ODESSA NATIONAL MEDICAL UNIVERSITY

Department of pediatric surgery

Methodical recommendations for students of VІ year
Congenital anomalies in children, which are followed with respiratory insufficiency

Approved at the methodical meeting of the chair 
Protocol № 1 from 27/08/2021
                                                                        Head of the department Losev O.O.

Odessa 2021

Concrete aims:
1.	To master classification of anomalies of development of the respiratory system, esophagus and diaphragm.
2.	To recognize the basic clinical symptoms of anomalies of development, which are accompanied with respiratory insufficiency. 
3.	To differentiate the anomalies of development.
4.	To interpret the auxiliary methods of examination: esophagus tube insertion, ultrasonic examination, fibroesophagogastroduodenoscopy, sciagraphy, bronchography, bronchoscopy, computer tomography, angiography, and others like the laboratory and biochemical analyses, indexes of hemodynamics (Р, BP,Нt, Hb), and immunological.
5.	To show the review of child with the anomaly of development of esophagus, diaphragmatic hernia and lobar emphysema.
6.	To identify the features of course of anomalies of development.
7.	To offer the algorithm of action of doctor and tactic of conduct of patients with the anomalies of development.
8.	To interpret general principles of medical treatment of anomalies of development.
4. The plan and organisation of lessons.
Work type	Time 	Activity	Equipment 	
		Students	Teacher		
Organisation of the practical class	 5	Listen 	Presence control	Journal 	
Aim setting	5	Listen	Explain 		
Checking of the knowledge of students 	15	Make 	Control 	Tests 	
Seminar 	60	Answer 	Control	X-ray-grams	
Clinical discussion	30	Listen	Discuss patients	Patients 	
Personal student’s work	60	Make 	Control	Patients 	
Results of the lesson	10	Listen	Appreciation of each activities		
Task for the next lesson	5	Listen	Explain the task. Indicates the literature.		

Congenital cysts of lungs, pulmonary hypoplasia.
Actuality of problem
1. The congenital cysts of lungs meet in 3 - 5% cases of patients with the unspecific diseases of lungs.
2. There are the single or multiple cysts of lungs depending on the term of influencing of endogenous and exogenous factors at violation of embriogenesis.
3. Due to their course the cysts are divided on complicated and noncomplicated.
Complications of the congenital cysts are suppuration of cyst, tension of cyst, drainage to pleural cavity or bronchial tree.
4. Clinical symptoms:
- limited action of the thorax in the act of breathing on the side of anomaly,
- percussion – tympanit,
- heart displacement in a healthy side.
5. Medical treatment of the congenital cysts of lungs is surgical after establishment of diagnosis.
In patients with the tension of cyst, followed with displacement of mediastinum, puncture of cyst and its drainage before a surgery shoud be done to decrease the intrathoracic pressure.
The volume of the operation depends on the localization of cyst and its distribution on adjoining tissues.
Pulmonary hypoplasia  - undevelopment of all elements of pulmonary structure. Among the congenital anomalies of lungs, it keeps 85%. Simple and cystic forms.
The clinical symptoms depend on the volume of undevelopment of lungs and presence of infection.
There are the important physical, functional methods of examination to make a diagnosis: bronchscopy, bronchography, angiopulmonography.
Methods of medical treatment: conservative or operative. It  depends on a volume, presence of complication, features of course of disease, function of the pulmonary tissue and breathing effectency.
Operative treatment: typical resection, limited resection, segmental resection, bronchi exsirpation, combined resections.
Congenital lobar emphysema.
Actuality of problem.
1. The congenital lobar emphysema is the enough rare anomaly of development of the respiratory system, the consequences of disease depend on the time of diagnostics. 
2. Etiology of congenital lobar emphysema consists of aplasia of the smooth and shiny muscles of terminal respiratory bronchioles, absence of intermediate generations of bronchial tree or aplasia of respiratory part of particle lungs.
3. The clinical symptoms depend on the form of the congenital lobar emphysema: compensated, subcompensated, decompensated.
The compensated form is diagnosed in children after one year age. A child has a shortness of breath, frequent pulmonary diseases, there is deformation of thorax with the explosion of the staggered half. This form can be diagnosed during roentgenologic examination.
The subcompensated form appears considerably earlier, in age 1-3 months, a  child has the disorders of breathing or attacks of cyanosis, which pass quickly, his growth and development are retardated. During roentgenologic examination the anomaly of development is found.
The decompensated  form (acute form) of the congenital lobar emphysema is diagnosed in newborn during the first days of life. This form is characterized by the  syndrome of intrapulmonary tension. Child  has a respiratory insufficiency, that  grows progressively. X-ray exposes darkening, the dome of diaphragm descends, there is a displacement of organs of mediastinum in a healthy side.
4. Medical treatment of the congenital lobar emphysema in newborn is only operative. In children with decompensated form the operation is performed in an urgent order, in case of subcompensated form the terms of operative treatment depend on the state of child and course of disease, at compensated form - medical treatment is performed in the plan order.
THORACIC INSUFFICIENCY SYNDROME ASSOCIATED WITH DIFFUSE SKELETAL DISORDERS
Thoracic insufficiency syndrome may be defined as any disorder that produces the inability of the thorax to support normal respiration or lung growth. It includes a spectrum of disorders including asphyxiating thoracic dystrophy (Jeune's syndrome), acquired asphyxiating thoracic dystrophy (after open pectus excavatum repair), spondylothoracic dysplasia (Jarcho-Levin syndrome), congenital scoliosis with multiple vertebral anomalies and fused or absent ribs (jumbled spine), and severe kyphoscoliosis. These disorders have been viewed and treated as separate entities, with little coordinated effort between specialties. However, they are best addressed with a unified approach integrating pediatric general and orthopedic surgeons as well as pediatric pulmonologists.
Jeune's syndrome is an autosomal recessive inherited osteochondrodystrophy with variable expres- sions. In mild forms, the chest may support adequate respiration. In more severe cases, the thorax is narrowed both transversely and vertically, with short, wide horizontal ribs and irregular costochondral junctions. This chest wall configuration produces a rigid chest with very little intercostal excursion for normal respiration, leading to ventilatory dependence and death from respiratory failure. Pathologic examination of pulmonary structures varies, with some findings of pulmonary hypertension. However, most patients have normal bronchial development with variable alveolar density. This suggests that the extrinsic chest wall plays a significant role in the underlying hypoplasia. Other associated skeletal abnormalities in Jeune's syndrome include short stubby extremities, fixed elevated clavicles, hypoplastic iliac wings, and a high incidence of C1 spinal stenosis. These patients also have varying degrees of renal dysplasia.
