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Ebstein Anomaly

Educational clinical summary of Ebstein Anomaly for doctors and students: definition, workup, management, and key caveats. Not a substitute for guidelines.

Maintained by Dr. Vivek Karn Review process: editorial policy

Overview

  • Definition: Ebstein anomaly is a rare congenital heart defect characterized by the apical displacement of the septal and posterior leaflets of the tricuspid valve into the right ventricle. This displacement leads to "atrialization" of a portion of the right ventricle, causing varying degrees of tricuspid regurgitation and right ventricular dysfunction. The anterior tricuspid leaflet, often described as "sail-like" or "fenestrated," is usually much larger and is typically tethered to the annulus.
  • Epidemiology:
    • Occurs in approximately 1 in 20,000 live births, representing less than 1% of all congenital heart diseases.
    • No significant sex predilection.
    • Familial cases are rare, but genetic associations with mutations in the NKX2.5 gene and other chromosomal abnormalities have been noted.
    • Associated with maternal lithium exposure during the first trimester (though the absolute risk is low).
  • Classification:
    • While various classifications exist, the Carpentier classification is commonly used, focusing on the degree of leaflet displacement and right ventricular dysfunction, which can guide surgical approach:
      • Type A: Large, mobile anterior leaflet; small atrialized RV; good functional RV.
      • Type B: Large, mobile anterior leaflet; moderate atrialized RV; RV pump function compromised.
      • Type C: Restricted anterior leaflet movement; large atrialized RV; significant RV dysfunction.
      • Type D: Completely adherent tricuspid leaflets with severe displacement; often associated with a patent ductus arteriosus (PDA) and functional pulmonary atresia (known as "neonatal Ebstein"). This is the most severe form.

Pathophysiology

  • Mechanism: The fundamental defect is a failure of delamination of the tricuspid valve leaflets from the underlying myocardium during cardiac development (typically weeks 4-6 of gestation). This results in:
    1. Apical displacement: The septal and posterior leaflets originate from the ventricular wall rather than the tricuspid annulus.
    2. Atrialization of the RV: The portion of the right ventricle proximal to the displaced leaflets functions as part of the right atrium, becoming thin-walled and poorly contractile.
    3. Tricuspid regurgitation (TR): The malformed and displaced leaflets are often insufficient, leading to varying degrees of TR.
    4. Right ventricular dysfunction: The functional right ventricle (distal to the displaced leaflets) is often hypoplastic and unable to effectively pump blood.
    5. Right-to-left shunting: Due to elevated right atrial pressure from severe TR and RV dysfunction, a patent foramen ovale (PFO) or atrial septal defect (ASD) often allows deoxygenated blood to cross into the left atrium, leading to cyanosis.
    6. Arrhythmias: The dilated right atrium and areas of abnormal myocardial tissue (e.g., accessory pathways, especially Wolff-Parkinson-White syndrome) are prone to supraventricular tachycardias (SVT) and atrial fibrillation.
  • Risk Factors:
    • Maternal lithium exposure during early pregnancy (increased risk, but still rare overall).
    • Genetic predisposition (e.g., NKX2.5 mutations, although most cases are sporadic).
    • Associated with other congenital heart defects in a minority of cases (e.g., VSD, pulmonary stenosis/atresia).
  • Protective Factors: None definitively identified. Early diagnosis and appropriate management are crucial for mitigating adverse outcomes.

Clinical Presentation

Signs and Symptoms

  • Cardinal Features: Vary widely depending on severity and age of presentation.
    • Cyanosis: Most common symptom, especially in neonates and severe cases, due to right-to-left shunting through a PFO/ASD.
    • Dyspnea/Fatigue: Progressive onset, particularly with exertion, due to reduced cardiac output and RV dysfunction.
    • Palpitations: Due to arrhythmias (SVT, atrial fibrillation).
    • Right-sided heart failure symptoms: Edema (lower extremity or abdominal), hepatomegaly (less common in children).
  • Early Signs (Neonates/Infants):
    • Severe cyanosis (often noticed immediately after birth).
    • Tachypnea, retractions, poor feeding.
    • Cardiomegaly on chest X-ray ("box-shaped" or "wall-to-wall" heart).
    • Peripheral edema in severe cases.
    • May present as cardiovascular collapse if severe TR and pulmonary outflow obstruction (functional pulmonary atresia) are present.
  • Advanced Signs (Adolescents/Adults with moderate-to-severe disease):
    • Progressive exertional dyspnea.
    • Increasing cyanosis.
    • Edema, ascites.
    • Syncope (especially with arrhythmias).
    • Symptoms of paroxysmal supraventricular tachycardia (SVT).
    • Sudden cardiac death (rare, but a risk with severe arrhythmias).
  • Atypical Presentations:
    • Asymptomatic until adulthood (mild cases).
    • Presentation solely due to arrhythmia without significant hemodynamic compromise.
    • Paradoxical embolism (stroke or peripheral embolism) due to right-to-left shunt.

