2.1.1. Gastric volvulus
Gastric volvulus is a rare, potentially life‐threatening condition . It may be defined as an abnormal rotation of one part of the stomach around another; the degree of the torsion varies from 180° to 360° and is associated with closed‐loop obstruction and the risk of strangulation.
220.127.116.11. Clinical features
Clinical features depend on the degree of rotation and obstruction. Persistent regurgitation and vomiting (sometimes unproductive) are common. The vomiting may or may not contain bile, depending on pyloric obstruction. Hematemesis and anemia are well described in this disease.
Plain abdominal pain and chest X‐rays are essential. A distended stomach in an abnormal position should suggest the possibility of gastric volvulus.
Contrast studies clarify the anatomy and the site of obstruction, which is usually at the pylorus, giving a so‐called “beak” deformity.
Acute gastric volvulus requires appropriate resuscitation and urgent surgery if ischemic necrosis and gastric perforation are to be avoided.
If possible, the stomach should be decompressed preoperatively by nasogastric suction but vigorous attempts to pass a tube must be avoided because of a risk of gastric perforation.
2.1.2. Gastric perforation
Gastric perforation in neonates can be broadly categorized as spontaneous (idiopathic), ischemic, and traumatic; however, in many instances, the etiology may be multifactorial .
Neonatal gastric perforation can occur in full‐term, premature, and small gestational age neonates.
Traumatic perforation results from pneumatic distention during mask ventilation, positive‐pressure ventilation, or iatrogenic injury during gastric intubation.
18.104.22.168. Clinical features
The majority cases present within the first 7 days of life. The neonates are often premature or have a history of asphyxia or hypoxia. They may present with feeding intolerance or emesis (sometimes bloody). Many develop abrupt onset of rapidly progressive abdominal distention.
The abdomen may rapidly become tense and tender with signs of peritonitis. Subcutaneous emphysema in the abdominal wall or pneumoscrotum may be perceived.
In infants with massive pneumoperitoneum, a plain abdominal X‐ray will demonstrate air under the diaphragm. Other plain X‐ray findings include subcutaneous emphysema, ascites, pneumoscrotum, or an oro‐nasogastric tube outside the confines of the stomach.
Open exploration (or laparoscopic) and repair is the essential part of treatment. However, infants with gastric perforation develop septic parameters and need to be well resuscitated preoperatively (respiratory supports, hydration, and broad spectrum antibiotics).
2.1.3. Duodenal obstruction
Congenital duodenal obstruction is the most common cause of intestinal obstruction in the newborn period .
Duodenal obstruction is the result of intrinsic lesions (atresia, stenosis, and “windsock” web), extrinsic lesions (annular pancreas, malrotation, preduodenal portal vein), or a combination of both.
22.214.171.124. Clinical features
About half of these patients are premature and have low birth weight. Vomiting is the most common symptom and is usually presented in the first day of life. There is minimal or no abdominal distension. The neonate may pass some meconium in the first 24 h of life.
The diagnosis of duodenal obstruction is confirmed on X‐ray examination. An abdominal X‐ray will show a dilated stomach and duodenum (double‐bubble sign), with no gas beyond the duodenum. In partial obstruction, there is usually some air in the distal intestine.
In some cases of partial duodenal obstruction, plain films may be normal. Upper gastrointestinal tract contrast X‐ray is indicated in these patients to establish the diagnosis.
Although duodenal atresia is a relative emergency, the patient should be hemodynamically stable preoperatively. Duodenoduodenostomy is the preferred procedure for patients with duodenal atresia.
2.1.4. Malrotation and midgut volvulus
Malrotation is the term used to denote an interference with normal process of orderly return of the fetal intestine from the physiological hernia to the abdominal cavity during which it undergoes systematic rotation and fixation .
126.96.36.199. Clinical features
Fifty‐five percent of malrotations present within the first week of life and 80% in the first month. Recurrent episodes of subacute obstruction with intermittent bilious vomiting are the main symptoms in neonatal period.
Strangulating intestinal obstruction as a consequence of midgut volvulus can present as bile‐stained vomiting, which may contain altered blood, abdominal distension and tenderness, the passage of dark blood per rectum, and shock. As the strangulation progresses to gangrene, perforation and peritonitis become evident.
The plain abdominal X‐ray in the infant with midgut volvulus typically shows a “gasless” appearance with air in the stomach and duodenum. Contrast studies are diagnostic (upper gastrointestinal contrast study). It shows the abnormal configuration of duodenum, (deviation of duodenojejunal junction to the right of midline). When volvulus has occurred, the duodenum and jejunum show a “corkscrew” appearance.
Ultrasonography to determine the relationship between the superior mesenteric vein (SMV) and the superior mesenteric artery (SMA) has been advocated.
The operative correction of a malrotation should be regarded as a surgical emergency. Neonates presenting with acute strangulating obstruction as a result of midgut volvulus require a short period of intensive resuscitation preoperatively.