Spondylothoracic dysplasia (Jarcho-Levin) syndrome occurs in two forms with different inheritance patterns. Type I is an autosomal recessive deformity characterized by multiple vertebral hemivertebrae and posterior rib fusions.85 This produces a marked shortening of the thoracic spine and a crab-like appearance of the chest on a standard radiograph . Associated malformations are noted in 30% of patients and include cardiac and renal anomalies. The type I form is often fatal by age 15 months, and a high incidence is reported in Puerto Rican families. 
Type II spondylothoracic dysplasia has an autosomal dominant inheritance pattern and is associated with near- normal longevity. It is seen most commonly in white children.
Thoracic insufficiency also may arise secondary to too early or too extensive pectus operations. Complex spine anomalies producing the so-called jumbled spine, unilateral thoracic hypoplasia seen with the VACTERL association, and kyphoscoliosis may be a cause of thoracic insufficiency.
Surgical techniques to correct the spectrum of these complex disorders have attempted to address the issue of thoracic volume by various approaches. In both congenital (Jeune's) and acquired (post-pectus) thoracic dystrophy, one approach has been an anterior longitudinal sternal split with widening of the sternum. This has been accomplished with methylmethacry- late, bone grafts or rib, and metal plates. A staged approach with a methylmethacrylate plate followed by secondary removal of the plate and latissimus dorsi flaps to cover the created sternal cleft also has been described. Sternal elevation has also been reported in cases of acquired thoracic dystrophy by both the open and the minimally invasive techniques used for standard pectus repair. A lateral staged approach with staggered rib osteotomies, staggered division of the chest wall, intercostal muscles, and pleura, with transposition of alternating ribs by using metal plate fixation, also has been described.
These approaches have had variable results because they are not easily revised to allow continued growth of the chest wall to allow lung expansion. The lateral thoracic expansion may also interfere with intercostal muscle function after division of multiple intercostal muscles and nerves. In regard to patients with Jarcho- Levin syndrome, jumbled spine, and kyphosis, pediat- ric general surgeons have done little to approach these problems that they considered either lethal or solely in the domain of the orthopedic surgeon.
A promising technique to address patients with the spectrum of causes for thoracic insufficiency syndrome rejoins the disciplines of pediatric general, thoracic, and orthopedic surgery. Expansion thoracoplasty and the use of a vertical expandable prosthetic titanium rib (VEPTR) developed by Campbell and Smith addresses many problems in the spectrum of these disorders. This technique allows serial expansion of the chest wall to allow continued growth of the thorax and spine until skeletal maturity is achieved. More than 300 patients with various disorders have been treated with this approach. In Jeune's asphyxiating thoracic dystrophy, 14 patients have undergone staged bilateral expansions. Anterior rib osteotomies adjacent to the costochondral junction and posterior osteotomies adjacent to the transverse process of the spine in the 3rd to 9th ribs are performed. This creates a mobilized segment of chest wall that is distracted posterolater- ally and anchored to a curved VEPTR that is attached to the 2nd and 10th ribs. The segment is anchored to the VEPTR with 2-mm titanium rings, stabilizing the segment and allowing reossification of the multiple osteotomies. The second stage is performed 3 months later, and then the devices are expanded every 6 months.
In patients with fused or absent ribs and scoliosis, a wedge thoracostomy through the fused segment of ribs not only allows expansion of the chest, but also correction of the scoliosis and the rotational spinal deformity (producing a windswept thorax). It also stimulates increased spinal height in both congenital scoliosis and Jarcho-Levin syndrome, in which bilateral devices are placed.
TRACHEAL OBSTRUCTION AND REPAIR
T) ediatric surgeons are often involved in the management of acute or chronic airway obstruction. Moreover, iatrogenic injury of the pediatric airway occasionally occurs. The large number of operative techniques for the treatment of tracheal stenosis shows that no single procedure or technique is universally applicable and successful. Prevention of, or prompt therapy for, injury is all-important.
PRACTICAL EMBRYOLOGY AND ANATOMY
A working knowledge of the embryonic development of mediastinal structures aids in understanding the etiology and associated anomalies of tracheal obstruction. Malformations of the great vessels (vascular rings) should be suspected and investigated when evaluating a child with complete tracheal rings. The most common vascular malformation associated with complete tracheal rings is a pulmonary vascular sling. This anomaly occurs when the left pulmonary artery arises to the right of the trachea, around which it curves and compresses just above the carina, and then passes between the trachea and esophagus before reaching the left lung. Other vascular ring malformations may produce varying degrees of tracheal, bronchial, and esophageal compression.
TRACHEAL MALFORMATIONS Congenital Subglottic Stenosis
The anatomy of the pediatric airway has been compared to an inverted cone, with the trachea fitting telescopically into the cricoid above it, the cricoid into the thyroid cartilage, and then the thyroid into the hyoid space, as illustrated in Figure 21-2. Congenital subglottic stenosis is the most common morphologic abnormality of the trachea and presents as a narrowing of the airway at the distal end of the larynx, just at the beginning of the trachea. This subglottic region lies at the junction of the cricoid cartilage and trachea and is the narrowest point of the child's airway. The cricoid cartilage is the only normally complete cartilaginous ring in the airway. Congenital abnormalities of this subglottic area consist of narrowing or malformation of the cricoid cartilage, the etiology of which is not truly known.
When compared with an adult, the anatomy of the trachea and larynx differs in several ways. The child's epiglottis is short and small, and the valleculae are very shallow. Also, the larynx points posteriorly toward the nasopharynx, and the arytenoid apparatus is large in relation to the lumen of the larynx. Finally, the narrowest point of the normal pediatric airway is the cricotracheal junction. In the adult, it is the glottis. Cricoid stenosis is exceeded only by laryngomalacia and vocal cord paralysis in the frequency of congenital airway anomalies.
In the normal trachea, the cartilaginous rings are horseshoe shaped, with the posterior wall composed of connective tissue and muscle. Thus, the lumen may change as the trachea expands or contracts with respiration. Long stenotic segments in the trachea usually consist of tracheal rings that are complete. When the cartilaginous rings are complete, the lumen is rigid and usually much smaller than the normal trachea. If it does not produce early respiratory distress, complete cartilaginous rings may be detected when an inflammatory process within the trachea produces mucosal edema, which further compromises the rigid lumen and results in acute airway obstruction. Occasionally, tracheal intubation for an elective operative procedure may be impossible and the narrowed segment is discovered.
Acquired Subglottic and Tracheal Stenosis
Acquired airway malformations usually result from intrinsic injury with subsequent inflammation, ulceration, and scarring, leading to severe subglottic or tracheal scarring and narrowing. Occasionally external trauma is the initiating event,2 but an iatrogenic event can exacerbate an unstable situation. For example, a child with a congenitally small airway might be asymptomatic until an endotracheal tube is inserted. The tube may be of an appropriate size but, because of the congenital stenosis, it will fit tightly and can lead to ulceration and stricture. Particularly difficult to treat are those injuries that occur well below the subglottic region, usually produced by an endotracheal balloon that has caused compression and ulceration in the trachea. Frequently, these areas of injury are below the usual site for a tracheostomy. The cuff may even erode into overlying vessels .
