C/ Intussusception To define it. To know its epidemiology. To know the etiology &pathogenesis. To distinguish its manifestations To diagnose a case. To manage it. What is the prognosis?
GER is defined as the effortless retrograde movement of gastric contents upward into the esophagus . GERD is the most common esophageal disorder in children of all ages. Although occasional episodes of reflux are physiologic, exemplified by the regurgitation of normal infants, the phenomenon becomes pathologic (GERD) in children who have episodes that are more frequent or persistent, and thus produce esophagitis or esophageal symptoms, or in those who have respiratory sequelae.
GERD
Physiologic GERspitting up is normal in infants younger than 12 months old. NATURAL HISTORY :reflux becomes evident in the 1st few months of life, nearly half of all infants are reported to spit up at 2 months of age. peaks at ≈4 mo resolves in most by 12 mo and nearly all by 24 mo.
Criteria for physiologic GER
Normal weight gain Have no signs of respiratory or peptic complications. The absence of bloody or bilious vomitingFactors involved in physiologic GER include
Liquid diet Frequent, relatively large volume feedings Horizontal body position Short, narrow esophagus Immature LES. Small, noncompliant stomachAs infants grow: They spend more time upright Develop a longer and larger diameter esophagus Have a larger and more compliant stomach Eat more solid foods Experience lower caloric needs per unit of body weight As a result, most infants stop spitting up by 9 to 12 months of age.
Pathologic GER
After 18 months of age or If there are complications in younger infants such as Esophagitis, This may present clinically as blood in the vomit or More insidiously with the development of anemia or stricture. Older children may complain of heartburn with reflux While smaller infants may develop feeding difficulties due to esophageal discomfort Respiratory symptoms : wheezing, aspiration pneumonia, hoarse voice chronic cough, or apneic spells. Failure to thrive
Diagnosis:
A clinical diagnosis is often sufficient in children with classic effortless regurgitation and no complications. Diagnostic studies are indicated for pathological GER A barium upper GI series: to exclude obstruction such as pyloric stenosis, hiatus hernia ,gastric antral web, duodenal stenosis, annular pancreas, and malrotation. Because of the brief nature of the examination, a negative barium study does not rule out GER. 24-hour esophageal probe : Data typically are gathered for 24 hours, following which the number and temporal pattern of acid reflux events are analyzed. Esophageal impedance monitoring, which records the migration of electrolyte rich gastric fluid in the esophagus. Endoscopy is useful to rule out esophagitis, esophageal stricture, and anatomic abnormalities. .Treatment
Treatment of uncomplicated GER In otherwise healthy young infants ("well-nourished, happy spitters"), The mother should be reassured and advised of simple measures to help with the problem. such as: Positional therapy: supine upright in seat, elevate head of crib with head up is helpful, Towel on caregiver's shoulder Cheap, effective. Useful only for physiologic reflux Thickened feedings :Reduces number of episodes, enhances nutrition,thickening of formula with a tablespoon of rice cereal per ounce of formula results in fewer regurgitation episodes, greater caloric density (30kcal/oz), and reduced crying time, Smaller, more frequent feedings :Can help some. Be careful not to underfeed child If there is a strong family history of atopy or signs of eczema the introduction of a hypoallergenic feed may be indicated.Treatment of complicated GER:Medical Therapy Proton-pump inhibitor (PPIs; omeprazole, lansoprazole, pantoprazole, rabeprazole, and esomeprazole) , effective medical therapy for heartburn and esophagitis H2 receptor antagonist(H2RAs :cimetidine, famotidine, nizatidine, and ranitidine) reduces heartburn, less effective for healing esophagitis Metoclopramide, enhances stomach emptying and LES tone. Real benefit is often minimal.Surgical Therapy: forEsophagitis unresponsive to medical therapy.Esophageal stricture Apneic spells or chronic pulmonary disease unresponsive to 2–3 months of medical therapy.Feeding jejunostomy, useful in child requiring tube feeds. Delivering feeds downstream eliminates GERD Nissen or other fundoplication procedure for life-threatening or medically unresponsive cases. Fundoplication procedures may be performed as open operations, by laparoscopy, or by endoluminal (gastroplication) techniques.
