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Operative Pediatric Surgery, 2e. Moritz M. Ziegler, MD, Richard G. Azizkhan, MD, PhD (Hon), Daniel von Allmen, MD, Thomas R. Weber, MD. Search Textbook. University of Puerto Rico, School of Medicine. University Pediatric Hospital. Chief – Pediatric Surgery. San Jorge Children Hospital. Pediatric surgery offers a unique opportunity to learn fluid and electrolyte Maintenance fluid volumes for the pediatric patient can be estimated using two.


Pediatric Surgery Books Pdf

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Download complete list of books in this Paediatric Surgery Collection .pdf) .xls) · RSS Feed Paediatric Surgery (Oxford Specialist Handbooks in Paediatrics). Professor. General & Thoracic Surgery. Topics for discussion. • What makes Pediatric Surgery unique? • Neonatal intestinal obstruction. • Abdominal wall defects. The Sages Manual of Pediatric Minimally Invasive Surgery. Danielle S. Lovell and Winter's Pediatric Orthopaedics Two-Volume Set, 7th Edition Retail PDF.

Postoperative management is very difficult. Due to hypoplastic lungs, there is frequently pulmonary hypertension leading to right-to-left shunting and progressive hypoxemia, hypercarbia, and acidosis that worsens the pulmonary hypertension. The use of chest tubes may cause overstretching of the already hypoplastic alveoli causing: increase pulmonary hypertension, reduce functional residual capacity and reduce lung compliance.

Postoperatively, the infant should be kept paralyzed and ventilated and only very slowly weaned from the ventilator. The severity of pulmonary hypoplasia, both ipsilaterally and contralaterally, is the main determinant of outcome.

ECMO extracorporeal membrane oxygenator has come to reduce somewhat the mortality of this condition. The mortality of CDH is directly related to the degree of lung hypoplasia associated. Death is caused by persistent pulmonary hypertension and right ventricular failure. Prospective studies of prenatally diagnosed fetus prior to 25 wk.

This unsolved problem has prompted investigators to develop new treatment options such as preoperative stabilization, jet-frequency ventilation, and ECMO. Another area of development is intrauterine fetal surgical repair.

Intrauterine repair has meet with limited success due to herniation of the fetal liver into the chest through the defect. Disturbance of the umbilical circulation during or after liver reduction causes fetal death. Positive-pressure ventilation after birth reduces the liver before the baby comes for surgical repair. Another less invasive approach is enlarging the hypoplastic lungs by reducing the normal egress of fetal lung fluid with controlled tracheal obstruction called PLUGS Plug Lung Until it Grows.

Infants and children will present with either respiratory or gastrointestinal symptoms such as: chronic respiratory tract infection, vomiting, intermittent intestinal obstruction, and feeding difficulty. Occasionally the child is asymptomatic. A rise intrabdominal pressure by coughing or vomiting transmitted to any defect of the diaphragm makes visceral herniation more likely.

Diagnosis is confirmed by chest or gastrointestinal contrast imaging. Management consists of immediate surgery after preop stabilization. Most defects can be closed primarily through an abdominal approach. Chest-tube placement in the non-hypoplastic lung is of help. Surgical results are generally excellent. A few deaths have resulted from cardiovascular and respiratory compromise due to visceral herniation causing mediastinal and pulmonary compression. Almost always asymptomatic, typically present in older children or adults with minimal gastrointestinal symptoms or as incidental finding during routine chest radiography mass or air-fluid levels.

Infants may develop respiratory symptoms tachypnea, dyspnea and cyanosis with distress. Cardiac tamponade due to protrusion into the pericardial cavity has been reported. US and CT-Scan can demonstrate the defect. Management is operative. Trans-abdominal subcostal approach is preferred with reduction of the defect and suturing of the diaphragm to undersurface of sternum and posterior rectus sheath.

Large defects with phrenic nerve displacement may need a thoracic approach. Results after surgery rely on associated conditions. Diagnosis is made radiologically always and in a number of patients endoscopically. The hiatal hernia HH refers to herniation of the stomach to the chest through the esophageal hiatus. The lower esophageal sphincter also moves. It can consist of a small transitory epiphrenic loculation minor up to an upside-down intrathoracic stomach major.

HH generally develops due to a congenital, traumatic or iatrogenic factor. Most disappear by the age of two years, but all forms of HH can lead to peptic esophagitis from Gastroesophageal reflux. Repair of HH is determined by the pathology of its associated reflux causing failure to thrive, esophagitis, stricture, respiratory symptoms or the presence of the stomach in the thoracic cavity. In the paraesophageal hernia PH variety the stomach migrates to the chest and the lower esophageal sphincter stays in its normal anatomic position.

