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Common surgical problems in children

This document summarizes several common surgical problems in children. It discusses conditions like cleft lip and palate, gastroesophageal reflux disease, infantile hypertrophic pyloric stenosis, and Hirschsprung disease. For each condition, it provides information on incidence, clinical features, investigations, and management. The goal is to provide pediatricians with sound knowledge of these common pediatric surgical issues.

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Common surgical problems in children Presented by Dr. Md. Ashik Kamal Alvee (MD resident, Phase A) Dr. Md. Mohsin Tareq (MD resident, Phase A)
Introduction Pediatric medicine and pediatric surgery are two distinct entity. But some surgical problems present in such a manner and with such complications that sometimes they need medical management at first. Sometimes these surgical conditions can also mimic various medical conditions. That is why sound knowledge about various common surgical problems of childhood is needed for every pediatrician.
Topic of discussion Today our topic of discussion is some of the most common surgical problems and their: • Incidence • Pathophysiology • Clinical features/ presentations • Complications • Investigations • Management
Common Surgical Problems in children • Cleft lip and Cleft palate • Gastroesophageal Reflux Disease • Hirschsprung disease • Oesophageal atresia with Tracheoesophageal fistula • Congenital diaphragmatic hernia • Infantile hypertrophic pyloric stenosis • Duodenal atresia. • Intussusception • Ureteropelvic junction obstruction • Posterior urethral valve • Hernia and Hydrocele • Hypospadias • Cryptorchidism • Phimosis and Paraphimosis
Cleft lip and cleft palate Incidence Highest amongst Asians (1 in 500) and Native Americans (1 in 300) Lowest among the black (1 in 2,500). Male: Female = 3:1 Cleft lip- Results from failure of fusion of medial nasal Process and maxillary process. Cleft palate- Result of failure of fusion of palatine Processes of two maxilla. Fig: development of face
Cleft lip may be- • Incomplete(small gap in the lip) or Complete(continues into the nose). • Unilateral or Bilateral. Cleft palate may be- • complete (soft and hard palate) or Incomplete(usually soft palate)
Problems associated with cleft lip and cleft palate • Difficulty in feeding.(Nasal regurgitation, inability to suck) • Recurrent respiratory tract infection. • Recurrent otitis media with subsequent hearing loss. • Speech difficulty. (Misarticulation and nasal intonation)
Management • Supportive Feeding : Help baby to ‘Latch on’ at the beginning of feed. Feeding with long handled spoon in upright position. Palatal shield to prevent nasal regurgitation. Treatment of infections with antibiotics • Specific Surgical correction. A conventional Rule of 10 is applied for surgery. Weight Age Hemoglobin Cleft lip 10 pounds(4.5 kg) 10 weeks 10 gm/dl Cleft palate 10 kg 10 months 10 gm/dl
Esophageal Atresia and Tracheoesophageal Fistula Esophageal atresia is the most common congenital anomaly of the esophagus, with a prevalence of 1.7 per 10,000 live births. Of these, >90% have an associated tracheoesophageal fistula (TEF).
Presentations • History of maternal polyhydramnios • Excessive frothing and bubbling at the mouth and nose after birth • Chocking on attempted feeding • Recurrent respiratory tract infection as a result of aspiration of saliva and gastric contents. • Failure to pass a NG tube to stomach.
Investigations • X ray of chest and abdomen presence of coiled NG tube in the upper pouch. in case of fistulae, gas shadow found in stomach and abdomen in case of no fistulae no gas shadow is seen in stomach or abdomen. • Barium swallow X-ray Isolated Tracheoesophageal fistulae (H type) can be demonstrated.
X ray of chest and abdomen showing coiled NG tube in esophagus and no gas shadow in gut X ray of chest and abdomen showing coiled NG tube in esophagus and gas shadow in gut
Barium swallow X-ray showing H-type fistula (arrow). Barium is seen to outline the tracheobronchial tree.
Management Supportive • Counselling • Prone positioning minimizes movement of gastric secretions into a distal fistula. • Placing a NG tube to do esophageal suctioning for minimizing aspiration. • Head to be kept elevated to minimize aspiration. • Antibiotics in suspected aspiration or RTI. Specific Surgery is definitive management.
Congenital diaphragmatic hernia It is as a communication between the abdominal and thoracic cavities due to congenital defect in diaphragm with herniation of abdominal contents in the thoracic cavity. Epidemiology • Incidence : between 1/2,000 and 1/5,000 live births • Female : Male = 2:1. • More common on the left (85%) and are occasionally (<5%) bilateral.
Types • Posterolateral (Bochdalek)- 90% • Esophageal hiatus (hiatal) • Paraoesophageal (adjacent to the hiatus) • Retrosternal (Morgagni) Depending on the position in diaphragm. It can be at-
Clinical features Symptoms Severe respiratory distress and cyanosis since birth Signs • Tachypnoea, tachycardia, cyanosis. • Respiratory system- Chest indrawing, bulged chest. Trachea and apex beat may be shifted. Diminished breath sound Bowel sound heard in chest. • Alimentary system- Scaphoid shaped abdomen.
Investigations • Chest X-ray Coils of intestine in chest with mediastinal shifting to opposite side. After inserting NG tube It may be visible in chest • Arterial blood gas analysis May show Respiratory and/or Metabolic acidosis. • Prenatal ultrasonography (between 16 and 24 weeks of gestation) Polyhydramnios, chest mass, mediastinal shift, gastric bubble or liver in the thoracic cavity.
Fig: plain Xray of chest showing coils of intestine in chest, shifting of mediastinum, left dome absent Fig: This chest radiograph shows a stomach, nasogastric tube, and coils of intestine in the thoracic cavity.(arrow
Management Supportive • Counselling • Nothing per oral • Keep the child warm • Rapid endotracheal intubation. • Giving oxygen in nasal cannula and avoid face mask. • Avoiding bag mask ventilation. • For ventilation-Conventional mechanical ventilation, ECMO Specific Surgical repair (at least 48 hours after stabilization)
Gastroesophageal Reflux Disease Gastroesophageal reflux (GER) is the retrograde movement of gastric contents across the lower esophageal sphincter (LES) into the esophagus, which occurs physiologically every day. The phenomenon becomes pathologic in infants and children who manifest various symptoms because of frequent Gastroesophageal Reflux.