VASCULAR COMPRESSIONS
Compression and partial obstruction of the trachea may be caused by abnormalities of the aortic arch that impinge on or encircle the trachea or esophagus or both. When both the trachea and esophagus are compressed, swallowing frequently produces acute airway compression and respiratory distress. Vascular rings are often asymptomatic in neonates and infants, yet can lead to significant airway obstruction in a child.
The physiologic impingement on the trachea by a vascular ring is similar to that seen in patients after repair of esophageal atresia. The persistently distended upper esophageal pouch can displace the trachea anteriorly, producing tracheomalacia, or softened tracheal rings. Particularly with swallowing, the distended esophageal pouch may compress the trachea against the innominate artery. This sequence of events is thought responsible for a condition called reflex apnea. Consequently, surgical correction of this problem consists of anterior mobilization and suspension of the innominate artery. The treatment of a pulmonary vascular sling usually requires not only relocation and reimplanta- tion of the pulmonary artery but also tracheal repair for the stenotic distal trachea. Stridor and dyspnea are symptoms that may be produced by vascular impingement on the trachea. Patients with severe compression from a double aortic arch are usually symptomatic, but their manifestations are variable. Some patients are initially seen with frequent coughing and stridor accompanied by dyspnea and cyanosis, whereas small infants may have reflex apnea. The symptoms of vascular impingement on the trachea are usually more dramatic than those of compression of the esophagus.
The diagnosis of vascular ring anomalies has classically been made or suspected from a barium esophagogram with indentations on the esophageal column of barium and a decrease in the tracheal air column. Offset of the axis of the barium column above and below the indentation is diagnostic of a double aortic arch. Newer imaging techniques with rapid computed tomographic (CT) scans allow a graphic reconstruction of the trachea and adjacent vessels. Magnetic resonance imaging (MRI) enhanced with intravenous administration of a contrast agent allows excellent visualization of the trachea and vessels.
Occasionally, a child will appear with acute airway obstruction or other medical problems requiring intensive care, during which endotracheal intubation and a concomitant nasogastric tube are inserted. The presence of tubes in both airway and esophagus makes detection of a vascular ring difficult and can generate complications. In a child who is already intubated, performance of contrast radiographic procedures may not be possible. Ultrasonography or CT and contrast- enhanced MRI may delineate the vascular abnormality. When both tracheal and esophageal intubations are necessary in a patient with a double aortic arch, the encircling vessels may sustain pressure necrosis. Erosion into the aortic arch produces an acute aorto- esophageal fistula that may not be manifest until either the endotracheal or the esophageal tube is removed. A sentinel hemorrhage may occur before a massive, and often fatal, hemorrhage into the esophagus. The passage of a Sengstaken-Blakemore tube with inflation of the esophageal balloon can be lifesaving by tam- ponading the fistula. Because no reliable diagnostic study is available to demonstrate an aortoesophageal fistula, the observation of a sentinel hemorrhage in such a patient with ultrasound confirmation of a double aortic arch is a clear indication for urgent cardio- pulmonary bypass and repair.
Vascular rings cause airway constriction and not vascular problems. Thus, simple division of the vascular ring is often not enough to relieve tracheal compression. Significant numbers of patients are now being treated by the thoracoscopic approach. A vessel that continues to compress the airway must not be dissected away from the trachea but suspended anteriorly, often to the back of the sternum, so that the vascular tracheal attachments will lift the anterior tracheal wall and enlarge the lumen . Regardless of the approach, from the right or from the left, or other technical variations, the recurrent laryngeal and phrenic nerves must be identified and protected. Flexible endoscopic observation of the trachea during these maneuvers can corroborate relief of the compression.
TRACHEOMALACIA
Often tracheomalacia is produced by the constant pressure of a cardiovascular structure. Thus, it is almost always necessary to suspend the offending vessel and utilize its attachments to the trachea to expand the tra- cheal lumen. Occasionally, tracheomalacia can be primary in nature and there is no obvious compression. In these cases, suspension of the large mediastinal vessels may enlarge the tracheal lumen.18-21 Interestingly in the United Kingdom (Scotland), guidelines have been promulgated for the use of thoracoscopic aor- topexy to treat severe primary tracheomalacia.22 The National Health Service believed that these guidelines were necessary because individual surgeons would operate infrequently on infants and children who are good candidates for operative correction.
INFLAMMATORY OBSTRUCTIONS
Viral laryngotracheitis (croup), bacterial or membranous tracheitis, and epiglottitis are inflammatory conditions that may require surgical intervention. The acute inflammatory airway process may progress rapidly to a life-threatening obstruction and require emergency tracheostomy. However, in all cases of inflammatory obstruction, endotracheal intubation before trache- ostomy is advisable, if at all possible. It is important to distinguish croup and bacterial tracheitis from epiglottitis because the treatments are quite different .
Children with epiglottitis characteristically tolerate endotracheal intubation without airway injury because the inflammation and edema are supraglot- tic and not circumferential. They do, however, present more risks of intubation failure because of the severe edema of the epiglottis. Some hospitals have strict protocols requiring diagnostic laryngoscopy in the operating room with anesthesia standby for suspected cases of epiglottitis because an emergency tracheostomy is occasionally necessary. Conversely, with viral or bacterial laryngotracheitis, the inflammatory process involves the entire circumference of the airway and prolonged intubation may lead to permanent scarring.
Croup characteristically occurs during viral seasons in children age 3 months to 3 years. Children in whom the classic "croupy" cough develops frequently have a history of an antecedent respiratory infection, usually with a high fever.24 Bacterial tracheitis, a nonviral infectious disease, is seen with fever and rapid development of upper airway obstruction, characterized by copious mucopurulent secretions. Epiglottitis typically affects children who are age 2 to 6 years and have sore throat and dysphagia. Consequently, speech may be slurred and drooling of saliva is prominent. Lateral radiographs of the neck may show an edematous epiglottis.
Fortunately, most of these inflammatory processes are now controlled with antibiotics and respiratory care without surgical intervention. Treatment includes oxygen with increased humidification and inhalation of racemic epinephrine. Endotracheal intubation is well tolerated in epiglottitis and usually causes no further injury while antibiotic therapy produces resolution of the epiglottic edema. However, in cases of viral or bacterial tracheitis, even brief (24-48 hours) intubation may cause ulceration in a trachea that is already acutely inflamed and swollen. Therefore, it may be best to use endotracheal intubation to establish a definitive diagnosis. If resolution does not occur within 48 to 72 hours, a temporary tracheostomy may be advisable.
