© Springer Science+Business Media New York 2015
Raymond S. Douglas, Allison N. McCoy and Shivani Gupta (eds.)Thyroid Eye Disease10.1007/978-1-4939-1746-4_88. Medical Management of Mild and Moderate to Severe Thyroid Eye Disease
(1)
Newcastle Eye Centre, Royal Victoria Infirmary, Newcastle upon Tyne, UK
(2)
Department of Endocrinology, Royal Victoria Infirmary, Queen Victoria Road, Elliott Building, Newcastle upon Tyne, NE1 4LP, UK
Keywords
Thyroid eye diseaseGraves’ diseaseGraves’ orbitopathyManagementTreatmentIntroduction
The distinction between “mild” and “moderate to severe” thyroid eye disease (TED) is blurred and definitions vary. Distinguishing “normal” from “mild” may be even harder. Clinicians who are newcomers to the field of TED are usually surprised by the disparity between the objective clinical findings and the patient’s perception, the latter often thought by the observer to be exaggerated. The reverse can also be true, though it is much rarer; in the authors’ experience, it tends to be associated with older patients. What is enlightening in every new case of TED is comparison of the present appearance with photographs of the patient prior to the onset of the eye disease. This should be regarded as an essential clinical assessment of no less importance than measuring proptosis or serum levels of thyroid antibodies. The definitions of mild and moderate-to-severe eye disease represent a combination of objective findings and the subjective impact of the disease for that individual [1].
Classification of disease severity of patients with TED [1]
Sight-threatening thyroid eye disease
Patients with compressive optic neuropathy (CON) and/or corneal breakdown. This category warrants immediate intervention.
Moderate to severe TED
Patients without sight-threatening disease whose eye disease has sufficient impact on daily life to justify the risks of immunosuppression (if active) or surgical intervention (if inactive). Patients with moderate to severe TED usually have any one or more of the following: lid retraction ≥2 mm, moderate or severe soft tissue involvement, exophthalmos ≥3 mm above normal for race and gender, inconstant or constant diplopia.
Mild TED
Patients whose TED signs and symptoms have only a minor impact on daily life. Patients usually have one or more of the following: minor lid retraction (<2 mm), mild soft tissue involvement, exophthalmos <3 mm above normal for race and gender, transient or no diplopia, and corneal exposure responsive to lubricants.
Clinical Assessment
The pertinent initial questions that need to be addressed include the following:
Is the diagnosis of TED correct?
How severe is the disease?
How active is the disease?
What is the impact of the disease on the patient?
Is the patient euthyroid?
Is the patient a smoker?
The diagnosis of TED is usually obvious, though atypical presentations (Chap. 9) can be challenging. A variety of other diagnoses may masquerade as TED [4]. The severity of the eye disease can be documented on the basis of the NOSPECS classification (Dickinson and Perros, 2001) [5]. Activity is one of the most difficult aspects of TED to quantify. The Clinical Activity Score (CAS) is widely used, especially in Europe (Bartalena et al., 2008) [1]. A CAS score of 4 out of 10 points or more has been associated with a positive predictive value of 80 % of responding to immunosuppressive treatments and a CAS <4 had a 68 % negative predictive value [6]. The VISA classification is used for grading severity and activity and is favored in North America [7]. The effects of the disease on the patient’s personal and professional life can be assessed adequately by any skilled clinician who is willing to listen and can ask relevant questions. It may be quantified by several questionnaires, the most validated of which is the GO-QOL [8]. Measuring the serum levels of thyroid hormones easily assesses thyroid status. Inquiring about smoking status is critical for determining the need for smoking cessation as well as the patient’s risk for developing more severe disease (Chap. 5)
Initial Management for Patients with Mild and Moderate to Severe TED
The first priority after initial assessment is for the clinician to communicate with the patient. TED is not an easy condition to explain, but it helps patients to understand the disease process and natural history, as well as the objectives of treatment. In order to achieve optimal outcomes, treatments are performed in a carefully choreographed sequence, a process that can be frustrating for patients, as it takes time. Written material and support from patient-led organizations are valuable resources.
Simple Measures
Some simple interventions can relieve troublesome symptoms. Ocular surface symptoms, such as dryness, foreign body sensation, and tearing, should be treated with artificial tear lubricants. Double vision can be managed with Fresnel prisms or occlusion as temporary measures (see Chap. 10). Chapter 13 discusses non-surgical interventions to improve patient symptoms, appearance, and quality of life in greater detail.
Botulinum Toxin
Botulinum toxin is a powerful neurotoxin that blocks the release of acetylcholine at the neuromuscular junction of cholinergic nerves, thereby weakening the force of muscular contraction. It is commercially available and licensed for treatment of a number of conditions characterized by muscle spasm or rigidity. Although the use of botulinum toxin for upper lid retraction in TED is widespread in clinical practice, only several small case series have been published [9, 10]. Both transcutaneous and transconjunctival routes of injection are reported to be efficacious. The mechanism of action is most likely a partial paralytic effect upon Muller’s muscle and levator palpebrae superioris.
Common side effects include local bruising and discomfort at the injection site. Ptosis (over-correction) and diplopia may occur due to the local spread of botulinum to extraocular muscles, most commonly the superior rectus muscle. More severe reactions have been reported, including muscle weakness, dysphagia, and aspiration, occurring rarely with all products that contain botulinum toxin. Extreme caution should be exercised in administering products that contain botulinum toxin to patients who have neurological disorders, or a history of dysphagia or aspiration. Only physicians with appropriate experience should administer products that contain botulinum toxin. Patients should be informed about the risk of spread of toxin and the symptoms, such as dysphagia or respiratory distress, that should prompt urgent medical attention [11].
Avoidance of Risk Factors that Exacerbate TED
Both hyper- and hypothyroidism are detrimental to patients; thus euthyroidism should be established as rapidly as possible and maintained (see Chaps. 1 and 3). Smoking cessation advice and support should be given to patients who smoke (see Chap. 5). The use of anti-oxidant supplements and other potential disease-limiting factors are discussed in detail in Chap. 6.
Specific Treatments for Mild, Active TED
Selenium plays an important role in health and disease and has antioxidant properties. Selenium supplements have been shown to reduce thyroid autoantibodies in patients with autoimmune thyroid disease [14]. A randomized placebo-controlled study in patients with mild, active TED has shown that 200 μg of sodium selenite daily for 6 months reduced disease severity and activity and improved quality of life [15] (Chap. 6). No side effects were reported. These data suggest that selenium is a disease-modifying treatment in TED. However, the study was conducted in Europe, where selenium deficiency is common. Whether the findings are applicable to selenium replete parts of the world is unclear at present.
Oral or intravenous steroids are effective, but the potential side effects are significant and generally not recommended for patients with mild disease [16]. The most notable exception is for patients who require radioiodine treatment for thyrotoxicosis, when a short course of oral steroids is well tolerated and may prevent worsening or new onset of TED, [17] (Chap. 4).
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