Homeostasis, Stress, Fluid-Electrolyte Imbalances and Surgery 2024-2025 Fall Semester PDF

SCHOOL OF HEALTH SCIENCES DEPARTMENT OF NURSING NURS212 SURGICAL DISEASES NURSING 2024-2025 FALL SEMESTER ASST. PROF. DR. UFUK KAYA  HOMEOSTASIS, STRESS, FLUID- ELECTROLYTE IMBALANCES AND SURGERY  HOMESOSTASIS - 01 The cell is the building block of all...

SCHOOL OF HEALTH SCIENCES DEPARTMENT OF NURSING NURS212 SURGICAL DISEASES NURSING 2024-2025 FALL SEMESTER ASST. PROF. DR. UFUK KAYA  HOMEOSTASIS, STRESS, FLUID- ELECTROLYTE IMBALANCES AND SURGERY  HOMESOSTASIS - 01 The cell is the building block of all tissues, organs and systems and is the basic unit of disease. Asst. Prof. Dr. Ufuk 3 KAYA  HOMESOSTASIS - 02 The fluid that circulates in blood vessels is plasma. Plasma carries oxygen and nutrients to cells for use in energy production and carries waste products resulting from metabolism out of cells. Asst. Prof. Dr. Ufuk 4 KAYA  HOMESOSTASIS - 03 The intercellular fluid surrounding the cell. This fluid creates an environment for the passage and exchange of substances between cells and vessels. The intracellular fluid inside the cell membrane creates the necessary fluid environment for cells to survive. Asst. Prof. Dr. Ufuk 5 KAYA  HOMESOSTASIS - 04 The maintenance of health depends on all systems in the body functioning in a way that keeps the chemical composition of plasma, interstitial and intracellular fluid, that is, the internal environment of the body, in balance. Asst. Prof. Dr. Ufuk 6 KAYA  HOMESOSTASIS - 05 Maintaining homeostasis depends on the performance of certain functions by the interstitial fluid. These functions are: Transportation of substances needed for energy production by cells Disposal of breakdown products produced during energy production Keeping the cell environment within the most appropriate limits in terms of fluid volume, distribution and composition to support energy production processes Asst. Prof. Dr. Ufuk 7 KAYA HOMESOSTASIS - 06 CLAUDE WALTER CANNON BERNARD (1929) (1813-1878)  HOMESOSTASIS - 07 The term homeostasis was coined by Walter B. Cannon in 1930. Cannon defined the concept of homeostasis as the balance of the internal environment of the body.  HOMESOSTASIS - 08 Homeostatic Imbalance: Homeostasis or disruption of the balance of the organism causes diseases. Destructive positive feedback can be stopped with strong negative feedback.  NEEDS OF THE CELL-01 The ability of a cell to grow, reproduce and perform certain functions in the body depends on its ability to create energy. Energy is obtained through various chemical reactions within the cell and all of these reactions are called "cell metabolism". Metabolism refers to the chemical combination of oxygen with nutrients to create energy and the formation of breakdown products during the reactions. All of these reactions take place in the intracellular fluid. Asst. Prof. Dr. Ufuk 11 KAYA  NEEDS OF THE CELL-02 Oxygen, nutrients and enzymes are essential for the formation of energy in the cell. In order for the cell to maintain its normal function, carbon dioxide, water and other breakdown products formed during metabolic processes must be removed from the environment. When looking at the body at the cellular level, there are four basic needs that serve to maintain homeostasis. These are oxygen, nutrients, the excretion of waste products and the mechanism that will maintain fluid-electrolyte balance. When these cellular needs are not met, the functions of the systems are disrupted and diseases occur. Asst. Prof. Dr. Ufuk 12 KAYA  STRESS-01 Environmental factors or agents that affect the body's adaptation capacity and cause the development of a stress response are called stressors. The body's response to stressors is stress. Stressors can be classified in various ways. Those that belong to the individual's body, such as genetic structure, age, and gender, are called "endogenous stressors"; those that come from outside the body, such as heat, cold, chemicals, radiation, and microorganisms, are called "exogenous stressors". Asst. Prof. Dr. Ufuk 13 KAYA  STRESS-02 Stressors can also be classified as biological, physical, chemical, psychological and sociological. Genetic structure and gender are examples of "biological stressors"; heat, cold, radiation and poisons are examples of "physical and chemical stressors"; loss of a loved one and pain are examples of "psychological stressors"; and an individual moving to a country with different cultural characteristics are examples of "sociological stressors". Asst. Prof. Dr. Ufuk 14 KAYA  GENERAL REACTIONS TO STRESS-01 In the face of stress, the individual generally gives a holistic response both physiologically and psychologically. Physiological response to stress occurs in two ways. These are; 1. General Adaptation Syndrome (GAS) 2. Local Adaptation Syndrome (LAS)  GENERAL REACTIONS TO STRESS-02 General Adaptation Syndrome: It is the body's response to stressors as a whole with homeostatic control mechanisms. The nervous system and the endocrine system have an important role in this response. Stressors that cause GAS: burns, cold, emotional causes, hemorrhage (bleeding) and infection can be counted. GENERAL REACTIONS TO STRESS-03 GAS consists of three separate but consecutive periods. These; 1. Alarm Period, 2. Resistance Period, 3. Extinction Period.  GENERAL REACTIONS TO STRESS-04 Alarm Period: It is the period when the body activates various defense mechanisms to cope with the stressor. It can take a few minutes to several hours. The purpose here is; It is to maintain the internal balance of the organism by fighting or escaping. FIGHT RUN  GENERAL REACTIONS TO STRESS-05 Alarm Period: Reactions in this period; increased arterial blood pressure, While the blood flow to the active muscles increases, the blood flow to the kidneys and gastrointestinal system organs, which is not needed for rapid motor activity, is decreased, Increased cellular metabolism rate increased blood glucose throughout the body, concentration, Increased glycolysis in muscle and increase in muscle strength, liver, increased mental activity, It is an increase in blood coagulation rate.  GENERAL REACTIONS TO STRESS-06 Alarm Period: During this period, paleness in color, sweating, frequent urination, dizziness, chest pain, nausea, vomiting, abdominal cramps, insomnia, weakness are observed. If the alarm period lasts for a long time, it can even cause death of the individual.  GENERAL REACTIONS TO STRESS-07 Resistance Period: If the efforts are successful in reducing stress, the symptoms during the alarm response disappear and the body returns to normal. If the individual can resist stress during this period, the general adaptation sign is working well, and if the stress is adapted, recovery occurs.  