Reflux is prevented by lower esophageal sphincter(LES) The LES is supported by • Right crus of the diaphragm • Angle of his. There is balance between intra-esophageal pressure and intra-abdominal pressure Normal anti-reflux mechanism
Diaphragm Causes of GERD • Esophagus Insufficient LES tone Abnormal LES relaxations • Hiatal hernia • Delayed gastric emptying Pyloric stenosis • Increased intra-abdominal pressure Obesity Ascites Intra-abdominal mass
Clinical features • Recurrent regurgitation • Weight loss or poor weight gain • Irritability in infants • Heartburn or chest pain • Hematemesis • Dysphagia, odynophagia • Stridor • Cough • Hoarseness • Recurrent pneumonia • Anemia • Dental erosion • Feeding refusal • Dystonic neck posturing (Sandifer syndrome) • Apnea spells
Investigations Investigations Findings Contrast X-ray of the esophagus and stomach • Esophageal strictures and stenosis • Hiatal hernia • Gastric outlet obstruction. pH monitoring of the distal esophagus pH<4 signifies distal esophageal acid exposure. Endoscopy with biopsy • Erosive esophagitis • Esophageal strictures • Grades of inflammation Esophageal manometry To detect LES closing pressure
Fig:Oesophageal reflux. Frontal (left) and oblique (right) X-rays of the chest and upper abdomen of a patient.The arrow at left points to the cardia, the region where the contents of the oesophagus empties into the stomach (across bottom). The X-ray shows reflux of contrast media from stomach to oesophagus.
Management Lifestyle modification • Food Infant- Thick frequent small feeds Children- Avoid reflux-inducing foods and beverages (tomatoes, chocolate, juices, carbonated and caffeinated drinks) • Proper positioning Infant-Seating position to be avoided. Prone position and Upright carried position recommended. Children-Lateral position and Head elevation during sleep.
• Drugs- Antacid H2 receptor antagonists Proton pump inhibitors • Endoscopic therapy Application of radiofrequency therapy to LES and cardia. • Surgery Fundoplication. During fundoplication, fundus is wrapped around the back of esophagus wrap is secured with suture to anchor lower esophagus below diaphragm
Infantile Hypertrophic Pyloric Stenosis Incidence • 1-3 per 1,000 infants Risk factors • Infants with B and O blood groups. • Male child (4-6 times more) • Use of erythromycin in the 1st 2 weeks of life. • Associated with- Tracheoesophageal fistula, Trisomy 18, Smith-Lemli-Opitz syndrome,Eosinophilic gastroenteritis.
Clinical features Symptoms • Nonbilious vomiting ,usually projectile, usually follows each feeding. • After vomiting, the baby is hungry and wants to feed again. Signs • May be dehydrated. • After feeding, there may be a visible gastric peristaltic wave. • On palpation, the enlarged pylorus , described as an ‘Olive mass’ is palpated specially after vomiting.
Investigations Findings Ultrasonography of abdomen • Pyloric muscle thickness 3-4 mm, • Pyloric channel length 15-19 mm, • Diameter of pylorus 10-14 mm. Barium meal X ray • Hugely dilated stomach • Contrast does not pass beyond pylorus • String sign, shoulder sign, double tract sign. S. Electrolyte Hypochloremic alkalosis, Hypokalemia, Hyponatremia S. Bilirubin Unconjugated hyperbilirubinemia. Investigations
Fig: barium meal X ray showing dilated stomach and elongated pyloric channel (string sign) Fig: barium meal X ray showing dilated stomach and elongated pyloric channel (string sign), bulge of the pyloric muscle into the antrum (shoulder sign)
Management Supportive • Counselling. • Correction of dehydration. • Correction of electrolyte imbalance. • Nasoduodenal feedings for patients who are not eligible for surgery. • Oral and I/V atropine sulfate (pyloric muscle relaxant). Specific Ramstedt pyloromyotomy.
Hirschsprung disease Otherwise known as Congenital Aganglionic Megacolon. It is a developmental disorder of the enteric nervous system, characterized by the absence of ganglion cells in the submucosal and myenteric plexus. • Incidence : 1 in 5,000 live births. • The male : female = 4 : 1 for short segment disease 2 : 1 for total colon involvement . • Uncommon in Prematurity.
Pathology Arrest of neuroblast migration in the gut from the proximal to distal bowel Absence of ganglion cells in the bowel wall, extending proximally from the anus for a variable distance. Inadequate relaxation of the bowel wall and bowel wall hypertonicity Failure to pass bolus leads to dilation of the bowel and abdominal distention, bowel obstruction. Intraluminal pressure increases, resulting in decreases blood flow (Stasis). Stasis allows proliferation of bacteria, which can lead to enterocolitis with associated diarrhea,sepsis.
Types • Ultra short segment: Aganglionosis limited to the internal sphincter • Short segment: Aganglionosis involving rectum and sigmoid colon. • Long segment: Aganglionosis extends proximal to sigmoid colon • Total segment: Aganglionosis affects entire large gut and portion of terminal ileum. Short segment Long segment Total segmentUltra-Short segment
Neonate Older children • Failure to pass meconium within 48 hours of life. • Distended abdomen. • Bilious vomiting. • Features of Enterocolitis , bowel obstruction, sepsis. • Failure to thrive (less common). • History of constipation since infancy, refractory to usual treatment. • Intermittent attacks of intestinal obstruction. • Distended abdomen with a palpable mass. • Rectal examination shows gripping of examining finger. (anal grip) • The rectum is usually empty of feces and when the finger is removed, there may be an explosive discharge of feces and gas. Clinical features
Investigations Plain X-ray of abdomen • Dilated proximal colon with absence of gas shadow in pelvic colon. Barium enema • Shows a transition zone in between dilated proximal colon and small caliber distal colon. • Rectal diameter is the same as or smaller than the sigmoid colon suggests Hirschsprung disease. Anorectal manometry Rectal biopsy • Absence of ganglionic cells in submucosal and myenteric plexus. • Hypertrophied nerve trunks.
Plain Xray abdomen: Dilated proximal colon with absence of gas shadow in pelvic colon Barium enema showing dilated proximal part (A), distal constricted part (B), and transition zone in between them(C).
Management Supportive • Counselling If there is feature of obstruction • Keep the child NPO • Intravenous fluid and antibiotics • NG decompression • Rectal irrigation Specific Surgery is the definitive treatment.
Congenital duodenal atresia • Incidence : 2.5-10 per 100,000 live Births • 50% of infants are premature. Associated abnormalities Congenital anomalies • Congenital heart disease (30%), • Annular pancreas (30%), • Renal anomalies (5-15%), • Esophageal atresia (5-10%), • Skeletal malformations (5%), Trisomy 21 (one-third of patients.)
Clinical features Symptoms Recurrent Bilious vomiting.(within hours of birth) Signs • Dehydration • Abdomen may be distended. • Peristaltic waves may be seen early in the disease process.
Investigations • Plain X ray abdomen : “double-bubble” sign. • Contrast X ray abdomen: no dye passes beyond duodenum. • S. electrolyte: Hypochloremic alkalosis, Hypokalemia, hyponatremia. • Echocardiography, renal ultrasound, and Chest Xray : Evaluation of associated anomalies. • Fetal ultrasonography: Double-bubble shadow, polyhydramnios.
Plain Xray of abdomen: showing double bubble shadow Stomach Duodenum
Management Supportive • Counselling • Patient kept NPO and I/V fluid is given. • Nasogastric/ Orogastric decompression. • Correction of dehydration. • Correction electrolyte imbalance. Specific Surgery. (Duodenoduodenostomy is done)
Anorectal malformation Incidence 1 per 3,000 live births. • Most patients presents with imperforate anus. • Others present with fistulous connection between anus and urethrae, vestibule, anal stenosis etc. • Here we discuss about imperforate anus.
