endocrine
Anatomy and Physiology of the Endocrine Glands (Box 43.1)
Functions
Maintenance and regulation of vital functions
Response to stress and injury
Growth and development
Energy metabolism
Reproduction
Fluid, electrolyte, and acid-base balance
Risk factors for endocrine problems (Box 43.2)
Hypothalamus (Box 43.3)
Portion of the diencephalon of the brain forming the floor and part of the lateral wall of the third ventricle
Activates, controls, and integrates the peripheral autonomic nervous system; endocrine processes; and many somatic functions, such as body temperature, sleep, and appetite
Pituitary gland (Box 43.4; Fig. 43.1)
The master gland; located at the base of the brain
Influenced by the hypothalamus; directly affects the function of the other endocrine glands
Promotes the growth of body tissue, influences water absorption by the kidney, and controls sexual development and function
Adrenal gland
One adrenal gland is on top of each kidney.
Regulates sodium and electrolyte balance; affects carbohydrate, fat, and protein metabolism; influences the development of sexual characteristics; and sustains the fight-or-flight response
Adrenal cortex
The cortex is the outer shell of the adrenal gland.
The cortex synthesizes glucocorticoids and mineralocorticoids and secretes small amounts of sex hormones (androgens, estrogens; Box 43.5).
Adrenal medulla
The medulla is the inner core of the adrenal gland.
The medulla works as a part of the sympathetic nervous system and produces epinephrine and norepinephrine.
Thyroid gland
Located in the anterior part of the neck
Controls the rate of body metabolism and growth and produces thyroxine (T4), triiodothyronine (T3), and thyrocalcitonin
Parathyroid glands
Located on the thyroid gland
Control calcium and phosphorus metabolism; produce parathyroid hormone (PTH)
Pancreas
Located posteriorly to the stomach
Influences carbohydrate metabolism, indirectly influences fat and protein metabolism, and produces insulin and glucagon
Ovaries and testes
The ovaries are located in the pelvic cavity and produce estrogen and progesterone.
The testes are located in the scrotum, control the development of the secondary sex characteristics, and produce testosterone.
Negative feedback loop
Regulates hormone secretion by the hypothalamus and pituitary gland
Increased amount of target gland hormones in the bloodstream decreases secretion of the same hormone and other hormones that stimulate its release.
Diagnostic Tests
Stimulation and suppression tests
Stimulation tests
In the client with suspected underactivity of an endocrine gland, a stimulus may be provided to determine whether the gland is capable of normal hormone production.
Measured amounts of selected hormones or substances are administered to stimulate the target gland to produce its hormone.
Hormone levels produced by the target gland are measured.
Failure of the hormone level to increase with stimulation indicates hypofunction.
Suppression tests
Suppression tests are used when hormone levels are high or in the upper range of normal.
Agents that normally induce a suppressed response are administered to determine whether normal negative feedback is intact.
Failure of hormone production to be suppressed during standardized testing indicates hyperfunction.
Overnight dexamethasone suppression test
Used to distinguish between Cushing's syndrome and Cushing's disease
In Cushing's disease, the source of excess cortisol is the pituitary gland rather than the adrenal cortex or exogenous corticosteroid administration.
Dexamethasone, a potent long-acting corticosteroid given at bedtime, would suppress morning cortisol in clients without Cushing's disease by suppressing adrenocorticotropic hormone (ACTH) production; in the client with Cushing's disease, this suppression will not occur.
Radioactive iodine uptake
This thyroid function test measures the absorption of an iodine isotope to determine how the thyroid gland is functioning.
A small dose of radioactive iodine is given by mouth or intravenously; the amount of radioactivity is measured in 4 to 6 hours and again at 24 hours.
Normal values are 3% to 10% at 2 to 4 hours and 8% to 25% at 24 hours. Some testing centers only measure at 24 hours. Values may vary depending on the client's iodine intake.
Elevated values indicate hyperthyroidism, decreased iodine intake, or increased iodine excretion.
Decreased values indicate a low T4level, the use of antithyroid medications, thyroiditis, myxedema, or hypothyroidism.
The test is contraindicated during pregnancy.
T3 and T4 resin uptake test
Blood tests are used to diagnose thyroid problems.
T3 and T4 regulate thyroid-stimulating hormone (TSH).
Normal values (normal findings vary between laboratory settings)
Triiodothyronine, total T3: 70 ng/dL to 205 ng/dL
Thyroxine, total T4: 5 mcg/dL to 12.0 mcg/dL
Thyroxine, free (FT4): 0.8 ng/dL to 2.8 ng/dL
The T3 level is elevated in hyperthyroidism, decreases with the aging process, and may be decreased in hypothyroidism.
The T4 level is elevated in hyperthyroidism and decreased in hypothyroidism.
Thyroid-stimulating hormone
Blood test is used to differentiate the diagnosis of primary hypothyroidism.
Normal value is 2 to 10 mcU/L.
Elevated values indicate primary hypothyroidism.
Decreased values indicate hyperthyroidism or secondary hypothyroidism.
Thyroid scan
A thyroid scan is performed to identify nodules or growths in the thyroid gland.
A radioisotope of iodine or technetium is administered before scanning the thyroid gland.
Reassure the client that the level of radioactive medication is not dangerous to self or others.
Determine whether the client has received radiographic contrast agents within the past 3 months because these may invalidate the scan.
Check with the primary health care provider (PHCP) regarding discontinuing medications that contain iodine for 14 days before the test and the need to discontinue thyroid medication before the test; check for allergy to iodine.
Reinforce instructions to the client to maintain NPO (nothing by mouth) status after midnight on the day before the test; if iodine is used, the client will fast for an additional 45 minutes after the ingestion of the oral isotope, and the scan will be performed in 24 hours.
If technetium is used, it is administered by the intravenous (IV) route 30 minutes before the scan.
The test is contraindicated during pregnancy and in those with an iodine allergy.
Needle aspiration of thyroid tissue
Aspiration of thyroid tissue is done for cytological examination.
No client preparation is necessary; NPO status may or may not be prescribed.
Light pressure is applied to the aspiration site after the procedure.
Glycosylated hemoglobin
HgbA1C is blood glucose bound to hemoglobin.
Hemoglobin A1c (glycosylated hemoglobin A; HbA1c) is a reflection of how well blood glucose levels have been controlled for the past 3 to 4 months.
Hyperglycemia in clients with diabetes is usually a cause of an increase in HbA1c.
Fasting is not required before the test.