GENERAL REACTIONS TO STRESS-08 Resistance Period: If this period is prolonged, the disease occurs. The individual has difficulty in adapting and if the disease cannot be cured, the exhaustion stage is passed.  GENERAL REACTIONS TO STRESS-08 Extinction Period: In situations where chronic stress is experienced, when the stressor cannot be resisted any longer or the amount of energy required to maintain the adaptation decreases, the organism cannot adapt and exhaustion/extinction occurs. Depending on the diseases that occurred in the previous period, irreversible organic disorders begin and various disease tables occur. GENERAL REACTIONS TO STRESS-09 Extinction Period: Physiological regulation is reduced and the condition can result in death.  GENERAL REACTIONS TO STRESS-10 Local Adaptation Syndrome: It is the response of a tissue, organ or part of the body to stress caused by trauma, illness or other physiological changes. Features; The response affects The answer is a single organ of the adaptive, body or certain parts of the body, The answer is short, The answer is restorative.  SURGICAL STRESS-01 The state of having surgery is a special situation in which the individual experiences anxiety at the highest level of physiological, psychological and social stress. Surgical intervention is physiologically a trauma for the organism. It causes disruption of homeostatic mechanisms.  SURGICAL STRESS-02 The main purpose when the organism is exposed to trauma; To maintain homeostasis by creating systemic and local responses to trauma. Neuroendocrine response, mediator release, intracellular and intercellular metabolic changes occur in trauma.  SURGICAL STRESS-03 Although surgical intervention is applied to eliminate the pain and suffering caused by the disease, the surgical procedure itself can be a source of pain and suffering. At the same time, surgical intervention is a frightening experience for patients.  SURGICAL STRESS-04 Patients undergoing surgical intervention may experience various problems such as not being able to wake up from anesthesia, losing the potential to work, dying, deterioration in body image, changing their lifestyle, being disabled, cancer, and experiencing financial difficulties.  SURGICAL STRESS-05 Stress response to surgery, decreased resistance to infection, deterioration of the vascular system, deterioration of organ functions, changes in body image and lifestyle, surgical intervention area, and physiological recovery cause all compensatory systems to come into play. Fluid-Electrolyte Imbalances 31 Water Content of the Body 32  Water Content of the Body - 01 Water is the primary component of the body, accounting for approximately 50% to 60% of body weight in the adult. The water content varies with gender, body mass, and age. 33 34  Water Content of the Body - 02 The percentage of body weight that is composed of water is generally greater in men than in women because men tend to have more lean body mass. The more fat present in the body, the less the total water content. Therefore obese individuals have a lower percentage of body water than slender people do. 35  Water Content of the Body - 03 Older adults, with less muscle mass and more fat content, have less body water for this same reason. In the older adult, body water content averages 45% to 55% of body weight, leaving them at a higher risk for fluid- related problems than young adults. 36  Body Fluid Compartments - 01 The two fluid compartments in the body are the intracellular space (inside the cells) and the extracellular space (outside the cells). 37 38  Body Fluid Compartments - 02 Approximately two thirds of the body water is located within cells and is termed intracellular fluid (ICF); ICF constitutes approximately 40% of body weight of an adult. The body of a 70-kg young man would contain approximately 42 L of water, of which 28 L would be located within cells. 39  Body Fluid Compartments - 03 The extracellular fluid (ECF) consists of interstitial fluid (the fluid in the spaces between cells), plasma (the liquid part of blood), and transcellular fluid (a very small amount of fluid contained within specialized cavities of the body). Transcellular fluids include cerebrospinal fluid; fluid in the gastrointestinal (GI) tract; and pleural, synovial, peritoneal, intraocular, and pericardial fluid. 40  Body Fluid Compartments - 04 ECF consists of one third of the body water; this would amount to about 14 L in a 70-kg man. About 20% of ECF is in the intravascular space as plasma (3 L in a 70-kg man), and 70% is in the interstitial space (10 L in a 70-kg man). The fluid in the transcellular spaces totals about 1 L at any given time. 41  Body Fluid Compartments - 05 However, because 3 to 6 L of fluid is secreted into and reabsorbed from the GI tract every day, loss of this fluid from vomiting or diarrhea can produce serious fluid and electrolyte imbalances. 42 Electrolytes 43  Electrolytes - 01 Electrolytes are substances whose molecules dissociate, or split into ions, when placed in water. Ions are electrically charged particles. 44  Electrolytes - 02 Cations are positively charged ions. Examples include sodium (Na+), potassium (K+), calcium (Ca2+), and magnesium (Mg2+) ions. Anions are negatively charged ions. Examples include bicarbonate (HCO3−), chloride (Cl−), and phosphate (PO43−) ions. 45  Measurement of Electrolytes The milliequivalent (mEq) is the commonly used unit of measure for electrolytes. 46  Electrolyte Composition of Fluid Compartments - 01 Electrolyte composition varies between ECF and ICF. The overall concentration of electrolytes is approximately the same in the two compartments. However, concentrations of specific ions differ greatly. 47 48  Electrolyte Composition of Fluid Compartments - 02 In ECF the main cation is sodium, with small amounts of potassium, calcium, and magnesium. The primary ECF anion is chloride, with small amounts of bicarbonate, sulfate, and phosphate anions. 49  Electrolyte Composition of Fluid Compartments - 03 In ICF the most prevalent cation is potassium, with small amounts of magnesium and sodium. The prevalent ICF anion is phosphate, with some protein and a small amount of bicarbonate. 50 51 52 FLUID AND ELECTROLYTE IMBALANCES 53  EXTRACELLULAR FLUID VOLUME IMBALANCES - 01 ECF volume deficit (hypovolemia) and ECF volume excess (hypervolemia) are common clinical conditions. ECF volume imbalances are typically accompanied by one or more electrolyte imbalances, particularly changes in the serum sodium level. 54  EXTRACELLULAR FLUID VOLUME IMBALANCES - 02 Fluid Volume Deficit (HYPOVOLEMIA) Fluid volume deficit can occur with abnormal loss of body fluids (e.g., diarrhea, fistula drainage, hemorrhage, polyuria), inadequate intake, or a shift of fluid from plasma into interstitial fluid. The term fluid volume deficit is not interchangeable with the term dehydration. Dehydration refers to loss of pure water alone without a corresponding loss of sodium. 