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UNIT 3: FLUID AND ELECTROLYTE IMBALANCE

Pages 80-89 - Complete Line-by-Line Explanation

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PAGE 80 - Functions of Body Fluids, Fluid Balance, Fluid Imbalance

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FUNCTIONS OF BODY FLUIDS

• Blood is the main transport vehicle in the body. It delivers oxygen and nutrients (like glucose, vitamins) to every cell. It also collects carbon dioxide and waste products (like urea, creatinine) and takes them away for excretion.

• The amount of fluid in blood vessels directly affects blood pressure. If blood volume is low (e.g., in dehydration), blood pressure drops. If it is high (e.g., in fluid overload), blood pressure rises.

• When the body overheats, sweat glands release fluid onto the skin. As that fluid evaporates, it carries heat away, cooling the body. This is how the body maintains a normal temperature (~37°C).

• All chemical reactions inside cells take place in a watery environment. Without adequate fluid, enzymes cannot work and metabolism stops.

• Hydrolysis means "breaking with water." Digestive enzymes use water molecules to break down large food molecules (proteins, fats, carbohydrates) into smaller, absorbable units.

• Kidneys use water to dissolve and flush out waste products as urine. Without adequate water, waste products accumulate in the blood (azotemia/uremia).

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FLUID BALANCE

• The body continuously loses fluid through urine, sweat, breathing, and feces. To stay healthy, a person must drink and eat enough to replace these losses (roughly 2-3 litres per day in an adult).

• Kidneys: The primary route - urine (approximately 1500 ml/day).
• Lungs: Breathing out water vapor (insensible loss, ~400 ml/day).
• Skin: Sweat (sensible) and insensible perspiration (~500 ml/day).

1. "The removal of body heat by evaporation of water through skin and lungs."
   • Heat is removed as water evaporates from the body surface and from breathing. This is a continuous process even when you are not visibly sweating.
2. "Excretion of urea and other metabolic wastes through kidney."
   • The kidneys need water to dilute toxic waste products and flush them out as urine. Without enough water, urine becomes concentrated and kidney stones/failure can develop.

• Then the text lists all types of body fluids: aqueous humour (eye fluid), vitreous humour (eye gel), bile, blood serum, breast milk, cerebrospinal fluid (CSF), cerumen (earwax), endolymph and perilymph (ear fluids), female ejaculate, gastric juice, mucus, peritoneal fluid, pleural fluid, saliva, sebum (skin oil), semen, sweat, tears, vaginal secretion, vomit and urine.
• Why this matters: All these fluids contribute to body fluid balance. Abnormal loss of any of them (e.g., vomiting = loss of gastric juice; diarrhea = loss of intestinal fluid) can cause imbalance.

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FLUID AND ELECTROLYTE IMBALANCE

• Diaphoresis = profuse sweating. In severe burns or wounds, large amounts of fluid and electrolytes (mainly sodium) pour out through the damaged skin. This can cause life-threatening dehydration.

• Fluid and electrolytes are inseparable. You cannot lose fluid without losing electrolytes and vice versa. This is why both must be monitored and replaced together.

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FLUID IMBALANCE

• Normal body water content is approximately 60% of body weight in adults. Anything above or below this range is an imbalance.

• Isotonic imbalance: Both water AND solutes (electrolytes) are gained or lost in equal proportions. The concentration (osmolarity) of body fluids does not change.
• Osmolar imbalance: Only water is gained or lost, so the concentration changes.

• If output exceeds intake, dehydration develops. If intake exceeds output, fluid overload develops.

1. Extracellular Fluid Volume Deficit (EFVD)
2. Extracellular Fluid Volume Excess (EFVE)
3. Extracellular Fluid Volume Shift (EFVS)
4. Intracellular Fluid Volume Excess (IFVE)
5. Intracellular Fluid Volume Deficit (IFVD)

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EXTRACELLULAR FLUID VOLUME DEFICIT (EFVD)

• Intravascular fluid = fluid inside blood vessels (blood plasma). Interstitial fluid = fluid surrounding cells in tissues. When both decrease, the total extracellular fluid (ECF) is reduced.

• EFVD is the most frequently encountered fluid problem in clinical practice (e.g., in dehydrated patients, surgical patients, burn patients).

• Both compartments shrink - blood vessels have less plasma (causing reduced blood pressure) and tissues have less fluid (causing sunken eyes, dry skin).

• EFVD can occur alone. But often, as fluid is lost, sodium concentration rises (because the same amount of sodium is now in less water). When this happens, it is called dehydration.

• Key definition to remember: Dehydration = EFVD + high sodium (hypernatremia). Just having low fluid is EFVD; when sodium also rises because water was lost more than sodium, it becomes dehydration.

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TYPES OF EXTRACELLULAR FLUID VOLUME DEFICIT

1. Hyperosmolar fluid volume deficit: Fluid loss is greater than solute (sodium) loss. The remaining fluid becomes more concentrated. Example: Fever, diabetes insipidus.
2. Iso-osmolar fluid volume deficit: Equal proportions of fluid and solute are lost. The concentration stays the same. Example: Hemorrhage, vomiting with loss of both fluid and salt.
3. Hypotonic fluid volume deficit: Electrolyte loss is greater than fluid loss. The remaining fluid becomes dilute. Example: Use of non-saline IV fluids after surgery.

