Diabetes insipidus is a disorder of the posterior lobe of the pituitary gland due to a deficiency of vasopressin, the antidiuretic hormone (ADH). it is characterized by polydipsia and polyuria. Diabetes insipidus may be (1) secondary, related to head trauma, brain tumor, or surgical ablation or irradiation of the pituitary gland or infection of the central nervous system or metastatic tumors (lung or breast); (2) nephrogenic (faliure of the renal tubules to respond to ADH), possibly related to hypokalemia, hypercalcemia, and a variety of medications (eg, lithium, demeclocycline); (3) primary (hereditary), with symptoms possibly beginning t birth (defect in pituitary gland).
The disease cannot be controlled by limiting the intake of fluids because loss of high volumes of urine continues even without fluid replacement. Attempts to restrict fluids cause the patient to experience an insatiable carving for fluid and to develop hypernatremia and severe dehydration.
Polyuria: enormous daily output of very dilute urine (specific gravity 1.001 to 1.005). Primary diabetes insipidus may have ab abrupt onset or an insidious onset in adults.
Polydipsia: patient experiences intense thirst, drinking 2 to 20 liters of fluid daily, with a special craving for cold water.
Polyuria continues even without fluid replacement.
Assessment and Diagnostic Findings
Fluid deprivation test: fluids are withheld for 8 to 12 hours until 3% to 5% of the body weight is lost. Inability to increase specific gravity and osmolality of the urine during test is characteristic of diabetes insipidus.
Urine specific gravity, serum osmolality, and serum sodium levels may be obtained.
Objectives of the therapy are to ensure adequate fluid replacement, to replace vasopressin, and to search for and correct the underlying intracranial pathology. Treatment for diabetes insipidus of nephrogenic origin involves using thiazide diuretics, mild salt depletion, and prostaglandin inhibitors (eg. ibuprofen, indomethacin, and aspirin).
Desmopressin (DDAVP), administered intranasally, 1 or 2 administrations daily to control symptoms.
Lypressin (Diapid), absorbed through nasal mucosa into blood; duration may be short for patients with severe disease.
Intramuscular administration of ADH (vasopressin tannate in oil) every 24 to 96 hours to reduce urinary volume (shake vigorously or warm; administer in the evening, rotate injection sites to prevent lipodystrophy)
Clofibrate, a hypolipidemic agent, has an antidiuretic effect on patients who have some residual hypothalamic vasopressin.
Chlorpropramide (Diabinese) and thiazide diuretics are used in mild forms to potentiate the aciton of vasopressin; may cause hypoglycemic reactions.
Encourage and support patient undergoing studies for possible cranial lesion.
Instruct patient and family members about follow-up care and emergency measures.
Advise patient to wear a medical identification bracelet and to carry medication information about the disorder at all times.
Use caution with administration of vasopressin if coronary artery disease is present because of vasoconstrictive action of this drug.
Joyce Young Johnson et. al Handbook for Brunner & Suddarth’s Textbook of Medical-Surgical Nursing 11th edition
Diabetes mellitus is a group of mtabolic disorders characterized by elevated levels of blood glucose (hyperglycemia) resulting from defects in insulin production and secretion, decreased cellular response to insulin, or both. Hyperglycemia may lead to metabolic complications, such as diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS). Long-term hyperglycemia may contribute to chronic microvascular complications (kidney and eye disease) and neuropathic disease. Diabetes is also associated with an increased occurrence of macrovascular disease, including coronary artery disease (myocardial infarction), cerebrovascular disease (stroke), and peripheral vascular disease.
Types of Diabetes
Type 1 (Formerly Insulin-Dependent Diabetes Mellitus)
About 5% to 10% diabetic patients have type 1 diabetes. Beta cells of the pancreas that normally produce insulin are destroyed by autoimmune process. Insulin injections are needed to control the blood glucose levels.
Type 1 diabetes has a sudden onset, usually before the age of 30 years.
