bubble_chart Overview

Vomiting refers to the reflexive action where stomach contents and part of the small intestine contents move backward through the digestive tract and are expelled through the mouth, which is a manifestation of digestive tract dysfunction. A typical vomiting episode consists of three steps: ① Peristalsis begins in the gastric body and propagates downward, stopping at the gastric angular notch, where strong contractions occur, preventing the stomach contents from advancing further; ② The epiglottis closes, and the soft palate elevates, isolating the pharynx from the trachea and nasal passages; ③ The cardia opens, the esophagus relaxes, the diaphragm remains fixed in a deep inhalation position, and the abdominal muscles suddenly contract, forcing the stomach contents through the esophagus for expulsion. In newborns, vomiting is less typical compared to adults or children. It occurs immediately after birth and worsens after feeding, presenting as non-projectile vomiting. The vomitus is foamy and mucus-like, and if it contains blood, it appears as a coffee bean-colored liquid. Typically, within the first 1–2 days after birth, the swallowed amniotic fluid and birth canal contents are completely expelled, and vomiting ceases. If there are no other complications, the infant's general condition remains normal without cyanosis or choking. Mild cases do not require special treatment, while severe cases may be resolved with 1–2 gastric lavages using a 1% sodium bicarbonate solution.

bubble_chart Etiology

There are many diseases that can cause vomiting in newborns, such as improper feeding, irritation of the gastric mucosa, gastrointestinal dysfunction, infectious diseases of the intestines, central nervous system disorders, inherited metabolic diseases, and gastrointestinal developmental abnormalities, all of which can lead to vomiting in newborns. Some diseases, such as gastric perforation, vascular compression of the esophagus, annular pancreas, duplication of the digestive tract, incarcerated hernia, intussusception, and appendicitis, can also cause vomiting.

bubble_chart Pathogenesis

The vomiting center is located at the base of the fourth ventricle in the medulla oblongata. The afferent nerves mainly include the vagus nerve, splanchnic nerve, vestibular nerve, glossopharyngeal nerve, optic nerve, and olfactory nerve. The efferent nerves are the vagus nerve, splanchnic nerve, phrenic nerve, spinal nerves of the abdominal muscles, glossopharyngeal nerve, etc. Afferent impulses from the gastrointestinal tract and other organs stimulate the vomiting center, reflexively triggering a series of coordinated movements in the stomach, diaphragm, abdominal muscles, as well as the pharynx, palate, and epiglottis, thereby forming the vomiting action. The vomiting center is adjacent to the respiratory center, autonomic nerve center, salivary nucleus, and vestibular nucleus, so before and during vomiting, symptoms such as pale complexion, sweating, excessive salivation, and changes in pulse and respiratory rate often occur.

Newborns are more prone to vomiting than children. The common causes and clinical manifestations of vomiting in newborns differ from those in other age groups, primarily due to the characteristics of newborns: ① The esophagus of newborns is more relaxed, the stomach capacity is small and horizontally positioned, the pyloric sphincter is well-developed while the cardiac sphincter is underdeveloped, the neural regulation of intestinal peristalsis is poor, and the intra-abdominal pressure is relatively high—all of which are anatomical and physiological reasons for the higher incidence of vomiting in newborns. ② Abnormal differentiation and development of organs during the embryonic stage, especially anomalies in the foregut, midgut, and hindgut, can easily lead to malformations of the digestive tract, preventing ingested food or digestive secretions from passing smoothly through the intestines and instead being expelled orally, resulting in vomiting. ③ Stimuli during birth, such as swallowing large amounts of amniotic fluid or blood, as well as the drastic changes in the internal and external environment after birth, can also easily trigger vomiting in newborns. ④ The vomiting center in newborns is not fully developed and is more susceptible to stimulation by toxins produced by systemic inflammation or metabolic disorders, leading to vomiting.

The significance of vomiting lies in expelling harmful substances from the body, which can be protective under certain conditions. However, frequent and severe vomiting can lead to the loss of large amounts of digestive fluids. Newborns have poor regulation of water and electrolyte metabolism, making them prone to dehydration, electrolyte imbalances, and acid-base disturbances. Prolonged vomiting can result in malnutrition and growth retardation. Moreover, newborns have weaker gag reflexes, and during vomiting, they may even aspirate vomitus into the respiratory tract, leading to aspiration pneumonia and asphyxia, which pose significant risks to newborns and should be taken seriously by clinicians.

bubble_chart Clinical Manifestations

1. Milk regurgitation

Most infants experience some degree of milk regurgitation during the neonatal period. Milk regurgitation is not true vomiting, as it lacks the neuromuscular reflex processes associated with vomiting. It can occur shortly after birth, primarily manifesting as the reflux of 1–2 mouthfuls of milk into the mouth or spitting up after feeding. Changing the baby's position after feeding can also easily trigger milk regurgitation. The regurgitated content is mainly white milk, and if the milk has stayed in the stomach for a longer time, it may contain curdled milk. Milk regurgitation does not affect the infant's growth and development, gradually decreasing with age and typically disappearing by around 6 months of age. It is generally believed that milk regurgitation is caused by underdeveloped elastic and muscular tissues in the newborn's esophagus and does not require special treatment.

2. Uncoordinated swallowing

This is also not true vomiting. It is primarily seen in premature infants or those with cranial or cranial nerve disorders, resulting from neuromuscular dysfunction in the pharynx and uncoordinated swallowing. It manifests as frequent retention of secretions in the pharynx, with some milk entering the esophagus during swallowing while some flows out through the nose or mouth, and some entering the respiratory tract, potentially causing neonatal pneumonia. Premature infants usually recover spontaneously as their function matures over weeks or months. The prognosis for those with neurological injuries depends on the recovery of the nervous system itself.