Physical Examination

  • Inspection:
    • Cyanosis (central or peripheral, degree variable).
    • Jugular venous distension (JVD) in severe cases.
    • Precordial bulge due to severe cardiomegaly.
  • Palpation:
    • Diffuse hyperdynamic precordium (RV heave) in severe TR.
    • Palpable liver edge.
  • Auscultation:
    • S1: Widely split, diminished, or cloaked by a holosystolic murmur.
    • S2: Widely split, P2 often diminished or single (due to reduced pulmonary blood flow).
    • S3: May be present, indicating RV dysfunction.
    • S4: May be present, especially with RV hypertrophy.
    • Murmurs:
      • Holosystolic murmur: Typically heard at the left lower sternal border, often radiating to the left upper sternal border, indicative of tricuspid regurgitation. Its intensity does not typically increase with inspiration (Carvallo's sign is often absent or inverted due to the fixed, displaced valve).
      • Diastolic murmur: May be present due to tricuspid stenosis or increased flow across the tricuspid valve.
      • Variable murmurs: From associated defects like PDA or VSD.
  • Special Tests: None specific during a bedside physical exam beyond general cardiac assessment.

Diagnostic Approach

History Taking

  • Key Questions:
    • Onset and progression of cyanosis (if present).
    • Exertional capacity, fatigue, dyspnea.
    • Episodes of palpitations, dizziness, or syncope.
    • Parental history of congenital heart disease or maternal medication exposure (e.g., lithium).
    • Symptoms of right-sided heart failure (edema, abdominal distension).
    • Any history of stroke or transient ischemic attack (TIA).
  • Red Flags:
    • Progressive cyanosis or dyspnea, especially at rest.
    • Frequent or sustained palpitations.
    • Syncope.
    • Signs of rapid decompensation (e.g., acute right heart failure).
    • Paradoxical embolism.

Laboratory Tests

  • First-Line:
    • Complete Blood Count (CBC): To assess for polycythemia (secondary to chronic hypoxemia) or anemia.
    • Arterial Blood Gas (ABG) / Pulse Oximetry: To assess oxygen saturation and degree of hypoxemia.
    • Electrolytes, Renal & Liver Function Tests: To assess organ function, especially in heart failure.
    • Brain Natriuretic Peptide (BNP)/N-terminal pro-BNP (NT-proBNP): Elevated levels may indicate myocardial stretch and heart failure, aiding in prognostication and monitoring.
  • Confirmatory: None specifically, diagnosis is primarily imaging-based.
  • Monitoring:
    • Repeat CBC for polycythemia (hematocrit > 60-65% may indicate hyperviscosity syndrome).
    • Follow-up electrolytes and organ function as clinically indicated.