Types • High lesion The rectum has not descended through the sphincter complex. • Low lesion The rectum has descended through the sphincter complex. • A persistent cloaca rectum, vagina and urinary tract are joined into a single channel.
Clinical features • Failure to pass meconium 24 hours after birth. • Examination of perineum High lesion • Perineum appears flat. • There may be air or meconium passed via the penis (urethra) Low lesion • Perineal fistula may be present. Male- along Median raphe across the scrotum/penile shaft. Female- may be in the vestibule • Covered anus- A thickened raphe or “bucket handle” covers anus.
Perineal fistula along median raphe across the scrotum Fig : “bucket handle” bridge over covered anus
Associated malformations GENITOURINARY • Vesicoureteric reflux • Renal agenesis • Cryptorchidism • Hypospadias VERTEBRAL • Spinal dysraphism • Presacral masses • Meningocele • Lipoma • Dermoid CARDIOVASCULAR • Tetralogy of Fallot • Ventricular septal defect • Transposition of the great vessels GASTROINTESTINAL • Tracheoesophageal fistula • Duodenal atresia • Malrotation • Hirschsprung disease CENTRAL NERVOUS SYSTEM • Spina bifida • Tethered cord
Investigations • Prone cross-table lateral plain x-ray Demonstrate rectal gas shadow below the level of coccyx. • Invertogram (the baby is turned upside down) A coin/metal piece is placed over the expected anus. The distance of the gas bubble in the rectum from the metal piece is noted: >2 cm denotes high type <2 cm denotes low type • Ultrasonography of abdomen • Voiding cystourethrogram
Fig : Prone cross-table lateral plain x-rayFig: Invertogram
Management Operative repair • If perineal fistula opens in good position, can be treated by simple dilation. (Hegar dilators) • In case of a low lesion - Perineal anoplasty. • In case of high lesion - Colostomy is performed to relieve bowel obstruction at first. Then definitive repair or posterior sagittal anorectoplasty (PSARP) is performed at about 1 year of age. Usually, the colostomy can be closed 6 weeks or more after the PSARP.
Introduction • Intussusception occurs when a portion of the alimentary tract is telescoped into an adjacent segment. • Most common cause of intestinal obstruction between 5 months to 3 years of age. • The male : female ratio is 3:1. • Incidence : 1-4/1000 live births. • Commonest area: ileocolic region.
Etiology • Idiopathic (90%) • Adenovirus or other upper respiratory tract infection. • Henoch-Schonlein Purpura and Gastroenteritis. Recognizable Lead points :- • Meckel diverticulum • Intestinal polyp • Neurofibroma • Lymphoma
Pathology
Clinical features • Sudden, severe and intermittent colicky abdominal pain with screaming and drawing up of the knees. • The child appears calm and relieved in between attack. • Vomiting and Diarrhoea. • Stool Looks like Red current Jelly. • Features Of Shock. • Advancing intestine prolapses through anus.
Abdomen Inspection : Distended Palpation : A tender sausage shaped mass is felt in upper mid abdomen. Auscultation : bowel sound may be absent. Digital Rectal Examination : Bloody mucus in fingers.
Investigations • Plain X ray abdomen May show intussusception, bowel obstruction, intestinal perforation. • Contrast X ray of abdomen Filling defect, coiled spring sign. • Ultrasonography of whole abdomen Longitudinal view shows a Reniform mass. Transverse view shows a Target appearance/Doughnut appearance.
Plain X-ray abdomen Small bowel dilatation Sausage shape density
FIG: plain X-ray abdomen showing sausage shaped density in the film reflecting intussusception FIG: contrast X-ray of abdomen showing coiled spring appearance. Contrast x-ray abdomen shows coiled spring sign and filling defect
USG of whole abdomen Transverse view shows a Target /Doughnut appearance Longitudinal view shows a Reniform mass
Treatment Medical Treatment • Counselling. • Nothing per oral. • Maintenance IV fluid e.g. 10% DA/Baby saline. • NG tube and decompress stomach. • Broad spectrum antibiotic. • Potassium correction if necessary. Surgical Treatment • Non operative Reduction with barium or Saline or Air(pneumatic reduction). • Laparotomy with Open Reduction • Resection of the intussusception with end to end anastomosis.
Ureteropelvic junction obstruction
Introduction • UPJ obstruction is the most common obstructive lesion in childhood. • It is the functional obstruction of junction between the renal pelvis and ureter. • Incidence is 1 in 2000 children with male female ratio is 2:1. • Bilateral in only 10% cases and 60% cases occurs on the left side.
Etiology • Congenital stenosis • Ureteral polyps • Ureteral folds • Crossing vessel causes Ureteral compression. • External compression.
Pathology Obstruction in the ureteropelvic junction Results in dilatation of pelvis and calyces due to collection of excessive urine Pressure upon the renal parenchyma Renal function begins to affected and parenchyma become thinner. Pyonephrosis
Clinical Features • A palpable renal mass. • Abdominal, flank or back pain(dull constant pain or severe spasmodic pain) • Febrile UTI. • Hematuria. • Dietl’s crisis. • Non-specific features such as anorexia, nausea, vomiting, failure to thrive, weakness, lethargy.
Investigations Investigations Characteristics Ultra sonogram of KUB Confirm the diagnosis and grade the hydronephrosis Intravenous urogram Shows dilatation of calyces and the pelvis and non visualization of the ureter on the affected side. Micturating cystourethrogram To see any ipsilateral vesicouretric reflux Antenatal Ultrasonography Fetal hydronephrosis may found CBC Urine R/E and C/S Renal function test
Intravenous urogram
USG of KUB
Table : Society of fetal urology grading for hydronephrosis. Grade Renal Pelvis Parenchymal thickness 0 Intact : no splitting Normal 1 Mild splitting Normal 2 Moderate splitting ( confined to renal border) Normal 3 Marked splitting (outside renal border, calyceal dilatation) Normal 4 Pelvicalyceal dilatation Thin
Treatment • Grade 1 or 2 hydronephrosis : observation • Grade 3 or 4 hydronephrosis : Pyeloplasty • Prophylaxis of UTI • Treatment of AKI • Treatment of CKD
Introduction • Posterior urethral valve is the most common obstructive uropathy. • These are tissue leaflets fanning distally from the posterior urethra to the external urinary sphincter. • It affects 1 in 8000 boys.
Pathogenesis Persistence of posterior urethral valves Narrowing of the bladder outlet with consequent obstruction of urine flow Increased pressure in proximal organs. Dilatation and enlargement. Vesico-uretric reflux, hydroureter, hydronephrosis and renal insufficiency.