55 56  EXTRACELLULAR FLUID VOLUME IMBALANCES - 03 Fluid Volume Deficit - Collaborative Care The goal of treatment for fluid volume deficit is to correct the underlying cause and to replace both water and any needed electrolytes. Balanced IV solutions, such as lactated Ringer’s solution, are usually given. Isotonic (0.9%) sodium chloride is used when rapid volume replacement is indicated. Blood is administered when volume loss is due to blood loss. 57  EXTRACELLULAR FLUID VOLUME IMBALANCES - 03 Fluid Volume Deficit – Nursing Diagnoses Deficient fluid volume related to excessive ECF losses or decreased fluid intake, Decreased cardiac output related to excessive ECF losses or decreased fluid intake, Risk for deficient fluid volume related to excessive ECF losses or decreased fluid intake, Potential complication: hypovolemic shock. 58  EXTRACELLULAR FLUID VOLUME IMBALANCES - 04 Fluid Volume Excess (HYPERVOLEMIA) Fluid volume excess may result from excessive intake of fluids, abnormal retention of fluids (e.g., heart failure, renal failure), or a shift of fluid from interstitial fluid into plasma fluid. Although fluid shifts between the interstitial space and plasma do not alter the overall volume of ECF, these shifts result in changes in the intravascular volume. 59 60  EXTRACELLULAR FLUID VOLUME IMBALANCES - 05 Fluid Volume Excess - Collaborative Care The goal of treatment for fluid volume excess is removing fluid without producing abnormal changes in the electrolyte composition or osmolality of ECF. The primary cause must be identified and treated. Diuretics and fluid restriction are the primary forms of therapy. 61  EXTRACELLULAR FLUID VOLUME IMBALANCES - 06 Fluid Volume Excess - Collaborative Care Restriction of sodium intake may also be indicated. If the fluid excess leads to ascites or pleural effusion, an abdominal paracentesis or thoracentesis may be necessary 62  EXTRACELLULAR FLUID VOLUME IMBALANCES - 07 Fluid Volume Excess - Collaborative Care Restriction of sodium intake may also be indicated. If the fluid excess leads to ascites or pleural effusion, an abdominal paracentesis or thoracentesis may be necessary 63  EXTRACELLULAR FLUID VOLUME IMBALANCES - 07 Fluid Volume Excess – Nursing Diagnoses Excess fluid volume related to increased water and/or sodium retention, Impaired gas exchange related to water retention leading to pulmonary edema, Risk for impaired skin integrity related to edema, Activity intolerance related to increased water retention, fatigue, and weakness, Disturbed body image related to altered body appearance secondary to edema, Potential complications: pulmonary edema, ascites. 64  EXTRACELLULAR FLUID VOLUME IMBALANCES - 08 Nursing Implementation (1) INTAKE AND OUTPUT. The use of 24-hour intake and output records gives valuable information regarding fluid and electrolyte problems. An accurately recorded intake-and-output flow sheet can identify sources of excessive intake or fluid losses. Intake should include oral, IV, and tube feedings and retained irrigants. 65  EXTRACELLULAR FLUID VOLUME IMBALANCES - 09 Nursing Implementation (2) INTAKE AND OUTPUT. Output includes urine, excess perspiration, wound or tube drainage, vomitus, and diarrhea. Estimate fluid loss from wounds and perspiration. Measure the urine specific gravity according to agency policy. Readings of greater than 1.025 indicate concentrated urine, whereas those of less than 1.010 indicate dilute urine. 66  EXTRACELLULAR FLUID VOLUME IMBALANCES - 10 Nursing Implementation (3) CARDIOVASCULAR CHANGES. Monitoring the patient for cardiovascular changes is necessary to prevent or detect complications from fluid and electrolyte imbalances. Signs and symptoms of ECF volume excess and deficit are reflected in changes in blood pressure, pulse force, and jugular venous distention. 67  EXTRACELLULAR FLUID VOLUME IMBALANCES - 11 Nursing Implementation (4) CARDIOVASCULAR CHANGES. In fluid volume excess the pulse is full, bounding, and not easily obliterated. Increased volume causes distended neck veins (jugular venous distention) and increased blood pressure. 68  EXTRACELLULAR FLUID VOLUME IMBALANCES - 12 Nursing Implementation (5) CARDIOVASCULAR CHANGES. In mild to moderate fluid volume deficit, compensatory mechanisms include sympathetic nervous system stimulation of the heart and peripheral vasoconstriction. Stimulation of the heart increases the heart rate and, combined with vasoconstriction, maintains the blood pressure within normal limits. 69  EXTRACELLULAR FLUID VOLUME IMBALANCES - 13 Nursing Implementation (6) CARDIOVASCULAR CHANGES. A change in position from lying to sitting or standing may elicit a further increase in the heart rate or a decrease in the blood pressure (orthostatic hypotension). If vasoconstriction and tachycardia provide inadequate compensation, hypotension occurs when the patient is recumbent. 70  EXTRACELLULAR FLUID VOLUME IMBALANCES - 14 Nursing Implementation (7) CARDIOVASCULAR CHANGES. Severe fluid volume deficit can cause flattened neck veins and a weak, thready pulse that is easily obliterated. Severe, untreated fluid deficit will result in shock. 71  EXTRACELLULAR FLUID VOLUME IMBALANCES - 15 Nursing Implementation (8) RESPIRATORY CHANGES. Both fluid excess and fluid deficit affect respiratory status. ECF excess can result in pulmonary congestion and pulmonary edema as increased hydrostatic pressure in the pulmonary vessels forces fluid into the alveoli. 72  EXTRACELLULAR FLUID VOLUME IMBALANCES - 16 Nursing Implementation (9) RESPIRATORY CHANGES. The patient will experience shortness of breath and moist crackles on auscultation. The patient with ECF deficit will demonstrate an increased respiratory rate because of decreased tissue perfusion and resultant hypoxia. 73  EXTRACELLULAR FLUID VOLUME IMBALANCES - 17 Nursing Implementation (10) NEUROLOGIC CHANGES. Changes in neurologic function may occur with fluid volume excesses or deficits. ECF excess may result in cerebral edema from increased hydrostatic pressure in cerebral vessels. Alternatively, profound volume depletion may cause an alteration in sensorium secondary to reduced cerebral tissue perfusion. 74  EXTRACELLULAR FLUID VOLUME IMBALANCES - 18 Nursing Implementation (11) NEUROLOGIC CHANGES. Assessment of neurologic function includes evaluation of (1) the level of consciousness, which includes responses to verbal and painful stimuli and determination of a person’s orientation to time, place, and person; (2) pupillary response to light and equality of pupil size; and (3) voluntary movement of the extremities, degree of muscle strength, and reflexes. Nursing care focuses on maintaining patient safety. 