Module 13 - Pharmacotherapy For Nutrition Hydration Electrolyte Disorders

Geriatric
Pharmacy Review Module 13: Pharmacotherapy for Nutri;on, Hydra;on, Electrolyte Disorders
Accreditation Information
ASCP is accredited by the Accreditation Council for Pharmacy Education as a provider of continuing pharmacy education.
This home study web activity has been assigned 3 credit hours. ACPE UPN: 0203-0000-10-007-H01-P Release Date: 3/23/2010 Expiration Date: 3/23/2013
To receive continuing education credit for this course, participants must complete an on-line evaluation form and pass the online assessment with a score of 70% or better. If you do not receive a minimum score of 70% or better on the assessment, you are permitted 4 retakes. After passing the assessment, you can print and track your continuing education statements of credit online.
Geriatric Pharmacy Review courses have not yet been approved for Florida consultant pharmacy continuing education.
Copyright 2011 American Society of Consultant Pharmacists
Content Experts
Current Content Experts:
Legacy Content Experts: Donna M. Lisi, PharmD, BS, BCPP, CGP Clinical Pharmacist, Geriatrics New Jersey VA Healthcare System & Adjunct Faculty, Rutger's University College of Pharmacy Lisa L. Larive, PharmD Assistant Clinical Professor University of Connecticut School of Pharmacy & Clinical Specialist, Critical Care Yale-New Haven Hospital
Michael L. Smith, PharmD, BCPS, CACP Clinical Coordinator William Backus Hospital
Kathryn Wheeler BS, PharmD, BCPS Assistant Clinical Professor - Internal Medicine Department of Pharmacy Practice School of Pharmacy University of Connecticut & Clinical Pharmacist William W. Backus Hospital
Content Experts
Faculty Disclosure: Michael L. Smith, PharmD, BCPS, CACP has no relevant financial relationships to disclose. Kathryn Wheeler BS, PharmD, BCPS has no relevant financial relationships to disclose. Donna M. Lisi, PharmD, BS, BCPP, CGP has no relevant financial relationships to disclose. Lisa L. Larive, PharmD has no relevant financial relationships to disclose. .
Malnutrition and Involuntary Weight Loss in the Elderly
Learning Objectives: By the end of this Review Concept you should be able to: Describe age-related changes which can affect the nutritional status of elderly individuals. Recognize the daily nutritional requirements of the elderly, how they differ from a younger individual and how illness can affect these nutritional requirements. Describe the incidence, etiology, physical and laboratory findings, and consequences of malnutrition and involuntary weight loss in the senior population. Identify medications which may cause nutritional deficiencies or involuntary weight loss. Design and monitor a management strategy for a senior with malnutrition or involuntary weight loss.
Age-Related Changes Affecting Nutritional Status in the Elderly

Changes in sense of taste and smell Decrease in salivary flow Poor dentition Decreased power of mastication Achlorhydria Decreased intrinsic factor Decreased pancreatic secretion Lactase deficiency Decreased gastric emptying
Nutrition is very important in the physiologic changes that take place in the aging process. By making nutritional interventions, it is estimated that 85% of the chronic diseases and disabilities could be prevented. The decline in appetite with advancing age is known as anorexia of ageing. This counterbalances the decline in physical activity and resting metabolic rate. Listed here are the age-related changes that occur which lead to malnutrition in the elderly. The enjoyment of food declines as we age, in part because the number of taste buds decline. Sweet and salty tastes decline first, and food begins to taste sour or bitter. The sense of smell tends to decline as well, leading to decreased food intake. Decreased salivary flow, poor dentition and decreased power of mastication limit the amount and variety of foods consumed. Dental problems may also contribute to having a bad taste in the mouth, thereby decreasing daily food intake. There may also be difficulty in swallowing, as a result of stroke, advancing Parkinson's disease or Alzheimer's disease. Achlorhydria occurs in about twenty-five percent of persons over the age of sixty. There are also decreases in intrinsic factor production and pancreatic secretions. Lactase deficiency is also common, and there is a decrease in gastric emptying.
Impact of Illness on Total Daily Energy Requirements

Total Energy Requirements = BMR + Activity-related Expenditure (BMR = basal metabolic rate) Successful nutritional management of the elderly patient depends on knowledge of the normal energy and nutrient requirements of older adults, as well as the impact of disease on these requirements. Estimates of total daily energy requirements are based primarily on basal metabolic rate and the energy of activity. Overall energy requirements decline after the age of 51. Basal metabolic rate is a measure of the amount of energy expended at rest without food, and is influenced by body size, age, gender, and level of activity. For a stable patient who weighs sixty to eighty kilograms, the basal metabolic rate is estimated to be 25 kcal/kg. However this equation may overestimate the basal metabolic rate in bedfast, chronically ill patients. When a person becomes ill, fever and inflammation increase internal heat production, increasing these energy requirements. The extent of the increase depends on severity of illness and level of activity. Fever increases the basal metabolic rate by seven percent for every degree Fahrenheit increase. For individuals with mild illness, the increase may be as little as ten percent of basal metabolic rate. For individuals with severe illness, this figure may be as high as fifty percent. Patients confined to bed need only twenty percent more energy, while ambulatory patients may need as much as thirty percent more energy. Protein requirements may also increase depending on the severity of illness.
Total Energy Requirements During Illness: BMR + Activity-related Expenditure + Illness-related Expenditure (BMR = basal metabolic rate)
Changes in Energy Requirements Due to Illness: Fever:+ 7% BMR Mild illness:+ 10% BMR Moderate illness:+ 25% BMR Severe illness:+ 50% BMR
Assessment of Nutritional Status

History Weight loss Chewing/swallowing Physical disability Mental confusion Medication Tools: 24 hour recall, food records, food frequency questionnaire, diet history Physical Exam Body composition analysis Laboratory tests Assessment of nutritional state can be made through history and observation, in addition to the physical exam and laboratory tests. A key component of the history is weight loss. A decline in appetite is expected with aging from a physiologic standpoint. The first step in the assessment of malnutrition is to determine the patient's capacity for nutrient intake and level of nutritional risk. This requires a thorough history, including medications, abdominal surgeries, anemia, diarrhea or constipation, chewing or swallowing problems, smoking habits, alcohol intake and diet. Assessment of cognitive function and activities of daily living are also important. Many patients will present with a chief complaint pointing to a specific organ. In the absence of a chief complaint, other areas to investigate include any gastrointestinal symptoms, hypermetabolic conditions, depression and dementia, and medications. Once risk factors for malnutrition have been identified, the patient should be thoroughly examined. The physical exam should establish whether or not there is true weight loss. It should also include a routine functional and mental status assessment. Anthropometric measures of height, weight, body fat and protein stores are required for comprehensive evaluation of nutritional status.
Definition and Incidence of Malnutrition

Definitions: Malnutrition is a deficit in calories, protein, carbohydrates, fat, vitamins, minerals, trace elements or any combination thereof Protein-energy malnutrition is the loss of lean body mass and adipose tissue due to an inadequate intake of amino acids and calories Incidence: 1% of independent, healthy elderly 52 85% of long term care facility (LTCF) residents 33 58% of acute care hospital patients When nutritional intake is insufficient to meet the physiologic needs of the body, malnutrition will occur. A greater risk exists with increased energy demands created by acute or chronic illness. Malnutrition is caused by an inadequate intake of calories, protein, carbohydrates, fat, vitamins, minerals, trace elements or any combination thereof. Protein-energy malnutrition is the specific loss of lean body mass and adipose tissue due to an inadequate intake of amino acids and calories. The effects of malnutrition depend on its severity, duration and which specific nutrients are lacking. In a broad sense, malnutrition may describe a state of under- or over-nourishment as malnutrition usually but does not always have to involve weight loss. Eating too much of one type of food may preserve body weight, but may leave the patient lacking various nutritional elements not found in that food. Protein-energy malnutrition affects as much as one percent of independent, otherwise healthy older adults, with estimates as high as eighty-five percent for long-term care residents and fifty-eight percent of acute care patients.
Etiology of Protein-Energy Malnutrition

Primary Inadequate Dietary Intake: Increased metabolic demands Increased nutrient losses Poor nutrient intake Secondary Medical Conditions and Drugs: Conditions associated with increased energy requirements or catabolic losses (e.g., fever, infection, trauma, pressure ulcers, burns, malignancy, COPD) Malabsorptive or maldigestive states Illnesses associated with excessive loss of nutrients (e.g., protein-losing enteropathy, nephrotic syndrome) Conditions or drugs associated with altered metabolism of nutrients or which cause anorexia, nausea, vomiting, diarrhea or constipation
In general, protein-energy malnutrition may be caused by illnesses associated with increased energy requirements and catabolic losses; by malabsorptive and maldigestive conditions; by diseases that involve the excessive loss of nutrients, and by drugs that alter metabolism. The most frequent causes among the elderly are acute infections, pressure ulcers, and traumatic injuries, such as hip fractures. Poor nutrient intake may be due to swallowing problems, chemotherapy, and inability to feed oneself due to a cognitive impairment. The rapidity with which the condition develops and its severity depends on the severity of the underlying illness, the patients nutrient reserves, and concurrent nutritional deficiencies. Many patients who are malnourished have elements of both protein and calorie deficiencies.
Medications Causing Weight Loss

Decreased appetite Digoxin, captopril, NSAIDs, antibiotics, phenothiazines, TCAs, fluoxetine, sertraline, antihistamines Malabsorption Laxatives, cholestyramine, colchicine, misoprostol Increased metabolism Thyroxine, pseudoephedrine Altered taste Captopril, penicillin, antihypertensives, metformin, vasodilators, metronidazole
Side effects of certain medications can be the cause of weight loss in the elderly. Some interfere with appetite, nutrient absorption, metabolism, or taste. Listed here are some of the more common offenders. Many others are not listed that decrease cognition, such as antihistamines, antiparkinsonian drugs, narcotics, and other sedatives. These drugs may decrease the ability for the elderly person to shop, prepare, and feed themselves. Drug-induced effects accounted for two to fourteen percent of involuntary weight loss depending on the study. Among nursing home residents, Morley and Kraenzle found that depression and medications were the most important causes of involuntary weight loss.
Definition and Incidence of Involuntary Weight Loss
Definition: weight loss >10% of body weight over 6 months, or >5% of usual body weight in 1 month, body weight of 20% over or under ideal body weight, especially in the presence of chronic disease, and inadequate nutrition intake including an impaired ability to ingest or absorb food adequately. Incidence: 13% of elderly 65 and older per year Independently predicts increased mortality Source: ASPEN Board of Directors and the Clinical Guidelines Task Force. Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients. JPEN 2002;26(1Suppl):9SA.
While not an inevitable consequence, unintentional or involuntary weight loss is closely related to malnutrition. Involuntary weight loss is described as weight loss of greater than ten percent of body weight over six months. It may also be greater than five percent of body weight in a period of one month. Presence of chronic diseases must also be considered to assess the ability to ingest or absorb the food. Involuntary weight loss can be a significant problem for the elderly. One study of community-dwelling male veterans sixty-five years and older showed an annual incidence of thirteen percent, and implicated involuntary weight loss as an independent predictor of increased mortality.
Etiology of Involuntary Weight Loss
Cancer, especially of the lung and GI tract GI problems (e.g., dysphagia, PUD, GERD, irritable bowel syndrome, constipation) Hyperthyroidism Uncontrolled diabetes Dyspnea due to COPD Heart failure Infections Neurological disorders (e.g., Parkinsons disease, stroke)
While involuntary weight loss is often a consequence of illness, not all patients with serious physical illness experience the condition. Various studies have been conducted to establish causes of involuntary weight loss. In 1981, Marton found that sixty-five percent of involuntary weight loss among elderly veterans was due to physical causes. In 1991, Thompson discovered that among community-dwelling elderly, cancer and benign gastrointestinal problems were the most common causes of involuntary weight loss. Patients with hyperthyroidism often lose weight, and uncontrolled diabetics may experience short-term weight loss secondary to osmotic diuresis. Patients with chronic obstructive pulmonary disease may experience weight loss due to dyspnea and the increased energy needed for respiration. Other physical causes of involuntary weight loss include heart failure, infections, and neurological disorders such as Parkinsons disease and stroke.
Other Causes of Malnutrition and Involuntary Weight Loss in the Elderly

Medications Emotional Problems (depression) Anorexia tardive (nervosa); alcoholism Late-life paranoia Swallowing problems Oral factors No money Wandering and other dementia-related behavior Hyperthyroidism, hyperparathyroidism, hypoadrenalism Enteric problems (malabsorption) Eating problems (inability to feed self) Low-salt, low-cholesterol diets Social problems (isolation, ethnic food preferences)
Source: Kamel HK, Morley JE. Anorexia of ageing. In: Oxford Textbook of Geriatric Medicine, 2nd Ed. Evans JG, Williams TF, Beattie BL Michel JP, Wilcock GK (Eds).Oxford University Press, New York, 2000.
In addition to the medical and pharmacological causes of malnutrition and involuntary weight loss, other explanations have been proposed to explain the persistence of nutritional deficiency among the elderly. Listed here is a mnemonic for treatable causes of malnutrition that may be present in the elderly. In the community, some older adults may not be able to afford high-nutrient foods or vitamin supplements. Others may simply forget to take them. With respect to psychosocial factors, depression is by far the most important factor. Depression due to bereavement or isolation can significantly suppress appetite.
Other Causes of Malnutrition and Involuntary Weight Loss in the Elderly

Other psychosocial conditions that may contribute to poor intake include dementia and alcoholism. Elderly people with dementia often dont recognize the need to eat. They may become paranoid about eating or develop apraxia of swallowing. Older adults who are more sociopathic may use their refusal to eat as a way to achieve another goal. Patients who require downgrading of their diet from solid or chopped food to puree or liquid because of dysphagia are at risk for malnutrition or weight loss. Altered sense of taste and smell may be age-related, drug-induced or may be secondary to neurological, endocrine, craniofacial or other disorders. Oral problems may be a factor, given that almost half of all Americans have lost a large percentage of their teeth by age sixty-five. In one study of veterans with an average age of seventy-seven, the number of oral problems was the best predictor of involuntary weight loss.
Consequences of Malnutrition
Behavioral: Confusion, somnolence, apathy, irritability, memory loss, decreased concentration Musculoskeletal: Weakness, decreased mobility, decreased work capacity, decreased potential for rehabilitation Pulmonary: Diaphragmatic atrophy, impaired secretion clearance, decreased vital capacity, tidal volume, respiratory rate, minute ventilation, decreased hypoxic ventilatory response Cardiovascular: Decreased cardiac reserve, ECG changes, decreased myocardial contractility and compliance Integumentary: Skin breakdown, increased risk of infection Pharmacological: The transport, metabolism and elimination of drugs Malnutrition can lead to numerous other problems. Behavioral changes include confusion, somnolence, apathy, irritability, memory loss and decreased concentration. Musculoskeletal system involvement is seen as weakness, decreased mobility, decreased work capacity, and decreased potential for rehabilitation. Wound healing can be impaired. Pulmonary involvement may take the form of diaphragmatic atrophy, impaired secretion clearance, decreased vital capacity, tidal volume, respiratory rate, and minute ventilation as well as decreased hypoxic ventilatory response.
Consequences of Malnutrition
The impact of malnutrition on the cardiovascular system may result in decreased cardiac reserve, produce ECG changes such as sinus bradycardia, or prolonged QT-interval and may produce decreased myocardial contractility and compliance. Increased risk of infections may result from altered anatomic barriers due to skin breakdown. Malnutrition also affects the transport, metabolism and elimination of drugs. Protein malnutrition leads to decreased albumin, reducing the protein binding of some drugs. In addition to protein deficiency, other nutrient deficits that can impair drug metabolism include ascorbic acid, niacin and riboflavin deficiencies. Starvation or prolonged fasting also slows drug metabolism. Renal excretion of drugs is decreased in the presence of edema, which may be associated with both protein malnutrition and congestive heart failure.
Micronutrient Deficiencies Seen in Elderly Patients After Vitamin Supplementation
NUTRIENT Vitamin C Thiamine Niacin Folate Vitamin B6 Vitamin B12
ALL ELDERLY (%) 6.7 10.0 30.1 11.3 28.0 14.8
INSTITUTIONAL (%) 2.1 2.5 33.1 13.1 33.8 13.2 25
NON-INSTITUTIONAL (%)
26.3 16.6 2.9 13.8 18.6
Source: Delafuente, J. C. & Stewart, R. B. (Eds.) Therapeutics in the elderly. Cincinnati: Harvey Whitney Books; 1998.
Low nutrient intake also leads to low vitamin intake. Reduced blood levels of vitamins A, D, and the water soluble vitamins are frequently found among long term care residents. Vitamin A is one of the only vitamins whose requirements decrease with age. This is due to an increase in absorption and a decrease in hepatic uptake. Studies have shown that although symptomatic deficiencies are rare, subclinical deficiencies are prevalent. In one study, mineral and vitamin deficiencies were reported in sixty-four percent of elderly taking multivitamin supplements and ninety-one percent of elderly not taking such supplements. The most common vitamin deficits among unsupplemented institutionalized elderly are B-6, niacin, and B-12. In unsupplemented community dwelling elderly, the most common deficits were in B-12, thiamine, and vitamin C, which is necessary to promote neutrophil function. Dietary folate absorption may decrease, which can lead to reduced thiamine levels. Deficiencies in iron and other trace minerals are common among nursing home residents. Homebound or long term care residents are at particular risk for Vitamin D deficiency due to low sunlight exposure especially those living in a colder climate. Vitamin D deficiency may also result from inadequate intake, impaired intestinal absorption, and age-related changes in the skin which impair sunlight-induced Vitamin D production. Drugs such as phenytoin, and altered hepatic and renal metabolism of Vitamin D to its active form, can also cause vitamin D deficiency.
Drugs that Can Cause Micronutrient Deficiencies

