Mar 1, 2011


Hyperthyroidism is a metabolic imbalance that results from overproduction of the 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.


Most people with classic hyperthyroidism rarely need hospitalization. Critically ill patients, those with extreme manifestations of thyrotoxicosis plus a significant concurrent illness, require inpatient acute care on a medical unit.


Heart failure: chronic

Psychosocial aspects of care


Patient Assessment Database

Data depend on the severity/duration of hormone imbalance and involvement of other organs.


May report: Nervousness, increased irritability, insomnia

Muscle weakness, incoordination

Extreme fatigue

May exhibit: Muscle atrophy


May report: Palpitations

Chest pain (angina)

May exhibit: Dysrhythmias (atrial fibrillation); gallop rhythm, murmurs

Elevated BP with widened pulse pressure

Tachycardia at rest

Circulatory collapse, shock (thyrotoxic crisis)


May report: Urinating in large amounts

Stool changes; diarrhea


May report: Recent stressful experience, e.g., emotional/physical

May exhibit: Emotional lability (mild euphoria to delirium); anxiety/depression


May report: Recent/sudden weight loss

Increased appetite; large meals, frequent meals; thirst


May exhibit: Enlarged thyroid; goiter

Nonpitting edema, especially in pretibial area


May exhibit: Rapid and hoarse speech

Mental status and behavior alterations, e.g., confusion, disorientation, nervousness, irritability, delirium, frank psychosis, stupor, coma

Fine tremor in hands; purposeless, quick, jerky movements of body parts

Hyperactive DTRs

Paralysis (thyrotoxic hypokalemia)


May report: Orbital pain, photophobia (eye movement)


May report: Difficulty breathing

May exhibit: Increased respiratory rate, tachypnea

Breath sounds: Crackles, wheezes (pulmonary edema associated with thyrotoxic crisis)


May report: Heat intolerance, excessive sweating

Allergy to iodine (may be used in testing)

May exhibit: Elevated temperature (above 100°F), diaphoresis

Skin smooth, warm, and flushed; hair fine, silky, straight

Exophthalmos, lid retraction; conjunctival irritation, tearing

Pruritic, erythematous lesions (often in pretibial area) that become brawny


May report: Decreased libido

Hypomenorrhea, amenorrhea



May report: Family history of thyroid problems

History of hypothyroidism, thyroid hormone replacement therapy or antithyroid therapy, premature withdrawal of antithyroid drugs, recent partial thyroidectomy

History of insulin-induced hypoglycemia, cardiac disorders or surgery, recent illness (pneumonia), trauma; x-ray contrast studies

Discharge plan DRG projected mean length of inpatient stay: 4.3 days

considerations: May require assistance with treatment regimen, self-care activities, homemaker/maintenance tasks

Refer to section at end of plan for postdischarge considerations.


Radioactive iodine (RAI) uptake test: High in Graves’ disease and toxic nodular goiter; low in thyroiditis.

Serum T4 and T3: Increased in hyperthyroidism. Normal T4 with elevated T3 indicates thyrotoxicosis.

Thyroid-stimulating hormone (TSH): Suppressed (except when etiology is a TSH-secreting pituitary tumor or pituitary resistant to thyroid hormone). Does not respond to thyrotropin-releasing hormone (TRH).

Thyroglobulin: Increased.

TRH stimulation: Hyperthyroidism is indicated if TSH fails to rise after administration of TRH.

Thyroid T3 uptake: Normal to high.

Protein-bound iodine: Increased.

Serum glucose: Elevated (related to adrenal involvement).

Plasma cortisol: Low levels (less adrenal reserve).

Alkaline phosphatase and serum calcium: Increased.

Liver function tests: Abnormal.

Electrolytes: Hyponatremia may reflect adrenal response or dilutional effect in fluid replacement therapy. Hypokalemia occurs because of GI losses and diuresis.

Serum catecholamines: Decreased.

Urine creatinine: Increased.

