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Hypothyroidism (Nursing)

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Last Update: February 18, 2024.

Learning Outcome

  1. List the causes of hypothyroidism
  2. Describe the clinical features of hypothyroidism
  3. Summarize the treatment of hypothyroidism
  4. Recall the nursing management plans for hypothyroidism

Introduction

The thyroid gland in the anterior neck secretes thyroid hormones and is essential for multiple metabolic functions spanning almost every organ system. Hypothyroidism results from low levels of thyroid hormone. However, the etiology and manifestations of hypothyroidism are varied. Clinicians treat hypothyroidism with levothyroxine. Untreated hypothyroidism increases morbidity and mortality. This article reviews hypothyroidism's etiology, clinical presentation, diagnosis, and management.

Nursing Diagnosis

  • Activity intolerance
  • Obesity
  • Overweight
  • Risk for constipation
  • Deficient knowledge
  • Imbalance in nutrition
  • Fatigue

Causes

The most common etiology is iodine deficiency in iodine-deficient geographic areas worldwide. Autoimmune thyroid diseases are the leading cause of hypothyroidism in the US and the iodine-sufficient regions. Etiology can be influenced locally by iodine fortification and the emergence of new iodine-deficient areas.[1]

Other common causes of hypothyroidism are drugs such as amiodarone and lithium, thyroid radioactive iodine therapy or thyroid surgery, radiotherapy to the head or neck area, and central hypothyroidism from neoplastic, infiltrative, inflammatory, or iatrogenic disorders of the pituitary or hypothalamus.[2][1][2]

Risk Factors

The National Health and Nutrition Examination Survey (NHANESIII) study found the prevalence of overt hypothyroidism among US adults aged 12 years and older to be 0.3% and subclinical hypothyroidism 4.3%. Female gender and increasing age were associated with higher thyroid-stimulating hormone (TSH) and prevalence of antithyroid antibodies.[3]

Assessment

A high index of suspicion should be maintained for hypothyroidism since the signs and symptoms can be mild and nonspecific, and different symptoms may be present in other patients.

Inquire about dry skin, voice changes, hair loss, constipation, fatigue, muscle cramps, cold intolerance, sleep disturbances, menstrual cycle abnormalities, weight gain, and galactorrhea.[2] Also, obtain a complete medical, surgical, medication, and family history. History of adverse pregnancy and neonatal outcomes should also be sought.[4]

Symptoms of depression, anxiety, psychosis, and cognitive impairments (eg, memory loss) can be present.[5] Rarely patients can present with ascites, rhabdomyolysis, and pericardial effusion.[6][7][6]

Patients can also present with carpal tunnel syndrome, sleep apnea, hyponatremia, hypercholesterolemia, congestive heart failure, and prolonged QT interval.[2]

A physical examination may reveal an enlarged thyroid gland, nodules, prolonged ankle reflex relaxation time, hoarse voice, and skin and hair changes.[2]

Evaluation

Serum TSH level is used to screen for primary hypothyroidism in most patients. In overt hypothyroidism, TSH levels are elevated, and free T4 levels are low. In subclinical hypothyroidism, TSH levels are elevated, and free T4 levels are normal.[2]

Central hypothyroidism is of pituitary or hypothalamic origin. The TSH produced can be biologically inactive and affect the levels of bioactive TSH; hence, the diagnosis of central hypothyroidism should be based on free T4 rather than TSH.[2]

Labs should include evaluation for autoimmune thyroid diseases with levels of anti-thyroid antibodies: the thyroid peroxidase antibodies and anti-thyroglobulin antibodies. Particularly in patients with thyroid nodules, fine-needle aspiration biopsy should be considered.[2]

Patients with subclinical hypothyroidism and thyroid peroxidase antibody positivity have a greater risk of developing overt hypothyroidism. These patients should be followed up periodically with clinical evaluation and lab tests. T3 levels are not a reliable or recommended test.[2] Hospitalized patients should undergo TSH testing only when thyroid dysfunction is suspected.[2] On labs, hyperlipidemia, elevated serum CK, elevated hepatic enzymes, and anemia can be present.[2] BUN, creatinine, and uric acid levels can also be elevated.[8]

Medical Management

Hypothyroidism is primarily treated with levothyroxine monotherapy.[9] The replacement levothyroxine dosage should be between 1.6 to 1.8 mcg/kg by mouth daily.[10] However, in patients who are older or with atrial fibrillation, reduction of the dose or starting at a low dosage and titrating up slowly as needed is essential.[9] 

When switching to the intravenous (IV) form, reduce the dose to 70% of the oral dose. Malabsorption syndromes, medications such as sucralfate, calcium preparations, and bile acid sequestrants can interfere with the absorption of levothyroxine.[2]

