eMedicine Specialties > Pediatrics: Surgery > General Surgery

Diaphragmatic Hernias

Nicola Lewis, MBBS, FRCS, Specialist Registrar, Department of Surgery, Birmingham Children's Hospital, UK
Philip Glick, MD, MBA, Professor, Departments of Surgery, Pediatrics, and Gynecology and Obstetrics, Vice-Chairperson for Research and Development, Department of Surgery, State University of New York at Buffalo

Updated: Oct 27, 2008

Introduction

History of the Procedure

In 1679, Lazarus Riverius (1589-1655) recorded the first reported case of a congenital diaphragmatic hernia (CDH); this was following postmortem examination of a 24-year-old male.¹ The first attempt at surgical repair for congenital diaphragmatic hernia was by Nauman of Sweden in 1888; the 19-year-old patient presented with acute respiratory distress and an acute abdomen, and a laparotomy was performed. In 1889, J. O'Dwyer, MD, carried out the first repair of congenital diaphragmatic hernia in an infant. The first successful repair occurred in 1905. The patient was aged 9 years, and Heidenhain (at the Municipal Hospital for Worms, Germany) reduced the hernia and closed the diaphragmatic defect through a midline laparotomy incision. Approximately 20 years later, Carl Hedbolm reported a 58% mortality rate for patients undergoing surgical intervention for congenital diaphragmatic hernia.

In 1940, William Ladd and Robert Gross based their diagnosis of congenital diaphragmatic hernia on history, physical examination findings, and findings on chest radiography with or without a barium meal.² They advocated early surgical intervention (within the first 48 h). Gross also described a 2-staged closure of the abdominal wall in difficult cases; closure of skin and subcutaneous fascia at the initial surgery and closure of the abdominal wall 5-6 days later. In 1950, C. Everett Koop and Julian Johnson suggested the transthoracic approach as a means of closing the defect under more direct vision.³

As surgical expertise improved, innovative strategies were developed to address large diaphragmatic defects and agenesis of the hemidiaphragm. These techniques included the use of rotational muscle flaps, perirenal fascia, and synthetic patch repairs.

The exponential elucidation of the pathophysiology of congenital diaphragmatic hernia was instrumental in improving the survival rate in infants. Congenital diaphragmatic hernia was no longer considered a primarily surgical disease but rather a disease associated with pulmonary hypoplasia, pulmonary hypertension, pulmonary immaturity, and an increased susceptibility of the lungs to ventilation-induced lung injury. This led to a delayed approach to surgical repair and to a gentle but more ingenious respiratory support.

Problem

Associated anomalies are present in 10-50% of patients with congenital diaphragmatic hernias; these anomalies confer a 2-fold relative risk of mortality when compared with patients with isolated congenital diaphragmatic hernias.⁴ Frequently associated anomalies include cardiac defects, chromosomal anomalies (ie. trisomies 21, 18, and 13), renal anomalies, genital anomalies, and neural tube defects.

Frequency

Congenital diaphragmatic hernia occurs in 1 per 3000 live births.⁵

Mortality

The Congenital Diaphragmatic Hernia Study Group recorded a 63% survival rate in 1995-1996 based on data from 62 centers in North America, Europe, and Australia.⁶ Survival rates are 60-90% for patients who present within the first few hours of life (see Media file 1).⁷

Etiology

Relevant embryology

The diaphragm is derived from 4 embryonic structures: the septum transversum, the pleuroperitoneal membranes, mesoderm of the body wall, and esophageal mesenchyme. Following folding of the fetal head at 4-5 weeks' gestation, the septum transversum comes to lie as a semicircular shelf, which separates the heart from the liver. The septum transversum does not completely separate the thoracic cavity from the peritoneal cavity but allows pericardioperitoneal canals to exist on either side of the esophagus.

