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chapter 12 Surgical Assessment of the Abdomen
Michael Giacomantonio
When unsure of the diagnosis, take the history again.
When you examine the abdomen of an infant or child, you need a clear understanding of the anatomic structures and physiologic phenomena involving the abdomen and its contents. In addition, special clinical skills are required to evaluate a child of any age with abdominal distress.
Abdominal symptoms can be manifestations of clinical problems that originate outside the abdomen, including various systemic and thoracic conditions (e.g., lower lobe pneumonia). Applying your knowledge methodically to the evaluation and management of a child with abdominal distress should allow you to diagnose most conditions correctly.
This chapter highlights clinical situations with which you should be familiar and offers some practical insights that should help you acquire the necessary clinical skills to evaluate a child with abdominal distress. It also includes selected topics that are encountered as part of the thorough evaluation of the abdomen and its related anatomical areas.
Key Point
The history is ultimately the story of the pathophysiology of the problem.
Most neonatal abdominal problems develop as a result of adapting to extrauterine life. Therefore, rather than defining the neonatal period as the first month corrected for gestational age, defining it as the first month of life ex-utero is more appropriate.
In necrotizing enterocolitis (NEC), which is a potentially serious disorder, a sequence of events combine in newborns (usually in those who are premature) to stress the infant bowel. Under stress of any kind, blood is shunted from less vital to more vital organs, threatening the infant’s gastrointestinal (GI) tract (the autonomic stress reflex). The tiny, highly reactive vessels of the GI tract allow the stress reflex to shunt blood away from the infant gut, particularly in the ileocecal region (furthest from the central vascular system), causing ischemic injury of the bowel to occur. This process, in turn, exposes deeper layers of the bowel wall to the enteric contents. The combination of ischemic injury and contamination by bowel contents can lead to bowel wall infection, progressive transmural injury, and, ultimately, necrosis and perforation. When the infant is fed, the added metabolic demands of digestion on an already ischemic bowel can further aggravate mucosal injury and accelerate the cascade of bowel wall injury. Premature infants are especially vulnerable to this sequence of events.
Feeding a stressed premature infant is a set-up for necrotizing enterocolitis.
Understanding the threat of this triad (i.e., prematurity, feeding, and stress) is essential when trying to prevent progression to severe bowel injury and perforation. The earliest clinical signs are those of bowel dysfunction, that is, unexpected abdominal distention and feeding intolerance. Plain abdominal radiographs may show early evidence of ileus, which should trigger an aggressive effort to prevent progression by putting the gut to rest, that is, by stopping feeding, initiating nasogastric decompression, and administering a broad-spectrum antibiotic. If the subtle early signs of ileus are missed and ischemic mucosal injury leads to sloughing and bleeding, bloody bowel movements may be seen, and with further progression, transmural injury and perforation can occur. Early transmural injury may be accompanied by pneumatosis intestinalis (air within the bowel wall), which can be seen on plain abdominal radiographs. Serial radiography may identify further signs of progression. Unremitting sepsis and bowel perforation are indications for surgical intervention.
While managing infants with NEC usually involves neonatologists and pediatric surgeons, general pediatricians and family physicians may be involved in the care of such infants. Awareness of the threat, timely evaluation, and intervention can make a big difference in the outcome.
Malrotation can occur when the midgut fails to position itself normally within the abdomen. As a result, the retroperitoneal attachments of the midgut, which usually extend from the fourth part of the duodenum to the ileocecal area, are narrow, resulting in close approximation of the duodenum and cecum. This phenomenon allows the midgut to hang from its pedicle at the level of the second part of the duodenum. This pedicle includes the cecum, duodenum, and superior mesenteric vessels. Midgut ischemia can be life-threatening.
Early in its progression, a volvulus, twisting around the second part of the duodenum, will lead to both duodenal and vascular obstruction, which is venous at first and later arterial, resulting in bilious vomiting—the typical presenting clinical feature. Progressive volvulus will cause venous obstruction first and then arterial obstruction, with subsequent clinical features of discomfort. At first, an affected infant may show no discomfort other than bilious vomiting, but that single feature demands immediate action. Plain abdominal radiographs may show no abnormality early in the process. However, an experienced pediatric radiologist looking specifically at the proximal duodenum may recognize the volvulus, which typically appears as a corkscrew type of partial duodenal obstruction. If this critical feature is missed, contrast in the more distal upper small bowel may appear entirely normal, and the diagnosis may be missed.
Malrotation with midgut volvulus requires urgent surgical intervention to untwist the bowel and separate the duodenum and ileocecal area sufficiently to minimize the risk of an anatomic pedicle at the mesenteric vessel level that could lead to recurrence of the volvulus.
Bilious vomiting in a newborn demands a full explanation.
