Pediatric Bowel Obstruction

Pediatric Bowel Obstruction

Pediatric Bowel Obstruction
Hypertrophic pyloric stenosis Atresia and stenosis Doudenal obstruction Malrotation and Volvous neonatorum Meconium Ileus Intussusceptions Hirsh sprung disease Duplications of the gut Neonatal necrotizing enter colitis Anorectal malformation

Hypertrophic pyloric stenosis
It is not truly a congenital disorder and is often called infantile hypertrophic pyloric stenosis 2nd common surgical problem in infancy after intussusception Affects 3 per 1000 live births Male: female 4:1 and most common in first born males

Hypertrophic pyloric stenosis (etiology)
In coordination between sympathetic and parasympathetic leading to continuous contraction of the circular muscle layer of pylorus leading to hypertrophy High level of maternal and child gastrin Variation in infant feeding

Hypertrophic pyloric stenosis (pathology)
Hypertrophy of circular muscle layer Mucosa become compressed and folded Lumen narrow admit little finger

Hypertrophic pyloric stenosis (Clinically)
Males presenting at 2 to 8 weeks of age however late presentation up to 6 months can occur Symptoms Vomiting Bile free, projectile and progressive in nature yet, Child hungry and often feeds immediately after vomiting Constipation Loss of weight

Hypertrophic pyloric stenosis (Clinically)
Signs General Dehydration and alkalosis are prominent clinical features. Wasting Sunken eyes Depressed fontanells Dry woody tongue Oligurea Abdominal Palpating an olive like tumor (pyloric tumor) Peristalsis from left to right seen

Hypertrophic pyloric stenosis (investigations)
Upper GIT series (Barium) Dilated stomach Hypertrophic gastric rugae Narrow elongated pyloric canal (string sign) Beak sign (ant rum gave rise to pylorus) Shoulder sign (pylorus bulge into ant rum) Delayed gastric empting time U/S Laboratory Repeated vomiting may lead to dehydration and hypochloremic hypokalemic alakalosis;

Hypertrophic pyloric stenosis (Treatment)
Pre-operative preparation Correct deficits dehydration hypochloremic hypokalemic alakalosis should be corrected before surgery (no urgency in surgery 24 to 72 hours for correction) Uses a nasogastric tube to decompress the stomach.

Operation is Frede- Ramstedt pyloromytomy Incisions used, either trans lateral part of the rectus, or entirely muscle splitting Traction on the omentum will bring out the stomach Ramstedt pyloromyotomy is completed Check out the integrity of the mucosa before closure

Hypertrophic pyloric stenosis

Post operative NG suction for 8-12 hour Feeding re-established within hours of surgery Stating with dextrose 10 % every 2 hours Increasing amount Half formula Full formula

Post operative complications Persistent vomiting Wrong diagnosis Gastritis Inadequate surgery perforation Burst abdomen Anesthetic complications

Intestinal Atresia and Stenosis

Intestinal Atresia and Stenosis
Incidence 95% Atretic 5% Stenotic 1:330 infants in USA Associated with Down’s syndrome Caused by an intrauterine vascular occlusion

Small bowel atresia Pathology
Can be single or multiple It can take different types Membrane atretic segment typically missing segment with V shaped defect in mesentery multiple segments (Chrismas tree)

Intestinal Atresia and Stenosis (clinically)
Classical triad of Bilious vomiting Distention Failure to pass meconium on first day of life.

Small bowel atresia Diagnosis Treatment
Can be diagnosed during pregnancy by U/S multiple fluid levels on X ray is diagnostic Gastrographin full through detect site of obstruction Treatment Excision of the non-propulsive area of the dilated segment is better to be done with end-to-end anastomosis

Duodenal atresia

Duodenal atresia It typically occurs at the second part of the duodenum When there is a missing part of the duodenum the pancreas gives the impression of annular pancreas The ampulla commonly drains into the proximal part (bile stained vomitus) Down’s syndrome is present in 30% of cases (not usually associated with other intestinal atresia)

