Diaphragmatic paralysis and eventration in infants

J

THoRAc CARDIOVASC SURG

91:490-497, 1986

Diaphragmatic paralysis and eventration in infants Twenty-six children with eventration (congenital in 10, resulting from birth trauma in four, and resulting from operative phrenic nerveinjury in 12) under 15 months of age were evaluatedat a single institution in a 5 year period. There was a high incidence of significant associated anomalies and prematurity. AU operative phrenic nerveinjuries occurred in patients under 3 months of age, and they were most common in patients undergoing Blalock-Taussig shunt. Plication (12 thoracic, nine abdominal) was performed in 21 patients, 19 of whom had respiratory distress or were ventilator dependent. Repeat plication was required in four patients. AU long-term survivors wereextubated within 1 weekof plication. Of 21 patients undergoing plication, 14 (67%) died. Death was attributed directly to complications of eventration in three patients and was a contributing factor in nine patients. We reached the foUowing conclusions: (1) The incidenceof operativephrenic nerveinjury in infants undergoing lateral thoracotomy, particularly for Blalock-Taussig shunt, is higher than generaUy appreciated; (2)plication is a safe procedureas performed by either an abdominal or thoracic approach; (3)failure to achieveextubation withina weekof plicationis an ominous prognostic sign; (4)mortality in patients with eventrationin the presence of major associated conditions may be high despite plication.

C. D. Smith, M.D. (by invitation), Robert M. Sade, M.D., Fred A. Crawford, M.D. (by invitation), and H. Biemann Othersen, M.D. (by invitation), Charleston, S. C.

In 1947, Bisgard' defined eventration of the diaphragm as "an abnormally high or elevated position of one leaf of the intact diaphragm as a result of paralysis, aplasia, or atrophy of varying degree of the muscle fibers" and reported the first successful diaphragmatic plication in an infant with congenital eventration. He noted that broad interpretation of the term included conditions that follow surgical interruption of the phrenic nerve or involvement of it by trauma, inflammation, or neoplasm, but he restricted his discussion to cases of congenital and idiopathic origin. Subsequently, the term eventration has been used in both its limited and broader interpretations"!' or has been qualified as congenital,I.12-14 nonparalytic," acquired,16.17 or iatrogenic. 18 Others have avoided the term and instead discussed "iatrogenic injury to the phrenic nerve,"19.20 "phrenic nerve paralysis,"21,22 "paralysis of the diaphragm.?":"

From the Division of Pediatric Surgery. Medical University of South Carolina, Charleston, S, C. Read at the Sixty-fifth Annual Meeting of The American Association for Thoracic Surgery, New Orleans, La., April 29-May I, 1985, Address for reprints: C. D. Smith, M.D" Division of Pediatric Surgery, Medical University of South Carolina, 171 Ashley Avc., Charleston, S. C. 29425,

490

"phrenic nerve palsY,"34,35 or "diaphragmatic malfunction,"36,37 all of which are encompassed in Bisgard's definition. Distinguishing acquired forms is important prognostically because they have potential for spontaneous recovery. However, since management decisions are necessarily based more on symptoms than cause, consideration together of patients with all forms of eventration seems justified. Eventration in pediatric patients is generally regarded as a rare condition that seldom requires intervention but that, in selected cases, responds well to diaphragmatic plication from either a thoracic or abdominal approach. Our recent experience with this entity in a tertiary referral center suggests that it is more common and potentially more dangerous than generally recognized.