DRUG Alcohol MICRONUTRIENT INTERACTION Zn, Vitamins A, B1, B2 B6, B12, folic acid Vitamin B1, folate, total calories Vitamin B12 Zn, total calories Zn, Vitamin B6, potassium Pyridoxine, niacin Calcium, Vitamins A, D, E, K, B2, B12 Total calories, Vitamin B12 Vitamin D Vitmain C, folate Total calories Total calories Folate
To diagnose micronutrient deficiencies it is essential to obtain a detailed medication history. Such a history is necessary because of the numerous drug-nutrient interactions. Drugs that can cause micronutrient deficiencies are listed on your screen. Each class of drug promotes nutritional deficiency through a different pathogenic mechanism. For example, antacids can cause aluminum-induced constipation or magnesium induced diarrhea. Diuretics can lead to electrolyte loss which may be manifested as asthenia.
Antacids Colchicine Digitalis Diure<cs Isoniazid (INH) Levodopa (L-dopa) MeMormin Phenytoin Salicylates SSRIs Theophylline Trimethoprim
Source: Morley, J. E. & Silver, A. J. (1995). Nutritional issues in nursing home care. Ann Intern Med; 123:859-9.
Physical Findings Associated with Nutrient Deficiencies

DEFICIENT NUTRIENT Calcium Calorie / protein Cyanocobalamin (Vitamin B12) Folate Iron Niacin(Vitamin B3) FINDINGS Tetany, muscle weakness, osteoporosis, osteomalacia Anorexia, apathy, irritability, flaking dermatitis, depigmentation, parotid enlargement, bradycardia, hypotension, respiratory depression, edema, transverse lines on nails, hepatomegaly, anemia Megaoloblastic anemia, glossitis, loss of position & vibratory sense, dementia Glossitis, macrocytic anemia, decreased thiamine absorption Microcytic anemia, nail spooning, tongue atrophy Flacking dermatitis, hyperpigmentation, diarrhea, dementia, glossitis (beef tongue), tongue fissuring, tongue atrophy
Pyridoxine(Vitamin B6) Peripheral neuropathy-paresthesia, loss of reflexes, wrist / foot drop Riboflavin(Vitamin B2) Thiamine(Vitamin B1) Vitamin A Vitamin C Vitamin D Vitamin E Zinc Flaking dermatitis, scrotal dermatosis, photophobia, blurring, glossitis, cheilosis, angular stomatitis, tongue atrophy Confusion, edema, muscle tenderness, peripheral neuropathy Follicular hyperkeratosis, night blindness, decreased recovery after glare, photophobia, xerosis, senile macular degeneration, poor wound healing Perifollicular petechiae, bruising, bleeding gums, poor wound healing Bone tenderness, muscle weakness Cerebellar degeneration, peripheral neuropathy Flaking dermatitis, hypogeusia, poor wound healing
Source: Jensen GL, Binkley J. Clinical manifestations of nutrient deficiency. JPEN 2002; 26:S29-S33. Copyright 2011 American Society of Consultant Pharmacists
Physical Findings Associated with Nutrient Deficiencies

The physical findings that may be associated with nutrient deficiencies are listed on your screen. For example, low Vitamin C levels have been associated with pressure ulcer formation and protein-energy malnutrition. Vitamin D deficiency may be an important factor in the pathogenesis of hip fractures. Both zinc and selenium deficiencies can aggravate immune deficits and delay wound healing.
Laboratory Studies for Assessment and Monitoring

Serum albumin Serum prealbumin Serum cholesterol Total lymphocytes Serum transferrin concentration Delayed cutaneous hypersensitivity Hematological tests (e.g. CBC) Chemistries with LFTs and serum calcium Serum TSH Chest X-ray Occult fecal blood Radiologic or GI studies (optional)
These laboratory studies can be useful in both screening for malnutrition and monitoring for progress following a change in the nutrition regimen. Laboratory studies such as complete cell count, liver function tests, and thyroid stimulating hormone levels are important in establishing or confirming a diagnosis of involuntary weight loss. A chest x-ray is often the most useful examination. Additional radiologic studies and more extensive laboratory testing should be directed by the initial evaluation. GI studies may be especially useful. If the initial evaluation is inconclusive, careful follow-up is usually more productive than undirected diagnostic testing. Because rapid protein losses decrease serum albumin but do not indicate the status of visceral protein, the use of albumin as an indicator of early malnutrition is limited. Its twenty-day half-life does make it unsuitable for determining early response to nutritional therapy. However, prealbumin has a shorter half-life than albumin, and is an earlier marker of nutritional status and change in nutritional status. Protein-energy malnutrition is usually accompanied by anemia and relative neutropenia. The total lymphocyte is also decreased. Initial laboratory tests should also include electrolytes, and calcium, magnesium, and phosphorus. Patients should be weighed at least monthly and labs should be obtained at least twice a year in patients with suspected malnutrition.
Managing the Malnourished Elderly Patient
Management of Nutritional Factors: Provision of sufficient calories Vitamin supplementation Protein-calorie supplements Dietary counseling Management of Social Factors: Social workers Other community resources Management of Psychological Factors: Psychotherapy Drug therapy Management of Medical Factors: Treatment of underlying condition Review and reduction of medications
Nutritional support of patients with protein-energy malnutrition or micronutrient deficiencies begins with the provision of enough proteins, vitamins and minerals to maintain body weight and immune system integrity, avoid catabolism of muscle mass, promote tissue repair, and prevent electrolyte disturbances. While nutritional supplements may be ineffective in the face of overwhelming pathology, such supplementation may delay further decline while the underlying disease is being treated. These supplements should be taken between meals to avoid reducing intake at mealtime. Management of the anorexic geriatric patient should focus on identification and treatment of the underlying medical, psychological, or social causes. Social causes of involuntary weight loss are best addressed through referrals to appropriate community resources; psychiatric causes are best addressed by psychotherapy. The management of medically-induced involuntary weight loss may involve a drug regimen review and reduction of the or changes in the patients medication regimen. It is important to recognize that involuntary weight loss may be unavoidable. Elderly patients may not fully recover their normal weight following stressful events such as surgery, acute illness and hospitalization. Early attention to nutrition and prevention of further weight loss at such times is key to avoiding further complications.
Managing Nutritional Deficiencies: Vitamin Supplements

Vitamin C: Promotes healing of pressure ulcers Thiamine: Improves cognitive functioning in patients with deficiency Calcium: Slows bone loss Vitamin D: Increases calcium absorption, stimulates both osteoblast and osteoclast activity
Vitamin supplementation can reduce the incidence of skin problems such as hemorrhage, cheilosis, and dryness in malnourished elderly patients.It has also been shown to reduce the incidence of infections. Vitamin C is often prescribed to promote the healing of pressure ulcers. Thiamin supplements have shown to improve cognitive functioning in elderly with established vitamin deficiency. Calcium supplements can slow bone loss significantly, and should be prescribed for patients on hormone replacement therapy with a calcium intake of less than one thousand milligrams per day. Vitamin D supplementation can increase calcium absorption and stimulate both osteoblast and osteoclast activity. Whether Vitamin D or an active metabolite is administered depends on the bodys ability to convert Vitamin D to 25-hydroxyvitamin D in the liver and to 1,25-dihydroxyvitamin D in the kidney. With aging there is less efficient conversion of 7-dehydrocholesterol to cholecalciferol in the skin.
Managing Nutritional Deficiencies: Pharmacological Options

Corticosteroids: may increase appetite, but not necessarily weight; side effect of steroid-induced psychosis Megestrol acetate (Megace): may increase appetite and weight, but side effects include adrenal insufficiency and confusion (esp. in elderly) Dronabinol (Marinol): may increase appetite and weight, but side effects include amnesia, ataxia, confusion and hallucinations (increased risk in elderly) Mirtazapine (Remeron) and other atypical antipsychotics: may increase appetite and weight as a side effect of the medication.
Pharmacological treatment of involuntary weight loss is limited. While randomized clinical trials have shown that corticosteroids can increase appetite in cancer patients, there is no evidence of weight gain. Megestrol acetate or Megace is a synthetic progestational agent that has been shown to increase both appetite and weight in advanced cancer patients. Drawbacks of the drug include adrenal insufficiency and confusion. Dronabinol is a cannabinoid antiemetic approved for appetite stimulation in AIDS patients. Mirtazapine and similar atypical antipsychotics have also been considered to help promote intake. Increased appetite and weight gain has been reported as a side effect of these drugs in as many as 17% of patients.
Managing Nutritional Deficiencies: Changing The Mechanics of Eating
In the long-term care setting, caloric intake in malnourished patients can also be improved by making simple changes in the way patients eat. Another is the use of special tableware that accommodates physical disabilities such as stroke and tremors. Patients who have difficulty swallowing should be seated as erect as possible.
Resources
For additional information, see: ASPEN Board of Directors and the Clinical Guidelines Task Force.Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients.JPEN 2002; 26(1 Suppl). American Society of Consultant Pharmacist. (1998). Enteral policy and procedure manual. Alexandria, VA: ASCP. Barnett, Y. A. (1994). Nutrition and the aging process. Brit J Biomed Sci; 51(3): 278-87. Beattie, B .L., Louie, V. Y., & Dwyer, J. (1995). Chapter 23: Nutrition and health in the elderly-. In: Reichel ,W. (Ed) Care of the Elderly-Clinical Aspects of Aging, 4th ed. Baltimore: Williams and Wilkins: 223-43. Berry, E. M. (1994). Chronic disease: how can nutrition moderate the effects. Nutrit Rev; 52(Pt 2): S28-30. Buchowski,M. S. & Sun, M. (1996). Nutrition in minority elders: current problems and future directions. J Health Care Poor Underserv; 7(3): 184-209. Casper, R. C. (1995). Nutrition and its relationship to aging. Experi Gerontol; 30(3-4): 299-314. Castle, S., et al (1995).Megestrol acetate suspension therapy in the treatment of geriatric anorexia/cachexia in nursing home patients.J. Am Geriatr Soc.43: 835. Chandra, R. (1995). Nutrition and immunity in the elderly: clinical significance. Nutrit Rev; 53(Pt 2): S80-3; discussion S83-5. Detsky, A. S., Smalley, P. S, & Chang, J. (1994). Is this patient malnourished? JAMA; 271:54-58.
Resources
Evans, W. J.(1996). Effects of aging and exercise on nutrition needs of the elderly. Nutrit Rev; 54(Pt 2): S35-9. Feinberg, M., et al. (1993). Enteral nutrition formulas and drug interactions:problems and solutions. Consult Pharm; 8(9): 975-983. Jensen GL, Binkley J.Clinical manifestations of nutrient deficiency.JPEN 2002; 26:S29-S33. Kamel HK, Morley JE.Anorexia of ageing.In: Oxford Textbook or Geriatric Medicine.2nd Ed. Evans JG, Williams TF, Beattie BL Michel JP, Wilcock GK (Eds).Oxford University Press, New York, 2000. Lipschitz DA. Nutrition and ageing.In: Oxford Textbook or Geriatric Medicine.2nd Ed. Evans JG, Williams TF, Beattie BL Michel JP, Wilcock GK (Eds).Oxford University Press, New York, 2000. Long, C. D., et al. (1993). Drug-induced nutritional complications among nursing home residents:a pilot study. Consult Pharm; 8(6): 637-641. Loprinsky, C. L.(1992). Megestrol acetate for anorexia and cachexia.Oncology, 49(Suppl): 46. Marton, K. I.(1981).Involuntary weight loss: Diagnostic and prognostic significance.Ann Int Med, 95: 568. Moore, S. A. (1994). Educating the family and the patient about nutrition. Prim Care Clin Office Pract; 21(1):69-83. Morley JE.Orexigenic and anabolic agents.Clin Geriatric Med 2002; 18(4):853-66. Morley, J. E. & Kraenzle, D. (1994).Causes of weight loss in a community nursing home.J AmGeriatr Soc, 42:583.
Resources
Morley, J. E. & Silver, A. J. (1995). Nutritional issues in nursing home care. Ann Intern Med; 123(11): 850-9. Omran ML, Morley JE.Assessment of protein energy malnutrition in older persons, Part I: History, examination, body composition, and screening tools.Nutrition 2000;16:50-63. Omran ML, Morley JE.Assessment of protein energy malnutrition in older persons, Part II: Laboratory evaluation.Nutrition 2000; 16-131-140. Pirlich M, Lochs H.Nutrition in the elderly.Best Pract Res Clin Gastroenterology 2001; 15:869-884. Wallace, J. T. & Schwartz, R. S. (1997). Weight loss in elderly outpatients. Clin Geriatr Med, 13(4): 717. Wallace, J. T. et al.(1995).Involuntary weight loss in older outpatients:Incidence and clinical significance.J Am Geriatr Soc, 43: 329.
Enteral Feeding of the Elderly

Learning Objectives:
By the end of this review concept, you should be able to:
Identify those elderly individuals in whom enteral feedings are indicated and appropriate, as well as those in whom enteral feeding is contraindicated Describe factors to be considered when administering enteral feeding in the elderly, including common access sites, administration rates, complications and medication administration via feeding tubes Describe ethical issues involved in withholding or withdrawing nutrition or fluids in the elderly
Introduction to Nutrition in the Elderly

Resting energy expenditure decreases Decrease in muscle mass Decrease in physical activity Less hungry and rapid satiety Delayed gastric emptying
Energy requirements decline due to a decrease in resting energy expenditure and decrease in muscle mass as we age. Reduced thyroid function does not appear to contribute to these reduced energy needs. As we age, there is also a decrease in physical activity. This may be due in part to concomitant disease states of angina, bone and joint disorders, lung disease, or loss of postural stability. Some older adults may also experience a decrease in gastric emptying leading to an early sensation of satiety which can result in a decrease in total calories.
Managing Nutritional Deficiencies with Enteral Feeding