75  EXTRACELLULAR FLUID VOLUME IMBALANCES - 19 Nursing Implementation (12) DAILY WEIGHTS. Accurate daily weights provide the easiest measurement of volume status. An increase of 1 kg (2.2 lb) is equal to 1000 mL (1 L) of fluid retention (provided the person has maintained usual dietary intake or has not been o nothing by-mouth [NPO] status). 76  EXTRACELLULAR FLUID VOLUME IMBALANCES - 20 Nursing Implementation (13) DAILY WEIGHTS. Obtain the weight under standardized conditions, that is, weigh the patient at the same time every day, wearing the same garments, and on the same carefully calibrated scale. Remove excess bedding and empty all drainage bags before the weighing. If the patient has items present that are not there every day, such as bulky dressings or tubes, note this along with the weight. 77  EXTRACELLULAR FLUID VOLUME IMBALANCES - 21 Nursing Implementation (14) SKIN ASSESSMENT AND CARE. Detect clues to ECF volume deficit and excess by inspecting the skin. Examine the skin for turgor and mobility. Normally a fold of skin, when pinched, will readily move and, on release, rapidly return to its former position. Skin areas over the sternum, abdomen, and anterior forearm are the usual sites for evaluation of tissue turgor. 78 79  EXTRACELLULAR FLUID VOLUME IMBALANCES - 22 Nursing Implementation (15) SKIN ASSESSMENT AND CARE. In older people, decreased skin turgor is less predictive of fluid deficit because of the loss of tissue elasticity. In ECF volume deficit, skin turgor is diminished, and there is a lag in the pinched skinfold’s return to its original state (referred to as tenting). 80  EXTRACELLULAR FLUID VOLUME IMBALANCES - 23 Nursing Implementation (16) SKIN ASSESSMENT AND CARE. The skin may be cool and moist if there is vasoconstriction to compensate for the decreased fluid volume. Mild hypovolemia usually does not stimulate this compensatory response. Consequently, the skin will be warm and dry. Volume deficit may also cause the skin to appear dry and wrinkled. 81  EXTRACELLULAR FLUID VOLUME IMBALANCES - 24 Nursing Implementation (17) SKIN ASSESSMENT AND CARE. These signs may be difficult to evaluate in the older adult because the patient’s skin may be normally dry, wrinkled, and nonelastic. Oral mucous membranes will be dry, the tongue may be furrowed, and the individual often complains of thirst. Routine oral care is critical for the comfort of a patient who is dehydrated or fluid restricted for management of fluid volume excess. 82  EXTRACELLULAR FLUID VOLUME IMBALANCES - 25 Nursing Implementation (18) SKIN ASSESSMENT AND CARE. Edematous skin may feel cool because of fluid accumulation and a decrease in blood flow secondary to the pressure of the fluid. The fluid can also stretch the skin, causing it to feel taut and hard. Assess edema by pressing with a thumb or forefinger over the edematous area. 83  EXTRACELLULAR FLUID VOLUME IMBALANCES - 26 Nursing Implementation (19) SKIN ASSESSMENT AND CARE. A grading scale is used to standardize the description if an indentation (ranging from 1+ [slight edema; 2-mm indentation] to 4+ [pitting edema; 8-mm indentation]) remains when pressure is released. Evaluate for edema in areas where soft tissues overlie a bone, with preferred sites being the tibia, fibula, and sacrum. 84  EXTRACELLULAR FLUID VOLUME IMBALANCES - 27 Nursing Implementation (20) SKIN ASSESSMENT AND CARE. Good skin care for the person with ECF volume excess or deficit is important. Protect edematous tissues from extremesof heat and cold, prolonged pressure, and trauma. Frequent skin care and changes in position will prevent skin breakdown. 85  EXTRACELLULAR FLUID VOLUME IMBALANCES - 28 Nursing Implementation (21) SKIN ASSESSMENT AND CARE. Elevate edematous extremities to promote venous return and fluid reabsorption. Dehydrated skin needs frequent care without the use of soap. Applying moisturizing creams or oils increases moisture retention and stimulates circulation. 86  EXTRACELLULAR FLUID VOLUME IMBALANCES - 29 Nursing Implementation (22) OTHER NURSING MEASURES. Carefully monitor the rates of infusion of IV fluid solutions. Be cautious about any attempts to “catch up,” particularly when large volumes of fluid or certain electrolytes are involved. 87  EXTRACELLULAR FLUID VOLUME IMBALANCES - 30 Nursing Implementation (23) OTHER NURSING MEASURES. This is especially true in patients with cardiac, renal, or neurologic problems. Patients receiving tube feedings need supplementary water added to their enteral formula. The amount of additional water depends on the osmolarity of the feeding and the patient’s condition. 88  EXTRACELLULAR FLUID VOLUME IMBALANCES - 31 Nursing Implementation (24) OTHER NURSING MEASURES. Do not allow the patient with nasogastric suction to drink water because it will increase the loss of electrolytes. Occasionally the patient may be given small amounts of ice chips to suck. 89  EXTRACELLULAR FLUID VOLUME IMBALANCES - 32 Nursing Implementation (25) OTHER NURSING MEASURES. Irrigate nasogastric tubes with isotonic saline solution, not with water. Water causes diffusion of electrolytes into the gastric lumen from mucosal cells. The suction then removes the electrolytes, increasing the risk of electrolyte imbalances 90  EXTRACELLULAR FLUID VOLUME IMBALANCES - 33 Nursing Implementation (26) OTHER NURSING MEASURES. Nurses in hospitals and long-term care facilities should encourage and help the older or debilitated patient to maintain adequate oral intake. Assess the patient’s ability to obtain adequate fluids independently, express thirst, and swallow effectively. Fluids should be easily accessible. 91  EXTRACELLULAR FLUID VOLUME IMBALANCES - 34 Nursing Implementation (27) OTHER NURSING MEASURES. Assist older adults with physical limitations, such as arthritis, to open and hold containers. A variety of types of fluids should be available, and assess for individual preferences. 92  EXTRACELLULAR FLUID VOLUME IMBALANCES - 35 Nursing Implementation (28) OTHER NURSING MEASURES. Serve fluids at the temperature preferred by the patient. Seventy percent to 80% of the daily intake of fluids should be with meals, with fluid supplements between meals. Older adults may choose to decrease or eliminate fluids 2 hours before bedtime to decrease nocturia or incontinence. 93  EXTRACELLULAR FLUID VOLUME IMBALANCES - 36 Nursing Implementation (29) OTHER NURSING MEASURES. The unconscious or cognitively impaired patient is at increased risk because of an inability to express thirst and act on it. In these patients, accurately document fluid intake and losses and carefully evaluate the adequacy of intake and output. 94 SODIUM IMBALANCES 95 96  Hypernatremia - 01 Hypernatremia, an elevated serum sodium, may occur with water loss or sodium gain. Because sodium is the major determinant of the ECF osmolality, hypernatremia causes hyperosmolality. In turn, ECF hyperosmolality causes a shift of water out of the cells, which leads to cellular dehydration. 