During the fifth week of gestation, the pleuroperitoneal membranes develop along a line connecting the root of the 12th rib with the tips of the 7th to 12th ribs. The pleuroperitoneal membranes grow ventrally to fuse with the posterior margins of the septum transversum and the dorsal mesentery of the esophagus. Hence, at 6-7 weeks' gestation, the pleuroperitoneal canals are closed; the left closes after the right. The mesentery of the esophagus condenses to form the left and right crura of the diaphragm, and the mesoderm of the body wall forms the outer rim of diaphragmatic muscle.

The posterolateral diaphragmatic defect is postulated to result from failure of closure of the pleuroperitoneal canals. The canal remains open when the intestines return to the abdomen at 10 weeks' gestation. Some intestine and other viscera enter the thorax and lead to compression of the developing lung at the crucial pseudoglandular stage and shifting of the mediastinum to the contralateral side. This causes compression of the heart and the contralateral lung as well.

In 1984, Iritani proposed a different concept of diaphragmatic development. He suggested that a posthepatic mesenchymal plate develops between the septum transversum and the pericardioperitoneal canals.⁸ Lateral growth of this plate leads to closure of the pericardioperitoneal canals, and congenital diaphragmatic hernia results from a disturbance in growth of the posthepatic mesenchymal plate.

Causes

• Genetic factors: The initiating factor responsible for the development of congenital diaphragmatic hernia is unknown. Wide variations have been noted in the reported prevalence of chromosomal abnormalities (7-31%) in patients with congenital diaphragmatic hernia. The prevalence is higher in cases of congenital diaphragmatic hernia associated with other defects.⁵ Familial occurrence has been noted in fewer than 2% of cases.
• Other causes: The role of drugs and environmental chemicals in the development of congenital diaphragmatic hernia is uncertain, but nitrofen, quinine, thalidomide, phenmetrazine, and polybrominated diphenyls have been used to induce congenital diaphragmatic hernia in various species. Current investigations are exploring the link between congenital diaphragmatic hernia and defects in the retinoid signaling pathway in experimental models.

Pathophysiology

The pathophysiology of congenital diaphragmatic hernia involves pulmonary hypoplasia, pulmonary hypertension, pulmonary immaturity, and potential deficiencies in the surfactant and antioxidant enzyme system.

Because of bowel herniation into the chest during crucial stages of lung development, airway divisions are limited to the 12th to 14th generation on the ipsilateral side and to the 16th to 18th generation on the contralateral side. Normal airway development results in 23-35 divisions. Because airspace development follows airway development, alveolarization is similarly reduced.

Development of the pulmonary arterial system parallels development of the bronchial tree, and, therefore, fewer arterial branches are observed in congenital diaphragmatic hernia. Abnormal medial muscular hypertrophy is observed as far distally as the acinar arterioles, and the pulmonary vessels are more sensitive to stimuli of vasoconstriction.⁹ Pulmonary hypertension resulting from these arterial anomalies leads to right-to-left shunting at atrial and ductal levels. This persistent fetal circulation leads to right-sided heart strain or failure and to the vicious cycle of progressive hypoxemia, hypercarbia, acidosis, and pulmonary hypertension observed in the neonatal period.

The surfactant system is demonstrably deficient in the lamb model of congenital diaphragmatic hernia.¹⁰ Postnatal administration of surfactant in these lambs is associated with dramatic increases in gas exchange, lung compliance, and pulmonary blood flow. However, in human neonates, reports on the status of the surfactant system are inconsistent.^11,12

Infants with congenital diaphragmatic hernias also have impairment of the pulmonary antioxidant enzyme system and are more susceptible to hyperoxia-induced injury.

In addition, a left ventricular smallness and hypoplasia are observed with congenital diaphragmatic hernia. This is believed to arise from decreased in utero blood flow to the left ventricle, the mechanical compression of the herniated viscus similar to that observed in the lungs, and/or a primary yet unidentified developmental defect that simultaneously causes the diaphragmatic hernia and lung problems.

Presentation

Prenatal

The diagnosis of congenital diaphragmatic hernia is frequently made prenatally prior to 25 weeks' gestation.

