Definition/Description[edit | edit source]

Hypothyroidism is caused by an insufficient amount of the thyroid hormone in the body resulting in an overall slowing of metabolism. There are two categories to classify Hypothyroidism which are primary and secondary. [1][2]

Below is a picture of the thyroid gland responsible for producing the thyroid hormones T4 and T3:


Prevalence[edit | edit source]

Hypothyroidism is more prevalent in women who have a four to ten times greater likelihood of developing this than men. Hypothyroidism can be present at birth, but has a higher occurrence rate between the ages of 30 and 60. It occurs in close to 10% of women and 6% of men over the age of 65. Primary Hypothyroidism is more common than secondary with approximately 95% of all people diagnosed categorized as the primary type. [1][2][3]


Characteristics/Clinical Presentation[edit | edit source]

Clinical signs are widespread and affect numerous body systems. With early onset of the disease, signs may be indistinct and go undetected such as general fatigue, slight weight gain from fluid retention and decreased metabolism, dry skin, or cold sensitivity.

Elderly patients have significantly fewer symptoms than do younger adults, and complaints are often subtle. Many elderly patients with hypothyroidism present with nonspecific geriatric symptoms like confusion, falling, incontinence, and decreased mobility.

With progression, clinical signs become more obvious and severe. Myxedema usually appears in the later stages if not treated resulting in nonpitting edema present around the eyes, hands, and feet. Myxedema may also cause thickening of the tongue and tissues of the larynx and pharynx, slurred speech and hoarseness.

Rarely, a goiter may be present if not medically treated and presents as a large swelling on the anterior neck resulting from marked thyroid gland growth. Although goiters are not frequently seen in the United States because its main cause is due to low iodine intake it can also be seen in elevated levels of TSH often present in progressed hypothyroidism. It is more commonly seen in other parts of the world where commercial foods containing iodine aren’t as abundant. Other frequent clinical manifestations are listed in the systemic involvement section of this page. [5][2][3][6]

Below is a picture of Myxedema of the hands and legs and a man before and after treatment for Myxedema[7]:

Image:Myxedema_2.jpg  Myxedema.jpg

Associated Co-morbidities[edit | edit source]

Medications[edit | edit source]

Synthetic hormone replacement therapy is the most common method of treatment for hypothyroidism. Artificial L4 hormone also known as L-thyroxine is used alone or in conjunction with a L3 hormone called liothyronine to supplement the deficient amounts of thyroid hormone that the thyroid is distributing throughout the body. Also, dehydrated animal thyroid hormone L-thyroxine may be used as another preferred method of hormone replacement.

The hormone replacement is started at a low dose and then is gradually increased until a proper level is achieved and maintained. This is especially true for the elderly population who may have heart comorbidities because this drug therapy can create temporary levels of hyperthyroidism for several hours and increases the risk for cardiac events.

The dose should be the lowest amount possible to return TSH blood levels close to normal range, although this is not the case for secondary hypothyroidism. L-thyroxine should not be given to someone with secondary hypothyroidism until they begin cortisol hormone therapy first to treat the underlying cause not due to the thyroid gland itself because this drug may hasten adrenal gland emergency. [5][2][3][8]

Below is a picture of the medication L-thyroxine typically used to treat hypothyroidism[9]:


Diagnostic Tests/Lab Tests/Lab Values[edit | edit source]

When the body senses that there is a decreased amount of thyroid hormone being produced the anterior pituitary gland increases the amount of thyroid-stimulating hormone (TSH) being released in an effort to promote thyroid hormone production. With Hypothyroidism, the thyroid gland does not respond properly to the TSH so the pituitary gland continues to increase its secretion causing elevated levels of TSH to be present in the blood. 

Elevated TSH levels found in the blood are used most often to diagnose Hypothyroidism because it is the most sensitive indication of the disorder. TSH levels are always elevated in Primary Hypothyroidism. In severe cases T4 hormone levels may be decreased in the blood. T3 levels are typically close to normal in most cases. Cholesterol and triglyceride levels may also be elevated. [5][2][3][6]

Causes[edit | edit source]

Primary Hypothyroidism[edit | edit source]

Primary Hypothyroidism is caused by hormone insufficiency related to the loss of productive thyroid tissue or defective hormone production.