97  Hypernatremia - 02 As discussed earlier, the primary protection against the development of hyperosmolality is thirst. Hypernatremia is not a problem in an alert person who has access to water, can sense thirst, and is able to swallow. Hypernatremia secondary to water deficiency is often the result of an impaired level of consciousness or an inability to obtain fluids. 98  Hypernatremia - 03 Several clinical states can produce hypernatremia from water loss. A deficiency in the synthesis or release of ADH from the posterior pituitary gland (central diabetes insipidus) or a decrease in kidney responsiveness to ADH (nephrogenic diabetes insipidus) can result in profound diuresis, thus producing a water deficit and hypernatremia. 99  Hypernatremia - 04 Hyperosmolality with osmotic diuresis can result from administration of concentrated hyperosmolar tube feedings and hyperglycemia associated with uncontrolled diabetes mellitus. Other causes of hypernatremia include excessive sweating and increased sensible losses from high fever. 100  Hypernatremia - 05 Excessive sodium intake with inadequate water intake can also lead to hypernatremia. Examples of sodium gain include IV administration of hypertonic saline or sodium bicarbonate, use of sodium- containing drugs, excessive oral intake of sodium (e.g., ingestion of seawater), and primary aldosteronism (hypersecretion of aldosterone) caused by a tumor of the adrenal glands. 101  Hypernatremia - 06 Clinical Manifestations (1) The manifestations of hypernatremia are primarily the result of water shifting out of cells into ECF with resultant dehydration and shrinkage of cells. 102  Hypernatremia - 07 Clinical Manifestations (2) Dehydration of brain cells results in neurologic manifestations such as intense thirst, agitation, and decreased alertness, ranging from sleepiness to coma. f there is any accompanying ECF volume deficit, manifestations such as postural hypotension, weakness, and decreased skin turgor occur. 103  Hypernatremia - 08 Nursing Diagnoses Risk for injury related to altered sensorium and seizures, Risk for fluid volume deficit related to excessive intake of sodium and/or loss of water, Risk for electrolyte imbalance related to excessive intake of sodium and/or loss of water, Potential complication: seizures and coma leading to irreversible brain damage. 104  Hypernatremia - 09 Nursing Implementation (1) The primary goal of treatment of hypernatremia is to treat the underlying cause. In primary water deficit, fluid replacement is provided either orally or IV with isotonic or hypotonic fluids such as 5% dextrose in water or 0.45% sodium chloride saline solution. 105  Hypernatremia - 10 Nursing Implementation (2) The goal of treatment for sodium excess is to dilute the sodium concentration with sodium-free IV fluids, such as 5% dextrose in water, and to promote excretion of the excess sodium by administering diuretics. 106  Hypernatremia - 11 Nursing Implementation (3) Monitor serum sodium levels and the patient’s response to therapy. Quickly reducing serum sodium levels can cause a rapid shift of water back into the cells, resulting in cerebral edema and neurologic complications. This risk is greatest in the patient who has developed hypernatremia over several days or longer. Dietary sodium intake is often restricted. 107  Hyponatremia - 01 Hyponatremia (low serum sodium) may result from a loss of sodium-containing fluids, water excess in relation to the amount of sodium (dilutional hyponatremia), or a combination of both. 108  Hyponatremia - 02 Common causes of hyponatremia from loss of sodium-rich body fluids include profuse diaphoresis, draining wounds, excessive diarrhea or vomiting, and trauma with significant blood loss. Hyponatremia causes hypoosmolality with a shift of water into the cells. 109  Hyponatremia - 03 A common cause of hyponatremia from water excess is inappropriate use of sodium-free or hypotonic IV fluids. This may occur in patients after surgery or major trauma or during administration of fluids in patients with renal failure. 110  Hyponatremia - 04 Patients with psychiatric disorders may have an excessive water intake. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) will result in dilutional hyponatremia caused by abnormal retention of water. 111  Hyponatremia - 05 Clinical Manifestations. Manifestations of hyponatremia are due to cellular swelling and first manifested in the central nervous system (CNS). The excess water lowers plasma osmolality, shifting fluid into brain cells, causing irritability, headache, confusion, seizures, and even coma. Severe acute hyponatremia, if untreated, can cause irreversible neurologic damage or death 112  Hyponatremia - 06 Nursing Diagnoses Risk for acute confusion related to electrolyte imbalance, Risk for injury related to altered sensorium and decreased level of consciousness, Risk for electrolyte imbalance related to excessive loss of sodium and/or excessive intake or retention of water, Potential complication: severe neurologic changes. 113  Hyponatremia - 07 Nursing Impelentation (1) In hyponatremia caused by water excess, fluid restriction is often the only treatment. If severe symptoms (seizures) develop, small amounts of IV hypertonic saline solution (3% sodium chloride) can restore the serum sodium level while the body is returning to a normal water balance. 114  Hyponatremia - 08 Nursing Impelentation (2) Treatment of hyponatremia associated with abnormal fluid loss includes fluid replacement with sodium-containing solutions. 115  Hyponatremia - 09 Nursing Impelentation (3) The drugs conivaptan (Vaprisol) and tolvaptan (Samsca) are given to block the activity of ADH. Conivaptan results in increased urine output without loss of electrolytes such as sodium and potassium. 116  Hyponatremia - 10 Nursing Impelentation (4) It should not be used in patients with hyponatremia from excess water loss. Tolvaptan is used to treat hyponatremia associated with heart failure, liver cirrhosis, and SIADH. Treatment with these drugs is started in a hospital setting so the patient’s clinical status and serum sodium levels can be carefully monitored. 117 POTASSIUM IMBALANCES 118  POTASSIUM IMBALANCES - 01 Potassium is the major ICF cation, with 98% of the body potassium being intracellular. For example, potassium concentration within muscle cells is approximately 140 mEq/L; potassium concentration in ECF is 3.5 to 5.0 mEq/L 119  Hyperkalemia - 01 Hyperkalemia (high serum potassium) may result from impaired renal excretion, a shift of potassium from ICF to ECF, a massive intake of potassium, or a combination of these factors. 