Causes of dependent edema ankles,red cross emergency first aid certificate,first aid level 2 melbourne courses,example op-ed articles - 2016 Feature

Please enable JavaScript in your browser to experience all the custom features of our site, including the ability to make a purchase. You must have JavaScript enabled in your browser to utilize the functionality of this website. Edema is the noticeable swelling resulting from fluid accumulation in certain body tissues.
The swelling, also referred to as dependent edema, is brought about by the accumulation of excess fluid beneath the skin in the interstitial spaces or compartments within the body tissues that are outside of the blood vessels. Occasionally pitting edema and non-pitting edema can occur without an underlying disease and it is then known as idiopathic edema. Pregnancy can cause edema in the legs as the uterus puts pressure on the vena cava, a major blood vessel that returns blood to the heart from the legs, and progesterone relaxes the walls of the blood vessels.
Standing or sitting for long periods of time particularly in hot weather can cause excess fluid to accumulate in feet, ankles and lower legs. Low protein levels in the blood caused by malnutrition, kidney and liver disease can also cause edema. Congestive heart failure is a condition in which the heart can no longer pump efficiently, and causes fluid buildup in the lungs and other parts of the body. Severe chronic (long-term) lung diseases, including emphysema and chronic bronchitis, increase pressure in the blood vessels that lead from the heart to the lungs. Tiny valves inside the veins of the legs can become weakened, causing a common problem called venous insufficiency. Most incidences of edema in children and infants are related to serious health conditions, so changes in your child should be monitored to avoid complications.
Children with acute or chronic upper airway obstruction are at risk for negative-pressure pulmonary edema, associated with upper airway obstruction. While quite rare, Nephrotic Syndrome (NS), a disorder of the kidneys, can cause edema in children.
Periorbital edema should be closely monitored, as it may be the result of a more serious condition, such as congestive heart failure and liver diseases.
Children and infants with diabetes may also experience edema as a side effect from insulin treatment.
The diagnosis of pitting and non-pitting edema are determined by the symptoms on physical examination.
Edema itself is usually a symptom of an underlying condition and can be noticed as swelling or puffiness of your face, hands, feet, legs, or around your eyes. If you experience shortness of breath, chest pain, redness or heat in a swollen edematous area, or a swelling of only one limb, consult a doctor immediately. Depending on the causes of edema and whether it is temporary or permanent, treating edema usually focuses on treating the condition that is causing it. If a blocked or damaged blood vessel is suspected as one of the causes of edema, surgery may be needed to improve the flow of blood.
Treating edema should include protecting any swollen, edematous areas of the body from pressure, injury and extreme temperatures. Thyroid (or thyrotoxic) storm is an acute, life-threatening syndrome due to an exacerbation of thyrotoxicosis.
Classic features of thyroid storm are indicative of a sudden and severe exacerbation of thyrotoxicosis, with fever, marked tachycardia, tremor, nausea and vomiting, diarrhea, dehydration, restlessness, extreme agitation, delirium or coma. Storm is typically associated with Graves’ disease, but it may occur in patients with toxic nodular goiter (1, 2) .
In Nelson and Becker’s series reported in 1969 (4) , there were 21 cases of thyroid storm among 2,329 admissions due to thyrotoxicosis (about 1%).
Thyroid storm classically began a few hours after thyroidectomy performed on a patient prepared for surgery by potassium iodide alone. Diagnosis of thyroid storm is made on clinical grounds and involves the usual diagnostic measures for thyrotoxicosis. Thyroid storm is an endocrine emergency that has to be treated in an intensive care unit (Table 12-1). The adrenal gland may be limited in its ability to increase steroid production during thyrotoxicosis.
Usually rehydration, repletion of electrolytes, treatment of concomitant disease, such as infection, and specific agents (antithyroid drugs, iodine, propranolol, and corticosteroids) produce a marked improvement within 24 hours. Antithyroid treatment should be continued until euthyroidism is achieved, when a final decision regarding antithyroid drugs, surgery, or 131-I therapy can be made. Graves’ orbitopathy (GO) is the complex of ocular manifestations that are often found in patients with Graves’ disease and, less frequently, in patients with Hashimoto’s thyroiditis or apparently without thyroid abnormalities (so-called Euthyroid Graves’ disease) (9, 10).
Clinical manifestations of GO reflect the enhanced orbital volume, due to an increase in retroocular fibroadipose tissue and swelling of extraocular muscles (30, 31).