Neonate Older Infants and children • Palpable distended bladder With or without palpable kidneys. • Weak urinary stream. • Sepsis • Straining during micturition • Poor urinary stream, dribbling of urine • Palpable bladder • Failure to thrive • UTI and Renal failure Clinical Features
Investigations Investigations Findings USG of Genito-urinary system • Bladder is thick-walled with an elongated and dilated posterior urethra • hydonephrosis • kidneys may be hyperechoic with loss of normal cortico-medullary differentiation MCUG- Diagnostic • Dilatation and elongation of posterior urethra. • Distal urethral stream is narrow • Bladder may show irregular border. Antenatal USG- • Bilateral hydronephrosis • Distended bladder • Oligohydramnios • Keyhole sign. Assessment of renal function
MCUG
Antenatal USG Postnatal USG Keyhole sign Hydronephrosi s
Treatment • Bladder drainage by insertion of feeding tube. • Correction of fluid, electrolyte imbalance, acid base irregularities and control of infection. • Vesicostomy • Percutaneous nephrostomy and haemodialysis. • Surgery - Transurethral ablation of valves
Hernia and hydrocele Introduction • Hernia and Hydrocele both results from patent processus vaginalis, a tongue like extension of the peritoneum. • Usually the processus closes down and there is no connection between abdomen and inguinoscrotal region. • If the processus remains patent and opening is large, abdominal viscera like intestines herniate into the scrotum.
• If the opening is small, only peritoneal fluid can enter, forming a hydrocele.
Epidemiology • The incidence of congenital indirect inguinal hernia in full-term newborn infants is estimated at 3.5-5.0%. • The incidence of hernia in preterm and low birth weight infants is considerably higher. • Male : female ratio inguinal hernia is approximately 8 : 1. • Approximately 60% of inguinal hernias occur on the right side, 30% are on the left side, and 10% are bilateral. • 1-2% neonate have a hydrocele.
Predisposing Factors Hernia Hydrocele • Prematurity • Cryptorchidism • Hypospadias/ epispadius • Raised intraabdominal pressure • Cystic fibrosis • Connective tissue disorders • Persistent patent processus • Testicular torsion • Epididymitis • Testicular Tumor • Trauma
Clinical Presentations Points Hernia Hydrocele Increase of size of swelling On crying or after activity. In the evening or after an active day. Decrease of size of swelling Can be reduce spontaneously and on gentle pressure. On waking up in the morning. Features of intestinal obstruction may present such as abdominal pain, distension. Absent Mobility Less mobile Mobile Character Hernia are smooth, firm and may be tender. smooth and non tender Reducibility Reducible Irreducible Get above the swelling Can not be done. Can be done. Trans illumination test negative Positive
Types of Hydrocele
Types of Inguinal Hernia 1. Indirect hernias (99%) 2. Direct hernia (0.5-1.0%) 3. Femoral hernia (<0.5%). Complications of hernia 1. Intestinal obstruction 2. Strangulation.
Investigation USG of the scrotum • Can help in distinguish between hernia and hydrocele. Plain X-Ray abdomen • Distended intestine with multiple air fluid level.
Treatment Hernia • Surgery as soon as diagnosed • Surgery Herniotomy with Herniorraphy. Hydrocele • Most congenital hydrocele resolves by 12 months of age. • If not resolved within 12-18 months then Surgical correction needed.
UNDESCENDED TESTIS (CRYPTORCHIDISM)
Introduction • Cryptorchidism means “Hidden Testis”. • It may be single or bilateral (10%). • When a boy is seen with single or no testicle in scrotum indicates the testis is undescended, absent or retractile. Aetiology • Unknown but may be related to genetic, hormonal or mechanical factor. • Prematurity.
Epidemiology • Most common disorder of sexual differentiation in boys. • At birth, approximately 4.5% boys have an undescended testis among them 30% are preterm and 3.4% are at term. • Majority of congenital undescended testis descend spontaneously during the 1st 3 months of life. • If the testis has not descended by 4 months, it will remain undescended.
Site of undescended and ectopic testis
Classification 1. Abdominal - Non-palpable 2. Peeping - Abdominal but can be pushed into the upper part of the inguinal canal. 3. Inguinal. 4. Gliding - Can be pushed into the scrotum but retracts immediately to the pubic tubercle. 5. Ectopic – Superficial inguinal pouch or rarely perineal.
Complications 1. Infertility 2. Testicular Malignancy 3. Poor testicular growth 4. Associated Hernia 5. Torsion of cryptorchid testis 6. Psychological effects. Investigations 1. Ultra sonogram of abdomen 2. MRI or CT scan of abdomen 3. Laparoscopy – Diagnostic.
Treatment Medical Hormonal therapy with hCG or LH-releasing hormones. Surgical • Should be treated surgically by 9-15 months of age. • Orchiopexy (success rate 98%). • Orchiectomy and implantation of testicular prosthesis
Hypospedias Introduction • Hypospadias is a urethral opening on the ventral surface of the penile shaft. • It affects 1 in 250 male newborn. • Cause is unknown. • Sometimes hypospadias is associated with Dorsal hood and chordae.
Clinical Presentations According to the position of the urethral meatus Hypospadias is classified as- 1. Glanular - on the glans penis. 2. Coronal 3. Subcoronal 4. Midpenile 5. Penoscrotal 6. Scrotal 7. Perineal 8. Megameatal
Treatment • Ideal age for repair in a healthy infant is 6-12 months. • Circumcision should be avoided. • The goal of any type of hypospadias surgery is to make a normal, straight penis with a urinary channel that ends at or near the tip. Surgery – • Tubularized incised plate repair. • Almost all cases are repaired in a single operation except Proximal cases.
Complications Untreated cases • Deformity of the urinary system. • Sexual dysfunction • Infertility • Meatal stenosis. After surgery • Urethro-cutaneous fistula. • Meatal stenosis.
Phimosis • Inability to retract the prepuce. • At birth, Phimosis is physiologic. • 80% of uncircumscribed boys the prepuce become retractable by 3 years of age. • In older child pathologic phimosis may occur due to inflammation and scarring at the tip of foreskin.
Treatment Medical • Application of topical corticosteroid cream to the foreskin 3 times daily for 1 month. Surgical • Circumcision • Minor operation to relieve foreskin tightness.
Paraphimosis It occurs when the foreskin is retracted proximal to the coronal sulcus and the prepuce can not be pulled back over the glans. Results in painful venous stasis and edema in the retracted foreskin leading to severe pain and inability to reduce the foreskin. Eventually gangrene and auto amputation of the distal penis Occurred.
Treatment • Lubricating the glans and foreskin and simultaneous Compressing the glans. • Topical application of granulated sugar • Injection of hyaluronidase into the edematous skin • Emergency circumcision.
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Common surgical problems in children

  • 1.
    Common surgical problems inchildren Presented by Dr. Md. Ashik Kamal Alvee (MD resident, Phase A) Dr. Md. Mohsin Tareq (MD resident, Phase A)
  • 2.
    Introduction Pediatric medicine andpediatric surgery are two distinct entity. But some surgical problems present in such a manner and with such complications that sometimes they need medical management at first. Sometimes these surgical conditions can also mimic various medical conditions. That is why sound knowledge about various common surgical problems of childhood is needed for every pediatrician.
  • 3.
    Topic of discussion Todayour topic of discussion is some of the most common surgical problems and their: • Incidence • Pathophysiology • Clinical features/ presentations • Complications • Investigations • Management
  • 4.
