by Hassan Chaudhary, INOVA Fairfax
Desiree Seeyave, Children's National on the Hot Seat
Case edited by Emily Willner
Here is the EKG in question:
Here's How You Answered Our Questions
What does this EKG suggest?
LESS than 3 yrs PEM experience n=12
MORE than 3 yrs PEM experience n=11
The distribution between pericarditis, early repolarization, and acute MI were similarly distributed between the the two experience groups. Most people thought this EKG reflected pericarditis with the smallest percentage thinking that this was an acute MI.
LESS than 3 yrs PEM experience n=9
MORE than 3 yrs PEM experience n=12
The largest portions of people in both groups wanted an emergent cardiology evaluation based on the history, exam, and EKG findings. But the second largest portion of people in both groups wanted only a non-emergent evaluation just prior to discharge. Another slightly smaller subset was comfortable with waiting until the cardiac enzymes to make a decision. Presumably, this means that results of cardiac enzymes would determine the level of concern for this patient.
Thank you to Dave and Jennifer for offering your opinions. One person thought it looked like an inferior MI while the other thought perhaps pericarditis. Desiree, our Hot Seat attending this week, breaks down what is worrying and reassuring about this patient, offers her approach to chest pain, gives her interpretation of the EKG, and notes the concern with using nitroglycerin and inferior wall MI. For their complete comments click here.
What does it look like?
"I'm no expert, but it looks like an inferior MI to me. I would go down the STEMI pathway and get the kid out of my ED in a timely fashion (to a place where he could potentially get a therapeutic cath)." -Dave Mathison, Children's National
"Quick ddx for pericarditis: viral (large majority), autoimmune illness (SLE, JIA), uremia, MI. He is adopted, so ask about TB status. Ask about exposure to histoplasmosis- as we learned yesterday, ask about barns and caves. Bacterial: he would be much sicker and febrile." -Jennifer Chapman, Children's National
A diagnostic and management approach
"My practical approach would be: IV, nitro-, morphine, oxygen, CXR." -Dave Mathison, Children's National
Labs: cbc, esr, crp, cmp, cardiac enzymes, no blood cx, ?viral titers for coxsackie, EBV, influenza, echovirus, HIV (check this with Cards, but probably not necessary). CXR. Echo from Cardiology colleague, may try myself first. -Jennifer Chapman, Children's National
Too call or not to call cardiology
"I wouldn't consult cardiology because I don't have a question for them." -Dave Mathison, Children's National
"Since the patient is uncomfortable but otherwise shows no tachycardia and no narrowed pulse pressure and no hypotension, I don't feel urgency about consulting Cardiology, but would put them in the loop while waiting for labs." -Jennifer Chapman, Children's National
From the Hot Seat
by Desiree Seeyave, Children's National
Red flags in the history of this patient that point to a possible cardiac cause of pain include:
1. Sudden onset
2. Radiation to the neck
3. “pressure”-like (I think ischemia with all of these)
4. SOB
Factors that point to a noncardiac cause include:
1. It started at rest
2. Worse with laying down (typical of pericarditis)
3. No diaphoresis
4. No syncope
The denial of substance abuse does not preclude getting a urine drug screen as cocaine, marijuana and amphetamines are well known to cause coronary vasospasm, angina, and ischemia.
Obtaining an EKG +/- CXR in most pediatric patients with chest pain are “low risk, high yield” in terms of ruling out pathology of the heart and lungs, as well as giving parental and patient reassurance if these are normal.
His VS are stable, with a bradycardia that may be normal due to his age and gender. The lack of reproducible chest wall tenderness raises another red flag for me, however not all cases of muscular pain have chest wall tenderness. The normal cardiovascular exam and lack of hepatomegaly is reassuring but does not rule out cardiac causes of chest pain.
The EKG shows normal sinus rhythm, HR 54, normal left inferior axis, normal PR interval, normal QTc of 0.34, and normal QRS duration of 0.08 seconds. The morphology of the QRS complex shows Q-waves in leads II, III and aVF, as well as ST elevation in these leads as well as aVR, aVF, V2-6. Pathologic Q-waves are > 0.04 seconds in duration and > 25% of the total QRS amplitude, hence the Q-waves seen in III and aVF seem to be pathologic.