Normal reference intervals: 4.0% to 6%, depending on physician preference
HgbA1C and estimated average glucose (eAG): Refer to Table 10.3 for these reference intervals.
Poor glycemic control in a client with diabetes mellitus is usually the cause of an increase in the HbA1c value. An HbA1c level greater than 7.0% is considered poor glycemic control.
24-hour urine collection for vanillylmandelic acid (VMA)
Diagnostic tests for pheochromocytoma include a 24-hour urine collection for VMA—a product of catecholamine metabolism, metanephrine, and catecholamines—all of which are elevated in the presence of pheochromocytoma.
The normal range of urinary catecholamines:
Epinephrine: <20 mcg/day
Norepinephrine: <100 mcg/dayPituitary Gland Problems (Box 43.6)
Hypopituitarism
Description: Hyposecretion of one or more of the pituitary hormones caused by tumors, trauma, encephalitis, autoimmunity, or stroke
Hormones most often affected are growth hormone (GH) and the gonadotropins (luteinizing hormone, follicle-stimulating hormone), but TSH, ACTH, or antidiuretic hormone (ADH) may be involved.
Data collection
Mild to moderate obesity (GH, TSH)
Reduced cardiac output (GH, ADH)
Infertility and sexual dysfunction (gonadotropins, ACTH)
Fatigue, low blood pressure (TSH, ADH, ACTH, GH)
Tumors of the pituitary also may cause headache and visual defects (pituitary is located near the optic nerve).
Interventions
Client may need hormone replacement for the specific deficient hormones.
Provide emotional support to the client and family.
Encourage the client and family to express feelings related to disturbed body image or sexual dysfunction.
Reinforce client education regarding the signs/symptoms of both hypofunction and hyperfunction related to insufficient or excess hormone replacement.
Hyperpituitarism (Acromegaly)
Description: Hypersecretion of GH by the anterior pituitary gland in an adult; caused primarily by pituitary tumors
Data collection
Large hands and feet
Thickening and protrusion of the jaw
Arthritic changes and joint pain; impingement syndromes
Visual disturbance
Diaphoresis
Oily, rough skin
Organomegaly
Hypertension atherosclerosis, cardiomegaly, heart failure
Dysphagia
Deepening of the voice
Thickening of the tongue, narrowing of the airway, sleep apnea
Hyperglycemia
Colon polyps, increased colon cancer risk
Interventions
Provide pharmacological interventions to suppress GH or block the action of GH.
Prepare the client for radiation of the pituitary gland or for stereotactic radiosurgery, if prescribed.
Prepare the client for hypophysectomy if planned.
Provide pharmacological and nonpharmacological interventions for joint pain.
Provide emotional support to the client and family, and encourage the client and family to express feelings related to disturbed body image.
Hypophysectomy (pituitary adenectomy, sublabial transsphenoidal pituitary surgery)
Description
The removal of the pituitary tumor via craniotomy or via sublabial transsphenoidal (endoscopic transnasal) approach (the latter approach is preferred because it is associated with fewer complications).
Complications for craniotomy include increased intracranial pressure, bleeding, meningitis, and hypopituitarism.
Complications for the sublabial transsphenoidal surgery include cerebrospinal fluid leak, infection, diabetes insipidus, and hypopituitarism.
If the sublabial approach is used, an incision is made along the gum line of the inner upper lip.
Postoperative interventions
Initiate postoperative care similar to craniotomy care.
Monitor vital signs, neurological status, and level of consciousness.
Elevate the head of the bed.
Monitor for increased intracranial pressure.
Reinforce instructions to the client to avoid sneezing, coughing, and blowing the nose.
Monitor for bleeding.
Monitor for signs of temporary diabetes insipidus; monitor intake and output and report excessive urinary output.
If the entire pituitary is removed, clients will require lifelong replacement of ADH, cortisol, and thyroid hormone.
Monitor for and report signs of infection and meningitis.
Administer antibiotics, analgesics, and antipyretics as prescribed.
Administer oral mouth rinse as prescribed. Clients may be instructed to avoid using a toothbrush or to brush teeth gently with an ultra-soft toothbrush for 10 days to 2 weeks after surgery.
Reinforce instructions to the client regarding the administration of prescribed medications.
After transsphenoidal hypophysectomy, monitor for and report postnasal drip or clear nasal drainage, which might indicate a cerebrospinal fluid leak. Clear drainage needs to be checked for glucose.
Diabetes insipidus
Description
Hyposecretion of ADH caused by stroke, surgery, or trauma, or may be idiopathic
The kidney tubules fail to reabsorb water.
In central diabetes insipidus, there is decreased ADH production.
In nephrogenic diabetes insipidus, ADH production is adequate but the kidneys do not respond appropriately to the ADH.
Data collection
Excretion of large amounts of dilute urine
Polydipsia
Dehydration (decreased skin turgor and dry mucous membranes)
Inability to concentrate urine
A low urinary specific gravity; normal is 1.003 to 1.030
Fatigue
Muscle pain and weakness
Headache
Postural hypotension that may progress to vascular collapse without rehydration
Tachycardia
Interventions
Monitor vital signs and the client's neurological and cardiovascular status.
Provide a safe environment particularly for the client with postural hypotension.
Monitor electrolyte values and for signs of dehydration.
Maintain client intake of adequate fluids; IV hypotonic saline may be prescribed to replace urinary losses.
Monitor intake and output, weight, serum osmolality, and specific gravity of urine for excessive urinary output, weight loss, and low urinary specific gravity.
Reinforce instructions to the client to avoid foods or liquids that produce diuresis.
Vasopressin tannate or desmopressin acetate may be prescribed; these are used when the ADH deficiency is severe or chronic.
Reinforce instructions to the client regarding the administration of medications as prescribed; desmopressin acetate may be administered by subcutaneous injection, intravenously, intranasally, or orally; watch for signs of water intoxication indicating overtreatment.
Reinforce instructions to the client to wear a Medic-Alert bracelet.
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Description
Condition of hyperfunctioning of the posterior pituitary gland in which excess ADH is released, but not in response to the body's need for it.
Causes include trauma, stroke, malignancy (often in the lungs or pancreas), medication, and stress.
The syndrome results in increased intravascular volume, water intoxication, and dilutional hyponatremia.
May cause cerebral edema and the client is at risk for seizures.
Data collection
Signs of fluid volume overload
Change in the level of consciousness and the client's mental status
Weight gain without edema
Hypertension
Tachycardia
Anorexia, nausea, vomiting
Hyponatremia
Low urinary output and concentrated urine
Interventions
Monitor vital signs and cardiac and neurological status.