Although it is widely accepted that GO is an autoimmune disorder, its pathogenesis is not completely clear. Other autoantigens, including several eye muscle antigens, acetylcholine receptor, thyroperoxidase, thyroglobulin, alpha-fodrin, have been proposed as putative shared antigens, but their true role is, to say the least, uncertain (42). The role of genetic factors in the pathogenesis of GO is not very well defined, and no striking differences have been observed between Graves’ patients with or without associated GO (61, 62). Clinical features of GO include soft tissue changes, proptosis, extraocular muscle dysfunction, corneal abnormalities, and optic nerve involvement (Figures 3-6).
Symptoms of GO (Table 4) include, in addition to changes in ocular appearance related to periorbital swelling and proptosis, excess lacrimation, photophobia, grittiness, pain in or behind the eyes, either spontaneous or with eye movements, diplopia of different severity with or without strabismus, blurred vision, which may clear with blinking (due to excessive lacrimation) or covering one eye (reflecting extraocular muscle impairment), or may persist (probably reflecting optic neuropathy, particularly if associated with gray areas in the field of vision). Clinical manifestations of GO have a profound negative impact on quality of life and daily activities of affected individuals (84).
Assessment of severity is particularly relevant to decide on whether a given patient should be treated by aggressive treatments (either medical or surgical) or simply by local or general supportive measures (see below).The other important feature of GO is its activity.
From Mourits et al (89), modified from an ad hoc Committee of the four Thyroid sister Societies (90).
Diagnosis of GO is usually easy on clinical grounds and by careful ophthalmological examination.
Management of GO is based on a multidisciplinary approach which involves endocrinologists, ophthalmologists, orbit surgeons, radiologists and radiotherapists.
Cogu bayanlar taraf?ndan kilo ald?m olarak alg?lanan odem asl?nda vucutta biriken suyun at?lmamas?ndan kaynaklanmaktad?r. Odem atmak icin yap?labilecekler aras?nda bitki caylar? vucudumuz icin onemli bir rol almaktad?r. Maydanoz Cay?: Diyet listelerinde en cok ad? gecen cayd?r ve vucudunuzdaki odemi atman?za cok buyuk bir katk? saglar. Bu kucuk ve basit odem atmak icin yap?labilecek yontemlerin ise yaramad?g?n? gordugunuz takdirde doktorunuzdan yard?m alarak bu tur sagl?k problerinden kurtulabilirsiniz. Bir onceki yaz?m?z olan Metabolizma h?z?n? artt?rma yontemleri basl?kl? makalemizde metabolizma h?z?n? art?rmak, metabolizma h?z?n? art?rmak icin ve metabolizma h?z?n? art?rmak icin ne yap?lmal? hakk?nda bilgiler verilmektedir. It is most commonly found in the feet, ankles and legs although it may also affect the face, hands and other parts of the body and body organs. Excess fluid accumulation in the lower regions of the body, such as the ankles, feet, and legs, is referred to as peripheral edema. Pitting edema is the term used to describe edema when pressure applied to the skin of the swollen area is released and an indentation is left behind (e.g. This is most common in women who experience it in their legs and feet when they are pre-menstrual or pre-menopausal – it is then often known as cyclical edema. Fluid retention during pregnancy also can be caused by a more serious condition called pre-eclampsia. The proteins help to hold water inside the blood vessels so fluid does not leak out into the tissues. This pressure backs up in the heart and the higher pressure causes swelling in the legs and feet. This makes it more difficult for the veins to pump blood back to the heart, and leads to varicose veins and a buildup of fluid. This condition may also occur after head injury, seizure, or accidental chemical ingestion or inhalation. As the main symptom of NS, edema is commonly seen around one or both of the eyes, also referred to as periorbital edema, but may be found in other parts of the body such as the legs. Other causes of periorbital edema in children and infants may include allergies or infections, such as conjunctivitis. However, children with diabetes should report this to their pediatrician, as it may be a symptom of cerebral edema (brain swelling), a rare but serious complication of diabetes. The doctor will examine the skin over the swollen area to check whether it may be stretched or shiny. Amongst others edema can indicate disease of the heart, liver, thyroid, lymphatic system or kidneys (causing salt retention). A low dose of a diuretic (water pill) may be prescribed to reduce the swelling and help you expel the excess fluid, but it is important to remember this just treats the symptom and is not necessarily addressing the cause. Edema is gravitational and will develop in dependent areas of the body, for example, in feet and legs when one is standing for prolonged periods.
