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CASE PRESENTATION Patricia Baile – PL1 December 16, 2009 16 year old male presents to the ER with chest pain HPI • Chest pain x 6 days ▫ ▫ ▫ ▫ ▫ ▫ Sharp, stabbing sensation on left side of chest Constant PS 7/10 Worse when lying on left side and on inspiration Radiating to back Mild improvement with aspirin and acetaminophen HPI • Chest pain ▫ Associated with nausea, dizziness and blurring of vision 2 days prior ▫ No diaphoresis • On day of admission, chest pain persistent, no improvement with acetaminophen hence BIB EMS to ER ROS • • • • • • Denies recent strenuous physical activity No fever No URI symptoms No sick contacts No joint pains No dyspnea Past Medical History • Asthma ▫ ▫ ▫ ▫ ▫ 9 previous hospitalizations, last 1 year prior No ICU, no intubation Advair BID Singulair 10 mg PO QD Albuterol PRN Family History • • • • • • • + Asthma + DM + Hypertension + CAD No sudden death No CVA No connective tissue disorders • Birth History ▫ FT, NSVD, no complication • Immunization History ▫ Up to date • Adolescent History ▫ ▫ ▫ ▫ ▫ Currently in 9th grade (behind 2 years) Lives with mother, stepfather and older brother No sport or after-school activity Denies drugs, alcohol, tobacco Sexually active, has had 8 partners, uses condoms, no STD history (never tested) Physical Examination • BP 102/58 HR 72 RR 18 O2 100%RA T 98.3 • Pain score: 6-7/10 • Wt: 76.9 kg (90%) Ht: 185 cm (90%) • GS: non-toxic appearing • HEENT: NCAT, congested turbinates, TMI, mild erythema OP, no CLAD • C/L: SCE, good air entry b/l, CTAB, no crackles, no rales, no tenderness on palpation of chest • CV: RRR, no m/r/g • Abdomen: soft, ND, NT, no organomegaly • Ext: well-perfused, good distal pulses EKG Labs • • • • • • • CBC: 6.9 > 13.7/39.1< 251 N 68 L 20 BMP: 138/3.8/100/26/7/0.6/104/8.3 LFT: 3.9/6.9/25/109/0.7/74 Lipase: 12 CPK: 1751 CKMB: 168.8 Troponin T: 8.77 Labs • Lipid profile ▫ ▫ ▫ ▫ Cholesterol: 106 TG: 49 HDL: 31 LDL: 65 • CRP: 7.5 • Urine Drug Screen: Negative Labs • • • • • • RSV/Flu: Negative Rapid strep test: negative Throat culture ASO: 165 Streptozyme: Positive Respiratory viral panel: Negative Ancillary Tests • Chest Radiograph ▫ Normal chest Ancillary Tests • Initial Echo ▫ ▫ ▫ ▫ ▫ Normal LV ejection fraction Normal RV function Mild inferolateral akinesis Inferior wall akinesis Small pericardial effusion Initial Impression • 16 year old male with Juvenile pattern pericarditis; Asthma exacerbation Hospital Course • • • • Admitted to PICU Cardiac enymes gradually decreased Repeat Echo done Cardiac catheterization done Ancillary Tests • Repeat Echo ▫ Myocarditis with LV inferior/posterior wall motion abnormality: persistent abnormal LV wall motion ▫ Suboptimal LV shortening fraction ▫ Normal diastolic LV function ▫ Trace inferior and posterior pericardial effusion Ancillary Tests • Cardiac catheterization ▫ Clear vessels ▫ Decreased ejection fraction ▫ Decreased motion of LV FINAL DIAGNOSIS • 16 year old male with chest pain secondary to Myocarditis; Asthma exacerbation MYOCARDITIS Introduction • Clinical syndrome characterized by inflammation of myocytes resulting from infectious, toxic, and autoimmune etiologies. • Ongoing viral infection, myocardial destruction, and adverse remodeling can lead to persistent ventricular dysfunction and dilated cardiomyopathy. Introduction • Infectious etiologies, particularly viral, are most common in children. • The most common causes of viral myocarditis are enterovirus (coxsackie group B) and adenovirus Incidence • Incidence of myocarditis in children is unknown ▫ Inflammatory infiltrates and myocardial cell damage were found at autopsy in 3 to 40% of infants and children who died suddenly unrelated to trauma ▫ 17 percent of infants who died of SIDS had histopathologic evidence of myocarditis Incidence • In one retrospective study from a single tertiary Canadian center, the estimated prevalence of myocarditis presenting to their emergency department was 0.5 cases per 10,000 visits • A review of all the autopsies performed at a single English pediatric tertiary center over a ten-year period (1996 to 2005) identified 28 of 1516 cases with myocarditis (1.8 percent) Pathophysiology • In susceptible patients: ▫ Viral RNA uptake cytotoxic necrosis rapid cell death • More common presentation ▫ 4-14 days post-infection immune response (macrophage activation and cytokine expression) natural killer cells target myocardium expressing the viral RNA and continue