Provide a safe environment, particularly for the client with a change in their level of consciousness or mental status.
Monitor for signs of increased intracranial pressure.
Implement seizure precautions.
Elevate the head of the bed a maximum of 10 degrees to promote venous return and decrease baroreceptor-induced ADH release.
Monitor intake and output and obtain weight daily.
Monitor fluid and electrolyte balance.
Monitor the serum and urine osmolality.
Restrict fluid intake as prescribed.
Assist to administer diuretics and IV fluids (usually normal saline [NS] or hypertonic saline) as prescribed; monitor IV fluids carefully because of the risk for fluid volume overload.
Loop diuretics may be prescribed to promote diuresis, but only if serum sodium is at least 125 mEq/L; potassium replacement may be necessary if loop diuretics are prescribed.
Vasopressin antagonists may be prescribed to decrease the renal response to ADH.
Adrenal Gland Problems (Box 43.7)
Adrenal cortex insufficiency (Addison's disease)
Primary adrenal insufficiency
Also known as Addison's disease, refers to hyposecretion of adrenal cortex hormones (glucocorticoids, mineralocorticoids, and androgen); autoimmune destruction is a common cause.
Requires lifelong replacement of glucocorticoids and possibly of mineralocorticoids, if significant hyposecretion occurs; the condition is fatal if left untreated.
Secondary adrenal insufficiency is caused by hyposecretion of ACTH from the anterior pituitary gland; mineralocorticoid release is spared.
Loss of glucocorticoids in Addison's disease leads to decreased vascular tone, decreased vascular response to the catecholamines epinephrine and norepinephrine, and decreased gluconeogenesis.
In Addison's disease, loss of the mineralocorticoid aldosterone leads to dehydration, hypotension, hyponatremia, and hyperkalemia.
Data collection (Table 43.1)
Interventions
Monitor vital signs (particularly for hypotension), for weight loss, and intake and output.
Monitor white blood cell (WBC) count; blood glucose; and potassium, sodium, and calcium levels.
Administer glucocorticoid or mineralocorticoid medications as prescribed.
Observe for Addisonian crisiscaused by stress, infection, trauma, or surgery.
Reinforce client education
Need for lifelong glucocorticoid replacement and possible lifelong mineralocorticoid replacement
Corticosteroid replacement will need to be increased during times of stress.
Avoid individuals with an infection.
Avoid strenuous exercise and stressful situations.
Avoid over-the-counter medications.
Diet needs to be high in protein and carbohydrates; clients taking glucocorticoids would be prescribed calcium and vitamin D supplements to protect against corticosteroid-induced osteoporosis; some clients taking mineralocorticoids may be prescribed a diet high in sodium.
Wear a MedicAlert bracelet.
Report signs and symptoms of complications such as underreplacement and overreplacement of corticosteroid hormones.
Addisonian crisis
Description (Box 43.8)
Data collection
Severe headache
Severe abdominal, leg, and lower back pain
Generalized weakness
Irritability and confusion
Severe hypotension
Shock
Interventions
Prepare to assist the registered nurse (RN) with the administration of IV glucocorticoids, as prescribed.
Prepare to assist the RN with the administration of IV fluids to replace fluids and restore electrolyte balance.
Following resolution of the crisis, administer glucocorticoids and mineralocorticoids orally, as prescribed.
Monitor vital signs, particularly blood pressure.
Monitor neurological status, noting irritability and confusion.
Monitor intake and output.
Monitor laboratory values, particularly sodium, potassium, and blood glucose levels.
Protect the client from infection.
Maintain bed rest and provide a quiet environment.
Clients taking exogenous corticosteroids need to establish a plan with their PHCP or endocrinologist for increasing their corticosteroids during times of stress.
Cushing's syndrome and Cushing's disease (hypercortisolism)
Cushing's syndrome
A metabolic disorder resulting from the chronic and excessive production of cortisol by the adrenal cortex or from the administration of glucocorticoids in large doses for several weeks or longer (exogenous or iatrogenic)
ACTH secreting tumors (most often of the lung, pancreas, or GI tract) can cause Cushing's syndrome.
Cushing's disease is a metabolic disorder characterized by the abnormally increased secretion (endogenous) of cortisol, caused by increased amounts of ACTH secreted by the pituitary gland.
Data collection (see Table 43.1)
Interventions
Monitor vital signs, particularly blood pressure.
Monitor intake and output and weight.
Monitor laboratory values, particularly WBC count, and serum glucose, sodium, potassium, and calcium.
Prepare to assist the RN with the administration of chemotherapeutic agents as prescribed, for inoperable adrenal tumors.
Prepare the client for radiation, as prescribed, if the condition results from a pituitary adenoma.
Prepare the client for the removal of pituitary tumor (hypophysectomy, sublabial transsphenoidal adenectomy), if the condition results from the increased pituitary secretion of ACTH.
Prepare the client for adrenalectomy, if the condition results from an adrenal adenoma; glucocorticoid replacement may be required following adrenalectomy.
Clients requiring lifelong glucocorticoid replacement following adrenalectomy need to obtain instructions from their PHCP about increasing their glucocorticoid prescription during times of stress.
Assess for and protect against postoperative thrombus formation; Cushing's syndrome predisposes to thromboemboli.
Allow the client to discuss feelings related to body appearance.
Instruct the client about the need to wear a MedicAlert bracelet.
Addison's disease is characterized by the hyposecretion of adrenal cortex hormones (glucocorticoids and mineralocorticoids), whereas Cushing's disease is characterized by a hypersecretion of glucocorticoids.
Primary hyperaldosteronism (Conn's syndrome)
Description
Hypersecretion of mineralocorticoids (aldosterone) from the adrenal cortex of the adrenal gland
Most commonly caused by an adenoma
Excess secretion of aldosterone causes sodium and water retention and potassium excretion, leading to hypertension and hypokalemic alkalosis.
Data collection
Symptoms related to hypokalemia, hypernatremia, and hypertension
Headache, fatigue, muscle weakness
Cardiac dysrhythmia
Paresthesia, tetany
Change in vision
Glucose intolerance
Elevated serum aldosterone level
Interventions
Monitor vital signs, particularly blood pressure.
Monitor for signs of hypokalemia and hypernatremia.
Monitor intake and output and urine for specific gravity.
Monitor for hyperkalemia, particularly for clients with impaired renal function or excessive potassium intake because potassium-retaining diuretics and aldosterone antagonists may be prescribed to promote fluid balance and control hypertension.
