Congenital Cardiac Anesthesia Society
A Section of the the Society for Pediatric Anesthesia

{“questions”:{“nm19a”:{“id”:”nm19a”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Nicholas Houska, DO – University of Colorado – Childrens Hospital Colorado\r\nA 7-year-old boy with a history of acute lymphoblastic leukemia treated with doxorubicin presents with symptoms of heart failure. Which of the following morphological subtypes of cardiomyopathy is MOST likely to be found in this patient? \r\n\r\n”,”desc”:”EXPLANATION \r\nAnthracyclines are a class of cytotoxic drugs extracted from the Streptomyces<\/em> bacterium. They are utilized as chemotherapeutic agents and include doxorubicin (the most commonly used), daunorubicin, and epirubicin. First used in the 1960s, anthracyclines remain one of the most commonly used and effective chemotherapeutics for solid and hematological cancers. Anthracyclines are inhibitors of the DNA topoisomerase II enzyme, leading to DNA double-strand breaks and subsequent upregulation of p53, which results in programmed cell death (apoptosis). \r\n\r\nAnthracyclines are thought to be the primary drugs related to chemotherapy-induced cardiotoxicity. The risk of cardiotoxicity increases as the total cumulative dose of doxorubicin (Dox) increases, with a 3-5% risk at 400 mg\/m^{2<\/sup> and 18-48% at 700 mg\/m2<\/sup>. Apoptosis-mediated loss of cardiomyocytes and oxidative stress are the main culprits of Dox-induced cardiomyopathy. Extremes of age (less than 5 years of age or greater than 65 of age), preexisting cardiac disease or cardiovascular risk factors, and radiation therapy are additional risk factors for Dox-induced cardiomyopathy. \r\n\r\nAnthracycline-induced cardiotoxicity can develop at various time points after the initiation of doxorubicin treatment, leading to a dated classification. Acute cardiotoxicity occurs after a single dose or course with the onset of symptoms within 2 weeks. Early-onset chronic occurs within 1 year and presents as a dilated-hypokinetic cardiomyopathy, with progressive development of heart failure. Late-onset chronic occurs years to decades after completion of doxorubicin therapy. Anthracycline-induced cardiotoxicity is defined as a decrease in left ventricular ejection fraction greater than 10% with a final value less than 53% after exposure. It is typically detected via cardiac imaging such as echocardiography and magnetic resonance imaging, along with monitoring of cardiac biomarkers. \r\n\r\nMost guidelines recommend serial monitoring after anthracycline use. While historically, doxorubicin-induced cardiotoxicity has been thought of as irreversible and associated with high mortality, more recent studies are suggesting that there may be some effectiveness of heart failure therapy. Primary prevention includes lifestyle modification of cardiovascular risk factors, limitations on total dosage, and the use of less cardiotoxic analogs such as epirubicin. Additionally, dexrazoxane, an iron-chelating agent that prevents the accumulation of oxygen-free radicals, is often included in chemotherapy regimens to protect against the cardiotoxic effects of anthracyclines. The mainstays of heart failure therapy for anthracycline-mediated dilated cardiomyopathy are angiotensin-converting enzyme inhibitors and beta blockers. \r\n\r\nAnthracyclines, and specifically doxorubicin-induced cardiotoxicity, are most commonly associated with a dilated hypokinetic cardiomyopathy (answer B). Hypertrophic cardiomyopathy (answer C) is typically associated with genetic disorders. While restrictive cardiomyopathy (answer A) can develop as a result of anthracycline use, it is much less common and presents years or decades after exposure. Restrictive cardiomyopathy is more commonly associated with deposition disorders such as amyloidosis and hemochromatosis. \r\n\r\n\r\n \r\nREFERENCES \r\nCardinale D, Iacopo F, Cipolla CM. Cardiotoxicity of Anthracyclines. Front Cardiovasc Med<\/em>. 2020;7:26. doi: 10.3389\/fcvm.2020.00026. \r\n\r\nRawat PS, Jaiswal A, Khurana A, Bhatti JS, Navik U. Doxorubicin-induced cardiotoxicity: An update on the molecular mechanism and novel therapeutic strategies for effective management. Biomed Pharmacother<\/em>.2021;139:111708. doi: 10.1016\/j.biopha.2021.111708. \r\n\r\nMancilla TR, Iskra B, Aune GJ. Doxorubicin-Induced Cardiomyopathy in Children. Compr Physiol<\/em>. 2019:12;9(3):905-931. doi: 10.1002\/cphy.c180017. \r\n\r\n”,”hint”:””,”answers”:{“kenij”:{“id”:”kenij”,”image”:””,”imageId”:””,”title”:”A.\tRestrictive cardiomyopathy”},”ggit0″:{“id”:”ggit0″,”image”:””,”imageId”:””,”title”:”B.\tDilated cardiomyopathy”,”isCorrect”:”1″},”huyfa”:{“id”:”huyfa”,”image”:””,”imageId”:””,”title”:”C.\tHypertrophic cardiomyopathy\r\n\r\n”}}}}}}

