Life-threatening emergencies calling for surgical intervention are a major cause of morbidity and mortality in the newborn. It is important for pediatricians to recognize the signs of emergencies requiring prompt surgical treatment and institute immediate lifesustaining measures, immediate consultation with a pediatric surgeon will be required in such cases, and often this will necessitate transferring the infant to a tertiary-care unit.
At times, the signs of an illness that does not require surgical intervention will mimic those of an illness that does. When there is uncertainty, consultation with a pediatric surgeon is warranted.
In the following article we propose to discuss those respiratory, gastrointestinal, and genitourinary abnormalities in the neonate that require prompt surgical intervention, indicate the signs that will alert the pediatrician to their presence, and comment on expected prognosis.
Among the life-threatening emergencies in the newborn are simple and tension pneumothorax, pneumohydrothorax, pneumomediastinum, lobar emphysema, and diaphragmatic hernias.
Pneumothorax. Pneumothorax is not an uncommon finding in the neonate. It may be related to airway-pressure changes occurring postnatally, or to vigorous resuscitative measures, or to meconium aspiration. Pneumothorax is a major complication of assisted ventilation, especially in the presence of a noncompliant lung.
Small pneumothoraces usually either are asymptomatic or present with minimal cardiorespiratory signs. When there is a larger amount of intrapleural air, tachycardia, tachypnea, cyanosis, flaring of the ala nasi, and substernal retractions may be observed. Breath sounds on the affected side may be decreased. A significant mediastinal shift is unusual.
Simple pneumothorax. A minor simple pneumothorax without significant clinical signs rarely requires aspiration or tube thoracostomy. Administration of supplementary oxygen will usually relieve the minor signs that are present.
When pneumothorax is followed by more serious signs, treatment with tube thoracostomy is required. This is especially true if the infant is receiving assisted ventilation.
The possibility that another pneumothorax may develop on the contralateral side should be kept in mind, since this could drastically increase the signs of respiratory distress.
Chest x-rays should be taken immediately whenever a diagnosis of pneumothorax is suspected.
Tension pneumothorax. In contrast to the slowly developing simple pneumothorax, with its minor signs of respiratory distress, a tension pneumothorax requires prompt treatment. Clinical signs can develop rapidly and often will require treatment before radiologic verification can be obtained.
SURGICAL EMERGENCIES IN THE NEONATE
When a tension pneumothorax occurs, there is a sudden expansion of intrathoracic air, with secondary mediastinal shift and compression of the contralateral lung; this decreases respiratory function of both lungs and diminishes cardiac return. The clinical signs consist of absent breath sounds on the affected side and a mediastinal shift to the contralateral side (Figure 1).
When the differential diagnosis is made, other space-occupying lesions (such as congenital diaphragmatic hernia - the posterolateral "Bochdalek" type - lobar emphysema, bronchogenic cyst, and pneumohydrothorax) should be ruled out. Clinical signs in infants with a posterior congenital diaphragmatic hernia may be identical to those of a tension pneumothorax, but in the herniated infant the abdomen is usually scaphoid. In children with lobar emphysema or lung cyst, signs usually develop at a slower rate than in those with tension pneumothorax.
When tension pneumothorax is suspected in an infant, immediate therapy and verification of the diagnosis can be accomplished by inserting a needle into the thoracic cavity, with aspiration of air. If the air is under pressure, tension pneumothorax has been established, and tube thoracostomy should follow immediately. Simple underwater drainage usually is sufficient for the infant with simple pneumothorax, but suction will usually be required for the infant with a tension pneumothorax in order to expand the lung.
Figure 1. Tension pneumothorax. Collapse of the right lung, with mediastinal shift to the left, can be seen on the radiograph. Such a tension pneumothorax results in the compression of the left lung, leading to marked respiratory distress and requiring prompt evacuation of the trapped air on the right side.
Pneumohydrothorax. Esophageal perforation in the neonate leads to sudden respiratory distress, which can be difficult to differentiate from tension pneumothorax. The combination of hydro- and pneumothorax differentiates it from chylothorax. It usually occurs on the right side. It may be either caused by trauma or secondary to sudden pressure changes at birth.2 Prompt tube thoracostomy and esophageal repair are essential.