Administer potassium supplements, as prescribed, to treat hypokalemia; clients taking potassium-sparing diuretics and potassium supplementation are at risk for hyperkalemia.
Prepare the client for adrenalectomy.
Maintain sodium restriction, if prescribed, preoperatively.
Administer glucocorticoids preoperatively, as prescribed, to prevent adrenal hypofunction and prepare for the stress of surgery.
Monitor the client for adrenal insufficiency postoperatively.
Reinforce instructions to the client regarding the need for glucocorticoid therapy after adrenalectomy.
Reinforce instructions to the client about the need to wear a Medic-Alert bracelet.
Pheochromocytoma
Description
Catecholamine-producing tumor usually found in the adrenal medulla, but extra-adrenal locations include the chest, bladder, abdomen, and brain; typically a benign tumor, but can be malignant
Excessive amounts of epinephrine and norepinephrine are secreted.
Diagnostic tests include a 24-hour urine collection for VMA.
Surgical removal of the adrenal gland is the primary treatment.
Symptomatic treatment is initiated if surgical removal is not possible.
The complications associated with pheochromocytoma include hypertensive crisis, hypertensive retinopathy and nephropathy, cardiac enlargement and dysrhythmia, heart failure, myocardial infarction, increased platelet aggregation, and stroke.
Death can occur from shock, stroke, renal failure, dysrhythmia, or dissecting aortic aneurysm.
Data collection
Paroxysmal or sustained hypertension
Severe headache
Palpitations
Flushing and profuse diaphoresis
Pain in the chest or abdomen with nausea and vomiting
Heat intolerance
Weight loss
Tremors
Hyperglycemia
Interventions
Monitor vital signs, particularly blood pressure and heart rate.
Monitor for hypertensive crisis; monitor for complications that can occur with hypertensive crisis such as stroke, cardiac dysrhythmia, and myocardial infarction.
Reinforce instructions to the client not to smoke, drink caffeine-containing beverages, or change position suddenly.
Prepare to administer a β-adrenergic blocking agent, as prescribed, to control hypertension; α-adrenergic blocking agents are started 7 to 10 days before β-adrenergic blocking agents.
Monitor serum glucose level.
Promote rest and a nonstressful environment.
Provide a diet high in calories, vitamins, and minerals.
Prepare the client for adrenalectomy.
For the client with pheochromocytoma, avoid stimuli that can precipitate a hypertensive crisis, such as increased abdominal pressure and vigorous abdominal palpation.
Adrenalectomy
Description (Box 43.9)
Preoperative interventions
Monitor electrolyte levels and correct electrolyte imbalances.
Monitor for dysrhythmia.
Monitor for hyperglycemia.
Protect the client from infection.
Administer glucocorticoids, as prescribed.
Postoperative interventions
Monitor vital signs.
Monitor intake and output; if the urinary output is less than 30 mL/hr, notify the RN because this may indicate acute kidney injury and impending shock. IV fluids will be prescribed to maintain blood volume.
Monitor weight daily.
Monitor electrolyte and serum glucose levels.
Monitor for signs of hemorrhage and shock particularly during the first 24 to 48 hours.
Monitor for manifestations of adrenal insufficiency (see Table 43.1).
Check the dressing for drainage.
Monitor for paralytic ileus.
Administer glucocorticoids and mineralocorticoids, as prescribed.
Administer pain medication as prescribed.
Provide pulmonary interventions to prevent atelectasis (coughing, deep breathing, incentive spirometry, splinting of incision).
Reinforce instructions to the client regarding the importance of hormone replacement therapy following surgery.
Reinforce instructions to the client regarding the signs and symptoms of complications, such as underreplacement and overreplacement of hormones.
Reinforce instructions to the client regarding the need to wear a Medic-Alert bracelet.
Thyroid Gland Problems
Hypothyroidism
Description
Hypothyroid state resulting from hyposecretion of thyroid hormones and characterized by a decreased rate of body metabolism
The T4 is low and the TSH is elevated.
In primary hypothyroidism, the source of dysfunction is the thyroid gland, and the thyroid cannot produce the necessary amount of hormones. In secondary hypothyroidism, the thyroid is not being stimulated by the pituitary to produce hormones.
Data collection (Table 43.2)
Interventions
Monitor vital signs, including heart rate and rhythm.
Administer thyroid replacement; levothyroxine sodium is most commonly prescribed.
Reinforce instructions to the client about thyroid replacement therapy and about the clinical manifestations of both hypothyroidism and hyperthyroidism related to underreplacement or overreplacement of the hormone.
Reinforce instructions to the client to consume a low-calorie, low-cholesterol, and low-saturated fat diet; discuss a daily exercise program such as walking.
Monitor the client for constipation; provide roughage and fluids to prevent constipation.
Provide a warm environment for the client.
Avoid sedatives and opioid analgesics because of increased sensitivity to these medications; may precipitate myxedema coma.
Monitor for overdose of thyroid medications characterized by tachycardia, chest pain, restlessness, nervousness, and insomnia.
Reinforce instructions to the client to immediately report episodes of chest pain or other signs of overdose.
Myxedema coma
Description (Box 43.10)
Data collection
Hypotension
Bradycardia
Hypothermia
Hyponatremia
Hypoglycemia
Generalized edema
Respiratory failure
Coma
Interventions
Maintain a patent airway.
Institute aspiration precautions.
Monitor IV fluids (normal or hypertonic saline), as prescribed.
Assist RN with the administration of IV levothyroxine sodium, as prescribed.
Assist RN with the administration of IV glucose, as prescribed.
Administer corticosteroids, as prescribed.
Monitor the client's temperature hourly.
Monitor blood pressure frequently.
Keep the client warm.
Monitor for any change in mental status.
Monitor electrolyte and glucose levels.
Hyperthyroidism
Description
Hyperthyroid state resulting from the hypersecretion of thyroid hormones T3 and T4
Characterized by an increased rate of body metabolism
A common cause is Graves' disease, also known as toxic diffuse goiter.
Clinical manifestations are referred to as thyrotoxicosis.
T3 and T4 are usually elevated and TSH level is low.
Data collection (see Table 43.2)
Interventions
Provide adequate rest.
Administer sedatives as prescribed.
Provide a cool and quiet environment.
Obtain weight daily.
Provide a high-calorie diet.
Avoid the administration of stimulants.
Administer antithyroid medications, such as methimazole or propylthiouracil, that block thyroid synthesis, as prescribed.
Administer iodine preparations that inhibit the release of thyroid hormone, as prescribed.
Administer propranolol for tachycardia as prescribed.