PYLORIC STENOSIS
Pyloric stenosis is an acquired condition caused by hypertrophy and spasm of the pyloric muscle, resulting in gastric outlet obstruction. Epidemiology : It occurs in 6 to 8 per 1000 live births 5:1 male predominance more common in first-born children.Clinical Manifestations
Vomiting: Nonbilious vomiting usually begins between ages 2 and 4 weeks and rapidly becomes projectile after every feeding; or it may be intermittent Vomiting in pyloric stenosis differs from spitting up(gastroesophageal reflux) because of its extremely forceful and often projectile nature. The vomited material never contains bile because the gastric outlet obstruction is proximal to the duodenum. This feature differentiates pyloric stenosis from most other obstructive lesions of early childhood. After vomiting, the infant is hungry and wants to feed again. Affected infants are ravenously hungry early in the course of the illness, but become more lethargic with increasing malnutrition and dehydration. As vomiting continues, a progressive loss of fluid, hydrogen ion, and chloride leads to hypochloremic metabolic alkalosis. Constipation: usually occur. Jaundice : associated with a decreased level of glucuronyl transferase is seen in approximately 5% of affected infants. The indirect hyperbilirubinemia usually resolves promptly after relief of the obstruction.Diagnosis is established bypalpating the pyloric mass: The mass is firm, movable, approximately 2 cm in length, olive shaped, hard, best palpated from the left side, and located above and to the right of the umbilicus in the mid epigastrium beneath the liver edge. After the infant vomits, the abdominal musculature is more relaxed and the “olive” easier to palpate. peristaltic wave: after feeding, there may be a visible gastric peristaltic wave that progresses across the abdomen . The diagnosis can be established clinically 60–80% of the time by an experienced examiner.Ultrasound examination: confirms the diagnosis in the majority of cases, allowing an earlier diagnosis .pyloric thickness greater than 4 mm or an overall pyloric length greater than 14 mm. Ultrasonography has a sensitivity of approximately 95%.Barium studies :Elongated pyloric channel A bulge of the pyloric muscle into the antrum (shoulder sign),Parallel streaks of barium seen in the narrowed channel, producing a (double tract sign) Diagnosis
Pyloric mass
Gastric peristaltic wave in an infant with pyloric stenosis.A, Transverse sonogram demonstrating a pyloric muscle wall thickness of >4 mm (distance between crosses.B, Horizontal image demonstrating a pyloric channel length >14 mm (wall thickness outlined between crosses) in an infant with pyloric stenosis
shoulder sign
TreatmentThe preoperative treatment : Before surgery, dehydration and hypochloremic alkalosis must be corrected, generally with an initial normal saline fluid bolus followed by infusions of half-normal saline containing 5% dextrose and potassium chloride when urine output is observed. Fluid therapy should be continued until the infant is rehydrated and the serum bicarbonate concentration is <30 mEq/dL, which implies that the alkalosis has been corrected. Correction of the alkalosis is essential to prevent postoperative apnea, which may be associated with anesthesia.
Surgical management: The surgical procedure of choice is the ramstedt pyloromyotomy. The procedure is performed through a short transverse incision or laparoscopically. The underlying pyloric mass is split without cutting the mucosa, and the incision is closed The surgical treatment of pyloric stenosis is curative, with an operative mortality of 0–0.5%.
INTUSSUSCEPTION
INTUSSUSCEPTION
Intussusception is the "telescoping" of a segment of proximal bowel (the intussusceptum) into downstream bowel (the intussuscipiens). Epidemiology :It is the most common cause of intestinal obstruction between 3 mo and 6 yr of age. Sixty percent of patients are younger than 1 yr, and 80% of the cases occur before 24 mo; it is rare in neonates.The incidence varies from 1– 4 in 1,000 live births. The male:female ratio is 4:1.
