Management

Management

Although most moles abort spontaneously, suction curettage offers a safe, rapid, and effective method of evacuating a hydatidiform mole if necessary (Cunningham et al., 2010; Gilbert, 2011). Induction of labor with oxytocic agents or prostaglandin is not recommended because of the increased risk of embolization of trophoblastic tissue. Post-evacuation administration of Rho(D) immune globulin to women who are Rh negative is necessary to prevent isoimmunization (Gilbert, 2011). The nurse provides the woman and her family with information about the disease process, the necessity for a long course of follow-up, and the possible consequences of the disease. The nurse also helps the woman and her family cope with the pregnancy loss and recognize that the pregnancy was not normal. In addition, the woman and her family are encouraged to express their feelings, and information is provided about local support groups or counseling resources as needed. Internet resources such as Share: Pregnancy and Infant Loss Support, Inc., at www.nationalshare.org and the International Society for the Study of Trophoblastic Disease at www.isstd.org may also be useful. Explanations about the importance of postponing a subsequent pregnancy and contraceptive counseling are provided to emphasize the need for consistent and reliable use of the method chosen. NURSING ALERT To avoid confusion in regard to rising levels of hCG that are normal in pregnancy but could indicate GTD, pregnancy should be avoided during the follow-up assessment period. Any contraceptive method except an IUD is acceptable. Oral contraceptives are preferred because they are highly effective.

Alterations in Thinking Delusions

Alterations in thinking can take many forms. Delusions are most often defined as false fixed beliefs that cannot be corrected by reasoning. They may be simple beliefs or part of a complex delusional system. In schizophrenia, delusions are often loosely organized and may be bizarre. Most commonly, delusional thinking involves the following themes: ideas of reference, persecution, grandiosity, somatic sensations, jealousy, and control. Table 17-1 provides definitions and examples of various delusions. TABLE 17-1 -- SUMMARY OF DELUSIONS[∗] TYPE OF DELUSION DEFINITION EXAMPLE Ideas of reference Misconstruing trivial events and remarks and giving them personal significance When Maria saw the doctor and nurse talking together, she believed they were plotting against her. When she heard on the radio that a hurricane was coming, she believed this was really a message that harm was going to befall her. Persecution The false belief that one is being singled out for harm by others; this belief often takes the form of people in power conspiring against the person or following the person, or being persecuted by friends or colleagues Sam believed that the Secret Service was planning to kill him. He believed that the Secret Service was poisoning his food. Therefore he would only eat food that he was certain was safe. Grandeur The false belief that one is a very powerful and important person, having special abilities, possessing great wealth or beauty Sally believed that she was Mary Magdalene and that Jesus controlled her thoughts and was telling her how to save the world. Somatic delusions The false belief that the body is changing in an unusual way (e.g., rotting inside, heart is no longer beating) David told the doctor that his brain was rotting away. Jealousy The false belief that one's mate is unfaithful; may have so-called proof Harry accused his girlfriend of going out with other men, even though this was not the case. His "proof" was that she came home from work late twice that week. He persisted in his belief, even when the girlfriend's boss explained that everyone had worked late. Erotomania The false belief that another person, usually a stranger, high-class, or famous, is in love with him or her Samantha is firmly convinced that Johnny Depp, the famous movie star, is madly in love with her. She imagines that callers who claim to have the wrong number are really from Johnny. She sends him love letters and flowers through his agent. She tries repeatedly to get his home address. Nihilistic The false conviction that a major catastrophe is about to happen Jason is becoming more preoccupied with the belief that the world will end soon from an impact by a meteorite. He is becoming more and more fearful with each passing day. Bizarre delusions Clearly implausible and incomprehensible false beliefs that do not derive from ordinary experiences Phoebe is obsessed with the idea that aliens are taking over her mind and are replacing parts of her brain with parts of an alien brain. ∗ A false belief held and maintained as true, even with evidence to the contrary. This does not include unusual beliefs maintained by one's culture or subculture. Approximately 75% of people with schizophrenia experience delusions at some time during their illness. The most common delusions are persecutory and grandiose, as well as those involving religious or hypochondriacal ideas. A person experiencing delusions is convinced that what he or she believes to be real is real. The person's thinking often reflects feelings of great fear and isolation: "I know the doctor talks to the FBI about ways to get rid of me without getting caught. They all want me dead." Delusions may reflect the person's feelings of low self-worth through the use of reaction formation (observed as grandiosity). "I have secret powers, and I am able to bend others to my will. One day I'll be famous for it." At times, delusions hold a kernel of truth. One patient came into the hospital acutely psychotic. He repeatedly told the staff that the mafia was out to kill him. Later, the staff learned that the patient had been selling drugs, had not paid his contacts, and gang members were trying to find him to hurt or even kill him. Other common delusions observed in schizophrenia include the following: • Thought broadcasting—belief that one's thoughts can be heard by others (e.g., "My brain is connected to the world mind. I can control all heads of state through my thoughts.") • Thought insertion—belief that thoughts of others are being inserted into one's mind (e.g., "They make me think bad thoughts.") • Thought withdrawal—belief that thoughts have been removed from one's mind by an outside agency (e.g., "The devil takes my thoughts away and leaves me empty.") • Delusion of being controlled—belief that one's body or mind is controlled by an outside agency (e.g., "There is a man from darkness who controls my thoughts with electrical waves") and made to feel emotions or sensations (e.g., sexual) that are not one's own. Concrete thinking Concrete thinking refers to an overemphasis on specific details and impairment in the ability to use abstract concepts. For example, during an assessment, the nurse might ask what brought the patient to the hospital. The patient might answer "a cab" rather than explaining the reason for seeking medical or psychiatric aid. When asked to give the meaning of the proverb "People in glass houses shouldn't throw stones," the person with schizophrenia might answer, "Don't throw stones or the windows will break." The answer is literal; the ability to use abstract reasoning is absent.