Duodenal atresia Causes
Complete obstruction Incomplete obstruction Intrinsic stenos is by diaphragm Extrinsic by Annular pancrease Band of Ladd

Duodenal atresia Clinical
Complete obstruction Vomiting (persistent bile stained ) Distention (sever) No passage of meconium May jaundice Incomplete obstruction Vomiting ( intermittent) Distention (minimal) Normal passage of meconium

Duodenal atresia Diagnosis
Antenatal U/S at weeks can diagnose the case Polyhydramnios may be present 60% Features of Down’ syndrome Plain X ray double bubble appearance Upper GIT series

Atresia and Stenosis Doudenal atresia oesphageal atresia

Duodenal atresia Management
A nasogastric tube should be passed Intravenous fluid resuscitation should be given Major cardiac and other defects should be excluded Duodenoduodenostomy should be performed when resuscitated Duodenojujnostomy

Malrotation and volvulus neonatoum

Non-fixation and Malrotation of the bowel
Around the 10th week bowel commences its return from the physiological hernia in the umbilical cord to the abdomen It rotates 270 counterclockwise This will lead to the formation of the C duodenal loop, which passes beneath the superior mesenteric vein. In a similar fashion the colon passes over the vessels bringing the cecum to the right iliac fossa

Anomalies of the bowel Rotation
Non rotation Incomplete rotation Midgut volvulus Band of Ladd causing duodenal obstruction Reversed rotation Anomalies mesenteric fixation Mobile caecum Paradoudenal hernia Internal mesenteric hernia

Failure of rotation may occur giving an S shaped duodenum absence of duodenojujenal junction presence of small bowel in the right side of the abdomen . The cecum lies in the left hypochondrium

Malrotation absence of duodenojujenal junction The cecum lies in
the left hypochondrium presence of small bowel in the right side

The incomplete or arrested rotation with the previous description will lead to either To midgut volvulus, due to the narrow attachment of the mesenteric base, and very long bowel loop Or will lead to the presence of a fibrous tissue band (Band of Ladd) that cross the duodenum, from the right hypochondrium to the cecum, causing duodenal obstruction

Presentations Two principal clinical presentations
Presents late with intermittent bile stained vomiting and distension (duodenal obstruction) Presents early with collapse and acidosis due to intestinal infarction Radiological investigations are often unhelpful Double bubble sign Multiple air fluid level Gastrographin detect site of obstruction

Management After resuscitation, early laparotomy may be required
Any volvulus should be reduced Resection may be required if there has been small bowel infarction Any Ladd's bands should be divided Colon should be placed on the left of the abdomen Small bowel should be placed on the right Inversion appendicectomy should be performed to prevent future diagnostic uncertainty

Malrotation and volvulus

Meconium ileus

Meconium ileus Commonest cause of neonatal intraluminal intestinal obstruction 80% cases are associated with cystic fibrosis on the other hand 15 % of patients with cystic fibrosis presents with meconium ileus Cystic fibrosis is an autosomal recessive trait Antenatal diagnosis is possible with U/S, showing dilated loops of bowel and abdominal distension

Meconium ileus Due to loss of pancreatic enzymes (cystic fibrosis)
Abnormal mucous thick and tacky meconium obstructs the lower ileum, The affected loops become heavy and dilated and thickened and become prone to volvulus . The colon is atrophic, microcolon with pellets of desquamated epithelium due to non use.

obstructs the lower ileum Proximal bowel dilated and thickened prone to volvulus The colon is atrophic, microcolon

Meconium ileus At birth, the baby is noted to have a markedly distended abdomen with The presence of large visible and palpable dilated loops of bowel filled with pultaceous rubbery meconium Then neoborn starts to vomit green. With delayed muconium passage.