Insertion of pharyngeal catheters, nasogastric tubes, and endotracheal tubes (especially when used with an indwelling metal stylet) may result in perforation of the pharynx. All of these procedures must be performed gently in small premature infants. Once such a pharyngeal injury is confirmed, conservative management with systemic antibiotics is usually sufficient. A tube gastrostomy under local anesthesia will solve the feeding problem and prevent further damage to the pharynx.3
Pneumomediastinum may be either simple or of the tension type. It usually follows the dissection of air along blood vessels into the mediastinum and is frequently combined with a pneumothorax. While tension pneumomediastinum rarely reaches the extent of a tension pneumothorax, drainage and evacuation of the air are occasionally indicated to relieve signs associated with the increased pressure.
There is recent evidence that genitourinary-tract anomalies occur with increased frequency in infants with spontaneous pneumothorax and pneumomediastinum.4 Therefore a careful investigation for such anomalies should be carried out in these infants.
Diaphragmatic hernias. The clinical signs of posterolateral diaphragmatic hernias often mimic those of tension pneumothorax. However, a scaphoid abdomen, due to presence of abdominal contents in the thoracic cavity, may point to the correct diagnosis.
The most severely affected infants show signs of severe respiratory distress immediately after birth because of hypoplasia (and often immaturity) of both the ipsilateral and contralateral lung. Mortality is highest in this group of infants when they have a very early onset of clinical signs. Less severely affected infants may be asymptomatic at birth. However, swallowing of air will cause distention of the intrathoracic intestine, with compression of first the ipsilateral and then the contralateral lung (Figure 2).
The immediate insertion of a nasogastric tube is required to prevent further intestinal dilatation. Immediate operative intervention, through an abdominal approach, with replacement of viscera into the abdominal cavity, is essential. Since the abdominal cavity is often small, primary closure of all layers of the abdominal wall may lead to excessive pressure on the diaphragm and renewed respiratory distress. Delayed closure, by either simple closure of skin or a Silastic covering (as is used in the treatment of omphalocele), is often required. If the clinical condition is complicated by a patent ductus arteriosus, ligation or pharmacologic closure with indomethacin is indicated.6
Lack of diaphragmatic movement may be secondary to either eventration (thinning) of the diaphragm or phrenic nerve paralysis. Abnormal respiratory signs may be slow to develop in these conditions, with operative intervention required (if at all) only after days or weeks.
Lobar emphysema. Signs of lobar emphysema (which usually involves the right upper or middle lobe) are similar to those of tension pneumothorax but develop more slowly. The insertion of a needle in an attempt to relieve a suspected tension pneumothorax will not harm the infant, and the lack of escaping air should suggest the correct diagnosis.
Figure 2. Diaphragmatic hernia. A left posterior lateral diaphragmatic defect, a "Bochdalek" hernia, has developed. Note small intestine in the left chest. Swallowed air, as outlined in stomach, leads to a distention of the intrathoracic intestine on the left side. Here it has resulted in a mediastinal shift to the right, with compression of the contralateral lung and severe respiratory distress.
The immediate treatment of an infant with advanced lobar emphysema consists of increased oxygenation, endotracheal intubation, and prompt operative intervention, with resection of the affected lobe. Some cases, however, will do well with conservative treatment.7
Ventilatory assistance. Many of these conditions requiring surgery are associated with hypoxemia, hypercarbia, and respiratory acidosis. Adequate ventilation and gastrointestinal decompression are vital in maintaining normal blood pH, oxygen (Po2) and carbon dioxide (PcO2) gas pressure levels. Sodium bicarbonate should be used with great caution in the presence of respiratory acidoses, since its administration may lead to a further accumulation of carbon dioxide.
Neonatal peritonitis, gastrointestinal perforation, necrotizing enterocolitis, Hirschsprung's enterocolitis, fetal ascites, intestinal obstruction or protrusion, esophageal and small-bowel atresia, meconium ileus, and meconium plug are among the gastrointestinal problems that may require immediate surgery in the neonate.
