36- neonatal intestinal obstruction - compatibility mode · 0 $1$*(0(17 7kh wuhdwphqw lv xowlpdwho\...
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NEONATAL INTESTINAL
OBSTRUCTION
Khaled Al-Omar1
Prof K
haled H.K
. Bahaaeldin
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الدكتور كان يقرا اغلب السلايدات ويسأل عند بعض النقاط او يركز عليها
3/23/2014
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Prof K
haled H.K
. Bahaaeldin
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NEONATAL INTESTINAL OBSTRUCTION
(NIO)
Definition:
An intestinal obstruction occurring during the first month of life.
Neonatal : first 28 days of life
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Prof K
haled H.K
. Bahaaeldin
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CAUSES OF NIO
Esophageal: Atresia (TOF)
GastricDuodenal:
Atresia Stenosis Diaphragm Malrotation with bands or volvulus Annular pancreas
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CAUSES OF NIO
Jeujunal & ileal obstruction: Obstructed inguinal hernia Intussusception Atresia Stenosis Meconium ileus Peritoneal bands or herniae Duplication cysts
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haled H.K
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CAUSES OF NIO
Large bowl obstruction: Hirschsprung’s disease Anorectal anomalies Meconium plug syndrome Atresia (rarest)
Necrotizing enterocolitis Complicated Inguinal Hernias
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GENERAL PRINCIPLES
neonate
Any baby presenting with persistent, bile stained vomiting should be considered to be surgical emergency until proven otherwise.
Clinical picture:
The cardinal signs are 2C, 2V, 2D
Colics, Constipation
Vomiting, Visible peristalsis
Distension, Dehydration 7
Prof K
haled H.K
. Bahaaeldin
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MANAGEMENT
First aid: for any intestinal obstruction
Gastric decompression (naso-gastric tube) IV line (for fluid replacement)
Deficit therapy Maintenance
Urinary catheter (to monitor urine output) Fluids:
Lactated Ringer’s solution 10-20ml/kg over an hour, to be repeated according to response
Drugs: To cover anaerobes as well as Gram stained bacteriaAntibiotics
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Definition:
The main pathology is atresia of the esophagus! Tracheoesophageal fistula is secondary to that.
Incidence:
•1-2500 to 1-10000•males slightly more affected than females•the second sibling of an affected child has 0.2-0.5% chance of being also affectedAssociations:
Other congenital anomalies occur in 50-70% of infants affected with esophageal atresia.These are most common with esophageal atresia and distal fistula. Anomalies includecardiovascular (the majority), genitourinary, gastrointestinal and skeletal.
VACTERL association consists of Vertebral, Anorectal, Cradiac, Tracheo-Esophageal,and radial Limb deformities. It is not correlated with a known genetic abnormality orsyndrome. Should scan for all possible anomalies
EA & TEFESOPHAGEAL ATRESIA & TRACHEOESOPHAGEAL FISTULA
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of esophageal atresiaTypes:
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C : most common, proximal atresia and distal fistula between trachea and esophagus
A: second most common is pure atresia, more difficult because of the gap between the
proximal and distal end
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D.Diagnosis
Antenatal:
Maternal ultrasound / polyhydromnios
Postnatal:
Tracheoesophageal fistula present within the first few hours of life by:
- excessive salivation
- respiratory distress because they are choking with saliva (asphyxiation)
- cyanosis
- inability to pass a nasogastric tube.
-Attempts at feeding cause choking, coughing, cyanosis, regurgitation.
Radiography:
•Plain X-ray
•Contrast study(pouchogram)
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Prof K
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. Bahaaeldin
Plain X-rayWith Ryle’s tube
NG tube
Note:•Coiling loop esophageal atresia
denotes approximate length of upper pouch of esophagus.•Presence of air in with distal fistula the abdomen denotes a distal fistula.