Type 2 (Formerly Non-Insulin-Dependent Diabetes Mellitus)
About 90% to 95% of diabetics have type 2 diabetes. It results from a decreased sensitivity to insulin ( insulin resistance) or from a decreased amount of insulin production.
Type 2 diabetes is first treated with diet and exercise, then oral hypoglycemic agents are needed.
Type 2 diabetes occurs more frequently in patients older than 30 years of age and in obese patients.
Gestational diabetes is characterized by any degree of glucose intolerance with onset during pregnancy (second or third trimester).
It occurs in women 25 years of age or older, women younger than 25 years of age who are obese, women with a family history of diabetes in first-degree relatives, or members of certain ethnic racial groups (eg, Hispanic American, Native American, Asian American, African American, or Pacific Islander). It increases their risk for hypertensive disorders of pregnancy.
Polyuria, polydipsia, and polyphagia
Fatigue and weakness, sudden vision changes, tingling or numbness in hands or feet, dry skin, sores that heal slowly, and recurrent infections.
Onset of Type 1 diabetes may be associated with nausea, vomiting, or stomach pains
Type 2 diabetes results from a slow (over years), progressive glucose intolerance and results in long-term complications if diabetes goes undetected for many years (eg, eye disease, peripheral neuropathy, peripheral vascular disease). Complications may developed before the actual diagnosis is made.
Signs and symptoms of DKA include abdominal pain, nausea, vomiting, hyperventilation, and fruity breath odor. Untreated DKA may result in altered level of consciousness, coma and death
Assessment and Diagnostic Methods
High blood glucose levels: fasting plasma glucose levels 126 mg/dL or more, or random plasma glucose levels more than 200 mg/dL on more than one occasion.
Evaluation for complications
For obese patients (especially those type 2 diabetes): weight loss is the key to treatment and the major preventive factor for the development of diabetes.
Complications of Diabetes
Complications associated with both types of diabetes are classified as acute or chronic. Acute complications occur from short-term imbalances in blood glucose and include:
Chronic complications generally occur 10 to 15 years after the onset of diabetes mellitus. They include:
Microvascular (small vessels) disease: affects the eyes (retinopathy) and kidneys (nephropathy); control blood glucose levels to delay or avoid onset of both microvascular and macrovascular complications.
Neuropathic disease: affects sensory motor and autonomic nerves and contributes to such problems as impotence and foot ulcers.
Because the incidence of elevated blood glucose levels increases with advance age, elderly adults should be advised that physical activity that is consistent and realistic is beneficial to those with diabetes. Advantages of exercise include a decrease in hyperglycemia, a general sense of well-being, metabolism of ingested calories, and weight reduction. Consider physical impairment from other chronic disease when planning an exercise regimen for elderly diabetic patients.
The main goal of treatment is to normalize insulin activity and blood glucose levels to reduce the development of vascular and neuropathic complications. The therapeutic goal within each type of diabetes is to achieve normal blood glucose levels (euglycemia) without hypoglycemia and without seriously disrupting the patients usual activities. There are five components of management for diabetes: nutrition, exercise, monitoring, pharmacologic therapy, and education.
Primary treatment of type 1 diabetes is insulin
Primary treatment of type 2 diabetes is weight loss
Exercise is important in enhancing the effectiveness of insulin
Use oral hypoglycemic agents if diet and exercise are not successful in controlling blood glucose levels. Insulin injections may be used in acute situations.
Because treatment varies throughout course because of changes in lifestyle and physical and emotional status as well as advances in therapy, continuously assess and modify treatment plan as well as daily adjustments in therapy. Education is needed for both patient and family.
Meal plan should be based on patient’s usual eating habits and lifestyle and should provide all essential food constituents (eg, vitamins, minerals)
Goals are to achieve and maintain ideal weight, meet energy needs, prevent wide daily fluctuations in blood glucose levels (keep as close to normal as is safe and practical), and decrease blood lipid levels, if elevated.
For patients who require insulin to help control blood glucose levels, consistency is required in maintaining calories ans carbohydrates consumed at different meals.
