Summary
The strabismus surgeon must realize that Graves’ orbitopathy is a bilateral disease with asymmetrical restrictive involvement of all the extraocular muscles. Orbital imaging should be considered a standard of care to identify restrictive forces. When vertical deviations occur, consider a frank or occult cyclotropia, a pattern deviation, and a misdirection of the muscle’s intended anatomical alignment. Surgical techniques should incorporate flexibility, along with meticulous forced duction testing to document muscle, orbital, and conjunctival restrictive forces, and utilization of adjustment techniques that firmly secure the muscle to the sclera with nonabsorbable sutures.
When the physician encounters a Graves’ disease patient, it requires a skill set and care commitment that is unique and demanding. This disease impacts many aspects of the patient’s health. Without proper treatment, the management outcome may be irreversible vision loss or serious health conditions. The patient is best served by a team approach of specialists including an endocrinologist, a radiologist, an oculoplastic surgeon, an internist knowledgeable in immunotherapy, and mental health specialists.
Advances in understanding of the pathogenesis of this autoimmune disease have led to promising treatment options that may eliminate the need for orbital decompressions or even strabismus surgery. The treating physician’s goal is to identify the disease and intervene early, in order to eliminate or diminish the restrictive complications seen from the disease’s congestive and fibrotic stages. Appropriate clinical and radiographic documentation, in addition to smoking cessation, immunotherapy, and stabilizing the patient’s endocrine and medical condition, requires expedient coordination between the specialties.
Good communication with these patients facilitates patient treatment compliance and satisfaction.
12 Thyroid Ophthalmopathy
12.1 Introduction
Of the many challenging patients medical professionals encounter in their careers, the Graves’ ophthalmopathy or orbitopathy (GO) patients require a time allocation and a skill set that separates them from other patients. These patients require not only your medical skills but also your emotional support. Graves’ disease (GD) can be disfiguring, vision threatening, and at times life threatening.
This author personally knows these associated clinical and emotional concerns. I was diagnosed 30 years ago with hyperthyroidism associated with atrial fibrillation. I later developed GO after radio-iodine thyroid ablation. I experienced the complications and anxieties of oral steroids, marked exophthalmos, a relative scotoma, orbital decompression surgery, three strabismus operations, and a lid procedure.
Robert J. Graves, an Irish physician, in 1835 first described the disease in females with tachycardia, goiter, and exophthalmos. 1 Today we characterize GD as an autoimmune disease associated with thyroid dysfunction and abnormal levels of circulating thyroid hormones that is usually hyperthyroid (90%) 2 but can be hypothyroid or even euthryoid.
The entity is labeled in the literature as thyroid-related eye disease (TED), Graves’ ophthalmopathy or orbitopathy (GO), or thyroid-associated ophthalmopathy (TAO) when eye signs are identified in these patients. A small proportion of GD patients (13%) have a dermopathy, most commonly pretibial myxedema with associated acropachy or clubbing of fingers and toes. 3 Graves’ disease has a 0.25% population prevalence that occurs in 16/100,000 females and 2.9/100,000 males. 4 GO usually occurs in concert with thyroid dysfunction, but in some patients the GO may lag years after, or even begin before the initial diagnosis of GD. 5 , 6
Although GO may clinically present unilaterally, careful imaging of these patients confirms asymmetrical bilateral involvement with enlarged muscles in 91% of patients. 7 Only 15% of GD patients present with strabismus, 8 and in Bartley’s series, 9.2% of patients required strabismus surgery. 9
GO is a unique disease entity that presents a clinical and therapeutic challenge to the strabismus surgeons and their consultants. Knowledge of GO’s distinctive pathophysiology, clinical presentation, and imaging, therapeutic, and surgical considerations will help the physician and patient achieve a desirable outcome.