{“questions”:{“gc68c”:{“id”:”gc68c”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Nicholas Houska, DO – University of Colorado – Children\u2019s Hospital Colorado \r\n\r\nA six-day-old boy with a prenatal diagnosis of D-transposition of the great arteries and ventricular septal defect presents for arterial switch operation and ventricular septal defect repair. Which of the following Society of Thoracic Surgeons and the European Association for Cardio-thoracic Surgery Congenital Heart Surgery Mortality Categories characterize this surgical procedure?\r\n”,”desc”:”EXPLANATION \r\nGiven the complexity and heterogeneity of congenital heart disease and surgical repair, comparison of procedures proves challenging when analyzing outcomes and data. Historically, procedure risk and complexity were categorized using methodologies based on expert opinion such as the Aristotle Basic Complexity Score (ABC Score) and ABC Level (ABC Level), in addition to the Risk Adjustment for Congenital Heart Surgery-1 (RACHS-1) methodology. With the creation of large databases of surgical outcomes, it became apparent that a more quantitative and validated scoring system was needed in recent decades. \r\n\r\nIn 2009 O\u2019Brien et al. analyzed the mortality risk of 148 types of operations that had been conducted on more than 77,000 patients who were entered into the European Association for Cardiothoracic Surgery (EACTS) Congenital Heart Surgery database and the Society of Thoracic Surgeons (STS) Congenital Heart Surgery database. Procedure-specific mortality rate estimates were calculated, and each procedure was assigned a numeric score, ranging from 0.1 to 5.0 based on the estimated mortality rate. This score was termed the STS-EACTS Congenital Heart Surgery Mortality Score or STS-EACTS score, more commonly referred to as STAT mortality categories. These surgical procedures were then grouped into five categories, referred to as the STS-EACTS Congenital Heart Surgery Mortality Categories (STS-EACTS categories). This scoring system categorizes procedures based on complexity and mortality, with category 1 being the lowest mortality risk and category 5 being the highest mortality risk. This model was then independently validated and compared with the ABC Score and the RACHS-1 score. The STS-EACTS scores and categories have demonstrated high discrimination (C-index) for predicting mortality as compared to the prior models. Although there are numerous congenital cardiac diagnoses for specific surgical procedures, representative examples of procedures and mortality categories are shown in Table 1 below.\r\n\r\n\r\n\r\nTable 1: Common examples of procedures in each STS-EACTS mortality category.\r\n\r\nThe STS-EACTS mortality categories have been increasingly utilized for both research and outcomes reporting. They are utilized in the STS Congenital Heart Surgery Database public reporting of mortality risk for participating hospitals. Given the expanded availability of this data, patients and parents are increasingly aware of and utilize this information when choosing a hospital for surgical care of congenital heart disease. \r\n\r\n \r\nREFERENCES \r\nO’Brien SM, Clarke DR, Jacobs JP et al. An empirically based tool for analyzing mortality associated with congenital heart surgery. J Thorac Cardiovasc Surg<\/em>. 2009;138(5):1139-53. doi: 10.1016\/j.jtcvs.2009.03.071. PMID: 19837218.\r\n\r\nJacobs JP, Jacobs ML, Maruszewski B et al. Initial application in the EACTS and STS Congenital Heart Surgery Databases of an empirically derived methodology of complexity adjustment to evaluate surgical case mix and results. Eur J Cardiothorac Surg<\/em>. 