Myxedema

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Synonyms and keywords: Myxoedema;

Overview

Myxedema is a skin and tissue disorder usually due to severe prolonged hypothyroidism. Hypothyroidism can be caused by Hashimoto’s thyroiditis, surgical removal of the thyroid, and rarer conditions. Partial forms of myxedema, especially of the lower legs (called pretibial myxedema), occasionally occur in adults with Graves’ disease, a cause of hyperthyroidism; or also Hashimoto’s thyroiditis without severe hypothyroidism.

Pathophysiology

Myxedema stemming from both the hyperthyroid and hypothyroid conditions, results from the accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis in both lesional and normal skin. The mechanism that causes myxedema is still not yet understood, although animal model studies suggest that thyroid hormones affect the synthesis and catabolism of mucopolysaccharides and collagen by dermal fibroblasts. The fibroblasts in the orbital and pretibial dermis share antigenic sites that underlie the autoimmune process that causes Grave’s disease. This cross-reaction may contribute to the development of myxedema long after normal levels of thyroid hormones have been restored by treatment.

Causes

Hashimoto’s thyroiditis
Drug side effects:

Potassium iodide

Differentiating myxedema from other diseases

Myxedema must be differentiated from other causes of lower limb edema like chronic venous insufficiency, acute deep venous thrombosis, lipedema, lymphatic filariasis, cellulitis and causes of generalized edema.

Diseases	Symptoms							Signs	Gold standard Investigation to diagnose
	History	Onset	Pain	Fever	Laterality	Scrotal swelling	Symptoms of primary disease	Signs	Gold standard Investigation to diagnose
Myxedema	History of untreated hypothyroidism. Infiltration of the skin with glycosaminoglycans with associated water retention.	Chronic	+	–	Bilateral	–	+ (hypothyroidism )	Pretibial myxedema	Thyroid function tests.
Lymphatic filariasis	History of living in endemic area or travelling to it	Chronic	+	+	Bilateral	+	–	Hepatomegaly Lymphedema Elephantiasis Lymphangitis Hydrocele Scrotal elephantiasis Lymphadenopathies Rhonchi may be present in patients with Pulmonary tropical eosinophilia syndrome.	Preparing blood smears Thick smears Thick smears consist of a thick layer of dehemoglobinized (lysed) red blood cells (RBCs). Thick smears allow a more efficient detection of parasites (increased sensitivity). Thin smears consist of blood spread in a layer such that the thickness decrease. By the ultrasound, the following findings can be observed: Dilated lymphatic channels Living worms tend to be in motion which called “filarial dance” sign.
Chronic venous insufficiency	History of untreated varicose veins Painful bilateral lower limb swelling that increases with standing and decreases by rest and leg elevation.	Chronic	+	–	Bilateral	+ (If congenial)	–	Typical varicose veins Skin change distribution correlate with varicose veins sites in the medial side of ankle and leg Reduction of swelling with limb elevation.	Duplex ultrasound will demonstrate typical findings of venous valvular insufficiency
Acute deep venous thrombosis	History of prolonged recumbency Classic symptoms of DVT include acute unilateral swelling, pain, and erythema	Acute	+	–	Unilateral	–	May be associated with primary disease mandates recumbency for long duration	Dilated superficial veins Difference in calf diameter is twice as likely to have DVT(most impotant sign )^[1] Calf pain on passive dorsiflexion of the foot (Homan’s sign) isn’t realiable sign.	Compression ultrasonography (CUS) with doppler is the diagnostic test of choice D-dimer level is used for unprobable cases
Lipedema	Family history especially in women; X-linked dominant or autosomal dominant condition.^[2] Abnormal deposition of fat and edema and easy bruising.	Chronic	+	–	Bilateral	–	–	Tender with palpation Negative Semmer sign to differentiate from lymphedema.^[3] Pinching the skin on the upper surface of the toes. If it is possible to grasp a thin fold of tissue then it is negative result. In a positive result, it is only possible to grasp a lump of tissue.	MRI offers strong qualitative and quantitative parameters in the diagnosis of lipedema ^[4]
(Cellulitis–erysipelas-skin abscess)	Acute painful swelling Fever	Acute	+	+	Unilateral	–	–	Tenderness, hotness, and may be fluctuation if abscess formed. Lymphangitis in nearby lymph nodes. Toxemia and fever in severe cases. Cellulitis involves the deeper dermis and erysipelas involves the upper dermis.^[5]	Usually it doesn’t need any laboratory tests to diagnose.^[6] Blood cultures are warranted for patients in the following circumstances:^[7] Systemic toxicity Extensive skin or soft tissue involvement Underlying comorbidities persistent cellulitis In patients with recurrent cellulitis, serologic testing for beta-hemolytic streptococci is a good diagnostic tool.^[8]
Other causes of generalized edema	History of chronic general condition (cardiac-liver-renal)	Chronic	–	–	Bilateral	–	+		According to the primary cause ( Echo- LFTs– RFT)