Consult dietitian for diabetes management planning to gradually increase or add fiber in meal plan (grains, vegetables).
Determine basic caloric requirements, taking into consideration age, gender, weight, and height and factoring in degree of activity (Harris-Benedict formula for basal energy expenditure)
Long-term weight reduction can be achieved (1 to 2 pound loss per week) by reducing basic caloric intake by 500 to 1000 calories from calculated basic caloric requirements.
The American Diabetes and American Dietitic Associations recommend that for all levels of caloric intake, 50% to 60% of calories be derived from carbohydrates, 20% to 30% from fat, and the remaining 10% to 20% from protein. Using food combinations to lower glycemic response (glycemic index) can be useful. Carbohydrate counting and the food guide pyramid can be useful tools.
NURSING PROCESS: The Patient with Newly Diagnosed Diabetes Mellitus
Focus on signs and symptoms of prolonged hyperglycemia and physical, social, and emotional factors hat affect ability to learn and perform diabetes self-care activities.
Ask for description of symptoms that preceded the diagnosis: polyuria, polydipsia, polyphagia, skin dryness, blurred vision, weight loss, vaginal itching, and nonhealing ulcers.
Assess for signs of DKA, including ketonuria, Kussmaul respirations, orthostatic hypotension, and lethargy
Question regarding DKA symptoms of nausea, vomiting and abdominal pain.
Monitor laboratory signs for metabolic acidosis (decreased pH, decreased bicarbonate) and electrolyte imbalance.
Assess patients with type 2 diabetes for signs of HHNS, hypotension, altered sensorium, seizures, decreased skin turgor, hyperosmolarity and electrolyte imbalance.
Assess physical factors that impair ability to learn or perform self-care skills: visual defects, motor coordination defects, neurologic defects
Evaluate patient’s social situation for factors that influence diabetic treatment and education plan (literacy, financial resources, health insurance, family support); evaluate typical daily schedule (eg, work, meals, exercise, travel plans).
Assess emotional status through observations of general demeanor (eg, withdrawn, anxious, body language).
Assess coping skills by asking how patient has dealt with difficult situations in the past.
Risk for fluid volume deficit related to polyuria and dehydration
Imbalanced nutrition related to imbalance of insulin, food, and physical activity
Deficient knowledge about diabetes self-care skills and information
Potential self-care deficit related to physical impairments or social factors
Anxiety related to loss of control, fear of inability to manage diabetes, misinformation related to diabetes, and fear of diabetes complications
The major goal of the patient may include attainment of fluid and electrolyte balance, optimal control of blood glucose, regaining weight lost, ability to perform basic (survival) diabetes skills ans self-care activities, reduction in anxiety, and absence of complications.
Maintaining Fluid and Electrolyte Balance
Measure intake and output
Administer intravenous fluids and electrolytes as ordered.
Measure serum electrolytes (sodium, potassium) and monitor closely.
Monitor vital signs to detect dehydration; tachycardia, orthostatic hypotension
Improving Nutritional Intake
Plan the diet with glucose control as the primary goal.
take into consideration patient’s lifestyle, cultural background, activity level, and food preference
Encourage patient to eat full meals and snacks as per diabetic diet.
Make arrangements for extra snacks before increased physical activity.
Ensure that insulin orders are altered as needed for delays in eating due to diagnostic and other procedures
Provide emotional support; set aside time to talk with patient.
Clear up misconceptions patient and family may have regarding diabetes.
Assist patient and family to focus on learning self-care behaviors.
Encourage the patient to perform skills feared most; self-injection or finger stick glucose monitoring.
Give positive reinforcement for self-care behaviors attempted.
Monitoring and Managing Potential Complications
Fluid overload: measure vital signs and monitor central venous pressure (CVP) and total hemodynamic status at frequent intervals; assess cardiac rate and rhythm, breath sounds, venous distention, skin turgor, and urine output; monitor intravenous fluid and other fluid intake.