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ETIOLOGY (Causes) of EFVD

1. Patients who are elderly, confused or debilitated - These patients cannot adequately express thirst or get their own water, leading to chronic dehydration.
2. Severe vomiting and diarrhea - Direct loss of gastrointestinal fluids rich in water and electrolytes.
3. Losing large volume of blood - Hemorrhage removes both fluid and red blood cells from circulation.
4. Difficulty in swallowing - Cannot take in fluids orally.
5. Loss of sodium containing body fluids:
   • a. Urine: Salt-wasting renal disorder (kidneys fail to hold sodium), excessive diuretic therapy (diuretics force extra urine output), prolonged bed rest.
   • b. GI fluids: Vomiting, diarrhea, and fistula drainage all remove sodium-rich fluids.
6. Diabetes ketoacidosis - High blood sugar causes osmotic diuresis (excess urine output), leading to fluid and electrolyte loss.

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RISK FACTORS (Table 3.4)

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PAGE 81 - Pathophysiology, Clinical Manifestations, Diagnostic Evaluation, Management of EFVD

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PATHOPHYSIOLOGY OF EFVD

• Sodium (Na+) is the main electrolyte of extracellular fluid. It acts like a magnet for water - where sodium goes, water follows. The kidneys regulate sodium to control fluid balance.

• When you lose more water than sodium (e.g., in fever, heat stroke), the sodium remaining in the blood becomes more concentrated. This high serum sodium signals dehydration.

• When blood sodium rises (hyperosmolality), the body tries to fix this by pulling water from the cells into the blood. But this still does not fully correct the deficit - it just moves fluid from one compartment to another.

• When water leaves cells to enter the blood, cells shrink. Shrunken brain cells cause neurological symptoms (confusion, headache). Shrunken skin cells cause decreased skin turgor.

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CLINICAL MANIFESTATIONS (Signs & Symptoms) of EFVD

1. Increased thirst - The body's first alarm signal. Dry mucous membranes stimulate the thirst center in the hypothalamus.
2. Decreased skin turgor - When you pinch the skin, it stays "tented" and does not spring back quickly. This shows the skin and underlying tissues are dehydrated.
3. Dry mucous membrane, cracked lips or tongue - The inside of the mouth and lips dry out because salivary glands do not produce enough saliva.
4. Eye balls soft and sunken - The fat and fluid around the eyeball are depleted, causing the eyes to appear sunken (enophthalmos).
5. Elevated temperature - Fluid is needed to cool the body through sweat. Without adequate fluid, the body cannot regulate temperature well and fever develops.
6. Postural systolic blood pressure fall >15 mm Hg and diastolic blood pressure fall >10 mm Hg - This is called orthostatic hypotension. When a dehydrated patient stands up, blood pressure drops (because there is not enough fluid to maintain pressure against gravity). A drop of >15 mmHg systolic is significant.
7. Narrowed pulse pressure - Pulse pressure = systolic BP minus diastolic BP. In EFVD, systolic drops more than diastolic (because the heart has less blood to pump out), so the gap narrows. Normal pulse pressure is 30-50 mmHg.
8. Weight loss - Each litre of fluid lost = 1 kg of body weight lost. Weight is the most accurate way to monitor fluid balance.
9. Oliguria <30 ml per hour - The kidneys conserve water by making very little, very concentrated urine. Urine output less than 30 ml/hour indicates the kidneys are not being adequately perfused.
10. Decreased central venous pressure - CVP measures pressure in the right side of the heart. When blood volume is low, CVP is low (normal is 2-8 mmHg).

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TABLE 3.5 - Clinical Manifestations with Their Pathophysiologic Basis

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DIAGNOSTIC EVALUATION

1. Extracellular fluid volume deficit determined through medical history and physical examination.
   • Ask: When did symptoms start? Any vomiting/diarrhea? How much fluid intake? History of diuretics?
2. Serum sodium imbalance is diagnosed from laboratory test on some form of blood (serum sodium <135 mEq/h).
   • Normal serum sodium = 135-145 mEq/L. Less than 135 = hyponatremia. In EFVD, sodium may be normal, high (dehydration), or low depending on the type.
3. Measure weight daily. - Daily weight is the gold standard for monitoring fluid balance in hospitalized patients.
4. Postural blood pressure measurements in adults and adolescents. - Check BP lying and standing to detect orthostatic changes.
5. BUN and hematocrit may be increased, if EFVD arises rapidly. - BUN (Blood Urea Nitrogen) rises because less blood flows to the kidneys. Hematocrit rises because red blood cells are now more concentrated in less fluid.
6. Serum osmolality <275 mOsm/kg. - Normal serum osmolality is 275-295 mOsm/kg. A low value can indicate EFVD in some contexts (though in hyperosmolar EFVD it would be high).
7. Assess small vein filling time (Box 3.1):
   • Place hand below heart level so veins fill.
   • Close off a vein with a finger.
   • Milk the vein toward the heart until flat.
   • Lift fingers and count seconds until vein refills.
   • If it takes more than 3 seconds to refill = EFVD (unless arterial disease is present).
8. Check skin turgor. - Pinch skin on forearm or forehead; if it stays tented >2 seconds, it indicates dehydration.
9. Assess dryness of opposing mucous membrane, e.g., between cheek and gums. - The fold between cheek and gum is a reliable place to check for dryness, as it is less affected by mouth breathing.