Neonatal peritonitis. Clinical signs of neonatal peritonitis may differ in the neonate, and its presence is much more difficult to detect than in the older child, even though the pathophysiology is similar. Abdominal guarding, presence or absence of bowel sounds, rebound tenderness, and referred tenderness are all difficult to determine in the neonate. The differential diagnosis between an adynamic ileus, intestinal obstruction, or peritonitis may be exceedingly difficult. With early peritonitis, the infant will resist an attempt to straighten out his legs. A continuous "fetal" position with knees drawn up may, therefore, be the first indication of peritonitis. With progressive peritonitis, the abdomen becomes "doughy" and the intraperitoneal fluid loss will lead to signs of hypovolemia.
Intravenous administration of isotonic fluids, gastrointestinal decompression, and a search for etiology are the first steps to be taken in treating these infants.
Gastrointestinal perforation. Spontaneous gastric perforation usually occurs at about the fourth or fifth day of life, often preceded by a history of stress or difficult delivery. While the cause of gastric perforation is unknown, it is thought to be related to a low-flow syndrome (the "diving reflex"), with local anoxia and necrosis, followed by perforation.8 The perforation, which is usually linear and extensive (Figure 3), leads to chemical peritonitis. Because of the large size of the gastric perforation, the infants are usually unable to vomit. The development of peritonitis and abdominal distention and the absence of vomiting are, therefore, clues to the diagnosis of gastric perforation.
Radiologic examination usually shows intraperitoneal free air, with the nasogastric tube outside the confines of the stomach. In contrast to distal intestinal perforation, especially necrotizing enterocolitis, there is usually a large amount of free air present, often with a typical "saddle-bag" deformity created by air around the liver (figure 4). In view of the often pronounced chemical peritonitis, a rapid hypovolemia develops, which requires immediate and continuous correction. Isotonic solutions, often in combination with colloid, are used at the onset of treatment. Prompt operative exploration and closure of the perforation after the infant is stabilized should lead to a survival rate of over 75 per cent in the absence of major coexistent problems.
Necrotizing enterocolitis. Necrotizing enterocolitis is usually observed in small and sick preterm infants who have required vigorous resuscitation and umbilical vessel cannulation. These infants have usually received an intravenous infusion of dextrose solution and an artificial formula rather than human milk.
Presenting signs vary widely, depending on the underlying extent and location of involvement. Gas develops within the intramural portion of the intestine, as in pneumatosis coli in older children and adults. In contrast tq pneumatosis coli, however, which is relatively harmless, intramural air in these infants represents a grave prognostic sign, especially if air advances through the portal system into the intrahepatic portal veins. Peritoneal signs accompany intestinal necrosis, which is usually diffuse and scattered, often leading to several sites of perforation. While the presence of intramural air is not uniformly accepted as indication for operative intervention, signs of peritonitis, especially with radiologic proof of perforation, are accepted as indications for operative intervention.9 Since enterocolitis is probably related to such factors as reduced perfusion and decreased oxygenation of the intestine, intestinal distention will further aggravate these conditions. The aim of both operative and nonoperative treatment should, therefore, be increased bowel perfusion and oxygenation, decrease of intestinal distention, control of bacterial flora, and prevention and treatment of sepsis.
Figure 3. Gastric perforation. Upper-gastrointestinal contrast study reveals a double density in the gastric area of this three-day-old. At operation, the serosa and muscularis of the stomach were necrotic, leading to distention and perforation of the distal gastric mucosa. Necrosis of the gastric mucosa had begun that would have eventually led to the typical longitudinal perforation in gastric perforation in the newborn.
Figure 4. Neonatal intestinal perforation. Sketch shows how perforation of a gastric ulcer in this five-day-old infant led to abdominal distention. Note "saddle-bag" deformity in x-ray, with free intraperitoneal air surrounding the liver. Fluid levels in the free peritoneal cavity indicate the marked isotonic fluid loss into the intraperitoneal space.
Intravenous administration of dextran may lead to decreased blood viscosity and increased perfusion.
If operative intervention is necessary, the necrotic areas are resected and enterostomies (several, if necessary) rather than anastomoses performed, to allow complete decompression of the intestine, followed by catheter installation of topical antibiotics.
