often the result of minimal force like bending over to pick something up off the floor
  • Use the same techniques as a native hip reduction
  • Do not need abduction bracing after the reduction
  • If the patient can walk after the reduction, they can be safely discharged (after discussion with their orthopedist)
  • Less urgency, no risk of avascular necrosis as the femoral head has already been replaced
  • Remember, these injuries are painful and although less urgent, the reduction should occur as soon as possible

 

Pain Pearls – Nitrous Oxide

Nitrous Oxide


Introduction to Nitrous in the ED

  • Tasteless colorless gas administered in combination with oxygen
    • Maximum concentration 70% N20
  • Absorbed via pulmonary vasculature and does not combine with hemoglobin or other body tissues
  • Rapid onset and elimination
    • <60 seconds
  • Analgesic and anxiolytic agent
    • Use along with local anesthetic or other non-opioid pain medications
  • Administered via facemask
  • Only monitoring needed is pulse oximetry
  • No NPO requirements, patient can drive after administration, no IV line needed, no RN necessary at bedside
  • Nitrous is NOT procedural sedation and should be thought of as a pain medication
  • Studies show it is similar to morphine 10 mg IM
  • It works only when the patient is breathing it in and stops working immediately when the gas is off

Contraindications

  • Severe COPD or asthma
  • Active Otitis Media/Sinusitis
  • Active Bowel Obstruction
  • 1st -2nd trimester pregnancy
  • Altered level of consciousness
  • Severe Psychiatric disease
  • EtOH
  • Head Injury
  • Complex Advanced Active Cardiac Disease

Indications (really any procedural pain)

  • Laceration repair
  • Incision & Drainage
  • Wound Care
  • Foreign body removal
  • Central Venous Access
  • Peripheral venous access
  • Fecal Disimpaction
  • Adjunct for
    • Dislocations
    • Splinting

Nitrous as an adjunct

  • If using nitrous to try and reduce a joint
    • Use IN ketamine
    • Intra-articular lidocaine
  • Concomitant admin of nitrous with opioids, benzos, or propofol is considered PSA
  • If giving an IV opioid you should wait 30-45 minutes before using nitrous to avoid excessive sedation or airway issues

What do we have?

Porter Standard Flowmeter

  • Stored in the trauma bay
    • Extra tank rack across from peds resus bed
  • Must use disposable breathing circuit
    • Located next to desk in trauma bay
    • There are adults small, youth medium, and peds small
Safety Features
  • Nitrous oxide flow stops if oxygen is shut off or supply becomes limited
    • Can never supply more than 70% nitrous oxide
  • Exhaled gas is scavenged away to avoid unnecessary exposure to providers

Getting started

  • Wheel to bedside
  • Plug green oxygen tube into oxygen port in the wall (may have to remove Christmas tree)
  • The gray tube scavenging tube plug into to the suction port in the wall
  • Breathing circuit only fits one way, push big lumen tube into top (by gray bag) and the clear little tube below breathing bag

Positioning

  • Position the patient comfortably
  • Bring unit close to the patient so you can reach the dials
  • Make sure pulse oximetry is connected and you can see the waveform
  • Once the mask is on…
  • Set oxygen flow rate then titrate nitrous oxide to desired percentage
  • Watch gray breathing bag as a guide to adjust flow (titrate flow)
    • If bag is fully collapsing, increase overall flow
    • If bag is not moving, decrease overall flow
    • Once nitrous oxide percentage is set, regardless of flow rate, percentage stays the same

During The Procedure

  • Titrate nitrous oxide up and down as needed for “desired analgesia”, watch breathing bag to determine overall flow
  • Once procedure is complete, turn off nitrous oxide, allow patient to breath oxygen only for 60 seconds
    • Continue to watch breathing bag
  • Then remove mask completely

Your Done!!

  • Patient can be discharged with no driving or work restrictions
  • Throw away the breathing circuit
  • Return it to the trauma bay

REFERENCES:
  • Becker 2008
  • Babl 2015
  • Zhang 1999
  • Champman 1979
  • Jastek 1991

Special thanks to Dr. Alexis LaPietra for her contribution! Watch out for next times pain pearls…….. Haldol as an analgesic!!!