It is now an infrequent condition, because of earlier diagnosis and treatment of thyrotoxicosis, better pre- and postoperative medical management.
At present, although still life-threatening, death from thyroid storm is rarer if it is promptly recognized and aggressively treated in an intensive care unit.
Other series, which included all cases with fever of 38.3 C or more in the postoperative period, reported an incidence of thyroid storm as high as 10% of patients operated on (5). Many such patients were not euthyroid and would not be considered appropriately prepared for surgery by current standards.



Semi-quantitative scales and related scores evaluating the presence and severity of clinical manifestations may be of some help in confirming the diagnosis (1, 3).
A variety of additional approaches have been reported, but indications for their use are not well defined. 1: Prevalence of GO in a series of 346 patients with newly diagnosed Graves’ hyperthyroidism. However, in a longitudinal cohort study, spontaneous amelioration was observed in two thirds of cases, while ocular involvement did not change with time in 20% and progressed in 14% (16). The prevalence of smokers among Graves’ women with orbitopathy is much higher than that in Graves’ women apparently without GO or in normal controls (Figure 2) (23). Prevalence of smokers among women with Graves’ disease with (GO) or without (GD) associated orbitopathy. Orbital tissues, including muscles, are infiltrated by inflammatory cells, including lymphocytes, mast cells, and macrophages. A still leading pathogenic hypothesis, based on the link between thyroid disease and eye disease (33), is that autoreactive T lymphocytes directed against one or more antigens shared by thyroid and orbit infiltrate the orbital tissue and the perimysium of extraocular muscles.
Because Graves’ hyperthyroidism is caused by TSH-receptor (TSH-R) antibodies (TRAb), TSH-R might be a plausible candidate autoantigen. An association between GO and Major Histocompatibility Complex (MHC), cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) or intercellular adhesion molecule 1 gene polymorphisms has been looked for (61-64), but results are not unequivocal.
In addition to reduced visual acuity, optic nerve involvement can be heralded by decreased color perception.
By the use of general health-related quality of life (HRQL) questionnaires, such as the SF-36 or its shorter forms, it was shown that GO is associated with significant changes in several functions, including physical functioning, role functioning, social functioning, mental health, general health perception, and bodily pain (85). Although, as stated above, GO natural history is not completely understood, it is commonly accepted that GO undergoes an initial phase of activity, characterized by progressive exacerbation of ocular manifestations until a plateau phase is reached; GO then tends to remit spontaneously, but remission is invariably partial. In a survey of GO management based on a questionnaire distributed among members of the European Thyroid Association, European Society of Ophthalmic Plastic and Reconstructive Surgery, and European Association of Nuclear Medicine, 96% of responders stated that a multidisciplinary setting for GO management is valuable, although 21% of patients were in the end not treated in a multidisciplinary setting (92). Most patients have mild GO, which does not require particularly aggressive treatments and often is self-limiting (9, 10, 13, 93).
Management of moderate-to-severe GO depends not only on severity, but also on activity of the orbitopathy (Table 8). Psikolojik nedenler, alerjik nedenler, baz? sagl?k sorunlar?da vucutta odem olusumunu saglar.
Duzenli ve doktor gozetimi alt?nda ilaclar?n?z? kullanarak odem olusmas?n? onleyebilirsiniz.
Stres ve uyku duzensizligi, hamilelik ve regl donemleride odem olusmas?na etkendir ve bu tur durumlar belirli zamanlarda gecer.
Pregnant women and older adults are often affected with this condition, but it can happen to anyone.
If a blood protein, called albumin, gets too low, fluid leaks out the blood vessels and edema occurs, especially in the feet, ankles and lower legs. Because edema can be a symptom of a serious underlying disorder, and can cause serious consequences itself, it is always important to seek medical advice. Cuts, scrapes and burns in areas that have edema take much longer to heal and are open to infection.
Pitting edema is a type of edema in which the skin surface, when pressed by a finger, leaves an indentation. However, acute exacerbation of thyrotoxicosis caused by intercurrent illness, especially infections, may still occur. Patients may present with a true psychosis or a marked deterioration of previously abnormal behavior.
Congestive heart failure may also occur, with peripheral edema, congestive hepatomegaly, and respiratory distress.
In a recent, nationwide study from Japan mortality rate was calculated to range between 9.5% and 11% (3).
