1. Premature babies. Any newborn whose gestational age is less than 37 weeks. Causes of preterm birth: premature rupture of membranes, low socioeconomic status, inappropriate perinatal care, poor nutrition, low education, unmarried status and sudden onset of untreated disease or infection. Other risk factors include maternal untreated bacterial vaginitis and previous history of preterm birth. Most complications in preterm infants are related to immature function of organs and systems. 2. Respiratory shutdown. The amount of lung surface active substance produced is usually not sufficient to prevent alveolar collapse and incomplete lung expansion, which leads to respiratory distress syndrome. Respiratory distress syndrome (RDS) almost always occurs in newborns born before 37 gestational weeks, and the younger the gestational age, the greater the chance of occurrence. Manifestations: increased and difficult breathing, breathing moans often immediately after birth or within a few hours, and nasal flapping. Immaturity of the brainstem respiratory center can lead to apnea episodes. 3. Hemorrhagic shutdown. In preterm infants, the periventricular embryogenic layer is prone to hemorrhage, which can enter the ventricles (intraventricular hemorrhage) . Periventricular white matter infarction (periventricular white matter softening) may be caused by several as yet incompletely understood causes. Hypotension, inadequate cerebral perfusion or unstable blood pressure, and a sudden rise in blood pressure (e.g., rapid intravenous injection of fluid or colloid) can cause cerebral infarction or hemorrhage. Bleeding in or around the brain is a fatal threat to preterm infants. Pulmonary hemorrhage, gastrointestinal hemorrhage. 4. Infection off. The incidence of sepsis or meningitis is almost four times higher in preterm infants than in full-term infants. Thin broken skin and significantly low serum immunoglobulin levels in preterm infants lead to an increased likelihood of infection. Premature infants are uniquely susceptible to necrotizing small bowel colitis. Manifestations: abdominal distension, vomiting, bloody stools. 5. Body temperature off. Premature infants have a large body surface area compared to body volume, so when exposed to an environment below neutral temperature, they will rapidly lose heat and have difficulty maintaining a normal body temperature. 6, feeding off. Premature babies have small stomach capacity, immature sucking and swallowing reflexes, which prevent adequate feeding via oral or nasal feeding tube and cause the risk of respiratory aspiration. Small preterm infants can be fed via nasal or oral feeding tubes. In very small or critically ill preterm infants, total parenteral hypernutrition is given by peripheral intravenous infusion, percutaneous or surgically placed catheters to provide adequate nutrition. 7. Hypoglycemia off. Hypoglycemia often occurs due to inadequate glycogen reserves at birth or secondary to hyperinsulinemia. Due to inadequate glycogen reserves in very low birth weight preterm infants, they are susceptible to hypoglycemia unless they receive a maintenance exogenous glucose infusion. Neonates with intrauterine malnutrition due to placental insufficiency (manifested as smaller than gestational age infants) also lack glycogen reserves, and if perinatal asphyxia hypoxia persists, all their glycogen reserves will be rapidly depleted in anaerobic enzymes, and hypoglycemia can occur in neonates with inadequate glycogen reserves at any time during the first few days after birth, especially in neonates with prolonged feeding intervals or inadequate nutrient intake. 8, jaundice off. Hyperbilirubinemia occurs more frequently in preterm infants than in term infants. In small, sick preterm infants kernicterus occurs even if the serum bilirubin is less than 10 mg/dl (170μmol/L). The high bilirubin levels in preterm infants should be attributed in part to immature hepatic excretory mechanisms, including defective uptake of bilirubin from the plasma, inadequate intracellular production of bilirubin-binding glucuronides, and inadequate excretion of bilirubin into the bile ducts. Reduced intestinal motility allows the conversion of bilirubin glucuronides into unconjugated bilirubin in the intestinal lumen by the intestinal luminal enzyme ;-glucuronidase, thereby increasing the reabsorption of free bilirubin (enterohepatic circulation of bilirubin). Conversely, early feeding increases intestinal peristalsis, thereby decreasing bilirubin reabsorption and therefore significantly reducing the incidence and severity of physiologic jaundice. In rare cases, late clamping of the umbilical cord leads to massive red blood cell input, increased red blood cell destruction and bilirubin production, which can significantly increase the risk of developing hyperbilirubinemia.