120  Hyperkalemia - 02 The most common cause of hyperkalemia is renal failure. Adrenal insufficiency with a subsequent aldosterone deficiency leads to retention of potassium ions. Factors that cause potassium to move from ICF to ECF include acidosis, massive cell destruction (as in burn or crush injury, tumor lysis, severe infections), and exercise. 121  Hyperkalemia - 03 Clinical Manifestations (1) Hyperkalemia increases the concentration of potassium outside of the cell, altering the normal ECF and ICF ratio and resulting in increased cellular excitability. 122  Hyperkalemia - 04 Clinical Manifestations (2) Initially, as the levels of potassium increase, the patient may experience cramping leg pain and weakness, followed by weakness or paralysis of other skeletal muscles, including the respiratory muscles. Abdominal cramping and diarrhea occur from hyperactivity of smooth muscles. 123  Hyperkalemia - 05 Clinical Manifestations (3) The most clinically significant manifestations of hyperkalemia are the disturbances in cardiac conduction. Cardiac depolarization is decreased, leading to flattening of the P wave and widening of the QRS complex. Repolarization occurs more rapidly, resulting in shortening of the QT interval and a T wave that is narrower and more peaked. Ventricular fibrillation or cardiac standstill may occur. 124  Hyperkalemia - 06 Nursing Diagnoses Risk for activity intolerance related to lower extremity muscle weakness, Risk for electrolyte imbalance related to excessive retention or cellular release of potassium, Risk for injury related to lower extremity muscle weakness and seizures, Potential complication: dysrhythmias. 125  Hyperkalemia - 07 Nursing Implementation (1) Eliminate oral and parenteral potassium intake. Increase elimination of potassium. This is accomplished with diuretics, dialysis, and ion-exchange resins such as sodium polystyrene sulfonate (Kayexalate). Kayexalate, administered orally or rectally, binds potassium in exchange for sodium, and the resin is excreted in feces. 126  Hyperkalemia - 08 Nursing Implementation (2) Force potassium from ECF to ICF. This is accomplished by IV administration of regular insulin (along with glucose so the patient does not become hypoglycemic) or IV sodium bicarbonate for the correction of acidosis. Occasionally, a β-adrenergic agonist (e.g., nebulized albuterol) is administered. This therapy is not indicated for patients with tachycardia or coronary artery disease 127  Hyperkalemia - 09 Nursing Implementation (3) Reverse the membrane potential effects of the elevated ECF potassium by administering IV calcium gluconate. Calcium ions can immediately reverse the membrane excitability. 128  Hyperkalemia - 10 Nursing Implementation (4) In cases in which the elevation of potassium is mild and the kidneys are functioning, it may be sufficient to (1) withhold potassium from the diet and IV sources and (2) increase renal potassium elimination by administering fluids and loop or thiazide diuretics. 129  Hyperkalemia - 11 Nursing Implementation (5) Patients with moderate hyperkalemia should additionally receive one of the treatments to force potassium into cells, usually IV insulin and glucose. Monitor the electrocardiograms (ECGs) of all patients with clinically significant hyperkalemia to detect dysrhythmias and to monitor the effects of therapy. 130  Hyperkalemia - 12 Nursing Implementation (6) The patient experiencing dangerous cardiac dysrhythmias should receive IV calcium gluconate immediately. Monitor blood pressure because rapid administration of calcium can cause hypotension. Hemodialysis is an effective means of removing potassium from the body in the patient with renal failure. 131  Hypokalemia - 01 Hypokalemia (low serum potassium) can result from increased loss of potassium, from an increased shift of potassium from ECF to ICF, or rarely from deficient dietary potassium intake. The most common causes of hypokalemia are abnormal losses from either the kidneys or the GI tract. 132  Hypokalemia - 02 GI tract losses of potassium are associated with diarrhea, laxative abuse, vomiting, and ileostomy drainage. Renal losses occur when the patient has a low magnesium level or is diuresing, particularly in the patient with an elevated aldosterone level. 133  Hypokalemia - 03 Aldosterone is released when the circulating blood volume is low, thus causing sodium retention in the kidneys with a loss of potassium in the urine. Low plasma magnesium stimulates renin release and subsequent increased aldosterone levels, which results in potassium excretion. 134  Hypokalemia - 04 Among the factors causing potassium to move from ECF to ICF are insulin therapy (especially in conjunction with diabetic ketoacidosis) and β-adrenergic stimulation (catecholamine release in stress, coronary ischemia, delirium tremens, administration of β-adrenergic agonist drugs). Alkalosis can cause a shift of potassium into cells in exchange for hydrogen, thus lowering the potassium in ECF and causing symptomatic hypokalemia 135  Hypokalemia - 05 Clinical Manifestations (1) Hypokalemia alters the resting membrane potential, resulting in hyperpolarization (an increased negative charge within the cell) and impaired muscle contraction. Therefore the manifestations of hypokalemia involve changes in cardiac and muscle function. 136  Hypokalemia - 06 Clinical Manifestations (2) The most serious clinical problems are cardiac changes, including impaired repolarization, resulting in a flattening of the T wave and eventually in emergence of a U wave. The P waves peak, and the QRS complex is prolonged. There is an increased incidence of potentially lethal ventricular dysrhythmias. 137  Hypokalemia - 07 Clinical Manifestations (3) Skeletal muscle weakness and paralysis may occur with hypokalemia. As with hyperkalemia, hypokalemia initially affects leg muscles. Severe hypokalemia can cause weakness or paralysis of respiratory muscles, leading to shallow respirations and respiratory arrest. 138  Hypokalemia - 08 Clinical Manifestations (4) Alterations in smooth muscle function may lead to decreased GI motility (e.g., paralytic ileus), decreased airway responsiveness, and impaired regulation of arteriolar blood flow, possibly contributing to smooth muscle cell breakdown. Finally, hypokalemia can impair function in nonmuscle tissue by impairing insulin secretion, leading to hyperglycemia. 139  Hypokalemia - 09 Nursing Diagnoses Risk for activity intolerance related to lower extremity muscle weakness, Risk for electrolyte imbalance related to excessive loss of potassium, Risk for injury related to muscle weakness and hyporeflexia Potential complication: dysrhythmias. 