Prepare the client for radioactive iodine therapy, as prescribed, to destroy thyroid cells.
Prepare the client for subtotal thyroidectomy, if prescribed.
Elevate the head of the bed of a client experiencing exophthalmos; in addition, instruct on a low-salt diet, administer artificial tears, encourage the use of dark glasses, and tape eyelids closed at night if necessary.
Allow the client to expressconcerns about changes in their body image.
Thyroid storm
Description (Box 43.11)
Data collection
Elevated temperature (fever)
Tachycardia
Systolic hypertension
Nausea, vomiting, diarrhea
Agitation, tremors, anxiety
Irritability, agitation, restlessness, confusion, and seizure as the condition progresses
Delirium and coma
Interventions
Maintain a patent airway and adequate ventilation.
Administer antithyroid medications, sodium iodide solution, propranolol, and glucocorticoids as prescribed.
Monitor vital signs.
Monitor continually for cardiac dysrhythmia.
Administer nonsalicylate antipyretics as prescribed (salicylates increase free thyroid hormone levels).
Use a cooling blanket to decrease the client's temperature as prescribed.
Thyroidectomy
Description
Removal of the thyroid gland
Performed when persistent hyperthyroidism exists
Subtotal thyroidectomy; removal of a portion of the thyroid gland is the preferred surgical intervention.
Preoperative interventions
Obtain vital signs and weight.
Monitor electrolyte levels.
Monitor for hyperglycemia.
Reinforce instructions to the client on how to perform coughing and deep-breathing exercises and how to support the neck during the postoperative period when coughing and moving.
Assist to administer antithyroid medications, iodides, propranolol, and glucocorticoids as prescribed to prevent the occurrence of thyroid storm.
Postoperative interventions
Monitor for respiratory distress.
Have a tracheotomy set, oxygen, and suction at the bedside.
Limit client talking and determine the level of hoarseness.
Avoid neck flexion and stress on the suture line.
Monitor for laryngeal nerve damage as evidenced by respiratory obstruction, dysphonia, high-pitched voice, stridor, dysphagia, and restlessness.
Monitor for signs of hypocalcemia and tetany, which can be the result of trauma to the parathyroid gland (Box 43.12).
Assist RN to administer calcium gluconate as prescribed for tetany.
Monitor for thyroid storm.
After thyroidectomy, maintain the client in a semi-Fowler's position. Monitor the surgical site for edema and for signs of bleeding, and check the dressing anteriorly and at the back of the neck. Monitor for inflammation, which could block the airway. An emergency tracheostomy kit must be at the bedside.
Parathyroid Gland Problems
Hypoparathyroidism
Description
Condition caused by hyposecretion of PTH by the parathyroid gland
Can occur following thyroidectomy because of the removal of parathyroid tissue
Data collection
Hypocalcemia and hyperphosphatemia
Numbness and tingling in the face
Muscle cramps and cramps in the abdomen or in the extremities
Positive Trousseau's sign or Chvostek's sign
Signs of overt tetany such as bronchospasm, laryngospasm, carpopedal spasm, dysphagia, photophobia, cardiac dysrhythmia, and seizure
Hypotension
Anxiety, irritability, depression
Interventions
Monitor vital signs.
Monitor for signs of hypocalcemia and tetany.
Initiate seizure precautions.
Place a tracheotomy set, oxygen, and suction at the bedside.
Assist RN with the administration of IV calcium gluconate for hypocalcemia.
Provide a high-calcium, low-phosphorus diet.
Reinforce instructions to the client regarding the administration of calcium supplements as prescribed.
Reinforce instructions to the client regarding the administration of vitamin D supplements as prescribed; vitamin D enhances the absorption of calcium from the GI tract.
Reinforce instructions to the client regarding the administration of phosphate binders, as prescribed, to promote the excretion of phosphate through the GI tract.
Reinforce instructions to the client in the use of thiazide diuretics, if prescribed, to protect the kidney if vitamin D is also taken.
Reinforce instructions to the client to wear a MedicAlert bracelet.
Hyperparathyroidism
Description: Condition caused by the hypersecretion of PTH by the parathyroid gland
Data collection
Hypercalcemia and hypophosphatemia
Fatigue and muscle weakness
Skeletal pain and tenderness
Bone deformities that result in pathological fractures
Anorexia, nausea, vomiting, epigastric pain
Weight loss
Constipation
Hypertension
Cardiac dysrhythmia
Renal stones
Interventions
Monitor vital signs, particularly blood pressure.
Monitor for cardiac dysrhythmia.
Monitor intake and output and for signs of renal stones.
Monitor for skeletal pain; move the client slowly and carefully.
Encourage fluid intake.
Administer furosemide, as prescribed, to lower calcium levels.
Normal saline may be prescribed intravenously to maintain hydration.
Assist with the administration of phosphates, which interfere with calcium reabsorption, as prescribed.
Assist to administer calcitonin, as prescribed, to decrease skeletal calcium release and increase renal excretion of calcium.
Assist with the administration of IV or oral bisphosphonates to inhibit bone resorption.
Monitor calcium and phosphorus levels.
Prepare the client for parathyroidectomy, as prescribed.
Encourage a high-fiber, moderate-calcium diet.
Emphasize the importance of an exercise program and avoiding prolonged inactivity.
Parathyroidectomy
Description: The removal of one or more of the parathyroid glands
Endoscopic radioguided parathyroidectomy with autotransplantation is the most common procedure.
Parathyroid tissue is transplanted in the forearm or near the sternocleidomastoid muscle allowing PTH secretion to continue.
Preoperative interventions
Monitor electrolytes, calcium, phosphate, and magnesium levels.
Ensure that calcium levels are decreased to near-normal values.
Inform the client that talking may be painful for the first day or two after surgery.
Postoperative interventions
Monitor for respiratory distress.
Place a tracheotomy set, oxygen, and suction at the bedside.
Monitor vital signs.
Position the client in a semi-Fowler's position.
Check the neck dressing for bleeding.
Monitor for hypocalcemic crisis as evidenced by tingling and twitching in the extremities and face.
Monitor for positive Trousseau's sign or Chvostek's sign, which signals the potential for tetany.
Monitor for changes in voice pattern and hoarseness.
Monitor for laryngeal nerve damage.
Reinforce instructions to the client regarding the administration of calcium and vitamin D supplements as prescribed.
Pancreas Problems
Diabetes mellitus
Description
Chronic disorder of impaired carbohydrate, protein, and lipid metabolism caused by a deficiency of insulin
An absolute or relative deficiency of insulin results in hyperglycemia.