Few patients are now seen with the classic pattern of thyroid storm, but patients are occasionally encountered with marked accentuation of symptoms of thyrotoxicosis in conjunction with infection. Exacerbation of thyrotoxicosis is still seen in patients sent too soon to surgery, but it is unusual in the antithyroid drug-controlled patient. For example, oral gallbladder contrast agents such as ipodate and iopanoic acid in doses of 1-2 g, which inhibit peripheral T4 to T3 conversion, might have value.
Moderate-to-severe GO includes one case of sight-threatening dysthyroid optic neuropathy (DON).
In a recent study of a large cohort of newly diagnosed Graves’ patients, about 75% had no ocular involvement at diagnosis, only 6% had moderate-to-severe GO, and 0.3% showed sight-threatening GO due to dysthyroid optic neuropathy (DON) (13) (Figure 1).
The observation that mild GO rarely progresses and often spontaneously remits was recently confirmed by a large prospective study of patients with recent onset Graves’ hyperthyroidism (13) and summarized in a review of published studies (19). Proliferation of orbital fibroblasts and adipocytes, both in the retroocular space and in the perimysial space, is also associated with an increased production of glycosaminoglycans, which are the ultimate responsible for edematous changes both in the connective tissue and the muscles, owing to their hydrophilic nature.
TSH-R expression has been shown in the orbital tissue of GO patients, both at the mRNA and protein levels (43, 44); however, TSH-R is also expressed in several other tissues not involved in Graves’ disease and orbitopathy (45), and, although at lower levels, in normal orbital fibroadipose tissue samples and cultures (46). GO likely stems from a complex interplay between endogenous factors and exogenous (environmental) risk factors (10, 65). Recommendations for GO assessment in clinical practice have recently been reviewed by EUGOGO (80) and other groups (VISA classification) (81) .
Note periorbital swelling, injection of conjunctival vessels, proptosis, marked lid retraction, and proptosis.
Note the superior eyelid edema, mild conjunctival vessel injection, marked proptosis, and marked upper lid retraction. Note marked periorbital swelling, palpebral hyperemia, conjunctival hyperemia, proptosis (particularly in the left eye), caruncle edema. Interestingly, these changes in HRQL parameters were similar to those found in patients with inflammatory bowel disorders, and even more marked than those observed in patients with diabetes mellitus, heart failure or emphysema (85). Modest extraocular muscle enlargement and increased fibroadipose tissue volume are often found in Graves’ patients without clinical manifestations of ocular involvement.
The therapeutic approach to a GO patient should be based on both severity and activity of the disease, the former being the feature to assess first.
If GO activity is modest, simple local measured can be suggested to obtain symptomatic relief until GO is burnt-out (Table 7).
Medical treatment is likely to be beneficial in patients with active GO, with florid signs and symptoms of inflammation, recent-onset extraocular muscle dysfunction, recent progression of the ocular abnormalities as a whole. Daha cok kad?nlarda gorunen oden her zaman gecici olmayabilir bazende kal?c? bir hastal?g?n habercisi olabilir. Thyroid storm in the past most frequently occurred after surgery, but now it is usually a complication of untreated or partially treated thyrotoxicosis, rather than a postoperative complication. Thyroid storm occasionally occurs in patients operated on for some other illness while severely thyrotoxic.
PTU, 150-250 mg every 6 hours should be given, if possible, rather than methimazole, since PTU also prevents peripheral conversion of T4 to T3, thus more rapidly reduces circulating T3 levels.
Pharmacological doses of glucocorticoids (2 mg dexamethasone every 6 h) acutely depress serum T3 levels by reducing T4 to T3 conversion. The relative contribution of the increase in fibroadipose tissue volume and extraocular muscle swelling is not always the same, and a predominance of either component may be observed in different patients with similar clinical features (32). Following shared antigen(s) recognition, facilitated by HLA class II antigen expression on antigen-presenting cells, CD4+ T lymphocytes secrete cytokines which amplify the immune response by activating either CD8+ T lymphocytes or autoantibody-producing B cells (34), and by stimulating orbital fibroblast proliferation (35). The latter are probably more important and include cigarette smoking, thyroid dysfunction, and, in a subset of patients, radioiodine therapy for Graves’ hyperthyroidism (10, 65).
