Life Saver Edition: Tranexamic Acid

By Christina Creel-Bulos, MD and Enyo Ablordeppey, MD MPH

TXA Background

Anti-fibrinolytics were first introduced by a husband and wife team of Japanese researchers searching for a product that would help prevent maternal mortality associated with postpartum hemorrhage. In the 1960’s, they invented the first anti-fibrinolytic agent, Episilon Aminocaproic Acid (eACA). Initial efforts demonstrated the need for more potent anti-fibrinolytics and lead to the identification of what is now known as Tranexamic Acid (TXA). Initially this was marked as a medication for menorrhagia and bleeding after dental extractions, but further research in the utilization of this medication proved to be significantly astounding!

TXA molecule, ball and stick representation

TXA molecule, ball and stick representation

What is TXA?

TXA was originally described as a chemical able to inhibit the enzymatic breakdown and degradation of fibrin by plasmin. It is an amino acid (lysine) analog that binds to the lysine-binding site on plasminogen; thus preventing the conversion of plasminogen into plasmin and blocking clot breakdown. Although its utilization began in the 1960’s, it was not until 2010 when studies demonstrated a mortality benefit in trauma patients.

TXA has the highest hypothetical benefit during the trauma induced “Lethal Triad” of death, which describes the implications of hypothermia and acidosis on coagulation. It has been cited that for every degree decrease from core temperature, coagulation factor activity decreases by 10%. Acidosis contributes to this triad by reducing Factor Xa, platelet counts, and fibrinogen levels; thus further highlighting the importance of fibrin clot preservation by using an antifibrinolytic such as TXA.

TXA stops the conversion of plasminogen to plasmin

TXA stops the conversion of plasminogen to plasmin


In 2010, the Clinical Randomization of an Antifibrinolytic in Significant Hemorrhage (CRASH-2) trial was released and its findings lead to its inclusion in the World Health Organization (WHO) list of essential medications. This international, randomized control and multi-centered trial enrolled 20,000 trauma patients-cited to be at risk for “significant hemorrhage”- from 274 hospitals and 40 different countries. It cited an absolute risk reduction (ARR) in mortality of 1.5% with a number needed to treat (NNT) of 65. A subgroup analysis further cited a mortality risk reduction (RR) from bleeding at different timelines from initial injury. Risk reductions at less than 1 hour, 1 to 3 hours, and greater than 3 hours were cited at: 0.68, 0.79, and 1.44 respectively with NNT 125. (CRASH 2 collaborators et al, 2010)

The (Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) study released in 2012 was a retrospective cohort analysis of 896 military trauma patients. A multivariate logistical analysis of a subgroup of patients who met criteria for activation of massive transfusion, demonstrated that TXA was independently associated with reduced mortality with an odds ratio (OR) for survival of 7.23 (Morrison et al, 2012).

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TXA for Peripartum Hemorrhage

The release of the World Maternal Antifibrinolytic (WOMAN) trial in 2017 marked increase interest in the utilization of TXA in obstetrical populations to reduced post partum hemorrhage (PPH). This randomized control trial consisting of 20,000 females diagnosed with PPH-after vaginal or cesarean delivery from 193 hospitals across 21 countries and found that death due to bleeding was reduced in patient who received 1g of TXA within three hours of delivery compared with placebo( ARR 0.4% and NNT 267).

Simonazzi et al performed a systemic review and meta-analysis of randomized control trials in 2016 regarding TXA in the peripartium population. Researchers identified 9 trials consisting of 2365 females and noted a significant decrease in: PPH rates, frequency of severe PPH, decrease in post partum blood loss, hemoglobin depreciation, and utilization of medications to increase uterine tone in those who received TXA prior to c-section compared with those who did not. Additionally there was not a significant difference in incidence of thromboembolic events between either group (Simonazzi et al 2016).


Expansion of TXA Utilization

Since these initial studies introducing TXA for traumatic indications, data evaluating expanded utilization of TXA has been cited in gynecological, gastrointestinal, orthopedic and Spinal literature. For example:

Wang et al noted trends towards reduced: total blood loss, transfusion requirements, and duration of surgery (Wang et al, 2017) in patients receiving TXA perioperatively after open myomectomy.  Orthopedic surgery literature has additionally begun investigating the utilization of anti-fibrinolytics in their practice. Although additional data is needed, a systematic review of randomized control trials also demonstrated a decrease in transfusion requirements and blood loss in patients undergoing total hip replacement or total knee arthroplasty given TXA without an increased risk in VTE  in both study groups (Kagoma et al, 2009). [EA1]  Finally, additional research to examine TXA utilization in Traumatic Brain Injury (TBI) patients after a systematic review of TXA utilization in patients with TBI/Intracerebral hemorrhage showed decreased ICH regression in patients receiving TXA but did not statistically change clinical outcomes (Zehtabchi et al, 2014).