140  Hypokalemia - 10 Nursing Implementation (1) Treatment of hypokalemia consists of oral or IV potassium chloride (KCl) supplements and increased dietary intake of potassium. Except in severe deficiencies, KCl is not given unless there is urine output of at least 0.5 mL/kg of body weight per hour. 141  Hypokalemia - 12 Nursing Implementation (2) SAFETY ALERT IV KCl must always be diluted and never given in concentratedamounts. Never give KCl via IV push or as a bolus. Invert IV bags containing KCl several times to ensure even distributionin the bag. Never add KCl to a hanging IV bag to prevent giving a bolus dose. 142  Hypokalemia - 13 Nursing Implementation (3) The preferred maximum concentration is 40 mEq/L. However, stronger concentrations (up to 80 mEq/L) may be given for severe hypokalemia, with continuous cardiac monitoring. The rate of IV administration of KCl should not exceed 10 mEq/hr and must be given by infusion pump to ensure correct administration rate. 143  Hypokalemia - 14 Nursing Implementation (4) Because KCl is irritating to the vein, assess IV sites at least hourly for phlebitis and infiltration. Infiltration can cause necrosis and sloughing of the surrounding tissue. Use a central IV line when rapid correction of hypokalemia is necessary. 144  Hypokalemia - 15 Nursing Implementation (5) Patients at risk for hypokalemia and those who are critically ill should have cardiac monitoring to detect cardiac changes related to potassium imbalances. Monitor serum potassium levels and urine output as appropriate. Because patients on digoxin therapy have an increased risk of toxicity if their serum potassium level is low, monitor the patient for digitalis toxicity. 145 CALCIUM IMBALANCES 146  Hypercalcemia - 01 Hypercalcemia (high serum calcium) is caused by hyperparathyroidism in about two thirds of the cases. Malignancy, especially from myeloma and breast, lung, and kidney cancers, causes the remaining third 147  Hypercalcemia - 02 Malignancies lead to hypercalcemia through bone destruction from tumor invasion or through tumor secretion of a parathyroid-related protein, which stimulates calcium release from bones. 148  Hypercalcemia - 03 Hypercalcemia is also associated with prolonged immobilization, which results in bone mineral loss and increased plasma calcium concentration. Rare causes include vitamin D overdose or increased calcium intake (e.g., ingestion of antacids containing calcium, excessive administration during cardiac arrest). 149  Hypercalcemia - 04 Nursing Diagnoses Risk for activity intolerance related to generalized muscle weakness, Risk for electrolyte imbalance related to excessive bone destruction, Risk for injury related to neuromuscular and sensorium changes, Potential complication: dysrhythmias. 150  Hypercalcemia - 05 Nursing Implementation (1) The basic treatment for hypercalcemia is promoting urinary excretion of calcium by administering a loop diuretic (e.g., furosemide [Lasix]) and hydrating the patient with isotonic saline infusions. 151  Hypercalcemia - 06 Nursing Implementation (2) The patient must drink 3000 to 4000 mL of fluid daily to promote the renal excretion of calcium and decrease the possibility of kidney stone formation. Other supportive measures include a diet low in calcium and an increase in weight-bearing activity to enhance bone mineralization. 152  Hypercalcemia - 07 Nursing Implementation (3) Bisphosphonates (e.g., pamidronate [Aredia], zoledronic acid [Zometa]) are the most effective agents in treating hypercalcemia caused by a malignancy. They inhibit the activity of osteoclasts (cells that break down bone and result in calcium release). Synthetic calcitonin given intramuscularly (IM) or subcutaneously lowers serum calcium levels; the intranasal form is not effective. 153  Hypocalcemia - 01 Hypocalcemia (low serum calcium) can be caused by any condition that decreases the production of PTH. This may occur with surgical removal of a portion of or injury to the parathyroid glands during thyroid or neck surgery. 154  Hypocalcemia - 02 Acute pancreatitis is another potential cause of hypocalcemia. Lipolysis, a consequence of pancreatitis, produces fatty acids that combine with calcium ions, decreasing serum calcium levels. The patient who receives multiple blood transfusions can become hypocalcemic because the citrate used to anticoagulate the blood binds with the calcium. 155  Hypocalcemia - 03 Sudden alkalosis may result in symptomatic hypocalcemia despite a normal total serum calcium level. The high pH increases calcium binding to protein, decreasing the amount of ionized calcium. Hypocalcemia can occur if there is increased loss of calcium due to laxative abuse and malabsorption syndromes. 156  Hypocalcemia - 04 Low calcium levels allow sodium to move into excitable cells, decreasing the threshold of action potentials with subsequent depolarization of the cells. This results in increased nerve excitability and sustained muscle contraction, or tetany. 157  Hypocalcemia - 05 Clinical signs of tetany include Chvostek’s sign and Trousseau’s sign. Chvostek’s sign is contraction of facial muscles in response to a tap over the facial nerve in front of the ear. Trousseau’s sign refers to carpal spasms induced by inflating a blood pressure cuff on the arm. 158 159  Hypocalcemia - 06 After the cuff is inflated above the systolic pressure, carpal spasms occur within 3 minutes if hypocalcemia is present. Other manifestations of tetany are laryngeal stridor, dysphagia, and numbness and tingling around the mouth or in the extremities. 160  Hypocalcemia - 07 Nursing Diagnoses Acute pain related to sustained muscle contractions, Ineffective breathing pattern related to laryngospasm, Risk for electrolyte imbalance related to decreased production of PTH, Risk for injury related to tetany and seizures, Potential complications: fracture, respiratory arrest. 161  Hypocalcemia - 08 Nursing Implementation (1) The primary goal of treatment of hypocalcemia is to treat the underlying cause. When severe manifestations of hypocalcemia occur, IV preparations of calcium (e.g., calcium gluconate, calcium chloride) are given. 162  Hypocalcemia - 09 Nursing Implementation (2) Treatment of mild hypocalcemia involves a diet high in calcium-rich foods along with vitamin D supplementation. Oral calcium supplements, such as calcium carbonate, can be used when patients are unable to consume enough dietary calcium, such as those who cannot tolerate dairy products. 163  Hypocalcemia - 10 Nursing Implementation (3) Measures to promote CO2 retention, such as breathing into a paper bag or sedating the patient, can control muscle spasm and other symptoms of tetany until the calcium level is corrected. Adequately treat pain and anxiety because hyperventilation-induced respiratory alkalosis can precipitate hypocalcemic symptoms. 164  Hypocalcemia - 11 Nursing Implementation (4) Closely observe any patient who has had thyroid or neck surgery in the immediate postoperative period for manifestations of hypocalcemia because of the proximity of the surgery to the parathyroid glands. 