General Indications: Patients who cannot consume sufficient nutrients alone or with assistance to maintain a stable weight Patients with a fully or partially functional GI tract Indications for Short-term Therapy: Patients who are alert and functional Examples: patients recovering from hip or knee surgery, pressure ulcers, COPD, depression Indications for Long-term Therapy: Patients who refuse to eat Patients who are unable to eat or swallow Patients with nonobstructive dysphagia
Managing Nutritional Deficiencies with Enteral Feeding
Enteral nutrition support via tube feedings should be considered for elderly patients who are unable to consume sufficient nutrients alone or with assistance to maintain a stable weight, have a fully or partially functional gastrointestinal tract, and have no contraindications to the use of tube feedings. It is important when considering the use of artificial methods of feeding whether the intake problem will be short or long term. Patients who are alert and functional may benefit from the use of a nasogastric tube for short course of supplementation. Examples include patients recovering from hip or knee surgery, pressure ulcers, or other kinds of acute conditions. Early enteral supplementation has been shown to decrease morbidity and mortality in patients recovering from orthopedic surgery, chronic obstructive pulmonary disease, and depression. The most common indications for chronic tube feeding in long term care include refusal or inability to eat or to swallow and nonobstructive dysphagia, such as in patients with endstage dementia, head and neck surgery, or stroke. There is a recent trend toward the early use of enteral supplements, especially among rehabilitation patients, and this may decrease morbidity and mortality.
Common Routes for Enteral Feeding

Short-term Therapy (< 3 months): Nasoenteric tube Long-term Therapy (> 3 months): Surgical gastrostomy for patients with esophagitis or pharyngitis, at high risk for aspiration, inability to use nasallyplaced tubes or undergo an endoscopic procedure Endoscopic or laproscopic gastrostomy Surgical or percutaneous jejunostomy patients with significant GERD, need to bypass stomach placement
Selection of the proper enteral feeding device is based on the patients gastrointestinal function and anatomy, anticipated duration, and the potential for aspiration. The most common access sites for enteral tube feedings include nasoenteric routes, gastrostomy and jejunostomy. The nasoenteric route is used for short term enteral therapy because of low complication rates, being relatively inexpensive and easy to place. Nasoenteric tubes are placed through the nose and may terminate in the stomach, duodenum, or jejunum.
Common Routes for Enteral Feeding
For long term therapy, it is best to obtain permanent access, which frequently means the placement of a gastrostomy tube. Gastrostomies may be placed surgically, endoscopically or laproscopically. Gastrostomy tubes are placed through the abdomen and are the most common method for long-term access. It eliminates nasal irritation and the psychosocial stress of a nasoenteric tube. A surgically placed gastrostomy tube may be indicated for those patients who experience complications with nasoenteric tubes such as esophagitis or pharyngitis; are at high risk for aspiration; have a physical condition that precludes the use of nasally-placed tubes; or are unable to undergo an endoscopic procedure. A PEG tube is a percutaneous endoscopically placed gastrostomy tube, which involves a non-surgical procedure and can be used to provide long term nutritional support. These tubes are favored because general aesthesia is not needed. Jejunostomy tubes may be useful for those patients who have significant gastroesophageal reflux and in whom gastrostomy feedings continue to pose an aspiration risk. Jejunostomy tubes may also be used when it is advantageous to bypass feeding placement in the stomach. Feeding jejunostomies may be placed surgically or percutaneously.
Contraindications to Enteral Nutrition
Intractable vomiting or diarrhea Diffuse peritonitis Severe small bowel ileus High output enterocutaneous fistula (> 500 mL/day) Acute pancreatitis (relative contraindication) Short bowel syndrome (<50% of small bowel remaining) Severe GERD Inability to obtain enteral access Complete intestinal obstruction (depending on location) Hypovolemia or septic shock Prognosis does not warrant aggressive nutrition support
Contraindications to the use of enteral feedings include intractable vomiting, severe diarrhea, and intestinal obstruction. Acute pancreatitis is a relative contraindication, because these patients can be fed enterally in the distal duodenum or jejunum, and bypass stimulating the pancreas. Enteral feedings should be avoided if the prognosis does not warrant aggressive nutrition support.
Factors to Consider When Preparing to Administer Enteral Feedings

Access site Tube caliber (1 French unit = 0.33mm) Formula volume and type Gastric emptying Gastrointestinal tolerance Ease of administration Clinical status of patient
There are various factors that must be considered when selecting a method and schedule for administering enteral feedings. Nasoenteric tubes may presidpose the patient to nasopharyngeal ulcers, sinusitis, nasal septum necrosis, otitis, hoarseness, and vocal cord paralysis. They may compromise lower esophageal sphincter competency, thereby increasing the risk of gastric reflux and aspiration. In patients being fed via the nasogastric route, the use of an isotonic enteral formula may be preferred over a hyperosmolar formula since gastric emptying is quickest with isotonic preparations. Small-bore feeding tubes made of silicone or polyurethane, in sizes from 5 French to 12 French, are soft, smooth, and flexible compared to the large-bore, stiff, nasogastric tubes. The smaller tubes lower the risk of nasal-tissue necrosis and are much more comfortable for the patient.
Types of Administration Schedules for Enteral Feeding

Continuous Feeding: Indications: preferred for initial feeding, patients who have not been fed for 3 days, patients who are unstable or chronically ill, patients with duodenal or jejunal feeding sites Administration: total volume required delivered at a slow continuous rate Monitoring: check for gastric residuals every 4 8 hours Drawbacks: requires frequent interruptions for drug administration Bolus Feeding: Indications: patients who require gastric feedings Contraindications: patients with high risk of aspiration, patients with GI complaints Administration: 200 400 mL delivered over a short period several times a day (4-6) to mimic usual eating patterns Drawbacks: nausea, abdominal bloating, cramping, diarrhea, higher risk for aspiration Monitoring: check for gastric residuals prior to and 2 hours after feeding Intermittent Feeding: Indications: patients who require gastric feedings Contraindications: patients with high risk of aspiration Administration: 250 400 mL over 30 60 minutes, x 5 8 times/day Monitoring: check for gastric residuals prior to and 2 hours after feeding Cyclic Feeding: Indications: stable patients at low risk for aspiration, patients who are progressing to oral feedings, patients unable to tolerate intermittent or bolus administration Administration: continuous over 8 16 hours/day Monitoring: check for gastric residuals every 4 8 hours
Types of Administration Schedules for Enteral Feeding
Enteral feedings may be administered continuously, intermittently, cyclically or by bolus. Continuous administration is preferred when tube feeding is being initiated; the patient has not been fed for three or more days; the patient is unstable or is critically ill, including patients at risk for aspiration; and when duodenal or jejunal feeding sites are used. Cyclic administration is continuous feeding for a finite time period. It is generally indicated for stable patients at lower risk for aspiration and patients who are progressing to oral feedings. This method is also used for patients who are unable to tolerate intermittent or bolus administration, but who need to be periodically disconnected from the feeding pump. Enteral feeding is provided over eight to sixteen hours a day. For example, in a patient who complains of fullness during the day and lack of appetite, stopping the enteral feeding during the day and infusing only at night may improve their feeding. Bolus administration involves delivery of two hundred to four hundred milliliters of formula via a feeding tube over a short period several times a day. This method is poorly tolerated and can result in nausea, abdominal bloating, cramping, diarrhea, and it may increase the risk for aspiration. Bolus feedings are restricted to gastric feedings and are contraindicated in patients at high risk for aspiration or patients currently experiencing gastrointestinal complaints. Gastric residuals should be checked every four to eight hours for patients receiving either continuous or cyclic feedings, and prior to and two hours after intermittent or bolus feedings. Intermittent feeding is similar to the bolus feeding except the prescribed feeding is administered over a longer period of time, usually 30-60 minutes. This is usually infused by gravity drip. Administering the tube feeding in this way may be warranted in patients that experience high gastric residuals or abdominal discomfort with bolus feeding.
Selection of Enteral Feeding Formulas

Proportion of carbohydrate, protein, and fat Disease-state specific formulations Lactose-intolerance Fiber-containing Osmolarity
Many enteral nutrition products are on the market currently, and there are a few that are commonly used. There are also specialty formulas to target specific disease states, such as diabetes, renal or hepatic disease, that have entered the market in recent years. This has made finding a cost-effective formula a challenge. Most standard formulations contain 1 kilocalorie per mL and have a well-proportioned mix of carbohydrate, protein, and fat. Most formulas are lactose-free, so lactose intolerance is less of an issue. The intent of fiber-containing products is to regulate bowel function. Patients who develop either constipation or diarrhea on a fiber-free product may be a candidate for a fiber containing formula. Finally, some of the higher calorie formulas have a higher osmolarity which can cause diarrhea.
Enteral Feeding Formulas

Standard Isotonic Formulas: (Osmolite, Isocal) Balanced nutrient composition Made of isolated sources of intact protein, carbohydrates, fat Low osmolality (300 500 mOsm/L) Lactose-free Standard Fiber-Containing Formulas: (Ultracal, Jevity) Same composition as isotonic formulas Soy polysaccharide is the protein source Fiber content can vary from 4 20 g/L
There are several types of commercially available enteral formulas which meet general or specific nutritional needs. Polymeric formulas are made of isolated sources of intact protein, carbohydrates, and fat. They usually have low osmolality and usually do not contain lactose. Standard enteral products when given in amounts recommended supply the RDA for nutrients. Many of the formulas in this category are unsweetened in order to maintain their osmolarity, and are therefore not palatable for oral supplementation.
Elemental/Peptide-Based Enteral Formulas

(Vivonex, Peptamen) Amino-acid/peptide based containing hydrolyzed nutrients Indicated for patients with maldigestion or malabsorption, small bowel Crohn's disease, enterocutaneous fistula, small bowel resection Low residue Lactose free
Elemental formulas are amino-acid/peptide based formulas which contain smaller, predigested nutrients. The protein is in the form of dipeptide and tripeptides and a lower proportion of free amino acids. This optimizes the protein absorption. These formulations are also higher in fat content, and use medium chain triglycerides as the fat source. These are low residue and lactose free. They are usually indicated for patients with maldigestion or malabsorption. They may also be used in patients with small bowel Crohn's disease, enterocutaneous fistula, shortly after small bowel resection, and in other conditions in which diarrhea may be a problem.
High-Protein Formulas
(Promote, Traumacal) Useful in patients who require increased protein (trauma, burns, pressure sores, surgical wounds)
Patients with disease states that require high amounts of protein may benefit for specialty high-protein formulas. Often with standard formulas, in order to meet the protein needs necessary for these disease states, the volume needed would lead to overfeeding with excessive non-protein calories.
High-Calorie Formulas
(Deliver 2.0, Two-cal HN) Concentrated to provide less fluid and electrolyte intake Provides 2 kcal/mL Similar proportions of carbohydrate, protein, and fat as standard formulas, but 50% less volume Increased osmolarity (>600 mOsm/L)
High-calorie enteral formulas are indicated for patients who require less fluid and electrolyte intake as in congestive heart failure or renal failure. They are half the volume with the same nutrient proportions as the standard formulas. These formulas are higher in osmolarity and this increases the risk adverse GI effects,, but they are still a well-tolerated tube feeding formula.
Disease / Condition-Specific Enteral Formulas

Renal disease: Modified protein and electrolyte composition and low fluid and mineral content (e.g., Suplena, Nepro) Immunodeficiency: Supplemented with arginine, fish oils and nucleotides (Advera) Hepatic disease: High branched chain amino acid to aromatic amino acid ratio (e.g., Hepatic-Aid) Metabolic stress: Fortified with branched chain amino acids, glutamine, arginine, and omega-3 fatty acids (e.g., TraumaCal) Pulmonary disease: High percentage of calories from fat (e.g., Pulmocare) Diabetes: Low in carbohydrates, high in fat and are supplemented with fiber (e.g., Glucerna) HIV / AIDS: High in calories and protein but low in fat (e.g., Immun-Aid)
Disease / Condition-Specific Enteral Formulas
Disease or condition-specific formulas are designed to meet the special metabolic demands associated with different disease states. Renal preparations contain modified protein composition and low fluid and mineral content. Formulas designed for immunosuppressed patients are supplemented with arginine, fish oils and nucleotides. However, the value of these preparations has not been proven. Hepatic disease formulas contain a high branched chain amino acid to aromatic amino acid ratio. Branched chain amino acids do not undergo liver metabolism. Immune-modulating tube feedings are fortified with branched chain amino acids to support increased muscle proteolysis along with glutamine, arginine and omega-3 fatty acids. Pulmonary formulas have a high percentage of calories from fat to minimize carbon dioxide production. Formulations designed for patients with diabetes mellitus are low in carbohydrates, high in fat and are supplemented with fiber to improve glycemic control. HIV/ AIDS formulations are high in calories and protein but low in fat.
Complications of Enteral Feeding
Gastrointestinal: Increased gastric residuals Nausea/vomiting/abdominal distention Aspiration Diarrhea Constipation Metabolic: Hyperglycemia Dehydration Mechanical: Tube occlusion Tube positioning
Gastric residual volumes refers to the volume of gastric contents obtained by aspirating from a nasogastric or gastrosomy tube. Patients with increased residuals are prone to vomiting and aspiration. Nausea, vomiting, and abdominal distention occurs from gastric residuals and decreased gastric emptying. Pulmonary aspiration is the most serious complication and potentially life-threatening. Rapid bolus of enteral nutrition may be associated with higher risk of aspiration compared to continuous infusion. Before concluding that the enteral feed itself is the cause of GI upset, other possibilities must be ruled out. Medications are a common cause of diarrhea, most often due to antibiotics which change the intestinal flora. Sorbitol is another agent that is found in liquid forms of medications, usually elixirs, such as acetaminophen and can cause diarrhea. Rapid advancement or introducing large amounts of tube feeding in the small bowel can also cause diarrhea and intolerance. Bowel function may be improved by increasing fluid intake and switching to a fiber-containing formula. Impaction and obstruction should be ruled out. Metabolic complications are easily prevented or managed with proper monitoring and treatment.
Complications of Enteral Feeding
Hyperglycemia may occur in those patients that are glucose intolerant, have diabetes, are receiving corticosteroids, or those with severe metabolic stress. Dehydration may also occur with tube feed administration because the formulas do not supply much free water. It is imperative, especially in those receiving a higher calorie formulation to also have adequate fluid intake. This may require the administration of free water intermittently throughout the day. Electrolyte imbalance from enteral nutrition alone is uncommon and requires much less stringent monitoring compared to parenteral nutrition. Tube occlusion is most commonly caused by medications improperly administered through the tube. The tube can also kink causing an occlusion and interruption in feeding. Finally, The patient themselves may remove or reposition the feeding tube, especially if they are agitated or confused.
Medication Administration via Feeding Tube

Factors in Deciding Whether to Administer Medications via the Feeding Tube: Availability of liquid medications Whether solid dosage forms can be crushed Compatibility of medication with enteral feeding Potential for drug-nutrient and drug-drug interactions Cost and comfort compared to other available routes General Guidelines: Consider an alternative route for medication administration Use liquid rather than solid dosage forms when possible Pellets of some microencapsulated dosage forms can be used provided that the pellets themselves are not crushed and will fit through the tube lumen. Dilute liquid medications with 10 mL of water prior to administration Never add medications directly to the feeding formula With high osmolality drugs, dilute with a higher volume of water and watch for signs of diarrhea To avoid interactions that reduce their effectiveness, stop feedings and flush tubes before and after administering medications
Medication Administration via Feeding Tube
Several factors need to be considered when administering medications via a feeding tube. They include the availability of commercial liquid medications, whether the medications can be crushed, whether the medications are incompatible with the enteral feeding, and the potential for drug-nutrient interactions. When possible, an alternative route of medication administration should be considered before opting to administer a medication via a feeding tube. If tablets are used, they should be crushed prior to administering down the feeding tube. However, crushed medications can clog a feeding tube, especially smaller bore tubes. If available, liquid medications should be used. The pellets inside of some microencapsulated dosage forms can be administered via a feeding tube provided that the pellets themselves are not crushed. Liquid medications should be diluted with ten milliliters of water prior to administration. Medications should never be added directly to the formula since the medication may interact with the formula to form a gel or insoluble precipitate. Enteral feedings may interfere with the absorption or therapeutic effect of some medications. For example, when phenytoin suspension is given concomitantly with enteral feedings, the bioavailability of the antiepileptic medication is reduced fifty to seventy percent. Enteral feedings should be stopped for two hours before and after the administration of phenytoin, and the feeding tube should be flushed before and after each dose of medication. Warfarin may bind to the components of enteral feedings, thereby decreasing its absorption. Therefore, feedings should be held before and after administration as well.
Medications that are Physically Incompatible with Enteral Formulas