PH is a frequent problem after antireflux operations in patients without posterior crural repair. Small PH can be observed. With an increase in size or appearance of symptoms reflux, gastric obstruction, bleeding, infarction or perforation the PH should be repaired. The incidence of PH has increased with the advent of the laparoscopic fundoplication. For groin inguinal or femoral hernias, this protrusion is into a hernial sac. Whether or not the mere presence of a hernial sac or processus vaginalis constitutes a hernia is debated.

Inguinal hernias in children are almost exclusively indirect type. Those rare instances of direct inguinal hernia are caused by previous surgery and floor disruption.

An indirect inguinal hernia protrudes through the internal inguinal ring, within the cremaster fascia, extending down the spermatic cord for varying distances.

The direct hernia protrudes through the posterior wall of the inguinal canal, i. The embryology of indirect inguinal hernia is as follows: the duct descending to the testicle is a small offshoot of the great peritoneal sac in the lower abdomen.

During the third month of gestation, the processus vaginalis extends down toward the scrotum and follows the chorda gubernaculum that extends from the testicle or the retroperitoneum to the scrotum. During the seventh month, the testicle descend into the scrotum, where the processus vaginalis forms a covering for the testicle and the serous sac in which it resides. At about the time of birth, the portion of the processus vaginalis between the testicle and the abdominal cavity obliterates, leaving a peritoneal cavity separate from the tunica vaginalis that surrounds the testicle.

The typical patient with an inguinal hernia has an intermittent lump or bulge in the groin, scrotum, or labia noted at times of increased intra-abdominal pressure. A communicating hydrocele is always associated with a hernia. This hydrocele fluctuates in size and is usually larger in ambulatory patients at the end of the day. If a loop of bowel becomes entrapped incarcerated in a hernia, the patient develops pain followed by signs of intestinal obstruction.

If not reduced, compromised blood supply strangulation leads to perforation and peritonitis. Most incarcerated hernias in children can be reduced. Associated to these episodes of incarceration are chances of: gonadal infarction the undescended testes complicated by a hernia are more vulnerable to vascular compromise and atrophy , bowel obstruction and strangulation.

Symptomatic hernia can complicate the clinical course of babies at NICU ill with hyaline membrane, sepsis, NEC and other conditions needing ventilatory support.

Repair should be undertaken before hospital discharge to avoid complications. Prematures have: poorly developed respiratory control center, collapsible rib cage, deficient fatigue-resistant muscular fibers in the diaphragm that predispose then to potential life-threatening post-op respiratory complications such as: need of assisted ventilation most common , apnea and bradycardia, emesis, cyanosis and re-intubation due to laryngospasm.

Postconceptual age sum of intra- and extrauterine life has been cited as the factor having greatest impact on post-op complications. These observation makes imperative that preemies with post conceptual age of less than 45 weeks be carefully monitored in-hospital for at least 24 hours after surgical repair of their hernias.

Outpatient repair is safer for those prematures above the 60 wk. The very low birth weight infant with symptomatic hernia can benefit from epidural anesthesia. At times, the indirect inguinal hernia will extend into the scrotum and can be reduced by external, gentle pressure.

Occasionally, the hernia will present as a bulge in the soft tissue overlying the internal ring. Elective herniorrhaphy at a near convenient time is treatment of choice. Since risk of incarceration is high in children, repair should be undertaken shortly after diagnosis. Simple high ligation of the sac is all that is required. Pediatric patients are allowed to return to full activity immediately after hernia repair.

Bilateral exploration is done routinely by most experienced pediatric surgeons. Recently the use of groin laparoscopy through the hernial sac permits visualization of the contralateral side.

Testicular feminization syndrome TFS is a genetic form of male pseudohermaphroditism patient who is genetically 46 XY but has deficient masculinization of external genitalia caused by complete or partial resistance of end organs to the peripheral effects of androgens.

This androgenic insensitivity is caused by a mutation of the gene for androgenic receptor inherited as an X-linked recessive trait. In the complete form the external genitalia appear to be female with a rudimentary vagina, absent uterus and ovaries. The incomplete form may represent undervirilized infertile men. Evaluation should include: karyotype, hormonal assays, pelvic ultrasound, urethrovaginogram, gonadal biopsy and labial skin bx for androgen receptor assay.

This patients will never menstruate or bear children. Chronic Intestinal Pseudo-Obstruction is a rare disorder of intestinal motility in infants and children characterized by recurrent attacks of abdominal pain, distension, vomiting, constipation and weight loss in the absence of obvious mechanical lesions.

The disease can be familial or sporadic. Suggested etiology is degeneration of enteric nervous or smooth muscle cells. The diagnosis is based on history, physical exam, radiographies and motility studies.

X-Ray hallmarks are: Histologic pattern portrayed: Management is primary supportive: Motility agents are unsuccessful. Venting gastrostomy with home parenteral nutrition has shortened the high hospitalization rate associated to this disease process. A similar condition can be seen in early fed prematures due to immaturity of intestinal motility. Bezoars are rare foreign body concretions formed in the stomach and small bowel composed mainly of hair tricho , vegetable matter phyto or milk curds lacto.