ECG: Atrial fibrillations; shorter systole time; cardiomegaly, heart enlarged with fibrosis and necrosis (late signs or in elderly with masked hyperthyroidism).

Needle or open biopsy: May be done to determine cause of hyperthyroidism, differentiate cysts or tumors, diagnose enlargement of thyroid gland.

Thyroid scan: Differentiates between Graves’ disease and Plummer’s disease, both of which result in hyperthyroidism.


1. Reduce metabolic demands and support cardiovascular function.

2. Provide psychological support.

3. Prevent complications.

4. Provide information about disease process/prognosis and therapy needs.


1. Homeostasis achieved.

2. Patient effectively dealing with current situation.

3. Complications prevented/minimized.

4. Disease process/prognosis and therapeutic regimen understood.

5. Plan in place to meet needs after discharge.

NURSING DIAGNOSIS: Cardiac Output, risk for decreased

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; presence of signs and symptoms establishes an actual diagnosis.]


Circulatory Status (NOC)

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.


Hemodynamic Regulation (NIC)


Monitor BP lying, sitting, and standing, if able. Note widened pulse pressure.

Monitor central venous pressure (CVP), if available.

Investigate reports of chest pain/angina.

Assess pulse/heart rate while patient is sleeping.


General/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).

Provides more direct measure of circulating volume and cardiac function.

May reflect increased myocardial oxygen demands/ischemia.

Provides a more accurate assessment of tachycardia.


Hemodynamic Regulation (NIC)


Auscultate heart sounds, noting extra heart sounds, development of gallops and systolic murmurs.

Monitor ECG, noting rate/rhythm. Document dysrhythmias.

Auscultate breath sounds, noting adventitious sounds (e.g., crackles).

Monitor temperature; provide cool environment, limit bed linens/clothes, administer tepid sponge baths.

Observe signs/symptoms of severe thirst, dry mucous membranes, weak/thready pulse, poor capillary refill, decreased urinary output, and hypotension.

Record I&O. Note urine specific gravity.

Weigh daily. Encourage chair rest/bedrest; limit nonessential activity.

Note history of asthma/bronchoconstrictive disease, sinus bradycardia/heart blocks, advanced HF, or current pregnancy.

Observe for adverse side effects of adrenergic antagonists, e.g., severe decrease in pulse, BP; signs of vascular congestion/HF; cardiac arrest.


Administer IV fluids as indicated.

Administer medications as indicated:

[beta]-blockers, e.g., propranolol (Inderal), atenolol (Tenormin), nadolol (Corgard), pindolol (Visken);


Prominent S1 and murmurs are associated with forceful cardiac output of hypermetabolic state; development of S3 may warn of impending cardiac failure.

Tachycardia (greater than normally expected with fever/increased circulatory demand) may reflect direct myocardialstimulation by thyroid hormone. Dysrhythmias often occur and may compromise cardiac function/output.

Early sign of pulmonary congestion, reflecting developing cardiac failure.

Fever (may exceed 104°F) may occur as a result of excessive hormone levels and can aggravate diuresis/dehydration and cause increased peripheral vasodilation, venous pooling, and hypotension.

Rapid dehydration can occur, which reduces circulating volume and compromises cardiac output.

Significant fluid losses (through vomiting, diarrhea, diuresis, diaphoresis) can lead to profound dehydration, concentrated urine, and weight loss.

Activity increases metabolic/circulatory demands, which may potentiate cardiac failure.

Presence/potential recurrence of these conditions affects choice of therapy; e.g., use of [beta]-adrenergic blocking agents is contraindicated.

Indicates need for reduction/discontinuation of therapy.

Rapid fluid replacement may be necessary to improve circulating volume but must be balanced against signs of cardiac failure/need for inotropic support.

Given to control thyrotoxic effects of tachycardia, tremors, and nervousness and is first drug of choice for acute storm. Decreases heart rate/cardiac work by blocking [beta]-adrenergic receptor sites and blocking conversion of T4 to T3. Note: If severe bradycardia develops, atropine may be required.