Patients and methods The charts of children with a diagnosis of diaphragmatic eventration at the Medical University of South Carolina between January of 1979 through December of 1984 were reviewed. Tabulations of the following were made: age, sex, associated conditions, cause of eventration, portion of diaphragm affected, means of diagnosis, interval between time of probable onset of eventration and its diagnosis, time of diagnosis and plication in symptomatic patients, number of patients

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Diaphragmatic paralysis and eventration

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Table I. Definitions Type of eventration

History

Congenital

No trauma

Acquired: Birth trauma

Difficult birth

Acquired: Operative phrenic nerve injury

Surgical trauma

Fluoroscopic findings

Appearance of diaphragm

Paradoxical movement of affected portion, normal contraction of remainder Paradoxical movement of entire hemidiaphragm Paradoxical movement of entire hemidiaphragm

undergoing plication, indication, surgical approach, complications of plication, interval between time of plication and extubation, survival, and role of diaphragmatic malfunction in deaths of nonsurvivors. Results Demographics and cause. Twenty-six children with diaphragmatic eventration, whose ages ranged from 1 day to 15 months, were identified during the study period. These patients were divided into three groups on the basis of history of birth or operative trauma, preoperative fluoroscopic findings, and intraoperative appearance of the diaphragm (Table I). The first group comprised 10 patients (four boys and six girls) with congenital eventration (three right, one left, and six anterior and bilateral); the second group, four patients (one boy and three girls) with diaphragmatic paralysis apparently caused by birth trauma (two right, one left, and one bilateral); and the third group, 12 patients (three boys and nine girls) with diaphragmatic paralysis caused by operative phrenic nerve injury (seven right and five left). In the birth trauma group, there were two breech deliveries and two prolonged, difficult forceps deliveries in primigravida mothers. All 12 children having operative phrenic nerve injury were 3 months old or less at the time of nerve injury. The procedures leading to nerve injury were Blalock-Taussig shunt (six), coarctation with repair of patent ductus arteriosus (PDA), coarctation with PDA repair and pulmonary artery banding, PDA ligation, Senning procedure for transposition, long-segment cartilage graft tracheobronchoplasty, and attempted PDA ligation. The last of these operations, performed at another hospital, consisted of inadvertent ligation of the left pulmonary artery, which originated anomalously from the left subclavian artery. Associated conditions. In the congenital eventration group, seven of the 10 patients had significant associated problems: congenital heart disease in four patients (PDA; ventricular septal defect; aortic valvular stenosis; and ventricular septal defect, coarctation, and PDA), porencephalic cyst with hydrocephaly, dysgenesis with

Affected portion membranous Normal except for elevation Normal except for elevation

Table II. Associated conditions in 12 patients with operative phrenic nerve injury Case No.

2

3 4 5 6

7

8

9 10 II

12

Associated conditions Single ventricle, pulmonary atresia, TGA, endocardial cushion defect, PDA Tetralogy of Fallot, anomalous hypoplastic left pulmonary artery from left subclavian artery, perinatal asphyxia, prematurity Tetralogy of Fallot, hypoplastic pulmonary arteries, choana I atresia and stenosis, dysmorphic appearance, prematurity Mitral atresia, pulmonary atresia, single ventricle, TGA. PDA TGA, PDA, malrotation with duodenal obstruction Pulmonary atresia, hypoplastic pulmonary arteries, VSD, multiple skeletal deformaties, prematurity Coarctation of the aorta, VSD, spina bifida, dysmorphic appearance, abnormality of chromosome I Coarctation of the aorta, VSD, PDA, single kidney, hypospadius VSD, prematurity Ebstein's anomaly, pulmonary stenosis, PDA PDA, severe necrotizing enterocolitis, cholestatic jaundice with portal hypertension and esophageal varices, prematurity Complete rings of trachea, right main-stem bronchus, and right upper lobe bronchus, pulmonary artery sling, PDA

Legend: TGA, Transposition of the great arteries. PDA, Patent ductus arteriosus. VSD, Ventricular septal defect.

multiple anomalies, severe tracheal malacia owing to hypoplastic segmented tracheal rings, perinatal asphyxia, severe gastroesophageal reflux in two patients, chromosomal abnormalities (ring chromosome of chromosome 18, addition to long arm of chromosome 6), and prematurity (less than 2,500 gm) in five patients. Two of the four patients with birth trauma were premature; none had Erb's palsy. Of the 12 patients with operative phrenic nerve injury, 11 had congenital heart disease

49 2

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Smith et af.

Table ID. Reoperations

Case No.