As this data and clinical implications continue to be discovered and developed, be on the look out for more exciting discoveries in this realm and keep in mind that TXA is not simply limited to cases with Trauma!

As always….Happy Resuscitating!

Works Cited

CRASH-­‐2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-­‐2): a randomised, placebo-­‐controlled trial. Lancet. 2010 Jul3;376(9734):23-­‐32.

CRASH-­‐2 collaborators. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-­‐2 randomised controlled trial. Lancet. 2011 Mar 26;377(9771):1096-­‐101, 1101.

Morrison JJ, Dubose JJ, Rasmussen TE, Midwinter MJ. Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study. Arch Surg. 2012 Feb;147(2):113-­‐9.

Simonazzi G, Bisulli M, Saccone G, Moro E, Marshall A et al. Tranexamic acid for preventing postpartum blood loss after cesarean delivery: a systematic review and meta-analysis of randomized controlled trials. Acta Obstet Gynecol Scand. 2016 Jan;95(1):28-37.

Wang D, Wang L,  Wang Y, Lin X. The efficiency and safety of tranexamic acid for reducing blood loss in open myomectomy: A meta-analysis of randomized controlled trials. Medicine. 2017; 96 (23): e7072.

Shakur H, Roberts I, Fawole B, Chaudhri R et al. Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial. Lancet Glob Health. 2018 Feb;6(2):e222-e228. doi: 10.1016/S2214-109X(17)30467-9.

Kagoma YK, Crowther MA, Douketis J, Bhandari M, Eikelboom J, Lim W. Use of antifibrinolytic therapy to reduce transfusion in patients undergoing orthopedic surgery: a systematic review of randomized trials. Thromb Res. 2009 Mar;123(5):687-96.

Winter SF, Santaguida C, Wong J, Fehlings M. Systemic and Topical Use of Tranexamic Acid in Spinal Surgery: A Systematic Review. Global Spine Journal. 2016; 6 (3): 284-95.

Zehtabchi S, Abdel Baki SG, Falzon L, Nishijima DK. Tranexamic acid for traumatic brain injury: a systematic review and meta-analysis. Am J Emerg Med. 2014 Dec;32(12):1503-9.

Kini RM, Koh CY. Metalloproteases Affecting Blood Coagulation, Fibrinolysis and Platelet Aggregation from Snake Venoms: Definition and Nomenclature of Interaction Sites. Toxins. 2016; 8(10):284.


Epoprostenol in the ED--Go with the Flolan?

By Emily Harkins, MD MPH & Brian Fuller, MD MSCI

The Setting

It’s the middle of one of the worst influenza seasons on record, and your hospital is packed to the gills. The private physician dining area of the cafeteria has been repurposed to treat patients. Every ICU bed is taken, and there are fourteen patients boarding in the ED while waiting on an ICU bed.

EMS then arrives to your ED with a 47-year-old woman who has a peripheral oxygen saturation (SpO2) of 91% on 15 liters per minute via non-rebreather mask. She was recently admitted for an ERCP, and her husband called 911 after she had two days of worsening abdominal pain at home and finally collapsed in the bathroom this evening. When EMS arrived, she was pale, diaphoretic, and her SpO2 on room air was 85%. She opens her eyes to voice and intermittently follows some commands, but she’s somnolent and breathing 40 times per minute. A quick portable chest x-ray shows this:

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Your early working diagnosis is that this patient is septic, likely from an intra-abdominal source. Her bedside cardiac ultrasound shows hyperdynamic ventricular function, with under-filled ventricles. Your interpretation of her chest x-ray is: bilateral alveolar infiltrates; this xray, along with the hypoxia and preserved cardiac function means your patient has acute respiratory distress syndrome (ARDS).