Duodenal atresia or stenosis are simply different degrees of the same abnormality. They usually occur at the level of the ampulla of Vater and are thought to be a result of compromised development of the segment of the duodenum where the ventral anlage of the pancreas develops and rotates to join its posterior segment. Thus, it can occur in association with an annular pancreas, resulting in a partial or complete duodenal obstruction. The annular pancreas in this situation is incidental and not clinically significant. A significant proportion of affected infants also have Down syndrome (trisomy 21). Prenatal diagnosis of both conditions is now possible.
Postnatally, duodenal stenosis or atresia causes feeding intolerance and vomiting, which may be bilious or nonbilious, depending on where the obstruction is in relation to the ampulla of Vater. Diagnosis is usually made with a radiograph of the abdomen with the infant upright, demonstrating the classic “double-bubble” sign. This sign is the result of dilation of both the stomach and the proximal duodenum, each being partially filled with fluid, and thus demonstrating two air fluid levels. Immediate surgical correction is required.
Intestinal atresia is thought to result from an in-utero vascular accident in a mesenteric segment of the bowel beyond the duodenum, causing loss of a segment of bowel, with sealing of the ends of the remaining bowel. A membrane may develop between the proximal (obstructed) segment and distal (unused) bowel segment. In severe cases, the vascular insult can result in loss of a significant segment of bowel between the proximal (atretic) and distal (unused) bowel. When this phenomenon occurs in utero, continuing fetal bowel function leads to bulbous distention of the proximal obstructed segment. The infant presents with abdominal distention, with or without bilious vomiting. Plain abdominal radiographs demonstrate obstruction and a bulbous proximal dilated bowel. Management is surgical, anastomosing the proximal dilated and distal unused segments to restore bowel continuity. The outcome varies but is usually favorable, depending on the amount of bowel lost.
Meconium ileus is a congenital small bowel obstruction caused by plugging of the distal small bowel with meconium. Most infants with meconium ileus are found to have cystic fibrosis on subsequent investigation or neonatal screening. Such infants present with signs of distal bowel obstruction—that is, abdominal distention and possibly bile-stained vomiting. Plain abdominal radiographs demonstrate the obstruction. Management may be nonsurgical if it is possible to promote (with contrast enemas) the wetting and loosening of the meconium plug to allow its spontaneous passage. If the promotion of spontaneous passage is not possible, surgical intervention is required.
Hirschsprung disease results from incomplete development of the distal enteric nervous system in the large bowel. The result is an absence of peristalsis and loss of reflex relaxation of the distal affected bowel, creating a functional partial large bowel obstruction. The rectum is the usual area involved, but it can extend to include the sigmoid or more proximal colon. In extreme cases, it can involve most of the colon. Histologically, there is an absence of ganglion cells in the affected bowel, and thus the disorder also is referred to as aganglionosis. The usual clinical presentation includes failure to pass meconium during the first 2 days of life in an otherwise normal full-term infant, with subsequent evidence of partial or complete distal bowel obstruction.
Failure to pass meconium spontaneously within the first few days of life should raise concerns of possible aganglionosis.
When Hirschsprung disease is suspected, a contrast enema should be performed, in which one looks specifically for an inverse ratio between the diameter of the rectum and that of the sigmoid colon. Normally, the rectal diameter is larger than that of the more proximal sigmoid colon; that is, the normal rectosigmoid ratio is greater than 1. (Note that the contrast enema must be done with isotonic [NOT hyperosmotic] contrast material, because instillation of hyperosmotic material into a colon that cannot evacuate may draw fluid into the colon, causing severe hypovolemia.)
Diagnosis is confirmed by a distal rectal biopsy to demonstrate the absence of ganglion cells and the presence of hypertrophied nerves.
Management requires distal intestinal decompression, resection of the aganglionic segment of distal bowel, and anastomosing the proximal (normally innervated) bowel to the area just above the anus.
Imperforate anus is part of a spectrum of anal maldevelopment. In its mildest form, anal stenosis can occur. In its most severe form, the anus is absent. In embryologic development, the most distal (endodermal) portion of the GI tract blends precisely within the complex anal muscular apparatus (a product of the ectodermal layer). If the GI tract does not end precisely within the anal muscular structures, it usually ends in a fistulous tract anterior to its normal relationship to the anus. The more anterior the fistula, the more severe the maldevelopment. In male infants, such a fistula can occur at the anterior aspect of the anal dimple, anteriorly along the perineum, or internally, along the posterior aspect of the urologic structures, such as the posterior urethra or even higher. In female infants, the fistulous opening can occur, as in male infants, along the perineal raphe or along the posterior aspect of the vagina. The most common fistula in female infants is at the posterior fourchette of the vagina, just distal to the hymenal ring.
As with any embryologic event that compromises normal development, more than one system may be involved. Thus, imperforate anus may occur in association with a constellation of abnormalities, referred to as the VACTERL syndrome, a mnemonic for Vertebral, Anal, Tracheal, Esophageal, Renal and Radial Limb syndrome. Therefore, any infant with imperforate anus must be carefully assessed for associated abnormalities.