Indications for reoperation

3

Suspected suture line breakdown Could not be weaned; recurrent diaphragmatic elevation Could not be weaned

4

Could not be weaned

2

Reoperation

Interval between plications (days)

Abdominal

Abdominal

II

Thoracic

Thoracic

Abdominal

Abdominal

10

Thoracic

Thoracic

25

Approach Initial

I

Findings at

reoperation

5

Outcome

Suture line Intact, residual left-sided eventration Suture line intact, further plication needed

Extubated 3 days postop.

Right-sided diaphragmatic plication incomplete laterally Diaphragm floppy, appeared to have stretched

Extubated 5 days postop. Improved but could not be weaned

Recovered

Table IV. Role of eventration in death of 21 patients undergoing plication Type of eventration Congenital (n = 8) Acquired: Birth trauma (n = 3) Acquired: Operative phrenic nerve injury (n

Directly related

Partially related

Unrelated

4

= 10)

(Table 11). In addition, one of these patients had an abnormality of chromosome 1, one had malrotation with duodenal obstruction, and another had necrotizing enterocolitis necessitating a massive small bowel and partial colon resection. The twelfth patient had complete rings involving most of the trachea, right main-stem bronchus, and right upper lobe bronchus with a pulmonary artery sling." Four of these babies were premature. Diagnosis. Diagnosis was first suspected from chest x-ray films in all patients and was confirmed by fluoroscopy in 18 patients and/or by peritoneography in nine. Liver/spleen scan showed an anterior eventration of the liver in two patients. Five patients had chest x-ray films only. One had respiratory distress at birth, underwent immediate laparotomy for suspected diaphragmatic hernia, but was found to have anterior eventration. Perioperative factors. Twenty-one patients underwent plication, 12 by a thoracic and nine by an abdominal approach. One of these patients had separate thoracotomies for plication to correct bilateral diaphragmatic paralysis. Indications for operation were respiratory distress in three (all congenital), inability to wean from the respirator in 16 (three congenital, three birth trauma, 10 operative phrenic nerve injury) and "prophylactic" in two asymptomatic patients with congenital anterior eventration and cardiac defects for which surgical therapy was anticipated. Time from probable onset to diagnosis in the 19 symptomatic patients who eventually had plication was less than 8 days in 13

I

2

5

2

patients and between 15 days and 3V2 months in six patients. Interval between diagnosis and plication in these same patients was less than 2 weeks in 14 and between 18 and 30 days in five. Five patients had been supported by the ventilator less than 2 weeks,seven from 2 to 4 weeks, and four from 1 to 3 months. Postoperative course. Complications included recurrent or residual eventration necessitating reoperation in four patients (Table III), hematoma over the diaphragm in a patient with thoracic plication, and a smalliaceration of the dome of the liver in a patient with abdominal plication. An unsuspected subphrenic abscess caused by Staphylococcus aureus was found at autopsy 3 months after abdominal plication in a patient dying of complications of severe tracheal malacia. Among the six symptomatic patients with congenital eventration who had plication, the indications for operation were respiratory distress in three and ventilator dependence in three. Two in the former group were extubated within 24 hours. The remaining four could not be weaned and died 17 days, 23 days, 1V2 months, and 3Vz months postoperatively. The two asymptomatic patients with congenital eventration who had plication "prophylactically" did not require postoperative intubation, but one had a second plication because of suspected recurrence (Table III). The three patients with birth trauma undergoing plication were ventilator dependent preoperatively. Two were extubated at 3 and 6 days; the third, who had bilateral paralysis (Case 2), was not weaned until the

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April. 1986

age of 7 months and died at home at 12 months of age because of tracheostomy tube obstruction. All 10 patients with operative phrenic nerve injury had plication because of ventilator dependence. Five could not be extubated and died 26 days, 47 days, 3 months, 3'12 months, and 1 year after plication. Of the remaining five, one was extubated 3 days after the second plication and survived. Four were weaned at 3 days, 5 days, 7 days, and 13 days after plication but died 6 weeks, 8 months, 3'12 months, and 6 days later, respectively. The five patients not undergoing plication survived. Of the remaining 21, 14 died (four congenital, one birth trauma, nine operative phrenic nerve injury). Nine of the 14 were born prematurely, and 13 had serious associated problems. The role of diaphragmatic malfunction in each death was analyzed (Table IV). Nine of the 10 patients undergoing plication for operative phrenic nerve injury died: In seven, diaphragmatic malfunction was at least partially responsible for the death.