Meconium ileus Abnormal radiographs show a granular appearance in dilated small bowel loops of variable diameter, with no fluid levels. Eventually full blown picture of intestinal obstruction in the upper loops develop Contrast enema reveals micro colon with pellets. 40% are associated with complications, either volvulus neonatorum, atresia or meconium peritonitis, giving physical signs of acute intra-abdominal process

Meconium Ileus

Treatment In 50% of non complicated cases the gastrografin enema (highly osmolar wetting agent) rapidly passing through the microcolon, can dislodge the meconium sufficiently to overcome the obstruction Two indications of laparatomy Residual obstruction The presence of complications

Meconium Ileus

Laparotomy An attempt is made to liquefy the meconium by intraluminal injection of Gastrographin Saline Plus bowel massage More frequently it is necessary to resect the dilated meconium filled loops back to bowel of a normal diameter then Either end to end anastomosis +wash out the distal bowel or Bishop Koop operation

Mikulicz Swenson Distal Chimney Proximal Chimney

Intussusception

Intussusception The term describes telescopic invagination of bowel within itself . As it advances more bowel is dragged through giving more bulky and tight mass. The mesentery invaginated will be compressed leading to congestion and strangulation.

Intussusception It is the commonest abdominal emergency between 3 months and 2 years Peak incidence is between 6 and 9 months Commonest site involved is the ileocaecal junction

Intussusception Etiology
Most cases are idiopathic Weaning Gastrorentritis in 50% of cases with the lead point due to enlarged Peyer's patches usually due to a viral infection Mobile ileocacecal junction Long bloodless fold of trves 5% are due to polyp, Meckel's diverticulum, duplication cyst or tumor

Intussusception Obstruction is complete from beginning
95% begin at ileocecal valve 2-8% have a lead point (polyp, Meckel’s, lymphoid patch) Edema produces lymph node enlargement Fluid, blood and mucus into the lumen Current Jelly Stool

Intussusception Symptoms
Early Intermittent colicky abdominal pain and vomiting in a well-nourished baby colicky spasmodic pain with legs drawn towards the abdomen pallor, sweating and retching vomiting Passage of blood - 'red currant jelly' per rectum Each episode classically last 1-2 min and recurs every min Late Symptoms of peritonitis and intestinal obstruction

Intussusception Signs
Early General well-nourished baby Abdomen Sausage shaped abdominal mass Danse’s sign (empty RT lower abdomen) Increase peristalsis PR Passage of blood - 'red currant jelly' per rectum Apex of intussesption Late General dehydration and electrolyte disturbances Abdomen peritonitis

Diagnosis Typical history and clinically felt mass current jelly stools Plain X abdomen (small bowel obstruction) empty right iliac fossa, opacity over the mass After resuscitation, barium enema (diagnosis confirmed with water soluble contrast enema or ultrasound) will outline the apex as Copra head or spring coil appearance

Intussusception

Intussusception - Treatment
NG Tube, IVF, Antibiotics, Surgical Consultation Hydrostatic Reduction (65%): Foley inserted into rectum, balloon inflated Barium run in from 3’ 6” above patient Fluoroscopy: meniscus lengthens, reduces If no free flow into ileum - surgery (Johns Hopkins series, 1965)

Intussusception - Treatment
Indications of surgery are Signs of peritoneal irritation Incomplete reduction Failure of reduction all together Suspected perforation (if high pressure is used) Surgery A gridiron approach in the right iliac fossa No pulling is allowed Resection with end-to-end anastomosis for suspected vitality

Hirschsprung disease

Hirschsprung disease Accounts for 10% of neonatal intestinal obstruction It is a congenital aganglionosis the most frequently involves the rectosigmoid segment There is definite genetic influence especially in long segment and total colonic types and in association with Down’ syndrome. It results due to failure of intrauterine migration of ganglion cells from the neural crest distally along the vagus nerve pathways

Hirschsprung disease Failure of development of local autonomic innervation leads to absent peristalsis within the affected bowel with consequent adynamic obstruction. The bowel proximal to the congenital obstruction becomes markedly dilated and hypertrophied, eventually tapering distally into the aganglionic segment. This tapered (transition zone) accounts for the cone effect noted on contrast radiography and at operation

Hirschsprung disease Pregnancy and the full term baby are normal in the first hours. Bile tinged vomiting Abdominal distension Failure to pass meconium within the first 24 hours. (80% of cases)