The outcome for such infants is usually good, although reconstruction can compromise anorectal function. Most children who have had surgical correction require bowel management programs to assist with evacuation and fecal continence. Aggressive bowel management can help minimize the social stigmata of fecal incontinence.
Careful inspection of the anal and perineal area of newborns is an important part of the newborn’s initial examination.
An omphalocele results from a failure of complete closure of the abdominal wall around the umbilical structures. Small omphaloceles represent incomplete closure of the abdominal wall so that an amniotic membrane remains at the umbilical site from which the umbilical vessels extend. Surgical repair is easily accomplished.
Larger (giant) omphaloceles also represent incomplete closure of the abdominal wall, with the central area having an amniotic covering from which the umbilical vessels emanate. In giant omphaloceles, the amniotic membrane covers a significant portion of the central abdominal cavity. In infants with a giant omphalocele, it is believed that the abdominal wall, although seemingly fully developed, is inadequate to contain the otherwise normal abdominal viscera. Management often requires a staged repair.
Here, too, it is important to look for associated congenital abnormalities, particularly in the cardiovascular system.
Outcome depends on the size of the omphalocele and/or associated anomalies. Infants with giant omphaloceles may require multiple interventions, and prognosis is more guarded.
Gastroschisis represents an in utero developmental defect in which a significant portion of midgut, including small bowel and proximal colon, extrudes through the abdominal wall to the right of the umbilical cord.
In infants with gastroschisis, the bowel is at risk of injury from exposure to amniotic fluid and from twisting of the bowel at its mesentery. Fortunately, vascular compromise is rare; however, inflammation of the bowel is common because of exposure within the amniotic fluid.
The clinical priority is to protect the bowel with gauze soaked in saline solution, covering it with a plastic membrane to minimize evaporative heat and water loss. The infant usually is placed on the right side, because the defect typically is to the right of the umbilical cord, and the bowel is propped up to avoid traction at the mesentery. The infant will require transfer to an appropriate facility for evaluation and surgical intervention. Prenatal diagnosis of this condition is now possible, with transfer of the expectant mother for delivery at a facility that can provide appropriate care for the infant.
The outcome is usually favorable if the bowel has not been significantly compromised. Most affected infants have some swelling of the bowel due to inflammation caused by exposure within the amniotic fluid. Resolution of edema and inflammation usually occurs over a few days following repair of the defect. In a few infants, however, inflammatory injury of the bowel can be sufficiently severe that functional bowel loss can be a significant threat. Associated anomalies with gastroschisis are no more common than in the general population.
Inguinal hernias are not uncommon in neonates, especially in premature infants and in male neonates. These hernias result from persistent patency of the processus vaginalis and often are asymptomatic. Premature infants with an inguinal hernia that remains asymptomatic often can wait until they are older to have the hernia repaired when administration of an anesthetic is less of a risk. The risk of postanesthetic apnea is a very real concern in newborn infants, especially premature infants, and this risk persists until after approximately 3 months corrected gestational age.
Asymptomatic hernias in neonates should be left alone and repaired electively after 3 months corrected gestational age.
Symptomatic hernias, that is, those causing irritability and those that include episodes of incarceration, demand more urgent attention.
In a premature infant it may be difficult to determine whether a hernia is causing discomfort, but when an inguinal hernia is present, it is reasonable to question if it is an aggravating factor. If the baby seems completely comfortable in spite of what looks like a large hernia, it is best to wait until the optimal time for repair (i.e., after 3 months corrected gestational age). Do not reduce an asymptomatic distended scrotum and inguinal area repeatedly. This procedure will cause unnecessary discomfort, and the hernia often reappears immediately after reduction.
On the other hand, if the baby seems symptomatic—for example, showing unexplained irritability—then reduction is appropriate. When incarceration occurs, careful reduction is absolutely required, and surgical repair is urgent.
Pyloric stenosis is caused by hypertrophy of the pyloric musculature, resulting in partial gastric outlet obstruction. It has a tendency toward familial occurrence. Most affected infants present clinically between the third and fifth week of life with “spitting up” that progresses to projectile vomiting of nonbilious material in an otherwise healthy infant.
Emesis of chloride-rich gastric contents, combined with the inability to consume an adequate amount of fluid, can lead to dehydration and metabolic alkalosis due to the hypochloremia. Thus hypochloremic metabolic alkalosis with possible hypokalemia and paradoxical aciduria are typical of this condition.
Diagnosis can be confirmed unequivocally by palpating the thickened musculature that feels like an olive in the upper abdomen to the right of the midline, which is best palpated from the infant’s left side. The “olive” often can be difficult for inexperienced clinicians to palpate, and because modern abdominal ultrasound technology is so accurate with regard to diagnosis of pyloric stenosis, it frequently is used to confirm the diagnosis.
Following correction of fluid and electrolyte disturbances, treatment is by surgical pyloromyotomy. The thickened musculature is divided along its entire length to relieve the luminal obstruction. This procedure allows the pylorus to relax, and when healing is complete, the muscle often returns to a normal state, as does gastric function.
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