The decreasing incidence of epiglottitis is probably due to the increasing use of immunization against Haemophilus influenzae type b, the most common causative organism. Other infectious organisms, however, may produce the typical epiglottic swelling. Intubation is usually not necessary for more than 24 to 48 hours until antibiotics can control the infection. Croup also is now more easily treated without intubation with racemic epinephrine inhalation combined with administration of dexamethasone, 0.6 mg/kg, either orally, intramuscularly, or intravenously.
Regardless of the cause of the inflammatory process, rapid obstruction of the airway can occur in a small child. The surgeon must be prepared to work with the anesthesiologist and pediatrician to establish an airway by endotracheal intubation, bronchoscopy, or tracheostomy.
TRACHEOSTOMY
Our experience has been that tracheostomy with a linear tracheal incision through the second, third, and, possibly, fourth rings without excising any of the anterior wall of the trachea is the preferred technique in children. Cruciate incisions should not be used because the flaps created may be inverted and narrow the lumen. However, some surgeons continue to espouse a technique called Starplasty. Cruciate incisions in the skin and the anterior tracheal wall are sutured together to produce a permanent ostomy. This technique should be reserved for permanent tracheostomy because operative closure is necessary when a tracheostomy tube is no longer needed.
Tracheostomy is best performed with an endotracheal tube in place so that the airway is controlled. A transverse incision made in the lower neck is deepened to allow lateral retraction of the strap muscles after the midline is opened. This dissection is then carried down to the trachea. In small children, palpation of the ridges of the tracheal cartilages is frequently more valuable than visualization for determining the appropriate level of tracheotomy. The incision in the trachea is made below the thyroid isthmus, no higher than the second ring. The tracheostomy tube specifications are illustrated in Table 21-3. Traction sutures of polypropylene, left long and labeled "Left" and "Right," allow easier reintubation in the event of accidental dislodgement within the first week. If the tra- cheostomy has been in place for longer than 2 weeks, bronchoscopy can be helpful during decannulation.
A large granuloma frequently develops at the superior rim of the tracheostomy stoma and may need endoscopic excision.
TRACHEAL REPAIR Congenital Stenosis
Most congenital obstructions have a cartilaginous base but also have a fibrous tissue component. As mentioned earlier, many congenital stenotic lesions in the airway are asymptomatic until an acute event such as an injury, acute tracheal inflammation, or endo- tracheal intubation. At that point, the constriction of the airway becomes symptomatic. Complete tracheal rings may first be suspected when the child requires an anesthetic and an endotracheal tube meets a tra- cheal obstruction.
For treatment of long-segment obstruction from complete tracheal rings, we have devised a procedure in which either the KTP or CO2 laser is used to divide each complete cartilaginous ring in the posterior midline.41 With an endoscopic balloon, the trachea is gradually dilated as the rigid bronchoscope is advanced. When all complete rings have been divided, a tube is inserted to serve as a stent. If long-term stenting is required, a T-tube is used (see later). If this procedure is done carefully without forceful dilation, no air leak should occur because the esophagus posteriorly fills the gap in the posterior tracheal wall. With a short segment of complete rings, resection and anastomosis has been accepted as effective therapy, but few surgeons have a large experience with this technique. Other groups have used resection for long and short lesions but are now considering slide tracheoplasty. An improvement on standard resection procedures, slide tracheoplasty allows reconstruction without tension. The narrowed segment is transected in its midportion, and the remaining stenotic segments are incised. One end of the trachea is opened in the posterior midline, and the other is incised in the anterior midline. Long-term evaluation has been satisfactory. The diameter of the resulting anastomosis is broad enough to avoid airway narrowing.
Some surgeons have compared laryngotracheal reconstruction with cricotracheal resection and attempted to categorize the indications for each pro- cedure. The surgical therapy for these patients continues to evolve, as evidenced by a recent review of 50 patients treated for congenital tracheal stenosis at a single institution over an 18-year span (1982 - 2000). Although the operation originally preferred was peri- cardial tracheoplasty, four procedures were compared: pericardial-patch tracheoplasty (28 patients), tracheal autograft (12 patients), tracheal resection (8 patients), and slide tracheoplasty (2 patients). These authors concluded that their operation of choice for short segments would be resection. Resection with tracheal autograft was preferred for long-segment stenoses (more than eight rings). In this latter procedure, the stenotic trachea is incised anteriorly and the midportion is excised. A primary anastomosis is made posteriorly, and the anterior defect is closed with a free autograft fashioned from the excised trachea. Others have used human cadaver tracheal allografts for recon- struction. The ideal surgical treatment for congenital tracheal stenosis has not yet been devised.
Anterior cricoid split is a procedure that is useful in treating moderate subglottic stenosis in neonates and young infants. Infants selected for the anterior cri- coid split procedure should weigh more than 1500 g and require assisted ventilation or inspired oxygen of more than 35%. They should also not be in cardiac failure. This technique is illustrated in Figure 21-15. Proper selection of patients for anterior cricoid split is crucial. After anterior cricoid split, those infants who can be successfully extubated have excellent long-term outcomes, whereas those who continue to need intubation will require tracheostomy.
Open Laryngotracheoplasty
Many variations exist in the operative techniques of procedures available for tracheal reconstruction for a scarred and stenotic trachea. First, an open procedure can be done with or without cardiopulmo- nary bypass. Recently, there has been a tendency to avoid bypass and use only endotracheal anesthesia. Second, the repair can be performed with or without an augmentation graft. The grafts may include tra- cheal autografts, costal cartilage, cartilage from other sites such as thyroid or alar cartilage, autologous or allogeneic pericardium, skin, and tracheal allografts. Third, a stent may be used to maintain the lumen and can remain in place for hours, days, months, or years.
When open laryngotracheoplasty is performed without a cartilage graft, it is essentially a cricoid split or the expansion of the lumen with the use of a castellated
The classic cartilage laryngotracheoplasty utilizes a cartilage graft. An omental flap may help a long cartilaginous graft survive. The cartilage is inserted anteriorly after incising the stenotic seg- ment. Cartilage inserts also can be placed posteriorly and laterally in sites where the stenotic cricoid is incised. Ciliated mucosa has been found on the surface of a mature costal cartilage graft if the perichondrium faces the airway lumen. Another option is resection and primary anastomosis. The stenotic portion of the trachea is excised, and an end-to-end anastomosis is performed.
A slide tracheoplasty uses autologous trachea by dividing the trachea in the midportion of the stenotic segment. The upper and lower portions of the stenosis are incised in the midline, one anteriorly and the other posteriorly, and the anastomosis is then performed. Another option for repair of tracheal stenosis is by anterior incision and closure of the defect with pericardium. All pericardial patch operations are done on cardiopulmonary bypass. However, experience at some centers has not been as good because of complications secondary to patch collapse. The original proponents of pericardial patching have now reported improved results with a free tracheal autograft in which the excised stenotic segment is flattened and used as a free anterior autograft to expand the lumen at the anastomosis.