Hirschsprung disease Rectal examination induces explosive evacuation of gas and liquefied meconium as the finger is withdrawn. The most serious complication in missing the diagnosis is enterocolitis with life threatening septicemia. The condition can be presenting later in the preschool age with constipation and/or failure to thrive

Hirschsprung disease Definitive diagnosis depends on histological demonstration on a rectal biopsy Absence of ganglia Hypertrophy and proliferation of nerve fibrils Increased acetylcholinestrase content in Auerbach, and Meissner neural plexus Biopsy specimens are obtained by suction mucosal biopsy, or as formal operation (anorectal myectomy)

Hirschsprung disease Other investigations such as Contrast radiology
Manometry (lack of recto anal inhibitory reflex RAIR) are helpful in confirming and possibly demonstrating the level of the lesion, but are not as conclusive as histology

Hirshirprung disease

Hirshirprung disease (treatment)
Conservative Enema and glycerin suppositories tell the child is 9 kg and can stand surgery Surgical Single stage Tran anal repair 3 stages repair Colostomy Procedure Closure of colostomy

Management As any intestinal obstruction Nasogastric suction
I.V. fluids and electrolytes Antibiotics should be used with caution (sometimes initiate enterocolitis) 4-6 hour digital rectal dilatation of adynamic segment (rectal washouts are used with cautions to avoid retained volumes and isotonic solution should be used)

Management When the general condition improves, do
Left iliac fossa or transverse colostomy in a ganglionic segment. Few month’s later definitive operation is done with intra operative frozen section histology for determination of the level of resection. The three most commonly described operations are Swenson, Duhamel and Soave The principle is to bring ganglionic colon as far down as the perianal margin

Anorectal malformation

Anorectal malformation Classifications
Low anomalies Imperforate membrane Anal stenosis Covered anus Ectopic anus Intermediate anomalies Anal agenesis Anorectal stenosis High anomlies Without fistula With fistula

Anorectal malformation Ladd and Gross Classification
Anal stenosis Imperforate anal membrane Anal agenesis without fistula with fistula Rectal agenesis Rectal atresia

Imperforate anus (Covered anus)
The rectum and anal canal dilated down to the membrane The normal site is covered with operculum formed of a layer of skin lined with mucosa Clinical picture progressive abdominal distension with a greenish membrane bulging at the normal site Treatment is by excision of the membrane with frequent digital dilatation for few months

Imperforate anus Anal stenosis
There is enormous variation in the severity of this very common condition. The ribbon or toothpaste stools are diagnostic. There is usually delay in diagnosis with more symptoms after changing the baby’s food on weaning. Treatment is dilatation .

Covered anus incomplete Or anocutaneous fistula
The bowel passes through the external sphincter and then turns forwards a fistulous tract deep to the median raphae to open in front of the anus The usual presentation is progressive abdominal distension with passage of small amounts of meconium from the fistulous opening

Ectopic anus Physiologically and histologically the internal sphincter keeps its relation to the bowel lumen, which passes in front of the pelvic floor slings Clinically if there is no stenosis, incontinence is not a major problem and no treatment is required. Only in stenosis dilatation is required. Females should avoid vaginal delivery by all means. Incontinence will be irreparable

Intermediate anomaly Anal agenesis without a fistula
Presentation is indistinguishable from high anomaly The first step is to do colostomy. Rectopbulbar fistula Meconium and air pass per uretheram cannot be differentiated clinically from the high anomaly with rectouretheral fistula Colostomy is the initial treatment

Intermediate anomaly Rectovestibular or rectovaginal low fistula
Probing will differentiate anovestibular from recto vestibular fistulae; the latter is passing upward and backward The rectovaginal low is just above the hymen Colostomy is the initial step

Anorectal malformations diagnosis
Invert gram (Rice Wangensteen view) PC line Ischeal spine These represent Puborectalis and levator ani ( pelvic floor) Contrast studies IVU