myocyte necrosis Pathophysiology ▫ TNF is involved in rapidly clearing virus and signals additional proinflammatory cells, activates endothelial cells, and has direct negative inotropic effects ▫ Cytotoxic T lymphocytes infiltrate myocytes and trigger lysis of these cells Pathophysiology • In the chronic phases, the effects of either inadequate or inappropriately abundant immune response can lead to the long-term sequelae of dilated cardiomyopathy and heart failure Pathophysiology • Ongoing study has demonstrated the presence of antimyosin autoantibodies and other immunomodulators long after initial viral infection Clinical Manifestation • Nonspecific illness ▫ ▫ ▫ ▫ Fatigue Mild dyspnea Myalgias Fever (20%) • Chest pain (35%) ▫ most commonly described as a pleuritic, sharp, stabbing precordial pain ▫ may be substernal and squeezing Clinical Manifestation • In a 6-year study of pediatric ED patients, the most common presenting symptom was dyspnea and more than half of patients were initially diagnosed with asthma or pneumonia. • May be asymptomatic Clinical manifestation • • • • • Symptoms of heart failure Dyspnea on exertion Orthopnea Shortness of breath Palpitation Physical Findings • Tachypnea and retractions • S3 and occasionally S4 gallops may be present and are important signs of impaired ventricular function • If the right or left ventricular dilation is severe, auscultation may reveal murmurs of functional mitral or tricuspid insufficiency Physical Findings • Signs of low cardiac output • Pericardial friction rub and effusion may become evident in some patients with myopericarditis • A widely inflamed heart shows the classic signs of ventricular dysfunction including the following: ▫ ▫ ▫ ▫ Jugular venous distention Bibasilar crackles Ascites Peripheral edema Causes • Infectious • Toxic • Immunologic Infectious Causes • Viral myocarditis is the most common ▫ ▫ ▫ ▫ ▫ Parvovirus B19, 36.6% Enterovirus, 32.6% Human herpesvirus 6 (HHV-6), 10.5% Adenovirus, 8.1% Co-infection with HHV-6 and parvovirus B19, 12.6% • HIV Infectious Causes • Bacterial causes ▫ Most common worldwide is Diphtheria ▫ Streptococcal and staphylococcal species and Bartonella, Brucella, Leptospira, and Salmonella species can spread to the myocardium as a consequence of severe cases of endocarditis • Chagas disease • Parasitic myocarditis from trypanosomiasis Toxic Causes • Numerous medications (eg, lithium, doxorubicin, cocaine, numerous catecholamines, acetaminophen) may exert a direct cytotoxic effect on the heart • Zidovudine (AZT) has been associated with myocarditis Toxic causes • Environmental toxins include lead, arsenic, and carbon monoxide • Wasp and scorpion stings and spider bites, specifically black widows, may cause myocarditis • Radiation therapy Immunologic Etiology • Connective tissue disorders ▫ ▫ ▫ ▫ Systemic lupus erythematosus (SLE) Rheumatoid arthritis Scleroderma Dermatomyositis • Idiopathic inflammatory and infiltrative disorders such as Kawasaki disease, sarcoidosis, and giant cell arteritis may be a cause Differential Diagnoses • • • • • • • Acute Coronary Syndrome Pneumonia Congestive Heart Failure Aortic Dissection Pulmonary Embolism Esophageal Perforation, Rupture and Tears Viral syndrome Diagnostic Studies • • • • • • • EKG CXR Cardiac enzymes Echo MRI with contrast Cardiac catheterization Other tests EKG • Classical triad ▫ Sinus tachycardia (>100 in a child; >120 in an infant; >150 in a neonate) ▫ Low voltage complexes ▫ ST segment and T wave changes • Other abnormalities like, varying AV blocks, bundle branch blocks, both supraventricular and ventricular arrhythmias and an even an anterior wall myocardial infarction pattern Chest Radiograph • Typically include cardiomegaly, although heart size may be normal • Pulmonary vascular congestion is often present Cardiac Enzymes • Elevation reflects myocardial necrosis • Seen in some patients with myocarditis • Experimental and clinical findings in adults suggest that elevations of cardiac troponin I or T (cTnI or cTnT) levels may be more common than CK-MB elevations in patients with biopsyproven myocarditis Echocardiography • Enlarged Left Ventricular (LV) dimensions, left atrial enlargement and impaired ejection fraction (EF) and shortening fraction • Normal EF in children is 64+4% • 2D echo reveals a large, hypo contractile LV which is globular, with thin walls, mild pericardial effusion and occasional regional wall motion abnormalities MRI • Said to pick up earliest