Phenytoin Penicillin Tetracycline Isoniazid Rifampin Enoxacin Norfloxacin Warfarin
The drug-nutrient interactions to be aware of are those that alter the bioavailability of the drug. There are very few studies that have assessed the effect of enteral nutrition on the absorption and desired outcome. The drugs listed here require the tube feedings to be held two hours before and two hours after administration. Phenytoin and warfarin are two drugs that have published evidence in the literature of the effect of enteral nutrition on the bioavalibility of these agents. Many of the antibiotics listed here are based on case reports and theoretical concerns. In addition, many enteral products contain vitamin K, and higher dosing of warfarin may be required in tube feed patients despite most products containing only the recommended daily allowance of 200 micrograms per liter of vitamin K.
Ethical Issues: Withholding Food and Fluid

American Society Society on Parenteral and Enteral Nutrition Guidelines: Legally and ethically, parenteral or enteral nutrition should be considered a medical therapy Caregivers should be informed of the benefits and risks of parenteral or enteral nutrition, including the interventions required in order to receive it Patients should be encouraged to have living wills and/or advance directives to discuss their wishes with their families Adult patients or an authorized surrogate has the right to accept or refuse parenteral or enteral nutrition Institutions should have clear policies regarding the withdrawal or withholding of parenteral or enteral nutrition and communicate these policies to patients
The issue of withholding or withdrawing nutrition is always difficult and often controversial. Whether or not tube feedings in an elderly terminally ill, demented resident who has stopped eating is viewed as beneficial or harmful may depend most importantly on personal values. However, the current clinical and judicial position is that parenteral and enteral nutrition are medical treatments and thus are subject to the same risk versus benefit analysis as other therapies. They may be discontinued in accordance with the principles and practices governing the withholding and withdrawing of other medical treatments. The American Society on Parenteral and Enteral Nutrition has promulgated guidelines addressing these ethical concerns. These guidelines are listed above.
Resources
For additional information, see: American Society for Parenteral and Enteral Nutrition.Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients. JPEN 2002; 26(Suppl 1): 1SA-96SA. Gross, M. E. (1990). Phenytoin and enteral products. Consult Pharm; 5:484, 486. Janson DD, Chessman KH.Enteral nutrition.In: Pharmacotherapy: A pathophysiologic approach. 5th Ed.Dipiro JT, Talbert RL, Yee GC, etal (Eds.).New York:McGraw Hill, 1999. Kale-Pradhan PB, Elnabtity MH, Park NJ, Laus M.Enteral nutrition in patients with pancreatitis.Pharmacotherapy 1999; 19:1036-1041. Meyers, R. M. & Grodin, M. A. (1991). Decisionmaking regarding the initiation of tube feedings in the severely demented elderly: a review. J Am Geriatr Soc; 39: 526-31. Rollins C.Enteral nutrition.In: Pharmacotherapy Self-Assessment Program, Book 8, Gastroenterology & Nutrition. 4th Ed.Mueller BA, Bertch KE, Dunsworth TS, etal (Eds.) Kansas City: American College of Clinical Pharmacy, 2002.
Dehydration in the Elderly

By the end of this Review Concept you should be able to: Describe the effect of age-related physiological changes on homeostasis and fluid balance in the elderly, as well as risk
factors for dehydration
Describe the pathogenic mechanisms, clinical manifestations and complications associated with dehydration in the
elderly, in addition to strategies for prevention of dehydration and management of the dehydrated patient.
Assess the medical and pharmacological causes of excess fluid loss or decreased fluid intake in the elderly patient,
given a patient case.
Fluid Balance in the Elderly
Dehydration: A rapid weight loss of >3% of body weight Maintenance of Fluid Balance in the Elderly: Daily Fluid Balance = Urine Output + Insensible Water Losses - Water Produced from Endogenous Metabolism Normal fluid intake: 1500 mL/day minimum 2000 2500 mL/day recommended If volume overload: 1000 mL/day maximum 2000 3000 mL/d of water volume = 1500 mL of urine volume
There is not a true definition of dehydration, but a proposed definition is a rapid weight loss greater than 3% of body weight. Total body water decreases as we age, and as the medium in which virtually all of the bodys metabolic processes takes place, water is critically important for the elderly. To replace insensible losses and maintain renal function, older adults need a minimum water intake of approximately fifteen hundred milliliters, unless they have volume overload caused by heart failure, cirrhosis, or nephrotic syndrome. Patients with these disorders are usually on a fluid restricted diets and may only tolerate one thousand milliliters of fluid per day. In elderly nursing home residents, two thousand to twenty-five hundred milliliters per day is usually needed to help maintain urine flow, good skin turgor and to provide a safety range for excessive insensible losses. A water volume of two thousand to three thousand milliliters per day produces a urine volume of one thousand to fifteen hundred milliliters.
Age-Related Changes and the Disruption of Fluid Balance

Decline in total body water Decrease in sense of thirst and related drinking behavior Defect in urine concentrating ability
The reasons for this increased need for fluid intake in the elderly are related to the physiologic changes associated with the aging process. While these changes have little effect on basal levels of electrolytes and osmolarity, there is a natural decline in total body water due to the gradual replacement of lean body mass with body fat. A younger male is comprised of 60 to 65 % water, but in an elderly male the total body water composition declines to 50%. Since there is less amount of total body water in fat than muscle, the elderly have a greater loss of water compared to the young for a given decrease in body weight. Also, it appears that the subjective sense of thirst and consequent drinking behavior decrease somewhat with age, making it more difficult for older adults to compensate for the disruptions in fluid balance caused by serious illness or the extremes of physiological stress.
Age-Related Changes and the Disruption of Fluid Balance

In a landmark study by Phillips et. al, elderly persons in a setting of water deprivation consistently described less thirst despite a higher degree of dehydration, observed by decreased body mass, and increased plasma osmolarity. Once granted access to free water, plasma osmolarity normalized in young patients within one hour, while the osmolarity in elderly patients failed to normalize over several hours. The elderly have a limited ability to tolerate water boluses and water deprivation. Furthermore, they have a decreased ability to concentrate the urine. Anitdiuretic hormone (A-D-H) levels are not suppressed in the elderly. In younger individuals, there is a diurinal excretion of A-D-H, with increased secretion at night. The elderly are devoid of this nighttime secretion, which is noted clinically as nocturia. In addition to A-D-H, atrial naturetic peptide (A-N-P) is increased 5 times over basal levels in the elderly. This leads to the loss of water and sodium. Finally, there is a blunted renin response, and altered aldosterone secretion. The clinical response to these changes is seen with a loss of sodium and water, leading to dehydration.
Epidemiology of Dehydration
More than 1 million elderly admitted to acute care units per year One of the 10 most common reasons for hospitalization and death among Medicare patients Black elderly patients twice as likely to be hospitalized for dehydration as white elderly patients Alzheimers patients have higher incidence than other elderly Medicare costs nearly $ 0.5 billion dollars annually Associated with numerous adverse consequences such as renal failure, decreased skin turgor, confusion, lethargy, increased falls, constipation with impaction Complications include seizures, permanent brain injury and death Mortality rate among elderly = 40-70%
Source: Opus Communication, 1996
Dehydration is one of the most common reasons for hospitalization and death among Medicare recipients. Approximately one million elderly with the condition are admitted each year to acute care hospital units. Elderly black individuals are twice as likely to be hospitalized for dehydration as are elderly white individuals. The elderly with Alzheimers disease have a higher incidence than other elderly at a similar age, perhaps due to a decreased vasopressin response to dehydration. The costs of dehydration-related problems amount to nearly half a billion dollars annually, and the condition is a significant cause of morbidity. Adverse consequences of dehydration include renal failure, decreased skin turgor resulting in skin breakdown, confusion, lethargy, increased falls, and constipation with impaction. If left untreated, severe dehydration may result in seizures, permanent brain injury and death. The overall lmortality rate among the elderly with dehydration-related condition is between forty and seventy percent.
Risk Factors for Dehydration in the Elderly
Decreased fluid intake Increased fluid losses Changes in functional status Delirium Medications (i.e., diuretics, laxatives) Mobility disorders Dementia Home environment
In addition to some of the age-related changes we have discussed thus far, confusion and dementia may also contribute to a decreased fluid intake by impaired communication or feeding disorders. Patient immobility, including use of restraints, may contribute to dehydration. Many long-term institutionalized patients are vulnerable to dehydration because of the time required by the staff for feeding and the patients may not receive adequate hydration. For those patients that live in the community, particularly in the hot summer months, they may have little to no access to air conditioning leading to an increase in water loss secondary to excessive sweating. They may also have a poor dietary intake secondary to a lack of a spouse or caregiver.
Pathogenesis of Dehydration
Excess loss of water: Altered intrarenal vasculature and glomerular function Decline in urine concentrating ability (minimum urine flow 0.5 mL/min in young adults vs. 1.0 mL/min for older adults; maximum urine osmolarity in young adults 1100 mOsm/kg vs. 882 mOsm/kg in older adults) Failure to recognize need to increase water intake: Decline in renin-angiotensin levels and sensation of thirst Altered baroreceptor function Impaired ingestion of water: Alterations in taste Gastric distention Dehydration may occur through any of three mechanisms: Excessive loss of water, failure to recognize the need to increase water intake, and impaired ingestion of water. Older adults are susceptible to excessive loss of water because urine concentrating ability declines with age. Compared to younger adults, who can decrease urine flow to a minimum of point-five milliliters per minute, older adults are only able to decrease urine flow to one point zero milliliters per minute. Age-related changes in renin-angiotensin levels and baroreceptor function may contribute to diminished thirst. Oropharyngeal factors such as altered taste and gastric distention may also affect drinking behavior in the elderly. Decreased fluid intake is also a significant cause of dehydration in the elderly, which will be discussed later in this program.
Forms of Dehydration
Hypertonic: High serum Na+ (> 150 mEq/L) High serum osmolarity (> 300 mOsm/L) Isotonic: Normal serum Na+ (135 150 mEq/L) Normal serum osmolarity (280 290 mOsm/L) Hypotonic: Low serum Na+ (< 135 mEq/L) Low serum osmolarity (< 280 mOsm/L)
Dehydration may present in one of three forms. Hypertonic dehydration occurs when the loss of more water than sodium results in high serum sodium levels. This is most commonly due to febrile illness. Hypertonic forms of dehydration can also occur with the elderly when they are not taking in enough water per day. It is considered an isovolemic hypernatremia, and is associated with hypertonicity. Isotonic dehydration, by far the most common form of dehydration, occurs with the balanced loss of water and sodium, most commonly with vomiting and diarrhea. Hypotonic dehydration is characterized by a greater loss of sodium than water, and observed with the overuse of diuretics.
Clinical Manifestations Associated with Dehydration in the Elderly
Symptoms: Alteration in mental status/ confusion Lethargy Lightheadedness/ dizziness/ syncope Decreased urine output Constipation Fever
Physical Findings: Decreased skin turgor Dry mucous membranes Tachycardia Orthostatic hypotension
Laboratory Abnormalities: Increased hematocrit Increased BUN/CR ratio Variations in serum sodium excessive blood loss
Signs and symptoms may be vague or absent in the elderly. Physical findings associated with dehydration include decreased skin turgor, dry mucous membranes, and tachycardia. However, these findings are not diagnostic. Early diagnosis is sometimes difficult because the classical presenting signs of dehydration may be absent or misleading in the elderly. Skin turgor is often unreliable and daily weights may be impractical in the nursing home setting. Dry mucus membranes may be misleading because many times elderly persons are mouth-breathers or on anticholinergic medications. Significant orthostatic blood pressure changes are considered to be a decrease in the systolic blood pressure of 20 mmHg or more, or a decrease in diastolic blood pressure of 10 mm Hg or more at 1 minute or 3 minutes from supine to sitting, sitting to standing, or supine to standing. The patient may also have an orthostatic pulse increase of 10 to 20 beats per minute also suggesting volume depletion. Beta blockers or pacemakers may limit the utility of these orthostatic pulse measurements. Increased hematocrit and blood urea nitrogen to serum creatinine ratio are associated with significant volume depletion. Serum sodium may be high, normal or low depending on the cause of volume depletion. Urinary sodium excretion is usually less than twenty milliequivalents per liter when sodium intake has been chronically reduced, or when losses have occurred from vomiting or diarrhea.
Causes of Increased Fluid Loss in Elderly

Chronic or acute infections Excessive urinary loss e.g., hypercalciuria, glycosuria, elevated BUN, diabetes insipidus, hypoaldosteronism, postobstructive diuresis, Alzheimers disease, high protein enteral feedings, diuretics GI losses e.g., vomiting, NG drainage, diarrhea secondary to infection, ischemic bowel, surgery and colectomy Excessive blood loss Environment-related fluid loss e.g., heat wave, hypothermia Compartmental fluid shifts e.g., hypoalbuminemia, pancreatitis, ascites, anaphylaxis, burns
Increased fluid losses can be caused by conditions such as pneumonia or urinary tract infections. These kinds of infections are common in the elderly, accounting for up to twenty percent of acute hospitalizations. Fever associated with acute infections and other illnesses can cause increased sensible water loss from sweating, tachypnea, emesis, diarrhea, and increased cellular catabolism. Infections of the upper urinary tract can reduce the kidneys concentrating ability. Excessive urinary loss can result from obligate diureses, glycosuria secondary to diabetes, and hypercalciuria secondary to malignancy. Gastrointestinal losses can occur through vomiting, nasogastric drainage, diarrhea and bleeding. Obligate diuresis can also result from increased protein catabolism in the gut secondary to a gastrointestinal bleed or high protein enteral feedings. Prolonged sweating from fever or environmental changes may precipitate symptoms of heat exhaustion such as thirst, giddiness, and oliguria. These symptoms may be masked in patients with Alzheimers disease and other cognitive deficits.
Pharmacological Causes of Increased Fluid Loss
Misuse of diuretics Mannitol Radiographic contrast agents Phenytoin Ethanol Lithium Laxatives
Certain medications can have a profound effect on fluid balance. Diuretic drug therapy is a common source of preventable dehydration in the elderly population, afflicting as much as ten percent of hospitalized elderly. The use of intravenous mannitol and radiographic contrast agents can also cause diuresis. Drugs such as phenytoin and ethanol suppress vasopressin release, resulting in decreased tubular reabsorption of water. Diarrhea, caused by prolonged laxative use or aggressive bowel-cleansing regimens prior to radiographic study can also lead to excessive fluid loss.
Causes of Decreased Fluid Intake in the Elderly