CONGENITAL BRONCHOPULMONARY MALFORMATIONS
A variety of developmental abnormalities of the tracheobronchial tree and pulmonary parenchyma are found in the newborn. Some of these have a genetic basis and produce widespread physiologic abnormalities. Many of these, such as surfactant protein deficiency, alveolar capillary dysplasia, and generalized pulmonary hypoplasia, are newly described and are not in the traditional scope of care of the pediatric surgeon. Thus, they are not addressed in this chapter. In this chapter, the more focal anatomic abnormalities of the foregut and its anlagen, traditionally termed bronchopulmonary malformations (BPMs), are covered. Although these lesions have been recognized for years and grouped as related for discussion purposes, no uniform pathologic or embryologic reason exists for this clustering. Rather, this grouping remains appropriate to facilitate an understanding of the common clinical presentation and management of BPMs.
With the advent of near-routine prenatal ultraso- nography, a great deal has been learned about the natural history and pathophysiology of BPMs. Currently, ultrasound findings are altering many of the conventional beliefs and understanding of these lesions. Moreover, prenatal identification and a more accurate depiction of their natural history have given rise to advanced fetal interventions. The lessons learned from prenatal ultrasonography have also affected the postnatal management of cystic lung lesions, because previously unrecognized and likely clinically silent malformations are being detected with ever greater frequency. Still, despite these advances, BPMs defy a common embryologic classification and, as a whole, their pathophysiology remains varied.
EMBRYOLOGY AND CLASSIFICATION
The traditional understanding is that the tracheo- bronchial tree and proximal gastrointestinal tract arise from a common foregut anlagen. At the end of the third week of gestation, the laryngotracheal groove or diverticulum can be seen in the caudal end of the
embryonic foregut. This groove arises as a ventral enlargement of the foregut and then grows caudad to form the primordium of the trachea and lung bud. This outgrowth of endoderm is ventral and in parallel with the more dorsal portion of the foregut or future esophagus. Next, the lateral walls of the foregut, now called longitudinal ridges, begin to approximate in the midline, forming the tracheoesophageal septum. The separation of the dorsal esophagus and the more ventral tracheobronchial tree is thought to be caused by this tracheoesophageal septum and is complete by the sixth week of gestation. If this process fails or is incomplete, congenital defects affecting the trachea, conducting airways, or esophagus may result.
Some now question this traditional embryologic description.4 Several lines of evidence tend to refute these long-held beliefs. With the use of scanning electronic microscopy at various stages of development, findings in chick embryos have described a paired caudal "lung bud" diverticulum with no identifiable tracheal primordium.4 Even more elusive is the developmental program of the lung primordia after separation from the foregut anlagen, which occurs between 6 and 16 weeks' gestation. Current advances in molecular biologic techniques, including conditional mutants and transgenic mice, have allowed a more in-depth investigation and understanding of the molecular regulators of airway and pulmonary parenchymal development. In more generalized terms, the epithelium of the trachea, bronchi, and alveoli originate from endoderm, whereas muscle and cartilage originate from mesoderm.2 Subsequent epithelial mesenchymal interactions result in the changes of branching morphogenesis and yield site-specific specialized epithelia for air conduction and gas exchange. Studies in mice have established non-overlapping cell lineages of conducting airways (trachea and bronchi) as being distinct from those of peripheral airways (bronchioles, acini, and alveoli), well before formation of the definitive lung buds.78 Similarly, studies in knockout mice and conditional mutants have revealed the involvement of many of the secreted protein morphogens involved in organogenesis throughout mammalian development, such as members of the BMP, FGF, Hhh, and Wnt families.
Knowledge of this embryology serves to elucidate the reasons for the frequent consideration of the close relation between anomalies of the proximal gastrointestinal tract and pulmonary system. Congenital BPMs comprise a broad spectrum of clinical lesions from both systems, including esophageal duplications, cystic lung lesions, and anomalies of solid pulmonary parenchyma with abnormal vascular supply. Classification of congenital BPMs therefore is not easy from either a morphologic or an embryologic standpoint. A simplified listing of BPMs by anatomic location becomes the most useful classification system for the clinician charged with managing the myriad presentations and diagnoses.
POSTNATAL MANAGEMENT
Several fetal anomalies can be confused with CPAMs and BPSs.3 Chief among these are CDHs, broncho- genic and enteric cysts, mediastinal cystic teratomas, congenital lobar emphysema (CLE), and bronchial
atresia.31-34 Smaller lesions may be asymptomatic at birth. Before the increased use of prenatal ultrasonog- raphy, many of these lesions went unnoticed, even on perinatal chest radiography. Current practice is to obtain computed tomography (CT) of the chest either before discharge or in the first several weeks of life. Planned elective resection of asymptomatic CPAMs and BPSs is recommended, given the accumulating evidence for the risks of either infection or occult malignant transformation.3,35-38 However, this remains debatable and practice patterns are still evolving for the small asymptomatic lesions. Moderate-sized lesions may cause some respiratory embarrassment at birth, either from hyperinflation or from the secondary mass effects on normal lung. The traditional postnatal management of planned delivery with multidisciplinary neonatal evaluation, stabilization, and eventual excision has produced an excellent overall prognosis. On rare occasions when severe perinatal respiratory distress is anticipated, a strategy using ECMO has been described.1315
BRONCHOPULMONARY SEQUESTRATION
Sequestrations should be distinguishable from CPAMs by their pathologic, radiologic, and clinical characteristics. A pulmonary sequestration is classically described as a cystic mass of nonfunctioning lung parenchyma that lacks a demonstrable connection to the tracheobronchial tree. In addition, this sequestered mass of lung tissue receives its blood supply anomalously from the systemic circulation. However, as with many of these lesions, exceptions are common, with a wide variety of arterial supply and venous drainage combinations being described. Because of the anomalous blood supply, many believe the true embryologic derivation of these lesions should classify them as vascular anomalies. However, because the majority of the clinical symptoms are respiratory, we continue to classify these as lung lesions. Sequestrations are largely solid lesions. Pathologically, these lesions demonstrate parenchymal maldevelopment, reflected as microcys- tic abnormalities similar to type II microcystic CPAMs.
