Three wall orbital decompression







Table 64.1

Indications for surgery













Disfiguring proptosis
Compressive optic neuropathy unresponsive to maximally tolerated medical therapy
Exposure keratopathy unresponsive to maximally tolerated medical therapy
Preparation for strabismus surgery with large angle deviation
Deep aching pain and pressure from proptosis


Table 64.2

Preoperative evaluation















Exophthalmometry readings
Extraocular muscle movements and primary deviation
MRD1, MRD2, degree of upper and lower eyelid retraction, lagophthalmos
Optic nerve function – relative afferent pupillary defect (RAPD), color perception, visual field testing, optic nerve head examination
CT scan – sinus relationships, muscle size and bone volume
Thyroid status including thyroid function tests


Table 64.3

Algorithm for average proptosis reduction by degree of bone removal






















Area of decompression Proptosis reduction
Orbital fat 2 mm
Orbital fat and lateral wall 4 mm
Orbital fat, lateral wall, and medial wall 6 mm
Orbital fat, lateral wall, medial wall, and floor 8 mm
Orbital fat, lateral wall, medial wall, floor, and lateral rim removal 10 mm


Introduction


Thyroid-related orbitopathy (TRO) is the most common cause of proptosis in adults. TRO is caused by an autoimmune process that leads to deposition of extracellular matrix in the orbital soft tissues that attracts water, causing swelling. This primarily occurs in the extraocular muscles; however, some patients have activation of orbital fat, leading to adipogenesis and fat hypertrophy. As with most autoimmune diseases, women have a 6 : 1 predilection for the disease. Factors associated with worsening disease include smoking, but tobacco use is not causal.


The most common eye manifestation is eyelid retraction, but other findings include: proptosis, restrictive strabismus, chemosis, conjunctival injection, eyelid edema, eyelid erythema, and optic neuropathy in severe cases. Approximately 90% of patients with eye findings are hyperthyroid, with the remaining 10% being either euthyroid or hypothyroid. CT imaging can reveal enlarged extraocular muscles (type II disease) and/or enlarged fat compartments (type I disease) in the orbit. The most commonly enlarged extraocular muscles in decreasing order are: inferior, medial, superior and lateral rectus muscles. The tendon insertions are typically spared from enlargement compared to myositis seen with idiopathic orbital inflammation.


Treatment is based on symptoms and severity of disease. Patients with optic neuropathy require urgent medical treatment followed by orbital decompression if resistant. In patients requiring elective surgical intervention, a staged approach is recommended (with not all stages being required) in order: orbital decompression, strabismus surgery, and eyelid surgery.


The decision to perform orbital decompression depends on many factors. The most common indication is disfiguring proptosis ( Table 64.1 ). The orbital aspect of the autoimmune process is self-limited and many patients have spontaneous improvement once the active inflammatory phase ends. Elective surgical rehabilitation should occur in the quiescent phase. Orbital decompression is an effective operation to help restore the proptosis to the pre-disease state. The preoperative evaluation must include measurement of exophthalmos and imaging ( Table 64.2 ). Symptoms of deep ache and pressure often resolve after orbital decompression. Our algorithm for decompression is seen in Table 64.3 .




Figures 64.1A and 64.1B


Preoperative surgical planning

Figure 64.1A shows an anatomic representation of bone removal during orbital decompression. The lateral wall is depicted in “A” shaded yellow, medial wall in “B” shaded blue, and floor in “C” shaded red. Removal of the lateral orbit rim is covered in Chapter 65 . Access to the lateral wall is achieved through a temporal upper eyelid crease incision ( Figure 64.1B , “A”). Medial wall decompression is achieved through a transcaruncular incision ( Figure 64.1B , “B”). Access to the orbital floor is achieved via a lateral canthotomy and inferior transconjunctival incision ( Figure 64.1B , “C”).

May 16, 2019 | Posted by in Reconstructive surgery | Comments Off on Three wall orbital decompression
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