2012;42(5):775-779 i: 10.1093\/ejcts\/ezs026. \r\n\r\nJacobs JP, Jacobs ML, Lacour-Gayet FG et al. Stratification of complexity improves the utility and accuracy of outcomes analysis in a Multi-Institutional Congenital Heart Surgery Database: Application of the Risk Adjustment in Congenital Heart Surgery (RACHS-1) and Aristotle Systems in the Society of Thoracic Surgeons (STS) Congenital Heart Surgery Database. Pediatr Cardiol<\/em>. 2009;30(8):1117-1130. doi: 10.1007\/s00246-009-9496-0. PMID: 19771463.\r\n\r\nThe Society for Thoracic Surgeons Public Reporting. https:\/\/publicreporting.sts.org\/chsd. Accessed November 13, 2024.\r\n\r\n”,”hint”:””,”answers”:{“ft11c”:{“id”:”ft11c”,”image”:””,”imageId”:””,”title”:”A. 3″},”bedlj”:{“id”:”bedlj”,”image”:””,”imageId”:””,”title”:”B. 4″,”isCorrect”:”1″},”jctpe”:{“id”:”jctpe”,”image”:””,”imageId”:””,”title”:”C. 5″}}}}}

{“questions”:{“3ajp7”:{“id”:”3ajp7″,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Fernando F. Cuadrado, MD and Matthew Monteleone, MD – Cincinnati Children\u2019s Hospital Medical Center \r\n\r\nA seven-year-old boy with a history of orthotopic heart transplantation is undergoing cardiac catheterization and biopsy under general endotracheal anesthesia. He is erroneously administered a 15 mcg\/kg bolus dose of dexmedetomidine due to an infusion pump programming error. The heart rate immediately decreases to 67 bpm with a blood pressure of 72\/43. Which of the following side effects is MOST likely to be observed in this patient? “,”desc”:”EXPLANATION \r\nDexmedetomidine is a highly selective alpha_{2<\/sub> adrenergic receptor agonist that induces sedation, anxiolysis, and analgesia by inhibiting norepinephrine release, thereby reducing sympathetic tone and promoting sedation without respiratory depression. In pediatric anesthesia, it is frequently used for postoperative sedation, particularly following cardiac catheterization. Dexmedetomidine is preferred in this setting because it provides sedation with stable hemodynamics and minimal to no respiratory depression, making it an ideal choice for children with cardiac conditions.\r\n\r\nThe most common side effects include hypotension, bradycardia, and, less frequently, hypertension, which typically occurs shortly after rapid bolus administration. The hypotensive effects are mediated via stimulation of central alpha2A<\/sub> receptors, resulting in decreased catecholamine release and sympathetic outflow from the locus ceruleus of the brainstem. In heart transplant patients, the bradycardic effects may be diminished due to cardiac denervation, though hypotension and hypertension can still occur. While these side effects are well-documented, less common adverse events such as hypoglycemia and miosis may arise, particularly with high doses or prolonged high-dose infusions. In a 2009 case report, a 20 month-old, 11kg patient was accidentally administered 36 mcg\/kg of dexmedetomidine over 36 minutes. A blood glucose check prompted by several shaking episodes in the recovery unit was 26 mg\/dL. The authors speculate that the hypoglycemia was due to the drug\u2019s sympatholytic effects of reducing circulating norepinephrine levels with a reduction in gluconeogenesis and glycogenolysis. Additionally, a decrease in serum cortisol levels may blunt the stress response induced by surgery, further affecting glucose homeostasis. In another case report, a 3-year-old, 11 kg child was accidentally given 100 mcg of dexmedetomidine as a bolus. The child presented with significant bradycardia, hypotension, bradypnea, deep hypnosis, and miosis, requiring treatment with an epinephrine infusion. Although this patient\u2019s glucose remained normal, the authors speculate that this may have been due to the epinephrine counteracting the sympatholytic effects of dexmedetomidine. In summary, when there is concern about oversedation, blood glucose levels should be closely monitored because of the increased risk of hypoglycemia with the administration of high-dose dexmedetomidine.