Sequestrations are typically classified as either intralobar or extralobar. If the lesion is contained within the same investing pleura as normal lung, it is intralobar. Extralobar lesions are found outside the investing parietal pleura of adjacent normal lung. Intralobar sequestrations are usually found in the lower lobe basilar segments and are more common in the patient's left hemithorax. Extralobar lesions have a more variable occurrence pattern. However, their typical location is also basilar, below the more normally formed lung. Extralobar lesions also have been found in the upper thorax, below the diaphragm in the upper abdomen, throughout the mediastinum, and within the pericardium. Many sequestrations are asymptomatic. Given the lack of communication to the tracheobronchial tree, infectious complications most likely develop from hematogenous seeding. Extralobar sequestrations are frequently identified as an incidental finding, with approximately 15% occurring below the diaphragm and, not infrequently, in association with a left-sided CDH. The radiographic findings for either intralobar or extralobar sequestrations are usually that of an opacified solid lung mass or a cystic parenchymal lesion with an air-fluid level secondary to infection. Intralobar BPS accounts for the majority of lesions overall, yet extralobar lesions are more likely to have other associated anomalies in as many as 50% to 65% of cases. The most commonly recognized anomalies associated with BPS, in addition to CDH, include diaphragmatic eventration and other foregut malformations such as tracheoesophageal fistula and esophageal duplication.
Historically, angiography was performed to confirm the anomalous systemic blood supply and to help in planning surgical management. Currently, the hallmark anomalous vascular supply can be identified by Doppler ultrasonography, CT, or MR angiography or a combination of these modalities. Typically, a single large feeding vessel arising from the abdominal aorta is. This vessel can be typically found within a pedicle or stalk. However, not infrequently, more than one major vessel is found to supply the sequestration. The venous anatomy may be even more variable, with systemic, bronchial, and azygous system involvement. If a bronchus is found within the pedicle, communication with the gastrointestinal tract should be sought.
Atresia of esophagus
Development of esophagus in an embrionic period, violation of processes of vacuolization at the solid stage of development of intestinal tube. Frequency of supervision of anomaly of development. VACTERL- association.
Types of atresia of esophagus. Clinical symptoms: foamy excretions, excessive salivation, aspiration, asphyxia, respiratory disorders, respirator distress-syndrome, pneumonia.
Tracheoesophageal fistulasin newborns with atresia and without atresia of esophagus.
Diagnostics: insertion of gastric tube, Elephant's test, X-ray with contrast catheter, pН-metry.
Preoperative preparation, its volume and duration. Operative treatment: retropleural access, mobilization of segments of esophagus, direct anastomosis with liquidation of fistula. Indications for multistage operations: esophagostomy, gastrostomy, plastic operation on an esophagus with antireflux defence.
Postoperative period, possible complications: pneumonia, insolvency of anastomosis, mediastinitis, pleurisy, pyopneumothorax, atelectssis, fistule recanalisation, stenosis of anastomosis. Proper tactic at complications.
Gastroesophageal reflux, conservative and operative medical treatment.
Diaphragmatic hernia
Development of diaphragm and origin of defects in a diaphragm. Classification of diaphragmatic hernia by Dolesky. Degree of hypoplasia of pulmonary tissue.
Clinical symptoms: violation of breathing, disorders of digestion, cardiac  insufficiency,"asphictic obstruction " by Doletsky.
Hernia of the esophagus (hiatus hernia) is followed with a sick syndrome, anaemia as a result of bleeding. At hernia of anterior part of diaphragm there is a deformation of sternum, pain.
Diagnostics of application of roentgenologic examination with the contrast material, ultrasound.
Differential diagnostics: hemorrhagic syndrome, lobar emphysema, cysts of lungs, spontaneous pneumpthorax.
Diaphragmatic  hernia and absolute indications to operative interference. Accesses: laparotomy, thoracotomy.
Preoperative preparation during 12-32 hours till a stabilization of indexes of hemodynamics, blood gases and adequate diuresis.
The volume of operation is determined by the type of anomaly of development: plastic of diaphragm, suturing of diaphragm, its fixation to a  muscular tissues or ribs, in case of diaphragmatic aplasia – synthetic transplontat.
General mortality (14-30%) and its reasons.
SURGICAL MANAGEMENT OF CONGENITAL PULMONARY airway MALFORMATION AND BRONCHOPULMONARY SEQUESTRATION
Although somewhat debatable, the finding of a CPAM or BPS, regardless of symptoms, is an indication for resection, given the risk of either infection or malignant transformation. In an asymptomatic newborn, the resection can be electively performed at 3 to 6 months of age. Both pleuropulmonary blastoma and bronchoalveolar carcinoma have been reported in infants, children, and adults with known CPAMs. The preoperative chest CT can help in planning the operative approach. Traditionally, a lateral thoracotomy has been performed, depending on the location of the target lesion. Either a lobectomy, or less frequently, a segmentectomy allows complete removal of the majority of these lesions. For extralobar sequestrations, the preoperative imaging and localizing studies are even more important, given the possibility that some lesions are located below the diaphragm. Obviously, for extralobar lesions, a nonanatomic resection is possible and is facilitated by the stalk or pedicle-like nature of the feeding vessel.
Over the past decade, the thoracoscopic approach for resection of CPAMs and BPSs has been well described. The advantages of this approach include a reduction in postoperative pain, decrease in hospital stay, improvement in cosmesis, and, importantly, the avoidance of morbidities (namely, musculoskeletal complications) associated with a thoracotomy. The first large series of thoracoscopic pulmonary procedures in infants and children was reported in 2000. The vast majority of the 113 cases reported were pulmonary biopsies and wedge resections. Lobectomies were performed with a hybrid technique of directed thoracoscopy and mini-thoracotomy. This report predated many of the instruments that are currently used for hemostasis and tissue sealing. The Ligasure (Tyco, Inc., Norwalk, CT), for example, also can be used to seal neonatal lung parenchyma when an incomplete fissure is encountered. Since this initial review, numerous reports attesting to the safety and efficacy of the thoracoscopic technique in the management of BPS and CPAM have been published. In a recent report, 65 of the 97 patients underwent thoracoscopic resection for either CPAM or BPS.53 All but 4 of the 97 lobectomies performed were completed thoracoscopically. Three postoperative complications were described (pneumothorax, pneumonia, and persistent air leak). Postoperative hospitalization averaged 2.4 days in patients who underwent successful thoracoscopic surgery. In 2007, a two-surgeon experience was published detailing a series of 144 consecutive pediatric lobectomies, 112 of which were performed for CPAM/sequestrations. Lung abnormalities were diagnosed prenatally (by ultrasonography and/or MRI) and postnatally (by CT). The majority of these resections were lower lobectomies, which are technically less difficult than upper lobe resections. The median operating time was 125 minutes, and the median postoperative hospitalization was 2.8 days. Long-term follow-up (1-10 years) has not revealed any problems with musculoskeletal deformity or weakness.