    Common Surgical Problemsin children • Cleft lip and Cleft palate • Gastroesophageal Reflux Disease • Hirschsprung disease • Oesophageal atresia with Tracheoesophageal fistula • Congenital diaphragmatic hernia • Infantile hypertrophic pyloric stenosis • Duodenal atresia. • Intussusception • Ureteropelvic junction obstruction • Posterior urethral valve • Hernia and Hydrocele • Hypospadias • Cryptorchidism • Phimosis and Paraphimosis
  • 5.
    Cleft lip andcleft palate Incidence Highest amongst Asians (1 in 500) and Native Americans (1 in 300) Lowest among the black (1 in 2,500). Male: Female = 3:1 Cleft lip- Results from failure of fusion of medial nasal Process and maxillary process. Cleft palate- Result of failure of fusion of palatine Processes of two maxilla. Fig: development of face
  • 6.
    Cleft lip maybe- • Incomplete(small gap in the lip) or Complete(continues into the nose). • Unilateral or Bilateral. Cleft palate may be- • complete (soft and hard palate) or Incomplete(usually soft palate)
  • 7.
    Problems associated withcleft lip and cleft palate • Difficulty in feeding.(Nasal regurgitation, inability to suck) • Recurrent respiratory tract infection. • Recurrent otitis media with subsequent hearing loss. • Speech difficulty. (Misarticulation and nasal intonation)
  • 8.
    Management • Supportive Feeding :Help baby to ‘Latch on’ at the beginning of feed. Feeding with long handled spoon in upright position. Palatal shield to prevent nasal regurgitation. Treatment of infections with antibiotics • Specific Surgical correction. A conventional Rule of 10 is applied for surgery. Weight Age Hemoglobin Cleft lip 10 pounds(4.5 kg) 10 weeks 10 gm/dl Cleft palate 10 kg 10 months 10 gm/dl
  • 9.
    Esophageal Atresia andTracheoesophageal Fistula Esophageal atresia is the most common congenital anomaly of the esophagus, with a prevalence of 1.7 per 10,000 live births. Of these, >90% have an associated tracheoesophageal fistula (TEF).
  • 10.
    Presentations • History ofmaternal polyhydramnios • Excessive frothing and bubbling at the mouth and nose after birth • Chocking on attempted feeding • Recurrent respiratory tract infection as a result of aspiration of saliva and gastric contents. • Failure to pass a NG tube to stomach.
  • 11.
    Investigations • X rayof chest and abdomen presence of coiled NG tube in the upper pouch. in case of fistulae, gas shadow found in stomach and abdomen in case of no fistulae no gas shadow is seen in stomach or abdomen. • Barium swallow X-ray Isolated Tracheoesophageal fistulae (H type) can be demonstrated.
  • 12.
    X ray ofchest and abdomen showing coiled NG tube in esophagus and no gas shadow in gut X ray of chest and abdomen showing coiled NG tube in esophagus and gas shadow in gut
  • 13.
    Barium swallow X-rayshowing H-type fistula (arrow). Barium is seen to outline the tracheobronchial tree.
  • 14.
    Management Supportive • Counselling • Pronepositioning minimizes movement of gastric secretions into a distal fistula. • Placing a NG tube to do esophageal suctioning for minimizing aspiration. • Head to be kept elevated to minimize aspiration. • Antibiotics in suspected aspiration or RTI. Specific Surgery is definitive management.
  • 15.
    Congenital diaphragmatic hernia Itis as a communication between the abdominal and thoracic cavities due to congenital defect in diaphragm with herniation of abdominal contents in the thoracic cavity. Epidemiology • Incidence : between 1/2,000 and 1/5,000 live births • Female : Male = 2:1. • More common on the left (85%) and are occasionally (<5%) bilateral.
  • 16.
    Types • Posterolateral (Bochdalek)-90% • Esophageal hiatus (hiatal) • Paraoesophageal (adjacent to the hiatus) • Retrosternal (Morgagni) Depending on the position in diaphragm. It can be at-
  • 17.
    Clinical features Symptoms Severe respiratorydistress and cyanosis since birth Signs • Tachypnoea, tachycardia, cyanosis. • Respiratory system- Chest indrawing, bulged chest. Trachea and apex beat may be shifted. Diminished breath sound Bowel sound heard in chest. • Alimentary system- Scaphoid shaped abdomen.
  • 18.
    Investigations • Chest X-ray Coilsof intestine in chest with mediastinal shifting to opposite side. After inserting NG tube It may be visible in chest • Arterial blood gas analysis May show Respiratory and/or Metabolic acidosis. • Prenatal ultrasonography (between 16 and 24 weeks of gestation) Polyhydramnios, chest mass, mediastinal shift, gastric bubble or liver in the thoracic cavity.
  • 19.
    Fig: plain Xrayof chest showing coils of intestine in chest, shifting of mediastinum, left dome absent Fig: This chest radiograph shows a stomach, nasogastric tube, and coils of intestine in the thoracic cavity.(arrow
  • 20.
    Management Supportive • Counselling • Nothingper oral • Keep the child warm • Rapid endotracheal intubation. • Giving oxygen in nasal cannula and avoid face mask. • Avoiding bag mask ventilation. • For ventilation-Conventional mechanical ventilation, ECMO Specific Surgical repair (at least 48 hours after stabilization)
  • 21.
    Gastroesophageal Reflux Disease Gastroesophagealreflux (GER) is the retrograde movement of gastric contents across the lower esophageal sphincter (LES) into the esophagus, which occurs physiologically every day. The phenomenon becomes pathologic in infants and children who manifest various symptoms because of frequent Gastroesophageal Reflux.
  • 22.
    Reflux is preventedby lower esophageal sphincter(LES) The LES is supported by • Right crus of the diaphragm • Angle of his. There is balance between intra-esophageal pressure and intra-abdominal pressure Normal anti-reflux mechanism
  • 23.
    Diaphragm Causes of GERD •Esophagus Insufficient LES tone Abnormal LES relaxations • Hiatal hernia • Delayed gastric emptying Pyloric stenosis • Increased intra-abdominal pressure Obesity Ascites Intra-abdominal mass
  • 24.
    Clinical features • Recurrentregurgitation • Weight loss or poor weight gain • Irritability in infants • Heartburn or chest pain • Hematemesis • Dysphagia, odynophagia • Stridor • Cough • Hoarseness • Recurrent pneumonia • Anemia • Dental erosion • Feeding refusal • Dystonic neck posturing (Sandifer syndrome) • Apnea spells
  • 25.
    Investigations Investigations Findings Contrast X-rayof the esophagus and stomach • Esophageal strictures and stenosis • Hiatal hernia • Gastric outlet obstruction. pH monitoring of the distal esophagus pH<4 signifies distal esophageal acid exposure. Endoscopy with biopsy • Erosive esophagitis • Esophageal strictures • Grades of inflammation Esophageal manometry To detect LES closing pressure
  • 26.