12.2 Etiology of Graves’ Disease
The inciting factor or factors of GD are unknown, but genetic and environmental factors have been implicated. The genetic etiology is elusive and cannot be traced to one gene or allele, but more than 70% of GD patients are thought to have a genetic connection. 10 Smoking is a known risk factor for both development and increased severity of GD. 11 Hyperthyroid patients treated with radio-iodine (33%) are at greater risk to develop GO compared to those treated with surgical (16%) and medical intervention (10%). 12 Concomitant treatment with glucocorticoids negates the increased risk of GO due to I-131 treatment. 13 Patients who live in areas of iodine and selenium insufficiency and those exposed to medications such as lithium, interferon alpha, interleukin-2, and antiretroviral therapy have an increased risk of GD. 14 Studies have shown toxic effects to thyroid cells from environmental pollutants, such as hydrocarbons and perfluorinated chemicals. 14
12.3 Pathophysiology
The pathophysiology of this immune disorder is complex, and the eye surgeon should have a working knowledge of the biologic mechanisms that explain the inflammatory nature of this disease. Novel medical treatment modalities used in clinical trials are based on the model of GD’s pathophysiology.
GD patients have excessive production of thyrotropin receptor autoantibodies (TRAbs), which activate thyroid-stimulating hormone receptor (TSHR) antigens, which reside in thyroid gland follicular cells. This interaction causes unregulated production of thyroid hormone, similar to, but independent of, the TSH pituitary–thyroid gland axis. In GD, memory T and B cells that produce cytokines and antibodies migrate into the obit. The high TRAb levels seen in many GO patients are propagated by these lymphocytic T cells and lymphocytic B cells through interaction with plasma cells. 10 , 15
TRAbs target TSHR expressed on orbital fibroblasts and adipose tissue. The orbital fibroblasts appear to be the autoantigens that are key to initiating the immunogenic response in GO. 16 There are two subsets of fibroblasts found in the orbit. The bone marrow–derived CD34+ fibroblasts that are found in the orbit and thyroid tissue of GO patients, but absent in healthy orbits, are reactive fibroblasts. 17 They are armed with TSH receptors and insulinlike growth factor 1 receptors (IGF-lRs) that, once stimulated, may initiate an inflammatory cascade, along with hyaluronic acid production. 17 , 18 These CD34+ fibroblasts add to the normally found CD34– fibrocysts, which may differentiate into orbital fat cells.17 CD34+ fibroblasts have many surface receptors including Thy-1 that differentiate these cells into mature orbital fat cells (Thy-1–) or myofibrocytes (Thy-1+). 19 The expression of Thy-1 surface receptors may explain the marked orbital and extraocular muscle (EOM) fibrosis and fat seen in GO. 19
Through TSH receptors found on CD34+ fibroblasts, TRAbs activate the initiation of the inflammatory cascade. 18 Inflammatory cells collect in the orbit and produce proinflammatory cytokines and hyaluronan, which lead to the congestive orbital changes in GO. 20 Hyaluronic acid and inflammatory cells incorporate into the matrix of the EOM, resulting in the EOM enlargement.
IGF-1 and IGF-1R have been identified as other factors that participate in the inflammatory initiation of GD. 18 IGF-1R is found on orbital fibroblasts and circulating B and T cells. In addition to regulating hemopoietic cell growth, differentiation, and immune cell response, IGF-1 has been shown to regulate thyroid cell function by interacting with TSH. 18 IGF-1 has also been shown to participate in hyaluronan production, a component seen in GO. 18 IGF-1R forms interacting complexes with TSHR. 18 Additionally, there is evidence to suggest that IGF-1–regulated IGF-1R on orbital fibroblasts may produce T-cell chemoattractants that propagate the finding we see in GO. 21
12.4 Medical Treatment
Because of IGF-1R’s intimate relation with the TSHR, and its implication in the pathogenesis of GO, treatment modalities targeting IGF-1 are being studied.