Most cases are females children, years old, with bizarre appetite trichophagia and emotional disturbances. Originally the mass forms in the stomach and can move to the small bowel by fragmentation, extension or total translocation. The child can develop an asymptomatic palpable abdominal mass, pain, obstruction or perforation. Other children will reduce intake and develop weight loss. Predisposing conditions to bezoar formations are: Management can consist of mechanical or pulsating jet of water fragmentation via the endoscope, operative extraction, shock-wave lithotripsy ESWL with subsequent evacuation, or dissolution by oral ingestion of proteolytic enzymes papain, acetylcysteine, cellulase.

With ESWL the shock wave pressure needed is less than half used for urolithiasis cases.

Case Report

Clinically two different types of isolated IND have been described: Type A shows symptoms of abdominal distension, enterocolitis, bloody stools, intestinal spasticity in imaging studies Ba Enema since birth, is less common and associated with hypoplasia of sympathetic nerves. Type B is more frequent, symptoms are indistinguishable from that of HD, with chronic constipation, megacolon, and repeated episodes of bowel obstruction.

Management depends on clinical situation; conservative for minor symptoms until neuronal maturation occurs around the 4th year of life, colostomy and resectional therapy for life threatening situations.

The most common congenital diaphragmatic hernia CDH is that which occurs through the postero-lateral defect of Bochdalek. It is caused by failure of the pleuroperitoneal membrane to develop adequately and close before the intestines returning to the abdomen at the tenth week of gestation.

The intestines then enter the pleural cavity and cause poor lung development leading to pulmonary hypoplasia a reduced number of alveoli per area of lung tissue. This defect is postero-lateral in the diaphragm and may vary in size.

Stomach, liver or spleen may be partly in chest as well. Frequency is 1: The clinical presentation is that the newborn becomes rapidly cyanotic, acidotic, and has poor ventilation. Major findings relate to the degree of pulmonary maldevelopment. Chest films will show intestines in the chest. Placement of a radiopaque nasogastric tube may show the tube coiled in the lower left chest.

Higher risk factors are: Treatment consist of rapid intubation and ventilation with use of muscle relaxants, placement of a nasogastric tube to prevent gaseous distension of the intestines and preoperative stabilization of arterial blood gases and acid-base status.

Surgery can be undertaken when one of the following objectives are met: Operative management consist of abdominal approach, closure of hernia by primary repair or use of mesh, and correction of malrotation. Postoperative management is very difficult. Due to hypoplastic lungs, there is frequently pulmonary hypertension leading to right-to-left shunting and progressive hypoxemia, hypercarbia, and acidosis that worsens the pulmonary hypertension. The use of chest tubes may cause overstretching of the already hypoplastic alveoli causing: Postoperatively, the infant should be kept paralyzed and ventilated and only very slowly weaned from the ventilator.

The severity of pulmonary hypoplasia, both ipsilaterally and contralaterally, is the main determinant of outcome. ECMO extracorporeal membrane oxygenator has come to reduce somewhat the mortality of this condition.

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The mortality of CDH is directly related to the degree of lung hypoplasia associated. Death is caused by persistent pulmonary hypertension and right ventricular failure. Prospective studies of prenatally diagnosed fetus prior to 25 wk. This unsolved problem has prompted investigators to develop new treatment options such as preoperative stabilization, jet-frequency ventilation, and ECMO. Another area of development is intrauterine fetal surgical repair.

To achieve success fetal surgery should: Intrauterine repair has meet with limited success due to herniation of the fetal liver into the chest through the defect. Disturbance of the umbilical circulation during or after liver reduction causes fetal death.

Positive-pressure ventilation after birth reduces the liver before the baby comes for surgical repair. Another less invasive approach is enlarging the hypoplastic lungs by reducing the normal egress of fetal lung fluid with controlled tracheal obstruction called PLUGS Plug Lung Until it Grows.

Infants and children will present with either respiratory or gastrointestinal symptoms such as: Occasionally the child is asymptomatic. A rise intrabdominal pressure by coughing or vomiting transmitted to any defect of the diaphragm makes visceral herniation more likely. Diagnosis is confirmed by chest or gastrointestinal contrast imaging.

Management consists of immediate surgery after preop stabilization. Most defects can be closed primarily through an abdominal approach. Chest-tube placement in the non-hypoplastic lung is of help.

Surgical results are generally excellent. A few deaths have resulted from cardiovascular and respiratory compromise due to visceral herniation causing mediastinal and pulmonary compression. First described in , Morgagni Hernias MH are rare congenital diaphragmatic defects close to the anterior midline between the costal and sternal origin of the diaphragm. Almost always asymptomatic, typically present in older children or adults with minimal gastrointestinal symptoms or as incidental finding during routine chest radiography mass or air-fluid levels.