Chronic Kidney Disease

Chronic kidney disease (CKD) involves progressive, irreversible loss of kidney function. The Kidney Disease Outcomes Quality Initiative (KDOQI) of the National Kidney Foundation defines CKD as either the presence of kidney damage or a decreased GFR less than 60 mL/min/1.73 m2 for longer than 3 months. The classification of CKD is presented in Table 47-6. The last stage of kidney failure, end-stage kidney (renal) disease (ESKD), occurs when the GFR is less than 15 mL/min. At this point, RRT (dialysis or transplantation) is required to maintain life. TABLE 47-6 -- STAGES OF CHRONIC KIDNEY DISEASE Description GFR (mL/min/1.73 m2) Clinical Action Plan Stage 1 Kidney damage with normal or ↑ GFR ≥90 Diagnosis and treatment CVD risk reduction Slow progression Stage 2 Kidney damage with mild ↓ GFR 60-89 Estimation of progression Stage 3 Moderate ↓ GFR 30-59 Evaluation and treatment of complications Stage 4 Severe ↓ GFR 15-29 Preparation for renal replacement therapy (dialysis, kidney transplant) Stage 5 Kidney failure <15 (or dialysis) Renal replacement therapy (if uremia present and patient desires treatment) Source: National Kidney Foundation. www.kidney.org/kidneydisease/aboutckd.cfm. Although CKD has many different causes, the leading causes are diabetes (about 50%) and hypertension (about 25%). Less common etiologies include glomerulonephritis, cystic diseases, and urologic diseases.[14] (Diseases of the renal system that affect the kidney are discussed in Chapter 46.) CKD is much more common than AKI (see Table 47-1). The increasing prevalence of CKD has been partially attributed to the increase in risk factors, including an aging population, rise in rates of obesity, and increased incidence of diabetes and hypertension.[14,15] More than 26 million American adults have CKD, and a million more are at increased risk. One of every nine Americans has CKD. Over half a million Americans are receiving treatment (dialysis, transplant) for ESKD. Despite all the technologic advances in life-sustaining treatment with dialysis, patients with ESKD have a high mortality rate. As the stage of kidney disease progresses, the mortality rate also increases. Mortality rates are as high as 19% to 24% for individuals with stage 5 CKD on dialysis. About 20% of patients with ESKD receiving dialysis die each year.[14] Because the kidneys are highly adaptive, kidney disease is often not recognized until there has been considerable loss of nephrons. Because patients with CKD are frequently asymptomatic, CKD is underdiagnosed and undertreated. It has been estimated that about 70% of people with CKD are unaware that they have the disease.[14] The prognosis and course of CKD are highly variable depending on the etiology, patient's condition and age, and adequacy of health care follow-up. Some individuals live normal, active lives with compensated kidney failure, whereas others may rapidly progress to ESKD (stage 5). Since 1972, the United States has covered the majority of the costs of providing dialysis for those eligible for Medicare benefits. Under Title XVIII of the Social Security Act, ESKD was recognized as a disability. As such, more than 90% of individuals of any age who have ESKD are eligible for financial assistance for treatment through Medicare. Medicare pays for 80% of eligible charges, with the remaining being paid for by state or private insurance or out of pocket.[14] Cultural & Ethnic Health Disparities Chronic Kidney Disease • Chronic kidney disease (CKD) has a high incidence in minority populations, especially African Americans and Native Americans. • Hypertension and diabetes mellitus are also more common in African Americans and Native Americans. African Americans • The risk of CKD as a complication of hypertension is significantly increased in African Americans. • African Americans have the highest rate of CKD, nearly four times that of whites. Native Americans • Native Americans have a rate of CKD twice that of whites. • The rate of CKD is six times higher among Native Americans with diabetes than among other ethnic groups with diabetes. Hispanics • The rate of CKD in Hispanics is 1.5 times higher than in non-Hispanic whites. Clinical Manifestations As kidney function deteriorates, every body system becomes affected. The clinical manifestations are a result of retained substances, including urea, creatinine, phenols, hormones, electrolytes, and water. Uremia is a syndrome in which kidney function declines to the point that symptoms may develop in multiple body systems (Fig. 47-2). It often occurs when the GFR is 10 mL/min or less. Click to view full size figure FIG. 47-2 Possible clinical manifestations of chronic kidney disease. The manifestations of uremia vary among patients according to the cause of the kidney disease, co-morbid conditions, age, and degree of adherence to the prescribed medical regimen. Many patients are tolerant of the changes because they occur gradually. Urinary System. In the early stages of CKD, patients usually do not report any change in urine output. Since diabetes is the primary cause of CKD, polyuria may be present, but not necessarily as a consequence of kidney disease. Because most people continue to have sufficient urine output, it is often difficult to convince them that they have kidney disease. As CKD progresses, patients have increasing difficulty with fluid retention and require diuretic therapy. After a period on dialysis, patients may develop anuria. Metabolic Disturbances Waste Product Accumulation. As the GFR decreases, the BUN and serum creatinine levels increase. The BUN is increased not only by kidney failure, but also by protein intake, fever, corticosteroids, and catabolism. For this reason, serum creatinine clearance determinations (calculated GFR) are considered more accurate indicators of kidney function than BUN or creatinine. Significant elevations in BUN contribute to development of nausea, vomiting, lethargy, fatigue, impaired thought processes, and headaches. Altered Carbohydrate Metabolism. Defective carbohydrate metabolism is caused by impaired glucose metabolism, resulting from cellular insensitivity to the normal action of insulin. Mild to moderate hyperglycemia and hyperinsulinemia may occur. Insulin and glucose metabolism may improve (but not to normal values) after the initiation of dialysis. Patients with diabetes who develop uremia may require less insulin than before the onset of CKD. This is because insulin, which depends on the kidneys for excretion, remains in circulation longer. As a result, a number of patients who required insulin before starting dialysis will be able to discontinue insulin therapy when they start dialysis and their kidney disease progresses. The insulin dosing must be individualized and glucose levels monitored carefully. Elevated Triglycerides. Hyperinsulinemia stimulates hepatic production of triglycerides. Almost all patients with uremia develop dyslipidemia, with increased very-low-density lipoproteins (VLDLs), increased low-density lipoproteins (LDLs), and decreased high-density lipoproteins (HDLs). The altered lipid metabolism is related to decreased levels of the enzyme lipoprotein lipase, which is important in the breakdown of lipoproteins. Most patients with CKD die from CV disease.[15] Electrolyte and Acid-Base Imbalances Potassium. Hyperkalemia is a serious electrolyte disorder associated with kidney disease. Fatal dysrhythmias have been reported when the serum potassium level reaches 7 to 8 mEq/L (7 to 8 mmol/L). Hyperkalemia results from the decreased excretion of potassium by the kidneys, the breakdown of cellular protein, bleeding, and metabolic acidosis. Potassium may also come from the food consumed, dietary supplements, drugs, and IV infusions. Sodium. Sodium may be elevated, normal, or low in kidney failure. Because of impaired sodium excretion, sodium along with water is retained. If large quantities of water are retained, dilutional hyponatremia occurs. Sodium retention can contribute to edema, hypertension, and HF. Sodium intake must be individually determined but is generally restricted to 2 g/day. Calcium and Phosphate. Calcium and phosphate alterations are discussed in the section on the musculoskeletal system on p. 1110. Magnesium. Magnesium is primarily excreted by the kidneys. Hypermagnesemia is generally not a problem unless the patient is ingesting magnesium (e.g., milk of magnesia, magnesium citrate, antacids containing magnesium). Clinical manifestations of hypermagnesemia can include absence of reflexes, decreased mental status, cardiac dysrhythmias, hypotension, and respiratory failure. Metabolic Acidosis. Metabolic acidosis results from the kidneys' impaired ability to excrete the acid load (primarily ammonia) and from defective reabsorption and regeneration of bicarbonate. The average adult produces 80 to 90 mEq of acid per day. This acid is normally buffered by bicarbonate. In kidney failure, plasma bicarbonate, which is an indirect measure of acidosis, usually falls to a new steady state at around 16 to 20 mEq/L (16 to 20 mmol/L). The decrease in plasma bicarbonate reflects its use in buffering metabolic acids. The bicarbonate level generally does not progress below this level because hydrogen ion production is usually balanced by buffering from demineralization of the bone (the phosphate buffering system). Hematologic System Anemia. A normocytic, normochromic anemia is associated with CKD. The anemia is due to decreased production of the hormone erythropoietin by the kidneys. Erythropoietin normally stimulates precursor cells in the bone marrow to produce RBCs (erythropoiesis). Other factors contributing to anemia are nutritional deficiencies, decreased RBC life span, increased hemolysis of RBCs, frequent blood samplings, and bleeding from the GI tract. For patients receiving maintenance hemodialysis (HD), blood loss in the dialyzer may also contribute to the anemic state. Elevated levels of parathyroid hormone (PTH) (produced to compensate for low serum calcium levels) can inhibit erythropoiesis, shorten survival of RBCs, and cause bone marrow fibrosis, which can result in decreased numbers of hematopoietic cells. Sufficient iron stores are needed for erythropoiesis. Many patients with kidney failure are iron deficient and require oral iron supplements. Folic acid, which is essential for RBC maturation, is dialyzable because it is water soluble. It needs to be supplemented in the diet (folic acid 1 mg/day). Bleeding Tendencies. The most common cause of bleeding in uremia is a qualitative defect in platelet function. This dysfunction is caused by impaired platelet aggregation and impaired release of platelet factor III. In addition, alterations in the coagulation system with increased concentrations of both factor VIII and fibrinogen occur. The altered platelet function, hemorrhagic tendencies, and GI bleeding susceptibility can usually be corrected with regular HD or PD. Infection. Patients with advanced CKD have an increased susceptibility to infection. Infectious complications are caused by changes in leukocyte function and altered immune response and function. Both cellular and humoral immune responses are suppressed. Other factors contributing to the increased risk of infection include hyperglycemia and external trauma (e.g., catheters, needle insertions into vascular access sites). Cardiovascular System. The most common cause of death in patients with CKD is CV disease. Myocardial infarction, ischemic heart disease, peripheral arterial disease, HF, cardiomyopathy, and stroke are leading causes of death. Even a slight reduction in GFR has been associated with a higher risk for coronary artery disease.[15] CV disease and CKD are so closely linked that if patients develop cardiac events (e.g., myocardial infarction, HF), evaluation of kidney function is recommended. Traditional CV risk factors such as hypertension and elevated lipids are common in CKD patients. However, CV disease may also be related to nontraditional CV risk factors such as vascular calcification and arterial stiffness, which are major contributors to CV disease in patients with CKD. The calcium deposits in the vascular medial layer are associated with stiffening of the blood vessels. The mechanisms involved are multifactorial. They include (1) vascular smooth muscle cells changing into chondrocytes or osteoblast-like cells, (2) high total body amount of calcium and phosphate resulting from abnormal bone metabolism, (3) impaired renal excretion, and (4) drug therapies to treat the bone disease (e.g., calcium phosphate binders).[16] Hypertension is highly prevalent in patients with CKD because hypertension is both a cause and a consequence of CKD. Hypertension is aggravated by sodium retention and increased extracellular fluid volume.[17] In some individuals, increased renin production contributes to hypertension (see Fig. 45-4). Hypertension and diabetes mellitus are contributing risk factors for vascular complications. The vascular changes from long-standing hypertension and the accelerated atherosclerosis contribute to the higher rate of CV disease in CKD. Left ventricular hypertrophy (LVH) is present in about 75% of patients receiving dialysis. Long-standing hypertension, extracellular fluid volume overload, and anemia contribute to development of LVH that may eventually lead to cardiomyopathy and HF. Patients with CKD are susceptible to cardiac dysrhythmias that result from hyperkalemia and decreased coronary artery perfusion. Uremic pericarditis can develop and occasionally progresses to pericardial effusion and cardiac tamponade. Pericarditis is typically manifested by a friction rub, chest pain, and low-grade fever. Hypertension can cause retinopathy, encephalopathy, and nephropathy. Because of the many effects of hypertension, blood pressure (BP) control is one of the most important therapeutic goals in the management of CKD. Respiratory System. With severe acidosis, the respiratory system may attempt to compensate with Kussmaul breathing, which results in increased carbon dioxide removal by exhalation (see Chapter 17). Dyspnea may occur as a manifestation of fluid overload, pulmonary edema, uremic pleuritis (pleurisy), pleural effusions, and respiratory infections (e.g., pneumonia). Gastrointestinal System. Stomatitis with exudates and ulcerations, a metallic taste in the mouth, and uremic fetor (a urinous odor of the breath) are commonly found in CKD. Anorexia, nausea, and vomiting may develop if CKD progresses to ESKD and is not treated with dialysis. Weight loss and malnutrition may also occur. Diabetic gastroparesis (delayed gastric emptying) can compound the effects of malnutrition for patients with diabetes. GI bleeding is also a risk because of mucosal irritation and the platelet defect. Constipation may be due to the ingestion of iron salts or calcium-containing phosphate binders. Constipation can be made worse by limitations on fluid intake and physical inactivity. Neurologic System. Neurologic changes are expected as kidney failure progresses. They are the result of increased nitrogenous waste products, electrolyte imbalances, metabolic acidosis, and atrophy and demyelination of nerve fibers. The central nervous system (CNS) becomes depressed, resulting in lethargy, apathy, decreased ability to concentrate, fatigue, irritability, and altered mental ability. Seizures and coma may result from a rapidly increasing BUN and hypertensive encephalopathy. Peripheral neuropathy is initially manifested by a slowing of nerve conduction to the extremities. Individuals with advanced stage 5 CKD may complain of restless legs syndrome (see Chapter 59), described as "bugs crawling inside the leg." Paresthesias are most often experienced in the feet and legs and may be described by the patient as a burning sensation. Eventually, motor involvement may lead to bilateral footdrop, muscular weakness and atrophy, and loss of deep tendon reflexes. Muscle twitching, jerking, asterixis (hand-flapping tremor), and nocturnal leg cramps also occur. In patients with diabetes, uremic neuropathy is compounded by the neuropathy associated with diabetes mellitus. Dialysis should improve general CNS manifestations and may slow or halt the progression of neuropathies. However, motor neuropathy may not be reversible. The treatment for neurologic problems is dialysis or transplantation. Altered mental status, a late manifestation of CKD stage 5, is rarely seen unless the patient has chosen to forgo RRT. Musculoskeletal System. CKD mineral and bone disorder (CKD-MBD) develops as a systemic disorder of mineral and bone metabolism caused by progressive deterioration in kidney function (Fig. 47-3). As kidney function deteriorates, less vitamin D is converted to its active form, resulting in decreased serum levels. Activated vitamin D is necessary to optimize absorption of calcium from the GI tract; thus low levels of active vitamin D result in decreased serum calcium levels.[18] Click to view full size figure FIG. 47-3 Mechanisms of chronic kidney disease mineral and bone disorder (CKD-MBD). GFR, Glomerular filtration rate; PTH, parathyroid hormone. Normally serum calcium levels are tightly regulated. PTH is the primary regulator of serum calcium levels. When hypocalcemia occurs, the parathyroid gland secretes PTH, which stimulates bone demineralization, thereby releasing calcium from the bones. Phosphate is released as well, leading to elevated serum phosphate levels. Hyperphosphatemia also results from decreased phosphate excretion by the kidneys. Hyperphosphatemia decreases serum calcium levels and further reduces the kidneys' ability to activate vitamin D. Low serum calcium, elevated phosphate, and decreased vitamin D contribute to the stimulation of the parathyroid gland and excretion of PTH. The PTH acts on the bone to increase remodeling and increase serum calcium levels. The accelerated rate of bone remodeling causes a weakened bone matrix and places the patient at a higher risk for fractures. Normally plasma calcium is found ionized or free (physiologically active form) or bound to protein. In kidney failure, it is unusual for hypocalcemia to be symptomatic. The reason for this is that, in the acidotic state associated with renal failure, more calcium is in the ionized form than is bound to protein. However, a low ionized calcium level can lead to tetany (see Chapter 17). CKD-MBD is a common complication of CKD and results in both skeletal complications and extraskeletal complications (vascular and soft tissue complications). Skeletal complications include osteomalacia, which results from demineralization from slow bone turnover and defective mineralization of newly formed bone, and osteitis fibrosa, a decalcification of the bone and replacement of bone tissue with fibrous tissue. Extraskeletal complications result from vascular calcifications. As previously mentioned, vascular calcifications are a significant contributing factor to CV disease. "Uremic red eye" is caused by the irritation from calcium deposits in the eye. Intracardiac calcifications can disrupt the conduction system and cause cardiac arrest. CKD-MBD contributes significantly to a patient's increased morbidity and mortality risks.[18] Integumentary System. Pruritus is more prevalent in patients receiving dialysis than in the earlier stages of CKD. A small percentage of patients develop refractory pruritus that can have a devastating impact on their well-being and quality of life. Pruritus has multiple causes, including dry skin, calcium-phosphate deposition in the skin, and sensory neuropathy. The itching may be so intense that it can lead to bleeding or infection secondary to scratching. Uremic frost is an extremely rare condition in which urea crystallizes on the skin; this is usually seen only when BUN levels are extremely elevated (e.g., over 200 mg/dL). Reproductive System. Both men and women can experience infertility and a decreased libido. Women usually have decreased levels of estrogen, progesterone, and luteinizing hormone, causing anovulation and menstrual changes (usually amenorrhea). Menses and ovulation may return after dialysis is started. Men experience loss of testicular consistency, decreased testosterone levels, and low sperm counts. Sexual dysfunction may also be caused by anemia, which causes fatigue and decreased libido. In addition, peripheral neuropathy can cause impotence in men and anorgasmy in women. Additional factors that may cause changes in sexual function are psychologic problems (e.g., anxiety, depression), physical stress, and side effects of drugs. Sexual function may improve with maintenance dialysis and may become normal with successful transplantation. Patients that become pregnant while receiving dialysis have been able to carry a fetus to term, but there is significant risk to the mother and infant. Pregnancy in patients with a kidney transplant is more common, but there is still considerable risk to both the mother and fetus. Psychologic Changes. Personality and behavioral changes, emotional lability, withdrawal, and depression are commonly observed in patients with CKD. Fatigue and lethargy contribute to the feeling of illness. The changes in body image caused by edema, integumentary disturbances, and access devices (e.g., fistulas, catheters) may lead to anxiety and depression. Decreased ability to concentrate and slowed mental activity can give the appearance of dullness and disinterest in the environment. The patient must also deal with significant changes in lifestyle, occupation, family responsibilities, and financial status. Long-term survival depends on medications, dietary restrictions, dialysis, and possibly transplantation. The patient also grieves the loss of kidney function. This can be a prolonged process for some individuals. Diagnostic Studies Because persistent proteinuria is usually the first indication of kidney damage, screening for CKD involves a dipstick evaluation of protein in the urine or evaluation for microalbuminuria, which is not detected with routine urinalysis. Patients with diabetes need to have examination of their urine for microalbuminuria if none is detected on routine urinalysis. A person with persistent proteinuria (1+ protein on standard dipstick testing two or more times over a 3-month period) should have further assessment of risk factors and a diagnostic workup with blood and urine tests to evaluate for CKD. A urine test for albumin-to-creatinine ratio provides an accurate estimate of the protein and albumin excretion rate. A ratio greater than 300 mg albumin per 1 g creatinine signals CKD. A urinalysis can detect RBCs, WBCs, protein, casts, and glucose. An ultrasound of the kidneys is usually done to detect any obstructions and to determine the size of the kidneys. Other diagnostic studies (Table 47-7) help establish the diagnosis and cause of CKD. A kidney biopsy may be necessary to provide a definitive diagnosis. TABLE 47-7 -- COLLABORATIVE CARE Chronic Kidney Disease Diagnostic • History and physical examination • Identification of reversible kidney disease • Renal ultrasound • Renal scan • CT scan • Renal biopsy • BUN, serum creatinine, and creatinine clearance levels • Serum electrolytes • Lipid profile • Protein-to-creatinine ratio in first morning voided specimen • Urinalysis • Hematocrit and hemoglobin levels Collaborative Therapy • Correction of extracellular fluid volume overload or deficit • Nutritional therapy* • Erythropoietin therapy • Calcium supplementation, phosphate binders, or both • Antihypertensive therapy • Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) • Measures to treat hyperlipidemia • Measures to lower potassium† • Adjustment of drug dosages to degree of renal function • Renal replacement therapy (dialysis, kidney transplant) * See Tables 47-10 and 47-11. † See Table 47-5. Many consider serum creatinine the best indicator of kidney function, but in reality serum creatinine alone poorly reflects kidney function. GFR is the preferred measure to determine kidney function. Several GFR calculators are available. The two equations used most frequently to estimate GFR are the Cockcroft-Gault formula and the Modification of Diet in Renal Disease (MDRD) Study equation (Table 47-8). The National Kidney Foundation KDOQI guidelines recommend the MDRD Study equation to estimate GFR.[19] TABLE 47-8 -- INDICATORS OF KIDNEY FUNCTION This example shows why serum creatinine is a poor indicator of kidney function. Calculation of GFR is considered the best index to estimate kidney function as indicated by the following example. Type of Patient Estimation of GFR 76-Yr-Old African American Woman (Weight 56 kg) 28-Yr-Old African American Man (Weight 74 kg) Serum creatinine 1.4 mg/dL 1.4 mg/dL GFR, estimated by the Cockcroft-Gault formula* 30.2 mL/min 82.2 mL/min GFR, estimated by MDRD equation† 47 mL/min/1.73 m2 64 mL/min/1.73 m2 Cr, Creatinine; GFR, glomerular filtration rate; MDRD, modification of diet in renal disease. * Cockcroft-Gault GFR = (140 − Age) × (Weight in kilograms) × (0.85 if female)/(72 × Cr). † GFR as estimated by MDRD equation calculator can be accessed at www.mdrd.com. Collaborative Care The overall goals of CKD therapy are to preserve existing kidney function, reduce the risks of CV disease, prevent complications, and provide for the patient's comfort (Table 47-9). For many, early recognition, diagnosis, and treatment can deter the progression of kidney disease. It is important that patients with CKD receive appropriate follow-up and referral to a nephrologist early in the course of the disease. Every effort is made to detect and treat potentially reversible causes of kidney failure (e.g., HF, dehydration, infections, nephrotoxins, urinary tract obstruction, glomerulonephritis, renal artery stenosis). TABLE 47-9 -- RISK FACTORS FOR CHRONIC KIDNEY DISEASE Risk Factors Prevention and Management Diabetes Achieve optimal glycemic control. Hypertension Maintain BP in normal range with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). Age >60 yr Prevent insult or kidney injury. Cardiovascular disease Institute aggressive risk factor reduction. Family history of CKD Teach about increased risk and assist with appropriate screening (BP measurement, urinalysis). Exposure to nephrotoxic drugs Limit exposure and give sodium bicarbonate as treatment. Ethnic minority (e.g., African American, Native American) Teach about increased risk and assist with appropriate screening (BP measurement, urinalysis). Patients with CKD have a high incidence of CV complications. A higher percentage of patients will die from CV disease than live to need dialysis. When a patient is diagnosed as having CKD, therapy is aimed at treating the CV disease in addition to slowing the progression of kidney disease (see Table 47-7). A focus on stages 1 through 4 (see Table 47-6) before the need for dialysis (stage 5) includes the control of hypertension, hyperparathyroid disease, anemia, hyperglycemia, and dyslipidemia. The following section focuses primarily on the drug and nutritional aspects of care. Drug Therapy Hyperkalemia. Multiple strategies are used to manage hyperkalemia (see Table 47-5). Every effort is made to control hyperkalemia with the restriction of high-potassium foods and drugs. Acute hyperkalemia may require treatment with IV glucose and insulin or IV 10% calcium gluconate. Sodium polystyrene sulfonate, a cation-exchange resin, is commonly used to lower potassium levels in stage 4 and can be administered on an outpatient basis. Tell the patient to expect some diarrhea because this preparation contains sorbitol, a sugar alcohol that has an osmotic laxative action and ensures evacuation of the potassium from the bowel. Never give sodium polystyrene sulfonate to a patient with a hypoactive bowel (paralytic ileus) because fluid shifts could lead to bowel necrosis. As sodium polystyrene sulfonate exchanges sodium ions for potassium ions, observe the patient for sodium and water retention. If changes appear in the ECG such as peaked T waves and widened QRS complexes, dialysis may be required to remove excess potassium. Hypertension. For some, the progression of CKD can be delayed by controlling hypertension. (Control and treatment of hypertension are discussed in Chapter 33.) It is recommended that the target BP be less than 130/80 mm Hg for patients with CKD and 125/75 mm Hg for patients with significant proteinuria.[17] Treatment of hypertension includes (1) weight loss (if obese), (2) therapeutic lifestyle changes (e.g., exercise, avoidance of alcohol, smoking cessation), (3) diet recommendations (DASH Diet; see eTable 33-1), and (4) administration of antihypertensive drugs. Most patients require two or more drugs to reach target BP. Evidence-Based Practice Translating Research Into Practice Can Exercise Improve Physical Fitness in Chronic Kidney Disease? Clinical Question For adults with chronic kidney disease (P), what is the effect of exercise (I) on physical fitness and functioning (O)? Best Available Evidence Systematic review of randomized controlled trials (RCTs) Critical Appraisal and Synthesis of Evidence • Forty-five RCTs (n = 1863) of adults with chronic kidney disease (CKD) or kidney transplant. Physical exercise interventions lasted at least 8 wk. Most common intervention was aerobic exercise. • Fitness and cardiovascular parameters were measured. • Regular exercise improved muscle strength, walking ability, blood pressure and heart rate, and quality of life. • Exercise did not significantly affect total cholesterol or triglyceride levels. Conclusion • Exercise significantly improved physical fitness (aerobic capacity). Implications for Nursing Practice • Encourage regular aerobic exercise to counter muscle strength loss in patients with CKD. • Maintain contact with patient to promote and encourage adherence to recommended exercise. P, Patient population of interest; I, intervention or area of interest; O, outcomes of interest (see p. 12). Reference for Evidence Heiwe S , Jacobson SH: Exercise training for adults with chronic kidney disease . Cochrane Database Syst Rev 2011; 10:CD003236. The antihypertensive drugs most commonly used are diuretics, calcium channel blockers, ACE inhibitors, and angiotensin receptor blocker (ARB) agents. Prescribed medications depend on whether the patient with CKD has diabetes or not. The ACE inhibitors and ARBs are used with diabetics and those with nondiabetic proteinuria because they decrease proteinuria and possibly delay the progression of CKD. However, they must be used cautiously in patients with ESKD because they can further decrease the GFR and increase serum potassium levels. Periodically measure the BP with the patient in the supine, sitting, and standing positions to monitor the effect of antihypertensive drugs. Teach the patient and caregiver how to monitor the BP at home and what readings require immediate intervention. BP control is essential to slow atherosclerotic changes that could further impair kidney function. CKD-MBD. Interventions for CKD-MBD include limiting dietary phosphorus, administering phosphate binders, supplementing vitamin D, and controlling hyperparathyroidism.[18] Phosphate intake is not usually restricted until the patient requires RRT. At that time, phosphate is usually limited to about 1 g/day, but dietary control alone is usually inadequate. Phosphate binders include calcium-based binders: calcium acetate (PhosLo) and calcium carbonate (Caltrate). They bind phosphate in the bowel and are then excreted in the stool. The administration of calcium may increase the calcium load and place the patient at increased risk for vascular calcifications. Therefore, when calcium levels are increased or there is evidence of existing vascular or soft tissue calcifications, consider changing to noncalcium-based phosphate binders, such as lanthanum carbonate (Fosrenol) and sevelamer carbonate (Renvela). To be most effective, administer phosphate binders with each meal. Constipation is a frequent side effect of phosphate binders and may necessitate the use of stool softeners. Because bone disease (osteomalacia) is associated with excessive aluminum, aluminum preparations should be used with caution in patients with kidney failure. Do not use magnesium-containing antacids (e.g., Maalox, Mylanta) because magnesium depends on the kidneys for excretion. Hypocalcemia is a problem in the later stages of CKD because of the inability of the GI tract to absorb calcium in the absence of active vitamin D. If hypocalcemia persists even if the serum phosphate levels are normal, then supplemental calcium and vitamin D should be given. Assess vitamin D levels to determine the need for supplementation. If the levels are low (serum values less than 30 ng/mL), vitamin D supplementation is recommended in the form of cholecalciferol. Treatment of secondary hyperparathyroidism in ESKD patients requires the activated form of vitamin D because the kidneys no longer possess the ability to activate vitamin D. Active vitamin D is available as oral or IV calcitriol (Rocaltrol, Calcijex), IV paricalcitol (Zemplar), or oral or IV doxercalciferol (Hectorol), and can reduce the elevated levels of PTH. Hypercalcemia may occur with calcium and vitamin D supplementation. If hypercalcemia occurs, then reduce or discontinue vitamin D and calcium-based phosphate binders. Noncalcium-based phosphate binders can be substituted. Cinacalcet (Sensipar), a calcimimetic agent, is used to control secondary hyperparathyroidism. Calcimimetics mimic calcium and increase the sensitivity of the calcium receptors in the parathyroid glands. As a result, the parathyroid glands detect calcium at lower serum levels and decrease PTH secretion. If hyperparathyroid disease becomes severe despite medical management, a subtotal or total parathyroidectomy may be performed to decrease the synthesis and secretion of PTH. In most cases, a total parathyroidectomy is performed, and some parathyroid tissue is transplanted into the forearm. The transplanted cells produce PTH as needed. If production of PTH becomes excessive, some of the cells can be removed from the forearm. It is difficult to determine what type of bone disease a patient might have by just looking at the serum levels of calcium, phosphorus, PTH, and alkaline phosphatase. The gold standard for diagnosis is a bone biopsy. Anemia. The most important cause of anemia is a decreased production of erythropoietin. Exogenous erythropoietin (EPO) is used in the treatment. It is available as epoetin alfa (Epogen, Procrit), which can be administered IV or subcutaneously, usually two or three times per week. Darbepoetin alfa (Aranesp) is longer acting and can be administered weekly or biweekly. A significant increase in hemoglobin and hematocrit levels is usually not seen for 2 to 3 weeks. Higher hemoglobin levels (more than 12 g/dL) and higher doses of EPO are associated with a higher rate of thromboembolic events and increased risk of death from serious CV events (heart attack, HF, stroke). The recommendation is to use the lowest possible dose of EPO to treat anemia. Furthermore, treatment of CKD-related anemia should be individualized with the goal being to reduce the need for blood transfusions. There is no target hemoglobin or widely accepted EPO dosing strategy.[20] Teach people who are prescribed EPO about the risks and benefits and allow them to make an informed decision regarding their individual treatment. If EPO is used in the management of anemia, recognize that uncontrolled hypertension is a contraindication and that EPO may exacerbate an individual's hypertension. The underlying mechanism is related to the hemodynamic changes (e.g., increased whole blood viscosity) that occur as the anemia is corrected. Another side effect of EPO therapy is the development of iron deficiency from the increased demand for iron to support erythropoiesis. Iron supplementation is recommended if the plasma ferritin concentrations fall below 100 ng/mL. Some studies have supported the use of parenteral iron with a much higher ferritin value (e.g., 800 ng/mL) in order to optimize treatment. Most CKD patients receive iron supplementation either by mouth or parenterally. Nonadherence may be an issue with oral supplementation because iron has GI side effects such as gastric irritation and constipation. Orally administered iron should not be taken at the same time as phosphate binders because calcium binds the iron, preventing its absorption. Tell the patient that iron may make the stool dark in color. Most patients receiving HD are prescribed IV iron sucrose injection (Venofer) or sodium ferric gluconate complex in sucrose injection (Ferrlecit). Supplemental folic acid (1 mg/day) is usually given because it is needed for RBC formation and is removed by dialysis. Blood transfusions should be avoided in treating anemia unless the patient experiences an acute blood loss or has symptomatic anemia (i.e., dyspnea, excess fatigue, tachycardia, palpitations, chest pain). Undesirable effects of transfusions are the increased sensitization and development of antibodies, thus making it more difficult to find a compatible donor for transplantation. Multiple blood transfusions may lead to iron overload because each unit of blood contains about 250 mg of iron. Dyslipidemia. Dyslipidemia, a known traditional risk factor for CV disease, is a common problem in CKD. Statins (HMG-CoA reductase inhibitors), such as atorvastatin (Lipitor), are used to lower LDL cholesterol levels (see Table 34-5). Evidence supports the use of statins in patients with CKD (especially patients with diabetes) not yet on dialysis. However, simvastatin has been associated with a higher rate of myopathy. It is recommended that patients who develop myopathy on simvastatin be switched to atorvastatin, which has minimal renal clearance and less chance of causing myopathy. The effectiveness of statins in patients on dialysis is still being studied. Fibrates (fibric acid derivatives), such as gemfibrozil (Lopid), are used to lower triglyceride levels (see Table 34-5) and can also increase HDLs. Specific drugs of these classes that are used depend on the individual patient response and physician recommendation. Complications of Drug Therapy. Many drugs are partially or totally excreted by the kidneys. Delayed and decreased elimination leads to an accumulation of drugs and the potential for drug toxicity. Drug doses and frequency of administration must be adjusted based on the severity of the kidney disease. Increased sensitivity may result as drug levels increase in the blood and tissues. Drugs of particular concern include digoxin, diabetic agents (metformin, glyburide), antibiotics (e.g., vancomycin, gentamicin), and opioid medications. Nutritional Therapy Protein Restriction. The current diet is designed to be as normal as possible to maintain good nutrition (Table 47-10). Calorie-protein malnutrition is a potential and serious problem that results from altered metabolism, anemia, proteinuria, anorexia, and nausea. Additional factors leading to malnutrition include depression and complex diets that restrict protein, phosphorus, potassium, and sodium. Frequent monitoring of laboratory parameters, especially serum albumin, prealbumin (may be a better indicator of recent or current nutritional status than albumin), and ferritin, and anthropometric measurements are necessary to evaluate nutritional status. All patients with CKD should be referred to a dietitian for nutritional education and guidance. TABLE 47-10 -- NUTRITIONAL THERAPY Chronic Kidney Disease* Pre-End-Stage Kidney Disease Hemodialysis Peritoneal Dialysis Fluid allowance As desired or depends on urine output Urine output plus 600-1000 mL Unrestricted if weight and blood pressure controlled and residual renal function Calories 30-35 kcal/kg/day 30-35 kcal/kg/day 25-35 kcal/kg/day (includes calories from dialysate glucose absorption) Protein Individualized or 0.6-1.0 g/kg/day (low protein) 1.2 g/kg/day 1.2-1.3 g/kg/day Sodium Individualized or 1-3 g/day Individualized or 2-3 g/day Individualized or 2-4 g/day Potassium Individualized based on laboratory values Individualized or about 2-4 g/day Usually not restricted Phosphorus Individualized or 1.0-1.8 g/day Individualized or about 0.6-1.2 g/day Individualized or about 0.6-1.2 g/day Calcium About 1000-1500 mg/day Individualized Individualized Iron Supplement recommended if receiving erythropoietin Supplement recommended if receiving erythropoietin Supplement recommended if receiving erythropoietin * Diets must be individualized in accordance with needs. For the patient who is undergoing dialysis, protein is not routinely restricted (see Table 47-10). The beneficial role of protein restriction in CKD stages 1 through 4 as a means to reduce the decline in kidney function is being studied. Historically, dietary counseling often encouraged a restriction of protein for individuals with CKD. Despite some evidence that protein restriction has benefits, many patients find it difficult to adhere to these diets. For CKD stages 1 through 4, many clinicians just encourage a diet with normal protein intake. However, teach patients to avoid high-protein diets and supplements because they may overstress the diseased kidneys. Dietary protein guidelines for PD differ from those for HD because of protein loss in the dialysate. During PD, protein intake must be high enough to compensate for the losses so that the nitrogen balance is maintained. The recommended protein intake is at least 1.2 g/kg of ideal body weight (IBW) per day; this can be increased depending on the patient's individual needs. For patients with malnutrition or inadequate caloric or protein intake, commercially prepared products that are high in protein but low in sodium and potassium are available (e.g., Nepro, Amin-Aid).[21] As an alternative, liquid or powder breakfast drinks may be purchased at the grocery store. Water Restriction. Water and any other fluids are not routinely restricted in patients with CKD stages 1 to 5 who are not receiving HD. In an effort to reduce fluid retention, diuretics are often used. Patients on HD have a more restricted fluid intake than patients receiving PD. For those receiving HD, as their urine output diminishes, fluids are restricted. Recommended fluid intake depends on the daily urine output. Generally, 600 mL (from insensible loss) plus an amount equal to the previous day's urine output is allowed for a patient receiving HD. Foods that are liquid at room temperature (e.g., gelatin, ice cream) should be counted as fluid intake. The fluid allotment should be spaced throughout the day so that the patient does not become thirsty. Patients are advised to limit fluid intake so that weight gains are no more than 1 to 3 kg between dialyses (termed interdialytic weight gain). Sodium and Potassium Restriction. Patients with CKD are advised to restrict sodium. Sodium-restricted diets may vary from 2 to 4 g/day. Do not equate sodium and salt because the sodium content in 1 g of sodium chloride is equivalent to 400 mg of sodium. Instruct the patient to avoid high-sodium foods such as cured meats, pickled foods, canned soups and stews, frankfurters, cold cuts, soy sauce, and salad dressings (see Chapter 35, Table 35-8). Potassium restriction depends on the kidneys' ability to excrete potassium. Most salt substitutes should be avoided if patients have been instructed to restrict potassium because they contain potassium chloride. Dietary restrictions for potassium range from about 2 to 3 g (39 mg = 1 mEq). Teach patients receiving HD which foods are high in potassium and to avoid them (Table 47-11). TABLE 47-11 -- NUTRITIONAL THERAPY High-Potassium Foods* Fruits Vegetables Other Foods • Apricot, raw (medium) • Avocado ( whole) • Banana ( whole) • Cantaloupe • Dried fruits • Grapefruit juice • Honeydew • Orange (medium) • Orange juice • Prunes • Raisins • Baked beans • Butternut squash • Refried beans • Black beans • Broccoli, cooked • Carrots, raw • Greens, except kale • Mushrooms, canned • Potatoes, white and sweet • Spinach, cooked • Tomatoes or tomato products • Vegetable juices • Bran or bran products • Chocolate (1.5-2 oz) • Granola • Milk, all types (1 cup) • Nutritional supplements (use only under the direction of physician or dietitian) • Nuts and seeds (1 oz) • Peanut butter (2 tbs) • Salt substitutes, Lite Salt • Salt-free broth • Yogurt Source: National Kidney Foundation: Potassium and your CKD diet. www.kidney.org/atoz/content/potassium.cfm * Contain at least 200 mg/portion. Portion = cup unless otherwise noted. Patients using PD do not usually need potassium restrictions and may even be prescribed oral potassium supplementation because of the loss of potassium with dialysis exchanges. Phosphate Restriction. As kidney function deteriorates, phosphate elimination by the kidneys is diminished and the patient begins to develop hyperphosphatemia. By the time a patient reaches ESKD, phosphate should be limited to approximately 1 g/day. Foods that are high in phosphate include meat, dairy products (e.g., milk, ice cream, cheese, yogurt), and foods containing dairy products (e.g., pudding). Many foods that are high in phosphate are also high in protein. Since patients on dialysis are encouraged to eat a diet containing protein, phosphate binders are essential to control phosphate.