Teprotumumab is a human monoclonal antibody inhibitor of IGF-1R. A clinical trial was performed to assess the impact of teprotumumab on the activity and progression of moderate to severe GO. 22 Compared to the placebo group, those receiving teprotumumab intravenously every 3 weeks for 24 weeks showed a significant reduction in proptosis (similar to decompression surgery), reduced clinical activity score (spontaneous retrobulbar pain, pain on attempted eye movements, conjuctival hyperemia, eyelid redness, chemosis, swelling of the caruncle, swelling of the eyelids), and less diplopia. 22
Another approach to decrease the inflammatory cascade and reduce production of anti-thyrotropin receptor antibodies is to specifically target orbital B cells. Rituximab (RTX) is a monoclonal antibody that targets the CD20 antigen on the surface of lymphocytic B cells. 23 RTX prevents B-cell differentiation and promotes B-cell lysis. RTX has been reported to decrease TRAb levels, which should decrease T-cell activation, and B- and T-cell–derived inflammatory stimuli in GO patients. 23 One RTX GO clinical trial showed disease-modifying effects compared to methylprednisolone, but another RTX treatment trial showed no effect as compared to placebo. 24 , 25 Other immune modulating drugs such as methotrexate, cyclosporine A, and somatostatin analogues have been used with varying success. 26
Glucocorticoids provide nonspecific immunosuppression to suppress inflammation in GO patients with active disease. Oral steroids are commonly given to GO patients due to their ease of administration, but intravenous steroids appear to be more efficacious. 27 Bartalena et al have shown that moderate- to high-dose (4.98 or 7.47 g) intravenous methylprednisolone over a 12-week period will improve the clinical signs of GO, but up to 33% of these patients experienced relapse. 28 Selenium, an over-the-counter substance with antioxidative properties, in a dosage of 200 µg twice a day, has been shown to reduce inflammation and decrease progression of GO in mild cases. 29
12.5 Clinical Presentation
The ophthalmologist may be the first physician the GD patient encounters. Subtle complaints such as intermittent periorbital edema, red eyes, bulging eyes, or tearing may initiate the office visit. With careful questioning the patient may confirm blurred or fluctuating vison, periorbital edema worse in the morning, or brow pain. The patient with more advanced GO may initially present with diplopia or loss of vision. The history should include questions about weight fluctuation, temperature intolerance, dry skin and hair, sweating, constipation, frequency of stools, memory loss or confusion, rapid heart rate, tremors, and shortness of breath or fatigue, which point to possible thyroid dysfunction.
A social history about smoking is essential. Smokers have more aggressive disease, with a five times greater risk of GO as compared to nonsmokers. 30 Additionally, smokers don’t respond well to surgical or medical intervention and may experience a higher recurrence rate years after surgery. 11 , 31 , 32 GO patients must be informed of the risk of smoking and the negative association of smoking to the disease process and surgical options.
A positive family history for thyroid dysfunction is common in GD patients. 33
12.6 Graves’ Orbitopathy: Differential Diagnosis
When the patient presents with the classic signs and symptoms of GO, along with supporting laboratory and imaging studies, diagnosis is straightforward. The euthyroid patient with inflammatory eye and orbital signs presents a greater diagnostic challenge. A number of orbital diseases mimic GO. These disorders include inflammatory, autoimmune, infectious, neoplastic, vascular, and neuromuscular entities (Table 12‑1). 34
Autoimmune |
|
Inflammatory |
|
Infectious |
|
Neoplastic |
|
Vascular |
|
Orbital infections are usually abrupt and are associated with fever and leukocytosis. Imaging may show an abscess formation or contiguous sinus disease.
Orbital pseudotumor is a nonspecific orbital disease, which can present with clinical findings similar to GO. Diffuse inflammation occurs and may include periorbital swelling, proptosis, and the restrictive motility patterns seen in GO. Imaging studies are not helpful in distinguishing this entity from GO, and specific laboratory findings to identify pseudotumor are lacking. Biopsy shows nonspecific inflammation. Pseudotumor patients typically respond to corticosteroid treatment and possibly other anti-inflammatory modalities. The diagnosis of orbital pseudotumor is one of exclusion; rule out other causes of orbital inflammation, and document a positive response to anti-inflammatory agents. IgG4-related disease is an orbital inflammatory entity with IgG4-bearing plasma cells that may represent a subset of idiopathic pseudotumor patients. 35
Sarcoid disease causes noncaseating granulomas, which can present with an orbital component. In addition to lacrimal gland infiltration, the eye muscles and associated orbital tissues can be involved and mimic GO. If the thyroid gland is infiltrated by sarcoid granulomas, the patient may present with hypothyroidism. Female patients with sarcoidosis have a higher incidence of clinical hypothyroidism. 36 Biopsy of a conjunctival nodule, a lacrimal gland, or orbital tissue confirms sarcoidosis.
