Pediatric congenital hypothyroidism, also known as cretinism, causes and manifestations can be due to congenital hypothyroidism or a disease of hypothyroidism caused by defects in enzymes in the synthesis of thyroid hormones, which is caused by an underdeveloped or underdeveloped thyroid gland, possibly due to some thyroid disease in the mother, thyroid antibodies produced in the blood stream, and this self-additive antibody passes through the placenta to the fetus and destroys the fetus or the application of antithyroid drugs during maternal pregnancy, which inhibit the synthesis of the thyroid system, and a deficiency of thyrotropin, commonly due to idiopathic hypopituitarism, or hypothalamus, a defect in pituitary development that reduces the production of thyrotropin by the pituitary gland, and possibly hypothyroidism or low target organ responsiveness. The period of physiological jaundice in the neonatal period is prolonged, so there is abdominal distension and constipation immediately after birth, much sleep, delayed reaction to the outside world, feeding difficulties, low cry, hoarseness, low body temperature, typical symptoms can appear six months after birth, with a special face, large head and short neck, dry skin, mucous edema on the face, eyelid edema, widening of the eye distance, flattened nose, large and thick tongue, often sticking out of the mouth, abdominal distention, umbilical hernia, short stature The patient has a short trunk, short limbs, slow movements, low intelligence, slow reaction, poor appetite, little movement, and dull expression. In the case of endemic hypothyroidism due to iodine deficiency, the child’s central nervous system is significantly affected, characterized by mental retardation, spastic paralysis, deafness and mute. At present, screening of children with hypothyroidism is done in our obstetrics department, and timely treatment of fever cases can leave no sequelae. Untreated or undiagnosed goiter in infants can have serious consequences on the development of the central nervous system, resulting in moderate to severe developmental delays that can jeopardize physical growth during childhood. The incidence of neonatal or congenital hypothyroidism is approximately 1 in 4000 live births. The most common cause is congenital absence of the thyroid gland (absence of the thyroid gland), which requires lifelong treatment. Signs and symptoms include cyanosis, persistent hyperbilirubinemia, feeding difficulties, hoarse crying, umbilical hernia, respiratory distress, giant tongue, large fontanelle, and delayed skeletal development. Less commonly, the newborn has temporary hypothyroidism. Screening with routine newborn filter paper screening procedures can detect the disease before the diagnosis is confirmed by clinical signs. Laboratory tests include measurement of serum thyroxine (T4) and thyroid-stimulating hormone (TSH). Immediately after diagnosis, treatment with L-thyroxine should be administered and closely monitored. The appropriate starting dose is 10-15 μg/kg per day orally (this allows rapid achievement of normal serum T4 concentrations), followed by adjustment of the drug dose during infancy to maintain serum T4 concentrations between 10-15 μg/dl (129-193 nmol/L). after 1 year of age, the usual dose is 4-6 μg/kg per day to maintain serum T4 and TSH titrated concentrations within normal within the normal range. Care must be taken to prevent drug overdose, which may produce medically induced hyperthyroidism. After treatment, most infants have normal motor and intellectual development. Juvenile hypothyroidism, or acquired hypothyroidism, is often caused by autoimmune thyroiditis (Hashimoto’s thyroiditis). Certain signs and symptoms are the same as in adults, including weight gain, constipation, dry, coarse hair, and yellow, cold or patchy rough skin. Symptoms that differ from those of childhood hypothyroidism include growth retardation, delayed bone development, and often delayed pubertal growth.