  • The most common cause for the development of Primary Hypothyroidism in the United States is autoimmune diseases, in particular, Hashimoto’s Thyroiditis. With this disease the body’s immune system attacks the thyroid gland cells and enzymes in an attempt to rid the body of invasion. This destroys the thyroid cells and leaves the gland with little ability to make the thyroid hormone.
  • Primary Hypothyroidism may also be caused by radiation treatment or surgical removal of the thyroid. This may be present in people treated for goiters, hyperthyroidism, Hodgkin’s disease, lymphoma, Grave’s disease or cancer of the head, neck, or thyroid gland.
  • Some medicines such as amiodarone, lithium, interferon-alpha, and interleukin-2 can prevent the thyroid gland from being able to make the thyroid hormone normally and can be another cause for Primary Hypothyroidism. These drugs usually only cause hypothyroidism in people with a higher genetic disposition to autoimmune diseases.
  • Rarely, primary hypothyroidism is congenital, or present at birth, or caused by deficient iodine intake in the diet.

Secondary Hypothyroidism[edit | edit source]

Secondary Hypothyroidism is caused by pathology to the pituitary gland or hypothalamic disease which causes under-stimulation to the thyroid gland secondary to inadequate amounts of TSH released to be utilized to make the thyroid hormone.[10][11][12]


Systemic Involvement [5][2][12][3][edit | edit source]

Common Systemic Clinical Manifestations of Hypothyroidism[edit | edit source]

Central Nervous System:

  • Hoarse Voice
  • Slurred Speech
  • Slowed mental function*
  • Fatigue
  • Headache
  • Ataxia
  • Depression

 *Slowed Mental function may include signs such as loss of interest or decreased short term memory.

Musculoskeletal System:

  • Proximal muscle weakness
  • Trigger Points
  • Myalgias
  • Stiffness
  • Carpal Tunnel
  • Syndrome
  • Slowed deep tendon reflexes
  • Parasthesias
  • Muscle or joint edema
  • Back Pain
  • Increase Bone Density

Cardiovascular System:

  • Bradycardia
  • CHF
  • Poor Peripheral Circulation**
  • Atherosclerosis
  • Hyperlipidemia
  • Angina
  • Pericardial effusion
  • Heart dilation
    ** Poor Peripheral Circulation may demonstrate as skin pallor, intolerance to cold, cool skin, or hypertension. 

Hematologic System:

  •  Anemia
  • Bruising

Integumentary System:

  • Myxedema
  • Thickened skin
  • Dry skin
  • Yellowing of skin
  • Coarse and thinning hair
  • Nonpitting edema
  • Poor wound healing
  • Thin/brittle nails

Respiratory System:

  • Dyspnea
  • Respiratory muscle weakness
  • Pleural effusion

Gastrointestinal System:

  • Anorexia
  • Constipation
  • Weight gain
  • Delayed Glucose uptake
  • Decreased Glucose absorption

Genitourinary System:

  • Infertility
  • Menstrual irregularity

Medical Management[edit | edit source]

There is still controversy about how to treat individuals who have subclinical hypothyroidism. Subclinical Hypothyroidism is when the person presents with high TSH levels and normal T4 levels and usually has little to no symptoms of the disorder. Some believe that this type of hypothyroidism should be treated medically just like primary hypothyroidism while others believe it has little benefit. One study included 350 women with subclinical hypothyroidism that were treated with either a placebo or L-thyroxine hormone replacement therapy. The results revealed that in these patients, symptoms of hypothyroidism, quality of life, blood lipid concentrations, and cardiac function did not change more in response to T4 therapy, as compared with the placebo. This supported the argument that these patients should be monitored for progression, but not medically treated with hormone therapy. [14]

Patients with hypothyroidism who are taking L-thyroxine are usually advised to take their daily dose before eating any food in the morning. One study was done to determine whether ingestion of L-thyroxine at different times throughout the day could result in different hormone concentrations in the blood. The results revealed that blood serum concentrations of both T4 and T3 are higher and blood serum TSH concentrations are lower when L-thyroxine is taken at bedtime instead of early in the morning. This suggests that L-thyroxine may be absorbed better when it is taken at night. [15]