With further evolution in the thoracoscopic technique, a broader range of lesions, such as bilateral disease and very large lesions, can be approached. On the other hand, it may be best to stage bilateral cases to give the remaining normal lung a period of accommodation between elective resections. Currently, the main limiting factor for the thoracoscopic approach is the child whose condition is unstable because of the mass effect, because the large size may eliminate the effective working space needed for thoracoscopic resection. On occasion, intraoperative cyst rupture has provided the necessary working space for resection by minimal- access techniques. An exceedingly large lesion requiring pneumonectomy also will require additional plans for managing potential pulmonary hypertension or the temporary respiratory insufficiency that can result from pulmonary hypoplasia. ECMO may be useful as a temporizing measure in such cases.
EMPHYSEMATOUS LESIONS
On occasion, CLE can be confused with a macrocystic CPAM. Radiographically, CLE appears as overdistention involving one or more lobes .This is believed to be caused by a variant of bronchomalacia with a focal cartilaginous deficiency of the tracheo- bronchial tree, leading to regional airway collapse with expiration.23 With postnatal air exchange, air trapping behind a structurally inadequate conducting airway leads to these emphysematous changes. Other rare causes include extrinsic compression from anomalous pulmonary vessels or by a very large ductus arterio- sus . In the premature infant with significant respiratory distress syndrome, pulmonary interstitial emphysema, in its more chronic form, can evolve into a variant of CLE. One third of cases remain classified as idiopathic.
The clinical presentation of CLE can be as varied as its numerous causes. With massive lobar overdistention, compression of the normal lung and the mediastinum can cause respiratory and cardiovascular collapse. In these cases, emergency thoracotomy is necessary as a lifesaving maneuver. In less dramatic presentations, progressive tachypnea and expansion lead to assisted ventilation and radio- graphic identification of the offending lesion. Plain chest radiographs and CT scans have been used both for diagnosis and for determining the appropriateness of surgical resection and the boundaries of normal lung. In most cases, resection of the abnormal lung allows re-expansion and compensatory growth of the normal lung. Expectant management is acceptable for the largely asymptomatic lesion. However, complete resolution of the radiographic findings is rare, and, for this reason, surgical resection is indi- cated. The aforementioned concerns of retained secretions as a nidus for infection exist with CLE as for CPAMs.
The acquired forms of emphysematous pulmonary lesions generally are first seen in a more time- dependent fashion than are the lesions caused purely by congenital structural defects. A history of chronic ventilation of a poorly compliant premature
lung precedes the development of pulmonary interstitial emphysema and its sequelae of lobar emphysema or parenchymal cysts. Many of these lesions will resolve spontaneously. However, if the mass effect produces some of the same clinical symptoms of compression of the normal lung and mediastinum, then surgical intervention is indicated. In the most chronic forms of CLE, operative therapy for cystic pulmonary lesions from prolonged ventilator barotrauma can be quite difficult because little residual normal lung will be available for continued gas exchange.
LOBULATION ANOMALIES AND ISOMERISM
Significant variations of lung anatomy occur with respect to the pattern of lung lobulation. The most common variability is an absent or incomplete fissure separating the anatomic lobes. Absent fissures occur in 30% of individuals, whereas incomplete fissures can be seen in more than half of the general population. However, these variations do not indicate disordered lobulation and, as such, have no clinical significance, other than to the operating surgeon. True lobulation and segmentation abnormalities can result in extra lobes such as a cardiac lobe (division of the left lower lobe into two separate lobes) or supersegmentation of the lower lobes. The majority of these anomalies are without clinical relevance. Lobulation anomalies can occur with abnormal bronchial patterns as seen with accessory tracheal lobes with direct airway connection to the trachea.
The azygos lobe is a malformation usually of the right upper lobe that is caused by an aberrant azygos vein that is suspended by pleura and acts as a mesentery that produces the defect. These lesions also most likely are clinically silent. Reports have mentioned esophageal lung, also termed communicating bronchopulmonary foregut malformation, in which a tract is preserved between the respiratory and alimentary systems. These anomalies are almost always seen in association with esophageal atresia and tracheal stenosis or fistula.
PULMONARY AGENESIS, APLASIA, AND HYPOPLASIA
Pulmonary agenesis is the complete failure of both airway and parenchymal development. Pulmonary aplasia is used to describe the incomplete development of lung parenchyma supplied by a rudimentary bronchus. Pulmonary hypoplasia is distinguished by a normal tracheobronchial tree and underdeveloped pulmonary parenchyma. Agenesis can occur either unilaterally or bilaterally. In the latter case this would be incompatible with life. In cases of unilateral agenesis, frequently other associated severe developmental abnormalities are also found. Most commonly, these include the elements of the VACTERL syndrome. The etiology and embryonic pathophysiology of aplasia and agenesis remain largely unknown.
Pulmonary hypoplasia is the most commonly encountered anomaly of underdeveloped lung parenchyma. There are a variety of known causes. The compressive effects of lung, mediastinal, or cardiac masses or herniated abdominal viscera, as seen with CDH, can result in arrested pulmonary parenchymal development. Other causes include the abnormal mechanical effects of fetal diaphragmatic excursion or fetal lung and amniotic fluid volume. Specifically, abnormal or absent fetal breathing or oligohydramnios, with or without renal dysgenesis or obstructive uropathy, can be causative of pulmonary hypoplasia.
The diagnosis and treatment of pulmonary hypo- plasia is dependent on the underlying etiology. For example, severe respiratory impairment can be seen with pulmonary hypoplasia from a CDH. In these cases, stabilization of the underlying physiologic impairment is the priority. In cases of aplasia or agenesis, the chest radiographs may demonstrate opacification of the ipsilateral hemithorax and an ipsilateral mediastinal shift with volume loss. In addition, asymmetry of the chest with obviously impaired respiratory movement of the affected side is seen. Treatment is initially directed at any associated anomalies, with particular focus on congenital cardiac lesions. If an operation is needed to remove a nonfunctioning lobe or lung, every effort is made to preserve functional parenchyma. In cases that render an empty hemitho- rax, consideration should be given to the intrathoracic placement of a tissue expander to prevent significant musculoskeletal disfigurement from the eventual mediastinal and skeletal shift toward the volume loss side.
MEDIASTINAL CYSTS
As has been discussed, many of the commonly recognized congenital bronchial malformations, such as bronchial agenesis, atresia, or stenosis, produce parenchymal abnormalities that distinguish these lesions clinically. However, a subset of congenital malformations is unique to the bronchial tree and has been traditionally grouped under the nomenclature of bronchogenic cysts or foregut duplication cysts. As discussed earlier, the embryologic derivation of these from a common foregut anlagen, their occurrence in the chest, and their most frequent clinical symptoms make their inclusion appropriate in a discussion of BPMs. The nomenclature in common usage remains confusing. In general, the term foregut duplication cyst appropriately links these lesions embryologically as arising from a common developmental structure. When one considers their histologic architecture, these lesions can be divided into three subdivisions: (1) bronchogenic cysts, (2) enteric duplication cysts, and (3) neuroenteric cysts, all of which reveal their common endodermal origins.