The inverted T waves in leads V1 and V2 are normal for age. The other T waves have normal morphology. There is normal R-wave progression from V1 to V6. There is also a deep S wave in V1, Q-wave in III but no T-inversion in III (the S1Q3T3 pattern typical of PE, but seen in only about 20% patients), and no R-axis deviation or diffuse T-wave inversions that are more typical of PEs.
The pattern shown on EKG could indicate an inferior wall MI (Q-waves in III and aVF, ST elevation in II, III and aVF), however the diffusely elevated ST elevation in most leads could indicate an inflammatory process such as pericarditis vs benign repolarization with J-point elevation seen commonly at this age. The lack of tachycardia or any other arrhythmias are reassuring but do not definitively rule out an MI.
Since the EKG points to a possible inferior wall MI, I would rule this out first. I would obtain cardiac enzymes, urine drug screen and inflammatory markers of ESR/CRP while consulting cardiology emergently. A CXR should be done to assess for cardiomegaly which could be due to dilated cardiomyopathy, a pericardial effusion, or pulmonary causes of chest pain such as pneumothorax.
The acute treatment of acute MI includes MONA (morphine, O2, nitroglycerin, aspirin). The patient should be placed on O2 to optimize cardiac muscle oxygenation and pain control with morphine if needed to decrease anxiety and improve cardiac coronary perfusion. I would consider giving nitroglycerin after cardiology consultation as nitrates in inferior wall MIs can precipitate profound hypotension. Although rare, cardiac ischemia in children can occur from undiagnosed coronary abnormalities such as ALCAPA or ALCA from the right coronary sinus, or coronary fistulas. Getting cardiology on board early to perform ECHO and cardiac catheterization is essential to preserving cardiac muscle and function.
If the cardiac enzymes are normal, they should be repeated in 3 hours, and serial EKGs should be obtained. If there is elevation in ESR/CRP, this may point to peri/myocarditis. If all the labs are normal, then the diffuse ST-elevation may just be caused by early repolarization and the patient can be reassured. If he continues to have chest pain and SOB despite proper pain medication with NSAIDS, further workup may be needed e.g. to rule out a PE.
Denouement
by Hassan Chaudhary, Inova Fairfax
This patient initially presented to an outside ED with the above EKG which was interpreted as infero-lateral STEMI. He had received aspirin, nitro and morphine at the outside hospital prior to his transfer. His troponin was positive at 0.72 ng/mL (normal less than 0.01), myoglobin was 271 ng/mL (normal less than 96), and CKMB was 37.4 ng/mL (normal less than 3.6). At the time of transfer, he was mostly pain free. A repeat EKG still showed significant infero-lateral ST segment elevations (more prominent than in other leads). At our hospital when it was repeated, the troponin I was 13.37 ng/mL (normal less than 0.09). He was seen by cardiologist and, in consultation with them and an adult Cardiologist, the decision was made to take him to cath (with an adult interventional cardiologist) for possible intervention in presumed STEMI. His coronaries were normal on cath other than a non-signifcant LAD muscle bridge, though he did have mild global hypokinesis noted, and some ectopy (run of Vtach), when they were injecting the LAD with contrast, that spontaneously resolved.
The patient was admitted to the pediatric intensive care unit where he remained pain free. A cardiac echo was performed the following day and was found to be normal with no cardiac artery anomalies. Infectious disease was also consulted for possible infectious causes, but none were identified. His troponin peaked at 19.87 ng/mL and on the day of discharge was 6.7 ng/mL. An electrocardiogram on discharge showed resolution of ST segment elevations with flipped T-waves in the inferior leads. The patient was discharged from the PICU after 2 days on famotidine and ibuprofen. The patient followed up with cardiology and infectious disease. In follow up with cardiology one week after discharge, the patient reported no new or recurrent symptoms. Echocardiography was normal. The EKG still showed inverted T waves in leads III and aVF, and the patient was ultimately thought to have myopericarditis.
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The Hot Seat is a recurrent online case series aimed at facilitating asynchronous sharing of PEM knowledge and experience. Faculty are placed on The Hot Seat and publish their opinions without knowing the case or its outcomes. Cases are based on real cases and written by PEM fellows at Children's National in DC, Johns Hopkins in MD, and INOVA Fairfax in VA to highlight teaching points. Emily Willner is the faculty advisor for the Hot Seat.
Huh. It seems as if the final diagnosis kind of includes everything. :)
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