Illustrative case reports Congenital eventration. CASE 1. A dysgenetic, chromosomally normal, small-fordates neonate weighing 2,210 gm was transferred to the Medical University Hosptial shortly after birth for management of gastroschisis. Pregnancy and delivery had been normal. The baby's deformities included dysmorphic facies, microcephaly, absence of lateral gaze and facial expression (Mobius syndrome), torticollis, flexion contractures of the wrists and elbows, and bilateral talipes equinovarus (Fig. I). He tolerated primary closure of the gastroschisis and was extubated 4 days postoperatively. A right diaphragmatic eventration was diagnosed before the operation but was not repaired because the greater need to restore the eviscerated intestines into the abdomen. Postoperatively, the baby fed poorly because of microstomia, hypoplastic mandible, and severegastroesophageal reflux. A gastrostomy was performed and he was transferred to the referring hospital for custodial care at 29 days of age. He was readmitted 6 days later because of recurrent regurgitation with aspiration. Bilateral eventration now appeared to be present on chest x-ray films and was confirmed by peritoneogram and fluoroscopy, which showed normal diaphragmatic excursion except for the elevated anterior and lateral portions of the right hemidiaphragm and the medial anterior portion of the left hemidiaphragm (Fig. 2). Bilateral diaphragmatic plication and an antirefiux anterior gastric fundoplication were performed by an abdominal approach at 60 days of age. He did not tolerate attempted extubation and died of respiratory insufficiency 3 weeks later. Necropsy findings included absence of the right sternocleidomastoid, pectoralis, and deltoid muscles, decreased muscle mass of biceps, triceps, and diaphragm, and extensive degeneration of the cervical spinal cord.

Comment. Eventration in this unusual case was the result of widespread central nervous and muscular abnormalities, including the diaphragm. An abdominal approach was chosen for this child to permit simulta-

Fig. 1. Case 1. Dysgenetic newborn infant with Mobius syndrome, bilateral congenital eventration, and multiple anomalies.

neous bilateral diaphragmatic plication and gastric fundoplication. The distinction between this type of anterior eventration from a subcostosternal diaphragmatic hernia of Morgagni is unclear. Thomas" suggested that this type of hernia may be a variant of eventration. Eventration owing to birth trauma. A 2,270 gm female infant was delivered by breech extraction to a 17-year-old primigravida mother. Apgar scores were 6 and 9 at I and 5 minutes. Because of increasing respiratory distress she required intubation and positivepressure ventilation. Chest x-ray films indicated bilateral eventration (Fig. 3). Fluoroscopy at I week of age was interpreted as showing ineffective but nonparadoxical movement of both hemidiaphragms. Ventilation/perfusion scan showed no evidence of pulmonary hypoplasia. Repeat fluoroscopy at 3 weeks documented paradoxical, symmetrical motion of the hemidiaphragms. Bilateral diaphragmatic plication by way of separate thoracotomies was performed at 28 and 32 days of age. Stimulation of a normal-appearing phrenic nerve at each procedure produced forceful diaphragmatic contraction. Tracheostomy was performed at 3 months and weaning from the respirator was not achieved until 7 months, by which time the patient had severe bronchopulmonary dysplasia. Diminishedbut nonparadoxical movement of both hemidiaphragms was documented by fluoroscopy at 7V2 months. Weighing only 7 kg after a very complicated 10 month hospitalization, she was discharged only to die at home 2 months later of a mucus plug obstructing the tracheostomy tube. CA SE 2.