Bronchogenic cysts are lined by respiratory bronchial epithelium, are mucus filled, and may contain cartilage in their walls. Enteric duplication cysts are lined by intestinal epithelium (either esophageal or gastric) and may contain smooth muscle. Most commonly, enteric cysts occur within the muscular wall of an otherwise intact esophagus without communication with the lumen. Neuroenteric cysts are the embryo- logic exception, arising from a failure of separation of notochord and foregut. These lesions contain gastrointestinal mucosa with well-developed smooth muscle walls and communicate with the central nervous system (CNS), spinal cord, and perhaps dura. This association explains their frequent coexistence with congenital vertebral defects, most commonly hemi- vertebrae. Neuroenteric cysts are, however, much rarer than either bronchogenic or enteric cysts.
Foregut duplications must be considered in the differential diagnosis of a cystic mediastinal lesion. Bronchogenic cysts can be diagnosed prena- tally, perinatally, or in an older child. The lesion may be seen in the newborn with acute respiratory distress because a large lesion can compress adjacent normal lung tissue. They may be totally asymptomatic in an older child or may occur with infection in an occult lesion. Occasionally, the lesion is discovered incidentally on chest radiography performed for unrelated reasons. Further studies should include CT of the chest to identify the lesion and its relation to surrounding structures. Mediastinal cysts also have been identified on prenatal ultrasonography and are followed up perinatally with these same imaging modalities. Close scrutiny of the mediastinal structures is indicated because all bronchogenic cysts, whether symptomatic or not, should be excised, given their propensity for expansion, infection, and hemorrhage. Because bronchogenic cysts are most commonly discrete lesions, they can be successfully approached thora- coscopically. Care must be taken to avoid injury to either the bronchial or esophageal wall, particularly when they share a common wall. The development of intracorporeal suturing techniques has enhanced our ability to excise these lesions endoscopically. Previous infection makes their removal more difficult by either the open or thoracoscopic approach, given the fibro- vascular reaction that occurs surrounding infected lesions.
Bronchogenic cysts also may occur within the pulmonary parenchyma separate from the hilar structures. Peripheral bronchogenic cysts may be multiple, in which case they are more appropriately termed bronchiolar cysts or cystic bronchiectasis. The more peripheral bronchogenic or pulmonary cysts are lined by ciliated respiratory epithelium and likely result from abnormalities during the latter portion of the pseudoglandular stage of lung development, as contrasted to the more central lesions that are true foregut abnormalities. These lesions invariably communicate with the airway and often create obstruction of accompanying bronchi. Peripheral lesions may initially be seen early from the accumulation of mucus that leads to obstruction, or they may be seen later as infected peripheral lesions. They may be confused with necrotizing pneumonia. Diagnostic evaluation almost always includes CT. The treatment is surgical resection, given the natural history of persistence with recurring symptoms. 
6.  Main literature:
1.	Pediatric surgery: textbook / Losev O.O., Melnychenko M.H., Dilanyan I.R., Samofalov D.O.; edited by Loseva O.O. – Odesa : ONMedU, 2011. — 224 pages
2.	Pediatric surgery (Textbook / Grif of the Ministry of Health of Ukraine / Odesa: ONMedU, 2019, 224 с.) Losev O.O., Melnychenko M.H., and others, 7 people altogether
3.	Kryvchenya D. Y., Lysak S.V, Plotnikov O.M Surgical diseases in children. - Vinnytsya: New book, 2008. - 256 p.
4.	Pediatric surgery. / Edited by Sushka V.I. and co-authors // K. Health. - 2002. - 718 p.
5.	Pediatric surgery. Tutorial. Part 2. Edited by Tolstanova O.K., Rybalchenko V.F., Danilova O.A. and others. Zhytomyr "POLISSYA". - 2016. - p. 225, 322-331

Additional literature:
6.	Emergency surgery of the abdominal cavity (standards of organization and professionally oriented algorithms for medical care) / Edited by Fomina P.D., Usenko O.Y., Bereznytsky Y.S. - Kyiv: ‘Health of Ukraine’ Library, 2018. - 354 p.
7.	Age aspects of acute appendicitis in children and the key to its recognition. Tutorial. 2019. 260 p. Edited by Bodnar B.M., Ribalchenko V.F., Bodnar O.B., Melnichenko M.H., and others. Publishing. ISBN 978-966-697-828-1
8.	Nedelska S.M. Diseases of the hepatobiliary system and pancreas in children. Textbook for 6th-year students of a medical faculty, interns, pediatricians, family doctors / Nedelska S.M., Mazur V.I., Shumna T.E.. - Zaporizhzhia: [ZDMU], 2017. - 113 p.
9.	Violation of defecation in children: constipation and encopresis: Textbook /  Rybalchenko V.F., Berezhnyy V.V. ,Konoplitsky V.S., and others; Edited by professor Rybalchenko V.F., Berezhnyy V.V., Konoplitsky V.S., Rusak P.S. - Kyiv: VIT-A-POL LLC, 2018. - 548 p .: illustrations
10.	Intestinal malrotation in children: from embryogenesis to consequences / Monograph. Edited by Pereyaslova A.A., Rybalchenko V.F., Loseva O.O - K .: PE "INPOL LTM" Printing House "000000000", 2019. - 226 p: illustrations
11.	Intestinal obstruction in children: a textbook for students of the 5th year of medical faculties (specialties: "Medical business", "Pediatrics"). Spahi O.V., Barukhovych V.Y., Kokorkin O.D., Lyaturynska O.V., Pakholchuk O.P., Zaporozhchenko A.H. - Zaporizhzhia. -2015.- 75 p.
12.	Developmental defects in children: a textbook for independent work of students of the VI course of the medical faculty (specialties "Medical business", "Pediatrics"). Solovyov A.E., Lyaturynska O.V., Barukhovych V.Y., Spahi O.V., Shchokin O.V., Makarova M.O., Anikin I.O. Zaporizhzhia, 2013. 165 p.
13.	Bachurin V.I. Malformations of the genitourinary system as a cause of urological pathologies: teaching methodology for independent work of fourth-year students in the specialty: 7.12010001 "Medical business", 7.12010002 "Pediatrics", 6.120102 "Laboratory diagnostics" / Bachurin V.I.. - Zaporizhzhia: ZSMU, 2017. - 86 p.
14.	Shmakov A.P. Workshop on pediatric surgery: manual / Shmakov A.P.- Vitebsk, VSMU, 2016 .-- 309 p.
15.	Makarov A.V. Examination of the respiratory organs in children. Training manual. Makarov A.V., Danilov O.A., Sokur P.P., Rybalchenko V.F., Yurchenko M.I. - C .: Business entity Kolyada O.P., 2005. - 160 p.