Hypokalemia: replace potassium cautiously, ensure that kidneys are functioning before administration; monitor cardiac rate, rhythm, electrocardiogram (ECG), and serum potassium levels
Hyperglycemia and DKA: monitor blood glucose levels and urine ketones; administer medications (insulin, oral hypoglycemic agents); monitor for signs and symptoms of impending hyperglycemia and DKA, administering insulin and intravenous fluids to correct.
Hypoglycemia: treat with juice or glucose tablets; encourage patient to eat full meals or snacks as prescribed; review signs and symptoms, possible causes, and measures to prevent or treat.
Cerebral edema: prevent by gradual reduction in blood glucose level’ monitor blood glucose level, serum electrolyte levels; urine output, mental status, and neurologic signs, minimize activities that increase intracranial pressure.
Joyce Young Johnson et.al Handbook for Brunner & Suddarth’s Textbook for Medical Surgical Nursing 11th edition
Cushing’s syndrome results from excessive adrenocortical activity. It may result from excessive administration of corticosteroids or adrenocorticotropic hormone (ACTH) or from hyperplasia of the adrenal cortex. It may be caused by several mechanism, including a tumor in the pituitary gland or less commonly an ectopic malignancy that produces ACTH. Regardless of the cause, the negative feedback mechanisms that control the functions of the adrenal cortex become ineffective, resulting in oversecretion of glucocorticoids, androgens, and possibly mineralocorticoid. Cushing syndrome occurs five times more often in women ages 40 to 60 years than in men.
Arrested growth, weight gain and obesity, musculoskeletal changes, and glucose intolerance
Classic features: central-type obesity, with a fatty “buffalo hump” in the neck and supraclavicular area, a heavy trunk, and relatively thin extremities; skin is thin, fragile, easily traumatized, with ecchymoses and striae
Weakness and lassitude; sleep is disturbed because of altered diurnal secretion of cortisol.
Excessive protein catabolism with muscle wasting and osteoporosis; kyphosis, backache, and compression fractures of the vertebrae are possible
Retention of sodium and water, producing hypertension and heart failure
“Moon-faced” appearance, oiliness of skin and acne
Increased susceptibility to infection; slow healing of minor cuts and bruises
Hyperglycemia or overt diabetes
Virilization in females (due to excess androgens) with appearance of masculine traits and recession of feminine traits (eg; excessive hair on face, breasts atrophy, menses cease, clitoris enlarges, and voice deepens); libido is lost in males and females
Changes occur in mood and mental activity; psychosis may develop and distress and depression are common
If Cushing’s syndrome is the result of a pituitary tumor, visual disturbances are possible cause of pressure on the optic chiasm
Assessment and Diagnostic Findings
Overnight dexamethasone suppression test to measure plasma corticol level (stress, obesity, depression, and medications may falsely elevate results)
Computed tomography (CT) or magnetic resonance imaging (MRI) scan or ultrasound may localize adrenal tissue and detect adrenal tumors
Treatment is usually directed at the pituitary gland because most cases are due to pituitary tumors rather than tumors of the adrenal cortex.
Surgical removal of the tumor (transsphenoidal hypophysectomy) is the treatment of choice (90% success rate.
Radiation of the pituitary gland is successful but takes several months for symptom control.
Adrenalectomy is performed in patients with primary adrenal hypertrophy
Postoperatively, temporary replacement therapy with hydrocortisone may be necessary until the adrenal glands begin to respond normally (may be several months)
If bilateral adrenalectomy was performed, lifetime replacement of adrenal cortex hormones is necessary
Adrenal enzyme inhibitors (eg, metyrapone or mitotane) may be used with ectopic ACTH-secreting tumors that cannot be totally removed; monitor closely for inadequate adrenal function and side effects
If Cushing’s syndrome results from exogenous corticosteroids, taper the drug to the minimum level or use alternate day therapy to treat the underlying disease.
