How to prepare an animal model of orbital fracture with invaginated eyeball?

  (1) Reproduction method Adult cats weighing 2.0 to 3.0 kg are anesthetized by intramuscular injection at a dose of 20 mg/kg body weight of ketamine and 2.5 mg/kg body weight of Diazepam. ①Medial orbital wall defect: select the inner adjoining skin incision, subperiosteal separation to expose the medial orbital wall, lightly press through the ethmoid floor with vascular forceps, and bite a bone wall defect with a width and height of 1.0 to 1.5 cm with a rongeur. Blunt separation destroys the periosteum and the orbital septum, so that the orbital contents are embedded into the ethmoid sinus. ② Anterior orbital floor defect: incision in the lower eyelid margin to expose the inferior orbital margin. The inferior orbital rim of the cat is intact, the anterior orbital floor is a bone wall, 1.0 to 1.5 cm from the inferior orbital rim, the middle and outer two-thirds of the orbital floor have no bone wall, only the masseter muscles close the orbital floor, and no maxillary sinus is seen. Resection part of the bony orbital floor and masseter muscle, so that the width and height of the defect are 1.0-1.5cm in size, blunt separation destroys the periosteum and orbital septum, so that the soft tissue in the orbit diverges to the subcutaneous. ③ Posterior orbital floor defect: Resection of the posterior masseter muscle results in a defect with a width and height of 1.0 to 1.5 cm.

  (2) Model characteristics During the production of this model, the proportion of animals with medial orbital wall fractures and defects was up to 85%, indicating that the medial orbital wall fractures caused the orbital contents to be embedded into the ethmoid sinus, and the eyeball axis was behind. The volume of the orbital cavity increases, resulting in a sunken eyeball. Most of the animals with anterior orbital floor defect did not develop ocular retraction, indicating that changes in the volume of the orbital cavity in front of the eyeball axis did not cause changes in the eyeball position and did not cause ocular retraction. Approximately 40% of animals with posterior orbital floor defects develop ocular enophthalmos, indicating that an increase in the volume of the orbital cavity behind the ocular axis can cause ocular enophthalmos.

  (3) Comparative Medicine Orbital fracture is a common clinical trauma, which often results in loss of visual function and craniofacial deformity. The occurrence and severity of ocular inset are not proportional to the severity of orbital fracture. To clarify the mechanism of enophthalmos, and to determine whether enophthalmos occurs after orbital fractures early has important guiding value for the selection of clinical treatment options for orbital fractures. It is generally believed that orbital fractures cause the soft tissue in the orbit to diverge into the sinuses, reduce the volume of the orbital content, and cause enophthalmos. The main reasons for the occurrence of enophthalmos: when the orbital floor and the inner wall of the orbit are fractured, the volume of the bony orbital cavity is enlarged; the bone wall is ruptured and the soft tissue in the orbit forks into the maxillary and ethmoidal sinus, and the volume of the orbital soft tissue is reduced ; Extraocular muscles, muscle sheaths and soft tissue scars and scar contractures. The method for the defect of the medial orbital wall in this model is similar to the clinical symptoms, and can be used as an ideal animal model for orbital fractures and ophthalmos.