Because of the hypoxia while on non-rebreather, you pre-oxygenate the patient with non-invasive ventilation (BiPap settings: 18/10 with FiO2 1.0) and flush-rate nasal cannula. After intubation, she initially improves and her SpO2 improves to 98%. You put in orders to maintain her on lung-protective ventilator settings, deeply sedated to a RASS of -4, and get back to the grind. A few minutes later, the respiratory therapist tells you she’s having trouble maintaining the SpO2 above 90% on a FiO2 of 1.0. The RT has attempted alveolar recruitment with PEEP, but still no improvement. You think back to your last month in the ICU, when you managed several patients with ARDS, and wonder if you should start an inhaled prostacyclin.

Acute Respiratory Distress Syndrome (ARDS)

ARDS is an inflammatory syndrome resulting in primarily non-hydrostatic, high-protein pulmonary edema. Following an inciting event (e.g. sepsis, trauma, inhalation injury, etc.), injury to the alveolar epithelium and capillary endothelium result in “leaky lungs”, and the resultant pulmonary edema, inflammation, and alveolar coagulation abnormalities, result in hypoxemia, and a situation of increased shunt and dead space.

The treatment of ARDS is largely supportive. Goals related to the mechanical ventilator should be to limit the potential for ventilator-associated lung injury while maintaining adequate enough oxygenation and ventilation. Tidal volume should be set around 6ml/kg predicted body weight (lower if plateau pressure goal exceeded, higher if hypercapnia results in life-threatening acidosis). There is no consensus on how to best set PEEP, but PEEP is increased for alveolar recruitment. Plateau pressure should be limited to <30 cmH2O, with an oxygenation goal of PaO2 55-80mmHg. (for this handy vent management card, check out ).

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Other physiologically sound and evidence-based treatment options include neuromuscular blockade and prone positioning, as demonstrated in the ACURASYS and PROSEVA trials.

When hypoxemia persists despite appropriate ventilator settings, neuromuscular blockade, and prone positioning, another treatment option to improve perfusion to ventilated alveolar units is the use of inhaled pulmonary vasodilators, such as epoprostenol.


Epoprostenol, a prostacyclin also known as Flolan, vasodilates the pulmonary capillaries around ventilated alveoli, thus reducing shunt. It also suppresses the production of several pro-inflammatory cytokines, and may increase surfactant production. When used as an infusion, it creates a substantially decreased systemic vascular resistance, as Bihari et al discovered in 1987. However, when inhaled at lower doses, prostaglandins selectively vasodilate the pulmonary vasculature with fewer effects on systemic pressure. In clinical trials by Walmrath and Zwissler, aerosolized PGI2 reduced the pulmonary artery pressure and increased oxygenation. Zwissler also found that inhaled epoprostenol produced the same reduction in pulmonary vascular resistance and increase in PaO2 at 10ng/kg/min as it did at 25ng/kg/min. Van Heerden’s clinical trial found the greatest increase in oxygenation occurred between 0-10ng/kg/min, without significant improvements at higher concentrations.

Inhaled nitric oxide has similar effects, reducing pulmonary vascular resistance and increasing PaO2 without a detrimental effect on systemic circulatory pressures or cardiac output. However, at higher concentrations, it theoretically induces the formation of methemoglobin, and generally costs an arm and a leg. De Wet and colleagues found that the average cost for Flolan was ~$150/day while inhaled Nitric Oxide was in the neighborhood of $3000/day.  


So where’s the rub with inhaled prostacyclins? The take away is that they will improve oxygenation and reduce pulmonary artery pressures, but there is VERY little outcome data to support inhaled epoprostenol use in ARDS (certainly it does not support its routine use). As Fuller et al discovered, the research that exists on inhaled prostacyclins is sparse. The results of these many RCTs are pretty heterogenous, many of them do not compare the results of iEPO to placebo, and few if any demonstrate a clinical outcome benefit. Even in patients with pulmonary arterial hypertension leading to hypoxemia in the ICU, the survival benefit of inhaled prostacyclins is unknown.

Coming back to our ARDS patient, her oxygenation improved significantly with bag and suction, during which RT was able to remove copious secretions. We performed similar lung recruitment measures every few hours and got our patient into an ICU after a twelve-hour board in the ED.


Bihari, D., Smithies, M., Gimson, A., & Tinker, J. (1987). The effects of vasodilation with prostacyclin on oxygen delivery and uptake in critically ill patients. New England Journal of Medicine, 317(7), 397-403.

Charl, J., Affleck, D. G., Jacobsohn, E., Avidan, M. S., Tymkew, H., Hill, L. L., ... & Smith, J. R. (2004). Inhaled prostacyclin is safe, effective, and affordable in patients with pulmonary hypertension, right heart dysfunction, and refractory hypoxemia after cardiothoracic surgery. The Journal of thoracic and cardiovascular surgery, 127(4), 1058-1067.

