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Attendings:
Jen Reed & Nathan Timm

Holly Hanson, Adam


Vukovic & Paria Wilson

D.H.

Setting

Liberty Emergency Department

HPI

17 yo previously-well male with no significant


PMH
URI symptoms x 1 week
Rhinorrhea
Nasal

congestion

Three days of vomiting and diarrhea


Progressive decreased activity

D.H.
Vomiting

Has become regular


Cant keep anything down, including clears
NBNB
UOP now decreased and concentrated

Diarrhea

Loose, BID
No mucous, no blood
Watery

D.H.
Now with decreased activity, progressive shortness
of breath and difficulty breathing
Mid- to upper-back pain with deep inspiration
Pleuritic chest pain
Feels as though heart is racing at times
PMH

Healthy, no chronic medical conditions, no daily


medications
ASA

with most recent illness x 2, nasal decongestant


No recreational drug or steroid usage

Immunizations UTD

D.H.
FHx

Family recalls taking turns being ill with similar URI


symptoms over the last week, described as viral cold
Symptoms typically lasted 2-3 days, then progressively
improved

ROS

Other than stated, notes mild headache and dizziness


with standing. No fever.

Vital

signs

T 36.7 C, HR 146, BP 113/73, RR 30, SpO2 98%

At this point
We

asked Jen and Nathan if they had


any clarifying questions theyd like to
ask our patient
Additionally, we asked what key physical
examination findings they would be
looking for

Jen
History Clarification
Any travel?
Any

trauma?

History

of rash?

Difficulty
What

breathing?

is mild orthostatic symptoms..dizziness,


syncope, etc. Orthostatic by HR or BP, both or neither.

Jen
Most Important PE Findings
Overall Appearance
Cardiovascular (esp M/R/G)
Pulmonary
Abdomen
GU Examination

Additionally:

Hydration status?
Edema?
Rash?

Nathan
History Clarification
Does position make breathing worse?
How

did he sleep?

What
Why

is his weight?

the aspirin? Any other possible


ingestion? Exposures? Organophosphates?

10

Nathan

Temp source?
Skin/eyes (icterus?)
HEENT (big erythematous tonsils?)
Abdomen (HSM?)
Edema of extremities?
Cardiac (MRG?)
Pulmonary (Edema?)

11

What we asked
Differential

Diagnosis
Top Diagnosis
What labs?
What imaging?
What would you do in the meantime?

12

Labs

13

D.H.s Labs

14

15

16

17

Discussion with Jen & Nathan

18

D.H.s Course in ED
Initially

given degree of tachycardia,


concern for shock so given 1L NS bolus
with response in HR to 130s-140s
Initial labs: CBC, renal, LFTs, CXR, EKG,
screening labs for sepsis (lactate/PCT)
Given additional 500ml bolus when
response in HR seen and perfusion
improved

19

D.H.s Course in ED
Signed

out to oncoming provider


After review of imaging/labs, D-dimer
ordered
Concern for PE
Bedside echo with concern for
depressed LV function
After speaking with cardiology, transfer
to base ED

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Additional Labs in ED

21

Echo
Dilated

cardiomyopathy
Severely dilated LV with global severely depressed left
ventricular function (left ventricular ejection fraction 1015%)

Abnormal parameters of left ventricular diastolic function

Severely

dilated left atrium (left atrial volume =


60mL/m^2)
Qualitatively mildly dilated right atrium and right ventricle
Qualitatively severely depressed RV systolic function
Mild MR & TR
Bidirectional PFO
Trivial posterior pericardial effusion

22

D.H.s Hospital Course


Admit

to CICU
LVAD placement 1/29/15 (10 days post
arrival)

EF 20% despite LVAD

Underwent

heart transplant (4/25/15)

23

Causes of Pump Dysfunction


Cardiomyopathy
Myocarditis
Myocardial infarction/ischemia

Arrhythmogenic

Anthracycline

Noncardiac causes

Neonatal Complete heart block with bradycardia (think SLE)


Supraventricular or ventricular tachycardia

Drug/toxin exposure

Anomalous left coronary artery arising off the pulmonary artery (ALCAPA)

Sepsis
Renal failure

Congenital heart disease

Hsu DT, Pearson GD. Heart failure in children: part I: history, etiology, and pathophysiology. Circ Heart Fail 2009; 2:65.

24

Cardiomyopathy
Most

common cause of heart failure in


children with structurally normal hearts
51% dilated, 42% hypertrophic, 3%
restrictive, 4% unspecified

Myocarditis
Viral inflammation of heart muscle leading to
either complete recovery of LV function or dilated
cardiomyopathy
At least of all cases of DCM are caused by
myocarditis

Lipshultz SE, Sleeper LA, Towbin JA, et al. The incidence of pediatric cardiomyopathy in two regions in the United States. N Eng J Med 2003;
348:1647.

25

Classification of
Myocarditis

Fulminant: preceded by viralprodromethen


followed by sudden onset severe HD compromise

Acute: less distinct onset, less severe HD


compromise but worse outcome

Better outcomes so early recognition is necessary


Death or resolves spontaneously

Present with established ventricular dysfunction


Complete resolutionvsDCM

Chronic: > 3months, insidious, recurrent & latent

Becomes fibrotic and progresses to DCM

Rose, N.R., Myocarditis: infection versus autoimmunity. J Clin Immunol, 2009. 29(6): p. 730-7.

