UMEM Emergency Cardiology Symposium PEARLS

Posted on by David Traficante

View the recorded lectures here: https://livestream.com/UMEmergencyMed/EMCard2018

LBBB and Chest Pain in Acute MI…What Should I Do?

Dr. William Brady – University of Virginia

  • Patients with new LBBB on EKG is not common in the setting of Acute MI (AMI). It is, however, the most common pseudo-infarction pattern.
  • 80% of AMIs with LBBB are not detectable by ECG

Rational approach to AMI in patients with LBBB:

https://pdfs.semanticscholar.org/f80b/9983005179f4718bb1326963c722d4f80e58.pdf

Wonder Women: Exploring the Gender Gap in ACS

Dr. Susanne DeMeester – University of Michigan

  • Average age of women presenting with ACS is 71. This age lags men by about 7-9 years.
  • Women have a higher 1 and 5 year post ACS mortality compared to men
  • 20% of women with acute STEMI on their ECG will have a clean cath
    • Cardiac microvascular dysfunction more common in women
      • Smaller epicardial vessels
      • Increased stiffness
      • Smooth muscle dysfunction
    • Rupture embolic plaque causing STEMI more common in men
    • Coronary vasospasm equal between men and women
  • NSTEMI is more common in women
  • Dyspnea is the most common angina presentation in women and geriatric patients (not chest pain!)
  • Women more likely to complain of chest “discomfort” rather than “chest pain” or “chest pressure”
  • Women have additional risk factors that have a greater association with ACS:
    • Depression, anxiety, psychosocial environment
  • Women with low risk HEART Score have lower risk of 6 week major acute cardiac event (MACE) compared to men (2% vs 6.5%).
  • Women have a smaller degree of ST elevation in acute STEMIs compared to men and are likely to produce lower levels of troponin.
  • Remember the diagnosis of spontaneous coronary artery dissection (SCAD) in the young peripartum woman
    • Risk factors include pregnancy, OCPs, vascular and connective tissue disorders
    • High recurrence rate ~20%
  • Fibrinolytics in ACS – Women are more likely to bleed
  • Women historically have had delays to treatment, and have received non-guideline treatment: Be careful to recognize and appropriately treat ACS in men and women

“Un-Break My Heart”: 2018 NSTEMI Updates

Dr. Tarlan Hedayati – Cook County, Chicago

  • Not all elevated troponin equals ACS
    • PE, dissection, myocarditis, pericarditis
    • History and clinical context are extremely important
  • Some NSTEMIs will have complete vessel occlusion (~25% of the time)
    • These patients are more likely to have higher troponins
  • Main risk factors for ACS: HTN, DM, Hypercholesterolemia (including HDL<40), Family Hx, Tobacco use
    • Others risk factors: Cocaine abuse, HIV/AIDS, ESRD, SLE, RA, stress, exogenous testosterone
  • Clopidogrel (Plavix: pro-drug, needs activation) vs. ticagrelor (Brilinta: works immediately)
    • PLATO trial
      • Lower risk of MACE with Brilinta
      • No difference in bleeding complications between two groups
    • Lovenox vs Heparin
      • No major differences in outcomes
      • Consider using Heparin if patient will be going for upcoming catheterization
  • Three options of NSTEMI management
    • Ischemic guided (conservative management)
      • Wait, trend troponins and serial EKG
      • Better for low risk patients
    • Immediate invasive (Cath ASAP, should be within 1-2 hours)
      • Patients with: refractory angina, recurrent angina, sustained Vtach/Vfib, or those who are clinically or hemodynamically unstable
    • Routine invasive (cath within 24-72 hours)
      • Early (cath within 24 hours)
        • Patients with dynamic EKG changes, new ST depressions or rising troponins
      • Late/delayed (within 72 hours)
        • Patients with DM, CKD/ESRD, LVEF < 40%, CABG/PCI within last 6 months, patients who are post recent MI with chest pain
      • TIMACS study
        • Benefit with early cath only seen with high risk patients