3. Improper feeding

This accounts for about one-fourth of neonatal vomiting. Causes include feeding too frequently or in excessive amounts; nipple holes that are too large or too small, or inverted nipples, leading to the ingestion of excessive air; inserting the nipple too far into the mouth, irritating the pharynx; milk that is too hot or too cold; changes in formula or inappropriate concentration; excessive crying after feeding; or moving the baby too much or too soon after feeding. Vomiting may vary in severity and does not occur after every feeding. The vomitus consists of milk or milk curds without bile. These issues are more common in firstborns due to the mother's lack of feeding experience and can be prevented by improving feeding methods.

4. Swallowing syndrome

This accounts for about one-sixth of neonatal vomiting. Normally, by the fourth month of gestation, the digestive tract is fully formed, and the fetus swallows amniotic fluid, which does not significantly irritate the gastric mucosa. However, during childbirth, conditions such as post-term pregnancy, difficult delivery, intrauterine distress, or asphyxia may lead to the fetus swallowing excessive amniotic fluid, contaminated amniotic fluid, or secretions/blood from the birth canal, which can irritate the gastric mucosa and cause vomiting. Vomiting may begin immediately after birth and worsen after feeding, presenting as non-projectile vomiting. The vomitus is foamy and mucous, or coffee-colored if it contains blood. Vomiting usually stops within 1–2 days after the swallowed amniotic fluid and birth canal contents are expelled. If there are no other complications, the infant's condition remains normal without cyanosis or choking. Mild cases require no special treatment, while severe cases may be resolved with 1–2 gastric lavages using 1% sodium bicarbonate.

5. Gastric bleeding

Gastrointestinal bleeding caused by neonatal hemorrhage, stress ulcers, or disseminated intravascular coagulation can irritate the gastric mucosa and lead to vomiting. Vomiting is often accompanied by symptoms and signs of the underlying condition. Appropriate laboratory tests can confirm the diagnosis.

6. Drug effects

Bitter-tasting medications can irritate the gastric mucosa and cause vomiting in newborns, such as certain Chinese herbal preparations. Some drugs, like erythromycin, chloramphenicol, amphotericin B, ipecac syrup, and calcium chloride, can directly induce vomiting, which usually resolves after discontinuation. If pregnant or breastfeeding women use drugs such as digitalis or emetine, these substances can enter the newborn's system via the placenta or breast milk, causing vomiting.

7. Infection

Vomiting caused by infection is the most common condition encountered in neonatal medicine. The infection can originate from within or outside the gastrointestinal tract, with gastrointestinal infections being more common. Almost all infections within the gastrointestinal tract can cause neonatal enteritis, with vomiting being an early symptom of neonatal enteritis. The vomitus consists of gastric contents, with a small amount containing bile. Subsequently, diarrhea occurs, often accompanied by water and electrolyte imbalances. With treatment, vomiting usually disappears first. Pathogens causing neonatal gastrointestinal infections include bacteria, viruses, fungi, etc. Common bacteria include Escherichia coli, Salmonella, Proteus, Staphylococcus aureus, etc. Among viral infections, rotavirus is the most common, but coronavirus, astrovirus, adenovirus, coxsackievirus, echovirus, etc., can also cause infections. The most common fungus is Candida albicans, which often causes neonatal thrush and fungal esophagitis, directly leading to neonatal vomiting. Fungal enteritis may also cause neonatal diarrhea and vomiting. Due to the widespread use of antibiotics, fungal infections are showing an increasing trend in clinical practice.

Vomiting caused by gastrointestinal external contraction infection is also very common. Various infections such as upper respiratory tract infections, bronchitis, pneumonia, omphalitis, skin, mucous membrane, soft tissue infections, myocarditis, meningitis, urinary tract infections, and sepsis can all lead to vomiting. The severity of vomiting varies, and the vomitus consists of gastric contents, usually without bile. Vomiting subsides once the infection is controlled.

8. Neonatal Hepatitis

The incidence of neonatal hepatitis is relatively high in China, so it is listed separately. Many pathogens can cause neonatal hepatitis, but viral infections are the most common, primarily cytomegalovirus and hepatitis B virus. EB virus, bacteria, Listeria, Staphylococcus aureus, and Escherichia coli can also cause liver lesions. Toxoplasma, Treponema pallidum, and Leptospira can also lead to neonatal hepatitis. Neonatal hepatitis occurs within 28 days after birth in the Inner Mongolia Autonomous Region, so most infections likely occur in utero or during childbirth. Mother-to-child transmission is the primary route of neonatal infection. The onset of neonatal hepatitis is often slow and insidious. Some infants may present with jaundice, fever, hepatomegaly, vomiting, poor appetite, and failure to thrive during the neonatal period, while others may only exhibit vomiting. However, a few may progress to severe chronic liver disease. In rare cases, symptoms can be severe, including intense jaundice, clay-colored stools, hepatosplenomegaly, ascites, and even massive hemorrhage or hepatic coma.

9. Necrotizing Enterocolitis

Currently, infection is considered to play a major role in the pathogenesis of this condition. It is more common in premature infants and low-birth-weight infants, with symptoms primarily including abdominal distension, diarrhea, vomiting, and hematochezia. Severe cases often present with systemic toxic symptoms and may be complicated by sepsis, shock, peritonitis, or intestinal perforation. X-ray plain films may reveal generalized intestinal distension, rigid intestinal loops, pneumatosis intestinalis, and portal venous gas. Recent studies suggest that ultrasound is more sensitive than X-ray in detecting portal venous gas, hepatic vascular gas, ascites, and pneumoperitoneum, making it an important diagnostic tool for this condition.