Euglycemic DKA

Hi all. I wanted to bring to your attention a great case. The case was a young woman with relative euglycemic diabetic ketoacidosis. This diagnosis used to be quite rare and associated with pregnancy or very poor PO intake. However, with the use of SGLT2 inhibitors (which this young woman was taking) the incidence is increasing. The diagnosis highlights some very important factors about the treatment of DKA:

  • Don’t just look at the blood sugar. Calculate your anion gap. Look at the bicarb. Calculate the strong ion difference. Check for ketones. A VBG is fine for a rough estimate of pH. If you really want to get fancy, an ABG will give you an accurate base deficit that can help you figure out (along with your lactic acid, strong ion gap, or delta-delta) exactly what else is going on with the patient in the setting of multiple competing metabolic processes. But that’s only if you want to get fancy. I think you can provide great initial resuscitation without it.
  • Remember why we do what we do in DKA and all the complications you can get from treatment. The treatment is based on exactly the same principles that guide the treatment of “regular” DKA. However, they are not starting at the exact same metabolically disturbed place as most patients do. They can be just as sick, if not more, but the initial treatment has to take into consideration exactly where they are in their metabolic disarray. Things to think about as you are coming up with a treatment plan:
  • These patients need fluid. Fluid will be your friend (more on that later)
  • These patients need glucose. From the start. For a glucose less than 100-125, consider starting D10 instead of D5.
  • They need glucose because they need insulin too. They still may have some relative insulin resistance so giving them glucose alone won’t help them if they cannot get the glucose into any cells. However, as you are already starting from a lower glucose, be very gentle. If you still bolus insulin in DKA (which I do- in selected cases- and would be glad to have conversation about whether we should or not at another time) do NOT bolus these patients. I don’t have great evidence as to where to start a drip so I pick a low number. Like 1 low. I can always move up. If anyone has a better scientific explanation on how to pick your infusion rate, I’d love to hear it.
  • They need insulin so you better be sure you aren’t going to cause a malignant arrhythmia if you give it to them. Make sure your potassium isn’t going to plummet when you start insulin. Rough guideline is to make sure it is >3.3 . This is true for all DKA.
  • They don’t have a sodium correction because the glucose is normal. If their sodium is already on the higher side (around >140), think of starting with ½ NS as your base.

The attending on the case did an excellent job with this patient. He focused on fluid and recognized her severe metabolic disturbance, despite the fact that her blood sugar was trying to hide it.

I’ve included two articles below. One is two case reports on euglycemic DKA and the other talks specifically about cases involving SGLT2 inhibitors. They aren’t the best articles I’ve ever read but they are more official than I am so felt I should include them. As a said, this is a relatively new class of medications and a relatively new phenomenon.


Euglycemic diabetic ketoacidosis: a diagnostic and therapeutic dilemma, EDM Case Reports, September 2017

Posted by:

Ruth Lamm, MD FACEP
Assistant Professor
Emergency Medicine
Critical Care Medicine
Saint Joseph’s Hospital Medical Center
lammr@sjhmc.org

EM Conference Pearls (9/20)

Pediatric congenital heart disease

  • Congenital HD: Two types: Neonates with ductal dependent lesions and infants (2-6months) presents with CHF
  • Cyanosis presentation: When ductal-dependent lesion is required for pulmonary blood flow (Will not respond to oxygen)
  • Shock presentation: When ductal-dependent lesion is required for systemic blood flow (appear septic and not response to fluids, may get worse with fluids)
  • Hypoxic/cyanotic or shocky/acidotic baby treatment = Prostaglandin E1 (PGE1) and transfer to facility with pediatric cardiovascular surgeon.
  • PGE1 treatment may cause apnea (monitor closely and consider intubation)
  • CHF in infants = wheezing, retractions, tachypnea, sweating/crying, difficulty feeding

EBM in the ED

  • EBM = What the evidence shows in the literature + What the physician wants for the patient + what the patient wants for themselves
  • Just like we need to practice intubation, central lines –> Learning to read and interpret literature is a skill that needs to be practiced.