\r\n\r\nThe correct answer is B, hypoglycemia. Dexmedetomidine offers effective sedation with a favorable safety profile in pediatric patients, particularly after cardiac procedures. However, there is a potential for hypoglycemia with higher-than-usual clinical doses. Notably, dexmedetomidine does not cause hyperglycemia. Additionally, xerostomia, rather than sialorrhea, is a common side effect due to reduced salivary gland activity. Finally, dexmedetomidine produces pupillary constriction in awake volunteers, possibly due to absent inhibition of the pupilloconstrictor nucleus and reduced sympathetic tone of the iris muscles. \r\n\r\n\r\n \r\nREFERENCES \r\nBernard PA, Makin CE, Werner HA. Hypoglycemia associated with dexmedetomidine overdose in a child? J Clin Anesth<\/em>. 2009; 21:50\u201353.\r\n\r\nG\u00f6rges M, Poznikoff AK, West NC, Brodie SM, Brant RF, Whyte SD. Effects of Dexmedetomidine on Blood Glucose and Serum Potassium Levels in Children Undergoing General Anesthesia: A Secondary Analysis of Safety Endpoints During a Randomized Controlled Trial. Anesth Analg<\/em>. 2019;129:1093-1099\r\n\r\nNath SS, Singh S, Pawar ST. Dexmedetomidine overdosage: An unusual presentation. Indian J Anaesth<\/em> 2013; 57(3):289-291.\r\n\r\nJooste EH, Muhley WT, Ibinson JW, et al. Acute hemodynamic changes after rapid intravenous bolus dosing of dexmedetomidine in pediatric heart transplant patients undergoing routine cardiac catheterization. Anesth Analg<\/em>. 2010;111(6):1490-1496.\r\n\r\n”,”hint”:””,”answers”:{“fbw95”:{“id”:”fbw95″,”image”:””,”imageId”:””,”title”:”A.\tSialorrhea “},”whv28”:{“id”:”whv28″,”image”:””,”imageId”:””,”title”:”B.\tHypoglycemia”,”isCorrect”:”1″},”fgzhl”:{“id”:”fgzhl”,”image”:””,”imageId”:””,”title”:”C.\tMydriasis”}}}}}}

{“questions”:{“xf629”:{“id”:”xf629″,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Nicholas Houska, DO – University of Colorado – Children\u2019s Hospital Colorado\r\nA 16-year-old girl who recently emigrated to the United States from Venezuela presents with dyspnea, fatigue, and dependent edema. Two years ago, her mother died in her sleep after exhibiting similar symptoms. An electrocardiogram shows sinus node dysfunction with bradycardia. A transthoracic echocardiogram reveals dilated cardiomyopathy with severely depressed biventricular function. Which of the following infectious organisms is the MOST likely cause of her dilated cardiomyopathy?\r\n\r\n”,”desc”:”EXPLANATION \r\nAmerican trypanosomiasis, commonly referred to as Chagas disease, is a protozoal infection caused by Trypanosoma cruzi<\/em>, which is endemic to Central and South America. Increased international migration is responsible for a growing number of cases worldwide. It is responsible for the highest parasitic disease burden in the Western Hemisphere, with an estimated 6 million people infected worldwide and 300,000 infected in the United States. Nearly 1.2 million people are suspected to have Chagas cardiomyopathy, which is one of the most serious complications of chronic Chagas disease. Despite the widespread burden of disease, it is poorly recognized outside of endemic regions. \r\n\r\nThe vector for transmission of Trypanosoma cruzi (T. cruzi)<\/em> is the triatomine insect commonly referred to as the \u201ckissing bug\u201d. The triatomine insect becomes infected with T. cruzi<\/em> after feeding on an infected animal host. The infected insect draws blood during feeding and simultaneously deposits feces. The resulting bite causes itching, and when scratched, T cruzi<\/em>-laden feces may be introduced into the bite wound, resulting in protozoal transmission. Transmission also occurs via the fecal-oral route or consumption of food or drink infected with insects and\/or their waste. It can also occur during blood transfusion, organ transplantation, or placental transfer, resulting in congenital Chagas disease. \r\n\r\nAcute Chagas disease is a multi-organ inflammatory disease presenting with lymphadenopathy, hepatomegaly, and splenomegaly. Cardiovascular involvement can lead to myocarditis, vasculitis, pericarditis complicated by pericardial effusion, and\/or dilated cardiomyopathy. Chagas disease may also cause myocardial and endocardial necrosis, in addition to inflammation of and damage to the cardiac conduction system. The acute phase of infection persists for eight to twelve weeks. The majority of patients exhibit mild or nonspecific symptoms, such as fever or fatigue. The electrocardiogram most often shows sinus tachycardia and PR\/QT prolongation. Rarely, patients may present with fulminant disease exhibiting myocarditis, pericardial effusion, meningitis, or death.