Congenital diaphragmatic hernia is usually detected in the antenatal period (46-97%), depending on the use of level II ultrasonography techniques. Ultrasonography reveals polyhydramnios, an absent intra-abdominal gastric air bubble, mediastinal shift, and hydrops fetalis. Ultrasonography demonstrates the dynamic nature of the visceral herniation observed with congenital diaphragmatic hernia. The visceral hernia has moved in and out of the chest in several fetuses.

Differential diagnoses on prenatal ultrasonography are as follows:

• Congenital cystic adenomatoid malformation
• Pulmonary sequestration (This can be an associated finding in CDH) 
• Mediastinal cystic processes (eg, cystic teratoma, thymic cysts, foregut duplication cysts)
• Neurogenic tumors

Postnatal

History and clinical findings vary with the presence of associated anomalies and the degree of pulmonary hypoplasia and visceral herniation. In the infant presenting in the neonatal period without prenatal diagnosis, variable respiratory distress and cyanosis, feeding intolerance, and tachycardia are noted.

In the physical examination, the abdomen is scaphoid if significant visceral herniation is present (see Media file 2).

Upon auscultation, breath sounds are diminished, bowel sounds may be heard in the chest, and heart sounds are distant or displaced.

Late presentation

Patients may present outside of the neonatal period with intestinal obstruction, bowel ischemia, and necrosis following volvulus.

Indications

No time for repair of congenital diaphragmatic hernia (CDH) is ideal, but the authors suggest that the window of opportunity is 24-48 hours after birth to achieve normal pulmonary arterial pressures and satisfactory oxygenation and ventilation on minimal ventilator settings.

Relevant Anatomy

The diaphragm is a musculotendinous structure that separates the thoracic cavity from the abdominal cavity. It is composed of a central nonmuscular portion (central tendon) surrounded by a muscular rim in addition to the right and left diaphragmatic cura. The right and left diaphragmatic cura are 2 muscular bands that originate from vertebral bodies L1-L3 and L1-L2 respectively. These muscular bands insert into the dorsomedial diaphragm.

Most diaphragmatic defects are posterolateral, with 85-90% of these occurring on the left. The label "posterolateral" may be a misnomer because, frequently, much larger areas of the diaphragm are missing and only a posterior rim of muscle can be found. A hernial sac is present in 10-20% of cases.

The Morgagni defect occurs posterior to the sternum and results from failure of sternal and costal fibers to fuse at the site where the superior epigastric artery crosses the diaphragm. The Morgagni defect is rare and is rarely a cause for surgery in the newborn.

Contraindications

The association of congenital diaphragmatic hernia (CDH) with lethal congenital abnormalities is a relative contraindication to repair of the diaphragmatic defect.

Workup

Laboratory Studies

• Antenatal
  • Amniocentesis for karyotype analysis should accompany a diagnosis of congenital diaphragmatic hernia (CDH).
  • Maternal serum alpha-fetoprotein may be low in cases of congenital diaphragmatic hernia.
• Postnatal
  • Assess ABG.
  • Hypoxemia, hypercarbia, and respiratory or metabolic acidosis depend on the degree of pulmonary hypoplasia, persistent pulmonary hypertension of newborn (PPHN), right-to-left shunting, and ventricular function.

Imaging Studies

Level III ultrasonography and echocardiography should accompany a diagnosis of congenital diaphragmatic hernia. Prenatal echocardiography may identify cardiac anomalies (more commonly, ventricular hypoplasia, atrial septal defects, and ventricular septal defects).¹³

• Chest radiography
  • An early chest radiograph is obtained to confirm the diagnosis of congenital diaphragmatic hernia.
  • Findings include loops of bowel in the chest, mediastinal shift, paucity of bowel gas in the abdomen, and presence of the tip of a nasogastric tube in the thoracic stomach (see Media file 3). Repeated chest radiography may reveal a change in the intrathoracic gas pattern.
  • Right-sided lesions are difficult to differentiate from diaphragmatic eventration and lobar consolidation.
• Echocardiography
  • Further investigations should include early echocardiography, which may reveal cardiac defects, decreased left ventricular mass, poor ventricular contractility, pulmonary and tricuspid valve regurgitation, and right-to-left shunting.
  • Repeated echocardiography is recommended to measure changes in the pulmonary artery pressure, left-to-right shunt, and flow across the ductus arteriosus.

