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Graves Disease Orbital Decompression

Editor: Craig N. Czyz Updated: 10/7/2022 5:37:41 PM


Thyroid eye disease (TED), or thyroid-associated ophthalmopathy (TAO), thyroid orbitopathy, Graves’ orbitopathy, or Graves’ ophthalmopathy, causes orbital congestion and proptosis due to extraocular muscle and orbital fat enlargement with fibrosis[1]. These anatomical alterations can result in compressive optic neuropathy, exposure keratopathy, and ocular motility disorders. Treatment of proptosis from thyroid eye disease consists of orbital decompression, taking advantage of the adjacent sinus spaces to expand orbital volume. Based on patient presentation, the amount of decompression required is determined on a case-by-case basis. For example, in cases of moderate to severe proptosis, medial wall, lateral wall, and floor decompression can be done, taking advantage of the adjacent ethmoid sinuses, maxillary sinus, and orbital trigone, respectively.

Anatomy and Physiology

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Anatomy and Physiology

The orbits contain the globes, extraocular muscles, nerves, fat, and blood vessels. The orbits are relatively cone-shaped, tapering from anterior to posterior. The average adult orbit is approximately 35mm in height, 45mm in width, and 45 mm in length, with a volume of 30 cm3. The bony orbit is made up of 7 different bones[2]:

  1. The frontal bone and the lesser wing of the sphenoid form the orbital roof.
  2. The maxillary, palatine, and zygomatic bones form the orbital floor.
  3. The ethmoid, lacrimal, and greater wing of the sphenoid form the medial orbital wall.
  4. The zygomatic bone's frontal process and the sphenoid's greater wing form the lateral orbital wall.

Medical wall decompression can be done via a transcaruncular approach[3], while a transconjunctival approach can be performed to access the orbital floor. Lateral wall decompression involves removing the deep lateral orbital wall bone, known as the trigone. Alternatively or additionally, the inner surface of the super and/or lateral walls can be thinned using a burr.


Compressive optic neuropathy, exposure keratopathy, and proptosis are key indications for orbital decompression in general[4]. Three-wall decompression can benefit those with moderate to severe symptoms, including compressive optic neuropathy[5].


Patients who are systemically unstable for a surgical procedure or who are unwilling to accept the potential surgical complications. Relative contraindications include chronic sinusitis, orbital infection, immunocompromise, bleeding disorders, and atretic sinuses.


Equipment varies depending on the approach and procedure.


Oculofacial Plastic Surgeon or any surgeon with advanced training in orbital surgery.


Complete ophthalmic evaluation, including dilated fundus exam. Orbital imaging (CT/MRI) is used to evaluate anatomy and disease status[6]. Routine preoperative history and physical for surgical clearance should include evaluation of thyroid function and acetylcholine receptor antibody testing in selected cases.

Technique or Treatment

Below is a 3-wall decompression with lateral orbital rim advancement. General endotracheal anesthesia is administered. A mixture of 2% lidocaine with 1:100,000 epinephrine and .75% Marcaine in a 1:1 is injected into the caruncle and inferior conjunctiva via a transconjunctival approach. The patient is then prepped and draped in a standard sterile fashion suitable for oculofacial surgery. Place a corneal shield. A lid-splitting incision starting at the lateral canthus is performed with a No. 15 Bard-Parker blade. Cutting electrocautery is used to incise the periosteum of the lateral orbital rim. A Freer elevator is used to free the periosteum from the underlying bone of the external lateral orbital rim. The temporalis muscle and fascia are separated from the lateral orbital rim with a No. 9 elevator. A similar maneuver frees the periorbita from the intra-orbital lateral orbital rim.

Attention is then placed on the orbital floor, where a Desmarres retractor is used to retract the lower lid while a Jaeger lid plate is used to protect the globe. Cutting electrocautery was used to dissect through the conjunctiva, lid retractors, and inferior orbital rim periosteum. A Freer elevator freed the orbital floor periosteum from the underlying orbital floor. Attention is then placed on the medial wall via a trans-caruncular approach. Westcott scissors create a surgical plane between the caruncle and plica semilunaris. Blunt dissection with Steven scissors is directed to the posterior lacrimal crest, and a Freer elevator is used to open the medial periosteum. A Freer elevator is then used to free the periosteum from the underlying medial wall. A malleable retractor retracts the orbital contents and exposes the subperiosteal plane. The subperiosteal dissection is continued until the lamina papyracea of the medial wall is visualized and the appropriate amount of the medial wall is exposed. Once exposure of the medial wall and the orbital floor is complete, attention is returned to the lateral wall.