Hemodynamic Regulation (NIC)


Thyroid hormone antagonists, e.g., propylthiouracil(PTU), methimazole (Tapazole);

Strong iodine solution (Lugol’s solution) or supersaturated potassium iodide (SSKI) PO;

RAI (Na131I or Na125I) following NRC regulations for radiopharmaceutical;

Corticosteroids, e.g., dexamethasone (Decadron);

Digoxin (Lanoxin);

Furosemide (Lasix);

Potassium (KCl, K-Lyte);

Acetaminophen (Tylenol);


Blocks thyroid hormone synthesis and inhibits peripheral conversion of T4 to T3. May be definitive treatment or used to prepare patient for surgery; but effect is slow and so may not relieve thyroid storm. Note: Once PTU therapy is begun, abrupt withdrawal may precipitate thyroid crisis.

Acts to prevent 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. May be used as surgical preparation to decrease size and vascularity of the gland or to treat thyroid storm. Note: Should be started 1–3 hr after initiation of antithyroid drug therapy to minimize hormone formation from the iodine.

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. Note: 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 glucocorticol support. Decreases hyperthermia; relieves relative adrenal insufficiency; inhibits calcium absorption; and reduces peripheral conversion of T3 from T4. Note: 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/safely intiated.

Diuresis may be necessary if HF occurs. Note: It also may be effective in reducing calcium level if neuromuscular function is impaired.

Increased losses of K+ through intestinal/renal routes may result in dysrhythmias if not corrected.

Drug of choice to reduce temperature and associated metabolic demands. Aspirin is contraindicated because it actually increases level of circulating thyroid hormones by blocking binding of T3 and T4 with thyroid-binding proteins.


Hemodynamic Regulation (NIC)


Sedative, barbiturates;

Muscle relaxants.

Monitor laboratory/diagnostic studies, as indicated, e.g.:

Serum potassium;

Serum calcium;

Sputum culture;

Serial ECGs;

Chest x-rays.

Provide supplemental O2 as indicated.

Provide hypothermia blanket as indicated.

Administer transfusions; assist with plasmapheresis, hemoperfusion, dialysis.

Prepare for surgery.


Promotes rest, thereby reducing metabolic demands/cardiac workload.

Reduces shivering associated with hyperthermia, which can further increase metabolic demands.

Hypokalemia resulting from intestinal losses, altered intake, or diuretic therapy may cause dysrhythmias and compromise cardiac function/output. Note: 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.

Elevation may alter cardiac contractility.

Pulmonary infection is most frequent precipitating factor of crisis.

May demonstrate effects of electrolyte imbalance or ischemic changes reflecting inadequate myocardial oxygen supply in presence of increased metabolic demands.

Cardiac enlargement may occur in response to increased circulatory demands. Pulmonary congestion may be noted with cardiac decompensation.

May be necessary to support increased metabolic demands/O2 consumption.

Occasionally used to lower uncontrolled hyperthermia (104°F and higher) to reduce metabolic demands/O2 consumption and cardiac workload.

May be done to achieve rapid depletion of extrathyroidal hormone pool in desperately ill/comatose patient.

Subtotal thyroidectomy (removal of five-sixths of the gland) may be treatment of choice for hyperthyroidism once euthyroid state is achieved.


May be related to

Hypermetabolic state with increased energy requirements

Irritability of central nervous system (CNS); altered body chemistry

Possibly evidenced by

Verbalization of overwhelming lack of energy to maintain usual routine, decreased performance

Emotional lability/irritability; nervousness, tension

Jittery behavior

Impaired ability to concentrate


Endurance (NOC)

Verbalize increase in level of energy.

Display improved ability to participate in desired activities.


Energy Management (NIC)


Monitor vital signs, noting pulse rate at rest and when active.

Note development of tachypnea, dyspnea, pallor, and cyanosis.

Provide for quiet environment; cool room, decreased sensory stimuli, soothing colors, quiet music.