The Crashing Kid

Dr. Mimi Lu – University of Maryland

  • There are 1 million adults with congenital heart defects.
  • 60% of congenital defects are missed on prenatal ultrasounds
  • Clinical findings of pediatric patients with congenital heart defects:
    • Central cyanosis, diastolic murmurs, delayed or difference pulses
    • Hepatomegaly is more common physical exam finding in pediatric patients with CHF (more common than lower extremity edema which is typically seen in adults)
    • Grunting = BAD in children
  • Cyanosis, poor feeding and/or tachypnea in first 7-14 days
    • Think sepsis, sepsis, sepsis (most common cause)
    • But also consider if this is a ductal dependent lesion
      • Typically present within the first 2 weeks of life
      • Hyperoxia test – check ABG on RA à apply 100% FiO2 for 10-15 min à recheck ABG
        • If PaO2 > 150mmHg = Lung problem
        • If PaO2 < 150mmHg = Cardiac problem
      • Quick and dirty hyperoxia test
        • Apply supplemental O2
        • If sats increase at least 5-10% = think Lung problem
        • If sats remain the same = think Cardiac problem
    • Workup
      • EKG – look for hypertrophy, abnormal axis, arrhythmias
      • CXR – look for cardiomegaly or pulmonary edema
        • It can be difficult to appreciate cardiomegaly in neonates (because of thymus, etc.)
        • Get a lateral film and use the anterior tracheal line to help determine if cardiomegaly
          • line parallel to anterior tracheal wall inferiorly to diaphragm – should NOT intersect heart; should NOT be pushed back to “hit” spine above diaphragm
      • Labs
        • BNP literature is weak, but can be considered
    • Initial Management of the Congenital Heart Disease pediatric patient
      • IV fluids – 10cc/kg
      • Maintain SpO2 80-85%
      • Prostaglandin (PGE-1) if considering ductal dependent lesion
        • Dose is 0.1mcg/kg/hr
        • Works within 10-15 minutes
        • Side effects: apnea, hypotension, fever
        • Historically most pts receiving PGE-1 are intubated however recent data supports watch and wait to see how the patients respond, but have RSI equipment ready
          • If transferring the patient to another facility after starting PGE-1 you should secure airway to avoid pt becoming apneic en route
      • Inotropes if shock (did not get into detail on which to use)
      • Furosemide if pulmonary edema (1mg/kg/dose)
      • Make sure to check blood sugar
      • Correct acidosis – early bicarb!
      • Optimize ionized calcium 

Diuretics in Acute Heart Failure: The Dark Side of the Force?

Dr. Peter Pang – Indianapolis EMS

  • Treatment of heart failure has not changed much over the past 40 years
    • Only additions are use of inotropes and nesiritide (recombinant BNP)
  • Patient outcomes have only slightly improved over past 40 years
    • Current data:
      • 75% = 5 yr mortality for patients admitted for CHF
      • 22% = 30 day rehospitalization rate of patients admitted for CHF
      • 8% = 30 day mortality for patients admitted for CHF
  • DOSE trial (2011)
    • No difference in patient outcomes using bolus vs. infusion of Lasix
    • Doubling (2-2.5x) the dose of patients home dose of Lasix ( continuing patients home dose) was associated with better symptom improvement and increased weight change at 72 hours. However there was no difference in mortality, hospital readmission, or ED visit. And there was increased risk of worsening renal failure with the higher dose.
  • Best practice appears to be doubling the oral dose of Lasix. You achieve better sx improvement and better urine output.  You may get a bump in the Creatine but this doesn’t seem to be worrisome as the patients do well.
  • Prospective Cohort Study ~1300 pts.  Loops that were given within 60 mins of arrival have less in Hosp mortality then delayed therapy. This study is suggestive that early therapy may benefit and is at least safe. Will need more studies to duplicate this finding.
  • The addition of captopril to combat the RAA system does not have sufficient evidence out at this time to recommend it.

