7 Hyperthyroidism Nursing Care Plans

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7 Hyperthyroidism Nursing Care Plans

Hyperthyroidism, also known as Grave’s disease, Basedow’s disease, or thyrotoxicosis is a metabolic imbalance that results from overproduction of thyroid hormones triiodothyronine (T3) and thyroxine (T4). The most common form is Graves’ disease, but other forms of hyperthyroidism include toxic adenoma, TSH-secreting pituitary tumor, subacute or silent thyroiditis, and some forms of thyroid cancer.

Thyroid storm is a rarely encountered manifestation of hyperthyroidism that can be precipitated by such events as thyroid ablation (surgical or radioiodine), medication overdosage, and trauma. This condition constitutes a medical emergency.

Nursing Care Plans

Nursing care management for patients with hyperthyroidism requires vigilant care to prevent acute exacerbations and complications.

Here are seven (7) nursing care plans (NCP) and nursing diagnosis for patients with hyperthyroidism:

  1. Risk for Decreased Cardiac Output
  2. Fatigue
  3. Risk for Disturbed Thought Processes
  4. Risk for Imbalanced Nutrition: Less Than Body Requirements
  5. Anxiety
  6. Risk for Impaired Tissue Integrity
  7. Deficient Knowledge
  8. Other Possible Nursing Care Plans
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Risk for Decreased Cardiac Output

Risk for Decreased Cardiac Output: At risk for Inadequate blood pumped by the heart to meet metabolic demands of the body.

Risk factors may include

  • Uncontrolled hyperthyroidism, hypermetabolic state
  • Increasing cardiac workload
  • Changes in venous return and systemic vascular resistance
  • Alterations in rate, rhythm, conduction

Possibly evidenced by

  • Not applicable. A risk diagnosis is not evidenced by signs and symptoms, as the problem has not occurred and nursing interventions are directed at prevention.