Comment. The death of this child with bilateral acquired eventration owing to birth trauma was a direct result of diaphragmatic paralysis. Diaphragmatic function returned, but only after extensive lung damage had been incurred by prolonged ventilator support. CASE 3. A 1,400 gm, 31-week-old infant required intubation after a precipitous breech delivery. On the second day of life he had placement of bilateral chest tubes after a cardiac arrest caused by bilateral tension pneumothoraces. He was

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Thoracic and Cardiovascular Surgery

Fig. 2. Case 1. Peritoneograms, at age 2 months, show extensive, bilateral anterior eventration.

weaned from the respirator on several occasions but each time required reintubation. He was referred to the Medical University Hospital at 3 months of age because of inability to wean and to reexpand an atelectatic right lower lobe. Fluoroscopy and peritoneograms documented paralysis of the right hemidiaphragm. He underwent right hemidiaphragmatic plication by an abdominal approach on the second hospital day and was extubated 6 days later. Bronchoscopic observations during plication were normal.

Comment. Extubation failed repeatedly in this premature infant with bronchopulmonary dysplasia until eventration was diagnosed and plication performed. This case shows the critical difference eventration can make in a patient with marginal pulmonary reserve. Because of the history of precipitous breech delivery, we assumed that eventration was due to birth trauma, although chest tube placement may have been responsible.P" Eventration owing to operative phrenic nerve injury. 4. A 15-day-old male infant was referred for evaluation of respiratory distress with progressive evidence of congestive heart failure and cardiomegaly. Weighing 2,7 kg after a normal birth, he had done well until 10 days of age, when he was noted to be dusky and to feed poorly. He required respiratory assistance and maximal medical support including digoxin, diuretics, hydralazine, and dopamine for 4 days before he could be extubated. His course was complicated by atelectasis of the left lung, which responded to physical therapy and endotracheal suctioning (Fig. 4). Echocardiogram showed a PDA. Because of continuing respiratory distress, he underwent left thoracotomy for PDA ligation. In addition, he had patch aortoplasty of a coarctation, which was identified during that procedure. He had persistent collapse of the left lung. Six days postoperatively, fluoroscopy showed poor movement of both hemidiaphragms but "essentially almost no CASE

movement of the left hemidiaphragm." He underwent repeat left thoracotomy for diaphragmatic plication on the eighth postoperative day. The diaphragm was elevated but otherwise normal in appearance. He continued to have moderate respiratory distress and persistent atelectasis of the left lung. Three weeks later bronchoscopy showed compression of the left main-stem bronchus and repeat fluoroscopy showed some paradoxical movement of the left diaphragm. Airway study showed left vocal cord paralysis. Forty-five days after plication he was discharged in stable condition, weighing 200 gm less than on admission, but he died suddenly and unexpectedly at home the next day.

Comment. This case of operative phrenic nerve injury illustrates the complexity of the clinical picture in this group of patients. Congestive heart failure was severe and nutrition was poor. Atelectasis of the left lung was present intermittently before and after operative phrenic nerve injury and after diaphragmatic plication. Diaphragmatic movement was marginal even on the unaffected side. Unilateral vocal cord paralysis and compression of the left main-stem bronchus further compromised the airway. Since survival would have been anticipated if operative phrenic nerve injury had not occurred, this death was attributed directly to diaphragmatic paralysis.

Discussion This collection of 26 pediatric cases of eventration in a single institution in 5 years is the largest series for a comparable period in the literature. Our hospital is a referral center for a state that had approximately 50,000 births per year during this period. The incidence of

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Diaphragmatic paralysis and eventration

495

Fig. 3. Case 2. Bilateral eventration caused by birth trauma: Left. Preoperative chest x-ray film. R ight. X-ray film after bilateral plication. Note lower level of plicated hemidiaphragms.