Imaging

  • Recommended:
    • Echocardiography (Transthoracic Echocardiogram - TTE): Diagnostic modality of choice.
      • Confirms diagnosis: Demonstrates apical displacement of the septal and posterior tricuspid leaflets (>8 mm/m² body surface area in adults, or quantitative measures relative to mitral valve annulus in children).
      • Assesses severity: Quantifies global and regional RV size and function (functional RV, atrialized RV).
      • Evaluates tricuspid regurgitation (TR): Degree, mechanism, and presence of tethering or fenestrations.
      • Identifies associated lesions: PFO/ASD, VSD, pulmonary stenosis/atresia, LV dysfunction.
      • Estimates pulmonary artery pressures and RV systolic pressure.
      • Evaluates for accessory pathways: May show pre-excitation or evidence of WPW.
    • Chest Radiograph (CXR):
      • "Box-shaped" or "wall-to-wall" heart due to massive cardiomegaly (dilated right atrium and atrialized RV).
      • Reduced pulmonary vascular markings in severe cases.
  • Advanced:
    • Cardiac Magnetic Resonance Imaging (CMR):
      • Highly recommended for comprehensive assessment: Provides superior tissue characterization, precise quantification of RV volumes, ejection fraction, and TR fraction, especially when echocardiographic windows are suboptimal.
      • Can accurately delineate the atrialized and functional RV.
      • Identifies myocardial fibrosis/scarring via late gadolinium enhancement.
      • Useful for pre-operative planning.
    • Cardiac Computed Tomography (CCT):
      • Less commonly used than CMR unless CMR is contraindicated (e.g., pacemaker).
      • Provides excellent anatomical detail, particularly for defining the tricuspid valve anatomy and its relation to the RV.
      • Useful for surgical planning.
    • Electrocardiogram (ECG):
      • Often shows right atrial enlargement (tall, peaked P waves in lead II: "P tricuspidale").
      • Right bundle branch block (RBBB) is common, particularly incomplete RBBB.
      • WPW syndrome: Common (up to 25% of patients), manifested by a short PR interval, delta wave, and wide QRS. Can lead to SVT.
      • Low voltage QRS in precordial leads may be seen due to extreme cardiomegaly.
      • Atrial arrhythmias (AF, atrial flutter) are common in older patients.
    • Holter Monitoring / Event Recorder:
      • To detect and characterize arrhythmias (SVT, atrial fibrillation, ventricular ectopy).
      • Essential for patients presenting with palpitations or pre-syncope.
    • Electrophysiology Study (EPS):
      • Indicated if accessory pathways are suspected (WPW on ECG) and for risk stratification or ablation planning for recurrent symptomatic tachyarrhythmias.

Management

Acute Management

  • Immediate:
    • Neonates with severe cyanosis: Maintain PDA patency with prostaglandin E1 (PGE1) infusion (initial dose 0.05-0.1 mcg/kg/min IV, titrated down to 0.01-0.03 mcg/kg/min IV) if severe pulmonary hypoperfusion/functional pulmonary atresia is present. This may be life-saving by providing pulmonary blood flow.
    • Acute heart failure: Diuretics (e.g., Furosemide 0.5-1 mg/kg IV) for pulmonary congestion or systemic edema.
    • Acute arrhythmias: Manage according to ACLS/PALS guidelines. Procainamide or synchronized cardioversion for unstable SVT.
  • Stabilization:
    • Optimize oxygenation and ventilation: Supplemental oxygen, mechanical ventilation if necessary.
    • Fluid balance: Judicious fluid management, avoiding overload in individuals with RV dysfunction.
    • Inotropes/Vasopressors: May be required for cardiogenic shock (e.g., dopamine, dobutamine, milrinone).
  • Emergency:
    • Balloon atrial septostomy (BAS): In neonates with severe cyanosis, an intact atrial septum or highly restrictive PFO, and functional pulmonary atresia, BAS can improve systemic oxygenation by decompressing the right atrium and augmenting right-to-left shunting. This is a temporizing measure.
    • Emergency surgery: Rarely needed acutely, unless profound hemodynamic collapse not responsive to medical management, or for critical neonates requiring immediate unifocalization (cone repair) or a staged Norwood variant for single ventricle physiology.

Chronic Management

  • Pharmacological:
    • Diuretics: For symptoms of systemic venous congestion (e.g., furosemide, spironolactone).
    • ACE inhibitors/ARBs: May be considered for symptomatic systolic RV dysfunction or chronic heart failure.
    • Beta-blockers: For rate control in atrial fibrillation, or in some cases, to reduce catecholamine-mediated stress on the RV.
    • Antiarrhythmics:
      • Conduction system disease: Beta-blockers, flecainide, propafenone for SVT. Amiodarone for refractory cases.
      • Anticoagulation: For patients with atrial fibrillation/flutter who have increased risk of stroke (CHA2DS2-VASc score guidance generally applies). Consider in patients with severe right atrial dilation and right-to-left shunt, regardless of arrhythmia.
    • Endocarditis prophylaxis: Generally not recommended unless there's a prosthetic valve or prior endocarditis.
  • Non-pharmacological:
    • Regular follow-up: With a congenital heart disease specialist.
    • Activity restriction: individualized based on severity, functional capacity, and presence of arrhythmias or pulmonary hypertension. Generally, mild-to-moderate unoperated Ebstein anomaly allows for most activities; severe forms require restriction from competitive sports or high-intensity exercise.
    • Counseling: Genetic counseling, psychosocial support.
    • Electrophysiology (EP) study and catheter ablation: For symptomatic or high-risk accessory pathways (e.g., WPW, especially if inducible arrhythmias or high-risk features are noted on EP study).
  • Monitoring:
    • Regular echocardiograms: Every 6-12 months typically, or more frequently if rapidly changing symptoms or severe disease, to assess RV function, TR severity, and chamber dimensions.
    • ECG and Holter monitoring: Annually or as symptoms dictate, to screen for arrhythmias.
    • Exercise stress testing: To assess functional capacity, exercise-induced arrhythmias, and oxygen desaturation.
    • CMR: Periodically, especially for comprehensive RV assessment or pre-surgical planning.