Crohn’s disease is a granulomatous autoimmune disease, which can present with an orbital inflammatory component. 37 Scleroderma, another autoimmune disease, can be associated with EOM fibrosis and mimic GO. 38 Lupus, an autoimmune vasculitis, is frequently associated with a rash and arthritis but may present with orbital inflammation. 39
Myasthenia gravis (MG) patients present with variable diplopia and can later develop restrictive ophthalmopathy, with motility restrictions similar to GO. Up to 10% of MG patients have associated GD, and 1% of GD patients experience MG. 40 , 41
Orbital myositis presents with pain, proptosis, and EOM restriction. Unlike GO, which spares the muscle tendon, magnetic resonance imaging (MRI) of myositis shows tendon involvement. These patients respond well to corticosteroid treatment but frequently relapse and may require other treatment modalities. 42 , 43
The euthyroid patient with painless proptosis needs to be evaluated for possible neoplasm. Orbital lymphomas may infiltrate the EOMs, causing a clinical presentation similar to GO. 44 Lesion biopsy will identify the cell line of this neoplasm. Other tumors infiltrating the orbit, both nonmalignant and malignant, must be considered when a patient presents with diplopia but proves negative for thyroid disease by testing.
Carotid-cavernous sinus fistula and arteriovenous malformations may present with engorged bulbar vessels and proptosis.
12.7 A Team Approach
GD patients require a multispecialty team approach. An endocrinologist or a primary care service assists in normalizing the patient’s thyroid function and GD-associated medical problems. An immunologist conversant in targeted and nonspecific immune therapy administration may be consulted. An experienced radiotherapy physician may be needed in special GO cases that are poor surgical candidates or don’t respond to medical treatment.
The radiologist provides the imaging information of EOM size, orientation, and inflammatory activity. Sequential MRIs establish disease progression or stability. Mental health professionals may be needed to address the depression or anxiety GD patients can experience, and tobacco cessation programs should be part of comprehensive GO treatment.
The oculoplastic surgeon addresses orbital congestion and lid malposition. Orbital decompression surgery may be needed to treat dysthyroid optic neuropathy (DON) or corneal exposure and excessive proptosis due to enlarged EOMs and orbital congestion. Tarsorrhaphy is needed at times to address corneal exposure. Sequential visions, MRIs, exophthalmometry readings, motility measurements, and external photographs monitor disease progression or stability.
12.8 Ophthalmic Examination
By concentrating on only the motility disturbance of a GO patient, subtle vision-threatening signs may be missed. The GD patient needs sequential measurement of refraction and vision, Hertel exophthalmometry, intraocular pressures (IOPs), perimetry, and optical coherence tomography (OCT).
Baseline refraction establishes the best-corrected vision, and is useful to document disease progression. A hyperopic refractive shift may occur due to globe-shortening axial pressure from the increased orbital volume. Conversely, the globe may experience sequential lengthening or a myopic shift if the muscles and orbital tissues compress the globe at its equator. Pressure from engorged orbital tissues or asymmetrical muscle enlargement can also induce astigmatism. These refractive changes can continue through the active inflammatory phase of GO and require frequent spectacle changes. Orbital decompression or strabismus surgery can also impact refraction. 45 , 46
Tonometry readings are recorded in primary gaze, upgaze, and side gaze, as a fibrotic or enlarged EOM can elevate the IOP. GO patients with elevated IOPs are at risk of open angle glaucoma. 47 Visual fields along with OCTs to establish nerve fiber layer thickness determine whether the patient needs medical or surgical intervention to lower the IOP.
The palpebral distance with upper lid margin to corneal reflex distance (margin reflex distance 1 [MRD1]) and lower lid margin to corneal light reflex distance (MRD2) measurements, in addition to Hertel exophthalmometry readings, documents progression of GO. The slit lamp identifies conjunctival chemosis, hyperemia, and superficial punctate keratopathy or frank corneal ulcerations.
The pupils are examined to rule out afferent pupillary defects. Diminished visual acuity and sequential red color desaturation indicate possible optic nerve compromise from the orbital congestion and muscle enlargement. 48 Central, paracentral, and enlarged blind spot scotomas on visual field testing are associated with compressive DON. The optic nerve is also monitored by OCT for progressive retinal nerve fiber damage or changes in optic nerve volume.