High anomalies Anorectal stenosis or atresia
Diagnosed by inability to insert the finger into the anus The clinical shape from outside looks normal Initial treatment is by colostomy Definitive reconstructive treatment is done at 3-12 month of age with the ultimate goal is achieving continence to stools and flatus. PSARP Abdominperineal approach

Neonatal respiratory distress syndrome
Tracheo esophageal fistula and esophageal atresia Diaphragmatic hernia Congenital lobar emphysema Vascular ring

Tracheo esophageal fistula and esophageal atresia

5 % 5 % 85% 5 %

A new borne premature and polyhydraminous A new borne with Excessive salivation Respiratory distress relieved temporarily by pharyngeal suction Regurgitation, choking, coughing and Cyanosis in trial of feeding Distended abdomen

Passage of a tube No.8 or 10 soft rubbers per mouth will be arrested at 10 cm from lips 1 ml water-soluble contrast.

Babygram is done to demonstrate air in GIT from the TEF, the pneumonic changes for vertebral and sacral anomalies U/S for heart, kidney and brain anomalies

Management Risk classification
Group A Birth weight > 2500 gm No pneumonia No other anomalis Survival 95 % Group B B W No pneumonia No other anomalis Survival 65 % Group B B W > 2500 gm Moderate pneumonia Non life threatening anomalis Survival 65 % Group C Birth weight < 1800 gm sever pneumonia life threatening anomalis Survival 6 %

Management Correct dehydration, pneumonia by fluids and antibiotics parentally Continue low suction of upper pouch, and keep baby on lateral side to decrease reflux into trachea. Plan for urgent operation, this is the only way to keep baby alive. This starts usually with treacheoscopy to evaluate the no and locations of the fistulae, and tracheitis and malicia status

Management In the operation cutting of the tracheoesophageal fistula is done first then the two ends of the esophagus are anastomosed in a tension free manner with assurance of the vascularity of the two ends

Management Complications Oesophageal dysfunction
Dilated proximal pouch Gastro-oesophageal reflux Anastomotic stricture Recurrent fistula

Anomalies of anterior abdominal wall
Exomphalus minor and major Gastroschisis Infantile umblical hernia Ectopia vesica Prune belly syndrome Anomalies of vitello intestinal duct Persistent vitello intestinal duct Patent urachus Urachal cyst Meckel’s diverticulum

Exomphalus minor Presents as an intact hernial sac within the structures of the umbilical cord It usually contains one or two loops of terminal ileum that can be adherent to the apex of the sac Minor surgery is done to replace the bowel and repair the defect, don’t excise the cord to keep the umbilical scar (for physic reasons)

Exomphalus major Large hernia of the cord with diameter at the base >5 cm The defect lies in the upper abdomen with the cord attached to the undersurface of sac (vs Ex. Minor) The sac can be intact or ruptured, with bowel and other organs out, with the ileum attached to the sac at the site of Meckel’s D Other anomalies should be searched for

Management Unruptured sac
The concept of delayed surgery is chosen. The child is electively paralyzed and ventilated, and the sac contents are slowly returned to the abdomen with gravity and sac plication over some days. Surgery is delayed until the contents of the sac have been accommodated within the abdomen. Repair is then done if abdominal wall closure is without undue tension to avoid impaired venous return, and respiratory embarrassment.

Trials of primary skin closure can be done child paralysis and ventilation is then adjuvant until the abdomen is more accommodated to avoid tension, furthermore a silo can be used if skin closure is impossible with again paralysis and ventilation until enough space exists

A trial of conservative treatment at hospital, with induction of cicatrisation of the sac with a cicatrizing agent until epithelium creeps to cover the sac avoids surgery, but needs more hospital stay and is endangered with rupture and sepsis.

Ruptured sac Emergency correction of the general condition is mandatory with the use of a silo and the procedure of primary or delayed repair described before is applied mortality is much higher with rupture.

Gastroschisis Infants borne with gastroschisis are smaller and with lower birth weight Low incidence of associated anomalies The defect is on the right of the umbilical cord, with no hernial sac Extruded viscera consists of midgut only The defect can take any size, with narrower defects worse as they are associated with intestinal atresia or loss of midgut.