Communication and Nursing Practice

Communication is a lifelong learning process. Nurses make the intimate journey with patients and their families from the miracle of birth to the mystery of death. As a nurse you communicate with patients and families to collect meaningful assessment data, provide education, and interact using therapeutic communication to promote personal growth and attainment of health-related goals. Despite the complexity of technology and the multiple demands on nurses' time, it is the intimate moment of connection that makes all the difference in the quality of care and meaning for a patient and a nurse. Communication is an essential part of patient-centered nursing care. Patient safety also requires effective communication among members of the health care team as patients move from one caregiver to another or from one care setting to another. Breakdown in communication among the health care team is a major cause of errors in the workplace and threatens professional credibility (World Health Organization, 2007). Effective team communication and collaboration skills are essential to ensure patient safety and high-quality patient care (Cronenwett et al., 2007). Competency in communication helps maintain effective relationships within the entire sphere of professional practice and meets legal, ethical, and clinical standards of care. The qualities, behaviors, and therapeutic communication techniques described in this chapter characterize professionalism in helping relationships. Although the term patient is often used, the same principles apply when communicating with any person in any nursing situation. Communication and Interpersonal Relationships Caring relationships formed among a nurse and those affected by a nurse's practice are at the core of nursing (see Chapter 7). Communication is the means of establishing these helping-healing relationships. All behavior communicates, and all communication influences behavior. For these reasons communication is essential to the nurse-patient relationship. Nurses with expertise in communication express caring by the following (Watson, 1985): • Becoming sensitive to self and others • Promoting and accepting the expression of positive and negative feelings • Developing helping-trust relationships • Instilling faith and hope • Promoting interpersonal teaching and learning • Providing a supportive environment • Assisting with gratification of human needs • Allowing for spiritual expression A nurse's ability to relate to others is important for interpersonal communication. This includes the ability to take initiative in establishing and maintaining communication, to be authentic (one's self), and to respond appropriately to the other person. Effective interpersonal communication also requires a sense of mutuality, a belief that the nurse-patient relationship is a partnership and that both are equal participants. Nurses honor the fact that people are very complex and ambiguous. Often more is communicated than first meets the eye, and patient responses are not always what you expect. By giving all of your attention to a patient, you attend to the patient's needs and aid the healing process (Tavernier, 2006). Most nurses embrace the profession's view of the holistic nature of people and experience synergy in human interaction. When patients and nurses work together, much can be accomplished. Therapeutic communication occurs within a healing relationship between a nurse and patient (Arnold and Boggs, 2011). Like any powerful therapeutic agent, the nurse's communication can result in both harm and good. Every nuance of posture, every small expression and gesture, every word chosen, every attitude held—all have the potential to hurt or heal, affecting others through the transmission of human energy. Knowing that intention and behavior directly influence health gives nurses tremendous ethical responsibility to do no harm to those entrusted to their care. Respect the potential power of communication and do not carelessly misuse communication to hurt, manipulate, or coerce others. Skilled communication empowers others and enables people to know themselves and make their own choices, an essential aspect of the healing process. Nurses have wonderful opportunities to bring about good things for themselves, their patients, and their colleagues through this kind of therapeutic communication. Developing Communication Skills Gaining expertise in communication requires both an understanding of the communication process and reflection about one's communication experiences as a nurse. Nurses who develop critical thinking skills make the best communicators. They draw on theoretical knowledge about communication and integrate this knowledge with knowledge previously learned through personal experience. They interpret messages received from others, analyze their content, make inferences about their meaning, evaluate their effect, explain rationale for communication techniques used, and self-examine personal communication skills (Balzer-Riley, 2007). Critical thinking in nursing, based on established standards of nursing care and ethical standards, promotes effective communication. When you consider a patient's problems, it is important to apply critical thinking standards to ensure sound effective communication (Chitty, 2010). For example, curiosity motivates a nurse to communicate and know more about a person. Patients are more likely to communicate with nurses who express an interest in them. Perseverance and creativity are also attitudes conducive to communication because they motivate a nurse to communicate and identify innovative solutions. A self-confident attitude is important because a nurse who conveys confidence and comfort while communicating more readily establishes an interpersonal helping-trusting relationship. In addition, an independent attitude encourages a nurse to communicate with colleagues and share ideas about nursing interventions. Such an attitude often involves risk taking because colleagues sometimes question suggested nursing interventions. At the same time, an attitude of fairness goes a long way in the ability to listen to both sides in any discussion. Integrity allows nurses to recognize when their opinions conflict with those of their patients, review positions, and decide how to communicate to reach mutually beneficial decisions. It is also very important for a nurse to communicate responsibly and ask for help if uncertain or uncomfortable about an aspect of patient care. An attitude of humility is necessary to recognize and communicate the need for more information before making a decision (Paul, 1993). It is challenging to understand human communication within interpersonal relationships. Each individual bases his or her perceptions about information received through the five senses of sight, hearing, taste, touch, and smell (Arnold and Boggs, 2011). An individual's culture and education also influence perception. Critical thinking helps nurses overcome perceptual biases, or human tendencies that interfere with accurately perceiving and interpreting messages from others. People often assume that others think, feel, act, react, and behave as they would in similar circumstances. They tend to distort or ignore information that goes against their expectations, preconceptions, or stereotypes (Beebe et al., 2010). By thinking critically about personal communication habits, you learn to control these tendencies and become more effective in interpersonal relationships. As communication skills develop, competence in the nursing process also grows. You need to integrate communication skills throughout the nursing process as you collaborate with patients and health care team members to achieve goals (Box 24-1). Use communication skills to gather, analyze, and transmit information and accomplish the work of each step of the process. Assessment, diagnosis, planning, implementation, and evaluation all depend on effective communication among nurse, patient, family, and others on the health care team. Although the nursing process is a reliable framework for patient care, it does not work well unless you master the art of effective interpersonal communication. Box 24-1 Communication Throughout the Nursing Process Assessment • Verbal interviewing and history taking • Visual and intuitive observation of nonverbal behavior • Visual, tactile, and auditory data gathering during physical examination • Written medical records, diagnostic tests, and literature review Nursing Diagnosis • Intrapersonal analysis of assessment findings • Validation of health care needs and priorities via verbal discussion with patient • Documentation of nursing diagnosis Planning • Interpersonal or small-group health care team planning sessions • Interpersonal collaboration with patient and family to determine implementation methods • Written documentation of expected outcomes • Written or verbal referral to health care team members Implementation • Delegation and verbal discussion with health care team • Verbal, visual, auditory, and tactile health teaching activities • Provision of support via therapeutic communication techniques • Contact with other health resources • Written documentation of patient's progress in medical record Evaluation • Acquisition of verbal and nonverbal feedback • Comparison of actual and expected outcomes • Identification of factors affecting outcomes • Modification and update of care plan • Verbal and/or written explanation of revisions of care plan to patient The nature of the communication process requires you to constantly make decisions about what, when, where, why, and how to convey a message. A nurse's decision making is always contextual (i.e., the unique features of any situation influence the nature of the decisions made). For example, the explanation of the importance of following a prescribed diet to a patient with a newly diagnosed medical condition differs from the explanation to a patient who has repeatedly chosen not to follow diet restrictions. Effective communication techniques are easy to learn, but their application is more difficult. Deciding which techniques best fit each unique nursing situation is challenging. Communication about specific diagnoses such as cancer or end of life and dealing with patient and family emotions can be challenging, and some nurses struggle to cope with their own reactions and emotions (Sheldon et al., 2006). Throughout this chapter brief clinical examples guide you in the use of effective communication techniques. Situations that challenge a nurse's decision-making skills and call for careful use of therapeutic techniques often involve the types of persons described in Box 24-2. Because the best way to acquire skill is through practice, it is useful for you to discuss and role-play these scenarios before experiencing them in the clinical setting. Consider who is involved in the situation to decide which communication will be most effective. Box 24-2 Challenging Communication Situations • People who are silent, withdrawn, and have difficulty expressing feelings or needs • People who are sad and depressed • People with special needs • People who are angry or confrontational and cannot listen to explanations • People who are uncooperative and resent being asked to help others • People who are talkative or lonely and want someone else to be with them all the time • People who are demanding and expect others to meet their requests • People who are frightened, anxious, and having difficulty coping • People who have difficulty seeing or hearing • People who are confused and disoriented • People who speak and/or understand little English • People who are flirtatious or sexually inappropriate Levels of Communication Nurses use different levels of communication in their professional role. A competent nurse uses a variety of techniques in each level. Intrapersonal communication is a powerful form of communication that occurs within an individual. This level of communication is also called self-talk, self-verbalization, or inner thought. People's thoughts strongly influence perceptions, feelings, behavior, and self-concept. You need to be aware of the nature and content of your own thinking. Self-talk provides a mental rehearsal for difficult tasks or situations so individuals deal with them more effectively and with increased confidence (Gibson and Foster, 2007; White, 2008). Nurses and patients use intrapersonal communication to develop self-awareness and a positive self-concept that enhances appropriate self-expression. For example, you improve your health and self-esteem through positive self-talk by replacing negative thoughts with positive assertions. Interpersonal communication is one-on-one interaction between a nurse and another person that often occurs face to face. It is the level most frequently used in nursing situations and lies at the heart of nursing practice. It takes place within a social context and includes all the symbols and cues used to give and receive meaning. Because meaning resides in persons and not in words, messages received are sometimes different from intended messages. Nurses work with people who have different opinions, experiences, values, and belief systems; thus it is important to validate meaning or mutually negotiate it between participants. For example, use interaction to assess understanding and clarify misinterpretations when teaching a patient about a health concern. Meaningful interpersonal communication results in exchange of ideas, problem solving, expression of feelings, decision making, goal accomplishment, team building, and personal growth. Transpersonal communication is interaction that occurs within a person's spiritual domain. Study of the influence of religion and spirituality has increased dramatically in recent years, and ongoing research helps us understand the role of nurses in addressing a patient's spiritual needs (Pesut et al., 2008). Many people use prayer, meditation, guided reflection, religious rituals, or other means to communicate with their "higher power." Nurses have a responsibility to assess a patient's spiritual needs and intervene to meet those needs (see Chapter 35). Small-group communication is interaction that occurs when a small number of persons meet. This type of communication is usually goal directed and requires an understanding of group dynamics. When nurses work on committees, lead patient support groups, form research teams, or participate in patient care conferences, they use a small-group communication process. Small groups are most effective when they are cohesive and committed and have an appropriate meeting place with suitable seating arrangements (Arnold and Boggs, 2011). A nurse's role varies with the function of a group. He or she frequently coordinates the group, provides recognition and acceptance of the contributions of each group member, and provides encouragement and motivation to help the group meet its goals (Townsend, 2009). Public communication is interaction with an audience. Nurses have opportunities to speak with groups of consumers about health-related topics, present scholarly work to colleagues at conferences, or lead classroom discussions with peers or students. Public communication requires special adaptations in eye contact, gestures, voice inflection, and use of media materials to communicate messages effectively. Effective public communication increases audience knowledge about health-related topics, health issues, and other issues important to the nursing profession.

Crisis Components

Crisis has four defining characteristics: (1) crises are specific, unexpected, and nonroutine events; (2) crises create uncertainty; (3) crises create perceptions of threat; (4) crises are processes of transformation during which the old system can no longer be maintained and the need for change is identified (Venette, 2003). Roberts (2005) states that all crises have five common components: (1) a hazardous or traumatic event; (2) a vulnerable state; (3) a precipitating factor; (4) an active crisis state; and (5) a resolution of the crisis. Often the crises that nurses encounter during their daily practice occur in the face of actual or perceived threats to an individual's physical/biologic, psychologic/emotional, social, or spiritual integrity, but they are time limited and without residual symptoms. Caplan (1964) identified four distinct phases of crisis: Phase 1: The individual is exposed to a stressor. This precipitant stressor triggers anxiety that leads to the use of problem-solving techniques and coping strategies in an effort to solve the problem and diminish the impact of the stressor. Phase 2: Previous coping and problem-solving strategies fail to relieve the stressor. As the threat posed by the stressor persists in the context of ineffective problem solving and coping, discomfort increases. The individual is often confused, and feelings of helplessness, disorganization, and distress prevail. Phase 3: Resources from within and outside of the individual are mobilized to resolve the problem and to alleviate the discomfort caused by the stressor. If all efforts at problem solving fail, anxiety may escalate to panic, and the individual may withdraw, flee the situation, and decline in function. Note that people may drop out of situations in numerous ways, including self-medication with alcohol, drugs, or other methods that have soothed them in the past. Alternatively, new problem-solving techniques may be used, and, if these are effective, a solution may be identified to lead to the resolution of the crisis. Phase 4: The absence of crisis resolution leads to major disorganization. During this phase, tension escalates to a breaking point, cognitive function declines substantially, emotions become labile, and behavior may become irrational, aggressive, or self-injurious (Lowry and Lating, 2002). Risk Factors for Crisis Risk factors may limit an individual's ability to cope or problem solve during stressful life events or situations. These may be present across a wide range of clinical settings and include the following: • The presence of concurrent or multiple biopsychosocial stressors • Multiple losses, unexpected life changes, and unresolved problems • Limitations in adaptive ability and coping skills • Chronic physical or psychologic pain or disability • Concurrent psychiatric disorders, substance abuse, and suicidality • Poor social support networks • Limited access to health care services Nurses across many clinical settings are in unique positions to identify individuals with risk factors for crisis as a result of their daily interactions with individuals and families who are experiencing disruptions in their lives. Nurses use the risk factors assessment criteria to identify individuals and families who are at high risk for the occurrence of crises and then intervene to prevent those crises from occurring. Types of Crises Four major types of crises may manifest in health care practices with individuals, families, and the community: (1) external crises result from actual events or circumstances in the environment; (2) internal crises are subjectively perceived and experienced; (3) maturational crises may occur during the course of normal growth and developmental phases and milestones; and (4) adventitious crises occur as a result of extraordinary events. External (Situational) Crises An external crisis is precipitated by a specific external situation or event that is apparent to another observer. It usually centers on real events that threaten physical health (e.g., the inability to obtain food, clothing, or shelter) or the loss of a loved one or a valued object. Examples include the loss of a job, the death of a loved one, a change in financial status, divorce, eviction, or foreclosure. External crises may affect individuals, families, or entire communities. In addition, one external event often results in multiple crises for an individual, a family, or a community. Internal (Subjective) Crises An internal crisis is triggered by a subjective perception of threat to one's well-being that may not be obvious to the outside observer. Examples of internal crises are responses to aging, loss, abandonment, or a breach of loyalty that results in profound feelings of betrayal, fear, or victimization. An internal crisis may also result from a threat to a deeply held belief or value, thereby triggering spiritual distress or a loss of faith. Any negative thought pattern or experience of emotional distress can act as an internal stressor and trigger an internal or subjective crisis. An individual or a family can view almost any situation as a crisis, depending on their own unique internal perception of the situation or event. What constitutes a crisis for one individual or family may not for another; it depends on the stressor itself and the family's internal perceptions of it. Other relevant factors include other stressors that the family is experiencing, the family's coping ability, the extent of available family resources, and prior experience with crises (Clark, 2008). Phase-of-Life (Maturational) Crises Humans experience normal and predictable changes throughout their lives, and these may precipitate phase-of-life or maturational crises for some individuals. Adolescence, career choices, marriage, parenthood, midlife, retirement, and aging represent some of the changes that are experienced along life's continuum. For example, a family may experience a crisis when the child leaves home for the first time for college or the military. The term midlife crisis describes the challenging transitions of middle adulthood. Age-related changes often bring a loss of strength, mobility, or balance; reduced memory; slower thinking; and other declining cognitive and physical abilities that may trigger crises. Each life phase brings with it expectations from oneself and others, challenges that often increase vulnerability to crisis, and the feeling that one needs to modify coping mechanisms accordingly. Differing beliefs about life changes, what they represent, and how they are experienced by the individual or family often determine whether or not a phase-of-life crisis occurs. Regardless of whether the crisis is internal or external, expected or unexpected, and actual or perceived, if coping abilities fail to remove the perception of threat to one's safety and restore equilibrium, a crisis will be experienced internally. It is this internal experience that becomes the focal point of crisis assessment and intervention. Disasters (Adventitious Crises) An adventitious crisis is precipitated by a disaster that is not part of everyday life. This type of crisis can arise from the following: • Natural disasters (e.g., hurricanes, fires, earthquakes) • National or global disasters (e.g., manmade disasters, including acts of terrorism, war, riots, and airplane crashes; environmental catastrophes, including oil spills and global disease outbreaks) • Crimes of violence (e.g. rape, assault, bomb threats, homicide, violence in school settings, abuse) (see Chapter 23). Since the 1990s, the mass media and the Internet have brought countless images of traumatic events and disasters into closer view for millions of people around the globe. The ongoing media coverage of events such as the New York terrorist attacks of September 11, 2001, and of the massive oil spill in the Gulf of Mexico in 2010 changed the landscape of awareness of the impact that multiple dimensions of adventitious crises have on people across the street as well as across the globe. Nurses and other health care personnel must be prepared when they are called to respond to manmade disasters and to natural disasters, which appear to be occurring with greater frequency and intensity than ever before. The increasing frequency and intensity of natural disasters are the result of multiple changing global factors (Landesman, 2005; Perry, 2007; Walström, 2010). Human Responses to Crisis A person's response to crisis is often an ordinary response to an extraordinary event. It does not represent psychopathology but rather a struggle to find strategies and solutions that will restore the balance and equilibrium of homeostasis. During a crisis, biologic, psychologic, social, and spiritual homeostasis are disrupted, and the individual perceives a sudden loss of his or her ability to use effective problem solving and coping skills. Physical, emotional, social, and spiritual distress may result, and the response to such distress can be either adaptive or maladaptive. When the response is adaptive, although the individual is temporarily unorganized, he or she is able to take action and seek a solution. When the response is maladaptive, the individual experiences prolonged or excessive periods of disorganization, tension, anxiety, hopelessness, and helplessness, and he or she is less likely to take action to find a solution. An individual's interpretation of the crisis is based on his or her perception of the event, prior learning, memory, and previous outcomes to similar situations. Nurses use the biopsychosocial-spiritual model when assessing a patient in a crisis situation to determine if the response is adaptive or maladaptive. Intervention for patients with adaptive responses is supportive, but maladaptive responses frequently require additional intervention. In each case, the opportunity for growth and change exists. In a crisis, an individual's coping abilities fail. Coping is an adjustment reaction or the use of habitual patterns of behavior by an individual in response to an actual or perceived threat in an effort to maintain psychologic integrity (Aguilera, 1998). Figure 21-1 illustrates the process and outcomes of crisis. Click to view full size figure FIGURE 21-1 A paradigm that illustrates the effects of balancing factors during a stressful event. Coping abilities emphasize various conscious and unconscious strategies that are used to deal with stress and tension. Human coping abilities manifest as fight-or-flight reactions or freeze reactions such as anxiety, hypervigilance, sleep disturbance, emotional or physical withdrawal, denial, emotional numbing, and impaired concentration and ability to focus during normal daily functioning (Flannery and Everly, 2000). During crisis, denial is a common defense mechanism and method of coping. Denial can help people to endure and process a reality that is psychologically overwhelming for them at the time, and it can lessen the intensity of the shock that often accompanies the early phase of crisis until other coping resources can be mobilized by the individual. Coping does not imply mastery over the crisis; rather, it is the process that is used to respond to the crisis and find resolution. During a crisis, biopsychosocial homeostasis or equilibrium is disrupted. The American Academy of Experts in Traumatic Stress (1999) identified the following immediate potential responses to crisis or trauma: • Shock • Numbness • Denial • Dissociative behavior • Confusion • Disorganization • Difficulty making decisions • Suggestibility • Physiologic symptoms, such as nausea, vomiting, tremors, profuse sweating, and dizziness Many individuals experience such symptoms immediately after a crisis or traumatic event, and they may continue for a limited time after the actual crisis event. According to the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision (DSM-IV-TR), an acute stress disorder (ASD) may manifest when a person is in crisis (American Psychiatric Association, 2000). ASD is an anxiety disorder that is characterized by a cluster of dissociative and anxiety symptoms that occur within 1 month of a major traumatic stressor. The immediate cause of ASD is exposure to an extreme stressor that involves a threat to life, physical integrity, or the potential for serious injury or witnessing an event that involves the death or serious injury of another person and reacting to the event with marked fear, helplessness, or horror. Either during or after the experience of the traumatic event, the individual has at least three of the following dissociative symptoms: 1 A subjective sense of numbing or detachment or the absence of emotional responsiveness 2 A reduction in the awareness of his or her surroundings (e.g., "being in a daze") 3 Derealization 4 Depersonalization 5 Dissociative amnesia (i.e., the inability to recall an important aspect of the trauma) In addition, the traumatic event is persistently reexperienced in at least one of the following ways: recurrent images, thoughts, dreams, or flashbacks; a sense of reliving the experience; or distress on exposure to reminders of the traumatic event. There is marked avoidance of stimuli that trigger recollections of the trauma (e.g., thoughts, feelings, conversations, activities, places, people) and marked anxiety symptoms or increased arousal symptoms (e.g., difficulty sleeping, irritability, poor concentration, hypervigilance, exaggerated startle response, motor restlessness). The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning or impair the individual's ability to pursue goals, complete activities of daily living, or mobilize the necessary personal help and assistance. The symptoms of ASD last for a minimum of 2 days and a maximum of 4 weeks, and they occur within 4 weeks of the traumatic event (American Psychiatric Association, 2000.) These symptoms are not necessarily cause for long-term intervention; most research indicates that the immediate response to the acute event is time-limited and responsive to crisis intervention and brief therapy in the majority of cases. However, if symptoms persist for more than 1 month, additional long-term therapy is usually indicated, and assessment for other diagnoses may be also be considered, such as posttraumatic stress disorder (PTSD). Several other diagnostic categories or symptom patterns are related to crisis. According to the DSM-IV-TR, crisis is not viewed as a distinct diagnostic category; rather, it is associated with several psychiatric disorders or categories of symptoms. In addition to ASD, the most common disorders include depression, anxiety, adjustment disorders, and PTSD. There has been a notable increase in the incidence of PTSD, which is due in large part to the numbers of military personnel who were diagnosed with the disorder. PTSD has been of great interest to clinicians and researchers over the past two decades, and it continues to receive attention for many reasons. PTSD is frequently associated with crises; a detailed description of the disorder appears in Chapter 10. Nurses use the biopsychosocial-spiritual model when assessing a patient in a crisis situation to determine if the response is adaptive or maladaptive. Interventions for patients with adaptive responses are usually supportive, but maladaptive responses frequently require additional intervention. In each case, the opportunity for growth and change exists. Psychological Stages after a Disaster According to New York State Office of Mental Health (2006), there are predictable phases that are experienced by groups of people or communities after any type of disaster: 1 Heroic phase. This occurs immediately after the event, and it is a time of altruism and heroic behavior in the community. 2 Honeymoon phase. This occurs 1 week to 3 to 6 months after the event, when feelings of community sharing and high social attachment exist. 3 Disillusionment phase. This occurs 2 months to 1 to 2 years after the event, and it is characterized by feelings of disappointment, anger, resentment, and bitterness regarding the expectations of support that were not met. 4 Reconstruction phase. This occurs 2 months to 1 to 2 years after the event, when physical and emotional reinvestment take place. Individuals proceed through these stages at their own pace. Nurses who are providing care need to recognize these stages and provide appropriate interventions that are closely matched to the phase that the patient or community is experiencing. Populations that are at special risk for adverse mental health conditions after a disaster or traumatic event include children and adolescents, the elderly, refugees and migrant groups, and the developmentally or mentally disabled (Langan and James, 2005). During Hurricane Katrina, the most affected population was the poor. They were stranded on highway overpasses, roofs, and in the Superdome and Convention Center without adequate food and water, and they became quickly overwhelmed with fear and a sense of hopelessness (Rhoads, 2006). However, even among the most vulnerable, some individuals perceive the stress associated with a disaster quite differently from others. Some individuals tend to feel empathy or survivor guilt after a disaster. It appears that a disaster often transforms behavior from isolation to increased interaction with others after the first response of shock and disbelief. Individual identities are set aside, altruism emerges, and, for a time, the focus is on the community (Dane, 2001). The literature documents that disaster experiences appear to promote personal growth and strengthen relationships in many cases (Friedman, 2005).