Closed lid eye palpation establishes whether the orbit is tight or soft. A globe that moves freely into the orbit without resistance may tolerate increases in thyroid orbital congestion without optic nerve compromise. A tight orbit increases the potential for optic nerve compromise. Patients with tight orbits, elevated IOP, and active signs of orbital inflammation need frequent clinical visits.
To control diplopia, the patient can be offered a patch or prisms. A Fresnel prism over one spectacle lens helps reestablish fusion if the patient has that capacity and torsion is not severe. Prisms help determine whether the deviation is stable or changing. A unilateral Fresnel prism can eliminate both horizontal and vertical deviation by tilting the prism from its horizontal or vertical orientation to neutralize the combined deviation. This eliminates the decreased vision when Fresnel prisms are placed on both spectacle lenses (Fig. 12‑1). Patients may wear Fresnel prisms indefinitely. If the GO patient has a stable motility pattern, permanent ground-in prism glasses are prescribed. In general, a maximum of 16 to 20 prism diopters or less, split equally between the two lenses, is tolerated on high-index spectacle lenses.
Botulinum toxin (BT) injections address diplopia in GO patients presenting without significant fibrosis. In some reports there has been permanent elimination of diplopia or improved deviation angle (Chapter 6). 50 , 51 Granet et al reported a better response to BT injections in GO patients with 20 diopters deviation or less, with elimination of surgical intervention in 32% of the 22 patients. 51
Strabismus surgery should be delayed while exophthalmometry readings, visual acuity, visual fields, and motility measurements are changing. However, orbital decompression, radiation, or medical intervention to treat optic nerve compromise or significant ocular exposure should not be deferred. A number of studies cite changes in motility patterns after orbital decompression surgery. 52 , 53 Variables contributing to strabismus after decompression surgery include which orbital bones are removed, how much bone and fat is removed, the operative approach, the degree of pre- and postoperative inflammation, and presence of preoperative strabismus. Patients requiring more proptosis reduction tend to have an increased risk of postoperative diplopia, as do smokers and patients with preoperative diplopia. 54 Medial orbital wall decompressions were associated with esotropia in 77% of patients, but there are also case reports noting improvement or elimination of diplopia after decompression surgery. 55 , 56
12.9 Surgical Planning
GO strabismus surgery requires careful planning and flexibility. The strabismus surgeon needs to identify all the restrictive forces and be willing to alter the initial surgical plan during the case.
Wallang et al cited 11 clinical studies analyzing surgical outcomes of strabismus surgery for GO. 57 Reoperation rates in these studies were as high as 45%. 58 Some of these studies predate the availability of orbital imaging and adjustable suture techniques.
12.9.1 Ocular Ductions Point to the Offending Muscle(s) or Orbital Tissues
Difficulty abducting an eye points to a tight medial rectus (MR) or adhesions in the medial orbit. A limitation of supraduction or infraduction suggests possible tight depressor or elevator muscles including the obliques, or adhesions within orbital tissue.
Grading restricted vertical or horizontal ductions as –4 (no movement past primary position), –3 (75% reduction limit past primary position), –2 (50% reduction), or –1 (25% reduction) gives reference points to the position of the eye for future documentation, aided by external photography (Fig. 12‑2).
To distinguish a paretic etiology from a tight muscle as the cause of motility limitation, in-office forced duction and force generation testing are performed (Section 3.2.2). In addition to the double Maddox rod test to measure torsion, the macular position (relative to the disc), as recorded with the indirect ophthalmoscope or fundus photography, establishes cyclotropia, which is especially useful in nonverbal patients (Chapter 11). With restrictive inferior rectus (IR) muscles, associated excyclotorsion is frequently encountered. 59 A tight superior rectus (SR) or superior oblique (SO) induces incylotorsion.
Prism and alternate cover testing (PACT) is performed in all cardinal fields of gaze for distance and near with the patient’s best-corrected vision. Incomitant horizontal or vertical prism measurements result from unequal restrictive EOMs or intraconal or extraconal adhesions. These restrictive forces may cause head posturing (face turning or chin up or down positioning) to maintain fusion. Tight IR muscles present with a chin up appearance. A tight MR directs a face turn in the direction of the offending muscle.