Infants may develop respiratory symptoms tachypnea, dyspnea and cyanosis with distress. Cardiac tamponade due to protrusion into the pericardial cavity has been reported. Associated conditions are: US and CT-Scan can demonstrate the defect. Management is operative. Trans-abdominal subcostal approach is preferred with reduction of the defect and suturing of the diaphragm to undersurface of sternum and posterior rectus sheath.

Large defects with phrenic nerve displacement may need a thoracic approach. Results after surgery rely on associated conditions. Two types of esophageal hernia recognized are the hiatal and paraesophageal hernia.

Diagnosis is made radiologically always and in a number of patients endoscopically. The hiatal hernia HH refers to herniation of the stomach to the chest through the esophageal hiatus. The lower esophageal sphincter also moves. It can consist of a small transitory epiphrenic loculation minor up to an upside-down intrathoracic stomach major. HH generally develops due to a congenital, traumatic or iatrogenic factor. Most disappear by the age of two years, but all forms of HH can lead to peptic esophagitis from Gastroesophageal reflux.

Repair of HH is determined by the pathology of its associated reflux causing failure to thrive, esophagitis, stricture, respiratory symptoms or the presence of the stomach in the thoracic cavity. In the paraesophageal hernia PH variety the stomach migrates to the chest and the lower esophageal sphincter stays in its normal anatomic position. PH is a frequent problem after antireflux operations in patients without posterior crural repair. Small PH can be observed.

With an increase in size or appearance of symptoms reflux, gastric obstruction, bleeding, infarction or perforation the PH should be repaired. The incidence of PH has increased with the advent of the laparoscopic fundoplication. A hernia is defined as a protrusion of a portion of an organ or tissue through an abnormal opening.

For groin inguinal or femoral hernias, this protrusion is into a hernial sac. Whether or not the mere presence of a hernial sac or processus vaginalis constitutes a hernia is debated. Inguinal hernias in children are almost exclusively indirect type. Those rare instances of direct inguinal hernia are caused by previous surgery and floor disruption. An indirect inguinal hernia protrudes through the internal inguinal ring, within the cremaster fascia, extending down the spermatic cord for varying distances.

The direct hernia protrudes through the posterior wall of the inguinal canal, i. The embryology of indirect inguinal hernia is as follows: During the third month of gestation, the processus vaginalis extends down toward the scrotum and follows the chorda gubernaculum that extends from the testicle or the retroperitoneum to the scrotum. During the seventh month, the testicle descend into the scrotum, where the processus vaginalis forms a covering for the testicle and the serous sac in which it resides.

At about the time of birth, the portion of the processus vaginalis between the testicle and the abdominal cavity obliterates, leaving a peritoneal cavity separate from the tunica vaginalis that surrounds the testicle. The typical patient with an inguinal hernia has an intermittent lump or bulge in the groin, scrotum, or labia noted at times of increased intra-abdominal pressure. A communicating hydrocele is always associated with a hernia.

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This hydrocele fluctuates in size and is usually larger in ambulatory patients at the end of the day. If a loop of bowel becomes entrapped incarcerated in a hernia, the patient develops pain followed by signs of intestinal obstruction. If not reduced, compromised blood supply strangulation leads to perforation and peritonitis.

Most incarcerated hernias in children can be reduced. Associated to these episodes of incarceration are chances of: Symptomatic hernia can complicate the clinical course of babies at NICU ill with hyaline membrane, sepsis, NEC and other conditions needing ventilatory support.

Repair should be undertaken before hospital discharge to avoid complications. Prematures have: Postconceptual age sum of intra- and extrauterine life has been cited as the factor having greatest impact on post-op complications.

These observation makes imperative that preemies with post conceptual age of less than 45 weeks be carefully monitored in-hospital for at least 24 hours after surgical repair of their hernias. Outpatient repair is safer for those prematures above the 60 wk. The very low birth weight infant with symptomatic hernia can benefit from epidural anesthesia. At times, the indirect inguinal hernia will extend into the scrotum and can be reduced by external, gentle pressure.

Occasionally, the hernia will present as a bulge in the soft tissue overlying the internal ring. Elective herniorrhaphy at a near convenient time is treatment of choice.

Since risk of incarceration is high in children, repair should be undertaken shortly after diagnosis. Simple high ligation of the sac is all that is required. Pediatric patients are allowed to return to full activity immediately after hernia repair.

Bilateral exploration is done routinely by most experienced pediatric surgeons. Recently the use of groin laparoscopy through the hernial sac permits visualization of the contralateral side. Testicular feminization syndrome TFS is a genetic form of male pseudohermaphroditism patient who is genetically 46 XY but has deficient masculinization of external genitalia caused by complete or partial resistance of end organs to the peripheral effects of androgens.