In infants in whom the viability of the entire intestine is in doubt, only the completely necrotic portions of the intestine are removed. Re-exploration within 24 to 48 hours, with re-evaluation of the remaining intestine, may allow the salvage of intestine previously thought to be nonviable.
Disseminated intravascular coagulation is a frequent complication of necrotizing enterocolitis. Coagulation studies are vital if this condition is suspected.
Hirschsprung's enterocolitis. Failure to recognize and treat congenital megacolon in the early neonatal period (see section below on Hirschsprung's disease), may lead to a lifethreatening enterocolitis with alternating obstipation and diarrhea, with signs similar to those of necrotizing enterocolitis.
In contrast to necrotizing enterocolitis, there is no gas in either intestinal wall or portal veins. Free fluid and occasionally free peritoneal air may be present following a colonic perforation. Hypovolemia must be corrected with isotonic solutions and colloid. The colon is decompressed with colonic irrigations if there is no evidence of intestinal perforation. The irrigation fluid consists of an isotonic (half saline, half bicarbonate) solution containing a topical antibiotic. Rapid improvement is usually seen within 24 hours, and a colostomy can then be performed electively. However, if there is no evidence of improvement of the enterocolitis, prompt operative intervention with a diverting colostomy in the ganglionic area is indicated.
Ascites. Fetal ascites occurs in four forms: hemorrhagic ascites, urinary ascites, chylous ascites, and ascites associated with ovarian lesions.
Hemorrhagic ascites is the most common of the four types and also potentially the most dangerous.10 It is often found in infants who have had a difficult delivery or who have coexisting anomalies or are of unusually large size. Hemorrhagic ascites may develop as late as four days after birth; it may be revealed by sudden abdominal distention or signs of peritonitis, hypovolemia, or shock, with a drop of hematocrit. The most common cause of intraabdominal hemorrhage is either a rupture of a subcapsular hematoma of the liver or an actual tear of the liver secondary to birth trauma. Adrenal hemorrhage and splenic rupture may also cause intra-abdominal bleeding.
The combination of abdominal distention, signs of peritonitis, and hemorrhagic shock is an indication for immediate paracentesis and, if positive, prompt laparotomy. In infants with splenic rupture in whom repair is impossible and splenectomy must be performed, continuous penicillin treatment should be started in view of the high incidence of meningococcal and pneumococcal septicemia following splenectomy.11
Urinary ascites is usually associated with obstructive uropathy (especially posterior urethral valves). A prompt genitourinary-tract work-up and treatment of the underlying disorder is mandatory.
Chylous ascites is not usually helped by surgery, and intravenous hyperalimentation, with complete avoidance of oral food intake, is the primary therapy.
Volvulus. In infants with intestinal malrotation, the formation of a volvulus can lead to a vascular compromise of the entire small intestine and ascending colon. Compression of the superior mesenteric vein leads to venous congestion, followed by hemorrhage into the intestine and into the peritoneum. A gasless abdomen is present on x-ray.
Suspicion of volvulus necessitates an immediate barium enema, followed by prompt operative intervention if the diagnosis is confirmed. Failure to immediately recognize and treat this life-threatening condition leads to increased loss of intestinal viability and, in many instances, death of the infant.
Omphalocele and gastroschisis. Omphalocele is a central-abdominal-wall defect of the umbilicus. In the type with an intact peritoneal covering over the extra-abdominal viscera, conservative therapy will allow the skin to slowly cover the entire defect. With small defects, primary closure of the abdominal wall may be possible. In some instances, only skin closure is possible. In cases where the defect is covered only by skin (following either conservative treatment or operative skin closure) a ventral hernia is formed. This can be repaired electively when the abdominal cavity has grown enough to accept the viscera comfortably.
In very large defects or those with ruptured sacs or associated obstruction,13 a staged closure using a Dacron-reinforced Silastic "silo" over the protruding viscera has been successfully employed.
Some degree of intestinal malrotation is always present, and this may lead to obstruction at any time.
Gastroschisis is a congenital anomaly of the abdominal wall lateral to the umbilicus. In this condition, eviscerated abdominal contents never have a peritoneal covering. Treatment is the same as that for omphalocele. In most instances, however, primary repair is not possible.