Fuller, B. M., Mohr, N. M., Skrupky, L., Fowler, S., Kollef, M. H., & Carpenter, C. R. (2015). The use of inhaled prostaglandins in patients with ARDS. Chest, 147(6), 1510-1522.

Guérin, C., Reignier, J., Richard, J. C., Beuret, P., Gacouin, A., Boulain, T., ... & Clavel, M. (2013). Prone positioning in severe acute respiratory distress syndrome. The New England journal of medicine368(23), 2159.

Kaisers, U., Busch, T., Deja, M., Donaubauer, B., & Falke, K. J. (2003). Selective pulmonary vasodilation in acute respiratory distress syndrome. Critical care medicine, 31(4), S337-S342.

Lee, K. (2017). The neuroICU book. McGraw Hill Professional.

NHLBI ARDS network. Updated 2014.

Papazian, L., Forel, J. M., Gacouin, A., Penot-Ragon, C., Perrin, G., Loundou, A., ... & Constantin, J. M. (2010). Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med363(12), 1107-1116.

Searcy, R. J., Morales, J. R., Ferreira, J. A., & Johnson, D. W. (2015). The role of inhaled prostacyclin in treating acute respiratory distress syndrome. Therapeutic advances in respiratory disease, 9(6), 302-312.

van Heerden, P. V., Barden, A., Michalopoulos, N., Bulsara, M. K., & Roberts, B. L. (2000). Dose-response to inhaled aerosolized prostacyclin for hypoxemia due to ARDS. Chest, 117(3), 819-827.

Walmrath, D., Schneider, T., Schermuly, R., Olschewski, H., Grimminger, F., & Seeger, W. (1996). Direct comparison of inhaled nitric oxide and aerosolized prostacyclin in acute respiratory distress syndrome. American journal of respiratory and critical care medicine, 153(3), 991-996.

Zwissler, B., Kemming, G., Habler, O., Kleen, M., Merkel, M., Haller, M., ... & Peter, K. (1996). Inhaled prostacyclin (PGI2) versus inhaled nitric oxide in adult respiratory distress syndrome. American journal of respiratory and critical care medicine, 154(6), 1671-1677.


The URI from Hell

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The URI From Hell: Pediatric Myocarditis

By Dr. Al Lulla, MD (PGY-2) and Dr. Melissa Puffenbarger, MD (PEM Attending and US Fellow)


A previously healthy 3-year-old girl presents to the ED with her mother. Her mother reports that she has had a cough and nasal congestion for the past 2 days. She reports she has been sleeping most of the day and “not acting like herself”. She denies her having any fevers at home. Mom also endorses her having a poor appetite and decreased urine output over the past 1-2 days. On arrival to the ED she presents with the following vital signs: T 36.4, P 150, BP 95/63, 98% RA. On exam she is lethargic. She is pale and diaphoretic appearing. She appears tachypneic but does not have any retractions. You identify crackles in the left lower lobe as well as nasal congestion.  You identify cool extremities with delayed capillary refill and thready peripheral pulses. Her CBC, BMP and UA are normal, however she has a lactate of 5.5. Chest X-ray demonstrates mild perihilar infiltrates with absence of cardiomegaly. You decide to administer a 20cc/kg normal saline fluid bolus. You obtain blood and urine cultures and start antibiotics. Soon after, you notice that she has worsened tachycardia, altered mental status and now hepatomegaly on exam. Her viral respiratory panel finally comes back positive for coronavirus. 

As you notice the child decompensating, you quickly fetch your trusty ultrasound machine to perform a bedside echo. What you notice befuddles you! 


Given what appears to be severe depressed biventricular function on your bedside US, your leading diagnosis is viral myocarditis!


Myocarditis can be described as an inflammatory condition of the heart muscle, which can progress to non-ischemic dilated cardiomyopathy and congestive heart failure [1]. While it has often been considered to be a rare disease, evidence from autopsies in the pediatric patient population indicates that 1.8% of patients have histological evidence consistent with myocarditis, of which 57% of those patients presented with sudden cardiac death [2]. It is thought to have a bimodal age distribution in both infancy and early childhood (<2 years) and in mid-adolescence (14-18 years) [1, 4]. 