The type of hormone therapy the patient is treated with is up to the preference of the doctor. Some doctors believe that L-thyroxine alone is sufficient enough to treat the symptoms of hypothyroidism while others use L-thyroxine, T4, in combination with triiodothyronine or T3. Some doctors will begin with T4 only and if symptoms are still bothersome then they will add T3 to the patient’s therapy. One study decided to compare the patient’s outcome when treated with T4 alone versus a combination of L4 and L3 hormone therapy. Approximately 1,216 patients were followed over 9 months and their symptoms were reported. The results revealed that T4 and T3 combination therapy is not more effective in decreasing pain symptoms throughout the body, fatigue, depression or improving quality of life than patients receiving T4 alone. [16]

Even though the American Thyroid Association advocates starting treatment at a low dose and building up to a proper maintenance dose to avoid adverse effects there is debate about whether the starting dose should be higher or, in other words, closer to the dose the patient is likely to need in the long term. One study decided to compare the effects of starting T4 with a high dose versus a low dose. The results revealed that starting hormone therapy with a full dose of T4 close to what would be needed in the long term was safe for the patient and did not cause adverse effects, but was not more effective in relieving symptoms than starting with a low dose. [17]

Because the elderly are at greater risk for developing hypothyroidism and they often have more severe co morbidities and symptoms related to the disorder, it is essential that the dosage of hormone treatment they receive is sufficient enough to properly treat them. As mentioned earlier, over-treating the symptoms of hypothyroidism in the elderly can lead to hyperthyroid like symptoms for several hours which can increase the likelihood for a cardiac event to occur. However, it is also important not to under-treat these elderly patients for fear of adverse effects because they are more susceptible to confusion, memory loss, muscle weakness and falls if their dosage is not adequate enough. One research study was done to find out how common over- and under-treatment is in elderly patients and what factors may cause this problem. This study included 339 patients over the age of 65 taking thyroid hormones that were divided into three groups which included low blood TSH levels, normal TSH levels, and high TSH levels. Only 43% of the patients had a normal TSH blood serum level while 41% had a low serum TSH and 16% had a high TSH. This study concluded that all elderly hypothyroid patients need to have their serum TSH levels more closely monitored and their hormone doses adjusted to result in a TSH in the normal range in order to avoid potential harmful side effects. [18]

Physical Therapy Management[edit | edit source]

Preferred Practice Patterns for Physical Therapy:

  • Impaired Muscle Performance
  • Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Connective Tissue Dysfunction.
  • Impaired Joint Mobility, Motor Function, Muscle Performance and Range of Motion Associated with Localized Inflammation.
  • Impaired Joint Mobility, Motor Function, Muscle Performance, Range of Motion and Reflex Integrity Associated with Spinal Disorders
  • Impaired Aerobic Capacity/Endurance Associated with Deconditioning.
  • Primary Prevention/Risk Reduction for Integumentary Disorders.

When myedematous hypothyroidism is treated it may cause the patient to develop pseudogout in the joints and may affect the spine as well. Pseudogout may cause crystals to be deposited into the ligamentum flavum and OA ligament causing spinal stenosis and other neurologic issues. The physical therapist’s role is like that when treating rheumatoid arthritis. The patient may have complaints of muscle aches, pain, or stiffness and may cause the development of trigger points. This will require hormone therapy to resolve the symptoms and cannot be helped with simple myofascial release.

The therapist working with a patient with hypothyroidism in the acute care setting must be aware that dry, edematous skin is prone to breakdown or tears. Prevention may be a key goal for the therapist to keep in mind and should work to monitor and relieve pressure points on the sacrum, coccyx, elbows and heels whenever necessary.

The therapist working in the outpatient setting must be aware that patients with hypothyroidism present with a multitude of varying symptoms that mimic musculoskeletal or neural disorders. When treating a patient with widespread muscle weakness, general fatigue, widespread trigger points, or overall decreased deep tendon reflexes it is important to take an in-depth history so that all symptoms can be reported, because the patient may not be able to connect symptoms to one another. Also, in cases of patient reported carpal tunnel it is important to get a thorough history to understand if the mechanism of injury is truly related to causes treatable by the therapist such as ergonomics or if the patient needs to be referred on so that the underlying issue may be resolved.

