Podcasts about hemodynamically

Show Notes Jeff: Welcome back to EMplify, the podcast corollary to EB Medicine’s Emergency Medicine Practice. I’m Jeff Nusbaum, and I’m back with my co-host, Nachi Gupta. This month, after a few months of primarily medical topics, we’re talking trauma, specifically Blunt Cardiac Injury: Emergency Department Diagnosis and Management. Nachi: With no gold standard diagnostic test and with complications ranging from simple ectopic beats to fulminant cardiac failure and death, this isn’t an episode you’ll want to miss. Jeff: Before we begin, let me give a quick shout out to our incredible group of authors from New York -- Dr. Eric Morley, Dr. Bryan English, and Dr. David Cohen of Stony Brook Medicine and Dr. William Paolo, residency program director at SUNY Upstate. I should also mention their peer reviewers Drs. Jennifer Maccagnano and Ashley Norse of the NY institute of technology college of osteopathic medicine and UF Health Jacksonville, respectively. Nachi: This month’s team parsed through roughly 1200 articles as well as guidelines from the eastern association for surgery in trauma also known as EAST. Jeff: Clearly a large undertaking for a difficult topic to come up with solid evidence based recommendations. Nachi: For sure. Let’s begin with some epidemiology, which is admittedly quite difficult without universally accepted diagnostic criteria. Jeff: As you likely know, despite advances in motor vehicle safety, trauma remains a leading cause of death for young adults. In the US alone, each year, there are about 900,000 cases of cardiac injury secondary to trauma. Most of these occur in the setting of vehicular trauma. Nachi: And keep in mind, that those injuries don’t occur in isolation as 70-80% of patients with blunt cardiac injury sustain other injuries. This idea of concomitant trauma will be a major theme in today’s episode. Jeff: It certainly will. But before we get there, we have some more definitions to review - cardiac concussion and contusion, both of which were defined in a 1989 study. In this study, cardiac concussion was defined as an elevated CKMB with a normal echo, while a cardiac contusion was defined as an elevated CKMB and abnormal echo. Nachi: Much to my surprise, though, abnormal echo and elevated ck-mb have not been shown to be predictive of adverse outcomes, but conduction abnormalities on ekgs have been predictive of development of serious dysrhythmia Jeff: More on complications in a bit, but first, returning to the idea of concomitant injuries, in one autopsy study of nearly 1600 patients with blunt trauma - cardiac injuries were reported in 11.9% of cases and contributed to the death of 45.2% of those patients. Nachi: Looking more broadly at the data, according to one retrospective review, blunt cardiac injury may carry a mortality of up to 44%. Jeff: That’s scary high, though I guess not terribly surprising, given that we are discussing heart injuries due to major trauma... Nachi: The force may be direct or indirect, involve rapid deceleration, be bidirectional, compressive, concussive, or even involve a combination of these. In general, the right ventricle is the most frequently injured area due to the proximity to the chest wall. Jeff: Perfect, so that's enough background, let’s talk differential. As you likely expected, the differential is broad and includes cardiovascular injuries, pulmonary injuries, and other mediastinal injuries like pneumomediastinum and esophageal injuries. Nachi: Among the most devastating injuries on the differential is cardiac wall rupture, which not surprisingly has an extremely high mortality rate. In terms of location of rupture, both ventricles are far more likely to rupture than the atria with the right atria being more likely to rupture than the left atria. Atrial ruptures are more survivable, whereas complete free wall rupture is nearly universally fatal. Jeff: Septal injuries are also on the ddx. Septal injuries occur immediately, either from direct impact or when the heart becomes compressed between the sternum and the spine. Delayed rupture can occur secondary to an inflammatory reaction. This is more likely in patients with a prior healed or repaired septal defects. Nachi: Valvular injuries, like septal injuries, are rare. Left sided valvular damage is more common and carries a higher mortality risk. In order, the aortic valve is more commonly injured followed by the mitral valve then tricuspid valve, and finally the pulmonic valve. Remember that valvular damage can be due to papillary muscle rupture or damage to the chordae tendineae. Consider valvular injury in any patient who appears to be in cardiogenic shock, has hypotension without obvious hemorrhage, or has pulmonary edema. Jeff: Next on the ddx are coronary artery injuries, which include lacerations, dissections, aneurysms, thrombosis, and even MI secondary to increased sympathetic activity and platelet activity after trauma. In one review, dissection was the most commonly uncovered pathology, occurring 71% of the time, followed by thrombosis, which occured only 7% of the time. The LAD is the most commonly injured artery followed by the RCA. Nachi: Pericardial injury, including pericarditis, effusion, tamponade, and rarely rupture, is also certainly on the differential. Jeff: In terms of dysrhythmias, sinus tachycardia is the most common dysrhythmia, with other rhythms, including PVC / PAC / and afib being found only 1-6% of the time. Nachi: And