\r\n\r\nChronic Chagas disease primarily affects the cardiovascular and gastrointestinal systems. The gastrointestinal manifestations are related to impaired esophageal or colonic motility. Megacolon and\/or megaesophagus and bowel ischemia are the most severe manifestations. Chronic Chagas heart disease typically presents decades after the initial infection. Chagas cardiomyopathy results in the majority of Chagas morbidity and mortality. It is generally classified as a dilated cardiomyopathy. However, Chagas cardiomyopathy has a distribution of fibrosis to the posterior and apical regions of the LV and involvement of the sinus node and electrical conduction system that distinguishes it from other types of cardiomyopathies. Chagas heart disease is considered an arrhythmogenic cardiomyopathy, characterized by atrial and ventricular arrhythmias, along with abnormalities of the conduction system. Sudden cardiac death is the most common overall cause of mortality. Chagas cardiomyopathy carries a poor prognosis when compared to other causes of cardiomyopathy, likely due to irreversible ventricular remodeling and damage before presentation.\r\n\r\nThe most sensitive test for acute infection is PCR testing, while chronic disease is best diagnosed via serology. Both of these tests are only available in the United States via the Center for Disease Control Division of Parasitic Disease (CDCDPD). Further diagnostic tests may include an electrocardiogram, echocardiogram, Holter monitoring, cardiac stress testing, magnetic resonance imaging, and\/or cardiac catheterization. Anti-parasitic treatment is with Benznidazole and\/or nifurtimox, both of which must be obtained via consultation with the CDCDPD. Treatment of acute Chagas disease and congenital Chagas disease is typically more successful than chronic Chagas disease. Treatment of cardiac manifestations typically includes medical management of heart failure, treatment of arrhythmias, pacemaker implantation, and prevention of sudden cardiac death with insertion of an implantable cardiac defibrillator. Chagas disease is NOT a contraindication to heart transplantation. Primary prevention against stroke is also commonly indicated. \r\n\r\nThe patient described in the stem emigrated from a region endemic to Trypanosoma cruzi<\/em> and has signs and symptoms of Chagas heart disease (Answer C). Plasmodium falciparum<\/em> (Answer A) is endemic to the African continent and causes malaria. Malaria typically presents with neurological, hematological, and respiratory manifestations. Zika virus (answer B) typically presents with fever, arthralgias, and rash. Infection during pregnancy can result in birth defects. \r\n\r\n \r\nREFERNCES \r\nNunes MCP, Beaton A, Acquatella H et al.American Heart Association Rheumatic Fever, Endocarditis and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young; Council on Cardiovascular and Stroke Nursing; and Stroke Council. Chagas Cardiomyopathy: An Update of Current Clinical Knowledge and Management: A Scientific Statement From the American Heart Association. Circulation<\/em>. 2018;138(12):e169-e209. doi: 10.1161\/CIR.0000000000000599. PMID: 30354432.\r\n\r\nEdwards MS, Stimpert KK, Bialek SR, Montgomery SP. Evaluation and Management of Congenital Chagas Disease in the United States. J Pediatric Infect Dis Soc<\/em>. 2019;8(5):461-469. doi: 10.1093\/jpids\/piz018. PMID: 31016324; PMCID: PMC10186111.\r\n\r\nChancey RJ, Edwards MS, Montgomery SP. Congenital Chagas Disease. Pediatr Rev<\/em>. 2023;44(4):213-221. doi: 10.1542\/pir.2022-005857. PMID: 37002357; PMCID: PMC10313159.\r\n\r\n”,”hint”:””,”answers”:{“glyvj”:{“id”:”glyvj”,”image”:””,”imageId”:””,”title”:”A. Plasmodium falciparum”},”8h1ed”:{“id”:”8h1ed”,”image”:””,”imageId”:””,”title”:”B. Zika virus”},”rfane”:{“id”:”rfane”,”image”:””,”imageId”:””,”title”:”C. Trypanosoma cruzi\r\n\r\n”,”isCorrect”:”1″}}}}}