Type 1 diabetes mellitus is a nearly absolute deficiency of insulin (primary beta cell destruction); if insulin is not given, fats are metabolized for energy, which results in ketonemia (acidosis).
Type 2 diabetes mellitus refers to a relative lack of insulin or resistance to the action of insulin; usually insulin is sufficient to stabilize fat and protein metabolism, but not carbohydrate metabolism.
Metabolic syndrome is also known as syndrome X and the individual has coexisting risk factors for developing type 2 diabetes mellitus; these risk factors include abdominal obesity, hyperglycemia, hypertension, high triglyceride level, and a lowered high-density lipoprotein (HDL) cholesterol level.
Diabetes mellitus can lead to chronic health problems and early death as a result of complications that occur in the large and small blood vessels in tissues and organs.
Macrovascular complications include coronary artery disease, cardiomyopathy, hypertension, cerebrovascular disease, and peripheral vascular disease. (Refer to Chapter 49 for information on cardiovascular problems)
Microvascular complications include retinopathy, nephropathy, and neuropathy.
Infection is also a concern because of reduced healing ability.
Male erectile dysfunction can also occur as a result of the disease.
Obesity is a major risk factor for diabetes mellitus.
Data collection
Polyuria, polydipsia, and polyphagia (more common with type 1 diabetes mellitus)
Hyperglycemia
Weight loss (common with type 1 diabetes mellitus, rare with type 2 diabetes mellitus)
Blurred vision
Slow wound healing
Vaginal infections
Weakness and paresthesia
Signs of inadequate circulation to the feet
Signs of accelerated atherosclerosis (renal, cerebral, cardiac, peripheral)
Diet
The diabetic client's diet would take into account weight, medication, activity level, and other health problems.
Day-to-day consistency in timing and amount of food intake helps control the blood glucose level.
As prescribed by the PHCP, the client may be advised to follow the recommendations of the American Diabetic Association diet or US dietary guidelines.
Carbohydrate counting may be a simpler approach for some clients; it focuses on the total grams of carbohydrates eaten per meal. The client may be more compliant with carbohydrate counting resulting in better glycemic control; it is usually necessary for clients using intense insulin therapy.
Incorporate the diet into individual client needs, lifestyle, and cultural and socioeconomic patterns.
Exercise
Exercise lowers the blood glucose level, encourages weight loss, reduces cardiovascular risks, improves circulation and muscle tone, decreases total cholesterol and triglyceride levels, and decreases insulin resistance and glucose intolerance.
Reinforce instructions to the client regarding dietary adjustments when exercising; dietary adjustments are individualized.
If the client requires extra food during exercise to prevent hypoglycemia, it need not be deducted from the regular meal plan.
If the blood glucose level is greater than 250 mg/dL and urinary ketones (type 1 diabetes mellitus) are present, the client is instructed not to exercise until the blood glucose is closer to normal and urinary ketones are absent.
The client should try to exercise at the same time each day and would exercise when glucose from the meal is peaking, not when insulin or glucose-lowering medications are peaking.
Insulin would not be injected into an area of the body that will be exercised following injection, as exercise speeds absorption.
Instruct the client with diabetes mellitus to monitor their blood glucose level before, during, and after exercising.
Oral hypoglycemic medications: Oral medications are prescribed for clients with type 2 diabetes mellitus when diet and weight control therapy have failed to maintain satisfactory blood glucose levels (see Chapter 44).
Insulin (refer to Chapter 44 for additional information on insulin)
Insulin is used to treat type 1 diabetes mellitus and may be used to treat type 2 diabetes mellitus when diet, weight-control therapy, and oral hypoglycemic agents have failed to maintain satisfactory blood glucose levels.
Illness, infection, and stress increase the blood glucose level and the need for insulin; insulin would not be withheld during illness, infection, or stress because hyperglycemia and diabetic ketoacidosis (DKA) can result.
The peak action time of insulin is important to explain to the client because of the possibility of hypoglycemic reactions occurring during that time.
Regular insulin (U-100 strength) can be administered via IV injection (IV push). Regular insulin (U-100 strength) and the short-duration insulins (lispro, aspart, and glulisine) can be administered via IV infusion.
Complications of insulin therapy
Local allergic reactions
Redness, swelling, tenderness, and induration or a wheal at the site of injection may occur 1 to 2 hours after administration.
Reactions usually occur during the early stages of insulin therapy.
Reinforce instructions to the client to cleanse the skin with alcohol before injection.
Insulin lipodystrophy
The development of fibrous fatty masses at the injection site caused by repeated use of an injection site; use of human insulin helps prevent this.
Reinforce instructions to the client to avoid injecting insulin into affected sites.
Reinforce instructions to the client about the importance of rotating insulin injection sites. Systematic rotation within one anatomical area is recommended to prevent lipodystrophy; the client would be instructed not to use the same site more than once in a 2 to 3 week period. Injections need to be 1 ½ inches (3.8 cm) apart within the anatomical area.
Dawn phenomenon
Dawn phenomenon is characterized by hyperglycemia upon morning awakening that results from excessive early morning release of GH and cortisol.
Treatment requires an increase in the client's insulin dose or a change in the time of insulin administration.
Somogyi phenomenon
Normal or elevated blood glucose levels are present at bedtime; hypoglycemia occurs at about 2:00 a.m. to 3:00 a.m., which causes an increase in the production of counterregulatory hormones.
By 7:00 a.m., in response to the counterregulatory hormones, the blood glucose rebounds significantly to the hyperglycemic range.
Treatment includes decreasing the evening (predinner or bedtime) dose of intermediate-acting insulin or increasing the bedtime snack, or both.
Clients experiencing the Somogyi phenomenon may complain of early morning headaches, night sweats, or nightmares caused by the early morning hypoglycemia.
Insulin administration
Subcutaneous injections and mixing insulin (see Chapter 44)
Insulin pumps
Continuous subcutaneous insulin infusion is administered by an externally worn device that contains a syringe attached to a long, thin, narrow-lumen tube with a needle or Teflon catheter attached to the end.
The client inserts the needle or Teflon catheter into the subcutaneous tissue (usually on the abdomen or upper arm) and secures it with tape or a transparent dressing; the pump is worn on a belt or in a pocket; the needle or Teflon catheter is changed at least every 2 to 3 days.
A continuous basal rate of insulin infuses; in addition, on the basis of the blood glucose level, the anticipated food intake, and the activity level, the client delivers a bolus of insulin before each meal.