Developing an exercise program for a patient with Hypothyroidism can be helpful in many ways. First, it helps to rebuild activity tolerance, increase muscle strength, and reduce apathy secondary to the decreased metabolism caused by the disorder. Exercise to help correct such problems should only be implemented once the patient has begun hormone replacement therapy, otherwise the issues cannot be resolved. Increasing the patient’s exercise tolerance can also be extremely helpful for patients who are severely constipated from the disorder. It helps increase the peristaltic activity and overall metabolism. Also, because many patients with hypothyroidism have co morbid heart conditions, increasing aerobic activity can have benefits on the cardiovascular health of the patient and reduce risk factors for cardiac events. [5][8][6]

Differential Diagnosis[edit | edit source]


Case Reports[edit | edit source]

  1. A case study of a 15 year old girl who was diagnosed with a rare triad of primary amenorrhea, hypothyroidism, and Addison disease :  An Unusual Cause of Primary Amenorrhea[19]
  2. Hypothyroidism can be linked to Sleep Apnea. A case study was done on an 84 year old woman with a history of hypothyroidism: Case Study: Obstructive Sleep Apnea[20]
  3. A case study of a woman who was diagnosed with hypothyroidism in her mid-twenties and now ten years later is pregnant with her first child: Case Study: Management of Hypothyroidism during Pregnancy[21]
  4. A case study presented to show how to deal with newly diagnosed hypothyroid patients: Newly Diagnosed Hypothyroidism[22]
  5. A case study presented about a 78 year old being treated for 6 chronic conditions including Hypothyroidism:  Rehabilitation of a Functionally Limited, Chronically Ill Older Adult: A Case Study[23]
  6. A case report about a 74 year old woman that presented with increasing abdominal swelling over four months: Hypothyroidism Mimicking Intra-abdominal Malignancy [24]
  7. A case report about how acquired ataxia has been described with hypothyroidism and is typically reversible by thyroid hormone replacement therapy: Ataxia associated with Hashimoto's disease: Progressive non-familial adult onset cerebellar degeneration with autoimmune thyroiditis[25]

Resources[edit | edit source]

American Thyroid Association: http://thyroid.org
Clinical Thyroidology for Patients: http://thyroid.org/patients/ct/index.html
Thyroid Foundation of Canada: www.thyroid.ca
American Association of Clinical Endocrinologists: www.aace.com
Clinical Center, National Institutes of Health: www.cc.nih.gov
Hormone Foundation: www.hormone.org

References[edit | edit source]