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MANAGEMENT of EFVD

1. Treatment for EFVD is the replacement of Isotonic Sodium Containing Fluid (ISCF).
   • a. Most common ISCF are normal saline and Ringer's solution and lactated Ringer's solution.
     • Normal saline (0.9% NaCl): Has the same sodium concentration as blood plasma. It expands blood volume without changing osmolality.
     • Ringer's solution / Lactated Ringer's: Contains sodium, potassium, calcium, and chloride - closely mimics the composition of plasma. Lactated Ringer's also contains lactate which is converted to bicarbonate in the liver.
   • b. Oral replacement can be accomplished by giving fluids which contains sodium, such as salty broth by providing salty foods.
2. Dietary management: Patient experiencing fluid loss from diarrhea should avoid fatty or fried food and milk products (these worsen diarrhea and further increase fluid loss).
3. If hemorrhage is the cause of EFVD, blood replacement may be essential, if blood is greater than 1L. - Blood transfusion is needed when the fluid lost is whole blood (not just plasma or water), especially if >1 litre has been lost.

1. Assess the patient's physical condition and medical history.
2. Monitor the vital signs every 2 to 4 hours.

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PAGE 82 - Nursing Management (EFVD continued), Extracellular Fluid Volume Excess (EFVE)

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NURSING MANAGEMENT OF EFVD (Continued)

1. Patient should be assessed for typical clinical manifestations.
2. Assess for skin turgor (Figure 3.2):
   • A & B (Normal): When normal skin is pinched, it resumes shape in seconds.
   • C (Poor turgor): If the skin remains wrinkled for 20-30 seconds, the patient has poor skin turgor - a sign of dehydration.
3. Nurse should assess the patient's ability to participate in the treatment plan. - Some patients (elderly, confused, children) cannot drink on their own and need assistance.
4. Weight of the patient should be monitored daily. - A loss of 1 kg = 1 litre of fluid lost. A gain of 1 kg = 1 litre of fluid retained.
5. Mild fluid volume loss can be corrected with oral fluid replacement. - Mild dehydration does not require IV fluids. Encouraging drinking (water, juice, broth) is sufficient.
6. Positional blood pressure should be assessed to determine the degree of orthostatic. - Check BP in lying, sitting, and standing positions.
7. Assess urine output hourly, if EFVD is severe. - Oliguria (<30 ml/hr) confirms severe EFVD and possible kidney impairment.
8. Monitor serum sodium, BUN glucose and hematocrit level. - Rising BUN and hematocrit, and abnormal sodium indicate worsening EFVD.
9. Manage the replacement of isotonic sodium containing fluid. - Ensure the right IV fluid is hung and running at the prescribed rate.
10. A nurse should apply lotion/emollient to the skin to preserve skin integrity. - Dehydrated skin is fragile and prone to cracking and breakdown.
11. Patient's position should be changed every 2 hours or more often, if skin assessment dictates. - Dehydrated, fragile skin breaks down quickly under pressure, causing pressure ulcers.
12. Oral care should be given every 2 hours. - Dry mouth causes discomfort and promotes bacterial growth; regular mouth care keeps mucous membranes moist.
13. If fluid loss is moderate or severe, administration of intravenous fluid is indicated. - Oral fluids may not be sufficient or possible; IV fluids deliver fluid directly into circulation.
14. Elderly patient must be rehydrated slowly because of frequent problems with renal and cardiac disease in that age group. - Fast rehydration in elderly patients can cause their weakened heart and kidneys to become overwhelmed, leading to fluid overload.
15. Encourage patient and family to talk about their concerns and ask questions. - Education and emotional support improve compliance with treatment.
16. Encourage patient to be as active as possible.
17. Instruct patient to make a chart to keep track of fluid intake. - Helps the patient self-monitor.
18. Indicate that cold or hot liquids often satisfy thirst better than lukewarm water. - Temperature affects palatability; patients drink more when they enjoy the taste.
19. Administer medications as ordered.

1. Renal failure - Prolonged poor kidney perfusion leads to acute kidney injury.
2. Heart failure - Low blood volume makes the heart work harder.

• Describe the processes that cause extracellular fluid volume deficit.
• Encourage the patient to be as active as possible within the limits of safety.
• Teach the patient to get up slowly and have something sturdy to hold onto in case of light-headedness.
• Teach how to prevent EFVD in the future.
• Teach how to detect early signs of extracellular fluid volume in case it recurs.
• Explain that reduction of signs and symptoms indicates that therapy is working well.
• Indicate that the patient should contact health care provider if symptoms worsen.

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EXTRACELLULAR FLUID VOLUME EXCESS (EFVE)

• EFVE is the opposite of EFVD. Too much fluid builds up in the blood vessels and tissues. Because it is isotonic (water and sodium are retained in the same proportion), the concentration of body fluids does not change.

• Blood vessels are overfilled (causing high blood pressure, bounding pulse) and tissues are waterlogged (causing edema).

• The osmolality is normal even though total volume is too high. This is the most common type of EFVE.

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ETIOLOGY of EFVE

1. Most commonly, it occurs in case of heart disease. - The failing heart cannot pump efficiently, so blood backs up in the venous system. The kidneys sense reduced blood flow and retain more sodium and water, making the problem worse.
2. Excessive intravenous infusion of sodium containing isotonic solutions:
   • a. Normal saline
   • b. Lactated Ringer's solution
   • Over-infusing these solutions adds excess sodium and water to the circulation.
3. Renal retention of sodium and water:
   • a. Primary hyperaldosteronism - Excess aldosterone hormone causes kidneys to retain more sodium (and water follows).
   • b. Chronic heart failure - Reduced cardiac output triggers aldosterone and ADH release, causing sodium and water retention.
   • c. Cirrhosis of liver - The liver cannot produce albumin normally; low albumin reduces oncotic pressure, causing fluid to leak into tissues. The kidneys compensate by retaining more fluid.
   • d. Cushing syndrome - Excess cortisol has mineralocorticoid effects, causing sodium retention.
   • e. Corticosteroid therapy - Same mechanism as Cushing syndrome.

