There are two main types of orbital decompression surgery: orbital wall decompression surgery and orbital fat decompression surgery. Orbital wall decompression surgery can be performed by removing the orbital wall to expand the volume of the orbit, effectively improving the protrusion of the eye and relieving orbital crowding. Orbital fat decompression surgery can be performed by removing orbital fatty tissue to achieve decompression and improve orbital protrusion to some extent. In recent years, orbital wall decompression surgery combined with orbital fat decompression surgery has begun to gain popularity and become the mainstream surgical approach. The safety of the combined procedure can be controlled and the results are significantly better than either single orbital wall decompression surgery or orbital fat decompression surgery. The “cycloplegic” approach, first described by McCord in the early 1980s, involves an external canthotomy combined with an inferior fornix conjunctival incision, which can be extended medially if required to provide adequate access to the orbital wall and orbital fat for most orbital decompression procedures. As an alternative, an inferior or medial conjunctival incision, and a double lid incision can be used alone or in combination. Orbital fat decompression surgery has never been as popular as orbital bone wall decompression surgery because of the theoretical high probability of complications, including injury to the motor ganglion, lacrimal nerve, orbital vessels, extraocular muscles, optic nerve, and ocular globe. Although there are theoretical risks associated with orbital bone wall decompression surgery, serious complications are rare in clinical practice. The major complications of orbital bone wall decompression surgery include: 1) permanent diplopia; 2) infraorbital nerve palsy; 3) paranasal sinusitis; 4) lower lid entropion; and 5) displacement of the eye. However, serious complications such as cerebrospinal fluid leakage, central nervous system infection, injury to the eye and optic nerve and its vessels, cerebral vasospasm, ischemia and infarction are very rare. Reactivation of thyroid-related eye disease is another rare complication of orbital decompression surgery. Reactivation presents with the same signs as the active phase in the weeks following surgery, with imaging showing thickening of the extraocular muscles, followed immediately by a normal recovery period. This is clinically referred to as delayed decompression-related reactivation (DDRR), which occurs in 1.3% of cases and can be managed by systemic immunosuppressive therapy and orbital radiation therapy. Most of the possible complications of orbital decompression surgery cannot be predicted Complication prevention is based mainly on guideline recommendations but is not specific and includes careful handling of orbital contents, precise dissection of orbital fat, and avoidance of vasodilator drugs and/or orbital transthermal therapy. Paranasal sinusitis can be prevented simply and effectively by ensuring adequate sinus cavity opening during decompression of the bony wall. Complications such as infraorbital nerve palsy and pain, ocular displacement, cerebrospinal fluid leakage, and central nervous system infection can be effectively prevented by measures such as 1) precise evaluation with preoperative imaging, 2) adequate design planning of surgical interventions, and 3) prophylactic antibiotic application as necessary. Strict adherence to methodological specifications for orbital decompression surgery can help assess the magnitude of the patient’s risk of complications. Patients with low septal paper-like plates who undergo medial orbital wall decompression surgery need to be alerted to the risk of cerebrospinal fluid leakage. When patients are at high anatomic risk, delayed entropion and inferior ophthalmoplegia can be prevented simply and effectively by avoiding medial inferior wall decompression.