Aortic Dissection

  • AD: Chest pain plus disease (ex: CP + Neurodeficit)
  • If you find your self giving large amounts of strong pain meds (narcotics) while treating what is seemingly ACS…STOP..think about AD or alternative diagnosis of chest pain
  • The 3 important questions, aortic dissection is the subarachnoid hemorrhage of the torso, migrating pain, colicky pain + opioids = badness and pain that comes and goes can still be a dissection.
  • Treatment: Treat pain, HR, BP
  • Pain: Fentanyl 25 – 50 mcg bolus
  • HR: Goal of 60 bbpm
  • Esmolol 0.5 mg/kg bolus then 50 – 300 mcg/kg/min or
  • Labetalol 10 – 20 mg bolus then 0.5-2 mg/minor
  • BP control: Goal SBP =110
  • Nitroprusside 0.25 – 0.5 mcg/kg/min then titrate (CN toxicity)
  • Nicardipine 5 mg/hr
  • Warning: Giving a vasodilator without concomitant reduction in ionotropy may cause progression of dissection. Start BB first before vasodilation meds.

ACEP Now Review on LVADs

Check out this excellent review on managing patients with LVADs from this month’s ACEP Now publication which was written by our own Dr. Yenisleidy Paez Perez, DO PGY-3 and one of our newly graduated residents, Dr. Terrance McGovern, DO. The article is entitled ‘How to Manage Emergency Department Patients with Left Ventricular Assist Devices.” Click the link below to be forwarded to the article.

http://www.acepnow.com/article/manage-emergency-department-patients-left-ventricular-assist-devices/

Breaking Bad News

One of the hardest roles of the emergency physician is giving bad news to a patient or their family members. Difficult topics that are often challenging for physicians to discuss include reporting the death of a family member or giving the diagnosis of a terminal illness. The optimal way to relay these topics is yet to be determined and each practitioner typically develops their own communication style. Some choose to deliver the message in a direct and succinct manner while others prefer a more drawn out and complete explanation. The Emergency Department provides a unique environment as there is often little time to develop any rapport with the patient and their family. This can make communicating these topics more challenging. In addition, breaking bad news involves more than just the verbal component of actually giving the bad news. It also requires the ability to respond effectively to patient’s and family’s emotional reactions and the dilemma of how to give hope when the situation is bleak.

Jurkovich et al studied the characteristics and methods of delivering bad news from the perspective of surviving family members. The chart below details the importance of various elements rated by respondents in the study. The attitude and clarity of the message delivered by the provider were deemed to be most important, while the attire of the provider had little importance to the respondents.

The duty of breaking bad news can be improved by understanding these characteristics and methods and then applying a step-wise method to effectively communicate and counsel patient’s and/or their families. In a recent Wednesday conference, Dr. Flannery, one of our core faculty attendings, introduced us to the SPIKES protocol for breaking bad news. The purpose of the protocol is to help the clinician fulfill the essential goals of gathering information, providing intelligible information, and supporting the patient or family by reducing their emotional impact and isolation. When we are informing our patients of an unfortunate diagnosis, the protocol also calls for collaborating in developing a strategy or treatment plan for the future. From the Emergency Department standpoint, this means guiding patients to the correct consultant for further workup and treatment options.

During our Wednesday conference, we broke into small groups and practiced situations that would be considered difficult to give bad news. The experience was positive and allowed us to give each other constructive criticism on ways to improve our approach to giving bad news. As a senior resident, I have unfortunately been involved in many of these situations throughout my residency. I have learned that despite the challenges involved in delivering bad news, there is also tremendous gratification in providing a therapeutic presence during a patient or family’s greatest need.

References:
1. Jurkovich et al. Giving bad news: the family perspective. J Trauma. May 2000
2. Baile W.F. et al. SPIKES – A Six-Step Protocol for Delivering Bad News: Application to the Patient with Cancer. The Oncologist. June 12, 2000.

EM Conference Pearls (8/2/17)

Pearl’s from Wed conference August 2nd 2017:

Agenda:
– Asthma/COPD: Baldino
– Sepsis Core Measures: Patel
– Pulmonary cases: Patel
– Medical student pearls (from Mike Taylor, one of our students)


Dr. Baldino: Asthma/COPD

-All that wheezes is not asthma (or COPD).
-Use diagnostics to rule out mimics such as pneumonia or ptx.
-Get the CXR in COPD exacerbation, not routinely in simple asthma exacerbation.
-Good evidence and NNT’s for benefit of ipratropium, systemic steroids, magnesium,  and BiPAP.
-Intubation last resort for asthma.  Remember to adjust I to E ratio on vent.
-Steroids at discharge for asthma/COPD.  Antibiotics at discharge for COPD.
-Discharge with a plan! (and a spacer)