Fig. 4. Case 4. Left, Recurrent atelectasis of the left lung in a patient with cardiac disease before operative phrenic nerve injury. Right. After operative phrenic nerve injury with the patient intubated but with the ventilator disconnected.

congenital eventration and eventration caused by birth trauma cannot be estimated accurately, however, since many other hospitals in the state treat newborn infants. In a review of 2,500 chest x-ray films of neonates, Beck and Motsay- found "about 4%" with "some diaphragmatic weakness" but only three with severe symptoms. Cavrot and Richard" found three cases of phrenic nerve palsy in 1,671 consecutive deliveries. To discover the incidence of operative' phrenic nerve injury at our institution, we reviewed all cardiovascular thoracotomies during the study period. We found that 10 of 176 (5.7%) newborn infants up to 3 months old undergoing lateral thoracotomy for heart disease had operative phrenic nerve injury; one such injury occurred

after 52 (2%) median sternotomies in neonates, whereas none occurred after 707 sternotomies and thoracotomies in older children. Six of 48 children (13%) up to 3 months old undergoing Blalock-Taussig shunt had operative phrenic nerve injury, although no such injuries occurred in 32 older patients who had the same procedure. Greene, L'Heureux, and Hunt" reported operative phrenic nerve injury in 19% of Blalock-Hanlon procedures in a 3 year period. Mickell and associates" reported a 1.7% incidence of operative phrenic nerve injury in pediatric cardiovascular procedures over an 8 year period: seven cases in 100 Blalock-Taussig shunts, four of 91 Mustard procedures, four of 239 atrial septal defect closures, and four of 297 PDA repairs. Others

The Journal of Thoracic and Cardiovascular

4 9 6 Smith et al.

have described operative phrenic nerve injury in tracheoesophageal fistula repair, lobectomy after staphylococcal pneumonia, excision of mediastinal tumors, and colon interposition for esophageal atresia. I I, 18, 19,23,33 In the infant chest, in which exposure is necessarily limited, the phrenic nerve is in close proximity to major structures requiring operative manipulation. Its identify may be obscured by scar tissue from previous procedures or inflammation or by tumor displacement. Allen? noted that the small artery that accompanies the phrenic nerve bleeds quite persistently when injured and is difficult to control with an adequate tie. He believed that use of cautery in this situation was probably the cause of operative phrenic nerve injury in many cases. As in our series, diaphragmatic plication has been reported to be a well-tolerated procedure with infrequent complications by either a thoracic or abdominal approach. Breakdown of diaphragmatic suture line can lead to recurrence, and, when a portion of the diaphragm has been excised, to free herniation of intestine into the chest." Insufficient plication may require reoperation if symptoms have not abated, but as in one of our cases (Table III), recurrence may be due to stretching of the diaphragm after initially satisfactory plication. Avoiding injury to the phrenic nerve branch in congenital eventration as a result of plication itself is theoretically possible, because the normal distribution of phrenic nerve branches is known." However, injuries to phrenic nerve branches as a complication of plication in such patients have been described II and may occur frequently, because these branches cannot be directly visualized. The possibility of recovery of diaphragmatic function after plication has been advocated as a reason to proceed with early plication in patients with phrenic nerve injury." However, there are few reports documenting such recovery after plication," 17,22 and there are no objective studies of the relative function of adequately plicated diaphragms with and without paralysis. The mortality (14/21, 67%) in our patients undergoing plication was distressingly high, but this seems due in large measure to the high incidence of major associated anomalies and prematurity. Furthermore, only three deaths were solely attributable to persistent diaphragmatic dysfunction. The view that plication is indicated in symptomatic patients is supported by many reports of progressive respiratory failure and death in such patients not undergoing operation- II, 16, 17,23,25,27,30,31,44 and by the dramatic results in selected patients undergoing operation.':" 10, 11, 16,19,21,22,28,30,32,33,36,37 A poor prognosis may be expected in patients with bilateral phrenic nerve paralysis, although management may be successful

Surgery

when nerve function recovers spontaneously. Similarly, when serious anomalies such as pulmonary hypoplasia, severe dysgenesis, chromosomal abnormalities, and complex congenital cardiac defects coexist, diaphragmatic dysfunction may play a critical role in a fatal outcome, despite plication. Our data do not permit a conclusion regarding the selection of patients for plication; however, we agree with empiric recommendations, such as those proposed by Haller and associates," to adopt a sequential approach to the evaluation and treatment of patients with eventration. The goal of such an approach is to treat associated parenchymal disease and cardiac dysfunction over a 2 to 6 week period, balancing the possibility of diaphragmatic recovery over time with that of producing iatrogenic complications related to mechanical ventilation. When there is known permanent nerve injury or associated gastric volvulus, earlier surgical intervention is probably indicated.