Treatment

Medical Therapy

In contrast to historic management patterns, which focused on the actual repair of the diaphragmatic hernia, the contemporary management of congenital diaphragmatic hernia (CDH) places emphasis on the management of pulmonary hypoplasia and persistent pulmonary hypertension. Current management uses various gentle alveolar recruitment strategies and a nonurgent approach to the operative treatment of congenital diaphragmatic hernia.^14,1

Immediately following delivery, the infant is intubated (bag and mask ventilation is avoided). A nasogastric tube is passed to decompress the stomach and to avoid visceral distention.

Adequate assessment involves continuous cardiac monitoring, ABG and systemic pressure measurements, urinary catheterization to monitor fluid resuscitation, and both preductal (radial artery) and postductal (umbilical artery) oximetry.

Pressure limited ventilation should be used, allowing the lowest airway pressures compatible with staying on the steep side of the pressure volume loop and preductal oxygen saturations greater than 90%. Peak inspiratory pressures (PIP) should be less than 30 cm H₂ O. Hypercarbia is allowed as long as the pH can be buffered.¹⁵

Alternative means of support (eg, high-frequency oscillatory ventilation [HFOV], extracorporeal membrane oxygenation (ECMO), and inhaled nitric oxide [iNO]) should be considered for patients who fail to stabilize on conventional ventilation.

HFOV is recommended for infants with hypercarbia and hypoxemia resistant to conventional ventilation or requiring high PIP (>30 cm H₂ O).¹⁶ HFOV uses an oscillating diaphragm to create a sinusoidal column of air within the airways. The diaphragm oscillates at a high frequency and improves gas exchange without increased ventilatory pressures. Increased gas exchange leads to elimination of carbon dioxide, which decreases the stimulus for pulmonary vasoconstriction and decreases pulmonary hypertension. At some institutions, HFOV is chosen as the primary means of ventilation.¹⁷

Surfactant rescue or prophylactic therapy is associated with an improvement in oxygenation in some neonates with congenital diaphragmatic hernia.^18,19 Surfactant used as rescue therapy is administered within 24 hours of birth in neonates with congenital diaphragmatic hernia and a poor prognosis. As prophylactic therapy, surfactant (50-100 mg/kg of Infasurf R) is administered prior to the first breath in neonates with congenital diaphragmatic hernia who were given a poor prognosis antenatally. Prophylactic surfactant therapy and natural surfactants are thought to be more efficacious. No definitive evidence of a surfactant deficiency in human neonates has been identified, and surfactant as rescue therapy has not been shown to improve outcome.²⁰

iNO has proven to be a highly selective pulmonary vasodilator and has been used as rescue therapy in infants with persistent pulmonary hypertension of newborn (PPHN). iNO produces pulmonary vasodilatation, decreases the ventilation-perfusion mismatch, and reverses the ductal shunting observed in PPHN. Limited success has been gained in the use of iNO in patients with congenital diaphragmatic hernia, but efficacy of iNO improves following surfactant therapy.²¹

The selection criteria for ECMO eligibility in congenital diaphragmatic hernia are the standard criteria used for other neonates with respiratory failure, as follows: a pH less than 7.15, oxygenation index greater than 40, and failure to respond to maximal medical treatment. ECMO should be reserved for patients who fail to respond to the alternative therapies if the extent of pulmonary hypoplasia is not considered to be lethal and when acute deterioration occurs in the postoperative period. ECMO in these cases provides respiratory support without additional barotrauma or oxygen toxicity. It allows time for the transition from fetal circulation, as well as the maturation of the pulmonary parenchyma (see Media file 4).