Since HRQL questionnaires are broad and may not address items speficic for a given disease, a GO-speficic quality of life (GO-QoL) questionnaire was developed and validated in clinical studies (84, 86-88). It is unknown how long this process takes to be completed, but it is widely believed that it takes between 6 months and two years. Orbital imaging is very useful to detect signs of optic nerve compression, which support the diagnosis of optic neuropathy.
Liver damage and jaundice may derive from congestive heart failure or a direct action of thyroid hormone on the liver coupled with malnutrition (Chapter 10). Severe exacerbation of thyrotoxicosis is rarely seen following 131-I therapy for hyperthyroidism; some of these may be defined as thyroid storm (6). Serum total T3 may be not particularly elevated or even normal, due to reduced T4 to T3 conversion as observed in nonthyroidal illness (1). This effect of glucocorticoids is beneficial in thyroid storm and supports their routine use in this clinical setting. Peritoneal dialysis can remove circulating thyroid hormone, and plasmapheresis can do likewise, but at the expense of serum protein loss. Ocular involvement is in most cases bilateral, although often asymmetrical, but it may be unilateral in up to 15% of cases (9).
A review of the first 100 consecutive patients seen at the same joint thyroid-eye unit in 1960 and 1990 revealed a decrease in the proportion of Graves’ patients with clinical relevant GO from 57% to 32% (18); likewise, a reduction in the proportion of severe forms of GO compared to milder forms was observed (18), likely reflecting an earlier diagnosis and treatment of both hyperthyroidism and orbitopathy. Analysis of T-cell clones from GO orbital tissues has shown both Th1 cytokine (interleukin-2, interferon-gamma, tumor necrosis factor-alpha) and Th2 cytokine (interleukin-4, interleukin-5, interleukin-10) secretory profiles, possibly related to different stages of the disease, with Th1 cytokines predominating early and Th2 cytokines late in the course of GO45. The relationship between cigarette smoking and GO has been discussed above (see paragraph on Epidemiology).
CT scan showed enlargement of extraocular muscles (particularly medial rectus and inferior rectus) in both eyes, but no relevant compression of the optic nerve at the orbit apex. Recognition of the different phases of the disease is important, because active disease, basically characterized by the presence of inflammation, can respond to immunosuppressive treatments, which are largely ineffective when GO is burnt-out. Imaging is required in asymmetrical or, particularly, unilateral forms of GO, to rule out that proptosis, periorbital swelling, inflammation, or diplopia be due to disorders other than GO (10).


Dysthyroid optic neuropathy, the most severe expression of the orbitopathy, is a clinical, sight-threatening emergency, which requires immediate treatment. Icerik ile ilgili herhangi bir sorun da lutfen Iletisim sayfam?zdan bizimle irtibata geciniz.
Thyroid storm appears most commonly following infection (1), which seems to induce an escape from control of thyrotoxicosis. Electrolytes, blood urea nitrogen (BUN), blood glucose, liver function tests, and plasma cortisol should be monitored. The onset of GO apparently has a bimodal peak in the fifth and seventh decades of life, but eye disease may occur at any age (15). It should be noted that a multicenter study carried out by the European Group on Graves’ Orbitopathy (EUGOGO) reported that 40% of GO patients had mild disease, 33% had moderate GO, and 28% had severe eye disease (20).
If proptosis, which can be considered a form of spontaneous decompression, is severe, subluxation of the eye may occur. Cytokines produced by T cells, macrophages and fibroblasts perpetuate the ongoing inflammatory process through several mechanisms, including induction of expression of HLA class II antigens, heat-shock proteins, CD40, prostaglandins, adhesion molecules, proliferation of fibroblasts, differentiation of preadipocyte fibroblasts into adipocytes, and stimulation of fibroblasts to synthesize and secrete glycosaminoglycans (30-32, 34). Both hyperthyroidism (66, 67) and hypothyroidism (68) seem to influence negatively the course of the orbitopathy.
Different indicators have been proposed to assess GO activity, including short duration of treatment (<18 months), positivity of octreoscan, decreased extraocular muscle reflectivity at orbital ultrasound, prolonged T2 relaxation time at MRI, increased urinary glycosaminoglycan levels, but they lack sufficient specificity and accuracy (88). Control of thyroid dysfunction is fundamental, because progression often is associated with hyper- or hypothyroidism (9, 10); refrain from smoking is also essential, because it is associated with a decreased chance of developing proptosis and diplopia (95), and decreases the likelihood to develop severe GO (21). If there is no response to medical treatment (high-dose intravenous glucocorticoids), orbital decompression is warranted (75, 76). Pneumonia, upper respiratory tract infection, enteric infections, or any other infection can cause this condition. It should be noted that these figures were clearly influenced by the fact that EUGOGO centers are all referral centers where it is likely to see more complicated cases of GO. In addition to direct irritative effects and modulation of immune reactions in the orbit (27), smoking was associated with an increase in the orbital connective tissue volume as assessed by MRI (28), and with an increased adipogenesis and hyaluronic acid production in in vitro cultured orbital fibroblasts (29).