10. Gastroesophageal Reflux

Many newborns experience reflux, but only about 1/300 to 1/1000 exhibit significant symptoms. The cause may be related to underdeveloped esophageal neuromuscular function, sometimes coexisting with hiatal hernia. Over 90% of affected infants develop vomiting within the first week of life, often occurring when lying flat. The vomitus consists of milk without bile but may contain traces of blood. Chronic gastroesophageal reflux can lead to reflux esophagitis and esophageal ulcers. Previously, semi-upright positioning was thought to reduce vomiting, but recent studies show limited efficacy, and it may even increase the risk of sudden infant death syndrome. Some suggest that small, frequent feedings can reduce gastric contents and alleviate reflux. If there are no anatomical abnormalities, the condition often resolves spontaneously within a few months.

11. Achalasia

This condition mostly occurs in adolescents and adults, with children under 4 years accounting for less than 5% of cases. Symptoms include intermittent dysphagia, milk regurgitation after feeding, and slow weight gain. Barium swallow studies may reveal esophageal dilation, a narrow cardia, absent or weak peristalsis, and occasionally fluid levels in the esophagus, with little or no gas in the stomach.

12. Pylorospasm

This is caused by temporary dysfunction of the pylorus. It typically occurs within the first week of life, presenting as intermittent projectile vomiting, not after every feeding. The vomitus consists of milk, possibly with curds, but no bile. It has minimal impact on overall nutrition. Physical examination rarely reveals gastric peristalsis or a palpable hypertrophic pyloric sphincter. Atropine treatment is effective.

13. Meconium Constipation

Normal newborns pass meconium within 48 hours after birth in 98% of cases. If there is no bowel movement or very little defecation within a few days after birth, it can lead to dysphoria, abdominal distension and fullness, refusal to feed, and vomiting. The vomitus may contain bile. The entire abdomen is distended, and sometimes intestinal patterns may be visible. Hard, dry fecal masses can be palpated, and borborygmi are active. Abdominal X-rays show dilated intestinal loops throughout the abdomen, with visible fluid levels and granular meconium shadows. During a rectal examination, dry and hardened meconium can be palpated. Symptoms are relieved after a large amount of thick meconium is expelled following a saline enema.

14. Neonatal constipation

is mostly caused by poor intestinal motility. A few newborns have bowel movements only once every 3 to 5 days, which is more common in formula-fed infants. Prolonged constipation can lead to abdominal distension and fullness and vomiting. The characteristics of vomiting are similar to those of meconium constipation. Symptoms resolve after defecation but soon reappear. Most cases naturally resolve after the first month.

15. Increased intracranial pressure

is relatively common in newborns. Conditions such as neonatal intracranial hemorrhage, intracranial hematoma, hypoxic-ischemic encephalopathy, and various infections causing meningitis or encephalitis can all lead to increased intracranial pressure. Vomiting due to increased intracranial pressure is projectile, with vomitus consisting of milk or milk curds, generally without bile, though sometimes containing coffee-ground-like bloody material. Affected infants often exhibit neurological symptoms and signs such as dysphoria, restlessness, drowsiness, unconsciousness, screaming, bulging fontanelle, and widened cranial sutures. Vomiting improves after dehydration and intracranial pressure reduction.

16. Inherited metabolic disorders

Most have a family history.

(1) Amino acid metabolism disorders: These include many conditions, such as phenylketonuria, cystinuria, congenital lysine intolerance, glycineemia, and valinemia, all of which can cause vomiting. Each disorder also has unique symptoms, such as light skin and hair color, urine with a peculiar musty odor, poor growth, unconsciousness, acidosis, and eye tremors. Blood tests can confirm the diagnosis.

(2) Carbohydrate metabolism disorders: Examples include galactosemia and maple syrup urine disease. Infants appear normal at birth but soon develop vomiting, diarrhea, and later jaundice, hepatomegaly, and cataracts.

(3) Congenital adrenal hyperplasia: There are many types, such as 21-hydroxylase deficiency, 11β-hydroxylase deficiency, 18-hydroxylase deficiency, 18-oxidase deficiency, 3β-hydroxysteroid dehydrogenase deficiency, 17α-hydroxylase deficiency, and 17,20-lyase deficiency. Among these, 21-hydroxylase deficiency is the most typical. Shortly after birth, symptoms such as drowsiness, vomiting, dehydration, electrolyte imbalance, and acidosis appear. Ambiguous genitalia are common, with males exhibiting a large penis or hypospadias and cryptorchidism, and females showing clitoral hypertrophy and partial fusion of the labia majora resembling male hypospadias or scrotal cryptorchidism. Diagnosis can be aided by measuring plasma corticosteroids and their precursor steroids, such as cortisol, 17-hydroxyprogesterone, dehydroepiandrosterone, and androstenedione.

17. Allergic diseases

Vomiting can occur in children allergic to medications, cow's milk protein, or soy protein. In newborns, cow's milk protein allergy is more common, typically manifesting 2 to 6 weeks after birth. The main symptoms include vomiting, abdominal distension and fullness, and diarrhea within 24 to 48 hours after milk feeding, with stools containing large amounts of milk curds and small amounts of mucus. Dehydration and malnutrition may also occur. Vomiting resolves after discontinuing milk.