while conduction blocks are rare, a RBBB is the most commonly noted, followed by a 1st degree AVB. Jeff: Though also rare, commotio cordis deserves it’s own section as its the second most common cause of death in athletes < 18 who are victims of blunt trauma. Though only studied in swine models, it’s hypothesized that the impact to the chest wall during T-wave upstroke can precipitate v-fib. Nachi: Aortic root injuries usually occur at the insertion of the ligamentum arteriosum and isthmus. Such injuries typically result in aortic insufficiency. Jeff: And the last pathology on the differential requiring special attention is a myocardial contusion. Again, no standard definition exists, with some diagnostic criteria including simply chest pain and increasing cardiac enzymes, and others including cardiac dysfunction, ecg abnormalities, wall motion abnormalities, and an elevation of cardiac enzymes. Nachi: Certainly a pretty broad differential… before moving on to the work up, Jeff why don’t you get us started with prehospital care? Jeff: Prehospital management should focus on rapid identification and stabilization of life threatening injuries with expeditious transport as longer prehospital times have been associated with increased mortality in trauma. Immediate transport to a Level I trauma center should be the highest priority for those with suspected blunt cardiac injury. Nachi: In terms of who specifically should be transporting the patient, a Cochrane review evaluated the utility of ALS vs BLS transport in trauma. There is reasonably good data to support BLS over ALS, even when controlling for trauma severity. Moreover, when airway management is needed, advanced airway techniques by ALS crews were associated with decreased odds of survival. Regardless of who is there, the message is the same: focus not on interventions, but instead on rapid transport. Jeff: And if it does happen to be an ALS transport crew, without delaying transport, pain management with fentanyl is both safe and reasonable and preferred over morphine. Post opiate hypotension in prehospital trauma patients is a rare but documented complication. Nachi: And if the prehospital team is lucky enough, or maybe unlucky enough, i don’t know, to have a credentialed provider who can perform ultrasound for those suspected of having a blunt cardiac injury, the general prehospital data on ultrasound is sparse. As of now, it’s difficult to conclude if prehospital US improves care for trauma patients. Jeff: Interestingly, the system I work in has prehospital physicians, who do carry US, but I can’t think of a major trauma where ultrasound changed any of the decisions we made. Nachi: Right, and I think that just reinforces the main point here: there may be a role, we just don’t have the data to support it at this time. Jeff: Great, let’s move onto ED care, beginning with the H&P. Nachi: On history, make sure to elucidate if there is any chest pain, and if it’s onset was before or after the traumatic event. In addition, make sure to ask about dyspnea, fatigue, palpitations, and lightheadedness. Jeff: And don’t forget to get the crash details from the EMS crew before they depart! As a side note, for anyone taking oral boards in a few months, don’t forget to ask the EMS crew for the details!!! Nachi: A definite must for oral boards and for your clinical practice. Jeff: In terms of the physical, tachycardia is the most common abnormality in blunt cardiac injury. In those with severe injury, you may note refractory hypotension secondary to cardiogenic shock. But don’t be reassured by normal vitals, especially in the young, who may be compensating well despite being quite ill. Nachi: Fully undress the patient to appropriately inspect and percuss the chest wall - looking for signs of previous cardiac surgeries or pacemaker placement, as well as to auscultate for new murmurs which may be a sign of valvular injury. Jeff: Similarly, as concomitant injuries are common, inspect the abdomen, looking for ecchymosis patterns, which often accompany blunt cardiac injury. Nachi: Pretty standard stuff. Let’s move on to diagnostic testing. Jeff: Lab testing should include a CBC, BMP, coags, troponin, lactate, and T&S. In one retrospective analysis, an elevated troponin and a lactate over 2.5 were predictors of mortality. Nachi: Additionally, in patients with chest trauma, a troponin > 1.05 was associated with a greater risk for dysrhythmias and LV dysfunction. Jeff: And it likely goes without saying, but an EKG is a must on all trauma patients with suspicion for blunt cardiac injury in accordance with the EAST guidelines. New EKG findings requires admission for monitoring. Unfortunately, on the flip side, an ECG cannot be used to rule out blunt cardiac injury. Nachi: Diving a bit deeper into the data, in a prospective study of 333 patients with blunt thoracic trauma, serial EKG and troponins at 0, 4, and 8 hours post injury had a sensitivity and specificity of 100% and 71%, respectively. However, of those with abnormal findings, all but one had them on initial testing, leading to a negative predictive value of 98%. Jeff: Well that’s an impressive NPV and has huge implications, especially in the era of heavily monitored lengths of stay... Nachi: Definitely. In terms of radiography, a chest x-ray should be obtained as rib fractures, hemopneumothorax, and mediastinal free air are all things you wouldn't want to miss and are also associated with blunt cardiac injury. Jeff: Keep in mind, however, that the chest x-ray should not be seen as a test for pericardial fluid as up to 200 mL of fluid can be contained in the pericardial space and remain undetectable by chest radiograph. Nachi: Which is why you’ll have to turn to our good friend the ultrasound, for more useful data. The data is strong that in the hands of trained Emergency Clinicians, when parasternal, apical, and subcostal views are obtained, US has an accuracy of 97.5% for pericardial effusion. Jeff: Not only is US accurate, it’s also quick. In one RCT, the FAST exam reduced the time from arrival in the ED to operative care by 64% in the setting of trauma. Nachi: That’s impressive -- for expediting patient care and for managing ED flow. Jeff: Exactly. The authors do note however that hemopericardium is a rare finding, so, while not the focus of this article, the real utility of the FAST exam may be in its expanded form, the eFAST, in which a rapid bedside ultrasonographic lung exam for pneumothorax is included, as this can lead to immediate changes in management. Nachi: And assuming you do your FAST or eFAST and have no management changing findings, CT will often be your next test. Jeff: Yeah, EKG-gated multidetector CT can easily diagnose myocardial rupture, pneumopericardium, pericardial rupture, hemopericardium, coronary artery insult, ventricular septal defects and even valvular dysfunction. Unfortunately, CT does not perform well for the evaluation of myocardial contusions. Nachi: This is all well and good, and certainly accurate, but let’s not forget that hemodynamically unstable trauma patients, like those with myocardial rupture, need to be in the operating room, not the CT scanner. Jeff: An important point that should not be understated. Nachi: And the last major testing modality to discuss is the echocardiogram. Jeff: The echo is a fantastic test for detecting focal cardiac dysfunction often see with cardiac contusions, hemopericardium, and valve disruption. Nachi: And it’s worth noting that transthoracic is enough, as transesophageal, despite the better images, hasn’t been shown to change management. TEE should be saved for those in whom a optimal TTE study isn’t feasible. Jeff: Great point. And one last quick note on echo: in terms of guidelines, the EAST guidelines from 2012 specifically recommend an echo in hemodynamically unstable patients or those with a persistent new dysrhythmia without other sources of ongoing hemorrhage or neurologic etiology of instability. Nachi: Perfect, so that wraps up testing and imaging for our blunt cardiac injury patient. Let’s move on to treatment. Jeff: In terms of initial resuscitation, there is an ever increasing body of literature to support blood transfusion over crystalloid in patients requiring volume expansion in trauma. There are no specific guidelines for transfusion in the setting of blunt cardiac injury, so stick to your standard trauma protocols. Nachi: It is worth noting, though, that there is literature outside of trauma for those with pericardial effusions, suggesting that those with a SBP < 100 have substantial benefit from volume expansion. So keep this in mind if your clinical suspicion is high and your trauma patient has a soft but not truly shocky blood pressure. Jeff: Operative management, specifically ED thoracotomy is a heavily debated topic, and it’s next on our list to discuss. Nachi: The 2015 EAST guidelines conditionally recommend ED thoracotomy for moribund patients with signs of life. The Western Trauma Association broadens the ED thoracotomy window a bit to include anyone with no signs of life but less than 10 minutes of CPR. The latter also recommend ED thoracotomy in those with refractory shock. Jeff: Though few studies exist on the topic, in one study of 187 patients, cardiac motion on US was 100% sensitive for predicting survivors. Nachi: Not great data, but it does support one's decision to stop any further work up should there be no cardiac activity, which is important, because the decision to pursue an ED thoracotomy is not an easy one. Jeff: And lastly, emergent pericardiocentesis may be another option in an unstable patient when definitive operative management is not possible. But do note that pericardiocentesis is only a temporizing measure, and not definitive for cardiac tamponade. Nachi: Treatment for dysrhythmias is standard, treat in accordance with standard ACLS protocols, as formal randomized trials on prophylaxis and treatment in the setting of blunt cardiac injury do not exist. Jeff: Seems reasonable enough. And in the very rare setting of an MI after blunt cardiac injury, you should involve cardiology, cardiothoracic surgery, and trauma to help make important management decisions. Data is, again, lacking, but the patient likely needs percutaneous angiography for appropriate diagnosis and potentially further intervention. Definitely hold off on ASA and likely nitroglycerin, at least until significant bleeding has been ruled out. Nachi: Yup, no style points for giving aspirin to a bleeding trauma patient. Speaking of medications, the last treatment modality to discuss here is pain control. Pain management is essential with chest injuries, as appropriate pain management has been shown to reduce mortality in pulmonary related complications. Jeff: And in line with every acute pain consult note I’ve ever come across, a multimodal approach utilizing opioids and nonopioids is recommended. Nachi: Perfect, so that sums up treatment, next we have one special circumstance to discuss: sternal fractures. Cardiac contusions are found in 1.8-2.4% of patients with sternal fractures, almost all of which were seen on CT and not XR according to the NEXUS chest CT study. Of these patients, only 2 deaths occured, both due to cardiac causes.  