1. Patients with heart, liver, kidney disorders are prone to sodium and water retention.
2. Patients with hyperaldosteronism or Cushing syndrome are at increased risk of EFVE.

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PATHOPHYSIOLOGY of EFVE

1. With fluid volume excess, fluid pressure is greater than usual at the arterial end of the capillary. - Normally, fluid moves from capillaries into tissues and back. In EFVE, the pressure in the capillary is so high that more fluid is pushed out into tissues than is reabsorbed.
2. Fluid is pushed into tissue spaces. Then, the edema of peripheral and pulmonary regions occurs. - Peripheral edema (swollen ankles, feet) and pulmonary edema (fluid in lungs) are the direct results.

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PAGE 83 - EFVE Continued (Pathophysiology, Clinical Manifestations, Management)

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PATHOPHYSIOLOGY of EFVE (Continued)

• Increased hydrostatic pressure in arterial end of capillary → Fluid movement into tissues → Edema → Increased peripheral vascular resistance → Increased left ventricular pressure → Increased left atrial pressure → Pulmonary edema

• Diseased kidneys cannot excrete sodium and water properly, so they accumulate.

• The heart tries to handle the extra load by beating harder and faster. Over time, this compensation fails, leading to congestive heart failure.

• Oncotic (colloid osmotic) pressure is the "pulling" force that keeps fluid inside blood vessels. Albumin provides this force. Low albumin = low pulling force = fluid leaks out into tissues = edema and ascites (fluid in the abdomen). (See Flowchart 3.5)

• Decreased production of plasma proteins → Decreased capillary oncotic pressure → Edema

• Lymph vessels normally drain excess fluid from tissues back into circulation. If they are blocked (e.g., cancer, surgery), fluid builds up in tissues.

• Lymphatic obstruction decreases absorption of interstitial fluid → Decreased transportation of capillary filtered protein → Increased tissue oncotic pressure which pulls fluid toward it → Edema

• Untreated fluid overload puts extreme strain on the heart, and eventually the kidneys and liver fail - this is multi-organ failure.

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CLINICAL MANIFESTATIONS of EFVE

1. Weight gain - The most early and reliable sign. Every kilogram gained overnight = approximately 1 litre of excess fluid.
2. Respiratory system:
   • a. Constant and irritating cough - Pulmonary edema irritates the airways.
   • b. Dyspnea (difficulty breathing) - Lungs fill with fluid, reducing gas exchange.
   • c. Crackles in lungs - Fine crackling sounds heard with a stethoscope when fluid-filled air sacs pop open with breathing. The hallmark sign of pulmonary edema.
3. Cardiovascular system:
   • a. Bounding pulse, elevated blood pressure - Overfilled vessels create a forceful pulse.
   • b. Sacral edema - Fluid collects in the sacrum (lower back area) in patients lying flat in bed.
   • c. Weight gain (mentioned again).
   • d. Neck vein engorgement in semi-Fowler's position - Jugular veins distend (bulge) because the right side of the heart is congested with excess fluid.
   • e. S3 gallop - An abnormal heart sound caused by the heart vibrating as blood hits an overfilled ventricle. It sounds like a galloping horse: "lub-dub-dub."
4. Neurologic: Change in the level of consciousness - Cerebral edema from fluid overload can cause confusion, drowsiness, or altered consciousness.

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TABLE 3.6 - Clinical Manifestations of EFVE with Pathophysiologic Basis

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DIAGNOSTIC EVALUATION of EFVE

1. Obtain complete history and physical examination.
2. Note the character of pulse - Is it bounding? This indicates excess volume.
3. Measure circumference of ankles to detect changes in amount of edema. - Ankle girth measurement tracks peripheral edema progression.
4. Serum sodium concentration does not change with an uncomplicated EFVE. - Because both sodium and water are retained equally (iso-osmolar), the concentration stays normal. Only the total amount changes.
5. If EFVE rises, the hematocrit may be decreased. - More fluid dilutes the red blood cells, making the hematocrit (percentage of blood that is red blood cells) appear lower.

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MANAGEMENT of EFVE

1. Loop and potassium wasting diuretics and digitalis preparations are prescribed for the treatment of EFVE.
   • Loop diuretics (e.g., furosemide): Act on the loop of Henle in the kidney, causing the most powerful diuresis (water and sodium excretion). Example: Furosemide (Lasix).
   • Potassium-wasting diuretics: These diuretics also flush out potassium, so potassium levels must be monitored.
   • Digitalis (e.g., digoxin): Strengthens the heart muscle, used when EFVE is from heart failure.
2. Digoxin is prescribed to increase the force of myocardial contraction or to slow the heart rate. - By strengthening the heart, more blood is pumped out each beat, reducing the backup of fluid.
3. Dietary management: Low sodium diet is ordered to reduce fluid retention.
   • Sodium attracts water. Restricting sodium intake reduces the kidneys' tendency to retain water.