{“questions”:{“pii3r”:{“id”:”pii3r”,”mediaType”:”image”,”answerType”:”text”,”imageCredit”:””,”image”:””,”imageId”:””,”video”:””,”imagePlaceholder”:””,”imagePlaceholderId”:””,”title”:”Author: Nicholas Houska, DO – University of Colorado – Children\u2019s Hospital Colorado \r\n\r\nA 13-year-old boy with tetralogy of Fallot and pulmonary atresia presents for right ventricle to pulmonary artery conduit replacement. Which of the following factors is a major risk for re-entry injury during repeat sternotomy?”,”desc”:”EXPLANATION \r\nRepeat sternotomy in pediatric cardiac surgery is associated with a variety of complications, including re-entry injury (RI) to cardiac and vascular structures, ventricular fibrillation, and venous air embolism. While the definition of re-entry injury varies, most studies categorize re-entry injuries as major or minor, with major injury typically requiring urgent initiation of peripheral cardiopulmonary bypass (CPB). Historical studies have demonstrated a five to ten percent rate of RI during repeat sternotomy, while more recent studies demonstrate a lower rate of less than two percent. Despite the low frequency of RI during repeat sternotomy, there is a significant risk of associated morbidity and mortality. \r\n\r\nRisk factors for RI during repeat cardiac surgery should be evaluated before surgery. Additionally, efforts to mitigate injury and reduce harm after a RI should be discussed by the perioperative team. A 2009 study by Kirshbaum et al., which included one thousand repeat sternotomies for congenital cardiac surgery, revealed an overall incidence of RI as 1.3%. Risk factors for major RI resulting in hemodynamic instability, emergent transfusion, or emergent femoral cannulation included the number of repeat sternotomies and the presence of a right ventricle to pulmonary artery conduit. Of note, RI was not associated with increased operative mortality. Preoperative planning, such as diagnostic imaging, to determine the relationship of critical structures to the sternum and the status of peripheral vessels for emergent CPB initiation is often warranted. Appropriately sized and situated vascular access for the rapid administration of blood products and inotropes should be present in the event of major vascular injury. Timely access to a large volume of blood products should be arranged between the operative team and the blood bank. Elective peripheral CPB initiation before sternotomy may be prudent in some patients deemed extremely high risk for RI. For patients with a high likelihood of requiring further sternotomies, some institutions routinely place a substernal membrane made of polytetrafluoroethylene to decrease the risk of RI, though data on efficacy is limited. \r\n\r\nRecent studies have shown that the risk of reentry injury (<2%) during repeat sternotomy has continued to decline in the last few decades. While there are few studies on risk factors for reentry injury, a retrospective study of a thousand repeat sternotomies concluded that the number of repeat sternotomies (answer A) and the presence of a right ventricular to pulmonary artery conduit are risk factors for RI. \r\n\r\n \r\nREFERENCES \r\nKirshbom PM, Myung RJ, Simsic JM et al. One thousand repeat sternotomies for congenital cardiac surgery: risk factors for reentry injury. Ann Thorac Surg<\/em>. 2009 Jul;88(1):158-61. doi: 10.1016\/j.athoracsur.2009.03.082. PMID: 19559217.\r\n\r\nMorales DL, Zafar F, Arrington KA et al. Repeat sternotomy in congenital heart surgery: no longer a risk factor. Ann Thorac Surg<\/em>. 2008 Sep;86(3):897-902; discussion 897-902. doi: 10.1016\/j.athoracsur.2008.04.044. PMID: 18721579.\r\n\r\nRussell JL, LeBlanc JG, Sett SS, Potts JE. Risks of repeat sternotomy in pediatric cardiac operations. Ann Thorac Surg<\/em>. 1998 Nov;66(5):1575-8. doi: 10.1016\/s0003-4975(98)00829-7. PMID: 9875754.\r\n\r\nJacobs JP, Iyer RS, Weston JS, Amato JJ, Elliott MJ, de Leval MR, Stark J. Expanded PTFE membrane to prevent cardiac injury during sternotomy for congenital heart disease. Ann Thorac Surg<\/em>. 1996 Dec;62(6):1778-82. doi: 10.1016\/s0003-4975(96)00610-8. PMID: 8957386.\r\n”,”hint”:””,”answers”:{“w69jk”:{“id”:”w69jk”,”image”:””,”imageId”:””,”title”:”A. Number of repeat sternotomies”,”isCorrect”:”1″},”nqk3a”:{“id”:”nqk3a”,”image”:””,”imageId”:””,”title”:”B. Patient age”},”d0td6″:{“id”:”d0td6″,”image”:””,”imageId”:””,”title”:”C. Presence of a substernal membrane “}}}}}