Limited access to fluids (e.g., physical restraints, impaired mobility) Alterations in sensorium (e.g., decreased level of consciousness or awareness secondary to illness, drugs) Dietary restriction (e.g., preop; prevention of incontinence, nocturia, aspiration; therapy for edema) GI disorders (e.g., swallowing disorders, bowel obstruction, anticholinergic medication) Alterations in thirst (e.g., primary adipsia, drug induced, focal CNS pathology) Psychosocial factors (e.g., fear of urinary incontinence)
Less appreciated than excess fluid loss are conditions that cause inadequate fluid intake in the elderly. Patients who are restrained or with impaired mobilility may not have easy access to fluids, while those who have altered levels of consciousness or awareness may not perceive the need for, or have access to, adequate fluids. Restriction of fluids may be necessary prior to diagnostic and surgical procedures. Elderly patients may restrict their own fluid intake to deal with problems of incontinence, nocturia, or pulmonary aspiration. Gastrointestinal disorders such as swallowing difficulty and bowel obstruction can limit fluid intake. Patients with ischemic bowel disease frequently find themselves in a vicious cycle in which the disease both exacerbates and is exacerbated by dehydration. Finally, cardiac glycosides and amphetamines can decrease the sense of thirst, along with conditions such as adipsia and stroke. It has been suggested that cerebrovascular accidents may permanently damage the feedback system between thirst and ADH, resulting in decreased fluid intake in patients who are both hypovolemic and hyperosmolar. Psychological factors such as fear of urinary incontinence may also result in limiting fluid intake.
Prevention and Treatment of Dehydration
Consequences of Severe, Untreated Dehydration: Seizures Permanent brain injury Death Strategies: Patient/family/NF staff education Recognition of nonspecific symptoms (e.g., anorexia, listlessness) Thorough medical history to determine etiology Thorough physical exam (e.g., BP, skin turgor, urine output (UO)) Relevant laboratory studies Accurate diagnosis
Prevention and early treatment are the most effective therapies for dehydration. In addition to patient, family, and nursing facility staff education, specific fluid prescriptions in the home or health care facility can be helpful. In the NF, water should be offered between meals. Patients who are susceptible to dehydration should be monitored for nonspecific symptoms such as anorexia and listlessness. For the patient who presents with dehydration, a thorough history should be conducted to establish the cause of fluid loss. A physical examination and laboratory studies are also essential. The severity of fluid deficit is determined by evaluation of blood pressure, orthostasis, skin turgor, and urine output. It may be helpful to compare the patients current weight with his or her premorbid baseline. It is imperative to ensure adequate oxygen delivery and perfusion to the organs and extremities.
Resident Assessment Protocol on Dehydration (RAP)
Sample Questions: Has there been a decrease in thirst perception? Is the patient/resident unaware of the need to intake sufficient fluids? Has the patient/resident or caregiver restricted intake to avoid urinary incontinence? Are fluids restricted because of diagnostic procedures or health reasons? Does sad mood, grief or depression cause the patient/ resident to refuse foods/ liquids?
The Resident Assessment Protocol or RAP part of the Minimum Data Sets helps long term care staff identify patients at risk for dehydration based on the presence of decreased fluid intake or increased fluid loss. For patients identified as being at risk for possible dehydration, the interdisciplinary care plan should state goals and interventions designed to alert staff to clinical signs of dehydration so that early interventions can be implemented. This form does not definitively identify patients suffering from dehydration but it is used as a screening tool. Some questions that the R-A-P advises the health care team to ask are: Has there been a decrease in thirst perception? Is the patient or resident unaware of the need to intake sufficient fluids? Has the patient or resident or caregiver restricted intake to avoid urinary incontinence? Are fluids restricted because of diagnostic procedures or health reasons? Does sad mood, grief or depression cause the patient or resident to refuse foods or liquids?
Calculating Fluid Deficit and Serum Osmolarity
Calculating Fluid Deficit and Serum Osmolarity Free Water Deficit or Total Body Fluid Vol (L) = weight (KG) x 0.45 x [(serum Na+/140) - 1] Serum Osmolality (mOsm)= 2(Serum Na+) + (Glucose/18) + (BUN/2.8)
When decreased extracellular fluid volume results almost entirely from water loss alone, free water deficit can be calculated using the equation shown on your screen. Zero-point-four-five is used in this equation instead of zero-point-six, because the elderly have decreased total body water relative to younger patients. Lean body mass decreases, fat increases, and total body water decreases. The calculation is not valid if the patient has also lost a large amount of sodium, resulting in hyponatremia. Serum osmolarity can be estimated using the second equation. If the measured osmolarity is significantly greater than the calculated value, the presence of abnormal unmeasured solutes such as ethanol, ethylene glycol or mannitol should be considered.
Methods of Fluid Replacement
Oral Rehydration: Preferred, if loss = 1 2 L/day Can administer free water or oral electrolyte solutions Contraindicated if patient has GI problems or altered mental status Subcutaneous Rehydration (hypodermoclysis): No longer used in practice Preferred infusion sites include abdomen, upper thigh 3 liters isotonic fluid per day (2 sites, 60 ml/hr) recommended May administer hyaluronidase to facilitate fluid absorption Intravenous Rehydration: Reserved for acute care setting If the patient is unable to drink between twenty five hundred and three thousand milliliters daily, water and electrolyte deficits can be made up through other routes. Three methods of fluid replacement may be used alone or in combination, depending on the severity of the condition and care setting. Oral rehydration with free water or electrolyte solutions is the preferred method. When the volume deficit is modest, say one to two liters, oral fluid replacement is preferred providing that the patient does not have altered mental status.
Methods of Fluid Replacement
This fluid may be provided by a variety of means. It can be ingested as fruit juices, broths, carbonated beverages, enteral formulas, intravenous fluids and foods with high water content. For patients requiring enteral feeds, supplemental free water should be provided. Sports replacement drinks are easily absorbed by the stomach, more palatable for the patient, and can correct hypertonic dehydration rapidly. If replacing fluids orally, the patients should also be monitored for signs of fluid overload. This may be observed as orthopnea, shortness of breath, alterations in sleep pattern or increased confusion. If the patient has a gastrointestinal problem or altered mental status, or if the volume deficit is more significant, intravenous fluids may be required. Hypodermoclysis is a subcutaneous infusion of fluids to treat dehydrated patients, but is no longer used in practice. Hypodermoclysis is no longer favored because of the severe adverse reactions associated with the use of electrolyte-free or hypertonic solutions. Whether or not hyaluronidase is required to promote subcutaneous fluid absorption remains controversial. Intravenous fluid replacement is usually reserved for the acute care setting by providing rapid correction and the patient can be closely monitored.
Treatment of Hypernatremic Dehydration
If patient shows signs of hemodynamic collapse: Infuse rapidly with isotonic saline until stabilized If the patient is hemodynamically stable: Replace half the fluid deficit over first 24 h using D5W in 0.45% normal saline Goals is to decrease serum osmolarity to 300 mOsm at a rate < 1 mOsm/kg/hr Gradually infuse to correct the total osmolar deficit over the next 48 72 hours
The first step in the treatment of hypernatremic dehydration is correction of hemodynamic collapse, which may manifest as hypotension, orthostasis and decreased urine output. Rapid infusion of isotonic saline can be used until the patient is stabilized. If the patient is hemodynamically stable, one-half of the fluid deficit should be replaced over the first twenty-four hours. A goal during rapid fluid replacement is to decrease the serum osmolarity to three hundred milliosmoles at a rate of no greater than one milliosmoles per kilogram per hour, followed by gradual infusion to correct the total osmolar deficit over the next forty-eight to seventy-two hours. The replacement fluid for these patients during this phase is D-5-W in point-fourfive percent normal saline.
Treatment of Isotonic Dehydration
Replace fluid deficit with isotonic saline Avoid rapid replacement of total fluid deficit (< 24 h); better to correct over 72 hours Altered mental status may persist for 2 weeks
Dehydrated patients with a normal or low serum sodium level should have their fluid deficit replaced with isotonic saline. Replacing fluids too rapidly may cause excessive movement of water into brain cells, resulting in death from cerebral edema. The fluid deficit of dehydration may be safely corrected over seventy-two hours, although altered mental status may persist for as long as two weeks.
Resources
For additional information, see: HCFA. Minimal Data Sets - Dehydration/ Fluid Maintenance- Resident Assessment Protocol Hodgkinson B, Evans D, Wood J.Maintaining Oral Hydration in Older Adults: A Systematic Review.Int J Nurs Pract 2003; 9:S19-S28. Kreimeir U.Pathophysiology of Fluid Imbalance.Crit Care 2000; 4(Suppl 2): S3-S7. Luckey AE, Parsa CJ.Fluid and Electrolyes in the Aged.Arch Surg 2003; 138; 1055-1060. Sansevero, A. C. (1997). Dehydration in the elderly: strategies for prevention and treatment Nurse Pract; 22(4): 41-2,51-7, 63-6. Weinberg, A. D. & Minaker, K. L. (1995). Dehydration: evaluation and management in older adults. Council on Scientific Affairs, American Medical Association. JAMA; 284:1552-6.
Disorders of Sodium Imbalence

By the end of this Review Concept you should be able to: Recognize common signs and symptoms, as well as possible causes, of hypernatremia and hyponatremia. Given a patient case, determine the differential diagnosis, possible causes and treatment options for an elderly individual presenting with SIADH.
Introduction to Hypernatremia
Na+: primary cation in the extracellular space Water loss accounts for the majority of cases of hypernatremia Water homeostasis is regulated by thirst, arginine vasopressin, and the kidneys Serum Osmolarity: 2 (Na+ + K+) + (Glucose/18) + (BUN/2.8)
Fluid and electrolyte imbalance disorders are commonly seen in the elderly. Age-related changes in homeostasis and adverse drug effects may contribute to this problem. Two electrolyte disorders based on alteration in sodium levels, hypernatremia and hyponatremia, are associated with dehydration. These disorders are of particular interest to the geriatrician. Sodium is the primary cation of the extracellular fluid, and determines the size of that compartment. In the elderly, there is a decrease in total body water content, decrease in glomerular filtration rate, decrease in the urine concentrating ability, and narrow limits for excreting water, sodium, potassium, and acid. Sodium contributes to tonicity and induces the water movement across cell membranes. Hypernatremia is caused by either a water deficit or sodium gain. Water loss accounts for the majority of the hypernatremia cases. Water homeostasis is regulated by thirst, arginine vasopressin, and the kidneys. Sodium is responsible for altering tonicity, but increases in serum glucose and urea may also change serum osmolarity as seen here with this equation.
Introduction to Hypernatremia
Defining Characterisics: Serum Na+ > 145 mEq/L Incidence: A retrospective analysis reported a 1% incidence of hypernatremia in over 15,000 hospitalized geriatric patients 57% of these hospitalized elderly developed hypernatremia during the hospital stay Surgery (21%) and febril illness (20%) were related to development of hypernatremia Institutionalized elderly are especially at risk
Hypernatremia is defined as a serum sodium concentration of greater than 145 mEq/L, and is associated with an increase in serum osmolarity. Hypernatremia is a common condition among the elderly, occuring in one-point-one to one-point-six percent of all elderly hospital admissions. A 1987 study by Snyder, et al, showed that fifty-seven percent of hospitalized elderly patients developed hypernatremia after admission. The factors related to the development of hypernatremia were surgery and febrile illness. Furthermore, patients who developed hypernatremia during their hospital stay had a higher mortality rate with the condition on admission. Institutionalized elderly are especially at risk for developing volume depletion with resultant hypernatremia. An acute increase in serum sodium concentration greater than 160 mEq/L has been found to be associated with a 75% mortality rate. Hypernatremia is often associated with other disease states, which may contribute to this high mortality rate.
Risk Factors for Hypernatremia in the Elderly

Age-related Changes in Renal Function: Decrease in the glomerular filtration rate (GFR) Increased incidence of renal disease Decreased ability to concentrate the urine Decrease in thirst mechanism Age-related Changes in Body Composition: Increase in body fat Loss of intracellular fluid Other Causes of Hypernatremia: Diabetes insipidus: Neurogenic: Impaired antidiuretic hormone (ADH) secretion Nephrogenic: Inadequate or lack of response from kidneys to intact ADH secretion Medications: lithium, demeclocycline, and amphotericin B Chronic renal insufficiency
When hypernatremia occurs in older adults it is usually iatrogenic, and is often a marker for severe associated systemic illness. One reason the elderly are at particular risk of developing hypernatremia is because of age-related changes in renal function. There is a decrease in the glomerular filtration rate, an increased incidence of renal disease with advancing age and a decreased ability to concentrate the urine, and impaired ability to conserve water. Age-related changes in body composition also play a role. A marked reduction in intracellular fluid and an increase in body fat associated with normal aging predispose the elderly to water loss with very little environmental prompting.
Risk Factors for Hypernatremia in the Elderly

Other causes of hypernatremia include diabetes insipidus, medications, and chronic renal insufficiency. Neurogenic diabetes insipidus results from impaired antidiuretic hormone secretion, causing the patient to excrete large volumes of dilute urine. On the other hand, nephrogenic diabetes insipidus is a lack of the kidneys to respond to intact anitdiuretic hormone secretion. Medications can also be the cause of the hypernatremia, resulting in a drug-induced diabetes insipidus, as seen with lithium, demeclocycline, and amphotericin B. Patients with chronic renal insufficiency from any cause may exhibit hypernatremia from antidiuretic hormone resistance. In addition to a decreased thirst mechanism, elderly patients may not be able to obtain free water secondary to decreased mobilty, poor visual acuity, cognitive impairment, swallowing disorders, and alterations in thirst from medications. Urinary incontinence may also limit their desire for water consumption to avoid embarrassment or inconvenience of daytime incontinence.
Types of Hypernatremia Seen in the Elderly
Hypovolemic Hypernatremia: Loss of sodium and water (water loss > Na+ loss) Caused by profound diarrhea, excessive sweating, drugs such as mannitol, diuretics or laxatives, glycosuria, acute or chronic renal failure, partial renal obstruction, adrenal deficiencies, and respiratory and skin losses Postural hypotension, tachycardia, decreased skin turgor Isovolemic Hypernatremia: Most common type of hypernatremia Isolated pure water loss; total body sodium content remains normal Caused by fever, diabetes insipidus, skin loss, failure to replace insensible water loss/replacement with hypertonic solution, insufficient water intake, and osmotic diuresis Hypervolemic Hypernatremia: Increase in total body sodium and water (Na+ gain > water gain) Extracellular fluid volume expands while intracellular fluid volume contracts May lead to volume overload and pulmonary edema Caused by administration of sodium bicarbonate, primary mineralocorticoid excesses There are three different presentations of hypernatremia. Hypovolemic hypernatremia is caused by losses of both sodium and water, especially water. Hypernatremia develops when sodium and water deficits are replaced with a fluid containing more sodium than the liquid that was lost. Causes of fluid loss that can lead to a hypovolemic hypernatremic state include profound diarrhea, excessive sweating, drugs such as mannitol, diuretics or laxatives, glycosuria, acute or chronic renal failure, partial renal obstruction, adrenal deficiencies, and respiratory and skin losses.
Types of Hypernatremia Seen in the Elderly
The most common type of hypernatremia, isovolemic hypernatremia, is characterized by an isolated pure water loss from both the extracellular and intracellular fluid compartments. The total body sodium content remains normal, and signs of extracellular fluid loss are only manifested when the serum sodium is in the range of one hundred sixty to one hundred seventy milliequivalents per liter. Causes of isovolemic hypernatremia include fever, diabetes insipidus, skin loss, failure to replace insensible water loss or replacement of insensible fluid loss with a relatively hypertonic solution, and insufficient water intake. Hypervolemic hypernatremia is characterized by an increase in total body sodium and water, with the increase in sodium greater than that of water. This condition produces a fluid shift resulting in expansion of the extracellular fluid volume and contraction of the intracellular fluid volume. If the patient cannot excrete the extra fluid, volume overload and pulmonary edema may result. Common iatrogenic causes of hypervolemic hypernatremia include the administration of sodium bicarbonate or primary mineralocorticoid excesses.
Etiology of Hypernatremia
Febrile illness (70%) Infirmity (40%) Surgery (21%) Nutritional supplements (20%) Intravenous solutes (18%) Diabetes mellitus (15%) Diarrhea (11%) GI bleeding (9%) Diuretics (9%)
Several clinical scenarios may contribute to the development of hypernatremia. In one study, forty-four percent of patients had three or more factors contributing to hypernatremia. One risk factor which is often overlooked in the elderly is the utilization of enteral feedings, especially if free water supplementation is inadequate. In the clinical situation of poorly controlled diabetes in older adults, it may not be severe enough to develop ketoacidosis, but spilling glucose into the urine leads to an osmotic water loss resulting in hypernatremia.
Signs and Symptoms of Hypernatremia in the Elderly
Weakness Decreased skin turgor Weight loss Dry mucous membranes Lethargy Orthostasis Restlessness Irritability Tremulousness Spasticity Hyperreflexia Obtundation Stupor Intracranial bleeding Coma
The symptoms of hypernatremia in the elderly may be very nonspecific, often leading to a delay in diagnosis. Hypernatremia causes a decrese in neuronal cell volume leading to weakness, restlessness, confusion and coma. Neurons adapt to hypertonicity by creating intracellular organic osmoles within 24 hours of onset. With the increase in intracellular tonicity, there is then an influx of water into the neurons in order to maintain cell volume. Intracranial bleeding can occur as a result of tearing of the cerebral blood vessels. The clinical signs of hypernatremia are those of volume depletion and dehydration. In more severe hypernatremia, symptoms may include obtundation, stupor, coma, seizures, and finally, death. Acute hypernatremia is associated with more morbidity and mortality than the chronic variety.
Laboratory Abnormalities Associated with Hypernatremia in the Elderly
HYPOVOLEMIC SERUM OSMOLALITY BUN / Cr RATIO URINE Na+ Increased Increased* Increased or Decreased Decreased or Increased
ISOVOLEMIC Increased Normal or Increased Normal or Decreased
HYPERVOLEMIC Increased Normal or variable Normal
URINE OSMOLARITY
Variable
Variable
*except in glycosuria or urea diuresis, when it is normal Laboratory findings associated with hypernatremia vary depending on the etiology. Unlike hyponatremia, which has been associated with low, normal or high osmolality, hypernatremia is always associated with hyperosmolality. In hypovolemic hypernatremia, the blood urea nitrogen-serum creatinine ratio is almost always elevated. Urinary sodium may be increased or, if gastrointestinal, respiratory or other losses are involved, it may be decreased. Remember that urine osmolality is inversely related to the urinary sodium. In isovolemic hypernatremia, the blood urea nitrogen-serum creatinine ratio is normal or increased, the urine sodium is usually normal, and urine osmolality is variable. In hypervolemic hypernatremia, the blood urea nitrogen-serum creatinine ratio is usually normal but, in the case of an iatrogenically-induced problem may be variable. Urine sodium is usually normal but urine osmolality may be variable.
Management Priorities in Patients with Hypernatremia