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MANAGEMENT
The treatment is ultimately surgical but management strategy include also preoperative, operative and postoperative measuresPreoperative evaluation includes a an Echo and Bronchoscopy: why? Echo: to make sure its normal left aortic arch , bronchoscopy: عشان نشوف وين مكان الfistula
Surgical treatment:Division and closure of the fisula and primary anastomosis of the two esophageal segments.If the “Gap” between the two segments is too long, the infant is managed temporarily with an esophagostomy and gastrostomy. Later in life an procedure to replace the esophagus is considered e.g. colon interposition bypass.
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Prof K
haled H.K
. Bahaaeldin
Ligate the fistula between the trachea and the distalesophagus and we do an anastomosis between theproximal and distal end , ال مرات anastomosis صعبة تكون
stages على نعملها فنضطرesophagostomy نسوي ممكن growth مايصير على مؤقت in two
ends and then we do anastomosis after few weeks
بس هذا المطلوب
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CONGENITAL HYPERTROPHIC
PYLORIC STENOSIS (CHPS)
Any neonate presenting with projectile, non bilious vomiting, associated with hunger and constipation should be considered CHPS
Incidence: 8:1000 M/F ratio=4:1 More in first born babies More in infants born to a mother who had suffered from
CHPS More during spring and autumn!In longitudinal and circular pyloric muscles
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Prof K
haled H.K
. Bahaaeldin
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Etiology: Unknown, but appears to be polygenic (environmental,
and genetic) theory : كل الاطفال ينولدون بCHPS ولكن ماتصير فيsymptoms الا الي عندهمobstruction and they gradually resolve
Drugs?
Pathology: Progressive hypertrophy of circular pyloric
muscles Persistent vomiting leads to development of
hypochloremic hyponatremic alkalosis and dehydration
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Prof K
haled H.K
. Bahaaeldin
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Clinical picture: Symptoms:
projectile, progressive, non bilious vomiting after which the baby is hungry and ready to suckle again. Classically the symptoms between 3-12 weeks after birth
Signs:Signs of dehydration which may be severe and life
threatening.Visible peristalsis in the upper abdomen can usually be
seen after the baby is given a test feed followed by projectile vomiting.
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Olive sign can feel it unless the baby is very cachectic or sedated
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Differential diagnosis: (any differential that has vomiting ) Gastroenteritis Gastro-esophageal reflux Other obstructive lesion of the gut Increased Intracranial tension
Investigations: Imaging: sonography and contrast X ray
pyloric channel length (normal 11 mm, pyloric stenosis > 15-18 mm),
pyloric muscle length (normal 13-17 mm, pyloric stenosis > 19-21 mm),
pyloric muscular wall thickness (normal < 2 mm, pyloric stenosis > 3-5 mm),
pyloric diameter (normal < 10-15 mm, pyloric stenosis > 10-15 mm)
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Laboratory: to detect and correct electrolyte and metabolic disturbances
Treatment: not a surgical emergency ,is a medical emergency
First aid treatment to correct dehydration and metabolic disturbances (metabolic alkalosis)
Definitive surgery, the Ramstad's pyloromyotomy ( pylorus نفتح ال ,splitting to muscle , mucosa intact then surgery is done )
Why we have to correct before we do the surgery?
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Ramstad's pyloromyotomy
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DUODENAL OBSTRUCTION
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DUODENAL ATRESIA
Due to failure to recanalize the lumen after the solid phase of intestinal development in the 4th and 5th wk of gestation.
The incidence of duodenal atresia is 1/10,000 births Accounts for 25–40% of all intestinal atresias. Half the patients are born prematurely. Down syndrome occurs in 20–30% of patients with
duodenal atresia. Other congenital anomalies that are associated with
duodenal atresia include malrotation (20%), esophageal atresia (10–20%), congenital heart disease (10–15%), and anorectal and renal anomalies (5%).
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Atresia Types:
Type I: mucosal diaphragmatic (web) membrane between proximaland distal part
Type II: short fibrous cord connects two atretic ends Type III: complete separation of two atretic ends An unusual cause of obstruction is a “windsock” web, which is a
distensible flap of tissue associated with anomalies of the biliarytract. like valve mechanism (vomiting and gastric distention )
membranous form of atresia is most common, with obstruction occurring distal to the ampulla of Vater in the majority of patients.