Based on the 2012 Clinical Practice Guidelines for Hypothyroidism in Adults by the American Association of Clinical Endocrinologists and the American Thyroid Association, therapy should be monitored and titrated based on serum TSH or free T4 measurements. Laboratory studies should be drawn every 4 to 8 weeks until target levels are achieved. Laboratory measurements should also be performed after starting treatment, after any dose change, after any change in the formulation or brand of levothyroxine, and after starting or stopping any medications that may affect the thyroid hormone levels.[2] If thyroid hormone levels are stable, then the monitoring interval can be extended to 6 months; if levels remain stable, then monitoring can be further extended to 12 months or done at shorter intervals on an individualized basis along with clinical evaluation.[2] Central hypothyroidism should be monitored based on free T4 rather than TSH.[2] For elderly patients and patients with cardiac diseases, starting at a lower dose and titrating slowly is recommended.[9]Patients with cardiac disease should be monitored for the development of any symptoms of angina and atrial fibrillation.[2] If a patient is overly treated with thyroid replacement for an extended period, screening for osteoporosis is warranted.[9]

Effective treatment should achieve a clinical improvement of signs and symptoms, along with an improved sense of patient well-being and normal TSH or free T4 levels.[11] A comprehensive differential diagnosis workup is recommended for unresolved symptoms in the presence of biochemical euthyroidism. There is a lack of strong evidence supporting the routine inclusion of triiodothyronine (T3) preparations with levothyroxine in the treatment of hypothyroidism.[12]

If symptoms persist despite normalization of TSH/free T4 levels, then consultation with an endocrinologist should also be considered. Thyroid replacement treatment can exacerbate coexisting adrenal insufficiency. Patients with known or suspected adrenal insufficiency should be tested and treated for the adrenal insufficiency while awaiting results.[2] Adrenal insufficiency can also be associated with subclinical hypothyroidism that is reversible with the treatment of adrenal insufficiency.[13] In patients who have confirmed adrenal insufficiency, consider a reassessment of thyroid tests following adequate treatment of adrenal insufficiency.

Nursing Management

  • Assess the client's weight and appetite
  • Consult with a dietitian to provide a menu for the patient (an increased fiber to counter constipation)
  • Educate the patient and family
  • Manage constipation with laxatives
  • Encourage the patient to use moisturizer if the skin is dry
  • Educate the patient on compliance with thyroid hormone therapy
  • Encourage exercise
  • Check labs for levels of thyroid hormone
  • Monitor fluid intake
  • Encourage the patient to follow up with a mental health nurse since depression is common in hypothyroidism.

Monitor for signs and symptoms of overtreatment with levothyroxine. Indications of overtreatment mimic signs and symptoms of hyperthyroidism, such as anxiety, palpitations, tachycardia, heat intolerance, fever, excessive sweating, changes in appetite, and weight loss. Report any signs of cardiac excitability, chest pain, and dysrhythmias to the medical provider. 

Coordination of Care

Hypothyroidism affects multiple organ systems across all age groups and affects patient well-being and ability to function daily. Treatment is with levothyroxine monotherapy.[2] Effective treatment calls for a team-based and patient-centered approach. An endocrinology consult should be obtained when patient symptoms are not adequately controlled.

Endocrinology consultation is also recommended in complex scenarios such as preconception, pregnancy, congenital and pediatric hypothyroidism, failure of treatment, co-existing cardiac or other endocrine disorders, difficulty in interpretation of thyroid test results, and drug-induced hypothyroidism.[2] Other specialists that may be needed are a psychiatrist, obstetrician-gynecologist, pediatrician, cardiologist, and intensivist.

Pharmacists help provide advice on medication and food interactions, the effect of changes in levothyroxine formulations, and investigating the causes for the requirement of unusually high doses of levothyroxine or fluctuating TSH levels. Prompt notification to physicians of unusually high levels of TSH by laboratory personnel and close monitoring of vital signs and mental status by nurses can facilitate early treatment and better outcomes, especially in the inpatient setting (eg, myxedema coma). Rapid response teams can be effectively utilized when severe long-term hypothyroidism causes hemodynamic instability from myxedema coma. Close interprofessional communication with all the involved teams is essential to improve patient outcomes.

Health Teaching and Health Promotion

Advise patients that treatment for hypothyroidism is lifelong. Instruct clients to take medications 30 to 60 minutes before the first meal of the day is essential. Also, inform patients not to take thyroid medications with other medications, as several food and medication interactions may occur.

Review Questions

 Pituitary Hyperplasia

Figure

 Pituitary Hyperplasia. The hyperplasia is due to primary hypothyroidism. Siddiqi AI, Grieve J, Baldeweg SE, Miszkiel K. Tablets or scalpel: pituitary hyperplasia due to primary hypothyroidism. Radiol Case Rep. 2016;10(2):1099. doi: 10.2484/rcr.v10i2.1099. (more...)

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Disclosure: Nikita Patil declares no relevant financial relationships with ineligible companies.

Disclosure: Anis Rehman declares no relevant financial relationships with ineligible companies.

Disclosure: Catherine Anastasopoulou declares no relevant financial relationships with ineligible companies.

Disclosure: Ishwarlal Jialal declares no relevant financial relationships with ineligible companies.

Disclosure: Angela Saathoff declares no relevant financial relationships with ineligible companies.

Copyright © 2025, StatPearls Publishing LLC.

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Bookshelf ID: NBK568746PMID: 33760505

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