Surgical Therapy

No ideal time for repair of congenital diaphragmatic hernia is recognized, but the authors suggest that the window of opportunity is 24-48 hours after birth to achieve normal pulmonary arterial pressures and satisfactory oxygenation and ventilation with minimal ventilator settings. However, surgical repair can be safely delayed in stable patients, and the operation can be scheduled on a semi-elective basis. Urgent surgical repair is almost never necessary and may worsen the pulmonary hypertension.

Preoperative Details

The priority of the preoperative care is focused on the ventilatory management of the newborn and determining if the patient has any other associated congenital anomalies, particularly cardiac abnormalities. Echocardiography should always be performed prior to surgical repair.

Intraoperative Details

• A subcostal incision is made. The abdominal viscera are examined, and the hernia is reduced by gentle traction. A hernia sac is sought and excised if found. Following careful dissection of the posterior leaf of the diaphragm, primary repair can be accomplished in a single layer using nonabsorbable sutures. If the diaphragmatic defect is large enough to preclude primary closure, a Gore-Tex patch, or rotational muscle flaps²² or fascial flaps^23,24 can be used. If the patient is stable, the malrotation is corrected and Ladd bands are lysed. The transthoracic repair of a left-sided and right-sided diaphragmatic hernia has been reported. However, this approach is not commonly used.
• If abdominal closure may interfere with chest wall or diaphragmatic compliance or lead to abdominal compartment syndrome, then a temporary silo with delayed primary closure of the fascia or skin can be safely accomplished.
• The use of chest tubes is controversial, as is the use of suction. The authors prefer to use a chest tube but limit suction to 5 cm H₂ O. Most authors in North America suggest avoiding the use of suction to minimize mediastinal shift.
• The patient with a right-sided defect and an intrathoracic liver presents unique problems to the surgeon. The neonatal liver is extremely friable, and kinking of the hepatic veins and the inferior vena cava can accompany the return of the liver to the abdomen. Careful manipulation of the liver into the abdomen must be accompanied by hemodynamic monitoring. Occasionally, a 2-cavity (right chest and abdomen) approach may be necessary to reduce the viscera. Another well-described technique is to repair the diaphragmatic hernia using thoracotomy. Such approach typically allows for reduction of the liver and viscera back into the abdomen with excellent exposure of the diaphragm.
• Surgical repair while the patient is on ECMO was initially associated with an increased mortality rate, surgical site hemorrhage, and intracranial hemorrhage.²⁵ To decrease the hemostatic complications, associated ECMO platelet counts are now maintained above 150,000/μ L, and the activated clotting times (ACT) are decreased to 160-180 seconds.
• Use of aminocaproic acid in the perioperative period decreases the fibrinolysis associated with use of the ECMO circuit and leads to decreased hemorrhagic complications. Intraoperative and postoperative blood loss is decreased with the following:
  • Use of electrocautery for skin incision
  • No dissection of the posterior leaf if primary repair is unlikely
  • Use of prosthetic patch repair
  • Limited blunt and sharp dissection
  • Judicious use of electrocautery
  • Application of topical thrombin to the suture line
• Repairing the diaphragmatic hernia after decannulation from ECMO avoids the hemostatic complications associated with ECMO. This leads to recurrent pulmonary hypertension in some patients. The authors prefer repair on ECMO when the patient is ready for decannulation. Therefore, the patient tolerates decannulation if bleeding occurs.

Follow-up

Continued care is provided for survivors of congenital diaphragmatic hernia by a multidisciplinary team consisting of a social worker, nutritionist, physiotherapist, pediatrician/neonatologist, neurologist, and pediatric surgeon.

The following screening tests could be performed prior to discharge:

• Chest radiography 
• ABG 
• Brain stem auditory evoked potentials
• Head CT scanning or head ultrasonography
• Developmental evaluation.

In the outpatient clinic, chest radiography, pulmonary function tests, nutritional and developmental assessments, and repeated auditory, ophthalmology, and neurology evaluations are performed.