The Evidence For and Against Epinephrine in CPR

Dr. Corey Slovis – Vanderbilt

  • Epi is a potent alpha and beta agonist
  • The evidence for use of epinephrine in cardiac arrest is weak and incomplete!
    • The case for or against epinephrine in CPR is embarrassingly not based on large randomized double-blind studies
    • Its use stems from a 1968 JAMA study on the use of epi in cardiac arrest of n=15 dogs
    • There is not good objective evidence, in controlled studies, that epinephrine is more effective than placebo
  • “High dose” epinephrine, of more than 1 mg per dose, significantly improves ROSC but not survival to discharge
    • The more you look into the data, the more higher dose of epinephrine looks bad
    • Also, reduced dose of epinephrine appears to offer no benefits
  • Early v. late use of epinephrine in cardiac arrest
    • Use epi as soon as possible (until its effectiveness is proven or disproven)
    • However, if patient is in VF/pVT, data supports waiting for the second shock prior to giving epi (better outcomes when compared to using after the first shock)
  • Try to space your repeat doses of epinephrine by longer intervals, not shorter ones
    • ACLS recommends epinephrine q3-5 min
    • It appears spacing doses out up to 8-10 minutes may be optimal, however this is a violation of current guidelines and no randomized study exists
    • Err on spacing out closer to the q5 minute mark
  • Epi given in shockable rhythms was 1/3 as effective in those patients that did not get epi in a post hoc analysis of a large trial (12% vs 32%)
  • Resuscitation 2018: 2255 pts got low dose epi in out-of-hospital cardiac arrest (0.5 mg).  Reduced dose didn’t cause a difference.
  • There is a London study coming out soon over >8,000 patients comparing epi vs. no epi for OHCA – should provide some useful information for use of epi in cardiac arrest.

Panel Discussion

  • RBBB does not prevent our ability to read an EKG like the LBBB does. You just have to look closely for the st elevation in that it can be more subtle. New RBBB in setting of an acute Mi is a bad prognostic sign.
  • Small group of pts who had pacers were studied with Sgarbossa criteria thus far. Seemed applicable to date. Bigger study by Dr Smith to be out soon that further looks into application of Sgarbossa criteria to paced individuals.
  • No data on continuous drip of epi verses bolus dose epi in cardiac arrest although some centers are doing this.
  • Cardiac Arrest with ROSC + NSTEMI – Should be indication for emergent cath (Also, Arrest with ROSC plus any of following: witnessed arrest with bystander CPR, initial rhythm VF/pVT)

Case of the Week COW #14

Posted on by David Traficante

Presenting Resident

Traficante

Chief Complaint

Cardiac arrest

Brief HPI

Hispanic male in his mid 30s who presented to the ED as John Doe after he was found unresponsive in the field with cardiac arrest. Unknown downtime. As per EMS endorsement from bystanders, the patient allegedly had a witnessed syncopal episode followed by seizure-like activity after which he became unresponsive. No bystander CPR. EMS arrived at the scene and found him pulseless, CPR started. On ALS arrival patient found to be in PEA. CPR, intubated, epi x 2, bicarb then ROSC achieved. Initial rhythm in ED was sinus tach on monitor. After 5 min in ED patient became bradycardic and went into PEA, compressions started, received epi x 1 w ROSC. Pt then went into wide complex tachycardia on monitor – SVT vs Vtach – pt was cardioverted 200J and given Amiodarone 150mg. Post cardioversion, rhythm changed to afib v aflutter. EKG was obtained after 10 min (below).

Pertinent PE and Vitals

On arrival: BP 81/50; P113; SpO2 95% ambubag 100% FiO2; Temp 37.0; BS 136

PE:
Gen: Unresponsive, intubated, occasional myoclonic jerks
HEENT: 2 cm hematoma right occiput, pupils constricted 1-2 mm b/l and non-reactive CV: tachycardic, s1/s2, no murmurs
Resp: Assisted breathing, good air entry b/l
Abd: Soft, NT
Neuro: GCS 3, has occasional myoclonic jerks

On admission: BP 153/83; P153; SpO2 98% on vent 100% FiO2

Pertinent Labs

ABG done on patient arrival = 6.80/86/253/14; Na+ 133; K+ 4.4, Ca++ 1.04; Glu 246, Lac 8.8, BE -10.2 These were the only labs available at the time of admission.