NURSING PROCESS: The Patient with Cushing’s Syndrome
Focus on the effects on the body of high concentrations of adrenal cortex hormones
Assess patient’s level of activity and ability to carry out routine and self-care activities
Observe skin trauma, infection, breakdown, bruising and edema
Note changes in appearance and patient’s response to these changes, family is good source of information about patient’s emotional status and changes in appearance
Assess patient’s mental function. including mood, response to questions, depression, and awareness of environment
Risk for injury related to weakness
Risk for infection related to altered protein metabolism and inflammatory response
Self-care deficits related to weakness, fatigue, muscle wasting, and altered sleep patterns
Impaired skin integrity related to edema, impaired healing, and thin and fragile skin
Disturbed body image related to altered appearance, impaired sexual functioning, and decreased activity level
Disturbed thought processes related to mood swings, irritability, and depression
Collaborative Problems/Potential Complications
Adverse effects of adrenocortical activity
Planning and Goals
Major goals include decreased risk for injury, decreased risk for infection, increased ability to carry out self-care activities, impaired skin integrity, improved body image, improved mental function, and absence of complications.
Decreasing Risk for Injury
Provide a protective environment to prevent falls, fractures, and other injuries to bones and soft tissues
Assist the patient who is weak in ambulating to prevent falls or colliding into furniture
Recommend foods high in protein, calcium, and vitamin D to minimize muscle wasting and osteoporosis; refer to dietitian for assistance
Decreasing Risk for Infection
Avoid unnecessary exposure to people with infections
Assess frequently for subtle signs of infections (corticosteroids mask signs of inflammation and infection)
Promoting Skin Care
Use meticulous skin care to avoid traumatizing fragile skin
Avoid adhesive tapes, which can tear and irritate the skin
Assess skin and bony prominences frequently
Encourage and assist patient to change positions ffrequently
Improving Body Image
Discuss the impact that changes have had on patient’s self-concept and relationships with others. Major physical changes will disappear in time if the cause of Cushing’s syndrome can be treated.
Weight gain and edema may be modified by a low-carbohydrate, low-sodium diet; a high in protein intake can reduce some bothersome symptoms
Improving Thought Processes
Explain to patient and family the cause of emotional instability and help them cope with mood swings, irritability, and depression
Report any psychotic behavior
Encourage patient and family members to verbalize feelings
Encouraging Rest and Activity
Encourage moderate activity to prevent complications of immobility and promote self-esteem
Plan rest periods throughout the day and promote a relaxing, quiet environment for rest and sleep
Preparing Patient for Surgery
Adrenal hypofunction ans addisonians crisis: monitor for hypotension; rapid, weak pulse, rapid respiratory rate; pallor; and extreme weakness. Note factors that may have led to crisis (eg, stress, trauma, surgery).
Administer intravenous fluids and electrolytes and corticosteroids before, during and after surgery or treatment as indicated.
Monitor for circulatory collapse and shock present in addisonian crisis; treat promptly.
Assess fluid and electrolyte status by monitoring laboratory values and daily weight.
Monitor blood glucose level, and report elevations to physician.
Joyce Young Johnson et.al Handbook for Brunner & Suddarth’s Textbook of Medical-Surgical Nursing 11th edition
Addison’s disease is caused by a deficiency of cortical hormone. It results when the adrenal cortex function is inadequate to meet the patient’s need for cortical hormones. Autoimmune or idiopathic atrophy of the adrenal glands is responsible for 80% to 90% of cases. Other causes include surgical removal of both adrenal glands or infection (tuberculosis or histoplasmosis) of the adrenal glands. Inadequate secretion of adrenocorticotrophic hormone (ACTH) from the primary pituitary gland results in adrenal insufficiency. Symptoms may also result from sudden cessation of exogenous adrenocortical hormone therapy, which interferes with normal feedback mechanisms.
Clinical manifestations include muscle weakness, anorexia, gastrointestinal symptoms, fatigue, emaciation, dark pigmentation of the skin and mucous membranes, hypotension, low blood glucose, low serum sodium and high serum potassium. The onset usually occurs with nonspecific symptoms. Mental changes (depression, emotional lability, apathy and confusion) are present in 60% to 80% of patients. In severe cases, disturbance of sodium and potassium metabolism may be marked by depletion of sodium and water and severe, chronic dehydration.