Gastroschisis Management is essentially similar to ruptured exomphalus major Unlike Exomphalus major, the return to intestinal function is delayed since the gut had been exposed to amniotic fluids, which is injurious and causes gut contraction over a granular membrane

Treatment Can often be treated by direct full-layer closure of abdominal wall May be associated with postoperative gut dysfunction Usually require postoperative nutritional and ventilatory support

Neuroblastoma and Wilms tumor

Most common extracranial childhood cancer sympathetic ganglia, adrenal medulla and other sites Adrenal and prarspinal tumors accounts for 65%, other sites are chest, neck and pelvis Most common childhood abdominal malignancy Pleuripotent nephroblastic cell Abdominal exclusively the kidneys

40% are younger than one year and these have a very good prognosis even in the presence of metastases further 35% between age of one and two years, and only 25% above two years. Affects children between one and five years. The age has no major effect on prognosis like neuroblastoma.

origin From the same cell of origin, there comes the ganglioneuroma (benign counterpart) ganglioneuroblastoma (semi malignant counterpart) Histologically there is a favorable histology type, which displays mature elements and very few anaplastic cells non-favorable type, which displays focal or diffuse anaplasia or clear cell sarcoma. This unfavorable histology type accounts for 15% of cases and at the same time 90% of deaths

Direct infiltration lymph nodes near by and bone and bone marrow, liver, skin and other organ Direct infiltration lymph nodes whether nearby or distant are next common. mainly lung and Liver

General symptoms of abdominal pains, emesis, weight loss fatigue bone pain and chronic diarrhea are common 50% present with advanced stage disease due to bone and bone marrow metastases Abdominal mass is another presentation Asymptomatic abdominal mass Hypertension gross hematuria fever

Neuroblastoma Paraspinal tumors can cause spinal cord compression by a dumbbell extension causing neurologic manifestations Horner syndrome is presentation in cervical tumors Mediastinal chest tumors are usually accidentally discovered during x raying the baby for irrelevant symptoms like chronic cough

Neuroblastoma Stage I localized tumor with complete excision
Stage II localized tumor with incomplete gross resection Stage III unresectable unilateral tumor infiltrating across the midline with regional LN affection Stage IV distant dissemination to bone, bone marrow and other organs Stage IVS localized primary tumor as in stage I or IIA or IIB with dissemination to skin liver and /or bone marrow (limited to infants below one year.)

Wilms tumor Stage I well encapsulated tumor completely removed by surgery Stage II extension outside renal capsule or to LN, no macroscopic residue after surgery Stage III positive macroscopic residue after surgery Stage IV distant metastases mainly to the lung Stage V bilateral disease

Urine collection for catecholamines (90% have elevated homovalnillic acid (HVA) and /or vanillylmandellic acid (VMA) detectable in urine) CBC kidney function urine analysis.

CT abdomen Chest X ray and CT chest (posterior mediastinum) MRI in para spinal tumors Bone scan and skeletal survey Bilateral bone marrow aspirate and biopsy Renal ultrasound, and /or CT X ray and CT chest to detect lung metastases and even CT guided biopsies from lung lesions since patients with lung lesions receive whole lung radiotherapy.

Tissue biopsy is essential which is obtained by FNABC Resection of the tumor As treatment depend on risk stratification of patients Histopathological confirmation is not essential in North America for any suspected Wilms T undergo Nephrectomy immedialy Explore the other kidney LN sampling not resection

Low risk (Stage 1,2,4s) Surgery only Intermediate risk (Stage 3,4) Multimodality therapy with surgery, chemo and selected radio Chemotherapy Vincristine Actinomycin D Radiotherapy Stage V Nephrectomy in the more affected side and heminephrectomy in the other side + chemoradiotheapy

High risk Unfavorable histology Mycin amplifed > 1 y stage 4 Surgery Multiagent chemotherapy Radiotherapy Followed by High dose chemotherapy and peripheral blood stem cell rescure

Pediatric Bowel Obstruction

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