165 MAGNESIUM IMBALANCES 166  Hypermagnesemia - 01 Hypermagnesemia (high serum magnesium level) usually occurs only with an increase in magnesium intake accompanied by renal insufficiency or failure. A patient with chronic kidney disease who ingests products containing magnesium (e.g., Maalox, milk of magnesia) will have a problem with excess magnesium. Magnesium excess could develop in the pregnant woman who receives magnesium sulfate for the management of eclampsia. 167  Hypermagnesemia - 02 Hypermagnesemia depresses neuromuscular and CNS functions. Initial clinical manifestations of a mildly elevated serum magnesium concentration include lethargy, nausea, and vomiting. As the levels of serum magnesium increase, deep tendon reflexes are lost, followed by somnolence, and then respiratory and, ultimately, cardiac arrest can occur. 168  Hypermagnesemia - 03 Management of hypermagnesemia should focus on prevention. People with chronic kidney disease should not take magnesium-containing drugs and should limit ingestion of magnesium containing foods (e.g., green vegetables, nuts, bananas, oranges, peanut butter, chocolate). 169  Hypermagnesemia - 04 The emergency treatment of hypermagnesemia is IV administration of calcium chloride or calcium gluconate to oppose the effects of the magnesium on cardiac muscle. If renal function is adequate, promoting urinary excretion with oral and parenteral fluids and IV furosemide decreases magnesium levels. The patient with impaired renal function requires dialysis because the kidneys are the major route of excretion for magnesium. 170  Hypomagnesemia - 01 Hypomagnesemia (low serum magnesium level) occurs in patients with limited magnesium intake or increased renal losses. Major causes of hypomagnesemia from insufficient food intake include prolonged fasting or starvation and chronic alcoholism. 171  Hypomagnesemia - 02 Fluid loss from the GI tract interferes with magnesium absorption. Another potential cause of hypomagnesemia is prolonged parenteral nutrition without magnesium supplementation. Many diuretics increase the risk of magnesium loss through renal excretion. In addition, osmotic diuresis caused by high glucose levels in uncontrolled diabetes mellitus increases renal excretion of magnesium. 172  Hypomagnesemia - 03 Hypomagnesemia produces neuromuscular and CNS hyperirritability. Clinical manifestations include confusion, hyperactive deep tendon reflexes, muscle cramps, tremors, and seizures. Magnesium deficiency predisposes to cardiac dysrhythmias, such as premature ventricular contractions and ventricular fibrillation. 173  Hypomagnesemia - 04 Clinically, hypomagnesemia resembles hypocalcemia and may contribute to the development of hypocalcemia resulting from the decreased action of PTH. Hypomagnesemia may also be associated with hypokalemia that does not respond well to potassium replacement. This occurs because intracellular magnesium is critical to normal function of the sodium potassium pump. 174  Hypomagnesemia - 05 The primary goal of treatment of hypomagnesemia is to treat the underlying cause. Management of mild magnesium deficiencies involves oral supplements and increased dietary intake of foods high in magnesium. If hypomagnesemia is severe or if hypocalcemia is present, IV magnesium (e.g., magnesium sulfate) is given. Monitor vital signs and use an infusion pump, since too rapid administration of magnesium can lead to cardiac or respiratory arrest. 175  Hypomagnesemia - 06 The primary goal of treatment of hypomagnesemia is to treat the underlying cause. Management of mild magnesium deficiencies involves oral supplements and increased dietary intake of foods high in magnesium. If hypomagnesemia is severe or if hypocalcemia is present, IV magnesium (e.g., magnesium sulfate) is given. Monitor vital signs and use an infusion pump, since too rapid administration of magnesium can lead to cardiac or respiratory arrest. 176 FLUID-ELECTROLYTE IMBALANCES IN SURGICAL PATIENS 177  Nursing Care - 01 Obtained-Extracted Tracking: Fluids taken, whether oral, parenteral, rectal, or by tube, should be recorded. This recording helps in recognizing imbalances, preventing them in a short time, and calculating fluid-electrolyte needs. Likewise, the removed fluids should be recorded. 178  Nursing Care - 02 Obtained-Extracted Tracking: It is important to record the character and volume of the urine. A few days after the surgery, the amount of urine is below normal. After major surgery, the amount of urine may be below 700 ml. In this case, excess fluid should not be given to increase the amount of urine. A 24-hour urine volume of less than 500 ml may suggest kidney failure. 179  Nursing Care - 03 Obtained-Extracted Tracking: All drainages in the body should be recorded. If the wound has excessive drainage, the weight between the dry dressing and the drained dressing should be calculated. As with paracentesis or thoracentesis, fluids aspirated from body cavities should be measured. Fluid loss occurs when body temperature rises. 180  Nursing Care - 04 Replacement of liquid-electrolytes: The ideal intake is oral. The integrity and mobility of the gastrointestinal tract is ensured. The most commonly used method in patients who cannot take it orally is the IV route. The amount to be given for adults without renal and circulatory problems should be between 2500-3000 ml. 181  Nursing Care - 05 Replacement of liquid-electrolytes: Patients receiving intravenous fluid therapy should be monitored for hypovolemia and hypervolemia. The catheter site should be observed frequently for inflammation and infiltration. When infiltration occurs, the infusion should be terminated. The infusion site should be changed every 72 hours. If the patient cannot take heavy fluids for a few days, it is requested to add KCl to the fluids to be given to the patient. 182  Nursing Care - 06 Replacement of liquid-electrolytes: More than 80% of potassium is excreted from the body through urine. KCl should not be added to the IV fluid of patients coming from surgery without first urinating. Electrolyte solutions containing K are irritating. Extravasation of these solutions causes tissue necrosis. 183  Nursing Care - 07 Preventing Nausea-Vomiting: Fluid-electrolyte imbalances cause nausea and vomiting, and vomiting causes fluid-electrolyte imbalance due to excessive loss of gastric secretion. Antiemetics are given parenterally. 184  Nursing Care - 08 Patient-family education: Education is important in diagnosing fluid-electrolyte imbalance. The signs and symptoms of fluid-electrolyte deficiency and excess are taught. Depending on the type of deficiency or excess, fluid intake is restricted or increased. A list of free or restricted foods should be given to the patient and family. 185 THANK YOU! 186