Thus, in patients with isolated sternal fractures, negative trops, ekg, and negative cxr - the patient can likely be discharged from the ED, as long as their pain is well-controlled. Jeff: And let’s talk controversies for this issue. We only have one to discuss: MRI. Nachi: The fact that MRI produces awesome images is not controversial, see figure 3. It’s role, however, is. In accordance with EAST guidelines, MRI may be most useful in differentiating acute ischemia from blunt cardiac injury in those with abnormal ECGs, elevated enzymes, or abnormal echos. It’s use in the hyperacute evaluation, however, is limited, in large part owing to the length of time required to complete an MRI Jeff: What a time to be alive that we even have to say that MRIs may not have a hyperacute role in trauma - absolutely crazy... Nachi: Moving on to disposition: any patient with aortic, pericardial, or myocardial injury and hemodynamic instability needs operative evaluation and likely intervention, so do not hesitate to get the consults coming or the helicopter in the air should such a patient arrive at your non-trauma center. Jeff: And in those that are hemodynamically stable, with either a positive ECG or a positive trop, they should be monitored on telemetry. There is no clear answer as to how long, but numerous studies suggest a 24 hour period of observation is sufficient. For those with persistent ekg abnormalities or rising trops - this is precisely when you will want to pursue echocardiography. Nachi: And if there are positive EKG findings AND a rising trop, they should be admitted to a step down unit or ICU as well -- as ⅔ of them will develop myocardial dysfunction. Similarly, those with hemodynamic instability but no active traumatic bleeding source - they too should be admitted to the ICU for a STAT echo and serial enzymes. Jeff: But in the vast majority of patients, those that are hemodynamically stable with negative serial EKGs and serial tropinins, they can effectively be ruled out for significant BCI after an 8 hour ED observation period, as we mentioned earlier with a sensitivity approaching 100%! Nachi: Though there are, of course, exceptions to this rule, like those with low physiologic reserve, mobility or functional issues, or complex social situations, which may need to be assessed on a more case-by-case basis. Jeff: Let’s wrap up this episode with some key points and clinical pearls. Cardiac wall rupture is the most devastating form of Blunt Cardiac Injury. The sealing of a ruptured wall may lead to a pseudoaneurysm and delayed tamponade. Trauma to the coronary arteries may lead to a myocardial infarction. The left anterior descending artery is most commonly affected. The most common arrhythmia associated with blunt cardiac injury is sinus tachycardia. RBBB is the most commonly associated conduction block. Commotio cordis is the second most common cause of death in athletes under the age of 18. Early defibrillation is linked to better outcomes. Antiplatelet agents like aspirin should be avoided in blunt cardiac injury until significant hemorrhage has been ruled out. An EKG should be obtained in all patients with suspected blunt cardiac injury. However, an EKG alone does not rule out blunt cardiac injury. Serial EKG and serial troponin testing at hours 0, 4, and 8 have a sensitivity approaching 100% for blunt cardiac injury. An elevated lactate level or troponin is associated with increased mortality in blunt cardiac injury. Perform a FAST exam to assess for pericardial effusions. FAST exams are associated with a significant reduction in transfer time to an operating room. Obtain a chest X-ray in all patients in whom you have concern for blunt cardiac injury. Note that the pericardium is poorly compliant and pericardial fluid might not be detected on chest X-ray. Transesophageal echocardiogram should be considered when an optimal transthoracic study cannot be achieved. CT is used routinely in evaluating blunt chest trauma but know that it does not evaluate cardiac contusions well. In acute evaluation, MRI is generally a less useful imaging modality given the long imaging time. There is evidence to suggest that a patient with an isolated sternal fracture and negative biomarkers and negative EKG findings can be safely discharged from the ED if pain is well-controlled. Trauma to the aorta, pericardium, or myocardium is associated with severe hemodynamic instability. These patients need surgical evaluation emergently. Hemodynamically stable patients with a positive troponin test or with new EKG abnormalities should be observed for cardiac monitoring. Nachi: So that wraps up Episode 26 on Blunt Cardiac Injury! Jeff: Additional materials are available on our website for Emergency Medicine Practice subscribers. If you’re not a subscriber, consider joining today. You can find out more at ebmedicine.net/subscribe. Subscribers get in-depth articles on hundreds of emergency medicine topics, concise summaries of the articles, calculators and risk scores, and CME credit. You’ll also get enhanced access to the podcast, including any images and tables mentioned. You can find everything you need to know at