abnormality in Myocarditis • Document the location and extent of inflammation • Gadolinium enhancement was greater in patients with myocarditis than in normal controls Cardiac Catheterization • Reveals depressed cardiac index, elevated left ventricular end diastolic pressure, and elevated mean atrial pressure • Angiography shows decreased left ventricular function with or without mitral regurgitation • Main purpose is to obtain samples by endomyocardial biopsy (EMB) for pathologic and microbiologic analysis Endomyocardial Biopsy (EMB) • Gold standard for the diagnosis of myocarditis • Dallas criteria ▫ Active myocarditis is defined as "an inflammatory infiltrate of the myocardium with necrosis and/or degeneration of adjacent myocytes not typical of the ischemic damage associated with coronary heart disease" EMB • Dallas criteria ▫ Borderline myocarditis is the term used if lymphocytic infiltration is present without myocyte destruction ▫ Ongoing Myocarditis – both inflammation and necrosis present. ▫ Resolving Myocarditis – inflammation may be present; cell necrosis not ▫ Resolved Myocarditis – No inflammation / cell necrosis. EMB • The American Heart Association, the American College of Cardiology, and the European Society of Cardiology released a scientific statement on the role of EMB ▫ Limited data are available on EMB in children ▫ EMB is reasonable in the setting of unexplained cardiomyopathy in children. ▫ Indications include fulminant or acute unexplained heart failure, cardiac transplant rejection monitoring, certain unexplained arrhythmias, and idiopathic dilated cardiomyopathy Treatment • Mainstays of therapy for acute or fulminant myocarditis are monitoring, supportive care, and standard regimens for heart failure • Patients should be monitored in a pediatric intensive care unit Treatment of Heart Failure • In the acute phase, diuretics, afterload reducing agents, and inotropic drugs are used to treat heart failure • Dopamine, dobutamine, and milrinone are used to prevent circulatory collapse in the case of acute fulminant myocarditis Treatment of Heart Failure • Mechanical ventilation • ECMO • Ventricular Assist Device • For patients who progress from acute myocarditis to chronic heart failure, diuretics, angiotensin inhibitors, digoxin, and aldosterone inhibitors (ie, spironolactone) are well-accepted therapies Anti-arrhythmic Drugs • Most antiarrhythmic drugs have negative inotropic activity and may therefore worsen cardiac function and lead to acute hemodynamic instability • Should be used only when the expected benefit exceeds the risk, and only in consultation with a pediatric cardiologist Immunosuppressive Therapy • Myocardial damage in infectious myocarditis is thought to be due to both direct viral damage and the immune response to infection. ▫ Myocarditis Treatment Trial: 111 patients with a histopathologic diagnosis of myocarditis and a left ventricular ejection fraction (LVEF) of less than 45 percent were randomly assigned to receive conventional therapy alone or immunosuppression with either cyclosporine or azathioprine for 28 weeks [7]. There was no difference in outcome in the two treatment groups. Immunosuppressive Therapy • Corticosteroids ▫ Case series and a small trial are inconclusive with respect to the beneficial effects of prednisone and/or other immunosuppressive agents (azathioprine, cyclosporine) on left ventricular function and ventricular arrhythmias in children with myocarditis, but definitive data are lacking Immunosuppressive Therapy • IVIG ▫ use is supported by experimental data in which polyclonal immunoglobulin protects against myocardial or arterial damage in mouse models of viral and autoimmune myocarditis ▫ no randomized controlled trials of IVIG for the treatment of myocarditis in children have been reported, some clinical evidence suggests it may be beneficial Pain control • Narcotic analgesic • Avoid NSAIDs which are relatively contraindicated in this condition PROGNOSIS • Most cases are believed to be clinically silent and resolve spontaneously without sequelae • Patients who present with CHF experience morbidity and mortality based on the degree of left ventricular dysfunction. • Patients who do not fully recover cardiac function may develop dilated cardiomyopathy. OUTPATIENT FOLLOW UP • Recovered patients should have restricted activity for 6 months because rapid return to activity has provoked recurrent inflammation in animal models • Follow-up visits with a cardiologist