Conclusions and recommendations 1. The incidence of operative phrenic nerve injury in infants under 3 months of age undergoing lateral thoracotomy, particularly Blalock-Taussig shunt, is higher than generally appreciated. 2. The mortality in patients with eventration and major associated anomalies may be high despite plication. 3. Respiratory compromise despite plication often causes or contributes to death (12/14, 86%). 4. Plication for eventration is a safe procedure as performed by either an abdominal or thoracic approach. 5. Failure to achieve extubation within a week of plication is an ominous prognostic sign. 6. Particular care should be taken to avoid operative phrenic nerve injury in infants undergoing lateral thoracotomy. 7. A sequential approach to the evaluation and treatment of patients with eventration is recommended.

2 3

4 5

REFERENCES Bisgard JO: Congenital eventration of the diaphragm. J THoRAc SURG 16:484-491, 1947 Beck WC, Motsay OS: Eventration of the diaphragm, Arch Surg 65:557-563, 1952 Carter REB, Waterson OJ, Aberdeen E: Hernia and eventration of the diaphragm in childhood. Lancet 1:656659, 1962 Chin EF, Lynn RB: Surgery of eventration of the diaphragm. J THoRAc SURG 32:6-14, 1956 Christensen P: Eventration of the diaphragm, Thorax 14:311-319,1959

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6 McNamara JJ, Paulson DL, Urschel HC, Razzuk MA: Eventration of the diaphragm. Surgery 64: 1013-1021, 1968 7 Michelson E: Eventration of the diaphragm. Surgery 49:410-422, 1961 8 Paris F, Biasco E, Canto' A, Tarazona V, Casillas M: Diaphragmatic eventration in infants. Thorax 28:66-72, 1973 9 Shah-Mirany J, Schmitz GL, Watson RR: Eventration of the diaphragm. Physiologic and surgical significance. Arch Surg 96:844-850, 1968 10 Symbas PN, Hatcher CR, Waldo W: Diaphragmatic eventration in infancy and childhood. J THORAC SURG 24:113-119,1977 11 Wayne ER, Campbell 18, Burrington JD, David WS: Eventration of the diaphragm. J Pediatr Surg 9:643-651, 1974 12 Thomas TV: Congenital eventration of the diaphragm. Ann Thorac Surg 10:180-192, 1970 13 Laxdal OE, McDougall H, Mellin GW: Congenital eventration of the diaphragm. J Med 250:401-408, 1954 14 Lee SS: Congenital eventration of the diaphragm in infancy. NC Med J 31:9-13, 1970 15 Thomas TV: Nonparalytic eventration of the diaphragm. J THORAC CARDIOVASC SURG 55:586-593, 1968 16 Bishop HC, Koop CE: Acquired eventration of the diaphragm in infancy. Pediatrics 22: 1088-1096, 1958 17 Stauffer UG, Rickham PP: Acquired eventration of the diaphragm in the newborn. J Pediatr Surg 7:635-640, 1972 18 Jewett TC, Thomson NB: Iatrogenic eventration of the diaphragm in infancy. J THORAC CARDIOVASC SURG 48:861-866, 1964 19 Mearns AJ: Iatrogenic injury to the phrenic nerve in infants and young children. Br J Surg 64:558-560, 1977 20 Iverson LIG, Mittal A, Dugan DJ, Samson PC: Injuries to the phrenic nerve resulting in diaphragmatic paralysis with special reference to stretch trauma. Am J Surg 132:263269, 1976 21 Mickell JJ, Oh KS, Siewers RD, Galvis AG, Fricker FJ, Mathews RA: Clinical implications of postoperative unilateral phrenic nerve paralysis. J THORAC CARDIOVASC SURG 76:297-304, 1978 22 Schwartz MZ, Filler RM: Plication of the diaphragm for symptomatic phrenic nerve paralysis. J Pediatr Surg 13:259-263, 1978 23 Blattner RJ: Unilateral paralysis of the diaphragm without involvement of the brachial plexus. J Pediatr 20:223-229, 1942 24 France NE: Unilateral diaphragmatic paralysis and Erb's palsy in the newborn. Arch Dis Child 29:357-359, 1954 25 Tyson RM, Bowman JE: Paralysis of the diaphragm in the newborn. Am J Dis Child 46:30-39, 1933 26 Adams FH, Gyepes MT: Diaphragmatic paralysis in the newborn infant simulating cyanotic heart disease. J Pediatr 78:119-121, 1971