Pertinent Imaging/EKG

Case d/w Cardio fellow who came to evaluate pt at bedside, decision made to transfer pt directly to cath lab. EKG was repeated after 5 minutes prior to patient being transferred, which is shown below.

Working Diagnosis at time of Disposition

Cardiac Arrest
STEMI – possible LMCA, LAD or Triple vessel dx

ED & Hospital Course

Interventional cardiologist advised immediate transfer to cath lab for diagnostic cath (did not want to wait for CT Head). Cath showed normal coronaries with LVEF 75%.

Patient transferred to the CCU post cath. He was noted to have no brainstem reflexes off sedation. CT Head showed findings c/w anoxic encephalopathy, no bleed. Neuro was consulted who stated patient’s exams and further diagnostic studies were significant for loss of all cortical and brain stem function, consistent with brain death. Patient was pronounced on Day 10 (delay with identifying patient and determining NOK).

Pearls & Takeaways

Is ST-Segment Elevation in Lead aVR Getting Too Much Respect?

Introduction

ECG reading is all about pattern recognition. And this particular pattern of ST-Elevation in aVR with diffuse ST Depression is a very important ECG pattern that you must be able to recognize. But what’s probably more important than being able to recognize the pattern, is understanding what it represents. There appears to be a common misconception that the ST-Elevation in aVR always represents “STEMI”, or acute transmural (full- thickness) ischemia. If this were the case the patient would most likely be dead or at the very least in profound cardiogenic shock. The key to understanding what this pattern represents lies in understanding that the ST-Elevation in aVR is reciprocal to the diffuse ST-Depression – and that this diffuse ST-Depression represents global subendocardial ischemia. So the real question that you must answer is: What is causing the global subendocardial ischemia?

What Else can Cause STE in aVR that Won’t Benefit from Going to the Cath Lab?

Worrisome Diagnoses:

  • –  Thoracic Aortic Dissection
  • –  Massive Pulmonary Embolism
  • –  Massive Gastro Intestinal Hemorrhage

Non-Worrisome Diagnoses:

  • –  Left Bundle Branch Block (LBBB)
  • –  Left Ventricular Hypertrophy (LVH) with Strain Pattern
  • –  Severe Atrial Tachydysrhythmias (i.e. SVT)

It is critical to realize that more often than not the cause is global myocardial strain from a Non-ACS etiology! (profound sepsis, tachycardia, anemia, hypoxemia, etc). In our patient above it may have been because of the SVT he was in during the code in addition to being in Afib w/ RVR at the time of the ECG. It is also very important to understand that in these Non-ACS settings, you can see this pattern with or without underlying coronary artery disease.

But of course it could be ACS. And if it is, then you are dealing with Left Main, Proximal LAD, or even multi-vessel plaque instability. But keep in mind that even if it is ACS you are still dealing with subendocardial and not transmural ischemia.