    Fig:Oesophageal reflux. Frontal (left)and oblique (right) X-rays of the chest and upper abdomen of a patient.The arrow at left points to the cardia, the region where the contents of the oesophagus empties into the stomach (across bottom). The X-ray shows reflux of contrast media from stomach to oesophagus.
  • 28.
    Management Lifestyle modification • Food Infant-Thick frequent small feeds Children- Avoid reflux-inducing foods and beverages (tomatoes, chocolate, juices, carbonated and caffeinated drinks) • Proper positioning Infant-Seating position to be avoided. Prone position and Upright carried position recommended. Children-Lateral position and Head elevation during sleep.
  • 29.
    • Drugs- Antacid H2receptor antagonists Proton pump inhibitors • Endoscopic therapy Application of radiofrequency therapy to LES and cardia. • Surgery Fundoplication. During fundoplication, fundus is wrapped around the back of esophagus wrap is secured with suture to anchor lower esophagus below diaphragm
  • 30.
    Infantile Hypertrophic PyloricStenosis Incidence • 1-3 per 1,000 infants Risk factors • Infants with B and O blood groups. • Male child (4-6 times more) • Use of erythromycin in the 1st 2 weeks of life. • Associated with- Tracheoesophageal fistula, Trisomy 18, Smith-Lemli-Opitz syndrome,Eosinophilic gastroenteritis.
  • 31.
    Clinical features Symptoms • Nonbiliousvomiting ,usually projectile, usually follows each feeding. • After vomiting, the baby is hungry and wants to feed again. Signs • May be dehydrated. • After feeding, there may be a visible gastric peristaltic wave. • On palpation, the enlarged pylorus , described as an ‘Olive mass’ is palpated specially after vomiting.
  • 33.
    Investigations Findings Ultrasonography of abdomen •Pyloric muscle thickness 3-4 mm, • Pyloric channel length 15-19 mm, • Diameter of pylorus 10-14 mm. Barium meal X ray • Hugely dilated stomach • Contrast does not pass beyond pylorus • String sign, shoulder sign, double tract sign. S. Electrolyte Hypochloremic alkalosis, Hypokalemia, Hyponatremia S. Bilirubin Unconjugated hyperbilirubinemia. Investigations
  • 34.
    Fig: barium mealX ray showing dilated stomach and elongated pyloric channel (string sign) Fig: barium meal X ray showing dilated stomach and elongated pyloric channel (string sign), bulge of the pyloric muscle into the antrum (shoulder sign)
  • 35.
    Management Supportive • Counselling. • Correctionof dehydration. • Correction of electrolyte imbalance. • Nasoduodenal feedings for patients who are not eligible for surgery. • Oral and I/V atropine sulfate (pyloric muscle relaxant). Specific Ramstedt pyloromyotomy.
  • 36.
    Hirschsprung disease Otherwise knownas Congenital Aganglionic Megacolon. It is a developmental disorder of the enteric nervous system, characterized by the absence of ganglion cells in the submucosal and myenteric plexus. • Incidence : 1 in 5,000 live births. • The male : female = 4 : 1 for short segment disease 2 : 1 for total colon involvement . • Uncommon in Prematurity.
  • 37.
    Pathology Arrest of neuroblastmigration in the gut from the proximal to distal bowel Absence of ganglion cells in the bowel wall, extending proximally from the anus for a variable distance. Inadequate relaxation of the bowel wall and bowel wall hypertonicity Failure to pass bolus leads to dilation of the bowel and abdominal distention, bowel obstruction. Intraluminal pressure increases, resulting in decreases blood flow (Stasis). Stasis allows proliferation of bacteria, which can lead to enterocolitis with associated diarrhea,sepsis.
  • 38.
    Types • Ultra shortsegment: Aganglionosis limited to the internal sphincter • Short segment: Aganglionosis involving rectum and sigmoid colon. • Long segment: Aganglionosis extends proximal to sigmoid colon • Total segment: Aganglionosis affects entire large gut and portion of terminal ileum. Short segment Long segment Total segmentUltra-Short segment
  • 39.
    Neonate Older children •Failure to pass meconium within 48 hours of life. • Distended abdomen. • Bilious vomiting. • Features of Enterocolitis , bowel obstruction, sepsis. • Failure to thrive (less common). • History of constipation since infancy, refractory to usual treatment. • Intermittent attacks of intestinal obstruction. • Distended abdomen with a palpable mass. • Rectal examination shows gripping of examining finger. (anal grip) • The rectum is usually empty of feces and when the finger is removed, there may be an explosive discharge of feces and gas. Clinical features
  • 40.
    Investigations Plain X-ray ofabdomen • Dilated proximal colon with absence of gas shadow in pelvic colon. Barium enema • Shows a transition zone in between dilated proximal colon and small caliber distal colon. • Rectal diameter is the same as or smaller than the sigmoid colon suggests Hirschsprung disease. Anorectal manometry Rectal biopsy • Absence of ganglionic cells in submucosal and myenteric plexus. • Hypertrophied nerve trunks.
  • 41.
    Plain Xray abdomen:Dilated proximal colon with absence of gas shadow in pelvic colon Barium enema showing dilated proximal part (A), distal constricted part (B), and transition zone in between them(C).
  • 42.
    Management Supportive • Counselling If thereis feature of obstruction • Keep the child NPO • Intravenous fluid and antibiotics • NG decompression • Rectal irrigation Specific Surgery is the definitive treatment.
  • 43.
    Congenital duodenal atresia •Incidence : 2.5-10 per 100,000 live Births • 50% of infants are premature. Associated abnormalities Congenital anomalies • Congenital heart disease (30%), • Annular pancreas (30%), • Renal anomalies (5-15%), • Esophageal atresia (5-10%), • Skeletal malformations (5%), Trisomy 21 (one-third of patients.)
  • 44.
    Clinical features Symptoms Recurrent Biliousvomiting.(within hours of birth) Signs • Dehydration • Abdomen may be distended. • Peristaltic waves may be seen early in the disease process.
  • 45.
    Investigations • Plain Xray abdomen : “double-bubble” sign. • Contrast X ray abdomen: no dye passes beyond duodenum. • S. electrolyte: Hypochloremic alkalosis, Hypokalemia, hyponatremia. • Echocardiography, renal ultrasound, and Chest Xray : Evaluation of associated anomalies. • Fetal ultrasonography: Double-bubble shadow, polyhydramnios.
  • 46.
    Plain Xray ofabdomen: showing double bubble shadow Stomach Duodenum
  • 47.
    Management Supportive • Counselling • Patientkept NPO and I/V fluid is given. • Nasogastric/ Orogastric decompression. • Correction of dehydration. • Correction electrolyte imbalance. Specific Surgery. (Duodenoduodenostomy is done)
  • 48.
    Anorectal malformation Incidence 1 per3,000 live births. • Most patients presents with imperforate anus. • Others present with fistulous connection between anus and urethrae, vestibule, anal stenosis etc. • Here we discuss about imperforate anus.
  • 49.
    Types • High lesion Therectum has not descended through the sphincter complex. • Low lesion The rectum has descended through the sphincter complex. • A persistent cloaca rectum, vagina and urinary tract are joined into a single channel.