Etiology:
Viral-induced lymphoid hyperplasia may produce a lead point in these children. In infants the lead point is presumed to be an enlarged Peyer’s patch, the lymphoid tissue presumably responding to a viral stimulant. This becomes the apex of the intussusception which then proceeds for a variable distance into the colonCorrelation with adenovirus infections has been noted, and the condition may complicate otitis media, gastroenteritis, Henoch-Schцnlein purpura, or upper respiratory tract infections.In older children(> 2years) the proportion of cases of patients caused by a pathologic lead point increases. the lead point may be Intestinal polyp, Meckel diverticulum,Neurofibroma,Hemangioma, or malignant conditions such as lymphoma.Intussusception may complicate mucosal hemorrhage as in henoch-schцnlein purpura or hemophilia.PATHOLOGY
Intussusceptions are most often ileocolic, less commonly cecocolic, and rarely exclusively ileal. Very rarely, the appendix forms the apex of an intussusception. The upper portion of bowel, the intussusceptum, invaginates into the lower, the intussuscipiens, pulling its mesentery along with it into the enveloping loop. Constriction of the mesentery obstructs venous return; engorgement of the intussusceptum follows, with edema, and bleeding from the mucosa leads to a bloody stool, sometimes containing mucus. Most intussusceptions do not strangulate the bowel within the 1st 24 hr but may later eventuate in intestinal gangrene and shock.Clinical Manifestations
In typical cases there is sudden onset, in a previously well child, of severe paroxysmal colicky pain that recurs at frequent intervals ,with legs and knees flexed and loud cries. pallor with a colicky pattern occurring every 15 to 20 minutes.The infant may initially be comfortable and play normally between the paroxysms of pain; but if the intussusception is not reduced, the infant becomes progressively weaker and lethargic.. Eventually a shocklike state may develop with fever. The pulse becomes weak and thready, the respirations become shallow and grunting, and the pain may be manifested only by moaning sounds.Vomiting occurs in most cases and is usually more frequent early. In the later phase, the vomitus becomes bile stained.Stools of normal appearance may be evacuated during the first few hours of symptoms. After this time, fecal excretions are small or more often do not occur and little or no flatus is passed. Blood generally is passed in the first 12hr but at times not for 1–2 days and infrequently not at all; 60% of infants pass a stool containing red blood and mucus, the currant jelly stool. Palpation of the abdomen usually reveals a slightly tender sausage-shaped mass, sometimes ill defined, most often in the right upper abdomen,. About 30% of patients do not have a palpable mass. P.R: The presence of bloody mucus on the finger as it is withdrawn after rectal examination supports the diagnosis of intussusception. Abdominal distention and tenderness develop as intestinal obstruction becomes more acute. On rare occasions, the advancing intestine prolapses through the anus.Diagnosis:
The clinical history and physical findings are usually sufficiently typical for diagnosis. Laboratory and Imaging Studies : Plain abdominal radiographs may show a density in the area of the intussusception. Ultrasonography is a sensitive diagnostic tool in the diagnosis of intussusception. A barium enema shows: coiled-spring signabdominal radiograph, showing a soft tissue mass (arrow heads) to the right of the midline
coiled-spring sign
doughnut or target appearanceTreatment
Admission: Therapy must begin with placement of an IV fluid and a nasogastric tube Surgical consultation should be obtained early . Reduction of an acute intussusception is an emergency procedure and performed immediately after diagnosis with preparation for possible surgery. Reduction in the theater either by : Nonoperative reduction pneumatic reduction Hydrostatic reduction If reduction is not complete, emergency surgery is required. Surgery The surgeon attempts gentle manual reduction, But may need to resect the involved bowel after failed reduction because of severe edema, perforation, a pathologic lead point (polyp, Meckel diverticulum), or necrosisManual Reduction
PROGNOSISUntreated intussusception in infants is almost always fatal; the chances of recovery are directly related to the duration of intussusception before reduction. Spontaneous reduction during preparation for operation is not uncommon.The recurrence rate after reduction of intussusceptions is ≈10%, and after surgical reduction it is 2–5%; none has recurred after surgical resection .Corticosteroids may reduce the frequency of recurrent intussusception.