18. Esophageal atresia and tracheoesophageal fistula

The incidence is 1/3000 to 1/4500, with premature infants accounting for about one-third of cases. This condition is classified into five types: Types I and II show no gastrointestinal air, while Types III, IV, and V all show gastrointestinal air. Clinically, Type III is the most common, accounting for 85–90% of cases. Due to fetal esophageal atresia, the inability to swallow amniotic fluid often leads to maternal polyhydramnios. After birth, infants may exhibit choking, cyanosis, aspiration pneumonia, or even asphyxia. Nasogastric tube insertion is obstructed or curls back in the mouth. X-ray examination clearly shows the obstruction and the position of the blind pouch. Further examination involves injecting 1–2 ml of iodized oil contrast to better visualize the atresia and any fistulas. The contrast should be promptly aspirated after imaging to prevent tracheal aspiration. The low surgical survival rate in China is mainly due to delayed diagnosis, with treatment often initiated only after aspiration pneumonia or severe infection develops. Some advocate inserting a nasogastric tube in the delivery room for suspected cases to enable timely diagnosis and treatment, thereby improving surgical survival rates.

19. Diaphragm hernia

The incidence is 3.1/1000 domestically and 1/2200 internationally. Clinically, it is classified into posterolateral diaphragm hernia, retrosternal hernia, and hiatal hernia. Posterolateral diaphragm hernia, also known as Bochdalek hernia, accounts for 70–90% of all diaphragm hernias and mostly occurs on the left side. It is often accompanied by intestinal malrotation, congenital heart disease, and pulmonary hypoplasia. After birth, symptoms such as paroxysmal tachypnea and cyanosis may appear. If intestinal malrotation or incarcerated intestinal loops enter the thoracic cavity, severe vomiting may occur, and in severe cases, the patient's overall condition may deteriorate rapidly, with a high mortality rate. Physical examination may reveal a scaphoid-shaped depression in the upper abdomen and paradoxical breathing. X-ray examination can confirm the diagnosis, showing air-filled intestinal loops and gastric bubble shadows in the thoracic cavity, atelectasis, mediastinal shift to the contralateral side, and reduced or absent abdominal gas shadows. Emergency surgery is required for posterolateral diaphragm hernia, though the optimal timing for surgery remains controversial. Due to frequent comorbidities with other malformations, the mortality rate remains relatively high.

20. Hiatal Hernia

It is a congenital defect in the development of the diaphragm, allowing part of the stomach to enter the thoracic cavity through the esophageal hiatus. Hiatal hernias are classified into sliding hiatal hernias, paraesophageal hernias, and mixed types. 85% of affected infants experience vomiting within the first week of life, and 10% develop symptoms within six weeks after birth. Vomiting does not occur when upright but is noticeable when lying down and may be projectile, with the vomitus consisting of milk and possibly containing brown or coffee-ground-colored blood. Some infants may develop secondary pyloric spasms, clinically resembling hypertrophic pyloric stenosis. One-third of infants may develop aspiration pneumonia. Paraesophageal hernias can lead to gastric ulcers and, occasionally, gastric necrosis, requiring emergency surgery. Vomiting may persist for 12–18 months, often resolving once the child begins to stand upright. Diagnosis primarily relies on X-ray examination; the presence of a gastric bubble or gastric mucosal shadow above the diaphragm on barium meal confirms the diagnosis. Sliding hernias may resolve spontaneously as the infant grows, and postural therapy is generally employed. Surgical intervention is recommended for cases with severe anemia, growth impairment, a large intrathoracic gastric bubble, or paraesophageal hernia.

21. Hypertrophic Pyloric Stenosis

Ranking as the third most common congenital digestive tract malformation, its incidence ranges from 0.3/1000 to 1/1000. It is more prevalent in male infants, with a male-to-female ratio of 4:1, and is often seen in full-term infants with a genetic predisposition. Vomiting typically begins around the second week of life, becoming persistent, progressive, and eventually projectile. The vomitus consists of milk and curds, is copious, sour-smelling, and may contain bile. Vomiting occurs shortly after or during feeding, yet the infant remains hungry and eager to feed. Repeated vomiting leads to failure to gain weight and reduced urine and stool output. Abdominal examination reveals prominent gastric peristaltic waves in both clockwise and counterclockwise directions. A firm, olive-sized mass—the hypertrophied pyloric sphincter—can be palpated at the lateral edge of the right rectus abdominis muscle. Severe vomiting may result in dehydration, hypochloremia, hypokalemia, and acid-base imbalances. Barium meal examination shows gastric dilation, delayed gastric emptying, and the characteristic "beak-like" narrowing and elongation of the pyloric canal, confirming the diagnosis. In recent years, ultrasound has increasingly replaced barium studies for diagnosing hypertrophic pyloric stenosis, as it directly visualizes the thickened pyloric sphincter. Diagnostic criteria include a pyloric muscle thickness exceeding 4mm or a pyloric canal length over 14mm. Surgical treatment is effective once the diagnosis is confirmed.

22. Pyloric Antral Web

A rare congenital anomaly, the web is typically located 1.5–3cm proximal to the pylorus, often with a central perforation. A non-perforated web presents with symptoms of complete upper gastrointestinal obstruction at birth, while a small perforation may cause symptoms in the neonatal period, manifesting as postprandial vomiting, often projectile, resembling hypertrophic pyloric stenosis in content and appearance. However, no mass is palpable on abdominal examination. Barium studies do not show the elongated, curved pyloric canal or duodenal bulb indentation characteristic of hypertrophic pyloric stenosis but reveal a narrowing defect 1–2cm proximal to the pylorus. Surgical resection of the web is required.