ebmedicine.net/subscribe. Nachi: It’s also worth mentioning for current subscribers that the website has recently undergone a major rehaul and update. The new site is easier to use on mobile browsers, has better search functionality, mobile-friendly CME testing, and quick access to the digest and podcast. Jeff: And as those of us in the north east say goodbye to the snow for the year, it’s time to start thinking about the summer and maybe start planning for the Clinical Decision Making conference in sunny Ponta Vedra Beach, Fl. The conference will run from June 27th to June 30th this year with a pre-conference workshop on June 26th. Nachi: And the address for this month’s credit is ebmedicine.net/E0319, so head over there to get your CME credit. As always, the [DING SOUND] you heard throughout the episode corresponds to the answers to the CME questions. Lastly, be sure to find us on iTunes and rate us or leave comments there. You can also email us directly at EMplify@ebmedicine.net with any comments or suggestions. Talk to you next month! Most Important References 7.* Clancy K, Velopulos C, Bilaniuk JW, et al. Screening for blunt cardiac injury: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg. 2012;73(5 Suppl 4):S301-S306. (Guideline) 22.* Schultz JM, Trunkey DD. Blunt cardiac injury. Crit Care Clin. 2004;20(1):57-70. (Review article) 23.* El-Chami MF, Nicholson W, Helmy T. Blunt cardiac trauma. J Emerg Med. 2008;35(2):127-133. (Review article) 27.* Bock JS, Benitez RM. Blunt cardiac injury. Cardiol Clin. 2012;30(4):545-555. (Review article) 34.* Berk WA. ECG findings in nonpenetrating chest trauma: a review. J Emerg Med. 1987;5(3):209-215. (Review article) 64.* Velmahos GC, Karaiskakis M, Salim A, et al. Normal electrocardiography and serum troponin I levels preclude the presence of clinically significant blunt cardiac injury. J Trauma. 2003;54(1):45-50. (Prospective; 333 patients) 73.* Melniker LA, Leibner E, McKenney MG, et al. Randomized controlled clinical trial of point-of-care, limited ultrasonography for trauma in the emergency department: the first sonography outcomes assessment program trial. Ann Emerg Med. 2006;48(3):227-235. (Randomized controlled trial; 262 patients)

Myocardial infarction (MI) in children is uncommon, but underdiagnosed.  This is due to two main factors: the etiologies are varied; and the presenting symptoms are “atypical”. We need a mental metal detector!  Case examples Congenital Two main presentations of MI due to congenital lesions: novel and known.  The novel presentation is at risk for underdiagnosis, due to its uncommonness and vague, atypical symptoms.  There are usually some red flags with a careful H&P.  The known presentation is a child with a history of congenital heart disease, addressed by corrective or palliative surgery.  This child is at risk for expected complications, as well as overdiagnosis and iatrogenia.  Risk stratify, collaborate with specialists. The fussy, sweaty feeder: ALCAPA Anomalous Left Coronary Artery from the Pulmonary Artery (ALCAPA) is an example of what can go wrong during fetal development: any abnormality in the number, origin, course, or morphology of the coronary arteries can present as a neonate with sweating during feeds (steal syndrome), an infant in CHF, or an older child with failure to thrive or poor exercise tolerance. The stable child with chest pain: myocardial bridge Normal coronary arteries run along the epicardial surface of the heart, with projections into the myocardium.  If part of the artery’s course runs within the myocardium (i.e. the artery weaves into and/or out of the myocardium), then there is a myocardial bridge of the coronary artery.  With every systolic contraction, the artery is occluded.  Although a myocardial bridge may not cause symptoms (especially at distal portions), the area it supplies is at risk. With any minor trauma or exertion, demand may outpace supply, resulting in ischemia.  Diagnosis is made on coronary angiography. The unwell child post-cardiac surgery: Fontan problems The child with single ventricle physiology may have a Norwood procedure at birth (creation of a neoaorta, atrial septectomy, and Blalock-Taussig shunt), a Bidirectional Glenn procedure at 3-6 months (shunt removed, superior vena cava connected to pulmonary arteries), and a Fontan procedure at about 2-3 years of age (inferior vena cava blood flow is shunted into the pulmonary arteries). These children depend on their preload to run blood passively into the pulmonary circuit; afterload reduction is also important to compensate for a poor left ejection fraction, as well as to avoid the development of pulmonary hypertension.  They are typically on an anticoagulant (often aspirin), a diuretic (e.g. furosemide), and an afterload reduction agent (e.g. enalapril).  Any disturbance in volume status (hyper- or hypovolemia), anticoagulation, or afterload may cause myocardial strain or infarction.  Take the child s/p Fontan seriously and involve his specialists early with any concerns. Autoimmune The body’s inflammatory-mediated reaction to a real or perceived insult can cause short- and long-term cardiac sequelae.  Find out how well the underlying disease is controlled, and what complications the child has had in the past. The red, hot, crispy, flaky child: acute Kawasaki disease Kawasaki disease (KD) is an acute systemic vasculitis, diagnosed by the presence of fever for five or more days accompanied by four or more criteria:  bilateral conjunctival injection, mucositis, cervical lymphadenopathy, polymorphous rash, and palmar or sole desquamation.  