Encourage patient to restrict activity and rest in bed as much as possible.

Provide comfort measures, e.g., judicious touch/massage, cool showers.

Provide for diversional activities that are calming, e.g., reading, radio, television.

Avoid topics that irritate or upset patient. Discuss ways to respond to these feelings.

Discuss with SO reasons for fatigue and emotional lability.


Pulse is typically elevated and, even at rest, tachycardia (up to 160 beats/min) may be noted.

O2 demand and consumption are increased in hypermetabolic state, potentiating risk of hypoxia with activity.

Reduces stimuli that may aggravate agitation, hyperactivity, and insomnia.

Helps counteract effects of increased metabolism.

May decrease nervous energy, promoting relaxation.

Allows for use of nervous energy in a constructive manner and may reduce anxiety.

Increased irritability of the CNS may cause patient to be easily excited, agitated, and prone to emotional outbursts.

Understanding that the behavior is physically based may enhance coping with current situation and encourage SO to respond positively and provide support for patient.


Energy Management (NIC)


Administer medications as indicated:

Sedatives, e.g., phenobarbital (Luminal); antianxiety agents, e.g., chlordiazepoxide (Librium).


Combats nervousness, hyperactivity, and insomnia.

NURSING DIAGNOSIS: Nutrition imbalanced, risk for less than body requirements

Risk factors may include

Increased metabolism (increased appetite/intake with loss of weight)

Nausea/vomiting, diarrhea

Relative insulin insufficiency; hyperglycemia

Possibly evidenced by

[Not applicable; presence of signs and symptoms establishes an actual diagnosis.]


Nutritional Status (NOC)

Demonstrate stable weight with normal laboratory values and be free of signs of malnutrition.


Energy Management (NIC)


Monitor daily food intake. Weigh daily and report losses.

Encourage patient to eat and increase number of meals and snacks, using high-calorie foods that are easily digested.

Avoid foods that increase peristalsis (e.g., tea, coffee, fibrous and highly seasoned foods) and fluids that cause diarrhea (e.g., apple/prune juice).


Consult with dietitian to provide diet high in calories, protein, carbohydrates, and vitamins.

Administer medications as indicated:

Glucose, vitamin B complex;

Insulin (small doses).


Continued weight loss in face of adequate caloric intake may indicate failure of antithyroid therapy.

Aids in keeping caloric intake high enough to keep up with rapid expenditure of calories caused by hypermetabolic state.

Increased motility of GI tract may result in diarrhea and impair absorption of needed nutrients.

May need assistance to ensure adequate intake of nutrients, identify appropriate supplements.

Given to meet energy requirements and prevent or correct hypoglycemia.

Aids in controlling serum glucose if elevated.

NURSING DIAGNOSIS: Anxiety [specify level]

May be related to

Physiological factors: hypermetabolic state (CNS stimulation), pseudocatecholamine effect of thyroid hormones

Possibly evidenced by

Increased feelings of apprehension, shakiness, loss of control, panic

Changes in cognition, distortion of environmental stimuli

Extraneous movements, restlessness, tremors


Anxiety Control (NOC)

Appear relaxed.

Report anxiety reduced to a manageable level.

Identify healthy ways to deal with feelings.


Anxiety Reduction (NIC)


Observe behavior indicative of level of anxiety.

Monitor physical responses, noting palpitations, repetitive movements, hyperventilation, insomnia.

Stay with patient, maintaining calm manner. Acknowledge fear and allow patient’s behavior to belong to patient.

Describe/explain procedures, surrounding environment, or sounds that may be heard by patient.

Speak in brief statements, using simple words.

Reduce external stimuli: Place in quiet room; provide soft, soothing music; reduce bright lights; reduce number of persons contacting patient.

Discuss with patient/SO reasons for emotional lability/psychotic reaction. (Refer to ND: Thought Processes, risk for disturbed, following.)

Reinforce expectation that emotional control should return as drug therapy progresses.