This androgenic insensitivity is caused by a mutation of the gene for androgenic receptor inherited as an X-linked recessive trait. In the complete form the external genitalia appear to be female with a rudimentary vagina, absent uterus and ovaries. The incomplete form may represent undervirilized infertile men. Evaluation should include: This patients will never menstruate or bear children.

Early gonadectomy is advised to: Vaginal reconstruction is planned when the patient wishes to be sexually active. These children develop into very normal appearing females that are sterile since no female organs are present. A hydrocele is a collection of fluid in the space surrounding the testicle between the layers of the tunica vaginalis.

Hydroceles can be scrotal, of the cord, abdominal, or a combination of the above. A hydrocele of the cord is the fluid-filled remnant of the processus vaginalis separated from the tunica vaginalis.

A communicating hydrocele is one that communicates with the peritoneal cavity by way of a narrow opening into a hernial sac. Hydroceles are common in infants. Some are associated with an inguinal hernia. They are often bilateral, and like hernias, are more common on the right than the left. Most hydroceles will resolved spontaneously by years of age. After this time, elective repair can be performed at any time.

Operation is done through the groin and search made for an associated hernia. Aspiration of a hydrocele should never be attempted. As a therapeutic measure it is ineffective, and as a diagnostic tool it is a catastrophe if a loop of bowel is entrapped. A possible exception to this is the postoperative recurrent hydrocele. The undescended testis is a term we use to describe all instances in which the testis cannot be manually manipulated into the scrotum.

The testes form from the medial portion of the urogenital ridge extending from the diaphragm into the pelvis. In arrested descent, they may be found from the kidneys to the internal inguinal ring. Rapid descent through the internal inguinal ring commences at approximately week 28, the left testis preceding the right.

Adequate amounts of male hormones are necessary for descent. The highest levels of male hormones in the maternal circulation have been demonstrated at week Thus, it appears that failure of descent may be related to inadequate male hormone levels or to failure of the end-organ to respond.

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The undescended testes may be found from the hilum of the kidney to the external inguinal ring. The undescended testis found in 0.

Testes that can be manually brought to the scrotum are retractile and need no further treatment. Parents should know the objectives, indications and limitations of an orchiopexy: To improve spermatogenesis producing an adequate number of spermatozoids surgery should be done before the age of two. Electron microscopy has confirmed an arrest in spermatogenesis reduced number of spermatogonias and tubular diameter in undescended testis after the first two years of life.

Other reasons to pex are: The management is surgical; hormonal Human Chorionic Gonadotropin treatment has brought conflicting results except bilateral cases. Surgery is limited by the length of the testicular artery. Palpable testes have a better prognosis than non-palpable. Laparoscopy can be of help in non-palpable testis avoiding exploration of the absent testis.

An umbilical hernia is a small defect in the abdominal fascial wall in which fluid or abdominal contents protrude through the umbilical ring. The presence of a bulge within the umbilicus is readily palpable and becomes more apparent when the infant cries or during defecation. The actual size of the umbilical hernia is measured by physical examination of the defect in the rectus abdominis muscle, and not by the size of the umbilical bulge.

The size of the fascial defect can vary from the width of a fingertip to several centimetres. Embryologically, the cause of an umbilical hernia is related to the incomplete contraction of the umbilical ring. The herniation of the umbilicus is a result of the growing alimentary tract that is unable to fit within the abdominal cavity. Umbilical hernias are more prevalent in females than in males and are more often seen in patients with African heritage.

The increased frequency of umbilical hernias has also been attributed to premature babies, twins and infants with long umbilical cords. Most umbilical hernias are asymptomatic; the decision to repair the umbilical hernia in the first years of life is largely cosmetic and is often performed because of parental request, not because of pain or dysfunction. In the past, some parents use to tape a coin over the umbilical bulge, however, manual compression does not have an effect on the fascial defect.

Treatment of umbilical hernia is observation. However, surgical repair is recommended if the hernia has not closed by the age of five. The incidence of incarceration trapped intestinal loop is rare, even in larger defects.

Females should especially have their umbilical hernia corrected before pregnancy because of the associated increased intra-abdominal pressure that could lead to complications. The procedure is simple and incidence of complication such as infection is extremely rare. The repair is usually done as outpatient surgery under general anesthetic. Embryology for surgeons: Inguinal and umbilical hernia repair in infants and children.

Surg Clinics of North Am 73 3: The developing human — 4th edition. Philadelphia, WB Saunders, pp. Some observations on umbilical hernias in infants. The comparative incidence of umbilical hernias in colored and white infants. J Natl Med Assoc The three most common abdominal wall defect in newborns are umbilical hernia, gastroschisis and omphalocele. Omphalocele is a milder form of primary abdominoschisis since during the embryonic folding process the outgrowth at the umbilical ring is insufficient shortage in apoptotic cell death.