An oscillating saw creates an osteotomy at the superior and inferior lateral wall margins. Kocher clamps are used to remove the lateral orbital wall carefully, and cutting electrocautery separates this wall from the underlying temporalis muscle and fascia. Kerrison rongeurs and a burr (piezoelectric bone saw/burr) are used to remove bone from the deep lateral wall. Care is taken to avoid any CSF leak. Bone wax is used for hemostasis. Attention is placed back to the orbital floor.

An osteotome and mallet create a bone window through the posterior medial orbital floor. The bone of the orbital floor is removed with pituitary forceps and up-biting Kerrison rongeurs. Care is taken to avoid the infraorbital nerve bundle and orbital strut. Once an adequate orbital floor decompression is performed, oxymetazoline is irrigated through the area for hemostasis. Attention is then placed on the medial wall.

A Freer elevator is used to fracture the medial orbital wall. The bone of the medial orbital is removed with a (pituitary/Takahashi) forceps. Underlying ethmoid air cells and mucosa are also removed. Once adequate medial bony decompression is performed, the area is irrigated with oxymetazoline for hemostasis.

A No. 12 Bard-Parker blade is used to incise the periorbita, allowing orbital fat to prolapse forward. A malleable retractor is placed as counter-traction in the subperiosteal plane while gentle pressure is placed on the globe, allowing orbital contents to prolapse into the decompressed medial orbit.

Attention is returned to the lateral orbit, where the periorbita is incised inferior to the lateral rectus to allow orbital fat to spill forward. The bone flap is thinned with a burr and then replaced with a 4-0 prolene suture through predrilled holes or a low-profile curvilinear plate with screws. The bone can be replaced further anteriorly if the surgeon desires to advance the lateral canthal angle.

The trans-caruncular incision is closed with a 6-0 plain gut suture in a buried interrupted fashion. The transconjunctival incision is not closed to prevent postoperative lid retraction. The lateral lower lid is secured to the common canthus and lateral orbital rim with a 5-0 vicryl suture. The deep subcutaneous tissue of our lid splitting incision is closed with 5-0 vicryl suture in a buried interrupted fashion. The skin is closed with 6-0 plain sutures in a running fashion.

After removing the corneal eye shield, an ophthalmic antibiotic ointment is placed on the ocular surface. The patient is extubated and taken to the recovery area in stable condition.


The complications that can manifest with Graves Disease orbital decompression include the following:

  • Orbital hemorrhage
  • Orbital compartment syndrome
  • Optic nerve injury
  • Infection
  • Diplopia
  • Restricted motility
  • Subconjunctival hemorrhage
  • Vision loss
  • Globe dystopia
  • Globe rupture
  • Hypoesthesia (V2)
  • Eyelid retraction or ptosis
  • Vitreous hemorrhage
  • Retinal detachment
  • Cerebrospinal fluid leak[7]
  • Lacrimal drainage system injury
  • Keratopathy
  • Scarring
  • Lid laxity/malposition
  • Canthal angle distortion

Clinical Significance

Thyroid eye disease is an autoimmune, inflammatory disorder associated most commonly with Graves' hyperthyroidism. TED's most common clinical feature is eyelid retraction[8], and TED is the most common cause of unilateral or bilateral proptosis. TED is associated with hyperthyroidism in 90% of patients, but euthyroid and hypothyroid disease states can also result in TED. About 30% of patients with Graves' hyperthyroidism have TED at the time of diagnosis or develop TED in the future, and the severity of the disease does not necessarily parallel serum levels of T4 or T3. Female gender and smoking are associated with increased risk and severity of TED, respectively[9]. Decreased vision due to optic nerve compression, present in approximately 2% of all patients with TED, requires urgent orbital decompression.

Enhancing Healthcare Team Outcomes

When patients with Graves' ophthalmopathy present with visual changes, a prompt referral to an ophthalmologist should be made. If surgery is necessary, the primary care provider, nurse practitioner, and endocrinologist should optimize the patient's functional status. In most patients with acute ocular symptoms, urgent decompression is required. The outcomes depend on the chronicity of the condition and the extent of optic nerve damage.



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