Intestinal obstruction. Congenital intestinal obstruction occurs in two forms: atresia (nonperforated), indicating a complete lack of intestinal continuity due to a diaphragm or the absence of a segment of intestine, and stenosis, representing a narrowing of the intestine, leading to a partial or incomplete obstruction.
In high intestinal obstruction - e.g., duodenal atresia or esophageal atresia without a tracheoesophageal fistula, inability of the fetus to swallow and absorb amniotic fluid via its gastrointestinal tract often leads to hydramnios.
Bilious vomiting, which occurs with most intestinal obstructions below the ampulla of Vater, requires a prompt diagnostic work-up to rule out intestinal obstruction, although it may be also seen in infants with sepsis or peritonitis. Only in infants with an intestinal obstruction proximal to the ampulla, such as pyloric stenosis or gastric or esophageal atresia, is vomiting nonbilious. The color of the vomitus not only is a clue to the site of the obstruction but may also indicate the type of metabolic derangement and, therefore, be suggestive of the required fluid therapy. Loss of clear gastric fluid usually leads to hypochloremic metabolic alkalosis, while the loss of alkaline bile-containing fluid (from a point distal to the ampulla of Vater) will usually cause a metabolic acidosis.
Abdominal distention, present in infants with peritonitis, ileus, or low intestinal obstruction, should be immediately treated with nasogastric suction to decompress the dilated bowel. In infants with high intestinal obstruction - e.g., duodenal atresia - only the upper abdomen may be distended, with a scaphoid lower abdomen.
Esophageal atresia. Excessive salivation should point to the diagnosis of esophageal atresia. Respiratory distress, when present, is usually due to reflux of stomach contents into the lung through an associated tracheoesophageal fistula. Aspiration of secretions into the right upper lobe of the lung usually occurs late. Inability to pass a nasogastric tube past the obstruction confirms the diagnosis. Lack of gas in the gastrointestinal tract points to the absence of an associated tracheoesophageal fistula.
In most infants, repair of an esophageal atresia and tracheoesophageal fistula can be performed with a transpleural or retropleural approach, with anastomosis of the esophagus and simultaneous ligation or transection of the tracheoesophageal fistula. When a long segment is missing between upper and lower esophagus, a direct repair may be difficult and either prolonged stretching or a colonic interposition at a later date may be necessary.
In small premature infants, the operative repair may have to be staged and long-term gastrostomy feeding may be necessary. Associated anomalies are commonly seen. These include imperforate anus, absent radius, and renal and cardiac anomalies.14 The prognosis will depend on the type of defect, associated anomalies, and maturity of the infant.
Duodenal obstruction. Infants with duodenal atresia usually develop early bilious vomiting without abdominal distention. The presence of a "double bubble" sign on x-ray, with a gas-fluid level evident in the stomach and duodenum, is diagnostic. Hypotonic dehydration is common if the diagnosis is not made promptly. Common associated defects include Down's syndrome and cardiac defects. Duodenojejunostomy, duodenoduodenostomy, and the excision of the diaphragm are accepted operative procedures. In the absence of associated anomalies, survival should be close to 100 per cent.15
Small-bowel atresia. Small-bowel atresia most commonly affects the ileum and less frequently the duodenum or jejunum. Rarely is more than one site involved, and colonic atresia is extremely uncommon.
Since the colon cannot be identified radiographically in neonates without the use of contrast material, the exact site of a low intestinal obstruction cannot be definitively identified on a plain abdominal film.
Regardless of location, findings are identical: abdominal distention and bilious vomiting. In a high jejunal obstruction, a "triple bubble" sign can be present on abdominal x-ray. It is rarely necessary to use barium orally in the presence of upper intestinal obstruction, since air alone will usually identify the site of obstruction. In a child with "low" intestinal obstruction, a barium enema may be helpful, however. Not only can it rule out malrotation by identifying the site of the cecum, but the presence or absence of a microcolon (Figure 5) may be of help in estimating the level of obstruction. The presence of a microcolon usually indicates that the obstruction is at the level of the distal ileum, since only very low, small-intestinal obstruction leads to microcolon. This finding also rules out the possibility of colonic atresia.