Duodenal obstruction can also be a result of an extrinsic compression such as an annular pancreas or from Ladd bands in patients with malrotation.
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Annular pancreas Incidence is around 1:7000 Failure of normal fusion of the two pancreatic buds which may obstruct the duodenum from
without
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CLINICAL MANIFESTATIONS
The hallmark is bilious vomiting without abdominal distention, which is usually noted on the 1st day of life.
Peristaltic waves may be visualized early in the disease process.
A history of polyhydramnios is present in half the pregnancies and is caused by a failure of absorption of amniotic fluid in the distal intestine.
Jaundice is present in one third of the infants.
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The diagnosis is suggested by the presence of a “double-bubble sign” on plain abdominal radiographs. because : air in stomach and air in duodenal cap
The appearance is caused by a distended and gas-filled stomach and proximal duodenum.
Contrast studies may occasionally be needed to exclude malrotation and volvulus because intestinal infarction may occur within 6–12 hr if the volvulus is not relieved.
Prenatal diagnosis of duodenal atresia is readily made by fetal ultrasonography
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Two bubbles لازم نتأكد ان مو حاطين NG tube evacuation
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TREATMENT
Initial - Nasogastric or Orogastric decompression and intravenous fluid replacement.
Echocardiogram and radiology of the chest and spine should be performed to evaluate for associated anomalies.
Definitive correction of the atresia is usually postponed to evaluate and treat these life-threatening anomalies.
Surgery duodenoduodenostomy.(side to side duodenal anastomosis) Duodenal diaphragmatic obstruction is managed by
duodenoplasty ( resection)
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JEJUNOILEAL ATRESIA Jejunoileal atresia involves an obstruction of the
jejunum or ileum of the small intestine. The segment of intestine just before the
obstruction becomes massively dilated, thus hindering its ability to absorb nutrients and peristalsis through the digestive tract.
Same principle but more distal , and more distention in abdomen
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Jejunoileal atresia have been attributed to intrauterine vascular accidents leading to ischemic necrosis of the sterile bowel and resorption of the affected segments.
Polyhydramnios occurs in 25% of affected patients
Monozygotic twins are at higher risk Premature birth occurs in 30% of infants. Atresia has also been associated with low
birthweight, multiple births, and maternal cocaine use and cigarette smoking.
Skip!
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Cystic fibrosis is also an associated disorder and may seriously complicate the management of jejunoileal atresia. Infants with jejunoileal atresia should be screened for cystic fibrosis.
Mostly associated with Meconium Ileus
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TYPES
Type I atresia (23%) is a transluminal septum with proximal dilated bowel in continuity with collapsed distal bowel. The bowel is usually of normal length. (there is membrane between proximal and distal part)
Type II atresia (10%) involves two blind-ending atretic ends separated by a fibrous cord along the edge of the mesentery with mesentery intact.
(there is fibrotic band between the 2 end)
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Type IIIa atresia (15%) is similar to type II, but there is a mesenteric defect and the bowel length may be foreshortened.
(complete sepration between proximal and distal part)
Type IIIb atresia (19%) (“apple peel”) consists of a proximal jejunal atresia, often with malrotation with absence of most of the mesentery and a varying length of ileum surviving on perfusion from retrograde flow along a single artery of supply.
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Type IV atresia is a multiple atresia of types I, II, and III, like a string of sausages. Bowel length is always reduced. The terminal ileum, as in type III, is usually spared.
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PRESENTATION
Infants with jejunoileal atresia, regardless of the subtype, usually vomit green bile within the first 24 hours of life.
However, those with obstructions farther down in the intestine may not vomit until two to three days later.
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Infants often develop a distended abdomen and may not have a bowel movement during the first day of life.
But!! Bowel movement dose not role out atresiabecause baby may pass meconium first 24-48 hour
Given the age of the patient and the symptoms, an abdominal X-ray is usually sufficient to establish a diagnosis.