23. Gastric Volvulus

Gastric volvulus is classified into two types: organoaxial (more common, accounting for 85%) and mesenteroaxial. Due to lax gastric ligaments and the horizontal positioning of the stomach in newborns, gastric volvulus occurs more easily. Many infants have a history of spitting up or regurgitation from birth, or vomiting may begin within weeks. Vomiting varies in severity, ranging from projectile to non-projectile, often occurring after feeding and worsening when the infant is moved. The vomitus does not contain bile. Severe cases may impair growth. Vomiting often ceases after a barium meal study; severe cases may require gastropexy.

24. Congenital Intestinal Atresia

is a common disease cause of intestinal obstruction in the neonatal period, accounting for about 1/3 to 1/4, with male infants more affected than female infants, and an incidence rate of 1/1500 to 1/2000. Low birth weight infants account for 1 to 3. Atresia can occur in any part of the intestine, most commonly in the ileum (50%), followed by the duodenum (25%), with the jejunum being less common and the colon rare. Some infants may have other associated malformations, such as the esophagus, which can be classified into membrane type, cord type, two-segment type, and multiple type. Atresia occurring in the duodenum and upper jejunum is referred to as high intestinal atresia, mostly of the membrane type. High atresia often has a history of polyhydramnios, and the higher the atresia site, the earlier vomiting appears. In duodenal atresia, vomiting occurs with the first feeding after birth, with vomitus consisting of gastric contents and duodenal secretions. Except for a few cases where the atresia occurs proximal to the ampulla, most vomitus contains bile. As feeding frequency increases, the infant's vomiting gradually worsens, becoming persistent and recurrent. A small amount of meconium may be passed, and the abdomen is not distended or shows grade I distension. Atresia occurring in the lower jejunum, ileum, and colon is called low intestinal atresia. Low intestinal atresia mainly manifests as abdominal distension and fullness, with vomiting usually starting 1–2 days after birth. The vomitus is fecal-like and foul-smelling, with no meconium or only mucus-like meconium. In high intestinal atresia, abdominal X-ray fluoroscopy or radiography may show 2–3 fluid levels, known as the double-bubble or triple-bubble sign. In low intestinal atresia, multiple dilated intestinal loops and fluid levels are visible, with no gas in the distal intestine. Barium enema reveals a fetal-type colon. Surgical treatment is the only effective method, but the mortality rate remains high. One reason is that infants often have other associated malformations, and another is late diagnosis, with infants often dying from secondary intestinal perforation, peritonitis, intestinal necrosis, or aspiration pneumonia. Therefore, some advocate that in cases of polyhydramnios, a gastric tube should be inserted immediately after birth. If 15–20 ml or more of bile-stained gastric fluid is aspirated, it indicates upper gastrointestinal obstruction, and aggressive measures should be taken.

25. Intestinal Stenosis

Intestinal stenosis is less common than intestinal atresia, with the majority being of the membrane type. The duodenum is the most frequently affected site, followed by the ileum, jejunum, and colon, which is relatively rare. The higher the location of the stenosis, the earlier the symptoms appear, and the more severe the stenosis, the more pronounced the symptoms. The main symptoms are vomiting and abdominal distension and fullness. In most cases, the vomitus contains bile, and normal stool may be passed. High intestinal stenosis presents with epigastric distension and visible gastric peristaltic waves, whereas low intestinal stenosis manifests as generalized abdominal distension and fullness, visible intestinal loops and peristaltic waves, accompanied by hyperactive bowel sounds. Abdominal X-rays reveal dilation proximal to the stenosis, and barium meal studies can confirm the diagnosis. After diagnosis, efforts should be made to improve the child's general condition, followed by surgical resection of the stenotic segment.

26. Malrotation of the Intestine

Malrotation of the intestine is a relatively common congenital anomaly of the digestive tract, ranking fourth among domestic digestive tract malformations. Over 70% of cases present symptoms during the neonatal period, and 30% occur in low birth weight infants. Around the 10th week of embryonic development, as the midgut returns to the abdominal cavity, it undergoes a counterclockwise rotation from left to right. If this rotation halts at any point, malrotation occurs. Depending on the timing of the halted rotation, the following scenarios may arise in the neonatal period: ① The cecum is located in the mid-upper or right upper abdomen, and the cecum or the cecal ligament extending from the cecum to the right posterior abdominal wall compresses the second or third part of the duodenum, causing incomplete obstruction. ② The cecum is situated in the upper or mid-abdomen, and the root of the small intestinal mesentery fails to fixate to the posterior abdominal wall, predisposing to volvulus. ③ The cecum reaches the right lower abdomen, but the mesentery does not fully fuse with the posterior abdominal wall, resulting in a "mobile cecum" prone to colonic volvulus and incomplete intestinal obstruction. ④ In rare cases, the duodenal loop lies anterior to the mesenteric vessels, and the first segment of the jejunum is compressed or entangled by peritoneal bands, leading to incomplete jejunal obstruction. ⑤ Reverse rotation of the intestine places the small intestinal mesentery anterior to the transverse colon, causing transverse colon obstruction. Due to the diversity of pathological structures, clinical manifestations vary widely. A minority of cases may remain asymptomatic for life, while most symptoms appear during the neonatal period. The primary presentation is high incomplete obstruction, typically beginning with intermittent vomiting 3–5 days after birth, which may vary in severity. The vomitus consists of milk and contains bile. Meconium is passed after birth. If volvulus resolves spontaneously, symptoms disappear. Gastrointestinal bleeding indicates intestinal necrosis, which may progress to intestinal perforation and peritonitis, with positive peritoneal irritation signs and toxic shock. Without timely surgery, death may occur rapidly. An upright abdominal X-ray shows gastric and duodenal dilation with a "double bubble" sign, and reduced or absent gas in the jejunum and ileum. A barium enema reveals most of the colon located in the left abdomen, with the cecum in the left upper or mid-abdomen, confirming the diagnosis.

