Auricular hypoplasia generally refers to congenital microtia, with genetic factors being the main factor in bilateral auricular hypoplasia. Congenital and birth trauma are also etiological factors. The causes of microtia are generally thought to be related to incidental events in early pregnancy, such as viral infections, taking y(a)o, mental stimulation, radiation, environmental pollution, and other factors. According to studies no one factor can play a major role. Current research suggests that microtia is an epidemic, random event and that parents must understand this condition. The incidence in relatives is only 5%, which means that the disease is not genetic. The etiology of bimacroglossia: The auricle originates from the embryonic first gill arch (mandibular arch) and the second gill arch (hyoid arch). During the 5th week of embryonic life, a portion of the gill arch will develop into the auricle, and roughly during the 5th-9th week of embryonic life the auricle develops and takes shape. During the 6th week of embryonic life, the ectoderm and mesenchyme are activated and proliferate in the mandibular and hyoid arches to form six small mound-like elevations. 1, 2 and 3 mounds appear caudally in the mandibular arch and later form the ear screen, pedicle and upper part of the external auditory meatus, while 4, 5 and 6 mounds appear at the head of the hyoid arch and develop into the opposite auditory meatus, opposite ear screen and earlobe. The first gill fissure is depressed inward to form the external auditory canal . During the developmental stages of the auricle, the embryo is susceptible to a variety of developmental malformations of the auricle due to genetic or external influences. Experimental studies on the embryonic development of the auricle have been conducted for many years, but the mechanisms are still unclear. The role of neural crest cells (CNCC) in the development of the ear is gaining attention, as CNCC is a kind of multi-differentiated potential stem cell, which is the main cellular component of the mesenchyme of the first and second parotid arches. It has been found that rupture of the stapedial artery during middle ear development in mice causes microtia, but CNCC do not have migratory properties. The administration of vitamin A in early gestation interferes with the migratory nature of CNCC. Purulent auricular chondromyelitis: This is a purulent inflammation of the auricular cartilage membrane and is usually caused by secondary infection from auricular injury, such as trauma, surgical injury, ear injection therapy or auricular puncture and aspiration. The causative organisms are mostly Pseudomonas aeruginosa and Staphylococcus aureus. When an abscess is formed, the surface is yellowish with a sense of fluctuation. If the abscess is not treated properly, the auricle will curl up and form a “cauliflower ear”-like deformity. Foreign body in the external auditory canal: Commonly found in children. Various small objects such as beans, beads and matchsticks are inserted into the external auditory canal. Deafness: It is generally considered that if the average hearing threshold at speech frequencies (0.5, 1.2 Hz) is 26 dB or more, then there is a hearing impairment, and those with hearing loss within 70 dB are weighed and those with hearing loss above 70 dB are deaf, which is clinically and conventionally referred to as deafness. Various acute infectious diseases, bacterial or viral infections, such as epidemic B encephalitis, mumps, septic meningitis, measles, scarlet fever, influenza, herpes zoster, typhoid fever, etc. can damage the inner ear and cause sensorineural deafness of different severity.