The fluid loss in a low intestinal obstruction usually is isotonic and leads to an isotonic dehydration, with a mild to moderate metabolic acidosis, depending on the duration of fluid loss. After adequate hydration, operative repair is indicated as soon as possible. It can consist of either end-to-end anastomosis (with resection of the dilated end, if necessary) or anastomosis with side vents, such as the Santulli or Bishop-Koop modifications.16
Figure 5. Microcolon. Radiograph shows barium-filled microcolon, with additional distended loops of small intestine. The combination of distended loops in the small intestine and microcolon indicates that a distal small-intestinal obstruction is present. Microcolon is usually not seen in high smallintestinal atresia.
Meconium ileus. Meconium ileus is the neonatal manifestation of cystic fibrosis.* Findings range from simple mechanical obstruction to intrauterine perforation with single or multiple sites of atresia, intrauterine peritonitis, or meconium cysts. A positive family history is useful in establishing the diagnosis.17
In the infant with intestinal obstruction due to meconium ileus, the radiologic features consist of variably dilated loops of intestine with an appearance characteristic of soap bubbles. In the absence of atresia, the installation of either Gastrografin or acetylcysteine may preclude the need for surgery. The effect of Gastrografin is based on its hyperosmolarity, pulling fluid into the intestine, and the additional effect of Tween 80, a detergent. If Gastrografin therapy fails, operative intervention, with mechanical removal of the meconium, is indicated.
The diagnosis of cystic fibrosis can be verified with a sweat test. The latter does not become reliable, however, until the infant is about four to six weeks old. Extreme care should be taken to avoid pulmonary infection in the early postoperative period.
Meconium plug. Inspissated meconium, leading to colonic obstruction, can mimic either Hirschsprung's disease or meconium ileus. In contrast to meconium ileus, where the obstruction usually occurs in the ileum, the obstruction due to meconium plugs is found primarily in the colon. It usually responds to saline enema, but occasionally a Gastrografin enema may be necessary. An association with Hirschsprung's disease or cystic fibrosis has been reported, however, in 10 per cent of infants with meconium plugs. When persistent obstipation or constipation is still present even after the removal of what appears to be a simple meconium plug, both of these entities should be ruled out.
Hirschsprung's disease. The absence of ganglion cells, with both parasympathetic and sympathetic intestinal dysfunction, leads to organic obstruction, most commonly seen in the left colon. Occasionally the entire colon or intestine may be affected. The lack of propulsion leads to obstruction, with signs of constipation or obstipation. In the neonate, obstipation with alternating diarrhea is the most suggestive finding, with explosive fecal evacuation after rectal examination.
The most serious complication of Hirschsprung's disease is enterocolitis. In an infant with Hirschsprung's disease, abdominal distention develops, with radiologic findings of low intestinal obstruction. A barium enema, which should be performed without prior cleansing enemas, shows the aganglionic segment to be relatively narrow or normal, with dilatation of the proximal aganglionic segment. With complete aganglionosis, the colon may appear to be normal, except for shortening and incompletely formed splenic and hepatic flexures.
The diagnosis can be established by rectal manometric examination. Distention of the rectum is followed by relaxation of the internal sphincter in the normal infant. In infants with Hirschsprung's disease, internal sphincter relaxation does not occur. A rectal biopsy confirms the diagnosis of aganglionosis, and in most infants a colostomy, placed into the ganglionic intestine, is indicated. A final repair with various modifications of abdominal perineal pull-throughs can then be performed after approximately six to 12 months of age.18
Imperforate anus. Although the term suggests a simple atresia of the anus, over 80 per cent of all infants with an "imperforate anus" have a fistulous connection between the rectum and the perineum or the genitourinary system.19 It is beyond the scope of this article to go into the many technical details, but several points should be stressed:
1. It is essential to differentiate a "low" from a "high" anomaly, since the therapy and prognosis vary.
2. In infants with high anomalies, associated anomalies, especially of the genitourinary system, are extremely common.
3. The first repair is the decisive one, with inadequacy of the first operative procedure usually necessitating subsequent, often fruitless, repairs and possibly lifelong anal incontinence.