Mild anxiety may be displayed by irritability and insomnia. Severe anxiety progressing to panic state may produce feelings of impending doom, terror, inability to speak or move, shouting/swearing.

Increased number of [beta]-adrenergic receptor sites, coupled with effects of excess thyroid hormones, produces clinical manifestations of catecholamine excess even when normal levels of norepinephrine/epinephrine exist.

Affirms to patient/SO that although patient feels out of control, environment is safe. Avoiding personal responses to inappropriate remarks or actions prevents conflicts/overreaction to stressful situation.

Provides accurate information, which reduces distortions/misinterpretations that can contribute to anxiety/fear reactions.

Attention span may be shortened, concentration reduced, limiting ability to assimilate information.

Creates a therapeutic environment; shows recognition that unit activity/personnel may increase patient’s anxiety.

Understanding that behavior is physically based enhances acceptance of situation and encourages different responses/approaches.

Provides information and reassures patient that the situation is temporary and will improve with treatment.


Anxiety Reduction (NIC)


Administer antianxiety agents or sedatives and monitor effects.

Refer to support systems as needed, e.g., counseling, social services, pastoral care.


May be used in conjuction with medical regimen to reduce effects of hyperthyroid secretion.

Ongoing therapy support may be desired/required by patient/SO if crisis precipitates lifestyle alterations.

NURSING DIAGNOSIS: Thought Processes, risk for disturbed

Risk factors may include

Physiological changes: increased CNS stimulation/accelerated mental activity

Altered sleep patterns

Possibly evidenced by

[Not applicable; presence of signs and symptoms establishes an actual diagnosis.]


Distorted Thought Control (NOC)

Maintain usual reality orientation.

Recognize changes in thinking/behavior and causative factors.


Delirium Management (NIC)


Assess thinking processes, e.g., memory, attention span, orientation to person/place/time.

Note changes in behavior.

Assess level of anxiety. (Refer to ND: Anxiety)

Provide quiet environment; decreased stimuli, cool room, dim lights. Limit procedures/personnel.

Reorient to person/place/time as indicated.

Present reality concisely and briefly without challenging illogical thinking.


Determines extent of interference with sensory processing.

May be hypervigilant, restless, extremely sensitive, or crying or may develop frank psychosis.

Anxiety may alter thought processes.

Reduction of external stimuli may decrease hyperactivity/reflexia, CNS irritability, auditory/visual hallucinations.

Helps establish and maintain awareness of reality/environment.

Limits defensive reaction.


Delirium Management (NIC)


Provide clock, calendar, room with outside window; alter level of lighting to simulate day/night.

Encourage visits by family/SO. Provide support as needed.

Provide safety measures, e.g., padded side rails, close supervision, or soft restraints as last resort as necessary.


Administer medication as indicated, e.g., sedatives/antianxiety agents/antipsychotic drugs.


Promotes continual orientation cues to assist patient in maintaining sense of normalcy.

Aids in maintaining socialization and orientation. Note: Patient’s agitation/psychotic behavior may precipitate family quarrels/conflicts.

Prevents injury to patient who may be hallucinating/disoriented.

Promotes relaxation, reduces CNS hyperactivity/agitation to enhance thinking ability.

NURSING DIAGNOSIS: Tissue Integrity, risk for impaired

Risk factors may include

Alterations of protective mechanisms of eye: impaired closure of eyelid/exophthalmos

Possibly evidenced by

[Not applicable; presence of signs and symptoms establishes an actual diagnosis.]


Tissue Integrity: Skin & Mucous Membranes (NOC)

Maintain moist eye membranes, free of ulcerations.

Risk Control (NOC)

Identify measures to provide protection for eyes and prevent complications.


Surveillance (NIC)


Encourage use of dark glasses when awake and taping the eyelids shut during sleep as needed.

Elevate the head of the bed and restrict salt intake if indicated.

Instruct patient in extraocular muscle exercises if appropriate.


Protects exposed cornea if patient is unable to close eyelids completely because of edema/fibrosis of fat pads.