During the PACT, the examiner should ask the patient whether he or she can establish a single binocular image with the neutralized prism in place. If there is an affirmative response, this confirms the appropriate angle of deviation and the presence of good fusional capabilities. If the patient notes diplopia with neutralized prisms in place, this may signify poor central fusion, a residual vertical or horizontal deviation, or a torsional component to the deviation.
Typically, IR restrictions are present in both eyes, but they may be asymmetrical. To determine if one or both IR muscles should be weakened surgically, fixation testing in the office may be useful. Head position is assessed while the more hypotropic eye is occluded. If the patient maintains a chin up fixation, then asymmetrical bilateral IR weakening is planned. If the head position straightens when the more hypotropic eye is covered, only unilateral IR recession is needed.
The potential impact of the “silent” tight SR and SO muscles should be considered when an IR is weakened. If the patient’s hypotropia increases when the hypotropic eye looks down and in adduction, the contralateral SR may be tight or the ipsilateral SO may be overacting.
The amount of excyclotorsion will help unmask a silent superior muscle. A tight SO reduces the expected degree of excyclotorsion caused by a tight IR. A fibrotic or overacting SO can cause marked incyclotorsion, vertical deviation, and a postoperative A pattern after IR muscle recession. Imaging is also useful in documenting the presence of an enlarged SO. 60
12.10 Imaging Studies
The imaging hallmark of GO is enlargement of the EOMs from their normal state with sparing of the muscles’ insertions. The average muscle thicknesses approximately 1 cm posterior to the globe can be used in conjunction with other clinical signs to establish the GO diagnosis and note disease progression. The established average diameters of normal EOMs are as follows: IR width 4.8 mm, MR width 4.2 mm, SR width 4.6 mm, and lateral rectus (LR) width 3.3 mm. 61 , 62
Computed tomography (CT) scans are superior for imaging the orbital bones and apex, and are therefore the preferred study of orbital surgeons. The unique properties of MRI allow better viewing of EOM detail, and can document active versus chronic disease without the risk of irradiation.
T1-weighted (T1W) MRI images analyze the size and configuration of the orbital structures, while T2-weighted (T2W) images assist in evaluating the composition of orbital structures. T1W coronal and axial images are used to measure proptosis, muscle diameter, and apex crowding. T2W images can estimate the water content of tissues. Normal weighted T2 images of rectus muscles with low water content may signify fibrotic, non-active disease. Prolonged or high weighted T2 images indicate a higher water content or edema, suggesting active muscle inflammation. Patients with T2W images indicating active inflammation have been shown to be more responsive to medical therapy than those with normal T2W images. 63
The horizontal diameters of the MR and LR muscles are reliably measured in the axial plane, while the SR, SO, and IR muscle vertical diameters are best measured in the sagittal plane.
Although conventional wisdom teaches us that the MR and IR muscles are frequently involved in GO, the LR, oblique, and SR muscles can also be involved in the generalized inflammatory response. Radiographic studies note generalized bilateral extraocular involvement in most GO patients that present with unilateral clinical signs and symptoms. 7 , 64 These “clinically silent” and minimally enlarged EOMs may cause problems after their antagonistic muscles are weakened surgically. Once an opposing tight muscle is surgically weakened, the silent tight antagonist muscle projects forces not anticipated and results in overcorrection. For example, a thickened ipsilateral SR documented by imaging in cases where the IR was recessed is associated with an overcorrection and decreased infraduction. 65 Postoperative A or V patterns that were not seen preoperatively may also be caused by these clinically silent tight muscles.
Thyroid ophthalmopathy may be associated with muscle displacements, which may be caused or exacerbated by orbital decompression. Diagnosis and correction of displaced muscles is discussed in Chapters 19 and 30.
12.11 Extraocular Muscle Involvement
12.11.1 Medial Rectus Muscle
GO patients presenting with esodeviation and abduction deficits need recession of the offending muscle(s). Tight MR muscles are recessed symmetrically or asymmetrically, depending on the preoperative motility measurements and intraoperative forced duction testing. Forced duction may identify a tight LR that could cause an unintended overcorrection, in which case the MR recession amount should be reduced slightly (Video 12.1).