Dr. Patel: Sepsis Core Measures

-Sepsis core measures are from CMS, not from SSC guidelines or Sepsis 3.0. They are not necessarily rooted in great evidence, but we have to follow them!
-Remember the 3 and 6 hour severe sepsis and septic shock bundles. Timing is based on presentation time (when chart displays severe sepsis, septic shock), not door time.  To make your life easy, just use door time to meet the metrics.
-The focused exam for septic shock can now just be documented with one statement, which is in Medhost.  Make sure to click that.
-Fluids from the field count (as your 30 cc/kg), as long as it is given as a bolus and documented on the chart.
-Antibiotic choice and timing both looked at for core measures. For choice, best to go with a monotherapy agent first to meet the metric.


Dr. Patel: Pulmonary Cases

-The term HCAP is not in the newest pneumonia guidelines from 2016.
-Treat HCAP like CAP unless the patient is going to the MICU.  If going to the MICU, cover for MRSA and Pseudomonas.

Hemoptysis:

-Minor hemoptysis (streaks in the sputum)–d/c unless CXR abnormal
-Moderate hemoptysis (frank hemoptysis)—admit for further work up and obs
-Massive hemoptysis (hemoptysis interfering with respirations)–intubate and consult pulmonary (for bronch) and IR (for possible bronchial artery embolization). If there is a suspicion of a bronchovesicular fistula or other arterial fistula, CT surgery may also need to be on board.


Medical Student Pearls

One of our current medical student’s Mike Taylor put together some info on questions that were raised in conference:

Intentional “L Main Bronchus Intubation:” (for hemoptysis)

Take Home Points from 1995 Anesthesiology Case Report:
 -Can use a double lumen ET tube with a endobronchial cuff
 -The inflated endobronchial cuff can tamponade the hemorrhaging R lung and occlude airflow into it. This allows only the L lung to be effectively intubated and the provider not have to be tasked with putting the tube in the L main bronchus
 Reference: http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1949905

Rate Control for MAT:

Take home points from Uptodate
 -Treat underlying cause
 -Maintain phos and mag levels
 -Can use CCBs or beta blockers for rate control in symptomatic pts
 Reference (requires access to UpToDate): https://www.uptodate.com/contents/multifocal-atrial-tachycardia

Bandemia Cut Offs:

Take home points from 2012 Retrospective Cohort Study:
 -With normal white counts, pts with bandemia of at least 11% had higher in hospital mortality
 -So 11% or higher could use as a cut off for admission, more aggressive treatment, etc.
 Reference: https://www.ncbi.nlm.nih.gov/pubmed/22939096

Special thanks to Chief Dan Poor PGY-4 for organizing this week’s Conference Pearls and for Mike Taylor MS-IV for his Medical Student Pearls

EM Conference Pearls (7/26/17)

Pediatrics Trauma Radiology Review (Dr. Flannery) – When in doubt splint

  • Salter Harris: Take home memorize classification and management
    • SH1: Clinical Dx – Splint and f/u
    • SH2: Splint and f/u, most common
    • SH3: Ortho consult
    • SH4: OR
    • SH5: OR
  • Supracondylar Fx : Take home: Type II/III requires OR
    • SC Fx type I: Look for posterior/anterior fat pads
      • Tx: Posterior splint, f/u ortho
    • SC Fx type II: Splint and Ortho consult
    • SC Fx type III: OR
  • Misc Fx
    • Greenstick fracture
    • Toddle Fx: Tx with posterior splint and out pt f/u (For non displaced)
      • When in doubt splint and f/u ortho
    • Buckle Fx: Volar splint
  • SCFE
    • Klein’s line should intersect the femoral head
    • Can be bilateral
  • SCIWORA
    • Always recheck spinal (ROM/focal findings) after a negative CT cervical

Trauma Board Review (Dr. Patel)