Defect may have liver, spleen, stomach, and bowel in the sac while the abdominal cavity remains underdeveloped in size. The defect is centrally localized and measures cm in diameter. A small defect of less than 2 cm with bowel inside is referred as a hernia of the umbilical cord. Epigastric localized omphalocele are associated with sternal and intracardiac defects i. All have malrotation. Cardiac, neurogenic, genitourinary, skeletal and chromosomal changes and syndromes are the cornerstones of mortality.

Cesarean section is warranted in large omphaloceles to avoid liver damage and dystocia. After initial stabilization management requires consideration of the size of defect, prematurity and associated anomalies. Primary closure with correction of the malrotation should be attempted whenever possible. Antibiotics and nutritional support are mandatory.

Manage control centers around sepsis, respiratory status, liver and bowel dysfunction from increased intraabdominal pressure. The protruding gut is foreshortened, matted, thickened and covered with a peel. The IA might be the result of pressure on the bowel from the edge of the defect pinching effect or an intrauterine vascular accident.

Rarely, the orifice may be extremely narrow leading to gangrene or complete midgut atresia. In either case the morbidity and mortality of the child is duplicated with the presence of an IA. Management remains controversial. Alternatives depend on the type of closure of the abdominal defect and the severity of the affected bowel. With primary fascial closure and good-looking bowel primary anastomosis is justified.

Angry looking dilated bowel prompts for proximal diversion, but the higher the enterostomy the greater the problems of fluid losses, electrolyte imbalances, skin excoriation, sepsis and malnutrition. Closure of the defect and resection with anastomosis two to four weeks later brings good results. Success or failure is related to the length of remaining bowel more than the specific method used.

Initially do an Apt test to determine if blood comes from fetal origin or maternal origin blood swallowed by the fetus. If this coagulation profile is normal the possibilities are either stress gastritis or ulcer disease. If the coagulation profile is abnormal then consider hematologic disease of the newborn and manage with vitamin K.

The apt test is performed by mixing 1 part of vomitus with 5 part H2O, centrifuge the mixture and remove 5 ml pink. If the coagulation profile is abnormal give Vit K for hematologic disorder of newborn.

A fissure could be the cause, if negative then consider either malrotation or Necrotizing enterocolitis.

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The stress includes prematurity, sepsis, hypoxia, hypothermia, and jaundice. These babies frequently have umbilical artery, vein catheters, have received exchange transfusions or early feeds with hyperosmolar formulas. The intestinal mucosal cells are highly sensitive to ischemia and mucosal damage leads to bacterial invasion of the intestinal wall. Gas-forming organisms produce pneumatosis intestinalis air in the bowel wall readily seen on abdominal films. Full-thickness necrosis leads to perforation, free air and abscess formation.

These usually premature infants develop increased gastric residuals, abdominal distension, bloody stools, acidosis and dropping platelet count. The abdominal wall becomes reddened and edematous.

There may be persistent masses and signs of peritonitis. Perforation leads to further hypoxia, acidosis and temperature instability. The acid-base status is monitored for worsening acidosis and hypoxia. The white blood cell count may be high, low or normal and is not generally of help. Serial abdominal films are obtained to look for evidence of free abdominal air, a worsening picture of pneumatosis intestinalis, or free portal air. Therapy consist initially of stopping feeds, instituting nasogastric suctioning and beginning broad-spectrum antibiotics ampicillin and gentamycin.

Persistent or worsening clinical condition and sepsis or free air on abdominal films require urgent surgical intervention. Attempts to preserve as much viable bowel as possible are mandatory to prevent resultant short gut syndrome. Complicated NEC is the most common neonatal surgical emergency of modern times, has diverse etiologies, significant mortality and affects mostly premature babies.

Consist of a right lower quadrant incision and placement of a drainage penrose or catheter under local anesthesia with subsequent irrigation performed bedside at the NICU. Initially used as a temporizing measure before formal laparotomy, some patient went to improvement without the need for further surgery almost one-third.

They either had an immature fetal type healing process or a focal perforation not associated to NEC? Some suggestion made are: PPD should be an adjunct to preop stabilization, before placing drain be sure pt has NEC by X-rays, persistent metabolic acidosis means uncontrolled peritoneal sepsis, do not place drain in pts with inflammatory mass or rapid development of intraperitoneal fluid, the longer the drainage the higher the need for laparotomy.

In the initial evaluation a history should be obtained for bleeding disorders, skin lesions, and aspirin or steroid ingestion. The physical exam for presence of enlarged liver, spleen, masses, ascites, or evidence of trauma or portal hypertension. Labs such as bleeding studies and endoscopy, contrast studies if bleeding stops.

Common causes of Upper GI bleeding are: Esophagus a Varices- usually presents as severe upper gastrointestinal bleeding in a year old who has previously been healthy except for problems in the neonatal period.