Decreases tissue edema when appropriate, e.g., HF, which can aggravate existing exophthalmos.

Improves circulation and maintains mobility of the eyelids.


Surveillance (NIC)


Provide opportunity for patient to discuss feelings about altered appearance and measures to enhance self-image.


Administer medications as indicated:

Methylcellulose drops;

Adrenocorticotropic hormone (ACTH), prednisone;

Antithyroid drugs;


Prepare for surgery as indicated.


Protruding eyes may be viewed as unattractive. Appearance can be enhanced with proper use of makeup, overall grooming, and use of shaded glasses.

Lubricates the eyes, reducing risk of lesion formation.

Given to decrease rapidly progressive and marked inflammation.

May decrease signs/symptoms or prevent worsening of the condition.

Can decrease edema in mild involvement.

Eyelids may need to be sutured shut temporarily to protect the corneas until edema resolves (rare) or increasing space within sinus cavity and adjusting musculature may return eye to a more normal position.

NURSING DIAGNOSIS: Knowledge, deficient [Learning Need] regarding condition, prognosis, treatment, self-care, and discharge needs

May be related to

Lack of exposure/recall

Information misinterpretation

Unfamiliarity with information resources

Possibly evidenced by

Questions, request for information, statement of misconception

Inaccurate follow-through of instructions/development of preventable complications


Knowledge: Illness Care (NOC)

Verbalize understanding of disease process and potential complications.

Identify relationship of signs/symptoms to the disease process and correlate symptoms with causative factors.

Verbalize understanding of therapeutic needs.

Initiate necessary lifestyle changes and participate in treatment regimen.


Teaching: Disease Process (NIC)


Review disease process and future expectations.

Provide information appropriate to individual situation.

Identify stressors and discuss precipitators to thyroid crises, e.g., personal/social and job concerns, infection, pregnancy.

Provide information about signs/symptoms of hypothyroidism and the need for continuing follow-up care.

Discuss drug therapy, including need for adhering to regimen, and expected therapeutic and side effects.

Identify signs/symptoms requiring medical evaluation, e.g., fever, sore throat, and skin eruptions.

Explain need to check with physician/pharmacist before taking other prescribed or OTC drugs.

Emphasize importance of planned rest periods.

Review need for nutritious diet and periodic review of nutrient needs; avoid caffeine, red/yellow food dyes, artificial preservatives.

Stress necessity of continued medical follow-up.


Provides knowledge base from which patient can make informed choices.

Severity of condition, cause, age, and concurrent complications determine course of treatment.

Psychogenic factors are often of prime importance in the occurrence/exacerbation of this disease.

Patient who has been treated for hyperthyroidism needs to be aware of possible development of hypothyroidism, which can occur immediately after treatment or as long as 5 yr later.

Antithyroid medication (either as primary therapy or in preparation for thyroidectomy) requires adherence to a medical regimen over an extended period to inhibit hormone production. Agranulocytosis is the most serious side effect that can occur, and alternative drugs may be given if problems arise.

Early identification of toxic reactions (thiourea therapy) and prompt intervention are important in preventing development of agranulocytosis.

Antithyroid medications can affect or be affected by numerous other medications, requiring monitoring of medication levels, side effects, and interactions.

Prevents undue fatigue; reduces metabolic demands. As euthyroid state is achieved, stamina and activity level will increase.

Provides adequate nutrients to support hypermetabolic state. A hormonal imbalance is corrected, diet will need to be readjusted to prevent excessive weight gain. Irritants and stimulants should be limited to avoid cumulative systemic effects.

Necessary for monitoring effectiveness of therapy and prevention of potentially fatal complications.

POTENTIAL CONSIDERATIONS following acute hospitalization (dependent on patient’s age, physical condition/presence of complications, personal resources, and life responsibilities)

Fatigue—hypermetabolic state diminishing body energy reserves, prolonged recovery.

Nutrition: imbalanced, risk for more than body requirements—change in BMR and metabolic needs.