Desired Outcomes

  • Maintain adequate cardiac output for tissue needs as evidenced by stable vital signs, palpable peripheral pulses, good capillary refill, usual mentation, and absence of dysrhythmias.
Nursing InterventionsRationale
Monitor BP lying, sitting, and standing, if able. Note widened pulse pressure.General or orthostatic hypotension may occur as a result of excessive peripheral vasodilation and decreased circulating volume. Widened pulse pressure reflects compensatory increase in stroke volume and decreased systemic vascular resistance (SVR).
Monitor central venous pressure (CVP), if available.Provides more direct measure of circulating volume and cardiac function.
Investigate reports of chest pain or angina.May reflect increased myocardial oxygen demands or ischemia.
Assess pulse and heart rate while patient is sleeping.Provides a more accurate assessment of tachycardia.
Auscultate heart sounds, note extra heart sounds, development of gallops and systolic murmurs.Prominent S1 and murmurs are associated with forceful cardiac output of hypermetabolic state; development of S3 may warn of impending cardiac failure.
Monitor ECG, noting rate and rhythm. Document dysrhythmias.Tachycardia (greater than normally expected with fever and/or increased circulatory demand) may reflect direct myocardial stimulation by thyroid hormone. Dysrhythmias often occur and may compromise cardiac output.
Auscultate breath sounds. Note adventitious sounds.Early sign of pulmonary congestion, reflecting developing cardiac failure.
Monitor temperature; provide cool environment, limit bed linens or clothes, administer tepid sponge baths.Fever (may exceed 104°F) may occur as a result of excessive hormone levels and can aggravate diuresis and/or dehydration and cause increased peripheral vasodilation, venous pooling, and hypotension.
Observe signs and symptoms of severe thirst, dry mucous membranes, weak or thready pulse, poor capillary refill, decreased urinary output, and hypotension.Rapid dehydration can occur, which reduces the circulating volume and compromises cardiac output.
Record I&O. Note urine specific gravity.Significant fluid losses through vomiting, diarrhea, diuresis, and diaphoresis can lead to profound dehydration, concentrated urine, and weight loss.
Weigh daily. Encourage chair rest or bedrest. Limit unnecessary activities.Activity increases metabolic and circulatory demands, which may potentiate cardiac failure.
Note history of asthma and bronchoconstrictive disease, sinus bradycardia and heart blocks, advanced HF, or current pregnancy.The presence or potential recurrence of these conditions affect the choice of therapy. For example use of [beta]-adrenergic blocking agents is contraindicated.
Observe for adverse side effects of adrenergic antagonists: severe decrease in pulse, BP; signs of vascular congestion/HF; cardiac arrest.Indicates need for reduction or discontinuation of therapy.
Administer IV fluids as indicated.Rapid fluid replacement may be necessary to improve circulating volume but must be balanced against signs of cardiac failure and need for inotropic support.
Administer medications as indicated:
  • Thyroid hormone antagonists: propylthiouracil (PTU), methimazole (Tapazole)
May be definitive treatment or used to prepare the patient for surgery, but the effect is slow and so may not relieve thyroid storm. Once PTU therapy is begun, abrupt withdrawal may precipitate a thyroid crisis. Acts to prevent the release of thyroid hormone into circulation by increasing the amount of thyroid hormone stored within the gland. May interfere with RAI treatment and may exacerbate the disease in some people.
  • [beta]-blockers: propranolol (Inderal), atenolol (Tenormin), nadolol (Corgard), pindolol (Visken)
Given to control thyrotoxic effects of tachycardia, tremors, and nervousness and is the first drug of choice for an acute storm. Decreases heart rate or cardiac work by blocking [beta]-adrenergic receptor sites and blocking the conversion of T4 to T3. If severe bradycardia develops, atropine may be required. Blocks thyroid hormone synthesis and inhibits the peripheral conversion of T4 to T3.
  • Strong iodine solution (Lugol’s solution) or supersaturated potassium iodide (SSKI) PO
May be used as surgical preparation to decrease the size and vascularity of the gland or to treat thyroid storm. Should be started 1–3 hr after initiation of antithyroid drug therapy to minimize hormone formation from the iodine. If iodide is part of treatment, mix with milk juice, or water to prevent GI distress and administer through a straw to prevent tooth discoloration.
  • RAI (Na131I or Na125I) following NRC regulations for radiopharmaceutical
Radioactive iodine therapy is the treatment of choice for almost all patients with Graves’ disease because it destroys abnormally functioning gland tissue. Peak results take 6–12 wk (several treatments may be necessary); however, a single dose controls hyperthyroidism in about 90% of patients. This therapy is contraindicated during pregnancy. Also, people preparing or administering the dose must have their own thyroid burden measured, and contaminated supplies and equipment must be monitored and stored until decayed.
Provides glucocorticoid support. Decreases hyperthermia; relieves relative adrenal insufficiency; inhibits calcium absorption; and reduces peripheral conversion of Tfrom T4. May be given before thyroidectomy and discontinued after surgery.
Digitalization may be required in patients with HF before [beta]-adrenergic blocking therapy can be considered or safely initiated.
  • Potassium (KCl, K-Lyte)
Increased losses of K+ through intestinal and/or renal routes may result in dysrhythmias if not corrected.
  • Acetaminophen (Tylenol)
Drug of choice to reduce temperature and associated metabolic demands. Aspirin is contraindicated because it actually increases the level of circulating thyroid hormones by blocking the binding of T3 and T4 with thyroid-binding proteins.
Promotes rest, thereby reducing metabolic demands and cardiac workload.
  • Furosemide (Lasix)
Diuresis may be necessary if HF occurs. It also may be effective in reducing calcium level if the neuromuscular function is impaired.
Reduces shivering associated with hyperthermia, which can further increase metabolic demands.
Provide supplemental O2 as indicated.May be necessary to support increased metabolic demands and/or O2 consumption.
Provide a hypothermia blanket as indicated.Occasionally used to lower uncontrolled hyperthermia (104°F and higher) to reduce metabolic demands/O2  consumption and cardiac workload.
Monitor laboratory and diagnostic studies: 
  • Serum potassium
Hypokalemia resulting from intestinal losses, altered intake, or diuretic therapy may cause dysrhythmias and compromise cardiac function/output. In the presence of thyrotoxic paralysis (primarily occurring in Asian men), close monitoring and cautious replacement are indicated because rebound hyperkalemia can occur as condition abates releasing potassium from the cells.
  • Serum calcium
Elevation may alter cardiac contractility.
  • Sputum culture
Pulmonary infection is the most frequent precipitating factor of crisis.
  • Serial ECGs
May demonstrate the effects of electrolyte imbalance or ischemic changes reflecting inadequate myocardial oxygen supply in the presence of increased metabolic demands.
Cardiac enlargement may occur in response to increased circulatory demands. Pulmonary congestion may be noted with cardiac decompensation.
Administer transfusions; assist with plasmapheresis, hemoperfusion, dialysis.May be done to achieve rapid depletion of extrathyroidal hormone pool in a desperately ill or comatose patient.
Prepare for possible surgery.Subtotal thyroidectomy (removal of five-sixths of the gland) may be the treatment of choice for hyperthyroidism once a euthyroid state is achieved.
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See Also

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