  • Hip/Femur fracture
    • Most are operative, recognize they are sick patients.
    • Fermoral head fx, neck fx, trochanteric (Inter/sub)
    • Pain control, Ortho consult, Most cases OR
  • Tibial plateau fracture
    • Maybe radiographically occult
    • Patella alta
  • Maisonneuve fracture
    • Proximal fibular fx + medial malleolar fracture ( or disruption of deltoid ligatment, IO membrane syndesmosis)
  • Lisfranc fracture
    • Tarso-metatarsal fracture-dislocation
    • Mal-alignment Metatarsals with cuneiforms.
  • Calcaneal fractures
    • 10% associated lumbar fractures
    • Boehler’s angle <20
  • Jones fracture: High rate on non-union
  • Pseudojones fractures: Bulky dressing and pain control
  • Hip dislocations
    • MC: Posterior dislocation (90%)
    • High rate of AVN femoral head, peroneal nerve dysfx, sciatic nerve injuries)
  • Knee dislocation
    • 50% will spontaneous reduce!!!
    • Need a good Neurovascular evaluation
    • ABI < 0.9
    • Vascular surgery/ortho eval à Arteriography or CT Angio
  • Ankle Sprain:
    • Ottawa ankle rule
  • Scapular fracture
    • Associated with concomitant injuries such as internal thoracic injuries
  • Clavicle fracture
    • Op: Open fx, unstable floating shoulder, NV compromise.
  • Radial head fx
  • Monteggia fracture
  • Galeazzi fracture
  • Scaphoid fx – Thumb spica, risk of non-union and AVN
  • Bannette’s fx – Thumb spica,
  • Rolando fx
  • Posterior shoulder dislocation: Light bulb / Drum stick appearance
  • Compartment syndrome
    • 6P’s. Money is on pain and paresthesia.
  • High pressure injury injection injury
    • Limb threatening
    • Surgical emergency

Trauma in pregnancy (Dr. Kashani)

  • Prepare for difficult airway
  • Be aware of Hemodynamic changes
  • Rh sensitization
  • >20 weeks with abdominal trauma monitor for 4 hrs
  • Peri mortem C-section best outcome if performed within 4 – 5 minutes of CPR 

Thanks to Chief Mike Hong, DO PGY-4 for writing up today’s CONFERENCE PEARLS

Take Home Pearls from 2017 UM EM Cardiac Arrest Symposium

Below is a review of the key points of each lecture from the 2017 University of Maryland Emergency Cardiology Symposium which was hosted by Amal Mattu, MD in Baltimore, MD. This year’s topic was Cardiac Arrest.

To view video and presentations of all of the lectures, visit: www.livestream.com/UMEmergencyMed.


How Far We’ve Come!

John M. Field, MD; Penn State University

  • JAMA 2016: trial showed LOWER likelihood of survival to discharge and worse neurological outcome for patients with in-hospital cardiac arrest treated with therapeutic hypothermia.
  • JAMA 2017: no mortality benefit for tracheal intubation during cardiac arrest – consider using LMA (quick placement and less compression interruption).

Running the Perfect Code

Michael Winters, MD; University of Maryland

  • Team leadership is key! (Take charge of your resuscitation. Assign roles prior to patient arrival.)
  • Early defibrillation
  • High-Quality CPR:
    • Highest rate of survival at 121-140 compressions/min.
      • Journal of Resuscitation: 120-140 compressions per minute (compared to ACLS taught 100-120) showed improved ROSC at this rate in the year 2017. Single center. Roughly 200 something patients.
    • 5-6 cm depth of compressions with appropriate recoil of chest wall.
    • Avoid leaning on the chest.
    • Chest compression fraction (percentage of time in which chest compressions are done by rescuers during cardiac arrest) should be greater than 60%; goal of 80%.
  • Hemodynamic-Directed CPR
    • Using femoral arterial line, aim for DBP >25-35 mmHg. This is also helpful for determining PEA vs pseudo-PEA.
    • Using end tidal CO2, aim for >20 mmHg.
    • Hold epinephrine if these parameters are met.
    • Aim for a coronary perfusion pressure (CPP = aortic diastolic pressure minus the left ventricular end-diastolic pressure) of >20 mmHg to attain ROSC. Need arterial and central line to obtain the CPP which may be difficult during a resuscitation. Instead, we can guide our resuscitations with the use of early arterial line placement and/or end tidal CO2.
  • Consider video laryngoscopy as first attempt in CPR because DL increases “no flow” time seen bc of holding compressions to optimize view.  Success rate is similar.
  • Code Medications: Epinephrine: ? evidence of efficacy.  There exists no definitive evidence of epi’s benefit to long term survival to date.
  • NEJM 2016:  Amiodarone vs Lidocaine vs Placebo in out of hospital cardiac arrest shockable rhythms:  NO DIFFERENCE.  However, there was a non-statistically significant trend towards benefit to hospital discharge in those getting amio or lido vs placebo.