There are a vast array of known causes of myocarditis, which can be broken up into infectious and non-infectious etiologies [3]. In the United States, viral myocarditis is by far the most common; other causes such as drug induced or autoimmune etiologies are exceedingly rare. 


The pathophysiology of myocarditis includes three distinct phases [1]:

  •  Phase 1: “Acute” phase, describes viral infiltration and direct injury of the myocardial cells causing necrosis, further potentiating an inflammatory response.
  •  Phase 2: “Subacute” phase, describes the autoimmune reactions mediated by virus-specific T cells, cytokine reaction and antibodies to viral and cardiac proteins. Cardiac contractility decreases.
  • Phase 3: “Chronic” phase describes the post inflammatory phase characterized by development of dilated cardiomyopathy.

Fulminant myocarditis, which is a terrifying entity of its own, is characterized by sudden onset of cardiogenic shock necessitating aggressive hemodynamic support. Ironically, patients with fulminant myocarditis have overall better long-term prognosis and decreased rates of cardiac transplantation than those with acute, subacute or chronic myocarditis [1]. 

Clinical Presentation

The presentation of myocarditis varies along a clinical spectrum from minimal symptoms suggestive of a viral syndrome to sudden cardiovascular collapse and death. No symptom is either pathognomonic or common, making the diagnosis of myocarditis extremely challenging for the emergency physician. The most common presenting complaints are: chest pain, shortness of breath, syncope, palpitations, gastrointestinal symptoms (anorexia, abdominal pain, vomiting), poor feeding, URI symptoms, fever and lethargy [1,3].

One study stratified patients with myocarditis as having moderate to severely depressed LV function versus mild-normal depressed LV function and identified that chest pain and respiratory distress were more likely in patients with mild/normal dysfunction compared to those with moderate/severe dysfunction. In addition, the diagnosis can often be elusive in infants who may not be able to verbalize their symptoms. Once again this supports (noticing a theme yet?) that this can be an extremely difficult diagnosis to make [4]. The key here is to always have a high index of suspicion.

On physical exam, patients may be noted to have tachycardia that is out of proportion to their fever. Tachycardia that does not respond to antipyretics or appropriate fluid resuscitation in a patient with viral symptoms warrants further evaluation for myocarditis.

Furthermore, patients may demonstrate evidence of respiratory distress including tachypnea, cyanosis and hypoxia. Patients who have moderate/severely depressed ejection fraction are more likely to show signs consistent with heart failure which include hepatomegaly, gallop, hypotension, edema, pallor and signs of diminished perfusion and end organ dysfunction [1,3,4]. 

Evaluation: [1,3]

  1. EKG: If there is suspicion of myocarditis, consider ordering an EKG. It’s cheap. It’s fast. Allthough there are no specific findings for myocarditis, many of these patients may have an EKG abnormality, which could help you hone in on a cardiac cause of their illness. EKG abnormalities that may be seen include sinus tachycardia (most common), ventricular hypertrophy, low-voltage QRS complexes and T wave inversions. 
  2. CXR: Radiation exposure is bad for children. But one may argue that myocarditis is badder (yes, I know that’s not a real word.). Consider ordering a chest xray in patients requiring increased respiratory support. Chest x-ray findings of pulmonary edema, cardiomegaly or pleural effusion should increase suspicion for myocarditis. 
  3. Cardiac Biomarkers: Studies show that troponin levels may be elevated among patients with myocarditis compared to those without myocarditis (sensitivity of 71% and specificity of 86% (when using a troponin T cut off value of 0.052 ng/mL). BNP levels are also more likely to be elevated in patients with myocarditis who have severely depressed LV function. That said, these tests are never diagnostic and should not be used to rule out myocarditis especially if clinical suspicion persists.
  4. Inflammatory Biomarkers: Given the inflammatory milieu created by viral myocardial injury, many patients may have elevated ESR or CRP levels, however these findings are neither sensitive nor specific. 
  5. Echocardiography: This is where the money is. Point of care ultrasound in the ED has started to play a significant role in the evaluation of undifferentiated shock in pediatric patients. Patients who have fulminant myocarditis may show global left ventricular or biventricular dysfunction, dilated cardiomyopathy and reduced ejection fraction. If the patient continues to deteriorate consider performing a lung ultrasound to evaluate for B-lines, which represent pulmonary edema (and may appear before the chest xray findings pop up). The utility of bedside ultrasound is that it can rapidly guide your resuscitation and inform you if you should or should not administer fluids to the patient. In the case of the above patient, giving fluids would likely do more harm than good.
  6. Other diagnostics: Cardiac MRI and endomyocardial biopsy (gold standard) may be used as well, but, they have little utility in the acute setting and are not routinely used.