Treatment Algorithms

  • First-Line (Surgical or Catheter Intervention):
    • Surgical Repair (Tricuspid Valve Repair): The preferred approach for symptomatic patients with moderate-to-severe TR, progressive RV dilation/dysfunction, or worsening cyanosis.
      • Cone Reconstruction (DeVega annuloplasty combined with leaflet plication and anterior leaflet mobilization and resuspension): The current gold standard, aiming to create a monocuspid valve from the anterior leaflet, restoring competence while preserving tricuspid tissue. Generally performed when TV leaflets are adequate.
      • Plication of atrialized RV + annuloplasty: Older technique, still used sometimes.
      • Tricuspid Valve Replacement: Considered when repair is not feasible due to severe leaflet dysplasia or destruction. Bioprosthetic valves are preferred due to the challenge of managing anticoagulation in children and young adults; however, they have limited durability. Mechanical valves require lifelong anticoagulation.
    • Accessory Pathway Ablation: For stable, symptomatic or high-risk WPW patients. Can be performed prior to or concurrent with surgical repair.
  • Second-Line:
    • Glen Shunt (Bidirectional Cavopulmonary Anastomosis): For palliative management in patients with severe RV dysfunction, significant cyanosis, and inability to undergo TV repair (e.g., severe Type D or advanced disease). Connects the superior vena cava to the pulmonary artery, offloading the RV and improving oxygenation. Not a definitive correction.
    • Fontan Procedure: Rarely performed, typically only in the most severe cases where the RV cannot sustain systemic output (e.g., functional single ventricle physiology after a Norwood variant procedure in infancy), converting to a single-ventricle circulation.
  • Refractory Cases:
    • Heart Transplantation: For end-stage RV failure, pulmonary hypertension, and severe symptoms despite maximal medical and surgical interventions. This is a last resort option.
    • Ventricular Assist Devices (VADs): May be considered as a bridge to transplant in severe biventricular failure.

Complications

  • Common:
    • Tricuspid Regurgitation: Varies from mild to severe, leading to RV volume overload.
    • Right Ventricular Dysfunction: Both the atrialized and functional RV can have impaired contractility.
    • Cyanosis: Due to right-to-left shunting (PFO/ASD).
    • Arrhythmias: SVT (WPW, AVNRT, atrial flutter, atrial fibrillation) are very common.
    • Progressive heart failure: Due to long-standing RV dysfunction and TR.
  • Serious:
    • Sudden Cardiac Death: Due to refractory ventricular arrhythmias or rapid atrial arrhythmias (e.g., AF with rapid conduction over an accessory pathway bypassing the AV node, leading to ventricular fibrillation). This risk is low but emphasized in risk stratification.
    • Paradoxical Embolism: Stroke or other systemic emboli due to venous clots crossing an ASD/PFO from right to left.
    • Pulmonary Hypertension: Can develop long-term, especially if there is significant left-to-right shunting or severe TR affecting pulmonary vascular resistance.
    • Acute RV failure: Rarely in crisis situations.
  • Long-term:
    • Chronic fatigue and exercise intolerance.
    • Polycythemia: Secondary to chronic hypoxemia, increasing risk of thrombotic events.
    • Recurrence of TR or arrhythmias after surgery.
    • Progressive chronic kidney disease from chronic heart failure and reduced cardiac output.