ACUTE GASTRITIS Etiology and Risk Factors

The acute form of gastritis may be seen with nausea and vomiting, epigastric discomfort, bleeding, malaise, and anorexia. It usually stems from ingestion of a corrosive, erosive, or infectious substance. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), digitalis, chemotherapeutic drugs, radiation therapy, steroids, acute alcoholism and cocaine use, food poisoning (typically caused by Staphylococcus organisms), and HIV/AIDS are common causes. In addition, food substances, including excessive amounts of tea, coffee, mustard, paprika, cloves, and pepper, can precipitate acute gastritis. Foods with a rough texture or those eaten at an extremely high temperature can also damage the stomach mucosa. Ingestion of corrosive agents, such as lye or drain cleaner, also causes acute gastritis with the damage/loss of the mucosal layer. Disorders linked with acute gastritis include uremia, shock, central nervous system lesions, hepatic cirrhosis, portal hypertension, and prolonged emotional tension. Acute gastritis is usually of short duration unless the gastric mucosa has suffered extensive damage, or is untreated, in which case it may evolve into chronic gastritis. Health promotion behaviors include limited use of NSAIDs, alcohol, and caffeine and avoidance of nicotine products, both smoking and chewing. Health maintenance behaviors include use of enteric-coated aspirin, cytoprotective agents (sucralfate [Carafate], misoprostol [Cytotec], and bismuth subsalicylate [Pepto-Bismol]) to protect the stomach lining, histamine-receptor antagonists to decrease gastric acidity, or proton pump inhibitors to block gastric acid production. Clients with medical disorders that may lead to gastritis should follow orders for prescribed medications to minimize stomach irritation. Pathophysiology The most common causes of acute gastritis are infectious. The pathogens include Helicobacter pylori, Escherichia coli, Proteus, Haemophilus, streptococci, and staphylococci. Bacterial infection of the stomach is rare but may be life-threatening. The mucosal lining of the stomach normally protects it from the action of gastric acid, and gastric acid may protect the stomach from bacterial infection. If this barrier is penetrated by inflammation and necrosis, infection occurs, with resultant injury to the mucosa. When hydrochloric acid comes into contact with the mucosa, injury to small vessels occurs with edema, hemorrhage, and possible ulcer formation. The damage associated with acute gastritis is usually limited if treated promptly. Clinical Manifestations Assessment typically reveals epigastric discomfort usually described as burning or aching, abdominal tenderness, cramping, belching, reflux, severe nausea and vomiting, and sometimes hematemesis. Sometimes GI bleeding is the only manifestation. When contaminated food is the cause of gastritis, diarrhea usually develops within 5 hours of ingestion of the offending substance. Diagnosis is based on a detailed history of food intake, medications taken, and any disorders related to gastritis. The physician may also perform a gastroscopic examination with a biopsy to determine histologic (cell) changes as well as epithelial degeneration (response to injury).

Plan of Care and Implementation

The nurse functions in the roles of teacher, encourager, and supporter rather than doer while implementing the psychosocial plan of care for a postpartum woman. Implementation of the psychosocial care plan involves carrying out specific activities to achieve the expected outcome of care planned for each individual woman. Topics that should be included in the psychosocial plan of care include promotion of parenting skills and family member adjustment to the newest member. These topics are discussed in Chapter 22. Cultural issues must also be considered when planning care. In contrast with allopathic medicine, many traditional health beliefs and practices occur among the different cultures within the North American population. Traditional health practices that are used to maintain health or to avoid illnesses deal with the whole person (body, mind, and spirit) and tend to be culturally based (Kim-Godwin, 2003; White, 2004). Women from various cultures may view health as a balance between opposing forces (e.g., yin versus yang), being in harmony with nature, or just "feeling good." Traditional practices may include the observance of certain dietary restrictions, clothing, or taboos for balancing the body; participation in certain activities such as sports and art for maintaining mental health; and use of silence, prayer, or meditation for developing spiritually. Practices (e.g., using religious objects or eating garlic) are used to protect oneself from illness and may involve avoiding people who are believed to create hexes, spells, or who have an "evil eye." Restoration of health may involve a person taking folk medicines (e.g., herbs or animal substances) or using a traditional healer (White, 2004). Childbirth occurs within this sociocultural context. Rest, seclusion, dietary restraints, and ceremonies honoring the mother are all common traditional practices that are followed for the promotion of the health and well-being of the mother and baby (Davis, 2001; Kridli, 2002; Lauderdale, 1999; Mattson, 2000). Women and their families use several common traditional health practices and hold various beliefs during the postpartum period. In Southeast Asia, for example, the body is thought to be in a "cold" state after birth because of the loss of blood, which is considered a "hot" substance. Therefore balance needs to be restored by increasing the return of yang forces present physically or symbolically in hot food, hot water, and warm air (Davis, 2001; Kim-Godwin, 2003; White, 2004). Vietnamese, Cambodian, and Hmong women believe that if they do not follow the traditional diet or get sufficient rest after childbirth, they will likely become ill or develop serious health problems later in life (Davis, 2001; White, 2004). Khmer women may practice "roasting" in which they lie on a bamboo bed for periods over a wood or charcoal fire to restore heat. Ghosts are attracted to blood, thus Khmer women are vulnerable to attack by ghosts in the postpartum period (White, 2004) (Cultural Awareness box). Another common belief is that the mother and baby remain in a weak and vulnerable state for a period of several weeks following birth (Davis, 2001; Mattson, 2000; White, 2004). During this time the mother may remain in a passive role, take no baths or showers, and stay in bed to prevent cold air from entering her body. Women who have immigrated to the United States or other Western nations without their extended families may not have much help at home, making it difficult for them to observe these activity restrictions (Davis, 2001). Box 21-8 lists some common cultural beliefs about the postpartum period and family planning. Box 21-8 Some Cultural Beliefs about the Postpartum Period and Family Planning Postpartum Care Chinese, Mexican, Korean, and Southeast Asian women may wish to eat only warm foods and drink hot drinks to replace blood loss and to restore the balance of hot and cold in their bodies. These women may also wish to stay warm and avoid bathing, exercises, and hair washing for 7 to 30 days after childbirth. Self-care may not be a priority; care by family members is preferred. The woman has respect for elders and authority. These women may wear abdominal binders. They may prefer not to give their babies colostrum. Haitian women may request to take the placenta home to bury or burn. Muslim women follow strict religious laws on modesty and diet. A Muslim woman must keep her hair, body, arms to the wrist, and legs to the ankles covered at all times. She cannot be alone in the presence of a man other than her husband or a male relative. Observant Muslims will not eat pork or pork products and are obligated to eat meat slaughtered according to Islamic laws (halal meat). If halal meat is not available, kosher meat, seafood, or a vegetarian diet is usually accepted. Family Planning Birth control is government mandated in mainland China. Most Chinese women will have an IUD inserted after the birth of their first child. Women do not want hormonal methods of contraception because they fear putting these medications in their bodies. Saudi Arabian and Hispanic women will likely choose the rhythm method because most are Catholic. (East) Indian men are encouraged to have voluntary sterilization by vasectomy. Muslim couples may practice contraception by mutual consent as long as its use is not harmful to the woman. Acceptable contraceptive methods include foam and condoms, the diaphragm, and natural family planning. Hmong women highly value and desire large families, which limits birth control practices. It is important that nurses consider all cultural aspects when planning care and not use their own cultural beliefs as the framework for that care. Although the beliefs and behaviors of other cultures may seem different or strange, they should be encouraged as long as the mother wants to conform to them, and she and the baby have no ill effects. The nurse must determine whether a woman is using any folk medicine during the postpartum period because active ingredients in folk medicine may have adverse physiologic effects on the woman when ingested with prescribed medicines (Mattson, 2000). However, the nurse should not assume that a mother desires to use traditional health practices that represent a particular cultural group just because she is a member of that culture. Many young women who are firstgeneration or second-generation Americans follow their cultural traditions only when older family members are present, or not at all.

Establishing a Therapeutic Relationship

The nurse must quickly establish a therapeutic relationship with the woman and her significant other. The woman's first impression influences her perception of the quality of her entire birth experience. Making the Family Feel Welcome. A warm greeting makes the woman and her significant other feel valued. Even if the unit is busy, the nurse should communicate interest, friendliness, caring, and competence. People understand if the nurse is busy, but they do not understand rudeness and insensitivity to their needs. Nurses often encounter women who speak a language other than English. Arranging for a culturally acceptable interpreter who is fluent in the woman's language makes the woman and her family feel welcome and promotes safety because it enhances understanding among the woman, her family, and the nurse. ▪ When caring for a woman who has not had prenatal care or childbirth classes, which are behaviors that most nurses value, the nurse must not be judgmental in either words or actions. The woman's priorities and values may be different from those of the nurse, but she deserves the same respect, support, and care as the woman who made every preparation for her baby's birth. Determining Family Expectations about Birth. Regardless of their number of children, women and their partners have expectations about the birth experience. The partners may have studied their options extensively and planned a birth that best fits their ideals. Those who have not made specific plans also have expectations shaped by contact with relatives and friends and previous birth experiences. A couple may want to repeat a previous satisfying experience or avoid repeating a poor experience. Sometimes one part of a past birth has negatively influenced the couple's impression of the entire experience. Conveying Confidence. From the first encounter, the nurse should convey confidence and optimism in the woman's ability to give birth and the ability of her significant other to support her. Women having their first baby may be overwhelmed by the power of normal labor contractions. The nurse can reassure these women that intense contractions are normal in active labor while helping them manage contractions and watching for true problems. ▪ Think about the different perspectives implied by the phrases give birth and be delivered. The woman who gives birth is an active and able participant; she is the principal action figure. However, the language of be delivered implies that the woman is passive. The nurse might ask "Who will attend you as you give birth?" rather than "Who will deliver your baby?" Assigning a Primary Nurse. Having one nurse give care during all of labor is ideal but often unrealistic. However, changes in caregivers should be as limited as possible. The woman should know the name of and what to expect from each caregiver. For example, the primary nurse might explain the role of a nursing student in the woman's care. Common roles of nursing students in the intrapartum area include promoting comfort, giving emotional support, and helping the primary nurse observe for maternal and fetal problems. Using Touch for Comfort. Touch can communicate acceptance and reassurance and provide physical and emotional comfort to many laboring women. Women who usually do not welcome touch may appreciate it during labor. Cultural norms and personal history influence a woman's comfort with touch from an unrelated person. The nurse should not assume that the woman desires touch but instead ask her if she welcomes or benefits from touch. As labor progresses, the woman's desire for touch may change, and touch may become irritating rather than comforting. Respecting Cultural Values. Cultural beliefs and practices give structure, meaning, and richness to the birth experience. They influence the behavior of both the childbearing family and the professional staff. Most cultural groups have specific practices related to childbearing. The nurse should incorporate a family's beneficial and neutral cultural practices into care as much as possible. ▪ People naturally believe that their own cultural values are best. The nurse should avoid using an attitude that is superior or diminishes the validity of another person's cultural beliefs. Trust in technology is a common value of many caregivers in the United States, but such reliance on technology is considered unnecessary, odd, and even harmful by many other cultures. Check Your Reading 1. What communication skills can the nurse use to establish a therapeutic relationship when the woman and her family enter the hospital or birth center? 2. How can the nurse incorporate a couple's cultural practices into intrapartum care?

Cognitive Strategies

When intervening in the cognitive area, nurses have three major aims, which require that they begin with the patient's conceptualization of the problem: • To increase the patient's sense of control over goals and behavior • To increase the patient's self-esteem • To help the patient modify dysfunctional thinking patterns Depressed Patients. Depressed patients often see themselves as victims of their moods and environment. They do not see their behavior and their interpretation of events as possible causes of depression. They assume a passive stance and wait for someone or something to lift their mood. One task of the nurse, therefore, is to move patients beyond their limiting preoccupation to other aspects of their world that are related to it. To do this, the nurse must progress gradually. The first step is to help patients explore their feelings. This is followed by eliciting their view of the problem. In so doing the nurse accepts the patient's perceptions but need not accept the patient's conclusions. Together they define the problem to give the patient a sense of control, a feeling of hope, and a realization that change may indeed be possible. Nursing actions should then focus on modifying the patient's thinking. Depressed patients are dominated by negative thoughts. Often, despite a successful performance, the patient will view it negatively. Cognitive changes may be brought about in a variety of ways, as described in Chapter 29. Often, negative thinking is an automatic process of which the patient is not even aware. The nurse can help patients identify their negative thoughts and decrease them through thought stopping or substitution. Concurrently, the patient can be encouraged to increase positive thinking by reviewing personal assets, strengths, accomplishments, and opportunities. Next, the patient can be helped to examine the accuracy of perceptions, logic, and conclusions. Misperceptions, distortions, and irrational beliefs become evident. The patient also should be helped to move from unrealistic to realistic goals and to decrease the importance of unattainable goals. All these actions enhance the patient's self-understanding and increase self-esteem. More detailed interventions related to alterations in self-concept, which are inherent in disturbances of mood, are explored in Chapter 17. Also, because the depressed patient tends to be overwhelmed by despair, it is important to limit the amount of negative evaluation in which the patient engages. One way is to involve the patient in productive tasks or activities; another way is to increase the level of socialization. These benefit the patient in two complementary ways: They limit the time spent on brooding and self-criticism, and they provide positive reinforcement. Manic Patients. Cognitive therapy and other focused psychosocial interventions have been found to enhance relationship functioning and life satisfaction among patients with bipolar disorder (Miklowitz et al, 2007). Manic patients need to gain control over their thoughts and behaviors. Here, however, the challenge is to bring together a patient's scattered thoughts and ideas to help the patient engage in adaptive, goal-directed behavior. The communication skills of focusing, clarifying, and confrontation are useful in redirecting a patient's self-expressions. Once this is accomplished, the nurse can begin to help the patient modify dysfunctional thinking. Manic patients often have problems of grandiose thoughts, overestimation of self, and unrealistic pursuits. As in depression, cognitive interventions can help the patient evaluate these thought problems and identify more realistic and ego-supportive goals. It is also important for the nurse to realize the meaning, nature, and value the manic patient places on behavior and mood change. For example, research has shown that patients with bipolar disorder receive pronounced short- and long-term positive effects from their illness. These include increases in productivity, creativity, sensitivity to surroundings, social friendliness, and sexual intensity. These effects can provide a great deal of secondary benefit from the illness and can be powerful reinforcers of maladaptive responses, thus making change more difficult. For some patients, at some times the perceived positive consequences of the illness may outweigh their perception of the negative consequences.

Implications for Nursing

According to Huff and Kline (1999), there are four areas of focus for culturally competent care: (1) developing cultural awareness or sensitivity to differences; (2) gaining cultural knowledge of values, beliefs, and lifeways of other groups; (3) developing skills in cultural assessment as a basis for intervention; and (4) engaging in direct cultural encounters or immersion in cultural experiences. These approaches build a basis for effective care strategies, enabling the nurse to promote self-care and effective lifestyle changes (Pender, Murdaugh, & Parsons, 2002). Cross-cultural experiences also present an opportunity for the health care professional to expand cultural sensitivity, awareness, and skills. All cultures maintain behavioral norms and expectations for each stage of the perinatal cycle. These norms and expectations evolve from a culture's view of how people stay healthy and prevent illness. A culture's economic, religious, kinship, and political structures pervade its beliefs and practices regarding childbearing. To practice with cultural competence, nurses must understand the ways in which people of different cultures perceive life events and the health care system. Patients have a right to expect that their physiologic and psychologic health care needs will be met and that their cultural and spiritual beliefs will be respected.