Proptosis is responsible for corneal exposure which may be particularly dangerous at night for the incomplete eyelid closure (lagophthalmos), and may result into sight-threatening corneal ulceration. The observation that immunoglobulins G from GO patients induce glycosaminoglycan synthesis in their orbital fibroblasts through the IGF-I receptor might suggest that the latter may represent a possible pathway in GO pathogenesis (36). In this model, some of the mice immunized by human TSH A-subunit by TSH receptor plasmid in vivo electroporation showed large infiltrates surrounding the optic nerve, increased adipogenesis, orbital muscle hypertrophy, exophtahlmos, and chemosis (48). TRAb are independent risk factors for GO and can help to predict severity and outcome of eye disease (69). A useful tool to assess GO activity is represented by the Clinical Activity Score (CAS), which can be calculated very easily and is recommended by EUGOGO in the assessment of GO in routine clinical practice, in specialist multidisciplinary clinics, and for clinical trials (80). Patients who do not succeed to quit smoking by themselves, should be helped by professional stop-smoking clinics, organizations, groups, where they can receive counseling, behavioral therapies, pharmacological treatments.
The clinical picture may be masked by a secondary infection such as pneumonia, a viral infection, or infection of the upper respiratory tract. The decreased incidence of thyroid storm can be largely attributed to improved diagnosis and therapy. There is a close temporal relationship between the onset of GO and the onset of hyperthyroidism. In summary, based on recent studies and reviews of the available literature, it can be concluded that GO is a rare disease, particularly in its severe expressions (19).
The enlarged muscle volume may cause optic nerve compression (dysthyroid optic neuropathy), especially if the orbital septum is tight and proptosis is minimal. Increased adipogenesis in the orbit of GO patients might be related to overexpression of adipocyte-related genes, such as secreted frizzled-related protein-1, PPAR-?, adiponectin (37), and immediate early genes which act as triggers of the subsequent transcriptional cascade leading to adipocyte phenotype (38). The role of the TSH receptor in GO development might also be supported by the finding of a correlation between GO activity, as assessed by the Clinical Activity Score, and TRAb (49).
Radioiodine therapy for Graves’ hyperthyroidism is associated with GO progression in about 15% of cases, although this effect may be transient (70-73). Lid retraction and proptosis are responsible for corneal exposure, which may lead to corneal epithelium damage (punctate keratopathy), corneal ulceration and perforation.
In its original formulation (89) it included 10 items, which were subsequently reduced to 7 when revised by an ad hoc Committee of the four sister thyroid societies (90).
Octreoscan may be useful to identify patients with active GO (78), but its role in clinical practice is limited, also in view of its high cost.
In a subset of patients with mild GO, the impact of GO on the quality of life is so pronounced as to justify the risk of immunosuppression (or surgery) as for moderate-to-severe GO (75, 76). Death may be caused by cardiac arrhythmia, congestive heart failure, hyperthermia, or other unidentified factors. In most cases, thyrotoxicosis is recognized early and treated by measures of predictable therapeutic value.
Unless congestive heart failure contraindicates it, propranolol or other beta-blocking agents should be given at once, orally or parenterally in large doses, depending on the patient’s clinical status.
In approximately 85% of cases GO and hyperthyroidism occur within 18 months of each other (15), although GO may both precede (about 20% of cases) or follow (about 40% of cases) the onset of hyperthyroidism (15). Optic nerve compression is particularly evident at the orbital apex and may be responsible for sight loss. Interestingly, ligands of PPAR-gamma, such as rosiglitazone, have been shown to stimulate adipocyte differentiation in orbital tissue in culture (39); in addition, progression of GO has been reported in a patient submitted to rosiglitazone treatment for diabetes mellitus type 2 (??). Thus, although evidence is not conclusive, TSH-R most likely has a role in GO pathogenesis (50). This effect is more frequently observed in patients who already have GO prior to radioiodine therapy, smoke, have high TRAb levels, or whose post-radioiodine hypothyroidism is not promptly corrected by L-thyroxine replacement therapy (10, 65).