Complications

Complications observed in the early postoperative period include recurrent pulmonary hypertension and deterioration in respiratory mechanics and gaseous exchange. Less commonly observed complications include recurrence of the congenital diaphragmatic hernia (CDH), which is more common with patch repair;²⁶ leakage of peritoneal fluid and blood into the thorax; and development of an ipsilateral hydrothorax. Small-bowel obstruction may occur secondary to adhesions or volvulus.

Outcome and Prognosis

Long-term outcomes and prognosis are as follows:

• Long-term pulmonary disease depends on the degree of pulmonary hypoplasia, barotrauma, and volutrauma sustained in the neonatal period. Bronchopulmonary dysplasia and restrictive and/or obstructive lung disease may be observed in patients who survive congenital diaphragmatic hernias (CDHs).
• Failure to thrive is often observed in the presence of optimal feeding regimes.
• Functional and anatomic esophageal abnormalities are associated with significant gastroesophageal reflux in 40% of survivors; less than half of these patients require antireflux surgery in the first 6 months of life.⁹
• The use of extracorporeal membrane oxygenation (ECMO), hyperventilation treatment, and ototoxic medication places this population at a higher risk for sensorineural hearing loss as well as neurodevelopmental abnormalities (ie, cognitive and developmental delay, cerebral palsy, seizure disorders, impaired vision).
• Altered musculoskeletal development results in thoracic scoliosis, pectus deformities, and a decreased thoracic cavity on the affected side.

For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center. Also, see eMedicine's patient education article Hiatal Hernia.

Future and Controversies

Liquid ventilation uses perfluorocarbon (PFC), which is an inert compound with low surface tension and greater solubility for respiratory gases than blood. In partial liquid ventilation (PLV), the lungs are filled with PFC to the functional residual capacity, and conventional ventilation is superimposed. PLV is associated with improved oxygenation and decreased peak inspiratory pressure (PIP) requirements. This may be due to recruitment of atelectatic lungs and decreased ventilation-perfusion mismatch. Theoretically, PLV decreases the requirements for ventilation and so decreases barotrauma-induced and hyperoxia-induced pulmonary injury associated with congenital diaphragmatic hernia (CDH).

Preliminary clinical trials were conducted on infants with congenital diaphragmatic hernias and a high predicted mortality rate; while these infants were on extracorporeal life support, their lungs were filled with PFC and continuous positive airway pressure was maintained at 7-10 cm H₂ O. Accelerated growth of the ipsilateral lung, improved gas exchange, and improved survival were observed after one week.

Experimental fetal surgery has been expanding rapidly over the last 2 decades. The fetus with congenital diaphragmatic hernia most likely to benefit from in utero intervention has lethal pulmonary hypoplasia and no coexisting other lethal congenital anomalies. To date, no prenatal parameter has been able to reliably predict the occurrence of lethal pulmonary hypoplasia. Hence, selection criteria for in utero intervention remain controversial. Current trends in fetal surgery for severe congenital diaphragmatic hernia focus on the manipulation of lung growth by temporary occlusion of the fetal trachea using minimal access surgery (see Media file 5). 

The immature lung in fetuses with congenital diaphragmatic hernia should benefit from antenatally administered corticosteroids. In the fetal lamb model, corticosteroid administration at 24 and 48 hours prior to delivery was associated with significant increases in lung compliance. Clinical trials using late prenatal steroids have failed to demonstrate improved survival, length of stay, and duration of ventilation.²⁷

Thoracoscopic repair of congenital diaphragmatic hernia in the neonatal period is now being attempted. This is associated with increased complication rates and longer operating times. As with most minimally invasive techniques, patient selection criteria prove to be the determining factor in successful thoracoscopic repair. Patients who require minimal ventilation support or those with an intra-abdominal stomach or delayed presentation are more likely to undergo a successful thoracoscopic repair.²⁸

Multimedia

Media file 1: Graph illustrating the concept of the hidden mortality of congenital diaphragmatic hernia. Image courtesy of Michael Harrison, MD.