ECHO Evaluation in Cardiac Arrest

Sarah A. Stahmer, MD; UNC

  • US can interrupt cardiac compressions. Need to use a focused approach to limit delay during CPR
  • Use ultrasound to evaluate pump, tank, pipes during the resuscitation
  • SHoC Study 
    • Look for the Four F’s:  Fluid (pericardial), Form (RV dilatation), Function (wall movement), Filling (IVC diameter
    • RUSH Exam – Rapid Ultrasound for Shock and Hypotension
    • FEEL Study
    • Asystole or PEA with any degree of wall movement had higher rate of survival
    • Use cardiac ultrasound to determine appropriate pacemaker capture; appropriate myocardial squeeze with capture.
    • A twitch in the heart muscle is not cardiac stand still.  Must be no cardiac muscle movement for standstill. However, valvular motion with cardiac stand still is considered cardiac death.
    • Sonographic asystole has a poor prognosis, but not no prognosis.  Small chance of survival exists.  If patient young, continue resuscitative efforts.  Older/Nursing home patients it may be reasonable to call the code.
    • Must consider all patient variables with continuation of resuscitative efforts.

A Rational Approach to PEA 

Laszio Littmann, MD; UNC

  • Almost impossible to remember all H’s and T’s during a code
  • New algorithm for PEA: Based on whether the QRS is Narrow or Wide
    • QRS Narrow:
      • Mechanical (RV) problem (tamponade, tension PTX, PE, mechanical hyperinflation) (US: hyperdynamic LV—PSEUDO PEA).  These patients may benefit from an intervention – fluids/phenylephrine/needle decompression etc. and not CPR.
    • QRS Wide:
      • Metabolic (LV) problem (HyperK, Na channel blocker tox) (US: Hypokinetic—TRUE PEA). These patients likely will benefit from CPR
      • Consider Phenylephrine (NOT Epinephrine) in pseudo-PEA (narrow QRS): 2-10 mcg/kg bolus. 200-500 mcg IVP over 10-30 seconds. May repeat in 10-15 minutes. Approximately 20-minute half-life. No scientific evidence behind using phenylephrine; Littmann’s personal experience.

Optimizing Post-Arrest Care

Joshua C. Reynolds, MD, MSU

  • Hard to share pearls considering detail of lecture
  • Best take home from this lecture is not to settle after initial resuscitation. Must consider domains of injury and phenotypes of injury. Direct care down to the cellular level.

Making ECMO a Reality in the ED

Zack Shinar, MD; San Diego

  • 8% survival to hospital discharge in cardiac arrests – number hasn’t moved in many years
  • JAHA 2016: 50% survival achieved by one hospital in Minnesota with wide use of ECMO
  • Arterial line for all cardiac arrest patients to monitor response
  • Getting ECMO in your ED: 1. Assess your capabilities; 2. Develop relationships (CT surg, Cardio, Intensive care); 3. Become a “professional proceduralist”

Where are we going?

Robert O’Connor, MD, MPH; University of Virginia

  • AHA 2012:  Dispatch pre-arrival instructions (on how to perform CPR until EMS arrives) improve survival in out of hospital cardiac arrest
  • Japan has a cardiac arrest registry. USA does not. Why??
  • Arterial line in codes – helpful in distinguishing PEA from pseudo-PEA.  Compressions may be harmful in the latter
  • What is a pulse?  Finger is not very accurate
  • Chain of Survival is key to appropriate care of out-of-hospital cardiac arrests
  • PulsePoint App for phone: allows those trained in BLS to know when they are close to an active cardiac arrest.
  • EMS Dispatcher guided CPR for bystanders
  • Prolonged prehospital care has increased patient mortality
  • Appropriate Cath lab activation for ROSC patients: refer to Mattu’s ECG weekly lecture.

Panel Discussion: 

  • Cool to 36 if mild sx moving around etc. Cool to 33 if in deep coma /sicker subset (Personal preference)
  • ECMO is reimbursed very well as long as your pt is insured
  • Fingers to palpate a pulse are not very good.  Ultrasound, arterial line, and end tidal may be better resources. One study done in prehospital setting with ultrasound in the field shows those with no pulse but ultrasound showing cardiac motion did better with Meds (pressors) verses starting compressions. These patients have “pseudo pea” bc they actually have a pulse you just can’t feel it.