Emergency department management of patients with myocarditis is largely supportive care. Specific therapies may be aimed at volume management, hemodynamic support, and antiarrhythmics in concert with emergent consultation with a pediatric cardiologist. Diuresis, most commonly with furosemide, is a mainstay of therapy and intravenous fluids should be avoided if possible. Afterload reduction can help augment cardiac output. Inotropic support should be considered in all patients with evidence of cardiogenic shock. Preferable agents include milrinone, epinephrine and dobutamine, however norepinephrine and dopamine have also been used historically. 

Immunosuppressive agents such as steroids have shown to have no benefit in primary outcome measures including death, transplant-free survival, or improvement in cardiac function. Other agents such as IVIG are considered to be controversial and not recommended in the acute phase of the illness. 

Patients who do not improve with pharmacotherapy may require mechanical circulatory support in the form of extracorporeal membrane oxygenation (ECMO) or a ventricular assist device (VAD). ECMO in particular has shown to be successful in the management of patients who require hemodynamic support from myocarditis. One small retrospective study of 28 patients examined outcomes of patients with fulminant myocarditis who were cannulated onto ECMO and found that 46% (n=13) of patients had complete recovery of myocardial function. 21% (n=6) of patients had chronic ventricular dysfunction, another 21% (n=6) underwent cardiac transplantation, and 11% (n=3) died prior to discharge [5]. It is vital to have ECMO resources “on standby” for any ED patient for whom there is concern of myocarditis.  (Side note: patients with myocarditis are at high risk for cardiac arrest during intubation. Intubation should be avoided if possible, but in the event that it is needed, having ECMO available may be a lifesaving intervention.)

Despite the fact that a significant proportion of patients will have full recovery with supportive therapies, or ECMO, a small percentage of patients may require cardiac transplantation. VADs are used as a bridge to transplantation, and it is estimated that approximately 88% of patients who are placed on a VAD will survive to receive successful cardiac transplantation [5].

With regards to management the bottom line is: myocarditis is a terrifyingly treatable condition with relatively good outcomes in children, IF you have a high index of suspicion. ED providers can make a huge difference.

Case Conclusion

After the patient was identified as likely having viral myocarditis, she quickly decompensated. She was intubated and then became pulseless. CPR was initiated simultaneously during cannulation with VA ECMO. The patient remained on vasopressor support for an additional 2 days and was successfully decannulated off ECMO 5 days later. She was discharged home on hospital day 21 with a normal ejection fraction. She was started on an ACE inhibitor and was noted to being doing very well at her follow up visit. 

Take Home Points

  • Fulminant myocarditis is a difficult diagnosis to make. The key is to have a high index of suspicion in the ED
  • The most common etiology of myocarditis is viral in origin
  • Point of care bedside ultrasound is one of the most important tools in your arsenal. Use it!
  •  Diuretics, vasopressors, and anti-arrhythmics are the mainstays of therapy
  • Consult a pediatric cardiologist. Consult them early
  • Patients who fail medical management should be emergently considered for mechanical support in the form of ECMO
  • Outcomes are favorable when aggressive supportive measures are initiated early


1.         Bergmann KR, Kharbanda A, Haveman L. Myocarditis And Pericarditis In The Pediatric Patient: Validated Management Strategies. Pediatr Emerg Med Pract. 2015;12(7):1-22.

2.         Weber MA, Ashworth MT, Risdon RA, Malone M, Burch M, Sebire NJ. Clinicopathological features of paediatric deaths due to myocarditis: an autopsy series. Arch Dis Child. 2008;93(7):594-8.

3.         Canter CE, Simpson KE, Simpson KP. Diagnosis and treatment of myocarditis in children in the current era. Circulation. 2014;129(1):115-28.

4.         Butts RJ, Boyle GJ, Deshpande SR, et al. Characteristics of Clinically Diagnosed Pediatric Myocarditis in a Contemporary Multi-Center Cohort. Pediatr Cardiol. 2017;38(6):1175-1182.

5.         Casadonte JR, Mazwi ML, Gambetta KE, et al. Risk Factors for Cardiac Arrest or Mechanical Circulatory Support in Children with Fulminant Myocarditis. Pediatr Cardiol. 2017;38(1):128-134.


-Dr Al Lulla