This medical emergency develops as the disease progresses. Signs and symptoms include:
Cyanosis, fever, and classic signs of circulatory shock: pallor, apprehension, rapid and weak pulse, rapid respirations, and low blood pressure
Headache, nausea, abdominal pain, diarrhea, confusion and restlessness
Slight overexertion, exposure to cold, and acute infections, decrease salt intake and may lead to circulatory collapse, shock and death
Stress of surgery or dehydration from preparation for diagnostic tests or surgery may precipitate addisonian or hypotensive crisis
Decreased blood glucose and sodium levels, increased serum potassium (hyperkalemia), and leukocytosis.
Assessment and Diagnostic Findings
Primary adrenocortical insufficiency:
greatly increased plasma ACTH (>22.0 pmol/L)
serum cortisol low normal or lower than normal (<165 nmol/L)
decreased blood glucose (hypoglycemia)
decreased sodium levels (hyponatremia)
increased serum potassium (hyperkalemia)
increased white cell count (leukocytosis)
Immediate treatment is directed toward combating shock.
Restore blood circulation, administer fluids, monitor vital signs, and place patient in a recumbent position with legs elevated
Administer intravenous hydrocortisone, followed by 5% dextrose in normal saline
Vasopressor amines may be required if hypotension persists
Antibiotics may be prescribed for infection
Oral intake may be initiated as soon as tolerated
If adrenal gland does not regain function, lifelong replacement of corticosteroids and mineralocorticoids is required
Dietary intake should be supplemented with salt during times of gastrointestinal losses of fluids through vomiting and diarrhea
NURSING PROCESS: The Patient with Addison’s Disease
Assessment focuses on fluid imbalance and stress
Check blood pressure from a lying to standing position; check pulse rate
Assess skin color and turgor
Assess history of weight changes, muscle weakness, and fatigue
Ask patient and family about onset of illness or increased stress that may have precipitated crisis
Deficient fluid volume related to inadequate fluid intake and fluid loss secondary to inadequate adrenal hormone secretion
Deficient knowledge about need for hormone replacement and dietary modification
Collaborative Problems/Potential Complications
Planning and Goals
Goals may include improving fluid balance, improving response to activity, decreasing stress, increasing knowledge about need for hormone replacement and dietary modifications, and ensuring absence of complications.
Record weight changes daily
Assess skin turgor and mucous membranes
Instruct patient to report increased thirst
Monitor lying, sitting, and standing blood pressures frequently
Assist patient in selecting, and encouraging patient to consume, food and fluids that assist in restoring and maintaining fluid and electrolyte balance (eg, foods high in sodium during gastrointestinal disturbances and very hot weather). Include a dietitian for added guidance.
Assist patient and family in learning to administer hormone replacement and to modify dosage during illness and stress
Provide written and verbal instructions about mineralocorticoid and glucocorticoid therapy.
Improving Activity Intolerance
Avoid unnecessary activities and stress that might precipitate a hypotensive episode
Detect signs of infection or presence of stressors that may have triggered the crisis
Provide a quiet, nonstressful environment during acute crises; carry out all activities for patient
Explain all procedures to reduce fear and anxiety
Explain rationale for minimizing stress during acute crisis
Monitoring and Managing Complications (Addisonian Crisis)
Assess for signs and symptoms of crisis: circulatory collapse and shock
Avoid physical and psychological stress, including exposure to cold, overexertion, infection, and emotional distress
Initiate immediate treatment with intravenous fluid, glucose, and electrolytes, especially sodium; corticosteroid supplements; and vasopressors
Avoid patient exertion; anticipate and take measures to meet patient’s needs
Monitor symptoms, vital signs, weight, and fluid and electrolyte balance to evaluate return to precrisis state
Identify factors that led to crisis
Joyce Young Johnson et.al Handbook for Brunner & Suddarth’s Textbook of Medical-Surgical Nursing 11th edition