The criteria may occur (and disappear) at any time during the illness. Infants are under double jeopardy with Kawasaki Disease.  They are more likely to have incomplete KD (i.e. not fulfill strict criteria) and if they have KD, they are more likely to suffer the dangerous consequences of aneurysm formation (chiefly coronary arteries, but also brain, kidney).  Have a low threshold for investigation. Treatment includes 2 g/kg/day IVIG and high-dose aspirin (30-50 mg/kg/day) acutely, then low-dose aspirin (5 mg/kg/day) for weeks to months.  Regular and long-term follow-up with Cardiology is required. The aftermath: sequelae of Kawasaki disease The family and child with a history of KD may have psychological trauma and continuous anxiety about the child’s risk of MI.  Approximately 4.7% of children who were promptly diagnosed and correctly treated will go on to have cardiac sequelae. Children who have no detected cardiac sequelae by 8 weeks, typically continue to be asymptomatic up to 20 years later.  Smaller aneurysms tend to regress over time, especially those < 6 mm. Thrombi may calcify, or the lumen may become stenotic due to myofibroblast proliferation.  Children with any coronary artery dilatation from KD should be followed indefinitely. Giant aneurysms (≥8 mm) connote the highest risk for MI.  Parents often are concerned about recurrence, and any subsequent fever can be distressing.  There is a low rate of recurrence for KD: approximately 2%.  Infants who have coronary aneurysms are at the highest risk for recurrence. The older child with vague chest complaints and hypercoagulability: Systemic Lupus Erythematosus and Anti-Phospholipid Syndrome Up to 15% of cases of SLE begin in childhood.  Adult criteria are used, with the caveat that the diagnosis of SLE in children can be challenging; many children only manifest a few of the criteria initially before going on to develop further systemic involvement. The Systemic Lupus International Collaborating Clinics (SLICC) revised the criteria in 2012.  The patient should have ≥4/17 clinical and/or immunologic criteria.  The clinical criteria are: acute cutaneous (malar); chronic cutaneous (discoid); oral; alopecia; synovitis; serositis; renal; neurologic; hemolytic anemia; leukopenia; or thrombocytopenia.  The immunologic criteria are: ANA; anti-dsDNA; anti-Sm; antiphospholipid; low complement; and/or Direct Coombs (in absence of hemolytic anemia).  At least one criterion should be clinical, and at least one should be immunologic.  Children with antiphospholipid syndrome (APS) may occur with or without SLE.  Patients are at risk for venous and arterial thrombi formation.  APS may also cause structural damage, such as valvular thickening and valvular nodes (Libman-Sacks endocarditis).  Mitral and aortic valves are at the highest risk. Although most children with chest pain will not have MI, those with comorbidities should be investigated carefully. Trauma Direct, blunt trauma to the chest can cause myocardial stunning, dysrhythmias, or an asymptomatic rise in Troponin I.  However, some children are at risk for disproportionate harm due to a previously unknown risk factor.  Clinically significant cardiac injury occurs in up to 20% of patients with non-penetrating thoracic trauma. The motor vehicle collision: blunt myocardial injury Direct trauma (steering wheel, airbag, seatbelt), especially in fast acceleration-deceleration injury, may cause compression of the heart between the sternum and the thoracic spine. Electrocardiography (ECG) should be performed on any patient with significant blunt chest injury.  A negative ECG is highly consistent with no significant blunt myocardial injury. Any patient with a new abnormality on ECG (dysrhythmia, heart block, or signs of ischemia) should be admitted for continuous ECG monitoring. Elevation in troponin is common, but not predicted.  A solitary elevated troponin without ECG abnormality is of unclear significance.  Author’s advice: obtain troponin testing if there is an abnormal ECG, more than fleeting suspicion of BCI, and/or the child will be admitted for monitoring. Hemodynamically labile children should be resuscitated and a stat transesophageal echocardiogram obtained. The high-velocity object: coronary artery dissection or thrombus Direct trauma (e.g. MVC, baseball, high-velocity soccer ball) may cause damage to the left anterior descending artery or left circumflex artery, at the highest risk due to their proximity to the chest wall.  Thrombosis and/or dissection may result, often presenting in a focal pattern of ischemia on the ECG. Echocardiography may reveal valvular damage related to the injury, as well as effusion and ejection fraction.  Since there is often a need to investigate the coronary anatomy, percutaneous coronary intervention (PCI) is recommended. The minor trauma with disproportionate complaint: myocardial bridge As mentioned in the congenital section (above), a known variation of a coronary artery’s course involves weaving in and out of the myocardium, creating a baseline risk for ischemia.  Even minor trauma in a child with a myocardial bridge may cause acute thrombus, or slow stenosis from resulting edema.  Unfortunately, the presence of myocardial bridging is often unknown at the time of injury.  