Correct hemodynamic collapse Resolve reversible causes Manage underlying conditions Normalize extracellular fluid volume Replace 30% of estimated water loss within the first 24 hours Replace remaining fluids over 72 hours Avoid complications due to over-rehydration: do not decrease osmolality > 2 mOsm/hour or 1 mEq/Na+/hour within first 48 72 hours Continuously reassess fluid status
Once a diagnosis of hypernatremic dehydration is established, the first step in treatment is the correction of hemodynamic collapse. This is usually manifested as hypotension, orthostasis and decreased urine output. Once the patient is stabilized, the next steps are to correct the reversible causes of hypernatremia, manage underlying conditions, such as congestive heart failure, and normalize the extracellular fluid volume. In the elderly, the recommended replacement for the first twenty-four hours is approximately thirty percent of the estimated water loss. Correction of fluid status over a seventy-two hour period may significantly improve recovery of mental function. As a general rule, the serum osmolality should not decrease faster than a rate of two milliosmoles per hour or one milliequivalent of sodium per liter per hour during a forty-eight to seventy-hour period. If the serum sodium is greater than one hundred seventy-five milliequivalents per liter, this should not be corrected by more than fifteen milliequivalents per liter in the first twenty-four hours. A fluid prescription with a defined amount of daily fluid intake may be an important component in preventing hypernatremia.
Differential Treatment of Hypernatremia

Hypovolemic Hypernatremia: 0.9% (isotonic) NaCl initially to stabilize and restore intravascular volume Then switch to D5W or 0.45% NaCl to correct free water deficit Water deficit = 0.6 x body weight (kg) x [(measured Na+/normal Na+) -1] Isovolemic Hypernatremia: D5W or 0.45% NaCl If due to central diabetes insipidus (DI), use ADH (vasopressin) Hypervolemic Hypernatremia: Replace water deficit and add diuretics Hemodialysis may be required if renal failure Specific treatment depends on the type of hypernatremia involved. In hypovolemic hypernatremia, the initial use of isotonic point-nine percent sodium chloride will help to restore intravascular volume until the blood pressure and tissure perfusion are adequate. Once the intravascular volume is repleted and the patient is more stable, the free water deficit can then be replaced. To replace the free water deficit use either D-5-W or point-four-five percent sodium chloride. For isotonic hypernatremia, the management is similar, except one does not have to initiate therapy with point-nine percent sodium chloride because the extracellular volume is usually not decreased. If the patient presents with central diabetes insipidus, antidiuretic hormone may be used. For nephrogenic diabetes insipidus caused by ADH resistance, therapy may include low salt diet, diuretics, and in the case of incomplete resistance, supplemental ADH to attain supraphysiologic levels capable of producing the desired effect. Hypervolemic hypernatremia is managed by replacing the water deficit and adding diuretic therapy to help eliminate the excess sodium that is present. In patients with renal failure, hemodialysis may be required. In patients with normal renal function, excess sodium and water are excreted rapidly. If renal excretion is impaired, a diuretic, such as furosemide, is useful.
Introduction to Hyponatremia
Defining Characterisics: Serum Na+ < 135 mEq/L Caused primarily by iatrogenic water overload Often undetected in mild form Incidence: 2.5% of all elderly hospital admissions 22% of nursing home residents (Sunderam & Mankikar, 1983) 7-fold increase in mortality compared to patients without condition
Hyponatremia is often asymptomatic as the serum sodium decreases below 135 mEq/L, and symptons are ofen absent until the sodium concentration is less than 125 mEq/L. Hyponatremia is also common among the elderly, occurring in two-pointfive percent of all hospitalized elderly patients and as much as twenty-two percent of nursing home residents. The condition is mainly due to water overload, often as a result of an iatrogenic event. In long-term care facilities, episodes of hyponatremia are frequently associated with increased intake of fluids either orally, intravenously or via low sodium containing tube feedings. The use of tap water enemas should also be discouraged in this population. Because mild hyponatremia often does not produce clinically apparent symptoms, it often goes unnoticed. Symptoms of hyponatremia are similar to those of hypernatremia and are reflective of the neurologic dysfunction that occurs as a result of cerebral edema.
Pathogenesis of Hyponatremia: Altered Renal Water Excretion
Most of the elderly patients with hyponatremia have a defect in the kidney that limits its capacity to excrete free water. While these individuals have normal total body water, their effective circulating volume is decreased due to poor tissue perfusion. This poor perfusion may be secondary to low cardiac output states or low plasma proteins from hepatic disease, inadequate protein intake or protein-losing diseases. The decrease in tissue perfusion causes hyponatremia by enhancing vasopressin release and by stimulating intrarenal mechanisms of water reabsorption.
Etiologyof Hyponatremia: Altered Renal Water Excretion
* Renal insufficiency * Antidiuretic hormone (ADH) excess Cortisol deficiency Hypothyroidism Syndrome of inappropriate antidiuretic hormone (SIADH) * Diuretics (esp. thiazides) * Decreased Na+ intake
Medical conditions such as renal insufficiency often predispose the older adult to hyponatremia. As the number of nephrons declines with age, the remaining nephrons must filter an increased solute load. The osmotic diuresis that results decreases the kidneys ability to excrete free water. Patients with cortisol deficiency and hypothyroidism also experience hyponatremia due to effective volume depletion and its effect on cardiac output. Volume depletion stimulates antidiuretic hormone release resulting in the retention of water in excess of sodium. A similar effect is produced by an excess of antidiuretic hormone secondary to central nervous system disorders. The syndrome of inappropriate antidiuretic hormone is another example of a medical condition that impairs water secretion in the presence of normal volume control. Diuretics can also cause hyponatremia by altering sodium chloride reabsorption and water excretion.
Etiology of Hyponatremia: Normal Renal Water Excretion

* Primary polydipsia (intake = 10 15 liters per day) Tricyclic antidepressants Phenothiazines * Reset osmostat Effective volume depetion Psychosis Quadriplegia Malnutrition
Not all patients with hyponatremia have defects in renal water excretion. Patients with primary polydipsia, for example, ingest an excessive amount of fluids, overwhelming the kidneys ability to excrete free water. This condition is most prevalent with elderly patients taking anticholinergic medications for psychiatric illness. The dry mouth experienced as a side effect of these medications stimulates the desire to drink more fluids. In other patients, the water regulating mechanism in the hypothalamus is set at a lower level, causing vasopressin to be released at a lower osmolarity. As many as one third of patients with SIADH may have an altered osmostat.
Types of Hyponatremia
Isotonic Hyponatremia: * Characterized by normal serum osmolality (280 mOsm) * Caused by hyperlipidemia, hyperproteinemia (pseudohyponatremia), IV infusion of isotonic sodium-free solution Hypertonic Hyponatremia: * Characterized by elevated serum osmolarity (> 280 mOsm) * Caused by hyperglycemia, administration of hyperosmolar solutions (e.g., glycerin or mannitol) * If caused by hyperglycemia, serum Na+decreases by 1.6 mEq/L for every 100 mg/dL increase in blood sugar Hypotonic Hyponatremia: * Characterized by low serum osmolarity (< 280 mOsm) * Three subclasses: Hypovolemic hypotonic hyponatremia Hypervolemic hypotonic hyponatremia * Isovolemic hypotonic hyponatremia
The first step in assessing hyponatremia is to obtain a serum osmolality. Isotonic hyponatremia is associated with a normal serum osmolality. Medical conditions that are associated with the development of isotonic hyponatremia include hyperlipidemia, hyperproteinemia, and intravenous infusion of isotonic sodium-free solution. Hyperlipidemia and hyperproteinemia result in a pseudohyponatremia. Sodium-free lipid or protein displaces sodium rich serum water.
Types of Hyponatremia
In addition, administration of sodium-free intravenous infusions of mannitol and glucose, are initially restricted to the intravascular space where they dilute the serum sodium concentration. Hypertonic hyponatremia is associated with an elevated serum osmolality. Common causes include hyperglycemia, or administration of hyperosmolar solutions. There is a fluid shift between the isotonic intracellular fluid volume and the hyperosmolar extracellular fluid compartment, which results in dilution of the serum sodium. As a general rule, when hyperglycemia is the cause of the hyponatremia, the serum sodium decreases by one-point-six milliequivalents per liter for every one hundred milligrams per deciliter increase in blood sugar. Hypotonic hypernatremia is defined by a low serum osmolality and it is much more complex. Hypotonic hypernatremia may be hypovolemic, hypervolemic or isovolemic.
Diagnosis of Hypotonic Hyponatremia

Hypovolemic Hypotonic Hyponatremia * Loss of extracellular fluid volume and greater deficit in sodium * Caused by: Use of sodium-free fluids GI, skin, and lung losses Third spacing Renal losses from diuretics, renal damage, or partial urinary tract obstruction Adrenal insufficiency Hypervolemic Hypotonic Hyponatremia: * Increase in total body sodium content and an expanded extracellular volume * Caused by: HF Liver disease Nephrosis Other hypoalbuminemic states
Diagnosis of Hypotonic Hyponatremia

Isovolemic Hypotonic Hyponatremia: * Normal total body sodium content and a small increase in the extracellular volume * Caused by: Water intoxication Renal failure Potassium loss A reset osmostat SIADH
Accurate diagnosis of hypotonic hypovolemia depends on assessment of extracellular volume. Hypovolemic hypotonic hyponatremia is associated with a deficit of extracellular fluid volume and sodium with a greater deficit in sodium. Causes include use of sodium-free replacement fluids, gastrointestinal, skin and lung losses, third spacing, renal losses (for example, from diuretics, renal damage, partial urinary tract obstruction) or adrenal insufficiency. Diuretic use is one of the most common etiologies of hyponatremia in the elderly, especially elderly women. Hypervolemic hypotonic hyponatremia is associated with an increase in total body sodium content and an expanded extracellular volume. This is clinically apparent as edema and weight gain. The disproportionate increase in water results in hyponatremia. Causes include congestive heart failure, liver disease, nephrosis and other hypoalbuminemic states, such as malnutrition. Isovolemic hypotonic hyponatremia is associated with normal total body sodium content and a small increase in the extracellular volume. It is due to an imbalance between water intake and excretion. Causes include water intoxication, defects in renal diluting mechanisms, potassium loss, a reset osmostat and Syndrome of Inappropriate Anti-diuretic Hormone.
Syndrome of Inappropriate Anti-diuretic Hormone (SIADH) a euvolemic hypotonic hyponatremia
Results from: Enhanced renal sensitivity to AntiDiuretic Hormone Increased release of ADH via non-osmotic &/or non-physiologic processes Presentation: Low serum plasma osmolality Elevated urine osmolality Signs and symptoms of hyponatremia Increased Production of ADH: * CNS disorders e.g., neoplasms, CVA, psychosis, infections * Drugs e.g., IV cyclophosphamide, carbamazepine, vincristine or vinblastine, thiothixine, thioridazine, haloperidol, amitriptyline, bromocriptine * Pulmonary disease e.g., infections, COPD * Postop state * Severe nausea * Idiopathic Ectopic Production of ADH: * Carcinoma * TB
Potentiation of ADH Effect: * Drugs e.g., chlorpropamide, carbamazepine, SSRIs, tolbutamide, IV cyclophosphamide, NSAIDs, intranasal vasopressin-analog, IV vasopressin
The inappropriate ADH activity causes water reabsorption resulting in concentrated urine, low plasma osmolality and hyponatremia. Successful treatment of hyponatremia depends on accurate diagnosis of the underlying disease state. In patients with Syndrome of Inappropriate Anti-diuretic Hormone there are several possibilities, ranging from central nervous system disorders to carcinoma. Identification of offending medications may be crucial to therapy. Intravenous cyclophosphamide and carbamazepine can increase production of antidiuretic hormone and potentiate its effects. Other drugs such as haloperidol, monoamine oxidase inhibitors and nonsteroidal anti-inflammatory drugs can also induce S-I-A-D-H. A little recognized cause of Syndrome of Inappropriate Anti-diuretic Hormone, especially in the elderly, is the use of selective serotonin reuptake inhibitors. Bouman and others found that use of these agents resulted in a high incidence of S-I-A-D-H in older patients. A complete medication history is important for determining any contributing factors. Oral water testing is useful in the diagnosis of S-I-A-D-H. A normal response to an oral water test is the elimination of greater than 80 % of the fluid load in 5 hours, and a decrease in the urine osmolarity to less than 100 milliosmoles per kilogram at 2 hours. Patients with S-I-A-D-H are unable to excrete the water load.
SIADH Treatment Acute treatment Discontinue any contributing medications Induce negative water balance: Water restriction; max 1,000-1,200 mL/day or less Slowly raise serum sodium 3% saline &/or water restriction. Loop diuretic conivaptan Chronic Treatment NaCl tablets loop diuretic (to treat expected ECF expansion) Demeclocycline Interferes with tubular ADH activity Delayed onset 3 - 6 days To treat patients presenting with SIADH, any medications that might be contributing to the condition should be discontinued. The goal is to induce a negative water balance. This can be achieved with water restriction. A maximum of 1200mL of water per day which is 300mL less that the normal daily obligate water loss of about 1500mL for a body. Additionally, slowly raising the serum sodium concentration to treat the signs and symptoms of hyponatremia if they are present can be achieved with the administration of a hypertonic saline solution. Normal saline in these patients risks worsening the hyponatremia. Remember that sodium is handled normally by the body, so sodium will be excreted by the kidney in response to the expanded volume.
The kidney however will continue to conserve fluid and maintain a high volume due to the ADH. A loop diuretic can be added to facilitate the removal of water and to avoid the risk of volume overload associated with hypertonic saline administration. A newer treatment available in the US is the aquaretic conivaptan. It has been approved for use in the treatment of euvolemic and hypervolemic hypontremia of hospitalized patients. It is administered intravenously, producing a diuretic effect within 1-2 hours. It blocks the receptor for ADH in the kidney thus increasing the excretion of water without dramatically effecting electrolytes. It is sometimes used in conjunction with hypertonic saline to more quickly increase the serum sodium concentration. This must be done with caution so as not to reverse the hyponatremia too quickly and induce neural injury.
Patients with chronic SIADH requiring treatment in addition to regulation of water intake have the option to increase the solute intake with salt tablets and/or increase their water loss with a loop diuretic. Increasing sodium intake addresses the low plasma solute concentration while the loop diuretic addresses the expected expansion of extracellular fluid secondary to increased plasma solute concentration.
Alternatively, demeclocycline is an option for patients requiring chronic treatment but are uncontrolled with fluid restriction alone. Due to the delay in onset of this medication, it is not for acute management. Renal function must be monitored as demeclocycline can cause nephrotoxicity.
Signs and Symptoms of Hyponatremia