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SURGERY The type of surgery depends on the type of
atresia, the amount of intestine present and the degree of intestinal dilation.
The most common operation involves removal of the blind intestinal segments, and the remaining ends are anastomosed. Similarly, a narrowed (stenosed) segment of the intestine can be removed and the bowel sutured together, thus establishing anastomosis.
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COLONIC ATRESIA
This rare form of intestinal atresia accounts for less than 15% of all intestinal atresias. The bowel becomes massively enlarged (dilated), and patients develop signs and symptoms similar to those associated with jejunoileal atresia. Colonic atresia may occur in conjunction with small bowel atresia, Hirschsprung's disease or gastroschisis.
The diagnosis is confirmed by an abdominal X-ray along with an X-ray contrast enema.
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SURGERY
Colonic Atresia: Babies with colonic atresia may undergo removal of the dilated colon in addition to a temporary colostomy. Less frequently, the ETE or STE anastomosis.
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Prenatal ultrasounds. Intestinal obstructions are
increasingly being identified through prenatal ultrasounds. This imaging technique may indicate excess amniotic fluid (polyhydramnios), which is caused by the failure of the intestine to properly absorb amniotic fluid.
Skip!
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MECONIUM ILEUS Obstruction of Ilieum due to thick inspissated
meconium Approximately 10% of infants with cystic fibrosis
develop meconium ileus; 80–90% of infants presenting with meconium ileus
have cystic fibrosis. simple meconium ileus
the last 20–30 cm of ileum is collapsed and filled with pellets of pale-colored stool, above which a dilated loop of varying length appears obstructed by meconium of the consistency of thick syrup or glue.
complicated meconium ileus Accompained by Volvulus, atresia, or perforation of the
bowel
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Perforation in utero produces meconium peritonitis. Intraperitoneal meconium can cause dense adhesions, leading postnatally to adhesive intestinal obstruction, and can rapidly become calcified.
Most symptomatic in the 1st day of life with abdominal distention and bile-stained emesis or gastric aspirate.
60 to 75% of the infants fail to pass meconium. Jaundice has been found in 20–30% of the
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DX Plain radiographs demonstrate many air-fluid levels or
peritoneal calcification associated with meconium peritonitis.
Contrast studies of the upper and lower bowel can delineate the level of obstruction and differentiate atresia from meconium ileus, meconium plug, and Hirschsprung disease.
Abdominal ultrasound can help distinguish meconium ileus from ileal atresia and identify intestinal malrotation.
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In meconium ileus- typical hazy or ground-glass appearance in the right lower
quadrant. Small bubbles of gas trapped in meconium are dispersed within this area.
Because of their viscid contents, moderately dilated loops of bowel do not have the air-fluid levels usually seen radiographically on the erect projection.
If there is meconium peritonitis, patchy calcification may be noted, usually in the flanks.
Pneumoperitoneum - as free air between the liver and the diaphragm on an upright radiograph of the abdomen; if there is a large amount of free air, the entire abdomen may look like a football from distention with air; the ligamentum teres is sometimes clearly visible in the midline.
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TREATMENT Initial -fluid and electrolyte balance Prophylactic antibiotics In uncomplicated meconium ileus,
Gastrografin enemas will diagnose the obstruction and wash out the inspissated material. Gastrografin is hypertonic and care must be taken to avoid dehydration, shock, and bowel perforation, may have to be repeated after 8–12 hr
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50% of patients with simple meconium ileus do not adequately respond to water-soluble enemas and need laparotomy.
Operative management is indicated when the obstruction cannot be relieved by repeated attempts at nonoperative management and for infants with complicated meconium ileus.
In simple meconium ileus, the plug can be relieved by manipulation or direct enteral irrigation with N-acetylcysteine following an enterotomy.
In complicated cases, bowel resection, peritoneal lavage, abdominal drainage, and stoma formation may be necessary.
Total parenteral is usually required.
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