Diagnosis

Symptoms

Myxedema usually presents itself with some of the following symptoms:

Skin thickening
Coarse skin
Change in facial appearance
Thickening nose
Swollen lips
Puffiness around the eyes
Jelly-like infiltrations in subcutaneous tissues
Slow speech
Mental dullness
Lethargy
Mental problems
Dry skin
Yellow skin
Swollen subcutaneous tissue
Weight gain
Constipation
Thinning hair
Brittle hair
Bald patches
Muscle pains
Deafness
Hearing impairment
Carpal tunnel syndrome

Treatment

Treatment for myxedema is difficult. Systemic or intralesional glucocorticoids, topical glucocorticoids under occlusion or high-dose intravenous immunoglobulin have been reported to offer some relief to patients. Treatment should follow correction of the original hyperthyroidism/hypothyroidism.

Related Chapters

Cretinism – congenital hypothyroidism

References

↑ Goodacre S, Sutton AJ, Sampson FC (2005). “Meta-analysis: The value of clinical assessment in the diagnosis of deep venous thrombosis”. Ann Intern Med. 143 (2): 129–39. PMID 16027455. Review in: ACP J Club. 2006 Mar-Apr;144(2):46-7 Review in: Evid Based Med. 2006 Apr;11(2):56
↑ Child AH, Gordon KD, Sharpe P, Brice G, Ostergaard P, Jeffery S; et al. (2010). “Lipedema: an inherited condition”. Am J Med Genet A. 152A (4): 970–6. doi:10.1002/ajmg.a.33313. PMID 20358611.
↑ Trayes KP, Studdiford JS, Pickle S, Tully AS (2013). “Edema: diagnosis and management”. Am Fam Physician. 88 (2): 102–10. PMID 23939641.
↑ Dimakakos PB, Stefanopoulos T, Antoniades P, Antoniou A, Gouliamos A, Rizos D (1997). “MRI and ultrasonographic findings in the investigation of lymphedema and lipedema”. Int Surg. 82 (4): 411–6. PMID 9412843.
↑ Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL; et al. (2014). “Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America”. Clin Infect Dis. 59 (2): 147–59. doi:10.1093/cid/ciu296. PMID 24947530.
↑ Raff AB, Kroshinsky D (2016). “Cellulitis: A Review”. JAMA. 316 (3): 325–37. doi:10.1001/jama.2016.8825. PMID 27434444.
↑ Woo PC, Lum PN, Wong SS, Cheng VC, Yuen KY (2000). “Cellulitis complicating lymphoedema”. Eur J Clin Microbiol Infect Dis. 19 (4): 294–7. PMID 10834819.
↑ Leppard BJ, Seal DV, Colman G, Hallas G (1985). “The value of bacteriology and serology in the diagnosis of cellulitis and erysipelas”. Br J Dermatol. 112 (5): 559–67. PMID 4005155.

Template:WikiDoc Sources

[pmid16027455-1] Goodacre S, Sutton AJ, Sampson FC (2005). “Meta-analysis: The value of clinical assessment in the diagnosis of deep venous thrombosis”. Ann Intern Med. 143 (2): 129–39. PMID 16027455. Review in: ACP J Club. 2006 Mar-Apr;144(2):46-7 Review in: Evid Based Med. 2006 Apr;11(2):56

[pmid20358611-2] Child AH, Gordon KD, Sharpe P, Brice G, Ostergaard P, Jeffery S; et al. (2010). “Lipedema: an inherited condition”. Am J Med Genet A. 152A (4): 970–6. doi:10.1002/ajmg.a.33313. PMID 20358611.

[pmid23939641-3] Trayes KP, Studdiford JS, Pickle S, Tully AS (2013). “Edema: diagnosis and management”. Am Fam Physician. 88 (2): 102–10. PMID 23939641.

[pmid9412843-4] Dimakakos PB, Stefanopoulos T, Antoniades P, Antoniou A, Gouliamos A, Rizos D (1997). “MRI and ultrasonographic findings in the investigation of lymphedema and lipedema”. Int Surg. 82 (4): 411–6. PMID 9412843.

[pmid24947530-5] Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL; et al. (2014). “Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America”. Clin Infect Dis. 59 (2): 147–59. doi:10.1093/cid/ciu296. PMID 24947530.

[pmid27434444-6] Raff AB, Kroshinsky D (2016). “Cellulitis: A Review”. JAMA. 316 (3): 325–37. doi:10.1001/jama.2016.8825. PMID 27434444.

[pmid10834819-7] Woo PC, Lum PN, Wong SS, Cheng VC, Yuen KY (2000). “Cellulitis complicating lymphoedema”. Eur J Clin Microbiol Infect Dis. 19 (4): 294–7. PMID 10834819.

[pmid4005155-8] Leppard BJ, Seal DV, Colman G, Hallas G (1985). “The value of bacteriology and serology in the diagnosis of cellulitis and erysipelas”. Br J Dermatol. 112 (5): 559–67. PMID 4005155.

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