  • 50.
    Clinical features • Failureto pass meconium 24 hours after birth. • Examination of perineum High lesion • Perineum appears flat. • There may be air or meconium passed via the penis (urethra) Low lesion • Perineal fistula may be present. Male- along Median raphe across the scrotum/penile shaft. Female- may be in the vestibule • Covered anus- A thickened raphe or “bucket handle” covers anus.
  • 51.
    Perineal fistula alongmedian raphe across the scrotum Fig : “bucket handle” bridge over covered anus
  • 52.
    Associated malformations GENITOURINARY • Vesicouretericreflux • Renal agenesis • Cryptorchidism • Hypospadias VERTEBRAL • Spinal dysraphism • Presacral masses • Meningocele • Lipoma • Dermoid CARDIOVASCULAR • Tetralogy of Fallot • Ventricular septal defect • Transposition of the great vessels GASTROINTESTINAL • Tracheoesophageal fistula • Duodenal atresia • Malrotation • Hirschsprung disease CENTRAL NERVOUS SYSTEM • Spina bifida • Tethered cord
  • 53.
    Investigations • Prone cross-tablelateral plain x-ray Demonstrate rectal gas shadow below the level of coccyx. • Invertogram (the baby is turned upside down) A coin/metal piece is placed over the expected anus. The distance of the gas bubble in the rectum from the metal piece is noted: >2 cm denotes high type <2 cm denotes low type • Ultrasonography of abdomen • Voiding cystourethrogram
  • 54.
    Fig : Pronecross-table lateral plain x-rayFig: Invertogram
  • 55.
    Management Operative repair • Ifperineal fistula opens in good position, can be treated by simple dilation. (Hegar dilators) • In case of a low lesion - Perineal anoplasty. • In case of high lesion - Colostomy is performed to relieve bowel obstruction at first. Then definitive repair or posterior sagittal anorectoplasty (PSARP) is performed at about 1 year of age. Usually, the colostomy can be closed 6 weeks or more after the PSARP.
  • 57.
    Introduction • Intussusception occurswhen a portion of the alimentary tract is telescoped into an adjacent segment. • Most common cause of intestinal obstruction between 5 months to 3 years of age. • The male : female ratio is 3:1. • Incidence : 1-4/1000 live births. • Commonest area: ileocolic region.
  • 58.
    Etiology • Idiopathic (90%) •Adenovirus or other upper respiratory tract infection. • Henoch-Schonlein Purpura and Gastroenteritis. Recognizable Lead points :- • Meckel diverticulum • Intestinal polyp • Neurofibroma • Lymphoma
  • 59.
  • 60.
    Clinical features • Sudden,severe and intermittent colicky abdominal pain with screaming and drawing up of the knees. • The child appears calm and relieved in between attack. • Vomiting and Diarrhoea. • Stool Looks like Red current Jelly. • Features Of Shock. • Advancing intestine prolapses through anus.
  • 61.
    Abdomen Inspection : Distended Palpation: A tender sausage shaped mass is felt in upper mid abdomen. Auscultation : bowel sound may be absent. Digital Rectal Examination : Bloody mucus in fingers.
  • 62.
    Investigations • Plain Xray abdomen May show intussusception, bowel obstruction, intestinal perforation. • Contrast X ray of abdomen Filling defect, coiled spring sign. • Ultrasonography of whole abdomen Longitudinal view shows a Reniform mass. Transverse view shows a Target appearance/Doughnut appearance.
  • 63.
    Plain X-ray abdomen Smallbowel dilatation Sausage shape density
  • 64.
    FIG: plain X-rayabdomen showing sausage shaped density in the film reflecting intussusception FIG: contrast X-ray of abdomen showing coiled spring appearance. Contrast x-ray abdomen shows coiled spring sign and filling defect
  • 65.
    USG of wholeabdomen Transverse view shows a Target /Doughnut appearance Longitudinal view shows a Reniform mass
  • 66.
    Treatment Medical Treatment • Counselling. •Nothing per oral. • Maintenance IV fluid e.g. 10% DA/Baby saline. • NG tube and decompress stomach. • Broad spectrum antibiotic. • Potassium correction if necessary. Surgical Treatment • Non operative Reduction with barium or Saline or Air(pneumatic reduction). • Laparotomy with Open Reduction • Resection of the intussusception with end to end anastomosis.
  • 67.
  • 68.
    Introduction • UPJ obstructionis the most common obstructive lesion in childhood. • It is the functional obstruction of junction between the renal pelvis and ureter. • Incidence is 1 in 2000 children with male female ratio is 2:1. • Bilateral in only 10% cases and 60% cases occurs on the left side.
  • 69.
    Etiology • Congenital stenosis •Ureteral polyps • Ureteral folds • Crossing vessel causes Ureteral compression. • External compression.
  • 70.
    Pathology Obstruction in theureteropelvic junction Results in dilatation of pelvis and calyces due to collection of excessive urine Pressure upon the renal parenchyma Renal function begins to affected and parenchyma become thinner. Pyonephrosis
  • 71.
    Clinical Features • Apalpable renal mass. • Abdominal, flank or back pain(dull constant pain or severe spasmodic pain) • Febrile UTI. • Hematuria. • Dietl’s crisis. • Non-specific features such as anorexia, nausea, vomiting, failure to thrive, weakness, lethargy.
  • 72.
    Investigations Investigations Characteristics Ultra sonogramof KUB Confirm the diagnosis and grade the hydronephrosis Intravenous urogram Shows dilatation of calyces and the pelvis and non visualization of the ureter on the affected side. Micturating cystourethrogram To see any ipsilateral vesicouretric reflux Antenatal Ultrasonography Fetal hydronephrosis may found CBC Urine R/E and C/S Renal function test
  • 73.
  • 74.
  • 75.
    Table : Societyof fetal urology grading for hydronephrosis. Grade Renal Pelvis Parenchymal thickness 0 Intact : no splitting Normal 1 Mild splitting Normal 2 Moderate splitting ( confined to renal border) Normal 3 Marked splitting (outside renal border, calyceal dilatation) Normal 4 Pelvicalyceal dilatation Thin
  • 76.
    Treatment • Grade 1or 2 hydronephrosis : observation • Grade 3 or 4 hydronephrosis : Pyeloplasty • Prophylaxis of UTI • Treatment of AKI • Treatment of CKD
  • 78.
    Introduction • Posterior urethralvalve is the most common obstructive uropathy. • These are tissue leaflets fanning distally from the posterior urethra to the external urinary sphincter. • It affects 1 in 8000 boys.
  • 79.
    Pathogenesis Persistence of posteriorurethral valves Narrowing of the bladder outlet with consequent obstruction of urine flow Increased pressure in proximal organs. Dilatation and enlargement. Vesico-uretric reflux, hydroureter, hydronephrosis and renal insufficiency.
  • 80.