4. Children with high anomalies should not have definitive repairs under the age of one year (or weight of 20 pounds).
Both radiologic examination of the spine and careful inspection of the perineum are vital. A deficiency of more than three sacral segments on x-ray suggests a high anomaly and absence of the levator sling, which is associated with a poor prognosis.
An ectopic opening in the perineum or the posterior fourchette in girls usually permits primary dilatation, and a definitive operative repair can be postponed. In children without an apparent fistula, a genitourinary work- up and radiological identification of the level of the ectopic or "imperforate anus" is essential. A perineal injection of dye may be used to outline the level of the rectal pouch in relation to the pubococcygeal line. A pouch above this line will require an abdominal perineal procedure and a pouch below the level usually can be repaired through perineal approach. A final abdominal-perineal repair of a high anomaly should not be attempted before the age of one year, or 20 pounds of weight, to assure the best possible result.
Gastrointestinal bleeding The presence of blood in the gastrointestinal tract of the neonate may be secondary to aspiration of maternal blood, a coagulation disorder, or bleeding originating in the gastrointestinal tract. The alkali denaturation test can differentiate between maternal and fetal red-blood cells. If the bleeding has originated in the infant, a coagulation work-up is indicated. If a clotting disorder is present, immediate corrective steps must be taken. If the clotting mechanism is normal, the site of bleeding must be determined. If there is blood in the nasogastric aspirate, the source is likely to be either esophagus, stomach, or duodenum.
In contrast to peptic ulcers in older children, single duodenal ulcers as a source of bleeding are uncommon. Bleeding in infancy usually is the result of multiple ulcers, usually superficial, involving stomach, duodenum, and esophagus.
In the vast majority of infants, nonoperative treatment with antacids is successful. Overtransfusion should be avoided, as this may cause recurrence of bleeding. Bleeding may occasionally precede perforation, however. If any infant loses more than his total blood volume within a 24-hour period, operative intervention is indicated.
If the bleeding is gastric or duodenal, the most conservative procedure adequate to control bleeding should be employed. This is most often a combination of vagotomy and antrectomy. This procedure has been shown not to interfere with the development of the child. In infants with a single, isolated bleeding ulcer, suture ligation of the ulcer may be sufficient.
In the absence of upper-intestinal bleeding, rectal bleeding is most often associated with anal fissure or enteritis. Hemorrhage secondary to volvulus is a dire prognostic sign. Bleeding secondary to intestinal polyps or Meckel's diverticulum is very rare in early infancy. A combination of clinical signs and radiologic studies will usually point to the correct diagnosis.
The most common cause of rectal bleeding is an anal fissure, with bright red blood coating the outside of the stool rather than being mixed with the stool. Gentle dilatation of the rectum and stool softeners are usually adequate treatment.
While any organ system can give rise to abdominal masses in the neonate, they are most often of genitourinary origin.
Hydronephrosis is usually caused by ureteropelvic or ureterovesical obstruction or posterior urethral valves. Intravenous pyelography may reveal a nonfunctioning or poorly functioning kidney, with dilation of collecting systems. Immediate treatment consists of decompression of the involved kidney or kidneys. While posterior urethral valves should be resected in the neonatal period, definite correction of other underlying defects is usually delayed until a later date.
Multicystic kidneys are usually unilateral and feel lobulated on palpation. Intravenous pyelography shows nonfunction on the affected side. Nephrectomy is the treatment of choice.
Masses of gastrointestinal origin may be either symptomatic or asymptomatic. Duplications may arise from any portion of the gastrointestinal tract and are capable of causing intestinal obstruction. Surgical correction is based on both the location and type of duplication.
Mesenteric cysts, which usually arise in the mesentary of the small bowel, may cause partial intestinal obstruction. Treatment consists of surgical excision.
Neoplasms represent a very small proportion of abdominal masses in the neonate. These include teratomas, neuroblastomas, mesoblastic nephromas, and Wilms' tumors. Surgical excision (together with chemotherapy and radiation when the tumor is malignant) is the treatment of choice.
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SURGICAL EMERGENCIES IN THE NEONATE