  1. 1.0 1.1 Goodman C, Snyder T. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis, Missouri: Saunders Elsevier, 2007.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Goodman C, Fuller K. Pathology: Implications for the Physical Therapist. St. Louis, Missouri: Saunders Elsevier; 2009.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 Porter R, Hypothyroidism. The Merck Manual Online Medical Library. 2008. Available at: http://www.merck.com/mmpe/index.html . Accessed February 17, 2010.
  4. Hypothyroidism:What is it, Causes, Symptoms and Treatments. Available from: https://www.youtube.com/watch?v=h9WIzDa9big [last accessed 29/12/19]
  5. 5.0 5.1 5.2 5.3 5.4 5.5 5.6 Goodman C, Snyder T. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis, Missouri: Saunders Elsevier, 2007.
  6. 6.0 6.1 6.2 6.3 Allahabadia A., Razvi S., Abraham P., Franklyn . Diagnosis and treatment of primary hypothyroidism. British Medical Journal (International Edition) [serial online]. 2009;338:1090. Available from: Health Module. Accessed February 19, 2010, Document ID: 1731734701.
  7. Types of Hypothyroidism. Available at: http://www.type2hypothyroidism.com/Type1VsType2.html. Accessed February 17. 2010.
  8. 8.0 8.1 8.2 Vaidya B., Pearce S.. Management of hypothyroidism in adults. British Medical Journal (International Edition) [serial online]. 2008;337:284. Available from: Health Module. Accessed February 19, 2010, Document ID: 1542959701.
  9. Sell.com Classified. L-thyroxine. Available at: http://www.sell.com/23C4FX. Accessed on: February 17, 2010.
  10. Goodman C, Snyder T. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis, Missouri: Saunders Elsevier, 2007.
  11. Goodman C, Fuller K. Pathology: Implications for the Physical Therapist. St. Louis, Missouri: Saunders Elsevier; 2009.
  12. 12.0 12.1 American Thyroid Association. Patient Resources Online.2009. Available at: http://thyroid.org/patients/patients.html . Accessed February 17,2010.
  13. Secondary Hypothyroidism. Available from: https://www.youtube.com/watch?v=zj1UZKtWgFM [last accessed 29/12/19]
  14. Villar HC, Saconato H, Valente O, Atallah AN. Thyroid hormone replacement for subclinical hypothyroidism. Cochrane Database Syst Rev 2007;(3):CD003419.
  15. Bolk N, Visser TJ, Kalsbeek A, van Domburg RT, Berghout A. Effects of evening vs morning thyroxine ingestion on serum thyroid hormone profiles in hypothyroid patients. Clin Endocrinol (Oxf) 2007;66:43-8.
  16. Grozinsky-Glasberg S, Fraser A, Nahshoni E, Weizman A, Leibovici L. Thyroxine-triiodothyronine combination therapy versus thyroxine monotherapy for clinical hypothyroidism: meta-analysis of randomized controlled trials. J Clin Endocrinol Metab 2006;91:2592-9.
  17. Roos A, Linn-Rasker SP, van Domburg RT, Tijssen JP, Berghout A. The starting dose of levothyroxine in primary hypothyroidism treatment: a prospective, randomized, double-blind trial. Arch Intern Med 2005;165:1714-20. (Erratum, Arch Intern Med 2005;165:2227.)
  18. Somwaru LL, Arnold AM, Joshi N, Fried LP, Cappola AR. High frequency of and factors associated with thyroid hormone over-replacement and under-replacement in men and women aged 65 and over. J Clin Endocrinol Metab 2009;94:1342-5.
  19. Persson E., Chapados I.. An Unusual Cause of Primary Amenorrhea. Clinical Pediatrics [serial online]. 2008;47:309. Available from: Health Module. Accessed February 19, 2010, Document ID: 1455542621.
  20. Berry D.. Case Study: Obstructive Sleep Apnea. Medsurg Nursing [serial online]. 2008;17:11-6; quiz 17. Available from: ProQuest Medical Library. Accessed February 19, 2010, Document ID: 1474547051
  21. Tammy J Bungard, Mary Hurlburt. Management of hypothyroidism during pregnancy. Canadian Medical Association. Journal [serial online]. 2007;176:1077-8. Available from: ProQuest Medical Library. Accessed February 19, 2010, Document ID: 1260001101.
  22. H U Rehman, T A Bajwa. Newly diagnosed hypothyroidism. British Medical Journal (International Edition) [serial online]. 2004;329:1271. Available from: Health Module. Accessed February 19, 2010, Document ID: 758626471.
  23. Robert Topp, Jessica Sobolewski, Debra Boardley, Amy L Morgan, et al. Rehabilitation of a functionally limited, chronically ill older adult: A case study. Rehabilitation Nursing [serial online]. 2003;28:154-8. Available from: ProQuest Medical Library. Accessed February 19, 2010, Document ID: 417139371.
  24. S T M Krishnan, Z Philipose, G Rayman. Hypothyroidism mimicking intra-abdominal malignancy. British Medical Journal (International Edition) [serial online]. 2002;325:946-7. Available from: Health Module. Accessed February 19, 2010, Document ID: 234072331.
  25. M Selim, D A Drachman. Ataxia associated with Hashimoto's disease: Progressive non-familial adult onset cerebellar degeneration with autoimmune thyroiditis. Journal of Neurology, Neurosurgery and Psychiatry [serial online]. 2001;71:81-7. Available from: ProQuest Medical Library. Accessed February 19, 2010, Document ID: 75203187.