Moderate Hyponatremia (< 125 mEq/L) * Malaise, lethargy, fatigue * Muscle cramps * Confusion * Headache * Nausea, anorexia Severe Hyponatremia (< 120 mEq/L) * Decrease in the deep tendon reflex * Hypothermia * Cheyne-Stokes respiration * Somnolence * Seizures * Coma Hypovolemic Hyponatremia * Poor skin turgor * Tachycardia * Orthostasis * Oliguria * Azotemia Hypervolemic Hyponatremia * Edema * Weight gain On the other hand, hypervolemic hyponatremia may present with edema and weight gain secondary to a fluid overload state. Isotonic hyponatremia is often asymptomatic. Isotonic Hyponatremia * May be asymptomatic
The severity and signs and symptoms of hyponatremia depend on how rapidly the serum sodium declines, the degree of sodium reduction, and the type of hyponatremia. Mild chronic hyponatremia may be asymptomatic. When the serum sodium level falls to less than one hundred twenty-five milliequivalents per liter, lethargy, muscle cramps, nausea and other nonspecific symptoms may occur. A serum sodium level of less than one hundred twenty may result in altered in mental status and neurological function, and changes in metabolic processes. If the serum sodium drops to less than one hundred fifteen milliequivalents per liter, death can occur. Hypovolemic hyponatremia may manifest as signs of dehydration: poor skin turgor, tachycardia, orthostasis, oliguria and azotemia.
Laboratory Findings in Hyponatremia
* Decreased serum Na+ * BUN/CR ratio may be increased, decreased or may remain normal * Urine Na+ may be increased or decreased based on the type of hyponatremia * Serum osmolality: In isotonic hyponatremia: normal In hypertonic hyponatremia: increased In hypotonic hyponatremia: decreased
In patients with hyponatremia, measured serum sodium levels are always decreased. If the patient is in a volume depleted state, the blood urea nitrogen-serum creatinine ratio will be elevated. This ratio may be normal or low in patients experiencing dilutional hyponatremia or S-I-A-D-H. The urinary sodium is usually less than twenty five milliequivalents per liter in patients with volume depletion secondary to gastrointestinal losses, whereas it may be greater than twenty in those who have S-I-A-D-H. Isotonic hyponatremia is associated with a normal serum osmolality whereas hypertonic and hypotonic hyponatremia are associated with an increased and decreased serum osmolality, respectively.
General Principles for Treating Hyponatremia

* Establish type of hyponatremia * Determine etiology * Assess severity of symptoms * Consider effect on concomitant disease states * Measure extracellular fluid volume and rate of decline in serum Na+ * Do not increase serum Na+ too rapidly to avoid osmotic demyelinization syndrome Nonemergent cases:< 12 mEq/d of replacement Na+ Emergent cases with rapid onset:15 mEq/L in 12 hours or 26 mEq/ L in 48 hours Emergent cases with seizures or coma: 3% sodium chloride IV and water restriction When establishing treatment goals for patients with hyponatremia, it is essential to establish the type of hyponatremia involved, determine its etiology if possible, and identify the severity of the symptoms based on laboratory findings, clinical presentation and rate of decline of the serum sodium. It is also important to consider the effect that management of hyponatremia may have on other concomitant disease states such as congestive heart failure. Regardless of which type of hyponatremia is present, the clinician must be careful about not increasing serum sodium too rapidly. Osmotic demyelinization syndrome refers to a neurologic syndrome characterized by quadriparesis, mutism and pseudobulbar palsy. This usually occurs in patients whose hyponatremia has been present for more than two days. To prevent this, the serum sodium in nonemergent patients should not increase more than twelve milliequivalents per liter per day. Rapid sodium correction may be attempted in emergent situations, such as seizures or coma, with an absolute change in serum sodium concentration of fifteen milliequivalents over twelve hours or of twenty-six milliequivalents over forty-eight hours, but this is not without risk of neurological injury. In an emergent situation characterized by the presence of seizures, coma, or impending death, more rapid sodium replacement can be achieved using three percent sodium chloride and water restriction.
Treatment of Hyponatremia
Hypovolemia Hyponatremia: replace with NS over 6 12 hours Isovolemic Hyponatremia * If serum sodium > 115 and asymptomatic:fluid restriction to 500 mL/day * If secondary to SIADH:fluid restriction + demeclocycline 600 1200 mg/day Hypervolemic Hyponatremia: * Correct underlying causes * Restrict salt and water * Loop diuretics For hypovolemic hyponatremia, fluid replacement with normal saline administered over six to twelve hours is usually sufficient to replace intravascular volume. For isovolemic hyponatremia, treatment is based on fluid restriction. If the serum sodium is one hundred fifteen milliequivalents or greater and the patient is asymptomatic, fluid restriction may be sufficient. One must allow for replacement of insensible water losses. If the patient has Syndrome of Inappropriate Anti-diuretic Hormone, fluid restriction and the use of demeclocycline may be tried, however, the onset of its effects may not occur for five to eight days. Demeclocycline is a tetracycline antibiotic that interferes with the action of antidiuretic hormone on the renal collecting duct. Its use is usually indicated for symptomatic patients who have failed fluid restriction and whose serum sodium is less than one hundred twenty-five milliequivalents per liter or if fluid restriction is not clinically feasible. The net effect of these efforts in SIADH is to make the patient's intake more concentrated than their urine output. The treatment of hypervolemic hyponatremia involves correcting the underlying disease, restricting sodium and water intake, and using loop diuretics, if necessary, to reduce excess fluid load.
Disorders of Potassium and Calcium Imbalance