Cultural Assessment

All health care professionals must develop skills in performing a cultural assessment so that they can understand the meaning of childbirth in different cultural groups. The following questions might be considered in making such an assessment: ▪ What is the family's ethnic affiliation? ▪ Is childbearing viewed as a normal process, a time of vulnerability, or a state of illness? ▪ What are the prescribed practices, customs, and rituals related to diet, activity, and behavior during pregnancy and childbirth? ▪ What maternal restrictions or precautions are considered necessary during pregnancy and childbirth? Are women exempted from any religious expectations at this time? ▪ Who provides support during pregnancy, childbirth, and beyond? ▪ What are the prescribed practices and restrictions related to care of the newborn? ▪ Who in the family hierarchy makes health care decisions? ▪ How is time marked—by minutes and hours, or by seasons and body needs? ▪ What are the views of life and death, including predestination and fatalism? ▪ How can health care professionals be most helpful? After such an assessment, plans for care should show respect for cultural differences and traditional healing practices. (Additional information is presented throughout this book relating to culture-specific areas such as nutrition, pregnancy, birth, and the postpartum period.) Check Your Reading 12. Why is it important for nurses to examine their own cultural values and beliefs? 13. How might communication be a source of conflict? 14. How is culture comparable to an iceberg?

Management

Although most moles abort spontaneously, suction curettage offers a safe, rapid, and effective method of evacuating a hydatidiform mole if necessary (Cunningham et al., 2005; Gilbert, 2007). Induction of labor with oxytocic agents or prostaglandins is not recommended because of the increased risk of embolization of trophoblastic tissue (Gilbert). Administration of Rho(D) immune globulin to women who are Rh negative is necessary to prevent isoimmunization. The nurse provides the woman and her family with information about the disease process, the necessity for a long course of follow-up, and the possible consequences of the disease. The nurse helps the woman and her family cope with the pregnancy loss and recognize that the pregnancy was not normal. In addition, the woman and her family are encouraged to express their feelings, and information is provided about support groups or counseling resources as needed. Explanations about the importance of postponing a subsequent pregnancy and contraceptive counseling are provided to emphasize the need for consistent and reliable use of the method chosen. NURSING ALERT To avoid confusion with signs of pregnancy, pregnancy should be avoided for 6 months to 1 year. Any contraceptive method except an IUD is acceptable. Oral contraceptives are preferred because they are highly effective.

Behaviors Associated With Delirium

Delirium is the behavioral response to widespread disturbances in cerebral metabolism. It should be considered any time there is an acute change in mental status. Although delirium can occur at any age, advanced age is probably the greatest risk factor. It often occurs in hospitalized patients but also can occur after hospitalization and in many cases may result from medications or medical procedures. QUALITY AND SAFETY ALERT • Delirium manifests as a sudden decline from a previous level of functioning. • It is often considered a medical emergency that can lead to death or permanent cognitive decline if not treated. Delirium results in disturbances in the following areas: • Consciousness—reduced clarity or awareness of the environment • Attention—impaired ability to direct and maintain mental focus, resulting in problems with processing stimuli into information • Cognition—recent memory impairment, disorientation to time and person, or language disturbance • Perception—misinterpretations, illusions, or hallucinations • Motor ability—poor balance, ambulation, or coordination The patient experiences a reduced awareness of the environment that involves sensory misperceptions and disordered thought (disturbed attention, memory, thinking, orientation) and also disturbances of psychomotor activity and the sleep-wake cycle. These disturbances develop rapidly (over hours to days) and tend to fluctuate over the course of the day, with occasional periods of mental clarity. The disturbances usually worsen at night. The clinical example that follows illustrates the behavior typical of a patient who is delirious. CLINICAL EXAMPLE Ms. S was brought to the emergency department of a general hospital by her parents. This 22-year-old single woman was described as having been in good health until 2 days before admission, when she complained of malaise and a sore throat and stayed home from work. She worked as a secretary in a small office and had a stable employment record. According to her parents, she had an active social life, and there were no significant conflicts at home. On admission, Ms. S was extremely restless and had a frightened facial expression. Her speech was garbled and incoherent. When approached by an unfamiliar person, she would become agitated, try to climb out of bed, and strike out aimlessly. Occasionally she would slip into a restless sleep. Her temperature on admission was 104° F (40° C), her pulse was 108 beats per minute, and her respirations were 28 per minute. Her skin was hot, dry, and flushed. According to her mother, Ms. S had only a few sips of water in the last 24 hours and had not urinated at all, but she had experienced several episodes of profuse diaphoresis. Ms. S's ability to cooperate with a mental status examination was limited. She would respond to her own name by turning her head. When her mother asked her where she was, she said "home," but she could not say where her home was. She would give only the month when asked for the date and said it was January (the actual date was February 19). She also refused to give the day of the week. A neurological examination was negative for signs of increased intracranial pressure and for localized signs of central nervous system (CNS) disease. The tentative medical diagnosis was delirium secondary to fever of unknown origin. Symptomatic treatment of the fever, including intravenous fluids, an aspirin suppository, and a cool water mattress, was begun immediately while further diagnostic studies were performed. Nurses caring for Ms. S noticed that she continued to be restless and disoriented and that her speech was still incoherent. They also noticed that she was picking at the bed clothing. Suddenly she became extremely agitated and tried to get out of bed while crying out, "Bugs, get away, get bugs away!" She was brushing and slapping at herself and the bed. As her mother and the nurse talked with her and held her, she gradually became calmer but periodically continued to slap at "the bugs" and needed reassurance and reorientation. Additional laboratory results became available later in the day. A lumbar puncture was performed, as was magnetic resonance imaging (MRI) of the head; results were normal. Results of a toxicological screening of the blood also were negative. However, the electroencephalogram (EEG) revealed diffuse slowing. In addition, the elevated white blood count and electrolyte imbalance were consistent with severe dehydration. Cultures of Ms. S's throat and blood were both positive for β-hemolytic streptococci, and intravenous antibiotic therapy was begun at once while other supportive measures were continued. Ms. S's mental state improved as the infection gradually came under control and the fever decreased. Her cognitive functioning was completely normal when she was discharged from the hospital, with the exception of amnesia for the time during which she was delirious. Selected Nursing Diagnoses • Hyperthermia related to infection, as evidenced by elevated temperature; hot, dry, flushed skin; and diaphoresis • Deficient fluid volume related to decreased fluid intake, as evidenced by anuria for 24 hours and hot, dry, flushed skin • Risk for injury related to fear and disorientation, as evidenced by agitated behavior and hallucination of bugs • Impaired verbal communication related to altered brain chemistry, as evidenced by garbled and incoherent speech Ms. S demonstrated many behaviors often seen in patients with delirium. These behaviors have a sudden onset and are related to alterations in neurochemical and electrical responses in the brain as a result of the stressor that causes the maladaptive response. Disorientation is generally present and sometimes in all three aspects of time, place, and person. Thought processes are usually disorganized. Judgment is poor, and there is a lack of sound decision-making. Stimuli may be misinterpreted, resulting in illusions or distortions of reality. An example of such an illusion is the perception that a polka-dot drape is actually covered with cockroaches. Delirious patients may hallucinate. These hallucinations are usually visual and often take the form of animals, reptiles, or insects. They are real to the person experiencing them and are very frightening. Assaultive or destructive behavior may be the patient's attempt to strike back at a hallucinated image. At times, patients with delirium also exhibit a labile affect, changing abruptly from laughter to tearfulness and vice versa for no apparent reason. A loss of usual social behavior also may be noted and may result in acts such as undressing, playing with food, and grabbing at others. Delirious patients tend to act on impulse. Other behaviors may be specifically related to the cause of the behavioral syndrome. For example, Ms. S's brain syndrome and the fever and dehydration she experienced were a result of her systemic streptococcal infection. It is very important that observations of behavior be described carefully, because this helps identify the stressor. Treatment is usually conservative until a specific stressor has been isolated. Although most patients recover, it is possible for the person to develop long-term disabilities or to die as a result of the severity of the stressor. Delirium is commonly found in hospitalized patients, particularly in intensive care units (ICUs), geriatric psychiatry units, emergency departments, alcohol treatment units, and oncology units (Fricchione et al, 2008; Uguz et al, 2010). In addition, a diagnosis of delirium can be missed because the symptoms are assumed to be caused by depression. If adequate intervention does not take place, delirium may become chronic and irreversible.

Acute Intervention.

During the acute phase, it is important to monitor vital signs. Hemodynamic stability may be compromised by hypotension, fever, and tachypnea. IV fluids are ordered, and the response to therapy is monitored. Fluid and electrolyte balance is closely monitored. Frequent vomiting, along with gastric suction, may result in decreased chloride, sodium, and potassium levels. Respiratory failure may develop in the patient with severe acute pancreatitis. It is important that respiratory function be assessed (e.g., lung sounds). If acute respiratory distress syndrome develops, the patient may require intubation and mechanical ventilatory support. Because hypocalcemia can also occur, the nurse must observe for symptoms of tetany, such as jerking, irritability, and muscular twitching. Numbness or tingling around the lips and in the fingers is an early indicator of hypocalcemia. The patient should be assessed for a positive Chvostek or Trousseau sign (see Fig. 17-15). Calcium gluconate (as ordered) should be given to treat symptomatic hypocalcemia. Hypomagnesemia may also develop, necessitating the observation of serum magnesium levels.[36] Because abdominal pain is a prominent symptom of pancreatitis, a major focus of nursing care is the relief of pain (see NCP 44-3). Pain and restlessness can increase the metabolic rate and subsequent stimulation of pancreatic enzymes. Morphine may be used for pain relief. The nurse should ascertain how long the pain medication provides relief. Measures such as comfortable positioning, frequent changes in position, and relief of nausea and vomiting assist in reducing the restlessness that usually accompanies the pain. Assuming positions that flex the trunk and draw the knees up to the abdomen may decrease pain. A side-lying position with the head elevated 45 degrees decreases tension on the abdomen and may help ease the pain. Nursing measures for the patient who is on NPO status or has an NG tube should be employed. Frequent oral and nasal care to relieve the dryness of the mouth and nose is comforting to the patient. Oral care is essential to prevent parotitis. If the patient is taking anticholinergics to decrease GI secretions, there will be additional dryness of the mouth. If the patient is taking antacids to neutralize gastric acid secretion, they should be sipped slowly or inserted in the NG tube. The nurse should observe for fever and other manifestations of infection in the patient with acute pancreatitis. Respiratory infections are common because the retroperitoneal fluid raises the diaphragm, which causes the patient to take shallow, guarded abdominal breaths. Measures to prevent respiratory infections include turning, coughing, deep breathing, and assuming a semi-Fowler's position.[34] Other important assessments are observation for signs of paralytic ileus, renal failure, and mental changes. Determination of the blood glucose level should be done to assess damage to the β-cells of the islets of Langerhans in the pancreas. After pancreatic surgery the patient may require special wound care for an anastomotic leak or a fistula. Measures to prevent skin irritation should be used. These include skin barriers such as Stomahesive, Karaya paste, or Colly-Seel; pouching; and drains. In addition to protecting the skin, pouching also provides a more accurate determination of fluid and electrolyte losses and increases patient comfort. Sterile pouching systems are available. The nurse may want to consult with a clinical specialist or an enterostomal therapy nurse, if available.

GESTATIONAL TROPHOBLASTIC DISEASE

Gestational trophoblastic disease includes hydatidiform mole, invasive mole, and choriocarcinoma. Hydatidiform mole (molar pregnancy) is a condition in which the trophoblastic tissue proliferates and the chorionic villi of the placenta become swollen and fluid filled, taking on the appearance of grapelike clusters (Figure 14-3). Molar pregnancies are classified into two types: complete and partial. Chromosome banding and enzyme analysis have demonstrated that in the complete mole all genetic material is paternally derived. The mechanism of the loss of the genetic material from the ovum is unknown. No inner cell mass develops embryonically, and there is no fetal vascularization, which explains the avascular villi (vesicles). With partial mole, genetic material is maintained but the fetus is abnormal and usually aborts. The mole is distinguished from an abortion in that the mole shows trophoblastic proliferation. Some moles may develop into choriocarcinoma. Click to view full size figure FIGURE 14-3 Gestational trophoblastic disease. Note the grape-like masses within the uterus containing a hydatidiform mole. The cause is unknown, but the incidence increases with maternal age and parity. In the United States this condition is fairly rare, occurring in approximately 1 in every 1000 pregnancies. Assessment and Management Early pregnancy appears normal. Then as gestation progresses, the uterus begins to grow rapidly because of the rapid proliferation of the trophoblastic cells. However, in 20% of the moles the uterus is found to be smaller than expected. Vaginal bleeding occurs, which often is brownish (like prune juice), as well as excessive vomiting (hyperemesis gravidarum), most likely because the serum hCG levels are higher than in normal pregnancy. Symptoms of gestational hypertension (GH) occur before 24 weeks, which strongly suggests a molar pregnancy. Serial b-hCG levels and ultrasound are the primary diagnostic tools and will reveal the characteristic pattern of vesicles. Treatment begins with the evacuation of the mole by suction aspiration. Follow-up care is extremely critical for these women because of the great risk of choriocarcinoma (cancerous growth). Continued assessment includes hCG levels and ultrasound scans of the abdomen. Continued rising hCG levels are abnormal. If malignant cells are found, chemotherapy for choriocarcinoma may be started. If therapy is ineffective, metastasis is often rapid. Administration of RhoGAM to women who are Rh negative is necessary to prevent isoimmunization (see Blood Incompatibility, p. 255). The woman is monitored for a year; if the hCG serum titers are within normal limits, the woman may be assured that she is healthy. The woman often takes oral contraceptives to prevent another pregnancy and to allow the hCG levels to return to normal. If the woman becomes pregnant immediately, it would make it impossible to monitor the decline in hCG, which is the significant part of follow-up care. Psychologic support should be provided in relation to the pregnancy loss, and another pregnancy should be delayed for at least 1 year. Subsequent pregnancies should be normal, since there is a low risk of recurrence.

Juvenile Hypothyroidism

Hypothyroidism is one of the most common endocrine problems of childhood. It may be either congenital (see Chapter 8) or acquired and represents a deficiency in secretion of TH (Foley, 2001). Hypothyroidism from dietary insufficiency of iodine is now rare in the United States, since iodized salt is a readily available source of the nutrient. Beyond infancy, a number of defects may cause primary hypothyroidism. For example, a congenital hypoplastic thyroid gland may provide sufficient amounts of TH during the first year or two but be inadequate when rapid body growth increases demands on the gland. A partial or complete thyroidectomy for cancer or thyrotoxicosis can leave insufficient thyroid tissue to furnish hormones for body requirements. Radiotherapy for Hodgkin disease or other malignancies may lead to hypothyroidism (Hudson, Krasin, Metzger, et al, 2011). Infectious processes may cause hypothyroidism. It can also occur when dietary iodine is deficient. Low levels of circulating thyroid hormones and raised levels of TSH at birth characterize congenital hypothyroidism. If left untreated, congenital hypothyroidism causes mental retardation. Improvements in newborn screening have led to earlier detection and prevention of cognitive dysfunction (American Academy of Pediatrics, Rose, Section on Endocrinology and Committee on Genetics of the American Thyroid Association, et al, 2006; Nebesio, McKenna, Nabhan, et al, 2010). Thyromegaly (enlarged thyroid gland) and growth deceleration are seen in children with hypothyroidism. Growth and development are less impaired when hypothyroidism is acquired at a later age. Because brain growth is nearly complete by 2 to 3 years of age, intellectual disability and neurologic sequelae are not associated with juvenile hypothyroidism. Clinical manifestations may include dry skin, puffiness around the eyes, sparse hair, constipation, sleepiness, lethargy, and mental decline. Growth failure, delayed puberty, and excessive weight gain can also be seen. Therapy is TH replacement, the same as for hypothyroidism in the infant. In children with severe symptoms, the restoration thyroid function is achieved more gradually with administration of increasing amounts of L-thyroxine over a period of 4 to 8 weeks. This is done to avoid symptoms of hyperthyroidism. Researchers have found that children treated early continue to have mild delays in reading, comprehension, and arithmetic but should catch up over time (Rovet and Ehrlich, 2000). Adolescents may demonstrate problems with memory, attention, and visuospatial processing. Nursing Care Management The importance of early recognition of congenital hypothyroidism in the infant is discussed in Chapter 8. Growth deceleration in a child whose growth has previously been normal should alert the observer to the possibility of hypothyroidism. Treatment is daily oral TH replacement. The importance of daily compliance and the need for periodic monitoring of serum thyroid levels should be stressed to patients and their families.