Approximately 25% of the population may have myocardial bridging, based on autopsy studies. Take the child seriously who has disproportionate symptoms to what should be a minor injury. Hematologic Coagulopathic and thrombophilic states may predispose children to focal cardiac ischemia.  The best documented cormorbidity is sickle cell disease, although other pro-thrombotic conditions also put the child at risk. The child with sickle cell disease and chest pain: when it’s not acute chest syndrome Sickle cell disease (SCD) can affect any organ system, although the heart is traditionally considered a lower-risk target organ for direct sickling and ischemia.  The major cardiac morbidity in sickle cell is from strain, high-output failure and multiple, serial increases in myocardial demand, causing left ventricular hypertrophy and congestive heart failure. However, there is mounting evidence that acute myocardial ischemia in sickle cell disease may be underappreciated and/or attributed to other causes of chest pain. Other cardiac sequelae from SCD include pulmonary hypertension, left ventricular dysfunction, right ventricular dysfunction, and chronic iron overload. Evidence of myocardial ischemia/infarction in children with SCD has been demonstrated on single-photon emission computed tomography (SPECT) scan. The puffy faced child with chest pain: nephrotic syndrome hypercoagulability Children who suffer from nephrotic syndrome lose proteins that contribute to the coagulation cascade.  In addition, lipoprotein profiles are altered: there is a rise in the very low-density lipoproteins (LDL), contributing to accelerated atherosclerosis.  Typically nephrotic patients have normal levels of high-density lipoproteins (HDL), unless there is profuse proteinuria. Children with difficult-to-control nephrotic syndrome (typically steroid-resistant) may form accelerated plaques that rupture, causing focal MI, as early as school age. The previously well child now decompensated: undiagnosed thrombophilia Asymptomatic patent foramen ovale (PFO) is the cause of some cases of cryptogenic vascular disease, such as stroke and MI.  However, the presence of PFO alone does not connote higher risk.  When paired with an inherited or acquired thrombogenic condition, the venous thrombus may travel from the right-sided circulation to the left, causing distal ischemia.  Many of these cases are unknown until a complication arises. The chronically worried, now with a reason: hypercholesterolemia A family history of adult-onset hypercholesterolemia is not necessarily a risk factor for early complications in children, provided the child does not have the same acquired risk factors as adults (e.g. obesity, sedentary lifestyle, smoking, etc).  Parents may seek help in the ED for children with chest pain and no risk factors, but adult parents who have poor cholesterol profiles. The exception is the child with familial hypercholesterolemia, who is at risk for accelerated atherosclerosis and MI. Infectious Myocarditis has varied etiologies, including infectious, medications (chemotherapy agents), immunologic (rheumatologic, transplant rejection), toxins (arsenic, carbon monoxide, heavy metals such as iron or copper), or physical stress (electrical injury, heat illness, radiation). In children, the most common cause of myocarditis is infectious (viruses, protozoa, bacteria, fungal, parasites).  Of these, viral causes are the most common (adenovirus, enterovirus, echovirus, rubella, HHV6). The verbal child may complain of typical chest complaints, or may come in with flu-like illness and tachycardia or ill appearance out of proportion to presumed viral illness. The most common presenting features in children with myocarditis are: shortness of breath, vomiting, poor feeding, hepatomegaly, respiratory distress, and fever. The infant in shock after a ‘cold’: myocarditis Beware of the poor feeding, tachycardic, ill appearing infant who “has a cold” because everyone else around him has a ‘cold’.  That may very well be true, but any virus can be invasive with myocardial involvement.  Infants are only able to increase their cardiac output through increasing their heart rate; they cannot respond to increased demands through ionotropy.  Look for signs of acute heart failure, such as hepatomegaly, respiratory distress, and sacral edema. The child with tachycardia out of proportion to complaint: myocarditis The previously healthy child with “a bad flu” may simply be very symptomatic from influenza-like illness, or he may be developing myocarditis.  Look for chest pain and tachycardia out of proportion to presumed illness, and constant chest pain, not just associated with cough. The “pneumonia” with suspicious chest x-ray: myocarditis Acute heart failure may mimic viral pneumonia.  Look for disproportionate signs and symptoms. Toxins Younger children may get into others’ medications, be given dangerous home remedies, take drugs recreationally, have environmental exposures (heavy metals), suffer from a consequence of a comorbidity (iron or copper overload) or have adverse events from generally safe medications. The hyperactive boy with a hyperactive precordium: methylphenidate Attention deficit hyperactivity disorder (ADHD) is growing in rate of diagnosis and use of medications.  As the only medical diagnosis based on self-reported criteria, many children are given stimulants regardless of actual neurologic disorder; with a higher proportion of children exposed to stimulants, adverse effects are seen more commonly. Methylphenidate is related to amphetamine, and they both are dopaminergic drugs.  