Prognosis

  • Factors:
    • Severity of Ebstein anomaly: As defined by degree of leaflet displacement, TR, RV dysfunction, and size of the functional RV. Neonatal presentation is associated with the worst prognosis.
    • Presence and severity of cyanosis: Severe cyanosis at birth indicates a poor prognosis without intervention.
    • Presence of associated lesions: Functional pulmonary atresia or severe LV dysfunction worsens prognosis.
    • Presence and control of arrhythmias: Uncontrolled supraventricular tachyarrhythmias increase morbidity and mortality.
    • Age at presentation: Neonatal presentation is associated with higher mortality.
    • Surgical intervention: Successful tricuspid valve repair, particularly cone reconstruction, significantly improves long-term prognosis and quality of life.
  • Survival:
    • Highly variable. Untreated severe cases have high mortality in infancy (up to 50% in the first year).
    • Mild cases may be asymptomatic and have a near-normal life expectancy.
    • After successful surgical repair (especially cone reconstruction), 20-year survival rates approach 80-90% for symptomatic patients, with significant improvement in functional capacity.
  • Quality of Life:
    • Often limited by fatigue, dyspnea, and recurrent arrhythmias, particularly before surgical intervention.
    • May improve significantly post-surgery with restored RV function and reduced TR.
    • Patients may require lifelong monitoring and management for arrhythmias and potential re-interventions.

Prevention

  • Primary:
    • Avoidance of known teratogens: Maternal lithium exposure during the first trimester. While lithium is a known risk factor, it's generally a low absolute risk, and the decision regarding its use in pregnant women needs to weigh the maternal psychiatric benefits against this small risk.
    • Genetic counseling: For families with a history of Ebstein anomaly or other congenital heart defects, though most cases are sporadic.
  • Secondary:
    • Early prenatal diagnosis: Fetal echocardiography can detect Ebstein anomaly in utero, allowing for planned delivery at a specialized center and early postnatal intervention if needed.
    • Newborn screening: Pulse oximetry screening for critical congenital heart disease can help detect cyanosis.
    • Early referral: Timely referral to a pediatric cardiologist upon suspicion of congenital heart disease for comprehensive evaluation.
  • Tertiary:
    • Prevention of complications: Aggressive management of arrhythmias, heart failure, and regular follow-up to monitor cardiac function.
    • Prophylaxis for paradoxical embolism: Consider anticoagulation in select high-risk patients with ASD/PFO and signs of venous thromboembolism.

Special Populations

  • Pediatric:
    • Neonates: Often present with severe cyanosis, requiring PGE1, BAS, or early surgical intervention (cone repair or single ventricle palliation). Mortality is highest in this group.
    • Infants/Young children: Closely monitored for growth, development, and exercise tolerance. Surgical indication varies with symptoms and severity.
  • Geriatric:
    • Rarely present de novo in this age group as it's a congenital defect.
    • Older adults with previously undiagnosed or uncorrected mild disease are more likely to present with new-onset heart failure symptoms or arrhythmias (e.g., persistent atrial fibrillation). Management focuses on symptom control and optimization of medical therapy. Surgical risk is higher due to age and comorbidities.
  • Pregnancy:
    • Risk stratification is crucial: Maternal risk is assessed based on NYHA functional class, exercise capacity, severity of TR, RV function, presence of cyanosis, and arrhythmias.
    • Increased risk: Pregnant women with Ebstein anomaly have an increased risk of arrhythmias (especially SVT), worsening heart failure, developing pulmonary hypertension, and cardiac complications during delivery.
    • Fetal risk: Increased risk of miscarriage, preterm delivery, and fetal growth restriction. The risk of recurrence of Ebstein anomaly in the offspring is low but higher than the general population (around 1-4%).
    • Management: Requires a multidisciplinary approach (cardiologist, maternal fetal medicine specialist, anesthesiologist). Close monitoring for arrhythmias and heart failure. Avoidance of medications potentially harmful to the fetus.
  • Comorbidities:
    • Down Syndrome: Increased incidence of congenital heart defects, but Ebstein anomaly is less frequently associated than VSD or AVSD.
    • Arrhythmias (WPW): Requires careful management, as ablation is often beneficial in preventing sudden cardiac death or symptomatic episodes.
    • Psychiatric disorders: Patients on lithium require careful monitoring for compliance and alternative medication strategies if considering pregnancy.