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Presentations of Mycocarditis

Respiratory (32%): rhinorrhea, cough, SOB

Tachypnea, retractions,gruntingbronchiolitis, asthma


MC presentation of kids < 10 years of age

Cardiac (29%): chest pain,palpitations, sudden death

Tachycardia was present in 73% of kids < 10 years of age

Hypoperfusion(22%): lethargy, lightheaded, dizzy,


syncope, seizure
Kawasaki associated (10%)
GI (6%): nausea, vomiting, diarrhea, abdominal pain

Nausea/vomiting +/- diarrheagastro (giving too much


fluids makes it worse)

Freedman, S.B., et al., Pediatric myocarditis: emergency department clinical findings and diagnostic evaluation, in Pediatrics2007: United States. p.
1278-85.

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Screening Tests in the ED

CXR: cardiomegaly, pulmonary venous congestion,


pleuraleffusion

EKG: axis deviation, decreased ventricular voltages, ST


segment or T wave abnormalities, atrial enlargement,
ventricular enlargement, heart block, infarction

Cardiomegaly is a late finding if it does occur


Sensitivity: 55%

Presence ofQTcprolongation, Q waves, or LBBBpoor outcome


Depending on the type of viral illness, the EKG findings may vary
Sensitivity: 93%

Utility of viral serology remains unproven

Mahfoudet al investigated viral serologyvsEMB viral genomes,


only 5/124 matched

Kindermann, I., et al., Update on myocarditis, in J Am Coll Cardiol2012, 2012 American College of Cardiology Foundation. Published by Elsevier Inc: United States. p. 779-

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Labs (n=31)

Freedman, S.B., et al., Pediatric myocarditis: emergency department clinical findings and diagnostic evaluation, in Pediatrics2007: United States. p.

29

Diagnosis

Echo: increased ventricular ESV or EDV, decreased


EF/shortening fraction, AV valveregurgitation,wall
motion abnormalities

If neither CXR or EKG demonstrate features of


myocarditis, then echo is likely unnecessary
Unless clinical suspicion for myocarditis is very high

Cardiac MRI: allows visualization of the myocardium


(edema within it) and identifies the patchy nature of
the lesions

Mahrholdtet al did a study of 32ptswith suspected


myocarditisEcho + MRI yielded a PPV of 71% and NPV
of 100%

Mahrholdt, H., et al.,Cardiovascular magnetic resonance assessment of human myocarditis: a comparison to histology and molecular pathology, inCirculation2004: United
States. p. 1250-8.

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Management Goals
Cardiovascular

Inotropic support
Afterload reduction
Arrhythmia management
Tissue oxygenation

Respiratory

Mechanical ventilation

FEN

Bolusesvsdiuretic therapy

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Inotropic Support
Dopamine:

1& 1dose dependent, renal

vasodilation
Dobutamine:1&SVR, increased oxygen
supply to the coronaries, significantHR is a SE
Epinephrine:1& 1dose
dependent,arrhythmogenic
Milrinone: PDE inhibitor that improves
contractility, diastolic function and afterload
reduction
Start thinking about mechanical support

Uhl, T.L.,Viral myocarditis in children, inCritCare Nurse2008: United States. p. 42-63; quiz 64.

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Arrhythmia management
Ventricularectopy,tachycardias, heart block
If occur, will cause further deterioration of
ventricular function
Adenosine: slows conduction through AV
node for SVT
Amiodarone: inhibits adrenergic stimulation
Lidocaine: suppresses automaticity of the
conduction system
Heart block for >2 weeks: pacemaker

Uhl, T.L.,Viral myocarditis in children, inCritCare Nurse2008: United States. p. 42-63; quiz 64.

33

Respiratory Management
Positive

Pressure Ventilation (PPV) or


mechanical ventilation
Decreases work of breathing & reduces
afterload
Monitor ABGs, ETCO2

Uhl, T.L.,Viral myocarditis in children, inCritCare Nurse2008: United States. p. 42-63; quiz 64.

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FEN Management
Preserve

preload and ventricular filling


without overloading
Lasixgttto slowly remove excess fluid
to improve intravascular volume

Uhl, T.L.,Viral myocarditis in children, inCritCare Nurse2008: United States. p. 42-63; quiz 64.

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Additional Management
Options
ECMO

Usually used in patients with sustained


ventricular arrhythmias or children whose
survival is thought to be less than 20%
ECMO can increase this survival rate to up to
60%
Generally effective only for 10-14 days, beyond
which the rate of transplant disqualifying
complications rises dramatically
Risks: clots (on heparin), infection, IVH, renal
failure

Morales, D.L., et al., Bridging children of all sizes to cardiac transplantation: the initial multicenter North American experience with the Berlin Heart EXCOR ventricular assist
device, in J Heart Lung Transplant2011, 2011 International Society for Heart and Lung Transplantation. Published by Elsevier Inc: United States. p. 1-8.

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Additional Management
Options

Left Ventricular Assist Device

Help to complement what little intrinsic


function the heart already has
There is a membrane separating the air
chamber from the blood chamber
Air pulses moves the membrane, allowing
blood to move in and out of the ventricle
Machine is heparinized to prevent clot
formation
Risks: high BP, stroke, infection

Jansen, P., et al., In vitro haemocompatibility of a novel bioprosthetic total artificial heart, in Eur J Cardiothorac Surg2012: Germany. p. e166-72.

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