    Neonate Older Infantsand children • Palpable distended bladder With or without palpable kidneys. • Weak urinary stream. • Sepsis • Straining during micturition • Poor urinary stream, dribbling of urine • Palpable bladder • Failure to thrive • UTI and Renal failure Clinical Features
  • 81.
    Investigations Investigations Findings USG ofGenito-urinary system • Bladder is thick-walled with an elongated and dilated posterior urethra • hydonephrosis • kidneys may be hyperechoic with loss of normal cortico-medullary differentiation MCUG- Diagnostic • Dilatation and elongation of posterior urethra. • Distal urethral stream is narrow • Bladder may show irregular border. Antenatal USG- • Bilateral hydronephrosis • Distended bladder • Oligohydramnios • Keyhole sign. Assessment of renal function
  • 82.
  • 83.
    Antenatal USG PostnatalUSG Keyhole sign Hydronephrosi s
  • 84.
    Treatment • Bladder drainageby insertion of feeding tube. • Correction of fluid, electrolyte imbalance, acid base irregularities and control of infection. • Vesicostomy • Percutaneous nephrostomy and haemodialysis. • Surgery - Transurethral ablation of valves
  • 85.
    Hernia and hydrocele Introduction •Hernia and Hydrocele both results from patent processus vaginalis, a tongue like extension of the peritoneum. • Usually the processus closes down and there is no connection between abdomen and inguinoscrotal region. • If the processus remains patent and opening is large, abdominal viscera like intestines herniate into the scrotum.
  • 86.
    • If theopening is small, only peritoneal fluid can enter, forming a hydrocele.
  • 87.
    Epidemiology • The incidenceof congenital indirect inguinal hernia in full-term newborn infants is estimated at 3.5-5.0%. • The incidence of hernia in preterm and low birth weight infants is considerably higher. • Male : female ratio inguinal hernia is approximately 8 : 1. • Approximately 60% of inguinal hernias occur on the right side, 30% are on the left side, and 10% are bilateral. • 1-2% neonate have a hydrocele.
  • 88.
    Predisposing Factors Hernia Hydrocele •Prematurity • Cryptorchidism • Hypospadias/ epispadius • Raised intraabdominal pressure • Cystic fibrosis • Connective tissue disorders • Persistent patent processus • Testicular torsion • Epididymitis • Testicular Tumor • Trauma
  • 89.
    Clinical Presentations Points HerniaHydrocele Increase of size of swelling On crying or after activity. In the evening or after an active day. Decrease of size of swelling Can be reduce spontaneously and on gentle pressure. On waking up in the morning. Features of intestinal obstruction may present such as abdominal pain, distension. Absent Mobility Less mobile Mobile Character Hernia are smooth, firm and may be tender. smooth and non tender Reducibility Reducible Irreducible Get above the swelling Can not be done. Can be done. Trans illumination test negative Positive
  • 90.
  • 91.
    Types of InguinalHernia 1. Indirect hernias (99%) 2. Direct hernia (0.5-1.0%) 3. Femoral hernia (<0.5%). Complications of hernia 1. Intestinal obstruction 2. Strangulation.
  • 92.
    Investigation USG of thescrotum • Can help in distinguish between hernia and hydrocele. Plain X-Ray abdomen • Distended intestine with multiple air fluid level.
  • 93.
    Treatment Hernia • Surgery assoon as diagnosed • Surgery Herniotomy with Herniorraphy. Hydrocele • Most congenital hydrocele resolves by 12 months of age. • If not resolved within 12-18 months then Surgical correction needed.
  • 94.
  • 95.
    Introduction • Cryptorchidism means“Hidden Testis”. • It may be single or bilateral (10%). • When a boy is seen with single or no testicle in scrotum indicates the testis is undescended, absent or retractile. Aetiology • Unknown but may be related to genetic, hormonal or mechanical factor. • Prematurity.
  • 96.
    Epidemiology • Most commondisorder of sexual differentiation in boys. • At birth, approximately 4.5% boys have an undescended testis among them 30% are preterm and 3.4% are at term. • Majority of congenital undescended testis descend spontaneously during the 1st 3 months of life. • If the testis has not descended by 4 months, it will remain undescended.
  • 97.
    Site of undescendedand ectopic testis
  • 98.
    Classification 1. Abdominal -Non-palpable 2. Peeping - Abdominal but can be pushed into the upper part of the inguinal canal. 3. Inguinal. 4. Gliding - Can be pushed into the scrotum but retracts immediately to the pubic tubercle. 5. Ectopic – Superficial inguinal pouch or rarely perineal.
  • 99.
    Complications 1. Infertility 2. TesticularMalignancy 3. Poor testicular growth 4. Associated Hernia 5. Torsion of cryptorchid testis 6. Psychological effects. Investigations 1. Ultra sonogram of abdomen 2. MRI or CT scan of abdomen 3. Laparoscopy – Diagnostic.
  • 100.
    Treatment Medical Hormonal therapy withhCG or LH-releasing hormones. Surgical • Should be treated surgically by 9-15 months of age. • Orchiopexy (success rate 98%). • Orchiectomy and implantation of testicular prosthesis
  • 101.
    Hypospedias Introduction • Hypospadias isa urethral opening on the ventral surface of the penile shaft. • It affects 1 in 250 male newborn. • Cause is unknown. • Sometimes hypospadias is associated with Dorsal hood and chordae.
  • 102.
    Clinical Presentations According tothe position of the urethral meatus Hypospadias is classified as- 1. Glanular - on the glans penis. 2. Coronal 3. Subcoronal 4. Midpenile 5. Penoscrotal 6. Scrotal 7. Perineal 8. Megameatal
  • 105.
    Treatment • Ideal agefor repair in a healthy infant is 6-12 months. • Circumcision should be avoided. • The goal of any type of hypospadias surgery is to make a normal, straight penis with a urinary channel that ends at or near the tip. Surgery – • Tubularized incised plate repair. • Almost all cases are repaired in a single operation except Proximal cases.
  • 106.
    Complications Untreated cases • Deformityof the urinary system. • Sexual dysfunction • Infertility • Meatal stenosis. After surgery • Urethro-cutaneous fistula. • Meatal stenosis.
  • 107.
    Phimosis • Inability toretract the prepuce. • At birth, Phimosis is physiologic. • 80% of uncircumscribed boys the prepuce become retractable by 3 years of age. • In older child pathologic phimosis may occur due to inflammation and scarring at the tip of foreskin.
  • 108.
    Treatment Medical • Application oftopical corticosteroid cream to the foreskin 3 times daily for 1 month. Surgical • Circumcision • Minor operation to relieve foreskin tightness.
  • 109.
    Paraphimosis It occurs whenthe foreskin is retracted proximal to the coronal sulcus and the prepuce can not be pulled back over the glans. Results in painful venous stasis and edema in the retracted foreskin leading to severe pain and inability to reduce the foreskin. Eventually gangrene and auto amputation of the distal penis Occurred.
  • 110.
    Treatment • Lubricating theglans and foreskin and simultaneous Compressing the glans. • Topical application of granulated sugar • Injection of hyaluronidase into the edematous skin • Emergency circumcision.
  • 111.