By the end of this Review Concept you should be able to: Recognize common signs and symptoms, as well as possible causes, of hypokalemia, hypercalcemia, hypocalcemia, hyperphosphatemia, and hypophosphatemia Given a patient case, determine the differential diagnosis, possible causes and treatment options for an elderly individual presenting with hyperkalemia or hypercalcemia
Potassium Homeostasis
Nomal K range = 3.5-4.8 mEq/L Recommended daily allowance of potassium = 50 mEq/d Primary intracellular cation Involved with cellular metabolism and cellular resting membrane potential 80-90% of K is excreted by kidneys (1 PPM p. 157) Potassium is the major intracellular cation and determines the intracellular osmolality. The difference between intracellular and extracellular potassium concentrations creates a gradient that establishes the resting membrane potentials required for normal impulse conduction of neuromuscular tissue. Potassium disorders are the most common electrolyte disorders of hospitalized patients and potassium is the most frequently monitored electrolyte. As potassium is primarily excreted by the kidneys, potassium disorders become more of a concern as renal function declines.
Introduction to Hyperkalemia
Serum potassium >5.5 mEq/L Signs and symptoms of hyperkalemia muscular weakness echocardiogram abnormalities Risks for hyperkalemia: Renal dysfunction Hypoaldosteronism Tissue damage Acidosis met acidosis assoc with uncontrolled diabetes Medications Salt substitutes Although defined as a serum potassium level greater than 5.5mEq/L, hyperkalemia may also be classified according to severity. Mild 5.5-6 mEq/L, moderate 6.1-6.9mEq/L and severe >7mEq/L. Alteration of the intracellular to extracellular potassium gradient would change the resting membrane potential and therefore the ability of the tissue to conduct impulses. Things to look for include muscular weakness and altered cardiac conduction determined by an electrocardiogram. There are a number of factors that would place a person at higher risk of developing hyperkalemia. Generally, they fall into 3 main categories: (1) impaired excretion leading to retention of higher levels of potassium. Examples include renal and any cause of altered aldosterone levels. Aldosterone regulates potassium concentration, such that decreased aldosterone can lead to hyperkalemia.
Introduction to Hyperkalemia
Medications that affect potassium excretion include ACE inhibitors, aldosterone antagonists, NSAIDS and heparin (2) Shifts in potassium from intracellular to extracellular space. Any cause of cellular damage, such as burns or surgery, can release intracellular potassium from the damaged tissue into the extracellular space resulting in an elevated potassium serum level. Acidosis produces a shift in potassium from the intracellular space to the extracellular space. This is most commonly seen in metabolic acidosis associated with uncontrolled diabetes. Digoxin and beta blockers are medications that may decrease the Na/K ATPase pump resulting in increased serum potassium levels. This may be an indication of toxicity associated with the medication. (3) Increased intake from diet or salt substitutes. Any combination of risk factors compounds a persons risk of developing hyperkalemia.
Treatment of Hyperkalemia
Quick onset treatments- Urgent treatment of hospitalized patients for acute symptomatic hyperkalemias Calcium gluconate Sodium Bicarbonate Insulin and glucose Nebulized Albuterol Slower onset Sodium polystyrene sulfonate orally or as retention enema onset of several hours - ~4 but duration of action 4-6 hours. Loop Diuretics Dialysis Treat the underlying cause as much as possible The treatment of hyperkalemia depends on severity of the disorder. Hyperkalemias severe enough to alter cadiac conduction must be stabilized to avoid arrhythmias that can result. For this, there are treatments with quick onset (less than 30 minutes) which work by shifting extracellular potassium into the cells. These urgent treatments stabilize the patients myocardial conduction but do not alter the total body potassium levels. The treatments with slower onset work by removing potassium from the body. Sodium polystyrene sulfonate is an ion exchange resin which removes potassium from the gut in exchange for sodium. Loop diuretics, like furosemide, increase excretion of potassium as does dialysis. Once the patient is stabilized, the underlying contributing factors which resulted in the increased potassium levels should be investigated and corrected. Of particular concern, are HF patients who are commonly on multiple medications which can impact potassium homeostasis. (i.e. ACE inhibitors, ARBs, diuretics, aldosterone antagonists, salt substitutes and may have some degree of renal dysfunction.)
Introduction to Hypokalemia
Serum potassium < 3.5mEq/L Hypokalemia risk factors Vomiting Diarrhea Hyperaldosteronism Medications Steroids Cisplatin Ticarcillin Amphoteracin therapy Poor diet S/sx of hypokalemia Muscle weakness Echocardiogram abnormalities KCl preferred for potassium repletion during hypokalemia Hypokalemia enhances digoxin effect PPM p. 158 Hypokalemia may be difficult to correct if pt is also hypomagnesemic hypomagnesemia may make it diffucult for the kidneys to conserve potassium. Hypokalemia is one of the most frequently encountered problems in clinical practice.
Introduction to Hypokalemia
The signs and symptoms of hypokalemia are similar to hyperkalemia in that both disorders result in muscular weakness and elctrocardiogram abnormalities. In general, hypokalemia is caused by 2 things: (1) the shift of extracellular potassium to the intracellular compartment which results in decreased serum potassium levels. Intracellular shifts in potassium may result from medications such as beta agonists or theophylline. (2) a deficit of total body potassium may have 2 possible causes: excessive loss of potassium or insufficient intake. Excessive loss of body potassium can occur from vomiting, diarrhea, excessive laxative use, hyperaldosteronism or diuretic use. Diuretics are the most common cause of hypokalemia. Prolonged vomiting and diarrhea is a particular concern in elderly patients who may have difficulty maintaining adequate fluid status. A deficit of total body potassium may also be the result of insufficient intake as with poor diet. Elderly who cannot cook for themselves or who may have difficulty chewing or swallowing should be monitored.
Hypokalemia Treatment
Determine and treat underlying cause Supplement with potassium chloride Correct hypomagnesemia Increase dietary intake
Oral supplementation is preferred for asymptomatic patients. Intravenous potassium should be reserved for patients exhibiting symptoms or who are severely depleted. Patients with concomitant hypomagnesemia can exhibit treatment refractory hypokalemia. This is because hypomagnesemia promotes renal potassium excretion. Note that hypokalemia can enhance the effect of digoxin. Therefore, maintaining appropriate serum potassium levels in patients taking digoxin is highly important. Increasing dietary intake can be accomplished by using a salt substitute instead of table salt and increased intake of foods rich in potassium such as molasses, nuts, fruits and vegetables.
Introduction to Calcium
Normal range = 8.5 10.2 mg/dL Ionized Calcium = 4.6-5.2mg/dL Important roles in bone metabolism cardiac function muscle contraction nerve conduction coagulation 98-99% of calcium in body is stored in bone and teeth Corrected Calcium = Serum Calcium concentration + 0.8 (4 Serum Albumin concentration) Calcium homeostasis Increase serum calcium Parathyroid Hormone (PTH) released when calcium levels are low, increases the release of calcium and phosphorus from bones stores into the plasma, promotes renal reabsorption and increases intestinal absorption of calcium. PTH is repressed when calcium levels are high. 1,25-dihydroxycholecalciferol Decrease serum calcium Calcitonin Phosphorus
Introduction to Calcium
Calcium is important electrolyte for the normal functioning of the body. The body primarily stores calcium in the bones. A calcium level measures the calcium content in the extracellular fluid, which corresponds to 0.5% of the bodys calcium stores. Of the extracellular calcium, roughly 50% is ionized and the rest is protein bound. For this reason, a corrected calcium level should be calculated in patients with hypoalbuminemia. For every 1g/dL decrease in serum albumin less than 4g/dL, the serum calcium level decreases by 0.8mg/dL. Alternatively, determining the ionized calcium level will assess calcium status in these patients. Calcium homeostasis is maintained by a number of other chemicals. Parathyroid hormone and 1,25 dihydroxycholecalciferol, the active form of vitamin D, both work to increase serum calcium levels. They increase calcium release from bone stores, decrease renal excretion of calcium and increase intestinal absorption. In contrast, calcitonin and phosphorus both decrease serum calcium levels. Calcitonin opposes parathyroid hormone actions by decreasing bone resorption, increasing renal excretion and decreasing intestinal absorption. Phosphorus has an inverse relationship with calcium. PTH increases bone resorption which releases both calcium and phosphorus from storage. However, PTH decreases the renal excretion of calcium thereby conserving the increase in serum calcium while increasing the renal excretion of phosphorus.
Hypocalcemia
Serum Calcium < 8.5mg/dL Causes of hypocalcemia: Insufficient dietary intake Recommended daily allowance = 800-1200 mg/d Malabsorption Excessive Ca loss Inactivity or immobility Hypomagnesemia Signs and symptoms Anxiety Confusion Irritability Increased seizure potential Paresthesias Muscle twitching, cramps or spasms Brittle nails and dry skin or hair Diarrhea Tetany Hypotension Arrhythmias / ECG changes Decreased myocardial contractility If an elderly person is unable to prepare their own meals or has a poor ability to chew and swallow, their calcium intake may be deficient. Any cause for intestinal malabsorption of calcium would also lead to insufficient intake of calcium by the body. This may include alcoholism, increased intestinal motility or diarrhea, pancreatic insufficiency or any disruption of PTH. Medications such as Phenobarbital, phenytoin, histamine receptor antagonists and proton pump inhibitors can decrease calcium absorption. Hypocalcemia may be further aggravated by concurrent bisphosphonate use is the patient is not adequately supplemented with calcium. Insufficient active vitamin D due to renal failure may not allow for sufficient calcium absorption. Excessive calcium loss may be a consequence of diuretic use. Prolonged inactivity or immobility of elderly patients can lead to decreased body stores of calcium as it is lost from bone. Serum calcium concentrations may be normal despite decreased stores in bone.
Hypocalcemia
The presenting signs and symptoms of hypocalcemia can depend upon whether the disorder is acute or chronic. The more severe presentations are often associated with acute hypocalcemia. Paresthesias are characteristically of the fingers, toes and the area around the mouth. Tetany is the typical feature of acute hypocalcemia.
Hypocalcemia Treatment
Identify and treat the underlying cause of the hypoCa Obtain Serum magnesium concentration Obtain 1,25 dihydroxycholecalciferol level Review daily medications Acute symptomatic with corrected serum Ca <8.5mg/dL Administer intravenous calcium gluconate or calcium chloride Evaluate patient continuously Obtain serum calcium concentration 4 or more times daily. Phosphate levels may need to be reduced or calcium will not be orally absorbed Asymptomatic hypocalcemia Calcium salt forms providing 1-3 grams of Calcium divided daily for hypocalcemia Obtain serum calcium concentration in 1-2 days Identification of the underlying cause of hypocalcemia is critical to avoid repeating the problem. Treating the underlying cause may require magnesium replacement, altering current medications therapies (for example stopping acid suppressing therapies if possible) and vitamin D supplementation as well as calcium supplementation. For acute symptomatic hypocalcemia IV is the preferred route of therapy. Calcium chloride or calcium gluconate are options. Calcium chloride delivers three times the calcium as the gluconate salt. For replacement purposes, calcium gluconate is the preferred therapy. It can be administered as a bolus and as a continuous infusion. Switch to oral therapy once serum calcium concentration rises above 8.5 mg/dL. For asymptomatic patients or for patients requiring calcium supplementation for maintenance of adequate serum levels, oral calcium therapy is recommended. There are multiple oral salt forms of calcium supplements on the market each providing different amounts of elemental calcium per dose. Regardless of salt form, administer 1-3 grams of elemental calcium in divided doses daily.
Hypercalcemia
Serum Calcium >10.5 mg/dL Causes of hypercalcemia Hyperparathyroidism Cancer adrenal insufficiency Prolonged Immobilization increased Ca release from bone. Excessive use of antacids Thiazide diuretics Lithium Vitamin A Vitamin D Signs and symptoms of hypercalcemia fatigue confusion depression altered mental status lethargy ECG changes Arrhythmia Nausea / vomiting / constipation Abdominal or flank pain / paralytic ilius Polyuria and dehydration polydipsia Kidney stones There are 3 primary causes of hypercalcemia: (1) insufficient excretion of calcium (2) increased bone resorption (3) increased intestinal absorption of calcium. The two most common reasons for hypercalcemia are excessive PTH production which increases resorption, promotes intestinal absorption and decreases excretion thereby increasing serum calcium, followed by malignancy which can alter calcium homeostasis. Hypercalcemia of malignancy can be a crisis. It can quickly progress to calcium concentrations >15mg/dL, requiring emergent treatment. With such severe hypercalcemia, arrhythmias, renal failure and coma threaten life. Mediations can increase the absorption of calcium or decrease the excretion causing the serum concentration to rise. Excessive use of antacids can deliver large doses of calcium. Prolonged immobilization may lead to increased serum calcium levels as it is released from bone. The signs and symptoms to look for are nonspecific. Polyuria and polydipsia occur as the body attempts to renally eliminate the excess calcium. Dehydration could quickly develop if the person cannot maintain adequate hydration. The patient may appear confused, tired, lethargic, reporting gastrointestinal discomfort which may be the result of hypercalcemia induced paralytic ilius. If elevated serum calcium concentration has been chronic, kidney stones may develop. Calcium deposits can develop and become imbedded in tissues throughout the body.
Treatment of Hypercalcemia
Hydration 0.9% NaCl Loop diuretics Dialysis Calcitonin Bisphosphonates Corticosteroids Treatment of hypercalcemia begins with hydration. Typically the patients kidneys have attempted to increase calcium removal and the patient may present dehydrated. Normal saline is a good fluid choice for rehydration and for calcium removal. The sodium inhibits the reabsorption of calcium. Once the fluid volume has been restored, the administration of loop diuretics can facilitate the removal of calcium by the kidneys. Thiazide diuretics are not useful, as they inhibit renal excretion of calcium. It is important to monitor potassium concentrations to avoid hypokalemia. Dialysis may be necessary if the hypercalcemia is life threatening or if severe insufficiency precludes adequate renal removal. Calcitonin is an option that works primarily by inhibition of bone resorption, but also inhibits renal reabsorption of calcium. In patients who may not tolerate hydration therapy (for example, patients with renal failure or congestive heart failure) calcitonin, can quickly initiate reduction in serum calcium. Bisphosphonates are indicated for hypercalcemia of malignancy as they are long acting and effective inhibitors of bone resporption. Corticosteroids inhibit bone resportion, increase renal excretion and decrease intestinal absorption of calcium. They are a good choice if hypercalcemia has been the result of excessive vitamin D or vitamin A. They are not for urgent treatment since their onset of effect may take 3-5 days.
Phosphorus
Normal levels = 2.5 - 4.5 mg/dL Primary anion of intracellular fluid 85% of phosphorus is bound to Calcium in bone Vital to body functions Recommended daily allowance = 800-1200 mg/d Kidneys excrete about 90% of ingested phosphorus Parathyroid gland excretes PTH in response to low serum calcium concentrations PTH Increases phos release from bone (increases Ca release as well) Increase P intestinal absorption Decrease P reabsroption in kidney Reduced PTH = increased P reabsorption by kidneys; increase serum levels Intra- or extracellular shifts in phosphate
Phosphorus
Phosphorus often used in the body as phosphate is the primary intracellular anion. The key to understanding phosphate disorders is that the measurable extracellular phosphate concentration may not accurately reflect the bodys phosphorus stores which are intracellular and unmeasurable. In other words, serum phosphate levels may not adequately assess a phosphate deficiency. Phosphate is vital to many of the bodys structures and functions including: cell membrane composition, bone health, muscle and neurological function, metabolism, buffering the balance of acids and bases in the body, energy production and oxygen delivery to tissues by red blood cells. Together the kidneys and the parathyroid gland via PTH production regulate phosphorus homeostasis. The kidneys are straightforward in the approach to phosphate regulation. Increased phosphate levels results in increased excretion. Decreased levels result in decreased excretion in order to maintain normal levels. PTH is released in response to low serum calcium levels. PHT increases phosphate levels by increasing bone resorption, increasing intestinal absorption and increasing renal excretion. Additionally, shifts in phosphorus from intracellular to extracellular or the reverse produce fluctuations in the serum phosphate levels. Insulin and alkalosis can shift phosphorus into the cells producing a decreased serum phosphate concentration. Older patients who already have a water deficit and renal insufficiency may have greater difficulty maintaining electrolyte balance.
Hypophosphatemia
Serum Phosphate < 2.5mg/dL Severe hypophosphatemia if serum phosphate <1 mg/dL Causes of hypophosphatemia Decrease in intestinal absorption Increased loss of P Chronic Diarrhea Excessive Laxative use Increased renal loss Shift of phosphorus from extracellular to intracellular fluid Respiratory alkalosis (produces hyperventilation) Refeeding Syndrome Signs and symptoms of severe hypophosphatemia Osteomalacia (chronic) Weakness Irritability Confusion Paresthesias Seizures Coma Organ failure There are generally 3 causes of hypophosphatemia. The first is a decreased intake or absorption of phosphate. Phosphate is a nutrient found in most foods, so hypophosphatemia is not commonly caused by poor intake alone unless intake is severely restricted as with starvation. More commonly, absorption can be decreased by the binding of phosphate with mediations while in the intestines such as antacids or sucralfate. Inadequate vitamin D can also decrease phosphate absorption. Hyperalimentation without adequate phosphate supplementation can sometimes be a cause of hyperphosphatemia. Second, an increased loss of phosphate can lead to low serum concentrations. Gastrointestinal loss of phosphate from chronic diarrhea or excessive use of laxative medications or increased renal excretion of phosphate due to diuretic use, alcohol, osmotic diuresis as occurs in diabetic ketoacidosis or excessive PTH production from hyperparathyroidism can all increase wasting of phosphorus and lead to hypophosphatemia.
Hypophosphatemia
The third cause for low serum phosphate levels is a shift from extracellular to intracellular fluid. This can occur with the use of insulin which drives glucose and phosphate into cells. More commonly referred to as the refeeding syndrome this must be anticipated in malnourished patients as they begin receiving adequate nutrition. Look for this in recently hospitalized alcoholic, debilitated or elderly patients who may not have been able to care for themselves well enough. Conditions resulting in respiratory alkalosis can also result in this intracellular phosphate shift producing low serum phosphate concentrations. Hypophosphatemia is most commonly asymptomatic unless it is severe. Severe hypophosphatemia better indicates a deficit in total body phosphorus store. Signs and symptoms of severe hypophosphatemia reflect the bodys inability to support its energy demands and the inability to deliver an adequate oxygen supply to the tissues. All of the bodys organ systems may be affected. Severe hypophosphatemia is more common in hospitalized critically ill patients.
Hypophosphatemia Treatment
Identify and treat the underlying cause Phosphorus replacement Nutritious diet Phosphate supplement Intravenous Monitor for hyperphosphatemia and hypocalcemia Oral Monitor for nausea or diarrhea
The first step toward rectifying a phosphate disorder is to identify the cause and correct it. Review the patients medications for any that may have led to the inadequate absorption or excessive excretion of phosphate. Treating the underlying cause for many patients is sufficient therapy. For patients with severe hypophosphatemia supplementation is warranted. Intravenous therapy is available as sodium or potassium phosphate salts. There is no consensus recommending appropriate dosing of phosphate for intravenous therapy. Monitor the patient closely and obtain serum levels multiple times daily. As the severe patient improves, or to initiate treatment of mild to moderate hypophosphatemia, oral supplementation can be instituted. There are various sodium phosphate an potassium phosphate oral supplements on the market.
Hyperphosphatemia
Phosphate > 4.5 mg/dL Severe hyperphos if P>/= 6 mg/dL Causes: Impaired renal excretion Increase in Phosphate load Medications Phosphate supplements laxatives or enemas vitamin D supplements Bisphosphonates Release of phosphate from tissues Shift from intracellular to extracellular fluid
The causes of hyperphosphatemia are due to impaired excretion, increase in phosphate load, or a shift from intracellular to extracellular fluid. Hyperphosphatemia is most commonly due to impaired excretion of phosphate by the kidneys. Excretion matches intake of phosphorus when the body is functioning normally, but when glomerular filtration rate drops to less than 30 mL/min the kidneys ability to rid the body of excess phosphate is compromised. Elevated serum phosphate levels is an uncommon finding in patients with normal kidney function. Hypoparathyroidism resulting in a lack of PTH can hinder phosphate homeostasis.
Hyperphosphatemia
Increasing the amount of phosphorus in the body and overwhelming the bodys ability to remove the excess is a second cause for hyperphosphatemia. Excessive use of phosphorus containing laxatives or supplements particularly if renal dysfunction is present can result in excess phosphate intake. A warning has been issued by the FDA regarding the risk of acute phosphate nephropathy associated with use of these products. At particular risk of this adverse event are the elderly, patients with renal disease and patients taking medications that affect renal perfusion or function. Excessive vitamin D can induce the absorption of phosphorus from the gastrointestinal tract. Tissue destruction resulting in the release of cellular contents as occurs during tumor lysis syndrome or rhabdomyolysis can elevate serum phosphate levels. Hyperphosphatemia can also result from the shift of phosphorus from intracellular to extracellular fluid. Acidosis is a cause.
Hyperphosphatemia Signs and Symptoms
Phosphate and Calcium have an inverse relationship; if P is high look for low Ca levels Hypocalcemia ; serum calcium concentration < 8.5 mg/dL paresthesia toes, fingertips, around mouth muscle spasm, cramps, pain, weakness hyperreflexia may progress to tetany confusion delirium seizures ECG changes Hypotension Heart failure Anorexia Nausea Vomiting Calcification of tissues red eye pruritis
The signs and symptoms of hyperphosphatemia are attributable to the correlated hypocalcemia that commonly occurs in conjunction with elevated phosphate levels. The first sign to look for is a low serum calcium concentration and then the sequelae of that condition. A major concern for patients with renal failure is the deposition of calcium phosphate crystals in tissues. The ischemia this can potentially cause is termed calciphylaxis. It is a dangerous adverse effect associated with an increase in mortality. It is best avoided by the constant management of phosphorus and calcium concentrations in renally insufficient patients.
Treatment of Hyperphosphatemia
Treat the underlying cause Treat symptomatic hypocalcemia Reducing phosphorus intake Dialysis to remove phosphate Phosphate binders Aluminum hydroxide Magnesium hydroxide Calcium acetate or calcium carbonate Sevelamer Lanthanum carbonate Goal: [Ca] x [P] <55
Treating severe hyperphosphatemia that presents as hypocalcemia may first require treatment with calcium salts. If hypocalcemia is manifest as the severe symptoms associated with this condition, treating this is the primary concern. Sources of phosphate should be identified and minimized. Dialysis can be utilized to remove excess phosphorus in symptomatic patients. For many patients with chronic kidney disease, hyperphosphatemia is a continuous concern. These patients often require a phosphate binder to minimize the amount of phosphate that is absorbed in the intestine. Calcium acetate and calcium carbonate are two common and less expensive binding agents. They are effective, but their use places the patient at risk of hypercalemia. Aluminum and magnesium based binders are generally avoided due to their associated toxicity and side effects. Sevelamer and lanthanum are newer agents that are not systemically absorbed. The goal of therapy for patients with chronic kidney disease is to maintain a calcium phosphate product less than 55. High phosphate levels and calcium phosphate products are associated with an increased mortality risk.
Resources
For additional information, see: Adrogue HJ, Madias NE.Hypernatremia.N Eng J Med 2000; 342: 1493-1499. Adrogue HJ, Madias NE.Hyponatremia. N Eng J Med 2000; 342: 1581-1589. Bouman, W., Pinner, G., & Johnson, H. (1998). Incidence of selective serotonin reuptake inhibitor (SSRI) induced hyponatremia due to the syndrome of inappropriate antidiuretic hormone (SAIDH) secretion in the elderly. Int J Geriatr Psychiatry; 13: 12-5. Chertow, G. M. & Brady, H. R. (1994). Hyponatremia from tap-water enema. Lancet; 344: 748. Letter. Hirshberg, B. & Ben-Yehuda A. (1997). The syndrome of inappropriate antidiuretic hormone secretion in the elderly. Am J Med; 103: 270-3. Joy MS, Hladik GA. Disorders of sodium, water, calcium and phosphorus homeostasis.In: Pharmacotherapy: A pathophysiologic approach. 7th Ed. Dipiro JT, Talbert RL, Yee GC, etal. New York: McGraw Hill, 2008. Kapoor M, Chan GZ.Fluid and electrolyte abnormalities.Crit Care Clin 2001; 17: 503-529. Kelleher CL.Disorders of water and electrolyte metabolism.In: Tallis RC, Fillit HM.Brocklehursts Textbook of Geriatric Medicine and Gerontology, 6th ed. London: Elsevier Science Limited, 2003. Luckey AE, Parsa CJ.Fluid and electrolytes in the aged.Arch Surg 2003; 138:1055-1060. Singer GG, Brenner BM. Fluid and electrolyte disturbances. In: Isselbacher, K. J., Braunwald, E., Wilson, I. D. (Eds.) Harrison's Principles of Internal Medicine. 15th ed. New York: McGraw-Hill, 2001. Synder, N. A., Feigal, D. W., & Arieff, A. I. (1987). Hypernatremia in elderly patient. A heterogeneous, morbid, and iatrogenic entity. Ann Intern Med; 107: 309-19.

Module 13 - Pharmacotherapy For Nutrition Hydration Electrolyte Disorders

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Module 13 - Pharmacotherapy For Nutrition Hydration Electrolyte Disorders

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Geriatric

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Malnutrition and Involuntary Weight Loss in the Elderly

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Age-Related Changes Affecting Nutritional Status in the Elderly

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Impact of Illness on Total Daily Energy Requirements

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Assessment of Nutritional Status

Definition and Incidence of Malnutrition

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Etiology of Protein-Energy Malnutrition

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Medications Causing Weight Loss

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Definition and Incidence of Involuntary Weight Loss

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Etiology of Involuntary Weight Loss

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Other Causes of Malnutrition and Involuntary Weight Loss in the Elderly

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Other Causes of Malnutrition and Involuntary Weight Loss in the Elderly

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Micronutrient Deficiencies Seen in Elderly Patients After Vitamin Supplementation

NUTRIENT Vitamin C Thiamine Niacin Folate Vitamin B6 Vitamin B12

ALL ELDERLY (%) 6.7 10.0 30.1 11.3 28.0 14.8

INSTITUTIONAL (%) 2.1 2.5 33.1 13.1 33.8 13.2 25

26.3 16.6 2.9 13.8 18.6

Drugs that Can Cause Micronutrient Deficiencies

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Physical Findings Associated with Nutrient Deficiencies

Physical Findings Associated with Nutrient Deficiencies

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Laboratory Studies for Assessment and Monitoring

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Managing the Malnourished Elderly Patient

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Managing Nutritional Deficiencies: Vitamin Supplements

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Managing Nutritional Deficiencies: Pharmacological Options

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Managing Nutritional Deficiencies: Changing The Mechanics of Eating

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Enteral Feeding of the Elderly

By the end of this review concept, you should be able to:

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Introduction to Nutrition in the Elderly

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Managing Nutritional Deficiencies with Enteral Feeding

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Managing Nutritional Deficiencies with Enteral Feeding

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Common Routes for Enteral Feeding

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