The volvulus occurs around the base of the narrowed midgut mesentery. The twist occurs in a clockwise direction and is untwisted by counter‐clockwise rotation. In patients with extensive intestinal gangrene, frankly necrotic bowel should be resected and the bowel ends either tide off or stomas fashioned with a view to a second‐look laparotomy in 24–48 h later.
In uncomplicated malrotation, Ladd's procedure (division of extensions of peritoneal folds across the bowel) is the preferred treatment.
2.1.5. Jejuno-ileal atresia
Jejuno-ileal atresia, defined as a congenital defect in continuity of the bowel, is a common cause of intestinal obstruction in the newborn .
188.8.131.52. Clinical features
Jejunoileal atresia presents clinically as neonatal intestinal obstruction with persistent bile‐stained vomiting. Abdominal distension is frequently present. Constipation is usually not absolute and the meconium passed.
Plain abdominal X‐ray will reveal distended small bowel loops and air‐fluid levels. When the abdominal X‐ray suggests a complete obstruction, a contrast enema may be performed to exclude colonic atresia. The classical appearance of the colon distal to jejunoileal atresia is an-used or microcolon.
The operation should not be delayed unduly as there is always a danger of further infarction of the bowel. The main surgical treatment in jejunoileal atresia is resection and anastomosis of bowel ends.
2.1.6. Meconium ileus
Meconium ileus is an early manifestation of cystic fibrosis (CF) due to abnormal, inspissated, and viscid mucus of intestinal origin. In children, the impacted meconium produces an intraluminal obstruction occurring in the mid‐ileum, leading to a progressive abdominal distention, intestinal volvulus, atresia, gangrene, perforation, peritonitis with abdominal calcifications, and meconial pseudocyst .
184.108.40.206. Clinical features
A family history of cystic fibrosis is clearly evident in 25% of patients. Main symptoms include abdominal distension, bilious vomiting, and delayed passage of meconium. Meconium ileus can be recognized clinically as two different conditions: a simple, uncomplicated type not requiring surgery and a complicated, severe type.
In the first type, symptoms of a distal ileal obstruction are seen not later than 48 h after birth. These generalized abdominal distention, bilious vomiting, and no stool.
In the second type, the progressive abdominal distension may culminate in respiratory distress. If a perforation occurs, a pneumoperitoneum and sepsis will be the unfavorable consequences.
Sometimes, the onset is directly with meconium peritonitis, which could involute in a giant meconial pseudocyst.
A water‐soluble contrast enema is useful for both diagnosis and therapeutic purposes. Contrast enema shows microcolon appearance and pellets in terminal ileum.
The first step of treatment includes medical management, such as nasogastric tube decompression, antibiotics, correction of dehydration, and contrast enema with water‐soluble contrasts (Gastrografin, Golytely, N‐Acetylcysteine).
When medical treatment is unsuccessful in spite of an uncomplicated meconium ileus, surgery is mandatory, and an open evacuation, resection, and ileostomy are the possible options.
The indication of operation for newborns with meconium peritonitis is a clear sign of intestinal obstruction or perforation. Infants with neonatal meconium calcifications, meconium ascites with hydrocele, or calcified meconium found in the hernia sac do not require operation.
2.1.7. Necrotizing enterocolitis (NEC)
NEC is the most common medical and surgical emergency affecting the gastrointestinal tract of infants in the neonatal intensive‐care unit (NICU) . Multiple risk factors that have been implicated in the pathogenesis of NEC include prematurity, hypoxia, initiation of enteral feeding, congenital heart disease, and bacterial infection. The majority of cases develop in infants less than 36 weeks of gestational age.
NEC is characterized by intestinal inflammation and mucosal destruction. In its most severe form, NEC is characterized by full‐thickness necrosis, intestinal perforation, peritonitis, sepsis, and death.
|Grade 1 ||Mild systemic signs (apnea, bradycardia, and temperature instability)|
|Mild intestinal signs (abdominal distension, gastric residual, And occult blood in stool)|
|Grade 2 ||Mild‐to‐moderate systemic signs|
|Additional intestinal signs (absent bowel sounds, abdominal tenderness)|
|Radiologic signs (pneumatosis intestinal, portal venous air)|
|Laboratory changes (metabolic acidosis, thrombocytopenia)|
|Grade 3 ||Severe systemic illness (hypotension, shock)|
|Intestinal signs (large abdominal distension, abdominal wall discoloration, peritonitis, perforation)|
|Severe radiologic signs (ascites, pneumoperitoneum)|
|Progressive laboratory derangement (metabolic acidosis, DIC)|
220.127.116.11. Clinical features
NEC may present as feeding intolerance, abdominal distension, bloody stool, hypoxia, and shock. The bell criteria (Table 3) allow for categorization of the severity of NEC for treatment guidelines.
Laboratory abnormalities in NEC include thrombocytopenia, leukocytosis or leukopenia, metabolic acidosis, hypercapnea, and hypoxia.