Their mechanisms of action are different, however.  Methylphenidate increases neuronal firing rate.  Methamphetamine reduces neuronal firing rate; cardiovascular sequelae such as MI and CHF are more common in chronic methamphetamine use. Although methylphenidate is typically well tolerated, risks include dysrhythmias such as ventricular tachycardia. The child with seizure disorder and chest pain: anti-epileptics Some anti-epileptic agents, such as carbamazepine, promote a poor lipid profile, leading to atherosclerosis and early MI.  Case reports include school-aged children on carbamazepine who have foamy cells in the coronary arteries, aorta, and vasa vasorum on autopsy.  It is unclear whether this is a strong association. The spice trader: synthetic cannabinoids Synthetic cannabinoids are notoriously difficult to regulate and study, as the manufacturers label them as “not for human consumption”.  Once reports surface of abuse of a certain compound, the formula is altered slightly and repackaged, often in a colorful or mysterious way that is attractive to teenagers. The misperceptions are: are a) synthetics are related to marijuana and therefore safe and b) marijuana is inherently “safe”. Both tend to steer unwitting teens to take these unknown entities.  Some suffer MI as a result. Exposure to tetrahydrocannabinol (THC) in high-potency marijuana has been linked to myocardial ischemia, ventricular tachycardia, and ventricular fibrillation.  Marijuana can increase the heart rate from 20-100%, depending on the amount ingested. K2 (“kush 2.0”) or Spice (Zohai, Genie, K3, Bliss, Nice, Black Mamba, fake weed, etc) is a mixture of plant leaves doused in synthetic chemicals, including cannabinoids and fertilizer (JWH-108), none of which are tested or safe for human consumption.  Synthetic cannabinoids have a higher affinity to cannabinoid receptors, conferring higher potency, and therefore worse adverse effects.  They are thought to be 100 to 800 times more potent as marijuana. Bath salts (Purple Wave, Zoom, Cloud Nine, etc) can be ingested, snorted, or injected.  They typically include some form of cathinone, such as mephedrone, similar to the substance found in the naturally occurring khat plant. Hallucinations, palpitations, tachycardia, MI, and dysrhythmias have been reported from their use as a recreational drug. Chest pain with marijuana, synthetic cannabinoid, or bath salt ingestion should be investigated and/or monitored. Riding that train: high on cocaine Cocaine is a well-known cause of acute MI in young people.  In addition to the direct stimulant causes acutely, such as hypertension, tachycardia, and impaired judgement (coingestions, risky behavior), chronic cocaine use has long-term sequelae.  Cocaine causes accelerated atherosclerosis.  That, in conjunction with arterial vasospasm and platelet activation, is a recipe for acute MI in the young. Cranky: methamphetamine Methamphetamine is a highly addictive stimulant that is relatively inexpensive and widely available.  Repeated use causes multiple psychiatric, personality, and neurologic changes.  Risky behavior, violence, and motor vehicle accidents are all linked to this drug.  Like cocaine, methamphetamine may cause fatal dysrhythmias, acute MI from demand ischemia, and long-term sequelae such as congestive heart failure. Summary Acute MI is a challenging presentation in children: Easily missed: uncommon and atypical Varied etiology Respect vague symptoms with a non-reassuring H&P Try to detect it: CATH IT! References Congenital AboulHosn JA et al. Fontan Operation and the Single Ventricle. Congenit Heart Dis. 2007; 2:2-11. Aliku TO et al. A case of anomalous origin of the left coronary artery presenting with acute myocardial infarction and cardiovascular collapse. African Health Sci. 2014; 14(1): 23-227. Andrews RE et al. Acute myocardial infarction as a cause of death in palliated hypoplastic left heart syndrome. Heart. 2004; 90:e17. Canale LS et al. Surgical treatment of anomalous coronary artery arising from the pulmonary artery. Interactive Cardiovascaulr and Thoracic Surgery. 2009; 8:67-69. Güvenç O et al. Correctable Cause of Dilated Cardiomyopathy in an Infant with Heart Failure: ALCAPA Syndrome. J Curr Pediatr. 2017; 15:47-50. Hastings RS et al. 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Cardiac Arrest following a Myocardial Infarction in a Child Treated with Methylphenidate. Case Reports Pediatr. 2015; AID 905097. Rezkalla SH et al. Cocaine-Induced Acte Mycardial Infarction. Clin Med Res. 2007; 5(3):172-176. Schelleman H et al. Methylphenidate and risk of serious cardiovascular events in adults. Am J Psychiatry. 2012 Feb;169(2):178-85. Sheridan J et al. Injury associated with methamphetamine use: a review of the literature. Harm Reduction Journal, 2006; 3(14):1-18. Stiefel G et al. Cardiovascular effects of methylphenidate, amphetamines and atomoxetine in the treatment of attention-deficit hyperactivity disorder. Drug Saf. 2010 Oct 1;33(10):821-42.   This post and podcast are dedicated to Edwin Leap, MD for his sanity and humanity in the practice of Emergency Medicine.  Thank you, Dr Leap for all that you do.

Hemodynamically unstable pelvic fractures are a talk-and-die situation. These folks require aggressive, rapid treatment if they are going to survive the injury. Inspired by my mentor, Thomas Scalea, I discuss the management of the unstable pelvic trauma patient.