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PAGE 84 - Nursing Management (EFVE), Extracellular Fluid Volume Shift (EFVS), Third Space Fluid

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NURSING MANAGEMENT of EFVE

1. Educate patient and family about extracellular fluid volume excess.
2. Monitor the vital signs.
3. Monitor 24-hours input and output daily.
4. Monitor the patient's weight daily.
5. For severe renal failure, perform hemodialysis. - If the kidneys are so damaged they cannot excrete excess fluid even with diuretics, hemodialysis mechanically removes fluid.
6. Observe the side effects of medications.
7. Position patient in semi-Fowler's to high-Fowler's position. - This upright position uses gravity to draw fluid away from the lungs, making breathing easier.
8. Observe the serum electrolyte values.
9. Assess neck vein engorgement every 8 hours.
10. Monitor laboratory values for changes.
11. Instruct patient about the fluid restriction and rationale for it.
12. Administer medications as ordered.
13. Manage the prescribed sodium restriction.
14. Carefully, monitor the pulmonary edema.
15. Provide careful skin care for edematous area, keeping them clean and dry.
16. Encourage patient and family to talk about their concerns.
17. Educate patient and family to read the labels on food, if sodium level is not evident.
18. Maintain a healthy diet.
19. Provide skin care to patient.
20. Provide psychological support to patient and family.

1. Delayed wound healing
2. Congestive heart failure
3. Pulmonary edema

• Teach patient about extracellular fluid volume excess and its treatment including its specific causes in each patient's case.
• Explain which food are rich in sodium.
• Teach how to manage a prescribed sodium restriction.
• Teach how to monitor daily weights and help the patient to prepare a chart for recording date and weight.
• Explain that edematous tissue is fragile and needs special care to keep it clean, dry and free from scratching.
• Explain that reduction of signs and symptoms indicates that therapy is working well.
• Indicate that patient should contact health care provider if symptoms worsen.

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EXTRACELLULAR FLUID VOLUME SHIFT (EFVS): Third Space Fluid

• Normal ECF moves between blood vessels (intravascular) and tissues (interstitial). A "shift" means fluid moves abnormally - either too much leaves the blood vessels or too much stays in the tissues.

• The fluid is still in the body, but it has moved to a space where it cannot be used (like the abdomen in ascites, or a wound cavity). It is "trapped" fluid.

• Injury releases chemicals (histamine, bradykinin) that make capillary walls more leaky, allowing fluid to pour into tissue spaces.

• These are the body cavities where third-space fluid most commonly accumulates.

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ETIOLOGY of EFVS

1. Renal failure
2. Heart failure
3. Cushing syndrome (handwritten note: "excess cortisol")
4. Long-term use of corticosteroids
5. Excessive isotonic or hypotonic IV fluids

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RISK FACTORS for EFVS

1. Major surgeries
2. Pancreatitis (inflammation of the pancreas causes massive fluid shift into the abdominal cavity)
3. Intestinal obstruction
4. Hypoalbuminemia (low albumin = low oncotic pressure = fluid leaks out)
5. Lymphatic obstruction
6. Crushing injuries
7. Excessive burns

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PATHOPHYSIOLOGY of EFVS

1. In extracellular fluid volume shift, injury of tissue causes the release of histamine and bradykinin. It increases the capillary permeability which allows fluid, protein and other solutes to shift into the interstitial space.
   • Histamine and bradykinin are inflammatory chemicals released after injury or allergic reaction. They make blood vessel walls "leaky," so fluid escapes into the surrounding tissue.
2. There are two phases of fluid shift:
   • a. First phase: Fluid shifts from vascular to interstitial space → leads to vascular (intravascular) volume deficit (the blood volume drops, causing shock-like symptoms).
   • b. Second phase: Fluid shifts from interstitial space back to the vascular space → leads to fluid volume excess (the blood volume rises, potentially causing overload).

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CLINICAL MANIFESTATIONS of EFVS

1. Skin pallor (paleness)
2. Cold extremities
3. Weak and rapid pulse
4. Hypotension (low blood pressure)
5. Oliguria (low urine output)
6. Decreased level of consciousness
7. Headache
8. Peripheral edema

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DIAGNOSTIC EVALUATION of EFVS

1. Laboratory test may indicate an elevated hematocrit measurement in relation to hemoglobin and elevated BUN measurements. - Rising hematocrit and BUN indicate blood is becoming concentrated (less fluid in circulation).

1. Abnormal findings may be seen depending on the area of body affected.

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MANAGEMENT of EFVS

1. Medical management begins with the determination of the cause of the fluid volume shift.

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PAGE 85 - EFVS Management, Intracellular Fluid Volume Excess (IFVE): Water Intoxication

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MANAGEMENT of EFVS (Continued)

1. A large volume of intravenous fluids is required when hypovolemia results from tissue injury. - IV fluids replace lost circulating volume.
2. Albumin is administered for protein deficit. - IV albumin helps restore oncotic pressure and draws fluid back into blood vessels.
3. Paracentesis or tapping for ascites or pleural effusion. - If fluid accumulates in the abdomen (ascites) or around the lungs (pleural effusion), it can be drained with a needle.
4. IV fluid intake is maintained after major surgery to maintain kidney perfusion. - After surgery, fluids keep the kidneys working adequately.

1. Monitor the vital signs every 1 to 8 hours depending upon the condition of patient.
2. Monitor the intravenous fluid replacement.
3. A nurse should frequently observe the patient for chest crackles, breathing and nerve vein engorgement (excessive filling). - These signs indicate the second phase of fluid shift (fluid overload).
4. Abdominal girth of patients with ascites should be measured every 8 hours. - Increasing girth = worsening ascites.
5. Peripheral pulses should be measured every hour, if the extremities are involved. - Checks circulation to the limbs.
6. Assess the level of consciousness.
7. Frequent skin care to edematous areas during fluid shift is essential to prevent skin breakdown.
8. Monitor urine output every hour.
9. Monitor the serum BUN levels and ammonia values in patient with ascites. - Rising ammonia in liver disease causes hepatic encephalopathy (brain dysfunction).
10. Administer medications as ordered.