Inborn Errors of Metabolism

Inborn errors of metabolism (IEMs) constitute a large number of inherited diseases caused by the absence or deficiency of a substance essential to cellular metabolism, usually an enzyme. When the normal metabolic process is interrupted as a result of a missing enzyme, an accumulation of substances precedes the interruption, the end product of the process is absent, or the process takes an alternate metabolic pathway. The consequence is manifested as an illness. Most IEMs are characterized by abnormal protein, carbohydrate, or fat metabolism. Newborn screening for IEMs varies from state to state; but all states test for at least seven core disorders, (i.e., phenylketonuria [PKU], CH, galactosemia, sickle cell disease, thalassemia, congenital adrenal hyperplasia [CAH], and cystic fibrosis [CF].* The purpose of screening is to identify children who may have a condition that benefits from early identification and treatment to prevent cognitive impairment. The screening test is most reliable if the blood sample is taken after the infant has ingested a source of protein for 24 hours. Because of early discharge of newborns, recommendations for screening include (1) collecting the initial specimen as close as possible to discharge or no later than 7 days, (2) obtaining a subsequent sample by 2 weeks of age if the initial specimen is collected before the newborn is 24 hours old, and (3) designating a primary care provider to all newborns before discharge for adequate newborn screening follow-up (Kaye and AAP Committee on Genetics, 2006). The nurse's responsibilities are to educate parents regarding the importance of screening and collect appropriate specimens at the recommended time (after 24 hours of age). With early newborn discharge before 24 hours, some authorities recommend a repeat screening for PKU within 2 weeks (Kaye and AAP Committee on Genetics, 2006). Accurate screening depends on high-quality blood spots on approved filter paper forms. The blood should completely saturate the filter paper spot on one side only. The paper should not be handled, placed on wet surfaces, or contaminated with any substance. A new screening test, tandem mass spectrometry, has the potential for identifying more than 20 IEMs in addition to the standard IEMs. With tandem mass spectrometry, earlier identification may prevent further developmental delays and morbidities in affected children (Wilcken, 2010). A major concern is that a significantly large number of infants are not rescreened for metabolic disorders after early discharge and are at risk for a missed or delayed diagnosis of a treatable disorder. Special consideration must be given to screening infants born at home who have no hospital contact. It is always necessary to confirm the screening results with diagnostic testing. Congenital Hypothyroidism CH may have a number of causes and can be either permanent or transient. Transient CH is frequently associated with maternal Graves' disease that was treated with antithyroid drugs. Most cases are sporadic (nonhereditary), but approximately 15% of all cases are transmitted as an autosomal dominant trait. The most common pathogenesis is thyroid dysgenesis, mostly with unknown causes. Worldwide the most common cause of CH resulting in hypothyroidism is iodine deficiency. However, no matter what the cause, the manifestations (Box 25-7) and management are similar. In some conditions the thyroid deficiency is severe, and manifestations develop early; in others the symptoms may be delayed for months or years. Early detection and prompt initiation of treatment are essential because their delay results in various degrees of cognitive impairment, in which the IQ loss has a direct relationship to the time that treatment is initiated. If treatment is implemented from 0 to 3 months of age, the mean IQ attained is 89 (range 64 to 107); if treatment begins at 3 to 6 months, mean IQ reaches 71 (range 36 to 96); treatment initiated after 6 months of age results in a mean IQ of 54 (range 25 to 80). Box 25-7 Clinical Manifestations of Congenital Hypothyroidism Birth* • Poor feeding • Lethargy • Prolonged jaundice (>2 weeks) • Respiratory difficulties • Cyanosis • Constipation • Bradycardia • Hoarse cry • Large anterior and posterior fontanels • Postterm • Birth weight over 4000 g (8 lbs 13 oz) Older Child • Short stature • Obesity • Varying degrees of intellectual deficits • Abnormal tendon reflexes • Slow, awkward movements Ages 6 to 9 Weeks† • Depressed nasal bridge • Short forehead • Puffy eyelids • Large tongue • Thick, dry, mottled skin • Coarse, dry, lusterless hair • Abdominal distention • Umbilical hernia • Hyporeflexia • Bradycardia • Hypothermia • Hypotension • Anemia • Widely patent cranial sutures * Clinical manifestations may not be obvious at birth, possibly because of maternal transfer of thyroid hormone to the fetus. Manifestations may be delayed in infants with certain types of familial hypothyroidism and in breastfed infants (may show after weaning). † If untreated, classical features. Results of screening tests in the United States indicate that CH occurs in approximately one in 4000 to one in 3000 newborns (Kaye and Committee on Genetics, 2006). It affects all races and ethnicities, but it is more prevalent among Hispanic and American Indian or Alaskan Native people (one in 2000 to one in 700 newborns) and less prevalent among African-Americans (one in 3200 to one in 17,000 newborns). Infants with Down syndrome have a much higher rate of either permanent or transient forms of the disorder (approximately one in 140 newborns) (Kaye and Committee on Genetics, 2006). In addition, a higher incidence of other congenital abnormalities has been observed in infants with CH. Many preterm infants have transient hypothyroidism (hypothyroxinemia) at birth as a result of hypothalamic and pituitary immaturity. Infants born before 28 weeks of gestation may require temporary thyroid hormone replacement. Some screening programs target both primary (thyroid-based) and secondary (pituitary-based) hypothyroidism. Because CH is one of the most common preventable causes of cognitive impairment, early diagnosis and treatment of this disease are essential interventions. Neonatal screening consists of an initial filter paper blood spot T4 measurement followed by measurement of thyroid-stimulating hormone (TSH) in specimens with low T4 values. Tests are mandatory in all U.S. states and territories. Although a blood sample obtained by heelstick for the spot test is best obtained between 2 and 6 days of age, specimens are usually taken within the first 24 to 48 hours or before discharge as part of a concurrent screen for other metabolic defects. Early screening can result in overdiagnosis (false positives) but is preferable to missing the diagnosis. For screening results that show a low level of T4 (<10%), TSH levels are obtained; if these are elevated (>40 mU/L), further tests to determine the cause of the disease should be administered (AAP and American Thyroid Association, 2006). Additional tests include serum measurement of T4, triiodothyronine (T3), resin uptake, free T4, and thyroid-bound globulin. Tests of thyroid gland function (thyroid scan and uptake) usually involve oral administration of a radioactive isotope of iodine (131I) and measurement of iodine uptake by the thyroid, usually within 24 hours. In CH protein-bound iodine, T4, T3, and free T4 levels are low; and thyroid uptake of 131I is decreased. Skeletal radiography is used to assess age. In newborns thyroid function studies are elevated in comparison with values in older children; therefore it is important to document the timing of the tests. In preterm and sick full-term infants, thyroid function tests are usually lower than in healthy full-term infants; a repeat T4 and TSH may be evaluated after 30 weeks (corrected age) in newborns born before that time and after resolution of the acute illness in sick full-term infants. Treatment involves lifelong thyroid hormone replacement therapy as soon as possible after diagnosis to abolish all signs of hypothyroidism and reestablish normal physical and mental development. The drug of choice is synthetic levothyroxine sodium (Synthroid, Levothroid). Optimum dosage of l-thyroxine should be able to maintain blood TSH concentration between 0.5 and 2 mU/L during the first 3 years of life (AAP and American Thyroid Association, 2006). Regular measurement of T4 levels is important to ensure optimum treatment. Bone age surveys are also performed to ensure optimum growth. The most important nursing objective is early identification of the disorder. Nurses caring for neonates must be certain that screening is performed, especially in infants who are preterm, discharged early, or born at home. Approximately 10% of cases are detected only by a second screening at 2 to 6 weeks of age. Nurses in community health need to be aware of the earliest signs of the disorder. Parental remarks about an unusually "quiet and good" baby and demonstrated symptoms such as prolonged jaundice, constipation, and umbilical hernia should lead to a suspicion of hypothyroidism, which requires a referral for specific tests. After the diagnosis is confirmed, parents need an explanation of the disorder and the necessity of lifelong treatment. The child should be referred to a pediatric endocrinologist for care. The importance of compliance with the drug regimen for the child to achieve normal growth and development must be stressed (Kaye and AAP Committee on Genetics, 2006). Because the drug is tasteless, it can be crushed and added to formula, water, or food. If a dose is missed, twice the dose should be given the next day. Unless there are maternal contraindicative factors, breastfeeding is acceptable and encouraged in infants with hypothyroidism (Lawrence and Lawrence, 2011). Parents also need to be aware of signs indicating overdose such as a rapid pulse, dyspnea, irritability, insomnia, fever, sweating, and weight loss. Ideally they should know how to count the pulse and be instructed to withhold a dose and consult their practitioner if the pulse rate is above a certain value. Signs of inadequate treatment are fatigue, sleepiness, decreased appetite, and constipation. If the diagnosis was delayed past early infancy, the chance of permanent cognitive impairment is great. Parents need the same guidance in caring for their child as do others who have an offspring with cognitive impairment. They need an opportunity to discuss their feelings regarding late recognition of the disorder. Although treatment will not reverse the intellectual deficit, it may prevent further damage. Genetic counseling is important for the rare families in which the etiology of CH is thyroid dyshormonogenesis, which is inherited in an autosomal recessive manner. Phenylketonuria PKU, an inborn error of metabolism inherited as an autosomal recessive trait (the PAH gene is located on chromosome 12q24), is caused by a deficiency or absence of the enzyme needed to metabolize the essential amino acid phenylalanine. Classic PKU is at one end of a spectrum of conditions known as hyperphenylalaninemia. Within the spectrum of hyperphenylalaninemia are conditions with varying degrees of severity, depending on the degree of enzyme deficiency. Because rarer forms are a result of a deficiency in other enzymes and are diagnosed and treated differently, the following discussion of PKU is limited to the severe, classic form. In PKU the hepatic enzyme phenylalanine hydroxylase, which normally controls the conversion of phenylalanine to tyrosine, is deficient. This results in the accumulation of phenylalanine in the bloodstream and urinary excretion of abnormal amounts of its metabolites, the phenyl acids. One of these phenylketones, phenylacetic acid, gives urine the characteristic musty odor associated with the disease. Another is phenylpyruvic acid, which is responsible for the term phenylketonuria. Tyrosine, the amino acid produced by the metabolism of phenylalanine, is absent in PKU. Tyrosine is needed to form the pigment melanin and the hormones epinephrine and T4. Decreased melanin production results in similar phenotypes of most individuals with PKU, which is blond hair, blue eyes, and fair skin that is particularly susceptible to eczema and other dermatologic problems. Children with a genetically darker skin color may be red haired or brunette. The prevalence of PKU varies widely in the United States because different states have different definition criteria for what constitutes hyperphenylalaninemia and PKU. The reported figures for PKU in the United States are one case per 15,000 live births. The incidence of the disease varies widely by ethnic groups. In Europe the incidence is one in 10,000 births; in Asia and Africa the prevalence is quite low (Blau, van Spronsen, and Levy, 2010). Clinical manifestations in untreated PKU include failure to thrive (growth failure); frequent vomiting; irritability; hyperactivity; and unpredictable, erratic behavior. Cognitive impairment is thought to be caused by the accumulation of phenylalanine and presumably by decreased levels of the neurotransmitters dopamine and tryptophan, which affect the normal development of the brain and CNS, resulting in defective myelinization, cystic degeneration of the gray and white matter, and disturbances in cortical lamination. Older children commonly display bizarre or schizoid behavior patterns such as fright reactions, screaming episodes, head banging, arm biting, disorientation, failure to respond to strong stimuli, and catatonia-like positions. The objective in diagnosing and treating the disorder is to prevent cognitive impairment. Every newborn should be screened for PKU. The most commonly used test for screening newborns is the Guthrie blood test, a bacterial inhibition assay for phenylalanine in the blood. Bacillus subtilis, present in the culture medium, grows if the blood contains an excessive amount of phenylalanine. If performed properly, this test detects serum phenylalanine levels greater than 4 mg/dL (normal value, 1.6 mg/dL), but it will not quantify the results. Other methods for testing include quantitative fluorometric assay and tandem mass spectrometry, which give an absolute value. Only fresh heel blood, not cord blood, can be used for the test. Nursing Alert Avoid "layering" the blood specimen on the special Guthrie paper. Layering is placing one drop of blood on top of the other or overlapping the specimen. This practice results in a falsely high reading, or false positive, which will lead the newborn screening department to call the family and health care provider to arrange for a diagnostic blood phenylalanine test to determine whether the newborn truly has PKU. Best results are obtained by collecting the specimen with a pipette from the heelstick and spreading the blood uniformly over the blot paper. Because of the possibility of variant forms of hyperphenylalaninemia, PKU cofactor variant screen should be performed in all children diagnosed with PKU. A major concern is that a significant number of infants are not rescreened for PKU after early discharge and are at risk for a missed or delayed diagnosis. Give special consideration to screening infants born at home who have no hospital contact and infants adopted internationally. Treatment of PKU involves restricting phenylalanine in the diet. Because the genetic enzyme is intracellular, systemic administration of phenylalanine hydroxylase is of no value. Phenylalanine cannot be eliminated from the diet because it is an essential amino acid in tissue growth. Therefore dietary management must meet two criteria: (1) meet the child's nutritional need for optimum growth, and (2) maintain phenylalanine levels within a safe range (2 to 6 mg/dL in neonates and children up to 12 years, 2 to 10 mg/dL through adolescence, and 2 to 15 mg/dL in adults) (Kaye and AAP Committee on Genetics, 2006). Professionals agree that infants with PKU who have blood phenylalanine levels higher than 10 mg/dL should be started on treatment to establish metabolic control as soon as possible, ideally by 7 to 10 days of age (Kaye and AAP Committee on Genetics, 2006). The daily amounts of phenylalanine are individualized for each child and require frequent changes on the basis of appetite, growth and development, and blood phenylalanine and tyrosine levels. Because all natural food proteins contain phenylalanine and are limited, the diet must be supplemented with a specially prepared phenylalanine-free formula (e.g., Phenex-1 for infants or Phenex-2 for children and adults). The phenylalanine-free formula is an amino acid-modified formula essential in the low phenylalanine diet to provide the appropriate protein, vitamins, minerals, and calories for optimal growth and development. Because tyrosine becomes an essential amino acid, the phenylalanine-free formula supplies an adequate amount; but in some cases additional supplementation may be needed. The phenylalanine-free amino acid-modified formula for infants has all the nutrients necessary for adequate infant growth. Because of the low phenylalanine content of breast milk, total or partial breastfeeding may be possible with close monitoring of phenylalanine levels (Lawrence and Lawrence, 2011). Most clinicians now agree that, to achieve optimal metabolic control and outcome, a restricted phenylalanine diet, including medical foods and low-protein products, most likely is medically required for virtually all individuals with classic PKU for their entire lives (Kaye and AAP Committee on Genetics, 2006). Such lifetime reduction of phenylalanine intake is necessary to prevent neuropsychologic and cognitive deficits because even mild hyperphenylalaninemia (20 mg/dL) would produce such effects. To evaluate the effectiveness of dietary treatment, frequent monitoring of blood phenylalanine and tyrosine levels is necessary. Phenylalanine levels greater than 6 mg/dL in mothers with PKU affect the normal embryologic development of the fetus, including cognitive impairment, cardiac defects, and LBW. It is recommended that phenylalanine levels below 6 mg/dL be achieved at least 3 months before conception in women with PKU (Kaye and AAP Committee on Genetics, 2006). The principal nursing considerations involve teaching the family regarding the dietary restrictions. Although the treatment may sound simple, the task of maintaining such a strict dietary regimen is demanding, especially for older children and adolescents. In addition, mothers of children with PKU may have to spend many hours preparing special foods such as low-phenylalanine snacks. Foods with low phenylalanine levels (e.g., vegetables; fruits; juices; some cereals, breads, and starches) must be measured to provide the prescribed amount of phenylalanine. High-protein foods such as meat and dairy products are eliminated from the diet. The sweetener aspartame (NutraSweet) should be avoided because it is composed of two amino acids, aspartic acid and phenylalanine, and if used decreases the amount of natural phenylalanine that is prescribed for the day. However, medications that use aspartame as the sweetener may be used if no other nonaspartame medications are available because the content of the artificial sweetener is minimal or can be counted in the total daily phenylalanine allowance. Maintaining the diet during infancy presents few problems. Solid foods such as cereal, fruits, and vegetables are introduced as usual to the infant. Difficulties arise as the child gets older. Studies show a gradual decline in diet compliance with consequent increases in blood phenylalanine levels during early adolescence and young adulthood (Channon, Goodman, Zlotowitz, et al., 2007). A decreased appetite and refusal to eat may reduce intake of the calculated phenylalanine requirement. The child's increasing independence may also inhibit absolute control of what he or she eats. Either factor can result in decreased or increased phenylalanine levels. During the school years peer pressure becomes a major force in deterring the child from eating the prescribed foods or abstaining from high-protein foods such as milkshakes and ice cream. Limitations of this diet are best illustrated by an example: a quarter-pound hamburger may provide a 2-day phenylalanine allowance for a school-age child. The assistance of a registered dietitian is essential. Parents need a basic understanding of the disorder and practical suggestions regarding food selection and preparation. Meal planning is based on weighing the food on a gram scale; a less accurate method is the exchange list. As soon as children are old enough, usually by early preschool, they should be involved in the daily calculation, menu planning, and formula preparation. Using a computer, voice-activated calculator, cards, or colored beads can help them keep track of the daily allowance of phenylalanine foods. A system of goal setting, self-monitoring, contracts, and rewards can promote compliance in adolescents. Preparation of the phenylalanine-free formula can present some challenges. The formula tends to be lumpy; mixing the powder with a small amount of water to make a paste and then adding the rest of the required liquid helps to alleviate this problem. A blender or mixer dissolves the powder more easily; a rechargeable hand mixer can be used when traveling. Although the taste is virtually impossible to camouflage, many new products are on the market today. Some of the complete formulas are chocolate, vanilla, strawberry, and orange flavored. Incomplete formulas that do not contain the vitamins and minerals and are plain tasting are also available; these can be added to cold foods instead of mixing them as a formula. Formula bars are convenient for active adolescents. Formula capsules are also available, but the patient would need to take 20 or more capsules per day. Galactosemia Galactosemia is a rare autosomal recessive disorder that results from various gene mutations leading to three distinct enzymatic deficiencies. The most common type of galactosemia (classic galactosemia) results from a deficiency of a hepatic enzyme, galactose 1-phosphate uridyltransferase (GALT), and affects approximately one of 50,000 births. The other two varieties of galactosemia involve deficiencies in the enzymes galactokinase (GALK) and galactose 4′-epimerase (GALE); these are extremely rare disorders. All three enzymes (GALT, GALK, and GALE) are involved in the conversion of galactose into glucose. As galactose accumulates in the blood, several organs are affected. Hepatic dysfunction leads to cirrhosis, resulting in jaundice in the infant by the second week of life. The spleen subsequently becomes enlarged as a result of portal hypertension. Cataracts are usually recognizable by 1 or 2 months of age; cerebral damage, manifested by the symptoms of lethargy and hypotonia, is evident soon afterward. Infants with galactosemia appear normal at birth, but within a few days of ingesting milk (which has a high lactose content) they begin to experience vomiting and diarrhea, leading to weight loss. E. coli sepsis is also a common presenting clinical sign. Death during the first month of life is frequent in untreated infants. Occasionally classic galactosemia is seen with milder, chronic manifestations such as growth failure, feeding difficulty, and developmental delay. This presentation is more frequent among African-American children with galactosemia (Kaye and AAP Committee on Genetics, 2006). Diagnosis is made on the basis of the infant's history, physical examination, galactosuria, increased levels of galactose in the blood, and decreased levels of GALT activity in erythrocytes. The infant may display characteristics of malnutrition (i.e., hypoglycemia, jaundice, hepatosplenomegaly, sepsis, cataracts, and decreased muscle tone) (Bosch, 2006). Newborn screening for this disease is required in most states. Heterozygotes can also be identified because heterozygotic individuals have significantly lower levels of the essential enzyme. During infancy treatment consists of eliminating all milk and lactose-containing formula, including breast milk. Traditionally lactose-free formulas are used, with soy-protein formula being the feeding of choice; however, some research suggests that elemental formula (galactose-free) may be more beneficial than soy formulas (Zlatunich and Packman, 2005). However, the AAP recommends the use of soy protein-based formula for infants with galactosemia, and it is considerably less expensive than elemental formula (Bhatia, Greer, and AAP Committee on Nutrition, 2008). As the infant progresses to solids, only foods low in galactose should be consumed. Certain fruits are high in galactose, and some dietitians recommend that they be avoided. Food lists should be given to the family to ensure that appropriate foods are chosen. If galactosemia is suspected, supportive treatment and care are implemented, including monitoring for hypoglycemia, liver failure, bleeding disorders, and E. coli sepsis. Nursing interventions are similar to those for PKU except that dietary restrictions are easier to maintain because many more foods are allowed. However, reading food labels carefully for the presence of any form of lactose, especially dairy products, is mandatory. Many drugs such as some of the penicillin preparations contain lactose as filler and also must be avoided. Unfortunately lactose is an unlabeled ingredient in many pharmaceuticals. Therefore instruct parents to ask their local pharmacist about galactose content of any over-the-counter or prescription medication. * Because newborn screening varies by state and policies change frequently, a good resource is the National Newborn Screening and Genetics Resource Center, www.genes-r-us.uthscsa.edu.

Therapeutic Management

Medical management includes two phases: (1) evacuation of the trophoblastic tissue of the mole and (2) continuous follow-up of the woman to detect malignant changes of any remaining trophoblastic tissue. At the same time the woman is treated for any other problems such as preeclampsia or HEG. Before evacuation, chest radiography, computed tomography (CT), or magnetic resonance imaging (MRI) may be performed to detect metastatic disease. A complete blood count, laboratory assessment of coagulation status, and blood type and screen or crossmatch are also necessary in case a transfusion is needed. Blood chemistries are done to evaluate renal, hepatic, and thyroid function. The mole usually is removed by vacuum aspiration followed by curettage. After tissue removal, IV oxytocin is given to contract the uterus. Avoiding uterine stimulation with oxytocin before evacuation is important. Uterine contractions can cause trophoblastic tissue to be pulled into large venous sinusoids in the uterus, resulting in embolization of the tissue and respiratory distress (Li, 2008). The tissue obtained is sent for laboratory evaluation. Although a hydatidiform mole is usually a benign process, choriocarcinoma may occur. Follow-up is critical to detect changes suggestive of trophoblastic malignancy. Follow-up protocol involves evaluation of serum beta-hCG levels every 1 to 2 weeks until undetectable. The test is then repeated every 1 to 2 months for a year. A persistent or rising beta-hCG level suggests continued gestational trophoblastic disease. Pregnancy must be avoided during the 1-year follow-up because the normal rise of beta-hCG level in pregnancy would obscure evidence of choriocarcinoma. Oral contraceptives are the preferred birth control method (Cahill & Wardle, 2006; Copeland & Landon, 2007; Li, 2008).

Biguanides ♦ metformin (Glucophage, Glucophage XR, Riomet); Fortamet, Glycon, Glucophage Indications

Metformin is an insulin-sensitizing drug with potent antihyperglycemic properties. It is used in combination with diet and exercise therapy for lowering blood glucose levels in patients with T2DM. Metformin is effective as monotherapy or in combination with sulfonylureas, insulin, and thiazolidinediones. Clinically, metformin lowers fasting and postprandial hyperglycemia. Metformin also decreases plasma very low-density lipoprotein (VLDL) triglycerides, resulting in modest decreases in plasma triglycerides and total cholesterol. Metformin reduces FBS by 50 to 70 mg/dL and A1c by 1.5% to 2%. Use of metformin is appropriate for patients who are overweight or obese and have insulin resistance. Pharmacodynamics Metformin acts primarily to reverse the defects of diabetes by reducing hepatic glucose production, but also by reducing intestinal glucose production and increasing insulin sensitivity (improved peripheral glucose uptake and utilization). Its major mode of action is to reduce hepatic glucose output, which is increased at least twofold in patients with T2DM. Metformin does not increase insulin secretion from the pancreas, and is not associated with hypoglycemia at therapeutic doses except in special situations. Metformin does not cause weight gain. Pharmacokinetics Metformin is not protein bound and is widely distributed through the body. Metformin does not undergo hepatic biotransformation or biliary excretion; rather it is excreted unchanged in the urine, with 90% of the drug eliminated within 24 hours. Peak serum levels are reached 1 to 3 hours after an oral dose. Bioavailability of metformin tablets is approximately 50% to 60%. Food decreases the extent and slightly delays the absorption of metformin; however, it is recommended that it be taken with food. Adverse Effects and Contraindications Diarrhea, nausea, vomiting, abdominal bloating, flatulence, anorexia may occur in about 30% of the patients during initiation of the drug. These effects are temporary and often diminish with continued treatment. To minimize effects, initiate therapy at low doses, and gradually increase at weekly or biweekly intervals. Hypoglycemia may occur if caloric intake is inadequate, with strenuous exercise, or in combination with other hypoglycemic drugs. Monitor patients for possible development of anemia since metformin can inhibit absorption of cyanocobalamin (vitamin B12). Metformin may increase blood lactate levels as a result of enhanced lactate production and carries an FDA-mandated black box warning regarding lactic acidosis. Metformin-associated lactic acidosis is common, but serious metabolic complications are more likely to occur in patients with renal insufficiency. Cardiovascular collapse from acute heart failure, myocardial infarction or other conditions characterized by hypoxia, or any other cause has been associated with lactic acidosis. Discontinue metformin if any of these events occur. Radiologic studies (e.g., computed tomography [CT]) that use intravenous iodinated contrast material has been associated in metformin-treated patients with lactic acidosis and can lead to acute renal failure. Discontinue metformin temporarily before these procedures and withhold for 48 hours following the procedure. Restart metformin after kidney function has been revaluated and found to be normal. Metformin is contraindicated for use in patients with renal disease, defined as serum creatinine levels greater than 1.5 mg/dL in men and greater than 1.4 mg/dL in women. Impaired kidney function slows elimination and may cause metformin accumulation. Metformin use is also contraindicated for patients with heart failure that requires drug therapy, in patients with hypersensitivity to metformin, and in the presence of acute or chronic metabolic acidosis including ketoacidosis. Drug Interactions Alcohol is known to potentiate the effect of metformin on lactate metabolism. Caution patients against drinking excessive amounts of alcohol, whether acutely or on a chronic basis, while using metformin. Cimetidine reduces the renal clearance of metformin. Other cationic drugs (amiloride, digoxin, morphine, procainamide, quinidine, quinine, ranitidine, triamterene, trimethoprim, and vancomycin) that compete for the common tubular transport system have the potential to increase plasma metformin levels and increase the risk for lactic acidosis. A number of other drugs may worsen hyperglycemia and lead to loss of glycemic control when taken with metformin (see Table 53-3). Close monitoring of blood glucose levels in patients who require these drugs will help to determine when dosage changes are needed for metformin. Concurrent administration of furosemide, a loop diuretic, and metformin may increase serum concentrations of metformin and decrease concentrations of furosemide. Concurrent use of nifedipine may increase serum concentrations of metformin without an effect on the level of nifedipine. Use of either drug with metformin increases the risk of hypoglycemia. Dosage Regimens There is no fixed dosage regimen for management of patients with T2DM who take metformin or metformin extended-release tablets. Treatment must be individualized for each patient. Initiate metformin therapy with a single dose (usually 500 mg), taken with the patient's largest meal to prevent gastrointestinal (GI) symptoms. After initiation of therapy, metformin is taken in divided doses with meals. Dosages may be increased by 500 mg every 1 to 2 weeks until blood glucose goals are reached, or until the maximum dosage of 2000 to 2550 mg is reached (2000 mg daily for children 10 to 16 years of age). Significant responses are usually not seen at levels below 1500 mg per day. The initial dose of extended-release metformin is 500 mg once daily with the evening meal. The dosage may be increased weekly in increments of 500 mg to a maximum dose of 2000 mg daily. In many cases the target dosage is 2000 mg daily. Lab Considerations The effectiveness of metformin therapy is determined through periodic measurements of blood glucose and A1c levels. Measure serum creatinine levels before starting therapy and at least yearly thereafter to verify that they are normal. Discontinue metformin if serum creatinine level is greater than 1.5 mg/dL in men or greater than 1.4 mg/dL in women. Monitor liver functions periodically. Avoid using metformin in patients with clinical or laboratory evidence of hepatic disease. Impaired hepatic function has been associated with some cases of lactic acidosis. Monitor serum vitamin B12 levels every 2 to 3 years in patients with inadequate vitamin B12 intake or absorption to assess for development of anemia.