27 Anognostakis D, Economou-Mavrou C, Moschos A, Vlachos P, Liakakos D: Diaphragmatic paralysis in the newborn. Arch Dis Child 49:977-979, 1973 28 Othersen HB, Lorenzo RL: Diaphragmatic paralysis and eventration. Newer approaches to diagnosis and operative correction. J Pediatr Surg 12:309-315, 1977 29 Bingham JAW: Two cases of unilateral paralysis of the diaphragm in the newborn treated surgically. Thorax 9:248-252, 1954 30 Harris GBC: Unilateral paralysis of the diaphragm in the newborn. Postgrad Med 50:51-54, 1971 31 Schifrin N: Unilateral paralysis of the diaphragm in the newborn infant due to phrenic nerve injury, with and without associated brachial palsy. Pediatrics 9:69-76, 1952 32 Greene W, L'Heureux P, Hunt CE: Paralysis of the diaphragm. Am J Dis Child 129:1402-1405, 1975 33 Haller JA, Pickard LR, Tepas JJ, Rogers MC, Robotham JL, Shorter N, Shermeta DW: Management of diaphragmatic paralysis in infants with special emphasis on selection of patients for operative plication. J Pediatr Surg 14:779-785, 1979 34 Smith BT: Isolated phrenic nerve palsy in the newborn. Pediatrics 49:449-451, 1972 35 Yasuda R, Nishioka T, Fukumasu H, Yokota Y: Bilateral phrenic nerve palsy in the newborn infant. J Pediatr 89:986-987, 1976 36 Sethi G, Reed W A: Diaphragmatic malfunction in neonates and infants. Diagnosis and treatment. J THoRAc CARDIOVASC SURG 62:138-143, 1971 37 Garbaccio C, Gyepes MT, Fonkalsrud EW: Malfunction of the infant diaphragm in infants and children. Arch Surg 105:57-61,1972 38 Pass HI, Sade RM: Tracheo-esophageal compressive syndromes of vascular origin. Rings and slings, Thoracic and Cardiovascular Surgery, ed 4, WW Glen, ed., New York, 1982, Appleton-Century-Crofts, pp 699-710 39 Ayalon A, Anner H, Moghilner M, Schiller M: Eventration of the diaphragm due to phrenic nerve injury caused by intercostal drainage. J Pediatr Surg 14:473-474, 1979 40 Marinelli PV, Ortiz A, Alden ER: Acquired eventration of the diaphragm. A complication of chest tube placement in neonatal pneumothorax. Pediatrics 67:552-554, 1981 41 Cavrot E, Richard J: Paralysie diaphragmatique obstetricale. Brux Med 37: 1366, 1957 42 Allen RG: Discussion of Haller et aP3 43 Merendino KA, Johnson RJ, Skinner HH, Maguire RX: The intradiaphragmatic distribution of the phrenic nerve with particular reference to the placement of diaphragmatic incisions and controlled segmental paralysis. Surgery 39: 189-198, 1956 44 Schwartz MZ: Discussion of Haller et aP3 45 Richard J, Chevalier V, Capelle R, Cavrot E, Contet J, Delforge J: La paralysie diaphragmatique obstetricale. Arch Franc Pediatr 14:563, 1957