• Teach patient about the extracellular fluid volume shift and its treatment.
• Explain that frequent care to edematous areas during fluid shift is essential to prevent skin breakdown.
• Instruct patient to take medicines as prescribed by physician.
• Explain that reduction of signs and symptoms indicates that therapy is working well and that therapy may need to be continued to keep signs and symptoms under control.
• Indicate that the patient should contact health care provider if symptoms of EFVS worsen.

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INTRACELLULAR FLUID VOLUME EXCESS (IFVE): Water Intoxication or Water Toxemia

• Too much water enters the cells, causing them to swell.

• When sodium in the blood is low (hyponatremia), the blood becomes "dilute" (hypoosmolar). Water then moves by osmosis from the dilute blood INTO the cells (which have a higher solute concentration).

• It is like adding too much water to a cup of tea - the tea (solutes) is still there, but it is very dilute.

• IFVE is less common than EFVD or EFVE in clinical practice.

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ETIOLOGY of IFVE

1. The most common cause of intracellular fluid volume excess is the administration of excessive amount of hypoosmolar intravenous fluid. - Example: Giving too much 5% dextrose (D5W) or distilled water IV. The dextrose is quickly metabolized, leaving essentially free water that enters cells.
2. Consumption of excessive amount of tap water without adequate nutritional intake. - Drinking excessive amounts of plain water (without electrolytes), especially in people who are malnourished.
3. Administration of excessive amount of hypoosmolar IV fluids.

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PATHOPHYSIOLOGY of IFVE (Flowchart 3.7)

• Most commonly caused by administration of excessive hypoosmolar intravenous fluid → Central nervous system changes (because hypoosmolar fluid is absorbed by cerebral cells more quickly than other cells) → Causes Increased intracranial pressure → Leads to: Headache, Nausea, Vomiting

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CLINICAL MANIFESTATIONS of IFVE

1. Vital signs:
   • a. Increased respiration
   • b. Increased systolic blood pressure
   • c. Flaccidity (loss of muscle tone)
   • d. Delirium (acute confusion)
   • e. Papilledema (swelling of the optic disc, seen on eye examination - indicates increased intracranial pressure)
2. Behavioral changes:
   • a. Confusion
   • b. Irritability
   • c. Drowsiness
   • d. Disorientation
3. Headache
4. Nausea/vomiting
5. Decreased muscle strength
6. Papillary changes
7. Weight gain

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PAGE 86 - Management of IFVE, Intracellular Fluid Volume Deficit (IFVD), Electrolyte Imbalance

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MANAGEMENT of IFVE

1. Intracellular fluid volume excess is treated by addition of solutes to intravenous fluids. - Adding sodium to the IV fluid raises blood osmolality, pulling water back OUT of the cells and reducing cerebral edema.
2. D5/0.45 percent NaCl help to correct intracellular fluid volume excess when the cause is water excess. - This is a hypertonic solution that helps restore osmotic balance.
3. Early administration of IV fluids containing sodium chloride can prevent Secretion of Inappropriate Antidiuretic Hormone (SIADH). - SIADH causes the body to retain too much water (because ADH is secreted when it should not be). Preventing SIADH prevents water intoxication.
4. Oral fluids, such as juice or soft drinks can be given orally every hour. - These contain both water and solutes (glucose, sodium) and are safer than plain water.
5. Antiemetics such as dexamethasone, ondansetron and prochlorperazine. - Used to control the nausea/vomiting caused by increased intracranial pressure.

1. Nurse should have a high index of suspicion for patients who have received excessive amount of D5-W or tap water.
2. Assess the reflexes and papillary response.
3. Intravenous therapy should be monitored every hour.
4. A nurse should offer fluids containing solutes every hour.
5. Monitor the vital signs every 1 to 8 hours.
6. Monitor the patient's weight daily.
7. Monitor intake and output every 1 to 8 hours.
8. A nurse should administer prescribed antiemetic to patient.
9. A nurse should closely observe the patient for protection from injury - keep the side rails up and properly padded. - Confused or seizing patients can fall; side rails prevent injury.
10. An oral airway and suction equipment should be kept at the bedside in the event of seizures. - Water intoxication can cause seizures; airway protection is essential.

1. Bradycardia (slow heart rate)
2. Widened pulse pressure
3. Cerebral edema
4. Seizures
5. Brain cell damage
6. Coma
7. Death

• Discuss about the intracellular fluid volume excess and its treatment.
• Teach how to manage fluid restriction.
• Frequent oral care to keep mucous membranes moist, which decreases thirst.
• Teach how to prevent intracellular fluid volume excess in the future.
• Teach how to detect early signs of intracellular fluid volume excess in case it recurs.
• Indicate the patient should contact health care provider if symptoms worsen.

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INTRACELLULAR FLUID VOLUME DEFICIT (IFVD)

• When blood sodium is very high (hypernatremia), the blood becomes hyperosmolar. Water is drawn OUT of cells by osmosis, shrinking them. This is intracellular dehydration.

• Elderly people have a diminished thirst sensation and may not drink enough water, making them prone to this condition.