The incomplete eye closure at night (lagophthalmos) and the absence of Bell’s phenomenon (no upward eye rotation on attempted eye closure) are risk factors for corneal damage (76, 80). A recent randomized controlled trial performed by EUGOGO in a large cohort of patients with mild GO showed that selenium supplementation for 6 months has beneficial effects on mild GO compared with placebo and can often prevent its progression to more severe forms (96). Permanent correction of the thyrotoxicosis by either 131-I or immediate thyroidectomy should be postponed until euthyroidism is restored.
Orbital inflammation and related anatomical changes may cause venous and lymphatic congestion that contribute to periorbital edema and chemosis. The role of PPAR-gamma agonists in GO pathogenesis is, however, not unequivocal, since in GO orbital fibroblasts and preadipocytes in culture rosiglitazone suppresses the release of IFN-gamma-inducible chemokine CXCL10, which plays an important role in the initial phases of autoimmune thyroid disorders (41).
Radioiodine-associated progression of GO can be prevented by a short course of prednisone (71, 74). Intraocular pressure is often increased, particularly in upward gaze, but this abnormality rarely progresses to true glaucoma. If one point is given to each item when present, CAS, which basically reflect eye inflammation, may range from 0 (absent activity) to 7 (maximal activity); GO is generally defined active if CAS is 3.
Thus, selenium, for its anti-inflammatory and immunomodulatory actions, should be considered both as a therapeutic tool for mild GO and a preventive measure (97). Using thionamides preoperatively, thyroid glands have only minimal amounts of stored hormones, thus minimizing thyroid hormone release due to manipulation. Other supporting measures should fully be exploited, including sedation, oxygen, treatment for tachycardia or congestive heart failure, rehydration, multivitamins, occasionally supportive transfusions, and cooling the patient to lower body temperature down.
With time inflammation subsides and muscle fatty degeneration and fibrosis may contribute to further extraocular muscle restriction and strabismus, which, at this stage, can only be corrected by surgery. As recently reviewed (51), increased IGF-1 receptor levels have been reported in orbital fibroblasts as well as in B and T lymphocytes from Graves’ patients, and immunoglobulins displacing IGF-1 from its binding to the IGF-1 receptor have also been found in these patients (52). Dysthyroid optic neuropathy, due to optic nerve compression at the orbit apex by swollen extraocular muscles, or, less frequently, to optic nerve stretching in cases of marked proptosis or eye subluxation, is a sight-threatening expression of GO. Whether selenium is also useful as an adjuvant therapy in patients with moderate-to-severe GO is presently unsettled. Antibiotics may be given on the presumption of infection while results of culture are awaited. Colocalization of TSH receptor and IGF-1 receptor has been shown both in orbital fibroblasts and thyrocytes, suggesting that the two receptors might form a functional complex (53). Neither thyroidectomy nor antithyroid drugs influence the course of the orbitopathy (76-78). It can be diagnosed by fundoscopy showing disc swelling, reduced visual acuity, abnormal color vision test, contrast sensitivity, perimetry, visual-evoked potentials, and pupillary responses (83).
Stimulation of the TSHR by the monoclonal TSHR-stimulating antibody, M22, could be inhibited by an IGF-1R-blockingmonoclonal antibody in orbital fibroblasts (54).
The above observations have important practical implications in terms of GO prevention (Table 2), because GO patients should be urged to refrain from smoking, their thyroid dysfunction (both hyper- and hypothyroidism) should be promptly corrected, and, in the case of radioiodine therapy, a short course of oral prednisone should be administered (10, 65, 76, 77). Involvement of the IGF-1R is not specific for Graves’ disease, since it is implicated in other autoimmune diseases, such as rheumatoid arthritis (55).
Thus, although involvement of the IGF-1R in the pathogenesis of GO seems likely (56), it is tempting to speculate, for the time being, that autoimmunity to the TSH receptor be the initiating mechanism, while subsequent increased expression of the IGF-1R might be fundamental to maintain ongoing reactions in the orbit (57). Interestingly, two recent reports found that, at variance with TRAb, only a minority of patients with GO have circulating antibodies to the IGF-1R (58, 59). This may be related to the low sensitivity and specificity of tests used to detect such antibodies (56).



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