Media file 2: Photograph of a one-day-old infant with congenital diaphragmatic hernia. Note the scaphoid abdomen. This occurs if significant visceral herniation into the chest is present.

Media file 3: Radiograph of an infant with congenital diaphragmatic hernia. Note shift of the mediastinum to the right, air-filled bowel in the left chest, and the position of the orogastric tube.

Media file 4: Newborn baby with congenital diaphragmatic hernia on venoarterial extracorporeal membrane oxygenation (ECMO). Note the arterial and venous cannulas connected to the bedside cardiovascular bypass machine.

Media file 5: Diagram illustrating the sheep model of PLUG, the trachea used for the fetal management of congenital diaphragmatic hernia. Image courtesy of Michael Harrison, MD.

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Keywords

congenital diaphragmatic hernia, CDH, posterolateral diaphragmatic hernia, Bochdalek hernia, retrosternal hernia, Morgagni's hernia, respiratory distress, pulmonary hypoplasia, pulmonary hypertension, pulmonary immaturity, neural tube defects, polyhydramnios, hydrops fetalis, cystic adenomatoid malformation, cystic teratoma, thymic cysts, foregut duplication cyst, neurogenic tumors, feeding intolerance, tachycardia, intestinal obstruction, bowel ischemia, necrosis, volvulus, ventricular hypoplasia, atrial septal defects, ventricular septal defects, metabolic acidosis, persistent-newborn pulmonary hypertension

Contributor Information and Disclosures

Author

Nicola Lewis, MBBS, FRCS, Specialist Registrar, Department of Surgery, Birmingham Children's Hospital, UK
Disclosure: Nothing to disclose.

Coauthor(s)

Philip Glick, MD, MBA, Professor, Departments of Surgery, Pediatrics, and Gynecology and Obstetrics, Vice-Chairperson for Research and Development, Department of Surgery, State University of New York at Buffalo
Philip Glick, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, American Thoracic Society, Association for Academic Surgery, Association for Surgical Education, Central Surgical Association, Federation of American Societies for Experimental Biology, Medical Society of the State of New York, Phi Beta Kappa, Physicians for Social Responsibility, Royal College of Surgeons of England, Sigma Xi, Society for Pediatric Research, Society for Surgery of the Alimentary Tract, Society of Critical Care Medicine, and Society of University Surgeons
Disclosure: Nothing to disclose.

Medical Editor

Robert K Minkes, MD, PhD, Professor of Surgery, University of Texas Southwestern; Chief of Surgical Services, Children's Medical Center of Dallas-Legacy
Robert K Minkes, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Andre Hebra, MD, Chief, Division of Pediatric Surgery, Medical University of South Carolina; Professor of Surgery and Pediatrics, Medical University of South Carolina
Andre Hebra, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, Association for Academic Surgery, Society of Laparoendoscopic Surgeons, South Carolina Medical Association, Southeastern Surgical Congress, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

H Biemann Othersen Jr, MD, Professor of Surgery and Pediatrics, Emeritus Head, Division of Pediatric Surgery, Medical University of South Carolina
H Biemann Othersen Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Association for the Surgery of Trauma, American Burn Association, American Cancer Society, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, American Society for Parenteral and Enteral Nutrition, American Surgical Association, American Thoracic Society, British Association of Paediatric Surgeons, Society for Surgery of the Alimentary Tract, Society of Critical Care Medicine, South Carolina Medical Association, Southeastern Surgical Congress, Southern Medical Association, Southern Society for Pediatric Research, and Southern Thoracic Surgical Association
Disclosure: Nothing to disclose.

Chief Editor

Marleta Reynolds, MD, Professor of Surgery, Feinberg School of Medicine, Northwestern University; Interim Head, Division of Pediatric Surgery, Department of Surgery, Children's Memorial Hospital of Chicago
Marleta Reynolds, MD is a member of the following medical societies: American Pediatric Surgical Association
Disclosure: Nothing to disclose.

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