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ETIOLOGY of IFVD

1. Vomiting
2. Diarrhea
3. Polyuria (excessive urination, e.g., diabetes insipidus)
4. Fever
5. Blood loss
6. Burns

1. Hemorrhage
2. Adrenal insufficiency (insufficient cortisol = cannot maintain fluid balance)
3. Liver dysfunction
4. Nausea

1. Confusion
2. Coma
3. Cerebral hemorrhage (in severe cases, shrinking brain cells can tear blood vessels)

1. Monitor vital signs.
2. Assess skin turgor and oral mucous membrane for signs of dehydration.
3. Assess color and amount of urine.
4. Monitor fluid status in relation to dietary intake.
5. Note the presence of nausea and vomiting.
6. Auscultate heart sounds.
7. Identify the possible cause of fluid disturbance or imbalance.
8. Monitor serum electrolyte and urine osmolality.
9. During treatment, a nurse should closely monitor the signs of circulatory overload.
10. Educate patient and family about possible cause and effect of fluid losses or decreased fluid intake.

1. Renal diseases
2. Multiple organ failure
3. Death

• Describe the processes that cause intracellular fluid volume deficit.
• Teach how to manage replacement of water.
• Teach how to detect early signs of intracellular fluid volume deficit in case it recurs.

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ELECTROLYTE IMBALANCE

• When salts dissolve in water, they break apart into charged particles called ions. These ions carry electric charges that are essential for nerve and muscle function.

1. Cations: Ions which carry a positive charge are called cations. The positively charged electrolytes are sodium (Na+), potassium (K+), calcium (Ca2+) and magnesium (Mg2+).
2. Anions: Ions which carry a negative charge are called anions. The negatively charged electrolytes are chloride (Cl-), phosphate (PO4-) and bicarbonate (HCO3-).

• Without the right electrolyte balance, nerves cannot fire, muscles (including the heart) cannot contract, enzymes cannot work, and the blood becomes too acidic or alkaline.

1. Sodium
2. Potassium
3. Calcium
4. Bicarbonate
5. Phosphorus imbalance
6. Chloride imbalance

1. Diminished ingestion - Not eating/drinking enough of a particular electrolyte.
2. Diminished elimination of an electrolyte - The body retains too much of an electrolyte (e.g., kidney failure retaining potassium).
3. Excessive ingestion - Eating too much of a particular electrolyte.
4. Excessive elimination of an electrolyte - Losing too much through urine, sweat, vomiting, etc.

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TABLE 3.7 - People at Risk for Electrolyte Imbalances

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SODIUM IMBALANCE

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HYPONATREMIA

• Normal sodium = 135-145 mEq/L. Below 135 = hyponatremia.

• Low sodium makes blood hypoosmolar. Water moves by osmosis into cells (which still have more solutes). Swelling of brain cells is particularly dangerous.

• Brain cells swell inside a rigid skull - there is nowhere for the brain to expand, causing increased intracranial pressure and the above symptoms.

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TYPES OF HYPONATREMIA (Table 3.8)

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PAGES 88-89 - Hyponatremia (Etiology, Pathophysiology, Management), Hypernatremia

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ETIOLOGY of HYPONATREMIA

1. The causative factor of hyponatremia is associated with fluid volume status.
2. Severe vomiting or diarrhea.
3. Excessive fluid intake, such as during endurance activities or excessive thirst.
4. Kidney failure.
5. Congestive heart failure.
6. Small cell lung cancer - Produces ADH-like substances (ectopic ADH) causing SIADH.

1. Age: Risk factors leading to hyponatremia are more prominent in elderly, infant and small children.
2. Certain medicines which increase the risk of hyponatremia:
   • a. Thiazide diuretics (cause sodium loss in urine)
   • b. Antidepressants (SSRIs can cause SIADH)
   • c. Pain relievers
3. Medical conditions:
   • a. Kidney disease
   • b. Heart failure
   • c. Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
   • d. Intensive physical activities

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PATHOPHYSIOLOGY of HYPONATREMIA

1. Hyponatremia occurs when some condition impairs normal free water excretion or sodium loss exceeds normal free water loss.
2. Water in the extracellular fluid moves into the cell by osmosis. It means there is less sodium to move across the excitable membrane which results in delayed membrane depolarization. - Nerve cells need sodium to "fire" (action potential). With low sodium, they cannot depolarize as quickly, causing sluggish nerve function.
3. Osmolality refers to the total concentration of solutes in water.
4. Plasma osmolality has a role in the pathophysiology of hyponatremia. It is maintained by strict regulation of arginine vasopressin known as antidiuretic hormone system.
5. When the plasma osmolality increases, ADH is secreted and water is retained by kidneys which decreases the serum osmolality. - ADH (antidiuretic hormone) tells the kidneys to conserve water. When plasma is too concentrated, ADH is released to dilute it.
6. Effective osmolality determines the osmotic pressure and flow of water.

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CLINICAL MANIFESTATIONS (Table 3.9)

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DIAGNOSTIC EVALUATION of HYPONATREMIA

1. Diagnosis of hyponatremia is based on the combination of clinical manifestation and serum laboratory values.
2. Complete medical history and physical examination.
3. Blood test and urine tests are performed to determine the level of sodium in blood.

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MANAGEMENT of HYPONATREMIA

1. The main aim of medical management is to correct the body water osmolarity and therefore, restore cell volume by raising the ratio of sodium to water in extracellular fluid.
2. If patient has hyponatremia due to excess fluid volume intake, fluid will be restricted to allow sodium to regain balance.
3. IV sodium solutions are recommended to raise the sodium level in blood.
4. Normal saline is administered in conjunction with the diuretic furosemide.
   • Furosemide removes water faster than sodium, helping to raise the sodium concentration.