27. Meconium Peritonitis

Fetal intestinal perforation leads to the leakage of meconium into the abdominal cavity, causing a sterile, chemical inflammation of the peritoneum, known as meconium peritonitis. The clinical manifestations vary depending on the timing of the intestinal perforation. Based on X-ray characteristics, it is generally classified into three types: ① Intestinal obstruction type: Obstruction symptoms such as vomiting, refusal to feed, abdominal distension and fullness, and constipation can be observed shortly after birth. An upright X-ray film shows dilated intestinal loops with multiple fluid levels and obvious calcified scattered ecchymosis shadows. ② Peritonitis type: Due to the intestinal perforation remaining open at birth, it rapidly leads to purulent peritonitis or pneumoperitoneum. Depending on the type of pneumoperitoneum, it can be further divided into two subtypes. One is free pneumoperitoneum, where the intestinal perforation is open. The infant's general condition is poor, possibly accompanied by dyspnea and cyanosis, with significant abdominal distension and fullness, red and shiny abdominal wall, and varicose veins. Sometimes, abdominal fluid may drain into the scrotum, causing scrotal redness and swelling. Abdominal percussion reveals tympany and shifting dullness. Bowel sounds are reduced or absent. Abdominal X-rays show calcified shadows, and sometimes calcifications are also visible in the scrotum. The other subtype is localized pneumoperitoneum, where the intestinal perforation is encapsulated by fibrous adhesions, forming a pseudocyst containing fluid and gas. Calcifications may be seen on the wall of the pseudocyst or elsewhere in the abdominal cavity. This type can progress to diffuse peritonitis or localized abdominal abscess. ③ Latent intestinal obstruction type: The intestinal perforation has healed at birth, but intestinal adhesions remain in the abdominal cavity, manifesting as recurrent intestinal obstruction after birth. Abdominal X-rays show calcified shadows. Mild cases may be relieved by fasting, gastrointestinal decompression, and enemas. If pneumoperitoneum or intestinal obstruction symptoms persist, surgical intervention should be performed as early as possible.

28. Congenital megacolon

is a common digestive tract malformation, ranking second among digestive tract malformations. Its incidence in China is approximately 1/2000 to 1/5000, with a male-to-female ratio of 4:1, and it has a familial predisposition. Due to the underdevelopment of the myenteric plexus in the terminal colon wall and the absence of ganglion cells, the affected intestinal segment remains in a constant state of spasm and narrowing. Feces accumulate in the proximal colon, causing the intestinal wall above the narrowing to expand and thicken, resulting in megacolon. Based on the extent of the aganglionic segment, it can be classified into five types: ① Short-segment type, where the lesion is confined to the lower rectum, accounting for about 8%; ② Common-segment type, the most prevalent, where the lesion extends from the anus to the distal sigmoid colon, accounting for about 75%; ③ Long-segment type, where the affected segment extends beyond the descending colon, accounting for about 20%; ④ Total colonic type, where the lesion involves the entire colon and the terminal ileum, accounting for about 2%; ⑤ Total intestinal aganglionosis, which is relatively rare. The initial symptom is delayed passage of meconium and constipation, with about 90% of cases failing to pass meconium within 24 hours after birth. Most cases develop symptoms of low intestinal obstruction 2–6 days after birth, including vomiting, which gradually increases in frequency. The vomitus contains bile or fecal matter, with abdominal distension, shiny skin, engorged veins, visible intestinal loops and peristaltic waves, and hyperactive bowel sounds. Digital rectal examination reveals an empty rectal ampulla and a palpable narrowing ring. Upon withdrawal of the finger, a large amount of feces and gas is expelled explosively under high pressure, providing temporary relief. After a few days, constipation, vomiting, and abdominal distension recur, often requiring enemas or digital examination for relief again. In advanced stages, complications such as enterocolitis and intestinal perforation may occur. X-ray abdominal examination in the upright position shows generalized intestinal distension without rectal gas. Barium enema is the primary diagnostic method, revealing a narrow distal rectum and sigmoid colon, with marked dilation of the proximal sigmoid and descending colon and weakened peristalsis. A follow-up after 24 hours often shows retained barium in the colon. Rectal manometry demonstrates persistently elevated anal pressure. Rectal biopsy and electromyography also aid in clinical diagnosis but are less commonly used in neonates. For mild or undiagnosed cases, medical therapy can be employed, such as daily or alternate-day warm saline enemas to prevent fecal accumulation, along with daily dilation of the spastic segment using a specialized dilator. In recent years, early-stage radical surgery during the neonatal period has been advocated for better outcomes. For children with concurrent infections or poor general condition, medical therapy should be initiated first, followed by radical surgery once the child's condition improves.