Importance of Culture and Religion to Nurses

A general agreement exists among nurses to raise the cultural competence of professional nursing practice. To begin to understand and to deal effectively with families in a multicultural community or in a unicultural community that is different from one's own, nurses must be aware of their own attitudes and values regarding a way of life, including health practices (Lipson, Dibble, Minarik, 2003). Nurses, too, are a product of their own cultural background. They also need to recognize that they are part of the "nursing culture." Nurses function within the framework of a professional culture with its own values and traditions and, as such, become socialized into their professional culture in their educational program and later in their work environments and professional associations. Frequently, nurses and other health care workers are not aware of their own cultural values and how those values influence their thoughts and actions. A model for self-examination on cultural competence is the ASKED model (Box 32-3). Recognizing that a behavior may be characteristic of a culture rather than an "abnormal" behavior places nurses at an advantage in their relationships with families. When nurses respect the cultural differences of a family, they are better able to determine whether the behavior is distinctive to the individual or a characteristic of the culture. Box 32-3 Exploring Your Cultural Competence ASKED Model of Cultural Competence A warceness: Am I aware of my personal biases and prejudices toward cultural groups different than mine? S kill: Do I have the skill to conduct a cultural assessment and perform a culturally based physical assessment in a sensitive manner? K nowledge: Do I have knowledge of the patient's worldview and the field of biocultural ecology? E ncounters: How many face-to-face encounters have I had with patients from diverse cultural backgrounds? D esire: What is my genuine desire to "want to be" culturally competent? Data from Campinha-Bacote J: Many faces: addressing diversity in health care, Online J Issues Nurs 8:1, 2003. Internet document available at www.nursingworld.org/ojin/topic20/tpc20_2.htm(accessed March 3, 2005). Cultural standards and values, the family structure and function, and experience with health care influence a family's feelings and attitudes toward health, their children, and health care delivery systems. It is often difficult for nurses to be nonjudgmental and objective in working with families whose behaviors and attitudes differ from or conflict with their own. The nurse needs to understand how one's own cultural background influences the way care is delivered (Lipson, Dibble, Minarik, 2003). Relying only on one's own values and experiences for guidance may result in frustration and disappointment. It is one thing to know what is needed to deal with a health problem; it is often quite another to implement a fruitful course of action unless nurses work within the cultural and socioeconomic framework of the family. It is beneficial to adapt ethnic practices to the health needs of the family rather than attempt to change long-standing beliefs. To aid their efforts to understand and respect the cultural beliefs of families, nurses should have a readily available resource file containing pertinent information about the cultural and subcultural characteristics of the community in which they practice (e.g., traditional practices related to infant feeding practices and the time and manner of weaning and toilet training). The nurse needs to develop knowledge on how cultural groups understand life processes, define health and illness, view the causes of illness, and have their healers care for the cultural group's members (Lipson et al, 2003). Some characteristics of selected cultures are outlined in Table 32-3. Tables 32-2 and 32-3 are presented as beginning frameworks for practicing transcultural nursing. Nurses must assess the cultural and religious practices of families to identify how these practices are similar to and different from those of their own cultural and religious backgrounds. Table 32-3 -- Cultural Characteristics Related to Health Care of Children and Families CULTURAL GROUP HEALTH BELIEFS HEALTH PRACTICES FAMILY RELATIONSHIPS COMMUNICATION African Illness classified as natural or unnatural: Self-care and folk medicine very prevalent Strong kinship bonds in extended family; members come to aid of others in crisis Alert to any evidence of discrimination Natural—affected by forces of nature without adequate protection (e.g., cold air, pollution, food and water) Folk therapies usually religious in origin Less likely to view illness as a burden Place importance on nonverbal behavior Folk therapies often not shared with the medical provider Place strong emphasis on work and ambition Affection shown by touching and hugging Silence may indicate lack of trust Unnatural—God's punishment for improper behavior Prayer is common means for prevention and treatment Elders cared for and respected Eye contact important to establish trust May see illness as the "will of God" Best to use direct, but caring, approach American Indian Believe health is state of harmony with nature and universe Distinction made between indigenous health problem requiring native healer or practice and Western disease requiring other medical care Cultures vary in kinship structure Most continue to speak their Indian language as well as English Respect of bodies through proper management Extended family structure—usually includes relatives from both sides of family Nonverbal communication Depend on individual belief in traditional culture Elder members assume leadership roles Individuals usually speak for themselves Traditional health beliefs holistic and wellness oriented Health practices include self-sufficiency and harmonious living Participation in religious ceremonies and prayer promotes health Chinese A healthy body viewed as gift from parents and ancestors and must be cared for Goal of therapy is to restore balance of yin and yang Extended family pattern common Open expression of emotions unacceptable Health is one of the results of balance between the forces of yin (cold) and yang (hot)—energy forces that rule the world Acupuncturist applies needles to appropriate meridians identified in terms of yin and yang Strong concept of loyalty of young to old Often smile when they do not comprehend Illness caused by imbalance Acupressure and tai chi replacing acupuncture in some areas Respect for elders taught at early age—acceptance without questioning or talking back Believe blood is source of life and is not regenerated Moxibustion is application of heat to skin over specific meridians Children's behavior a reflection on family Chi is innate energy Wide use of medicinal herbs procured and applied in prescribed ways Family and individual honor and "face" important Meals may or may not be planned to balance hot and cold Self-reliance and self-esteem highly valued; self-expression repressed Vietnamese Good health considered to be balance between yin and yang Concept of health based on harmony and balance Family uses all means possible before using outside agencies for health care Family is revered institution Many immigrants are not proficient in speaking and understanding English Many use rituals to prevent illness Regard health as family responsibility; outside aid sought when resources run out Multigenerational families May hesitate to ask questions Use herbal medicine, spiritual practices, and acupuncture Family is chief social network Questioning authority is sign of disrespect; asking questions considered impolite May use cupping, coin rubbing, or pinching skin Children highly valued May avoid eye contact with health professionals as a sign of respect May use inhaling aromatic oils, herbal teas, or wearing strings tied on body Individual needs and interests are subordinate to those of a family group Father is main decision maker Woman taught submission to men Parents expect respect and obedience from children Filipino Health is a result of balance Illness is a result of imbalance May not respond to illness until it is advanced Family is highly valued, with strong family ties Immigrants and older persons may not be able to speak or understand English To be able to be healthy again is to correct an evil deed May use herbal medicine Multigenerational family structure Eating well, not necessarily eating right, promotes good health common, often including collateral members Sensitive to tone and manner of speaker Physical ailment may be caused by the supernatural Members avoid any behavior that would bring shame on the family Limited direct eye contact Haitian Illness is a punishment Health is a personal responsibility Maintenance of family reputation paramount Recent immigrants and older persons may speak only Haitian Creole Natural cause (maladi bone die— disease of the Lord) caused by environmental factors, movement of blood within the body, changes between hot and cold, and bone displacement Foods have properties of "hot"/"cold" and "light"/"heavy" and must be in harmony with one's life cycle and bodily states Lineal authority supreme; children in a subordinate position in family hierarchy Often smile and nod in agreement when do not understand Natural illnesses treated by home and folk remedies first Children valued for parental social security in old age and expected to contribute to family welfare at an early age Quiet and gentle communication style and lack of assertiveness lead health care providers to falsely believe they comprehend health teaching and are compliant Supernatural (loa—spirits' anger) Good health is the maintenance of equilibrium Prayer and good spiritual habits very important May use religious medallions, rosary beads, or figure of saint to pray with May not ask questions if health care provider is busy or rushed Japanese Shinto religious influence Energy restored by means of acupuncture, acupressure, massage, and moxibustion along affected meridians Close intergenerational relationships Issei—born in Japan; usually speak Human inherently good Kampõ medicine—use of natural herbs Generational categories: Japanese only Evil caused by outside spirits Believe in removal of diseased parts Issei—first generation to live in Nisei, Sansei, and Yonsei have few language difficulties Illness caused by contact with polluting agents (e.g., blood, corpses, skin diseases) Trend is to use both Western and United States Health achieved through harmony and balance between self and society Asian healing methods Nisei—second generation Make significant use of nonverbal communication with subtle gestures and facial expression Disease caused by disharmony with society and not caring for body Care for disabled viewed as family's responsibility Sansei—third generation Tends to suppress emotions Take pride in child's good health Yonsei—fourth generation Will often wait silently Seek preventive care, medical care for illness Family tends to keep problems to self Value self-control and self-sufficiency Concept of haji (shame) imposes strong control; unacceptable behavior of children reflects on family Mexican-American Health controlled by environment fate and by will of God Seek help from curandero or curandera, especially in rural areas Strong kinship extended families include compadres (godparents) established by ritual kinship Spanish speaking or bilingual Children valued highly and desired, taken everywhere with family May have a strong preference for native language and revert to it in times of stress Certain illnesses considered hot and cold states and are treated with food that complement those states Curandero(a) receives position by birth, apprenticeship, or a "calling" via dream or vision Elderly treated with respect May shake hands or engage in introductory embrace Disease based on imbalance between individual and environment Treatments involve use of herbs, rituals, and religious artifacts Interpret prolonged eye contact as disrespectful Practice for severe illness—make promises, visit shrines, offer medals and candles, offer prayers Relaxed concept of time—may be late to appointments Adhere to "hot" and "cold" food prescriptions and prohibitions for prevention and treatment of illness Puerto Rican Subscribe to the "hot-cold" theory of causation of illness Infrequent use of health care system Family usually large and home centered—the core of existence Spanish speaking or bilingual Believe some illness caused by evil forces Seek folk healers (Espiritistas)—use of herbs, rituals Father has authority in family Strong sense of family privacy—may view questions regarding family as impudent Destiny (Si Dios quiere—if God wants) is in control of health Treatment classified as "hot" or "cold" Great respect for elders Many varieties of herbal teas used to treat illness and promote healing Children valued—seen as a gift from God Children taught to obey and respect parents Data from Lipson JG, Dibble SL, Minarik PA: Culture and nursing care: A pocket guide, San Francisco, CA, 2003, UCSF Nursing Press; Spector RE: Cultural diversity in health and illness, ed 5, Upper Saddle River, NJ,2000, Prentice-Hall. Nurse Alert These generalizations are presented to help nurses learn the unique beliefs and practices of various groups and are not meant to be stereotypes of any group. It is critical to remember that no cultural group is homogeneous; every racial and ethnic group contains great diversity, and knowledge of a culture may not reflect an individual member's beliefs (Nance, 1995).

Calcium Enhancers

A. Description 1. Calcium ion replacement directly increases serum calcium concentration 2. Vitamin D replacement improves absorption of calcium from intestines 3. Biphosphonates absorb calcium phosphate crystals in bone and may directly block dissolution of hydroxyapatite crystals of bone; inhibit resorption of bone 4. Parathyroid agents decrease bone resorption 5. Hormone replacement therapy (see Osteoporosis and Estrogens in Chapter 6) B. Examples 1. Calcium ion replacement: calcium carbonate (OsCal); calcium chloride; calcium gluconate 2. Vitamin D replacement: calcitriol (Rocaltrol) and cholecalciferol (Calciferol) 3. Biphosphonates: alendronate (Fosamax), pamidronate (Aredia), risedronate (Actonel) 4. Parathyroid agents: etidronate (Didronel) calcitonin (Miacalcin) C. Major side effects 1. Nausea, vomiting, renal calculi, muscle flaccidity (hypercalcemia) 2. Constipation (increased serum calcium delays passage of stool in GI tract) 3. Calcium preparations: cardiac disturbances (stimulation of cardiac conduction) 4. Vitamin D: dry mouth; metallic taste (early vitamin D toxicity associated with hypercalcemia) 5. Biphosphonates: bone pain, headache, abdominal pain, nausea 6. Parathyroid agents: diarrhea; nephrotoxicity and seizures (Didronel); headache, chest pressure, and dyspnea (Miacalcin) D. Nursing care 1. Assess for signs of hypercalcemia and tetany 2. Monitor serum electrolytes during course of therapy 3. Encourage increased fluid intake and acid ash diet to reduce potential of renal calculi and constipation; stress vitamin D and calcium-rich foods such as eggs, cheese, whole-grain cereals, and cranberries; limit milk, fruits, and vegetables 4. Calcium preparations: assess for potentiation of digitalis effect

Delegation and Supervision.

As a nursing leader, you will delegate certain nursing tasks and activities to unlicensed assistive personnel (UAP), such as patient care technicians (PCTs) or patient care assistants (PCAs). Delegation is the process of transferring to a competent person the authority to perform a selected nursing task or activity in a selected patient care situation. This process requires precise and accurate communication. The nurse is always accountable for the task or activity that is delegated! An important process that is sometimes not consistently performed by busy medical-surgical nurses is supervision of the UAP to whom the task or activity has been delegated. Supervision is guidance or direction, evaluation, and follow-up by the nurse to ensure that the task or activity is performed appropriately. Examples of delegated tasks are turning and positioning, vital signs, and intake and output measurements. Be sure to follow these five rights when you delegate and supervise a nursing task or activity to a UAP: • Right task: The task is within the UAP's scope of practice and competence. • Right circumstances: The patient care setting and resources are appropriate for the delegation. • Right person: The UAP is competent to perform the delegated task or activity. • Right communication: The nurse provides a clear and concise explanation of the task or activity, including limits and expectations. • Right supervision: The nurse appropriately monitors, evaluates, intervenes, and provides feedback on the delegation process as needed. Other activities or patient care responsibilities may be assigned by a registered nurse (RN) to another RN or to a licensed practical or vocational nurse (LPN/LVN). Each state designates which tasks may be safely delegated and assigned to nursing team members. Interventions that you can typically delegate or assign in any state are indicated throughout this text. Some of the Clinical Judgment and NCLEX Examination Challenges throughout this book will test your understanding of the delegation and supervision process.

Magnesium sulfate.

One of the important goals of care for the woman with severe preeclampsia is prevention or control of convulsions. Magnesium sulfate is the drug of choice in the prevention and treatment of convulsions caused by preeclampsia or eclampsia (ACOG, 2002; Cunningham et al., 2005; Nick, 2004). The routine use of magnesium sulfate is indicated for severe preeclampsia, HELLP syndrome, or eclampsia. However, no data support the routine use of magnesium sulfate for women diagnosed with mild preeclampsia or gestational hypertension (Working Group, 2000). Magnesium sulfate is administered as a secondary infusion (piggyback) to the main intravenous (IV) line by volumetric infusion pump. An initial loading dose of 4 to 6 g of magnesium sulfate per protocol or physician's order is infused over 15 to 20 minutes. This dose is followed by a maintenance dose of magnesium sulfate that is diluted in an IV solution per physician's order (e.g., 40 g of magnesium sulfate in 1000 ml of lactated Ringer's solution) and administered by infusion pump at 2 g/hr (Cunningham et al., 2005). This dose should maintain a therapeutic serum magnesium level of 4 to 7 mEq/L (Cunningham et al., 2005; Nick, 2004). Levels of magnesium sulfate are often checked daily (Gilbert & Harmon, 2003). After the loading dose, there may be a transient lowering of the arterial BP secondary to relaxation of smooth muscle by the magnesium sulfate. For the initial 24 hours postpartum, magnesium sulfate is usually continued intravenously (Box 23-5). BOX 23-5 Care of Patient with Preeclampsia Receiving Magnesium Sulfate PATIENT AND FAMILY TEACHING Explain technique, rationale, and reactions to expect • Route and rate • Purpose of "piggyback" Reasons for use • Tailor information to woman's readiness to learn • Explain that magnesium sulfate is used to prevent disease progression • Explain that magnesium sulfate is used to prevent seizures Reactions to expect from medication • Initially woman will feel flushed, hot, sedated, nauseated, and may experience burning at the IV site, especially during the bolus. • Sedation will continue Monitoring to anticipate • Maternal: blood pressure, pulse, DTRs, level of consciousness, urine output (indwelling catheter), presence of headache, visual disturbances, epigastric pain • Fetal: FHR and activity ADMINISTRATION • Verify physician order • Position woman in side-lying position • Prepare solution and administer with an infusion control device (pump) • Piggyback a solution of 40 g of magnesium sulfate in 1000 ml lactated Ringer's solution with an infusion control device at the ordered rate: loading dose—initial bolus of 4 to 6 g over 15 to 30 min; maintenance dose—1 to 3 g/hr MATERNAL AND FETAL ASSESSMENTS • Monitor blood pressure, pulse, respiratory rate, FHR, and contractions every 15 to 30 min, depending on woman's condition • Monitor intake and output, proteinuria, DTRs, presence of headache, visual disturbances, level of consciousness, and epigastric pain at least hourly • Restrict hourly fluid intake to a total of 100 to 125 ml/hr; urinary output should be at least 30 ml/hr REPORTABLE CONDITIONS • Blood pressure: systolic ≥160 mm Hg, diastolic ≥110 mm Hg, or both • Respiratory rate: ≤12 breaths/min • Urinary output <30 ml/hr • Presence of headache, visual disturbances, or epigastric pain • Increasing severity or loss of DTRs; increasing edema, proteinuria • Any abnormal laboratory values (magnesium levels, platelet count, creatinine clearance, levels of uric acid, AST, ALT, prothrombin time, partial thromboplastin time, fibrinogen, fibrin split products) • Any other significant change in maternal or fetal status EMERGENCY MEASURES • Keep emergency drug tray at bedside with calcium gluconate and intubation equipment • Keep side rails up • Keep lights dimmed, and maintain a quiet environment DOCUMENTATION • All of the above DTRs, Deep tendon reflexes; FHR, fetal heart rate; AST, aspirate aminotransferase; ALT, alanine aminotransferase. Intramuscular (IM) magnesium sulfate is rarely used because absorption rate cannot be controlled, injections are painful, and tissue necrosis may occur. However, the IM route may be used with some women who are being transported to a tertiary care center. The IM dose is 4 to 5 g given in each buttock, a total of 10 g (with 1% procaine possibly being added to the solution to reduce injection pain), and can be repeated at 4-hour intervals. Z-track technique should be used for the deep IM injection, followed by gentle massage at the site. PLAN OF CARE Severe Preeclampsia: Hospital Care NURSING DIAGNOSIS Risk for injury to woman and fetus related to CNS irritability Expected Outcome Woman will show diminished signs of CNS irritability (e.g., DTRs 2+, absence of clonus) and have no convulsions. Nursing Interventions/Rationales • Establish baseline data (e.g., DTRs, clonus) to use as basis for evaluating effectiveness of treatment. • Administer IV magnesium sulfate per physician's orders to decrease hyperreflexia and minimize risk of convulsions. • Monitor maternal vital signs, FHR, urine output, DTRs, IV flow rate, and serum levels of magnesium sulfate to assess for and prevent magnesium sulfate toxicity (e.g., depressed respirations, oliguria, sudden drop in blood pressure, hyporeflexia, fetal distress). • Have calcium gluconate at bedside to be available if needed as antidote for magnesium sulfate toxicity. • Maintain a quiet, darkened environment to avoid stimuli that may precipitate seizure activity. NURSING DIAGNOSIS Ineffective tissue perfusion related to preeclampsia secondary to arteriolar vasospasm Expected Outcome Woman will exhibit signs of increased vasodilation (i.e., diuresis, decreased edema, weight loss). Nursing Interventions/Rationales • Establish baseline data (e.g., weight, degree of edema) to use as basis for evaluating effectiveness of treatment. • Administer intravenous magnesium sulfate per physician order, which serves to relax vasospasms and increase renal perfusion. • Place woman on bed rest in a side-lying position to maximize uteroplacental blood flow, reduce blood pressure, and promote diuresis. • Monitor intake and output, edema, and weight to assess for evidence of vasodilation and increased tissue perfusion. NURSING DIAGNOSIS Risk for • excess fluid volume related to increased sodium retention secondary to administration of magnesium sulfate • impaired gas exchange related to pulmonary edema secondary to increased vascular resistance • decreased cardiac output related to use of antihypertensive drugs • injury to fetus related to uteroplacental insufficiency secondary to use of antihypertensive medications Expected Outcomes Woman will exhibit signs of normal fluid volume (i.e., balanced intake and output, normal serum creatinine levels, normal breath sounds); adequate oxygenation (i.e., normal respirations, full orientation to person, time, and place); normal range of cardiac output (i.e., normal pulse rate and rhythm); and fetal well-being (i.e., adequate fetal movement, normal FHR). Nursing Interventions/Rationales • Monitor woman for signs of fluid volume excess (increased edema, decreased urine output, elevated serum creatinine level, weight gain, dyspnea, crackles) to detect potential complications. • Monitor woman for signs of impaired gas exchange (increased respirations, dyspnea, altered blood gases, hypoxemia) to detect potential complications. • Monitor woman for signs of decreased cardiac output (altered pulse rate and rhythm) to detect potential complications. • Monitor fetus for signs of difficulty (decreased fetal activity, decreased FHR) to prevent complications. • Record findings and report signs of increasing problems to physician to enable timely interventions. Magnesium sulfate interferes with the release of acetylcholine at the synapses, decreasing neuromuscular irritability, depressing cardiac conduction, and decreasing CNS irritability. Because magnesium circulates in a free state and unbound to protein and is excreted in the urine, accurate recordings of maternal urine output must be obtained and monitored. Diuresis is an excellent prognostic sign; however, if renal function declines, all of the magnesium sulfate will not be excreted and can cause magnesium toxicity. Because magnesium sulfate is a CNS depressant, the nurse assesses for signs and symptoms of magnesium toxicity. Serum magnesium levels are obtained on the basis of the woman's response and if any signs of toxicity are present. Expected side effects of magnesium sulfate are a feeling of warmth, flushing, and nausea. Symptoms of mild toxicity include lethargy, muscle weakness, decreased DTRs, and slurred speech. Increasing toxicity may be indicated by maternal hypotension, bradycardia, bradypnea, and heart block (Nick, 2004). NURSE ALERT Loss of patellar reflexes, respiratory depression, oliguria, and decreased level of consciousness are signs of magnesium toxicity. Actions are needed to prevent respiratory or cardiac arrest. If magnesium toxicity is suspected, the infusion should be discontinued immediately. Calcium gluconate, the antidote for magnesium sulfate, may also be ordered (10 ml of a 10% solution, or 1 g) and given by slow IV push (usually by the physician) over at least 3 minutes to avoid undesirable reactions such as arrhythmias, bradycardia, and ventricular fibrillation (Cunningham et al., 2005; Nick, 2004; Sibai, 2002). NURSE ALERT Because magnesium sulfate is also a tocolytic agent, its use may increase the duration of labor. A preeclamptic woman receiving magnesium sulfate may need augmentation with oxytocin during labor. The amount of oxytocin needed to stimulate labor may be more than that needed for a woman who is not receiving magnesium sulfate.