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NURSING MANAGEMENT of HYPONATREMIA (Page 89)

1. A nurse should obtain a complete history of the cause of hyponatremia such as vomiting, diarrhea and decreased intake of sodium.
2. Assess the level of serum sodium.
3. A dietary history should be assessed to ascertain the amount of sodium consumed.
4. Patient and family members should be asked about behavioral changes, headache and increased sleepiness.
5. Physical assessment of patient includes height and weight with a calculation of ideal body weight for body frame.
6. Nurse should have a high index of suspicion for hyponatremia in patients who have NPO or NPO without sodium replacement intravenous fluid with nausea, vomiting or abdominal cramps.
7. Monitor the vital signs.
8. Nurse should monitor the type and amount of fluid intake.
9. Nurse should irrigate nasogastric tubes and wound sites with normal saline.
10. Nurse should promote the intake of fluid containing sodium, such as broth and juices.
11. Monitor input and output hourly.
12. Daily weight of patient should be obtained to monitor fluid balance.
13. Nurse should plan for fluid restriction, if hyponatremia is caused by fluid volume excess.
14. Nurse should provide mechanisms to reorient the patient as well as provide safety measures, if patient is confused or agitated.
15. Patient should be protected from injury during the seizure.

1. Brain disease
2. Cerebral edema
3. Seizure
4. Coma
5. Death

• Describe the process that causes hyponatremia and explain how the patient's sign and symptoms result from body fluids being too dilute.
• Explain the prescribed fluid restriction to patient and help the patient to make a chart to keep track of fluid intake.
• Indicate that cold and hot liquids often satisfy thirst better than lukewarm ones.

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HYPERNATREMIA

• Normal sodium = 135-145 mEq/L. Above 145 = hypernatremia.

• Hypernatremia is dangerous and associated with high death rates, making rapid identification and treatment important.

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ETIOLOGY of HYPERNATREMIA

1. Gastrointestinal loss:
   • a. Vomiting
   • b. Diarrhea
   • c. Intestinal fistula
2. Inadequate water intake:
   • a. Impaired thirst drive (especially in elderly)
   • b. Increased insensible loss (breathing, sweating without replacement)
   • c. Inability to swallow water
3. Medications:
   • a. Phenytoin (anti-seizure drug)
   • b. Sulphonylureas (diabetes medication)
   • c. Amphotericin (antifungal)
   • d. Alcohol
   • e. Lithium
4. Skin loss:
   • a. Burns
   • b. Sweating
5. Excessive sodium:
   • a. Iatrogenic (medically caused) sodium administration:
     • i. Sodium bicarbonate
     • ii. Hypertonic saline
   • b. Mineralocorticoid or glucocorticoid excess:
     • i. Cushing syndrome
     • ii. Ectopic ACTH production
   • c. Peritoneal dialysis: Loss of water in excess of sodium.

1. Vomiting
2. Fever
3. Dehydration
4. Delirium or dementia
5. Poorly controlled diabetes
6. Kidney disease
7. Larger burn areas on the skin

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PATHOPHYSIOLOGY of HYPERNATREMIA

1. Hypernatremia is not a problem of sodium homeostasis; it is usually a problem of water. - The sodium is not necessarily too high in absolute amount; there is just not enough water to dilute it.
2. Hypernatremia is always due to loss of hypotonic fluid and impaired access to free water. - Losing fluid that has less sodium than blood (like pure sweat) concentrates the blood sodium.
3. In this, high serum osmolality stimulates the hypothalamus and initiates the sensation of thirst. - The thirst center in the brain is activated to encourage drinking and correcting the imbalance.
4. Neurologic symptoms are the result of cerebral cellular dehydration. - Opposite of hyponatremia: in hypernatremia, water leaves brain cells (moving toward the hypertonic blood), causing brain cells to shrink.
5. Increased sodium concentration in extracellular fluid increases osmolality. - Higher concentration = higher osmotic pressure = water pulled out of cells.
6. Water leaves the cell by osmosis and enters into the extracellular compartments, i.e. dilution of fluid in extracellular fluid. - The body tries to compensate by moving water from cells to blood to dilute the high sodium.

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QUICK SUMMARY TABLE

1. Page 80 - Functions of body fluids, fluid balance basics, and the 5 types of fluid imbalance (with the flowchart explained)
2. Pages 80-81 - Extracellular Fluid Volume Deficit (EFVD) - types, causes, risk factors, pathophysiology, all 10 clinical signs with reasoning, diagnostic tests, and management
3. Pages 81-82 - Full nursing management of EFVD (21 nursing interventions explained), complications, and patient teaching (Box 3.2)
4. Pages 82-83 - Extracellular Fluid Volume Excess (EFVE) - all 3 pathophysiology flowcharts explained, clinical signs by system, diagnostic evaluation, and medical management (diuretics, digoxin, diet)
5. Page 84 - EFVE nursing management (20 interventions), Extracellular Fluid Volume Shift (Third Space Fluid) - both phases, causes, and clinical signs
6. Page 85 - EFVS management and nursing care; Intracellular Fluid Volume Excess (Water Intoxication) - pathophysiology flowchart, causes, and symptoms
7. Page 86 - IFVE management, Intracellular Fluid Volume Deficit (IFVD), and beginning of Electrolyte Imbalance with sodium, risk factor table, and Hyponatremia types
8. Pages 87-89 - Hyponatremia (full etiology, pathophysiology, symptoms by system, management), and Hypernatremia (etiology, all pathophysiology points explained)