29. Anorectal malformations

mainly refers to atresia or stenosis of the anus and rectum, which is the most common gastrointestinal malformation in newborns, with an incidence of approximately 0.75/1000. Clinically, it can be divided into four types: ① stricture of anus; ② anal membrane-type atresia, where a membranous structure separates the anal skin from the rectum, classified as low anal atresia; ③ anorectal agenesis, where only a dimple is present at the anal site, with a significant distance between the rectum and the anal dimple, classified as high anal atresia; ④ rectal atresia, where the anus and anal canal are normally present but separated from the rectum by varying distances, a relatively rare clinical condition. Approximately 50% of anorectal atresia cases are accompanied by various fistulas. Male infants may have rectovesical fistula, rectourethral fistula, or rectoperineal fistula, while female infants may have rectovaginal fistula, rectovestibular fistula, or rectoperineal fistula. Children with anorectal malformations often also have genitourinary tract malformations and malformations in other parts of the digestive tract. Due to the variety of malformations and the presence of fistulas or other anomalies, clinical manifestations can differ. Infants with anorectal atresia do not pass meconium after birth and gradually develop symptoms of low intestinal obstruction, such as abdominal distension and fullness, vomiting (with vomitus containing bile and fecal-like material), with symptoms progressively worsening. Most infants can be diagnosed through careful physical examination, revealing the absence of an anus or anal abnormalities. For clinically suspected cases, an inverted lateral radiograph can be performed 24 hours after birth. Before imaging, the infant is held upside down for several minutes, and a metal marker is placed on the skin at the anal dimple. This helps determine the type of atresia and its level. If the intestinal blind end is less than 2 cm from the anal fold, it is classified as low atresia, which is relatively simple to surgically correct. If the distance exceeds 2 cm, it is considered high atresia, requiring more complex surgery. If a fistula is present, fistulography can be performed. Ultrasound can also accurately measure the distance between the rectal blind end and the anal skin. Stricture of anus can be treated with anal dilation, while other types require surgical intervention.

bubble_chart Diagnosis

I. Diagnostic Methods

Neonatal systemic diseases can all present with vomiting symptoms. To diagnose the disease cause of vomiting, it is necessary to closely combine the disease history, maternal pregnancy and delivery history, feeding history, a thorough physical examination, necessary auxiliary tests, and close observation of vomiting conditions for comprehensive analysis to reach a clear diagnosis.

1. Age of Onset

Vomiting within a few hours after birth is often seen in swallowing syndrome. Vomiting after the first feeding should raise suspicion of esophageal atresia. Vomiting within a few days after birth is mostly due to congenital digestive system malformations or birth-related cranial brain injury. Advanced-stage neonatal vomiting is commonly caused by improper feeding or infectious diseases.

2. Nature of Vomiting

(1) Milk regurgitation: Milk regurgitation is not true vomiting and lacks the series of neuromuscular reflex excitations seen in vomiting. Most cases involve 1-2 mouthfuls of milk flowing back into the mouth or corners of the mouth after feeding.

(2) Typical vomiting: This involves the three-step vomiting process described above and is the most common clinically. It is mainly seen in non-obstructive digestive tract diseases and external infectious diseases of the digestive tract.

(3) Projectile vomiting: This is severe, typical vomiting where large amounts of stomach contents are forcefully expelled through the mouth and nose. It is seen in various intracranial lesions and high gastrointestinal obstructions.

3. Contents of Vomit

(1) Vomit without gastric acid or milk curds: Consider esophageal obstructive diseases.

(2) Vomit containing bile: Generally, mild vomiting does not contain bile. Large amounts of vomit with bile suggest obstruction distal to the duodenal ampulla.

(3) Feculent vomit: Seen in low organic intestinal obstruction.

(4) Bloody vomit or hematemesis: Seen in neonatal hemorrhagic disease, systemic hemorrhagic diseases, severe infectious diseases, and rare congenital gastric wall muscle defects.

4. Relationship Between Vomiting and Feeding

The higher the lesion in the digestive tract, the shorter the time between feeding and vomiting. Esophageal and cardia diseases often cause vomiting during or immediately after feeding. Vomiting due to non-digestive tract diseases has no clear relationship with feeding.

5. Relationship Between Vomiting and Body Position

Gastroesophageal reflux, hiatal hernia, and gastric volvulus often cause more pronounced vomiting in the supine position, which can be alleviated by changing position. Vomiting due to digestive tract obstruction or cranial diseases has no clear relationship with body position.

6. Accompanying Symptoms and Signs

Note the presence of other digestive symptoms such as abdominal pain, diarrhea, delayed meconium passage, constipation, hematochezia, etc., as well as systemic symptoms like mental state, appetite, growth, fever, and crying.

7. Maternal Pregnancy and Delivery History

Maternal infections in early pregnancy may affect embryonic differentiation and development, leading to malformations in the digestive tract and multiple organs. Polyhydramnios suggests fetal digestive tract atresia. Intrapartum fetal distress and asphyxia can cause cranial brain injury, leading to vomiting.

8. Feeding History

Inquire about feeding practices, maternal and neonatal medication history, as improper feeding can cause vomiting.

9. Physical Examination

Every vomiting neonate should undergo a comprehensive physical examination to observe signs of systemic infection, neurological disease, or metabolic disorders, with a focus on abdominal and neurological signs. Abdominal wall intestinal patterns, peristaltic sounds, or splashing sounds indicate organic intestinal obstruction. Generalized abdominal distension suggests infectious diseases, neonatal necrotizing enterocolitis, central nervous system diseases, or low intestinal obstruction. Upper abdominal distension with lower abdominal depression is seen in pyloric and duodenal obstructions. Hypertrophic pyloric stenosis, intussusception, and abdominal tumors may present as palpable masses. Loss of liver dullness suggests pneumoperitoneum. Also, check for abdominal tenderness, muscle rigidity, and inguinal hernias. Neurological examination should assess for cranial suture separation, meningeal irritation signs, and optic disc edema.

10. Auxiliary Examination

(1) Nasogastric tube examination is a simple and effective method for detecting upper digestive tract malformations. When encountering maternal polyhydramnios or when an infant exhibits crab-like foam vomiting shortly after birth, a nasogastric tube examination should be performed in the delivery room. Normally, the nasogastric tube can be smoothly inserted into the stomach, and a small amount of fluid can be aspirated. If the nasogastric tube encounters resistance during insertion or recoils from the mouth or nose, it suggests esophageal atresia.