This is a result of extrahepatic portal obstruction portal vein thrombosis most commonly , with resulting varices. The bleeding may occur after a period of upper respiratory symptoms and coughing. Management is initially conservative with sedation and bedrest; surgery ir rarely needed. Treatment consist of antacids, frequent small feeds, occasionally medications and if not rapidly improved, then surgical intervention with a fundoplication of the stomach.

This was thought to be uncommon in children because it was not looked for by endoscopy. It probably occurs more often than previously thought. Treatment initially is conservative and, if persistent, oversewing of the tear through an incision in the stomach will be successful.

They bleed when there is ectopic gastric mucosa present. Total excision is curative. Stomach a Gastric Erosions- managed medically in most cases. Duodenum a Duodenitis- associated to acid peptic disease.

Occasionally requires surgical intervention with local repair or ligation of hepatic vessels. Anal fissure is the most common cause of rectal bleeding in the first two years of life.

Outstretching of the anal mucocutaneous junction caused by passage of large hard stools during defecation produces a superficial tear of the mucosa in the posterior midline. Pain with the next bowel movement leads to constipation, hardened stools that continue to produce cyclic problems.

Large fissures with surrounding bruising should warn against child abuse. The diagnosis is made after inspection of the anal canal. Chronic fissures are associated with hypertrophy of the anal papilla or a distal skin tag.

Management is directed toward the associated constipation with stool softeners and anal dilatations, warm perineal baths to relax the internal muscle spasm, and topical analgesics for pain control. If medical therapy fails excision of the fissure with lateral sphincterotomy is performed.

MD can be the cause of: Diagnosis depends on clinical presentation. Rectal bleeding from MD is painless, minimal, recurrent, and can be identified using 99mTc- pertechnetate scan; contrasts studies are unreliable. Persistent bleeding requires arteriography or laparotomy if the scan is negative.

Obstruction secondary to intussusception, herniation or volvulus presents with findings of fulminant, acute small bowel obstruction, is diagnosed by clinical findings and contrast enema studies. The MD is seldom diagnosed preop. Diverticulitis or perforation is clinically indistinguishable from appendicitis. Mucosal polyps or fecal umbilical discharge can be caused by MD. Laparoscopy can confirm the diagnosis and allow resection of symptomatic cases.

Histology features a cluster of mucoid lobes surrounded by flattened mucussecreting glandular cells mucous retention polyp , no malignant potential.

Commonly seen in children age with a peak at age As a rule only one polyp is present, but occasionally there are two or three almost always confined to the rectal area within the reach of the finger. Most common complaint is bright painless rectal bleeding. Occasionally the polyp may prolapse through the rectum. Diagnosis is by barium enema, rectal exam, or endoscopy. Removal by endoscopy is the treatment of choice. Rarely colotomy and excision are required. Uncommon disorder in childhood.

Trauma compressed injury against spinal column and biliary tract disorders choledochal cyst, cholelithiasis are most common cause of pancreatitis. The most common congenital ductal anomaly leading to pancreatitis is pancreas divisum. Most common complaint is mid-epigastric abdominal trauma associated with nausea and vomiting.

Diagnosis is confirmed with elevated levels of amylase and lipase. Ultrasound is useful to determine degree of edema and presence of pseudocyst formation. Treatment consists of: NPO, NG decompression, decrease acid stimulation H-2 blockers , aprotinin, glucagon, and anticholinergics. Pain is relieved with meperidine. When pancreatic serum enzymes level return to near normal level patient is started in low-fat diet.

Antibiotic prophylaxis use is controversial. Surgery is indicated for: Pseudocysts are the result of major ductal disruptions or minor lacerations. Percutaneous aspiration and catheter drainage is another alternative in management.

Follow-up studies permit determine if cavity is decreasing in size. This can be done outpatient teaching parents to irrigate the catheter at home to assure patency.

Persistency beyond 6 months may need resectional therapy. Additional option is internal drainage cyst-gastrostomy, cyst-jejunostomy. Abscess should be drained and debride. Pancreatic pseudocyst formation is an uncommon complication of pancreatic inflammatory disease pancreatitis or trauma in children. More than half cases are caused by blunt abdominal trauma.

Ultrasound is the most effective and non-invasive way of diagnosing pancreatic pseudocysts. Acute pseudocysts are managed expectantly for wk.

Medical therapy consists of decreasing pancreatic stimulation and giving nutritional support. Rupture is the major complication of conservative management. Percutaneous catheter drainage under local anesthesia using Ultrasound or CT guided technique is an appropriate method of first-line therapy for non-resolving chronic or enlarging pancreatic pseudocysts.

The approach is transgastric or transcutaneous. Those cysts that fail to resolve with percutaneous drainage should go investigation of ductal anatomy to rule out disruption of the main pancreatic duct.

The need for further surgery drainage or resectional will depend on the status of the duct of Wirsung. Cholestasis means a reduction in bile flow in the liver, which depends on the biliary excretion of the conjugated portion.