Both rapid-acting and regular short-acting insulin (buffered to prevent the precipitation of insulin crystals within the catheter) are appropriate for use in these pumps.
Insulin pump and skin sensor
A skin sensor device can be used to monitor the client's blood glucose continuously; the information is transmitted to the pump, determines the need for insulin, and the insulin is then injected.
The pump holds up to a 3-day supply of insulin and can be easily disconnected for activities such as bathing.
Pancreas transplants
The goal of pancreatic transplantation is to halt or reverse the complications of diabetes mellitus.
Transplants are performed on a limited number of clients (in general, those clients who are undergoing kidney transplantation simultaneously).
Immunosuppressive therapy is prescribed to prevent and treat rejection.
Self-monitoring of blood glucose level
Self-monitoring provides the client with the current blood glucose level and information to maintain good glycemic control.
Some monitoring devices require a finger prick to obtain a drop of blood for testing; devices are also available that do not require a prick to test for glucose.
Alternative site testing (obtaining blood from the forearm, upper arm, abdomen, thigh, or calf) is now available using specific measurement devices.
Testing via finger or other site pricks needs to be done with caution in clients with diabetic neuropathy.
Client instructions (Box 43.13)
Urine testing
Urine testing for glucose is not a reliable indicator of blood glucose and is not used for monitoring purposes.
Reinforce instructions to the client regarding the procedure for testing urine ketones.
The presence of ketones may indicate impending ketoacidosis.
Urine ketone testing would be performed during illness and whenever the client with type 1 diabetes mellitus has persistently elevated blood glucose levels (higher than 250 mg/dL or as prescribed for 2 consecutive testing periods).
Acute Complications of Diabetes Mellitus
Hypoglycemia
Description
Hypoglycemia occurs when the blood glucose level falls below 70 mg/dL or when the blood glucose drops rapidly from an elevated level.
Hypoglycemia is caused by too much insulin or oral hypoglycemic agents, too little food, or excessive activity.
The client needs to be instructed to always carry some form of fast-acting simple carbohydrate with him or her (Box 43.14).
If the client has a hypoglycemic reaction and does not have any of the recommended emergency foods available, any available food should be eaten; high-fat foods slow the absorption of glucose, and the hypoglycemic symptoms may not resolve quickly.
Clients who experience frequent episodes of hypoglycemia, older clients, and clients taking β-adrenergic blocking agents may not experience the warning signs of hypoglycemia until the blood glucose level is dangerously low; this phenomenon is termed hypoglycemia unawareness.
Data collection (Box 43.15)
Mild hypoglycemia: The client remains fully awake but displays adrenergic symptoms; the blood glucose level is usually lower than 70 mg/dL.
Moderate hypoglycemia: The client displays symptoms of worsening hypoglycemia; the blood glucose level is usually less than 54 mg/dL.
Severe hypoglycemia: Client displays severe neuroglycopenic symptoms; the blood glucose level is usually lower than 40 mg/dL.
Priority Nursing Actions
Suspected Hypoglycemic Reaction (the 15/15 rule)
If a blood glucose monitor is readily available, check the client's blood glucose level. If the client is experiencing symptoms suggestive of hypoglycemia such as diaphoresis, hunger, pallor, and shakiness, and a blood glucose monitor is not readily available, assume hypoglycemia and treat accordingly.
For the client whose blood glucose is below 70 mg/dL, or for the client with an unknown blood glucose who is exhibiting signs of hypoglycemia, administer 15 g of a carbohydrate such as ½ cup of fruit juice or 15 g of glucose gel.
Recheck the blood glucose level in 15 minutes.
If the blood glucose remains below 70 mg/dL, administer another 15 g of a simple carbohydrate.
Recheck the blood glucose level in 15 minutes; if still below 70 mg/dL, treat with an additional 15 g of a simple carbohydrate.
Recheck the blood glucose level in 15 minutes; if still below 70 mg/dL, assist the registered nurse with treating with 25 to 50 mL of 50% IV dextrose or, if no IV equipment is present, treat with 1 mg of glucagon subcutaneously or intramuscularly.
After the blood glucose level has recovered, have the client ingest a snack that includes a complex carbohydrate and a protein.
Document the client's complaints, actions taken, and outcome.
Explore the precipitating cause of the hypoglycemia with the client.
Interventions: always follow agency protocols (see Priority Nursing Actions)
Do not attempt to administer oral food or fluids to the client experiencing a severe hypoglycemic reaction who is semiconscious or unconscious and is unable to swallow. This client is at risk for aspiration. For this client, an injection of glucagon is administered subcutaneously or intramuscularly. In the hospital or emergency department, the client may be treated with an IV injection of 25 to 50 mL of 50% dextrose in water.
Diabetic ketoacidosis
Description (Fig. 43.2)
DKA is a life-threatening complication of type 1 diabetes mellitus that develops when a severe insulin deficiency occurs.
The main clinical manifestations include hyperglycemia, dehydration, electrolyte imbalance, ketosis, and acidosis.
Data collection (Table 43.3)
Interventions
Restore circulating blood volume and protect against cerebral, coronary, and renal hypoperfusion
Dehydration will be treated with rapid IV infusions of 0.9% or 0.45% NS, as prescribed; dextrose is added to IV fluids when the blood glucose level reaches 250 to 300 mg/dL. Too rapid administration of IV fluids, particularly hypotonic solutions, and correcting the blood glucose too rapidly can lead to cerebral edema.
Hyperglycemia will be treated with regular insulin administered intravenously as prescribed.
Correct electrolyte imbalances (potassium level may be elevated as a result of dehydration and acidosis).
Monitor potassium level closely because when the client receives treatment for dehydration and acidosis, the serum potassium will decrease, and potassium replacement may be required.
Cardiac monitoring is necessary for the client with DKA because of the risks associated with abnormal serum potassium levels.
Insulin IV administration by the RN
Short-duration insulin only is used.
An IV bolus dose of short-duration regular U-100 insulin (usually 5–10 units) may be prescribed before a continuous infusion is begun.
The prescribed IV dose of insulin for continuous infusion is prepared in 0.9% or 0.45% NS as prescribed.
The insulin infusion is always placed on an IV infusion controller.
Insulin is infused continuously until subcutaneous administration resumes to prevent a rebound of the blood glucose level.
Monitor vital signs.
Monitor urinary output and for signs of fluid overload.
Monitor potassium and glucose levels and for signs of increased intracranial pressure.
The potassium level will fall rapidly within the first hour of treatment as dehydration and acidosis are treated.