Clinical Pearls

  • Diagnostic:
    • Think Ebstein with "box-shaped heart" on CXR, unexplained cyanosis in a neonate, or new-onset SVT with a congenital heart defect.
    • The degree of tricuspid regurgitation on echo is critical, but don't solely rely on it; assess RV size and function (atrialized and functional RV) holistically.
    • WPW and right atrial enlargement on ECG are strong clues.
  • Treatment:
    • Cone repair is the gold standard for surgical correction and aims to preserve TV tissue, offering superior long-term results compared to replacement.
    • Early referral to a specialized congenital heart disease center is paramount for optimizing management, especially for decision-making regarding surgical timing and technique.
    • Management of arrhythmias is a cornerstone, as they are frequent and can be debilitating or life-threatening.
  • Pitfalls:
    • Underestimating the severity of RV dysfunction due to compensatory mechanisms. CMR is invaluable here.
    • Delayed diagnosis or referral, especially in milder forms, can lead to progressive RV remodeling and worse surgical outcomes.
    • Misinterpreting the holosystolic murmur as a VSD or simple TR, overlooking other subtle findings.
    • Overlooking concomitant accessory pathways, leading to inadequate arrhythmia management and increased risk.
    • Aggressive management of polycythemia (phlebotomy) without proper indication can sometimes lead to iron deficiency and worsen exercise tolerance; conservative approach is often preferred.

Recent Updates

  • Guidelines:
    • Recent guidelines (e.g., ACC/AHA Adult Congenital Heart Disease Guidelines) emphasize the role of CMR for comprehensive anatomical and functional assessment and recommend Cone reconstruction as the preferred surgical technique.
    • Increased emphasis on multidisciplinary care for pregnant patients and those with complex arrhythmias.
  • Evidence:
    • Growing evidence supports the long-term superiority of tricuspid valve repair (especially cone reconstruction) over replacement, with excellent functional outcomes and improved survival.
    • Advancements in catheter ablation techniques have improved success rates and safety for accessory pathways associated with Ebstein anomaly.
    • Research into the genetic basis of Ebstein anomaly continues, identifying new gene associations beyond NKX2.5, though most cases remain sporadic.
  • Controversies:
    • Optimal timing of surgery: While symptomatic individuals clearly benefit, the optimal timing for asymptomatic or mildly symptomatic patients with objective evidence of progression (e.g., RV dilation, worsening TR) remains a topic of debate, balancing the risks of early surgery against the benefits of preventing irreversible RV damage.
    • Role of valve replacement vs. repair: While repair is generally preferred, debate continues on the type of prosthetic valve (mechanical vs. bioprosthetic) when repair is not feasible, especially in younger patients.

Key References

  • Guidelines:
    • 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: Offers comprehensive recommendations for diagnosis, risk stratification, and management of Ebstein anomaly in adults.
    • 2017 ESC Guidelines for the management of valvular heart disease: Includes sections relevant to Ebstein anomaly and tricuspid valve disease.
    • AHA/ACC Guideline for the Management of Patients With Supraventricular Tachycardia: Addresses management of arrhythmias, including WPW syndrome relevant to Ebstein anomaly.
  • Studies:
    • Carpentier A, Chauvaud S, Mace L, et al. A new reconstructive operation for Ebstein's anomaly of the tricuspid valve. J Thorac Cardiovasc Surg. 1988;96(1):92-101. (Landmark paper describing the original cone repair concept).
    • Ma L, Song N, Liu J, et al. Cone Reconstruction for Ebstein Anomaly: A 20-Year Experience. JACC Cardiovasc Interv. 2021 May 24;14(10):1135-1144. (Recent large series on cone reconstruction outcomes).
    • Attenhofer Jost CH, Connolly HM, Dearani JA, et al. Ebstein's Anomaly. Circulation. 2007 May 29;115(21):e662-e671. (Comprehensive review of the disease).
  • Reviews:
    • Burch TM, Saliba AN, Dearani JA, et al. Ebstein's Anomaly: An Update for the Clinician. Clin Cardiol. 2017 Jul;40(7):501-508.
    • Warnes CA. Ebstein's anomaly: not so benign. Heart. 2006 Jan;92(1):16-8.

Disclaimer: This information is intended for educational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Clinical judgment must always be exercised in the context of individual patient circumstances.

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