Take Home Points

    1. STE in aVR Should be Concerning IF you have a patient with:
      1. Worrisome/Concerning Symptoms (Cardiopulmonary Symptoms) AND…
      2. ST-Segment Depression in Several Other Leads
    2. Don’t worry so much about STE 0.5mm or less in lead aVR, because it lacks specificity. Using 1.0mm or greater in lead aVR, has better specificity
    3. Patients with ACS due to LMCA Blockage, Triple Vessel Disease, or Proximal LAD Blockage will look “sick” due to global cardiac ischemia. This narrows the number of patients we would consider activating the cath lab for with STE in aVR.
    4. The key to ECG reading is pattern recognition. The pattern of ST-Elevation of at least 1mm in lead aVR + diffuse ST-Depression with a maximal depression vector towards leads II & V5 is a pattern you must know. It represents global subendocardial ischemia.
    5. When you see this pattern you should divide the differential for the diffuse subendocardial ischemia into two main categories: ACS vs Non-ACS. Do not automatically assume that it is ACS. I have seen this mistake made many times as ACS becomes the focus, at the expense of appropriate resuscitation addressing the underlying cause. It is very important to keep in mind that the etiology is far more likely to be Non-ACS than ACS!
    6. The key to determining the etiology is through history, physical exam, clinical picture, laboratory data, Echo, and vigilant monitoring and frequent reassessment. If you have identified and addressed potentially reversible causes of the ischemia, and the ECG pattern persists then you are dealing with ACS until proven otherwise.
    7. Refrain from using dual-antiplatelet therapy in these patients as there is a high likelihood they will require CABG.
    8. Remember that if this ECG pattern does represent ACS, the ST-Elevation in aVR is not the result of direct injury (or transmural ischemia) and that the ST-Elevation in aVR is reciprocal to the diffuse ST-Depression. Therefore these ACS cases do not represent a clear “STEMI”. However, while there is not great data to guide the timing of cath for these patients, I would advocate going to the cath lab with a much stronger sense of urgency than for other “NSTEMIs”. The reasoning is that ACS is a very dynamic process and without the advantage of optimal medical therapy (a second platelet inhibitor should be withheld) there is a higher chance of the culprit vessel suddenly occluding and evolving to transmural ischemia. If this happens in the Proximal LAD, Left Main, or in the setting of Multi-vessel involvement the myocardial territory in jeopardy is so large that there is a good chance the patient will arrest and die before any reperfusion can be established! If your patient looks sick or has persistent chest pain, they should be going to the cath lab ASAP.
    9. With diffuse subendocardial ischemia, you may not see any wall motion abnormality. Global function can even be normal, although it may be globally depressed as well. A normal bedside echo does not help in:
      1. differentiating the cause of the STE in aVR
      2. ruling out ACS

References: http://hqmeded-ecg.blogspot.com/2018/02/st-elevation-in-avr-with-diffuse-st.html

Pediatric Pearls – Bronchiolitis

Posted on by David Traficante 
Pathophysiology
  • Disorder that is commonly caused by a viral lower respiratory tract infection in infants
  • Characterized by acute inflammation, edema and necrosis of epithelial cells lining small airways and increased mucus production

  • Etiology
    • Coronavirus
    • Influenza
    • Rhino virus
    • Adenovirus
    • Parainfluenza virus
    • RSV (respiratory syncytial virus) – MOST COMMON!
  • Incidence – December-March
      • Most infections occur within first 2 years of life
      • About 40% experience lower respiratory infection during initial infection
      • RSV doesn’t grant permanent or long-term immunity – RE-INFECTION COMMON
      • The risk of significant viral or bacterial lower respiratory tract infection or pneumonia in an infant is low
  • Transmission
    • Direct contact with secretions
    • Young children shed virus for >2 weeks
    • 30-70% of household contacts become ill
  • Natural history
    • Begins with URI – Rhinorrhea, congestion, cough
    • Progresses to LRI in 2-6 days – Airway obstruction (tachypnea, wheezing, respiratory distress)
    • Variable and dynamic course
    • Lasts 2-4 weeks
Case

7-month-old male presents to the emergency room with his parents due to cough, runny nose, congestion and SOB that started 3 days ago.

VS: RR – 65, HR – 140, Temp – 99.1°F, O2 sat – 93% on RA

History
  • Typical Presentation of Bronchiolitis
    • Viral URI and cough with signs of lower respiratory tract infection
      • Work of breathing – grunting, nasal flaring, intercostal/subcostal retractions
      • Tachypnea
      • Wheeze
      • Coarse rales
Physical Exam
  • TIPS for a better exam
    • Upper airway obstruction can contribute to work of breathing
    • Suctioning and positioning may decrease the work of breathing and improve the quality of your examination
    • Counting respiratory rate over the course of 1 min is more accurate than shorter observations
  • Assess mental status, respiratory rate, work of breathing, oxygen status, listen to breath sounds, and assess hydration status