Reduce flow causes retention of biliary lipoproteins that stimulates hypercholesterolemia causing progressive damage to the hepatic cell, fibrosis, cirrhosis and altered liver function tests. Biliary Atresia BA is the most common cause of persistently direct conjugated hyperbilirubinemia in the first three months of life. It is characterized by progressive inflammatory obliteration of the extrahepatic bile ducts, an estimated incidence of one in 15, live births, and predominance of female patients.

The disease is the result of an acquired inflammatory process with gradual degeneration of the epithelium of the extrahepatic biliary ducts causing luminal obliteration, cholestasis, and biliary cirrhosis. The timing of the insult after birth suggests a viral etiology obtained transplacentally. Histopathology is distinguished by an inflammatory process in several dynamic stages with progressive destruction, scar formation, and chronic granulation tissue of bile ducts.

Physiologic jaundice of the newborn is a common, benign, and self-limiting condition. In BA the patient develops insidious jaundice by the second week of life. The baby looks active, not acutely ill and progressively develops acholic stools, choluria and hepatomegaly. Non-surgical source of cholestasis shows a sick, low weight infant who is jaundiced since birth. The diagnostic evaluation of the cholestatic infant should include a series of lab tests that can exclude perinatal infectious TORCH titers, hepatitis profile , metabolic alphaantitrypsin levels , systemic and hereditary causes.

Liver function tests are nonspecific. The presence of the yellow bilirubin pigment in the aspirate of duodenal content excludes the diagnosis of BA.

Ultrasound study of the abdomen should be the first diagnostic imaging study done to cholestatic infants to evaluate the presence of a gallbladder, identify intra or extrahepatic bile ducts dilatation, and liver parenchyma echogenicity.

The postprandial contraction of the gallbladder eliminates the possibility of BA even when nuclear studies are positive. Nuclear studies of bilio-enteric excretion DISIDA after pre-stimulation of the microsomal hepatic system with phenobarbital for days is the diagnostic imaging test of choice. The presence of the radio-isotope in the GI tract excludes the diagnosis of BA.

Percutaneous liver biopsy should be the next diagnostic step. The mini-laparotomy is the final diagnostic alternative. Those infant with radiographic evidence of patent extrahepatic biliary tract has no BA. Medical management of BA is uniformly fatal. Kasai portoenterostomy has decreased the mortality of BA during the last 30 years. Kasai procedure consists of removing the obliterated extrahepatic biliary system, and anastomosing the most proximal part to a bowel segment.

Almost three-fourth of patients will develop portal hypertension in spite of adequate postoperative bile flow. They will manifest esophageal varices, hypersplenism, and ascites. Hepatic transplantation is reserved for those patients with failed portoenterostomy, progressive liver failure or late-referral to surgery. The etiology is related to an abnormal pancreatic-biliary junction common channel theory causing reflux of pancreatic enzymes into the common bile duct trypsin and amylase.

Symptoms are: Infants develop jaundice more frequently, causing diagnostic problems with Biliary Atresia. Older children may show abdominal pain and mass. By George W.

Pediatric Surgery HANDBOOK

Richardson Endowed Chair in Pediatric Surgery,[ By Chandrasen K. By Frank Hinman, Jr. By Mohan S. Pediatric Plastic and Reconstructive Surgery. Handbook of Pediatric Neurosurgery.

Pediatric Spinal Deformities. Atlas of Pediatric Cardiac Surgery Pediatric Digestive Surgery The Surgery of Childhood Tumors, 3rd Edition. Pediatric Orthopedic Deformities Volume 1: Paediatric Orthopaedics in Clinical Practice Paediatric Orthopaedics Operative General Surgery in Neonates and Infants Practice of Paediatric Orthopaedics, 3rd Edition. Pediatric Spots. Master Techniques in Orthopaedic Surgery: Pediatrics, 2nd Edition.

Paediatric Orthopaedic Diagnosis. Key Clinical Topics in Paediatric Surgery.Since risk of incarceration is high in children, repair should be undertaken shortly after diagnosis. Oxford Textbooks in Public Health. Undescended Testis. High lesions are more frequent in males, low ones in females. The three most common abdominal wall defect in newborns are umbilical hernia, gastroschisis and omphalocele. Recently the use of gas enema reduction has been successful in patients with: 1 symptoms less than 12 hours, 2 no rectal bleeding, 3 absence of small bowel obstruction, and 4 normally hydrated.

At about the time of birth, the portion of the processus vaginalis between the testicle and the abdominal cavity obliterates, leaving a peritoneal cavity separate from the tunica vaginalis that surrounds the testicle. Symptoms vary according to the size and location of the duplication. Chronic Intestinal Pseudo-obstruction L. Ultrasound confirms the cystic nature of the lesion muscular rim sign and CT the relationship to surrounding structures.

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