Potassium is administered intravenously in a diluted solution as prescribed; ensure adequate renal function before administering potassium.
Reinforcement of client education (Box 43.16)
Monitor the client being treated for DKA closely for signs of increased intracranial pressure. If the blood glucose level falls too far or too fast before the brain has time to equilibrate, water is pulled from the blood to the cerebrospinal fluid and the brain, causing cerebral edema and increased intracranial pressure.
Hyperosmolar hyperglycemic syndrome (HHS)
Description
Extreme hyperglycemia occurs without ketosis and acidosis.
The syndrome occurs most often among individuals with type 2 diabetes mellitus.
The major difference between HHS and DKA is that ketosis and acidosis do not occur with HHS; enough insulin is present with HHS to prevent the breakdown of fats for energy, thus preventing ketosis.
Data collection (see Table 43.3)
Interventions
Treatment is similar to that for DKA.
Treatment includes fluid replacement, the correction of electrolyte imbalances, and insulin administration.
Fluid replacement in the older client must be done very carefully secondary to the potential for heart failure.
Insulin plays a less critical role in the treatment of HHS than it does for the treatment of DKA because ketosis and acidosis do not occur; rehydration alone may decrease glucose levels.
Chronic Complications of Diabetes Mellitus
Diabetic retinopathy
Description
Chronic and progressive impairment of the retinal circulation that eventually causes hemorrhage
Permanent vision changes and blindness can occur.
The client has difficulty with carrying out the daily tasks of blood glucose testing and insulin injections.
Data collection
A change in vision is caused by the rupture of small microaneurysms in retinal blood vessels.
Blurred vision results from macular edema.
Sudden loss of vision results from retinal detachment.
Cataracts result from lens opacity.
Interventions
Maintain safety.
Early prevention via the control of hypertension and blood glucose levels
Photocoagulation (laser therapy) may be done to remove hemorrhagic tissue to decrease scarring and prevent the progression of the disease process.
Vitrectomy may be done to remove vitreous hemorrhages and thus decrease tension on the retina preventing detachment.
Cataract removal with a lens implantation improves vision.
Diabetic nephropathy
Description: Progressive decrease in kidney function
Data collection
Microalbuminuria
Thirst
Fatigue
Anemia
Weight loss
Signs of malnutrition
Frequent urinary tract infections
Signs of a neurogenic bladder
Interventions
Early prevention measures include the control of hypertension and blood glucose levels.
Monitor vital signs.
Monitor intake and output.
Monitor the blood urea nitrogen, creatinine, and urine albumin levels.
Restrict dietary protein, sodium, and potassium intake as prescribed.
Avoid nephrotoxic medications.
Prepare the client for dialysis procedures, if planned.
Prepare the client for kidney transplant, if planned.
Prepare the client for pancreas transplant, if planned.
Diabetic neuropathy
Description
A general deterioration of the nervous system throughout the body
Complications include the development of nonhealing ulcers of the feet, gastric paresis, and erectile dysfunction.
Classifications
Focal neuropathy or mononeuropathy: Involves a single nerve or a group of nerves, most frequently cranial nerves III (oculomotor) and VI (abducens), resulting in diplopia
Sensory or peripheral neuropathy: Affects the distal portion of the nerves, most frequently in the lower extremities
Autonomic neuropathy: Symptoms vary according to the organ system involved.
Cardiovascular: Cardiac denervation syndrome (heart rate does not respond to changes in oxygenation needs) and orthostatic hypotension occur.
Pupillary: Pupil does not dilate in response to decreased light.
Gastric: Decreased gastric emptying (gastroparesis)
Urinary: Neurogenic bladder
Skin: Decreased sweating
Adrenal: Hypoglycemic unawareness
Reproductive: Impotence (male) and painful intercourse (female)
Data collection: Findings depend on the classification.
Paresthesia
Decreased or absent reflexes
Decreased sensation to vibration or light touch
Pain, aching, and burning in the lower extremities
Poor peripheral pulses
Skin breakdown and signs of infection
Weakness or loss of sensation in cranial nerves III (oculomotor), IV (trochlear), V (trigeminal), and VI (abducens)
Dizziness and postural hypotension
Nausea and vomiting
Diarrhea or constipation
Incontinence
Dyspareunia
Impotence
Hypoglycemic unawareness
Interventions
Early prevention measures include the control of hypertension and blood glucose levels.
Careful foot care is required to prevent trauma (Box 43.17).
Administer medications, as prescribed, for pain relief.
Initiate bladder-training programs.
Reinforce instructions to the client regarding the use of estrogen-containing lubricants for women with dyspareunia.
Prepare the male client with impotence for penile injections or other possible treatment options, as prescribed.
Prepare for surgical decompression of compression lesions related to the cranial nerves as prescribed.
Care of the Diabetic Client Undergoing Surgery
Preoperative care
Check with the PHCP regarding withholding oral hypoglycemic medications or insulin.
Some long-acting oral antidiabetic medications are discontinued 24 to 48 hours before surgery.
Metformin may need to be discontinued 48 hours before surgery and may not be restarted until renal function is normal postoperatively.
All other oral antidiabetic medications are usually withheld the day of surgery.
Insulin dose may be adjusted or withheld if IV insulin administration during surgery is planned.
Monitor the blood glucose level.
Assist to administer prescribed IV fluids.
Postoperative care
Assist the RN with the administration of IV glucose and regular insulin infusions, as prescribed, until the client can tolerate oral feedings.
Administer supplemental short-acting insulin, as prescribed, based on blood glucose results.
Monitor blood glucose levels frequently, especially if the client is receiving parenteral nutrition.
When the client is tolerating food, ensure that the client receives an adequate amount of carbohydrates daily to prevent hypoglycemia.
Client is at higher risk for cardiovascular and renal complications postoperatively.
Client is also at risk for impaired wound healing.
What Would You Do?
Answer
Hypertensive crisis can occur as a complication of pheochromocytoma. This can result in stroke, cardiac dysrhythmia, or myocardial infarction. Manifestations include severe headache, extremely high blood pressure (BP), dizziness, blurred vision, shortness of breath, epistaxis (nosebleed), and severe anxiety. If the nurse suspects a hypertensive crisis, the nurse would place the client in a semi-Fowler's position and notify the RN immediately. The PHCP must also be notified immediately, and as prescribed, the nurse needs to prepare to administer oxygen, assist the RN with starting an IV infusion of 0.9% NS solution and infuse it slowly to prevent fluid overload (which would increase blood pressure), assist the RN with the administration of IV medications to lower the BP and monitor it