Rectus muscle recession technique is the same as the standard techniques (Chapter 23), except for a few important differences. These muscles require meticulous dissection due to their fibrotic and engorged character. Prior to disinsertion, the longitudinal orientation should be noted. If there is misdirection from their anatomical plane (muscle displacement), this should be corrected with myopexy, along with the recession (Chapter 30). It is important to perform forced ductions after the MR muscle is removed from its insertion. Posterior medial orbital restrictions contributing to the esotropia, or a tight LR, would be missed without this maneuver (Video 12.2).
12.11.2 Lateral Rectus Muscle
The LR muscles may need to be explored if the forced duction test confirms tightness. Muscle belly misdirection, or displacement, can occur from previous orbital decompression surgery, and should be addressed. A displaced LR could contribute vertical and torsional components to the deviation (Chapter 19).
12.11.3 Inferior Rectus Muscle
Because the IR actions include depression, excyclotorsion, and adduction, recession of these tight muscles can lead to downgaze A-pattern exotropia with incyclotorsion, which may be mitigated by a medial transposition of the insertion by one-half to one tendon width. However, when the IR is recessed and medially transposed, the SO is stimulated to depress and intort the eye, potentially also causing an A-pattern exotropia with incyclotorsion. Elevating the MR insertion will collapse the A-pattern exotropia but increase incyclotorsion. Weakening the tight SOs when simultaneously recessing the IRs can both collapse the A-pattern exotropia in downgaze and decrease incyclotorsion. If just one tight IR is recessed, the primary position may be aligned but with a resulting undesirable reverse diplopia in downgaze. There are several options to limit or prevent this while maintaining fusion in primary gaze. Either asymmetrical recession of both IRs is performed, or recession of the contralateral SR with reduced recession of the ipsilateral tight IR may help (Fig. 12‑3). A third option is to perform a restrictive procedure such as scleral or pulley posterior fixation to the contralateral IR (Chapter 33).
The average amount of excyclotorsion reduction with a single IR recession without nasal transposition in GO patients is 2.5 degrees (range 1–5 degrees). 66 Recession with a half tendon width transposition averages 4 degrees (range 3–8 degrees) excyclotorsion correction, while a full tendon transposition averages 11.7 degrees (range 8–15 degrees) reduction. 66
After the IR is disinserted, forced duction testing is again performed to identify restrictive forces unrelated to the muscle itself, as well as to uncover silent SR or SO restrictions.
Progressive late overcorrection after IR recession in GO was described by Sharma and Reinecke. 67 IR surgery overcorrection can be encountered in more than 40% of patients (Fig. 12‑4). 68 Kerr demonstrated that absorbable sutures were associated with a greater risk of late overcorrection in GO IR recessions, which was reduced by the use of nonabsorbable sutures. 68 She also found that unlike the IR, other recessed rectus muscles in GO did not experience postoperative shift or overcorrection when absorbable sutures were utilized.
There may be several mechanisms to explain the predisposition of a GO IR recession to late overcorrection. Sharma and Reinecke postulated that the Bell phenomenon places increased force on the IR during sleep. 67 Chatzistefanou et al imaged GO recessed IR muscles on the first day after surgery, and showed poor apposition of these suspended muscles to the globe. 69 If there is a reduced arc of contact with an absorbable suture, this could promote IR displacement posterior to the intended surgical position.
Ludwig has postulated that tension on the new surgical muscle insertion site, due to pull from the tight IR, causes lengthening or stretching of the scar between the muscle tendon and sclera. 70 , 71 If the GO muscle already has fibrosis or a residual inflammatory component, this would also weaken healing and increase scar stretch. A tight silent ipsilateral SR would also contribute to the tension across the IR insertion and contribute to late overcorrection. Sprunger and Helveston reported increased overcorrection after IR recession when adjustable sutures were used. 72
The use of nonabsorbable sutures may play a role in stabilizing late overcorrection of these tight muscles, which are subject to forces from restrictive ipsilateral antagonists not usually encountered in non-GO patients. The use of nonabsorbable sutures with direct scleral attachment (avoiding hang-back or adjustable sutures) during IR recession in GO patients may enhance the point of contact, potentially preventing posterior migration or stretch.
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