(2) X-ray examination

① Abdominal fluoroscopy and radiography: Abdominal fluoroscopy and radiography are the most commonly used diagnostic methods for neonatal vomiting. To better observe distended intestinal loops and fluid levels, upright fluoroscopy and radiography should be performed, or lateral horizontal projection radiography can be used.

In normal newborns, gas reaches the jejunum within 15–60 minutes after birth, the ileum within 2–3 hours, and the colon within 3 hours. By 5–6 hours, gas is distributed in the transverse and descending colon. After 24 hours, gas is present in the stomach, small intestine, and colon. Normal newborns have more intestinal gas than children, with a higher amount in the small intestine, which should not be considered a sign of intestinal obstruction. The focus should be on observing the distribution of intestinal gas, the presence of distended intestinal loops and fluid levels, and the morphology and distribution of distended loops to infer the nature and location of obstructive diseases. The timing of gas appearance in the intestines is also important; for example, the absence of gas in the rectum 24 hours after birth often indicates intestinal obstructive disease. The presence of free gas in the abdominal cavity suggests gastrointestinal perforation, while calcifications in the intestinal lumen or abdominal cavity aid in diagnosing meconium ileus and meconium peritonitis.

② Barium meal or barium enema examination: These can assess the morphology and function of the esophagus, stomach, and intestines, providing significant diagnostic value for digestive tract diseases. Barium contrast is contraindicated in neonates suspected of having complete gastrointestinal obstruction or perforation. For suspected esophageal atresia or tracheoesophageal fistula, water-soluble iodine contrast can be used, and the contrast agent should be promptly aspirated after the procedure.

③ Ultrasound examination: Ultrasound is highly sensitive and specific for detecting ascites, determining the location and nature of abdominal masses, and identifying free intraperitoneal gas. It outperforms X-ray in diagnosing conditions such as choledochal cysts, adrenal cortical hyperplasia, and neonatal necrotizing enterocolitis. Currently, ultrasound for hypertrophic pyloric stenosis has largely replaced barium meal examinations. Ultrasound not only reveals gastrointestinal changes but also directly observes alterations in the hepatobiliary, urinary, and circulatory systems and their impact on the digestive tract, greatly aiding in diagnosing the causes of vomiting.

④ Gastroscopy: Neonates often require general anesthesia for gastroscopy, limiting its clinical use. Gastroscopy allows direct observation of mucosal congestion, hemorrhage, edema, ulcers, scars, tumors, and congenital malformations, providing definitive diagnoses for certain esophageal and gastric diseases.

II. Key Diagnostic Points and Analysis

The causes of vomiting are highly complex, and a preliminary diagnosis can only be made after a detailed medical history, comprehensive physical examination, and necessary auxiliary tests. Broadly, two aspects should be considered: First, whether the primary cause of vomiting is a disease of the digestive system itself or an extra-digestive system disease. Second, whether the cause of vomiting is functional or organic in nature.

First, the affected system should be identified based on the neonate’s clinical manifestations, such as the nervous, respiratory, circulatory, hematologic, or urinary systems. Diseases in these systems are often non-organic vomiting and can be treated according to the principles of managing the respective system’s diseases.

If the vomiting is due to a digestive system disease, further localization should be based on the characteristics, timing, and nature of the vomitus, as well as accompanying symptoms.

1. Upper digestive tract

In cases of esophageal and cardiac diseases, vomitus does not contain bile or milk curds, often accompanied by regurgitation and dysphagia, and vomiting usually occurs on the first day after birth or shortly after feeding. Congenital upper gastrointestinal atresia is often associated with polyhydramnios. In gastric and pyloric diseases, the vomitus consists of milk curds or milk, which may be mixed with blood, but bile is not present. For upper gastrointestinal diseases, most cases can be definitively diagnosed through barium meal or gastroscopy.

2. Middle consumptive thirst digestive tract

Middle consumptive thirst digestive tract: When pathological changes occur in the digestive tract, the vomitus contains bile. Early-onset vomiting with mild or only gastric distension suggests lesions in the upper jejunum. If the vomitus is greenish-yellow fecal-like material with significant abdominal distension, the lesions are mostly located in the lower jejunum and ileum.

3. Lower consumptive thirst digestive tract

Mainly manifests as constipation and abdominal distension, with visible large intestinal loops and sometimes palpable fecal masses. Vomiting usually occurs one week after birth, and the vomitus is fecal-like. Lesions are mostly in the sigmoid colon, rectum, or anus. Digital rectal examination and barium enema aid in diagnosis.

Differentiating functional vomiting from organic vomiting: The timing, characteristics, nature of the vomitus, and its relationship with feeding are valuable for qualitative diagnosis. Early, severe, persistent vomiting containing bile, blood, or feces, along with significant extra-digestive symptoms and signs, often indicates functional vomiting.

Differentiating mechanical ileus from paralytic ileus: In mechanical obstruction, abdominal distension is accompanied by prominent intestinal loops, hyperactive bowel sounds, and audible splashing sounds. Newborns may exhibit paroxysmal crying, temporarily relieved after vomiting. In paralytic ileus, abdominal distension is present but intestinal loops are indistinct, bowel sounds are weakened or absent, and newborns often show no crying but painful moaning. However, neonatal presentations are atypical, especially in preterm infants, requiring clinicians to closely monitor changes and provide timely intervention.

4. Gastroscopy

Neonates often require general anesthesia, limiting its clinical use. Gastroscopy allows direct observation of mucosal congestion, hemorrhage, edema, ulcers, scars, tumors, and congenital anomalies, providing definitive diagnosis for certain esophageal and gastric diseases.