Diagnosis
  • DIAGNOSIS IS CLINICAL – NO LABS OR RADIOLOGICIAL STUDIES ARE NEEDED
    • When to consider CXR – if child has had >2 days of fever, an asymmetric chest exam, does not demonstrate improvement or has an unusually high O2 need
    • Diagnostic testing may be considered if:
      • Need cohorting – this is why we get testing for those we admit
      • Uncertain clinical diagnosis
      • Age <2 months
      • To assess for influenza – also needed this for those we admit
Management

Classify patient as mild, moderate, or severe based on the above physical exam

Mild Moderate Severe
1. Consider suction bulb

2. Discharge

 1. Suction bulb

2. No bronchodilators

3. Discharge or admit

 1. Suction bulb or wall

2. No bronchodilators

3. If no improvement consider starting high flow NC

4. Admit
  • Rehydration
    • IVF – moderately or severely dehydrated, secretions are thick and difficult to mobilize or severe respiratory distress
    • PO feeds – mildly to moderately dehydrated and can tolerate PO
  • Considerations for severely ill patients
    • Consider ONE TIME albuterol MDI trial if:
      • Severe respiratory distress OR
      • Increased risk for asthma
        • >12 months old, wheeze and once of the following
          • personal history of atopy or recurrent wheezing
          • strong family history of atopy or asthma
        • if responds to albuterol then consider switching to asthma pathway
      • Consider HFNC for significant hypoxia OR severe respiratory distress not improving with rigorous supportive care

 

Discharge criteria Admission criteria
–       Oxygen saturation >90%

–       Awake

–       Adequate oral intake

–       Mild/moderate work of breathing

–       Reliable caretaker

–       Able to obtain follow up care

–       MDI/spacer teaching if response to albuterol

 –       Admit if discharge criteria not met:

o   Inpatient: Requires 02 or progression expected

o   OBS: Mild disease with expected LOS < 24 hours

o   ICU: Apnea, severe distress; Requires HFNC / CPAP / intubation

–       Infants with these risk factors present early in the illness have higher risk of progression:

o   Gestational age < 34 weeks

o   Respiratory rate ≥ 70

o   Age < 3 months

 
Additional Notes
  • Differentiate infants with probable viral bronchiolitis from those with other disorders
  • The above management points to do take into consideration patients with significant medical history such as congenital heart disease, anatomic airway defects, neuromuscular disease, immunodeficiency, chronic lung disease – ADMIT, HIGH RISK!
  • The physical exam will vary from minute to minute depending on child’s position, level of alertness, response to treatment – CONSTANTLY RE-EVALUATE!
  • If patient presents within the first couple of days, they may worsen and need admission at a later point – PARENT EDUCATION IS KEY!
    • Viral illness, treated by hydration and suction
    • Signs of respiratory distress
    • How to suction
    • When to suction
    • Frequent feeds and watch hydration status
    • Cough may last 2-4 weeks, do not use OTC cough and cold medications
    • Avoid tobacco smoke
  • NOT RECOMMENDED!
    • Albuterol – Wheezing is due to the airways being clogged with debris not bronchospasm
    • Racemic epinephrine
    • Corticosteroids
    • Chest physiotherapy
    • Montelukast
    • Antibiotics
    • Hypertonic Saline
    • Routine testing
    • Chest X-rays

References

  1. http://pediatrics.aappublications.org/content/134/5/e1474
  2. http://www.chop.edu/clinical-pathway/bronchiolitis-emergent-evaluation-clinical-pathway
  3. http://www.cochrane.org/CD001266/ARI_bronchodilators-for-bronchiolitis-for-infants-with-first-time-wheezing
  4. http://www.seattlechildrens.org/healthcare-professionals/gateway/pathways/

Special thanks to Dr. Hima Khamar, MD PGY-2 for her contribution to this month’s Pediatric Pearls!

Varicella in Pregnancy

Posted on by David Traficante

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

Posted on by David Traficante

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

Posted on by David Traficante

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

Posted on by David Traficante

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

Euglycemic Diabetic Ketoacidosis: A Potential Complication of Treatment With Sodium–Glucose Cotransporter 2 Inhibition, Diabetes Care, Volume 38, September 2015

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)

Posted on by David Traficante

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

Posted on by David Traficante

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

Posted on by David Traficante

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.