Magnesium Sulfate

One of the important goals of care for the woman with severe preeclampsia is prevention or control of convulsions. Magnesium sulfate is the drug of choice in the prevention and treatment of convulsions caused by preeclampsia or eclampsia (ACOG, 2002b; Magpie Trial Collaborative Group, 2002). The use of magnesium sulfate in the management of preeclampsia halves the risk of eclampsia and probably reduces the risk of maternal death (Magpie Trial Collaborative Group, 2002). The routine use of magnesium sulfate is indicated for severe preeclampsia, HELLP syndrome, or eclampsia; however, no data support routine use of magnesium sulfate for women diagnosed with mild preeclampsia or gestational hypertension (Summary Report, 2000; Working Group, 2000). Magnesium sulfate is administered as a secondary infusion ("piggyback") to the main intravenous (IV) line by volumetric infusion pump. An initial loading dose of 4 to 6 g diluted in 100 ml of IV fluid per protocol or physician's order is infused over 15 to 30 minutes. This dose is followed by a maintenance dose of magnesium sulfate diluted in an IV solution per physician's order (e.g., 40 g of magnesium sulfate in 1000 ml of lactated Ringer's solution) and administered by infusion pump at 2 g per hour (Gilbert & Harmon, 2003). This dose should maintain a therapeutic serum magnesium level of 4 to 8 mg/dl. No data exist to support the routine drawing of serial serum magnesium levels, although levels are often checked daily (Gilbert & Harmon, 2003) (Box 14-6). Box 14-6 Protocol for Care of Patient with Preeclampsia Receiving Magnesium Sulfate Magnesium Sulfate Administration Patient and Family Teaching Explain technique, rationale, and reactions to expect • Route and rate • Purpose of "piggyback" Reasons for use • Tailor information to patient's readiness to learn • Explain that it is to prevent disease progression • Explain that it is to prevent seizures Reactions to expect from medication • Initially patient will feel flushed, hot, sedated, especially during the bolus • Sedation will continue Monitoring to anticipate • Maternal: blood pressure, pulse, DTRs, level of consciousness, urine output (indwelling catheter likely), presence of headache, visual disturbances, epigastric pain • Fetal: FHR and activity Administration • Verify physician order • Position woman in side-lying position • Prepare solution and administer with an infusion control device (pump) • Piggyback a solution of 40 g of magnesium sulfate in 1000 ml of lactated Ringer's solution with an infusion control device at the ordered rates: loading dose: initial bolus of 4-6 g over 15-30 min; maintenance dose: 1-3 g/hr Maternal and Fetal Assessments • Monitor blood pressure, pulse, respiratory rate, FHR, and contractions every 15-30 min, depending on patient condition • Monitor intake and output, proteinuria, DTRs, presence of headache, visual disturbances, and epigastric pain at least hourly • Restrict hourly fluid intake to a total of 100-125 ml/hr; urinary output should be ≥30 ml/hr Reportable Conditions • Blood pressure: systolic, 160 mm Hg; diastolic, 110 mm Hg, or both • Respiratory rate: 12 breaths/min • Urinary output <30 ml/hr • Presence of headache, visual disturbances, or epigastric pain • Increasing severity or loss of DTRs, increasing edema, proteinuria • Any abnormal laboratory values (magnesium levels, platelet count, creatinine clearance, levels of uric acid, AST, ALT, prothrombin time, partial thromboplastin time, fibrinogen, fibrin split products) • Any other significant change in maternal or fetal status Emergency Measures • Keep emergency drug tray at bedside with calcium gluconate and intubation equipment • Keep side rails up • Keep lights dimmed, and maintain a quiet environment Documentation • All of the above ALT, alanine aminotransferase; AST, aspartate aminotransferase; DTRs, deep tendon reflexes; FHR, fetal heart rate. After the loading dose, there may be a transient lowering of the arterial blood pressure secondary to relaxation of smooth muscle. Nurse Alert The woman's BP, pulse, and respiratory status should be monitored closely while the loading dose is being administered intravenously and every 15 to 30 minutes at other times, depending on the stability of the woman's condition. Administration of magnesium sulfate is continued for at least the first 12 to 24 hours postpartum to prevent seizures. Intramuscular (IM) magnesium sulfate is used rarely because the absorption rate cannot be controlled, injections are painful, and tissue necrosis can occur. The IM route may be used with some women who are being transported to a tertiary care center. The IM dose is 4 to 5 g given in each buttock, for a total of 10 g (1% procaine may be ordered to be added to the solution to reduce injection pain), and can be repeated at 4-hour intervals. Z-track technique should be used for the deep IM injection, followed by gentle massage at the site. Magnesium sulfate interferes with the release of acetylcholine at the synapses, decreasing neuromuscular irritability, depressing cardiac conduction, and decreasing CNS irritability. Because magnesium circulates free and unbound to protein and is excreted in the urine, accurate recordings of maternal urine output must be obtained. Diuresis within 24 to 48 hours is an excellent prognostic sign. It is considered evidence that perfusion of the kidneys has improved as a result of relaxation of arteriolar spasm. With improved perfusion, fluid moves from interstitial spaces to the intravascular bed and edema is reduced. Diuresis results in weight loss. Although diuresis generally indicates improvement, diuresis in the presence of worsening clinical status may indicate impending renal failure. As renal function declines and serum creatinine levels rise, renal filtration is compromised. The woman can excrete large volumes of urine (greater than 200 ml/hr) but will not excrete magnesium sulfate. Because magnesium sulfate is a CNS depressant, the nurse assesses for signs and symptoms of magnesium toxicity (see Box 14-6). Serum magnesium levels are obtained on the basis of the woman's response and if any signs of toxicity are present. Early symptoms of toxicity include decreased DTRs, nausea, a feeling of warmth, flushing, muscle weakness, decreased reflexes, and slurred speech. Nurse Alert Loss of patellar reflexes, respiratory depression, oliguria, and decreased level of consciousness are signs of magnesium toxicity. Actions are needed to prevent respiratory or cardiac arrest. If magnesium toxicity is suspected, the infusion should be discontinued immediately. Calcium gluconate, the antidote for magnesium sulfate, may also be ordered (10 ml of a 10% solution, or 1 g) and given by slow IV push (usually by the physician) over at least 3 minutes to avoid undesirable reactions such as dysrhythmias, bradycardia, and ventricular fibrillation. Because magnesium sulfate is also a tocolytic agent, its use may increase the duration of labor. Nurse Alert The labor of a woman with preeclampsia receiving magnesium sulfate may need augmentation with oxytocin. The amount of oxytocin needed to stimulate labor may be more than that needed for a woman who is not on magnesium sulfate. Magnesium sulfate does not seem to affect FHR variability in a healthy term fetus, and rarely is toxic in the healthy term newborn whose weight is within normal range for gestational age. Neonatal serum magnesium levels approximate those of the mother, and toxic levels can cause depressed respirations and hyporeflexia. The neonate with hypermagnesemia can be treated with calcium and exchange transfusion with citrated blood or may require assisted mechanical ventilation until serum levels normalize. A follow-up study is being conducted to determine whether there are long-term effects of magnesium administration on mothers and infants (Magpie Trial Follow Up Study Management Group, 2004). If eclampsia develops after the initiation of magnesium sulfate therapy, additional magnesium sulfate or another anticonvulsant (e.g., diazepam or phenobarbital) may be administered (Roberts, 2004) (Emergency box). Rarely, the woman will continue to experience seizures despite adequate blood magnesium levels. Diazepam has fetal and neonatal effects. The FHR loses variability, a reflection of fetal oxygenation. High levels of these medications in the newborn depress sucking ability, cause hypotonia, and may result in temperature instability. The newborn's respiratory rate may be decreased. Careful surveillance of both maternal and fetal or neonatal status is necessary.

IMPLEMENTATION for Intubating the Client with a Small-Bore Nasogastric or Nasointestinal Feeding Tube

STEPS RATIONALE 1 See Standard Protocol (inside front cover). 2 Explain procedure to client and how to communicate during intubation (e.g., raise a finger to indicate gagging or discomfort). It is important for client to have a method for communication during the procedure to alleviate stress. Nurse may need to pause during insertion to decrease gagging. COMMUNICATION TIP To help the client have a chance to participate and feel a sense of control, explain how to try to relax and communicate during tube insertion. "Now I will explain each step as we go along. The tube will cause a slight burning pain as it passes through your nose. I want you to raise one finger to tell me if it's too uncomfortable so that I can be gentle and at the same time get this done as quickly as possible." 3 Place towel over client's chest and position client in sitting or high-Fowler's position. If client is comatose, place in semi-Fowler's position with head propped forward using a pillow. It may be necessary to have an assistant help with positioning of confused or comatose clients. Position reduces risk of pulmonary aspiration in event client vomits. Assists with closure of airway and passage of the tube into the esophagus. When inserting the tube into the nose, avoid tipping the client's head back because it opens the airway and increases risk for aspiration. NURSE ALERT Place tissues and emesis basin within client's reach. 4 Check feeding tube for flaws: rough or sharp edges on distal end and closed or clogged outlet holes. Flaws in feeding tube hamper tube intubation and can injure client. 5 Determine length of tube to be inserted and mark with tape or indelible ink (see illustration). Determines approximate depth of insertion. NURSE ALERT Tip of tube must reach stomach. Measure distance from tip of nose to earlobe to xiphoid process of sternum (see illustration). Add an additional 20 to 30 cm (8 to 12 inches for NI tube ( Hanson, 1979; Lord and others, 1993; Welch, 1996). 6 Prepare NG or NI tube for intubation: a. Perform hand hygiene. Reduces spread of microorganisms. b. Inject 10 ml of water from 60-ml Luer-Lok or catheter-tipped syringe into the tube. Aids in guidewire or stylet insertion. c. Make certain to securely position guidewire against weighted tip and to snugly fit both Luer-Lok connections. Promotes smooth passage of tube into GI tract. Improperly positioned stylet can induce serious trauma. 7 Cut adhesive tape 10 cm (4 inches) long or prepare tube fixation device. 8 Dip tube with surface lubricant into a glass of room temperature water or apply water-soluble lubricant. Do not place tubes in cold or ice water. Activates lubricant to facilitate passage of tube into naris to GI tract. Ice or cold water causes tubes to become inflexible, causing trauma to mucous membranes. COMMUNICATION TIP Explain that you are now about to insert the feeding tube. Let client know how he or she can assist. "I will insert the tube through your nose toward the back of your throat. Swallowing will help advance the tube. Once the tip is in the back of your throat, I will ask you to begin to swallow. The water (ice chips) may help if you find it hard to swallow. I will tell you when to stop swallowing." 9 Hand the alert client a glass of water with straw or glass with crushed ice (if able to swallow). Client is asked to swallow to facilitate tube passage. 10 Gently insert tube through nostril to back of throat (posterior nasopharynx). This may cause client to gag. Aim back and down toward ear (see illustration). Natural contour facilitates passage of tube into GI tract. 11 Have client flex head toward chest after tube has passed through nasopharynx. Closes off glottis and reduces risk of tube entering trachea. 12 Emphasize need to mouth breathe and swallow. Helps facilitate passage of tube. Click to view full size figure STEP 5 Determining length of feeding tube. Click to view full size figure STEP 10 NG tube inserted through nose and esophagus into stomach. 13 When you insert tube to tip of the carina (approximately 25 cm [10 inches] in the adult), stop and listen for air exchange from distal portion of the tube. If air can be heard, tube could be in respiratory tract; remove tube and begin again ( Metheny and Titler, 2001). NURSE ALERT Do not force tube. If resistance is met or client starts to cough, choke, or become cyanotic, stop advancing tube and pull tube back. 14 Advance tube each time client swallows until desired length has been passed. Reduces discomfort and trauma to client. 15 Check for position of tube in back of throat with penlight and tongue blade. Tube may be coiled, kinked, or entering trachea. 16 Temporarily anchor tube to nose with small piece of tape and verify placement of tube (see Skill 31.2). Movement of tube stimulates gagging. Assesses general position before anchoring tube more securely. 17 After verifying tube placement by gastric aspirates, anchor tube to nose and avoid pressure on nares. Mark exit site on tube with indelible ink. Use one of the following options for anchoring: Properly secured tube allows client more mobility and prevents trauma to nasal mucosa. a. Apply tape (1) Apply tincture of benzoin sparingly to nose and allow it to become "tacky." (2) Remove gloves and split one end of the adhesive tape strip lengthwise 5 cm (2 inches). (3) Wrap each of the 5-cm strips around tube as it exits nose (see illustration). b. Apply tube fixation device (1) Apply wide end of shaped adhesive patch to bridge of nose (see illustration). (2) Slip connector around feeding tube as it exits nose (see illustration). Click to view full size figure STEP 17a.(3) Wrapping tape to anchor nasoenteral tube. Click to view full size figure STEP 17b.(1) Applying fixation device patch to bridge of nose. Click to view full size figure STEP 17b.(2) Slip connector around feeding tube. 18 Fasten end of NG tube to client's gown using piece of tape (see illustration). Do not use safety pins to pin tube to client's gown. Reduces traction on naris when tube is moved. Safety pins can become unfastened and cause injury to client. 19 Assist client to comfortable position. note: Positioning client on right side does not facilitate intestinal placement. Researchers indicate that placing patient on right side does not promote passage of tube into the small intestine ( Kittinger and others, 1987). NURSE ALERT Leave guidewire or stylet in place until x-ray confirmation of correct position is obtained. Never attempt to reinsert partially or fully removed guidewire or stylet while feeding tube is in place. Guidewire or stylet may perforate GI tract, especially the esophagus or nearby tissue, and seriously injure client. 20 Obtain x-ray film of abdomen. X-ray verifies placement of tube ( AACN, 2005). 21 Apply gloves and administer frequent oral hygiene. Cleanse tubing at nostril. Promotes client comfort and integrity of oral and nasal mucous membranes. 22 See Completion Protocol (inside front cover). Click to view full size figure STEP 18. Fasten feeding tube to client's gown.

Unlicensed Assistive Personnel

Supervision of unlicensed personnel is a growing responsibility of the licensed practitioner. Many hospitals use unlicensed assistive personnel (UAP); depending on the state this may include emergency medical technicians, paramedics, or certified nursing assistants. Delegation of nursing functions to these individuals can create legal problems for the licensed practitioner. A registered nurse may not delegate any task to UAPs that rightfully only a licensed practitioner should perform. These activities include tasks that involve professional clinical judgment related to the diagnosis and treatment of patients. This may include such nursing functions as assessment, planning, and evaluation, depending on the specific state NPA.[4]

Gestational Trophoblastic Neoplasia

These types of tumors are classified as nonmetastatic, metastatic low risk, and metastatic high risk. After the evacuation of a hydatidiform molar pregnancy, approximately 20% of women are treated for malignancy. Almost 50% of these tumors occur after a hydatidiform mole. Approximately 30% follow an ectopic pregnancy or miscarriage, and 20% occur after an apparently normal birth at term. There is an almost 100% cure rate after nonmetastatic and low risk metastatic GTN. Common sites of metastasis are the lungs, vagina, vulva/cervix, liver, and brain (Copeland & Landon, 2007). There is a 20% risk of maternal death after high risk metastatic GTN. Continued bleeding after evacuation of a hydatidiform mole is usually the most suggestive symptom of GTN. Other clinical signs include abdominal pain and uterine and ovarian enlargement. Signs of metastasis include pulmonary symptoms (e.g., dyspnea, cough). The diagnosis is usually confirmed by increasing or plateauing hCG levels after evacuation of a molar pregnancy. Once diagnosis is confirmed, other clinical studies (e.g., computed tomography scan of lungs and brain, chest x-ray, pelvic ultrasound, and liver scan) are done to determine the extent of the disease. Single-agent chemotherapy is usually effective. Methotrexate has been the treatment of choice for years. Dactinomycin also has been used with equally good results and is used for women with liver or renal disease, both of which are contraindications for methotrexate. Hysterectomy with adjuvant chemotherapy is often the choice of treatment for nonmetastatic tumors in women who have completed their childbearing. Therapy is continued until negative hCG levels are obtained. Follow-up after successful chemotherapy is by serum hCG levels obtained every month for a year (Gilbert, 2007). Physical examinations are done at least annually, and chest x-rays are done if indicated. Contraception is needed until the woman has been in remission for at least 6 months. Oral contraceptives are preferred, but barrier methods are acceptable if oral contraceptives are contraindicated. During a subsequent pregnancy, pelvic ultrasonography is recommended because the woman is at higher risk to develop another molar pregnancy. Serum hCG levels should be obtained 6 weeks after the birth.

Women of Varying Ethnic and Cultural Groups

Childbearing practices and rituals of other cultures may not be congruent with standard practices associated with bonding in the Anglo-American culture. For example, Chinese families traditionally use extended family members to care for the newborn so that the mother can rest and recover, especially after a cesarean birth. Some Native American, Asian, and Hispanic women do not initiate breastfeeding until their breast milk comes in. Haitian families do not name their babies until after the confinement month. Amount of eye contact varies among cultures, too. Yup'ik Eskimo mothers almost always position their babies so that eye contact can be made. Nurses should become knowledgeable of the childbearing beliefs and practices of diverse cultural and ethnic groups. Because individual cultural variations exist within groups, nurses need to clarify with the patient and family members or friends what cultural norms the patient follows. Incorrect judgments may be made about mother-infant bonding if nurses do not practice culturally sensitive care.

Biguanides

Metformin (Glucophage) is a biguanide glucose-lowering agent. The primary action of metformin is to reduce glucose production by the liver. It also enhances insulin sensitivity at the tissue level and improves glucose transport into the cells. Metformin is the first-choice drug for most people with type 2 diabetes.[9] Unlike sulfonylureas and insulin, metformin does not promote weight gain. It also has beneficial effects on plasma lipids. Metformin is also used in the prevention of type 2 diabetes in people with prediabetes, especially individuals who are obese and less than 60 years old, and have risk factors such as hypertension, low HDL, or a family history of diabetes in first-degree relatives. DRUG ALERT Biguanides • Do not use in patients with kidney disease, liver disease, or heart failure. • Do not use in people who drink excessive amounts of alcohol.