Dehydration

Introduction:

A state of having less-than-normal body fluids, due to an excess loss of fluids or
an inadequate intake of fluids. Dehydration may be actual or relative. A relative
dehydration exists when the amount of fluid and electrolytes in the body is cor-
rect, but the placement is not correct. If fluid shifting has occurred and the fluid
is now in the interstitial areas rather than in the circulating blood volume, the
patient may actually be experiencing a relative dehydration. Even though there is
adequate fluid within the body, it cannot be utilized at this time. More commonly,
dehydration is actual and due to loss of fluid from the body or lack of adequate
hydration.

PROGNOSIS
Adequate replacement of fluids with the appropriate fluid type is essential to ensure
adequate circulating blood volume.


SIGNS AND SYMPTOMS

• Thirst as the body wants more fluids
• Poor skin turgor due to fluid loss
• Tachycardia—heart rate increases to circulate remaining volume faster
• Tachypnea—respiratory rate increases in an attempt to obtain more oxygen
• Decreased urinary output—less volume available to leave the body
• Increased BUN as volume depletes
• Hypotension due to decrease in circulating blood volume

TREATMENT

• Intravenous and oral fluid replacement.
• Monitor serum electrolytes, BUN, creatinine, urine electrolytes.
• Monitor cardiac rhythm if there is an electrolyte disturbance.

NURSING DIAGNOSIS
• Deficient fluid volume
• Risk for impaired urinary elimination

NURSING INTERVENTION
• Monitor vital signs; check for orthostatic hypotension.
• Monitor intake and output.
• Assess intravenous access site for signs of redness, swelling, or pain.
• Assess skin and mucous membranes for dryness.
• Assess cardiovascular status—heart rate, heart sounds, peripheral pulses.
• Assess respiratory status—lung sounds, respiratory rate.
• Encourage oral fluid intake.
• Increase frequency of mouth care.
• Impaired oral mucous membrane

Hypermagnesemia

Introduction:

Hypermagnesemia is a greater-than-normal amount of magnesium in the blood.
Patients with poor renal function or long-term abuse of magnesium-containing
compounds have difficulty excreting magnesium. The excess of magnesium in the
blood causes the cell membranes to become less excitable than normal, requiring
a greater stimuli than would normally be needed to cause a required effect. As the
magnesium level continues to rise, the cell membrane becomes more resistant to
its natural stimuli.

PROGNOSIS
Correction of the magnesium level is necessary to prevent life-threatening com-
plications. Patients are at significant risk for cardiac arrest as the magnesium lev-
els continue to rise.

SIGNS AND SYMPTOMS

• Bradycardia due to slowed cellular response to normal stimuli
• Hypotension due to vasodilation
• Drowsiness or lethargy
• Weakness
• Less-than-normal deep tendon reflexes
• Confusion
• Urinary retention
• Cardiac arrest when level severely elevated

TREATMENT
• Administer magnesium antagonist intravenously:
• calcium chloride
• Administer Loop diuretic to reduce magnesium level:
• furosemide
• Dialysis—hemodialysis or peritoneal, to remove excess magnesium (espe-
cially in patients with renal failure).
• Reduce magnesium in diet (avoid meat, legumes, dark green leafy vegetables,
fish, whole grains, nuts).
• Increase fluid intake to maintain hydration.

NURSING DIAGNOSES

• Impaired gas exchange
• Risk for injury
• Reduced cardiac output

NURSING INTERVENTION
• Monitor intake and output.
• Monitor vital signs for changes.
• Monitor cardiovascular status for changes in heart rate, rhythm.
• Monitor labs for electrolyte balance.
• Explain to the patient:
• Avoid foods high in magnesium.
• Avoid magnesium-based medications.

Hypomagnesemia

Introduction:

Hypomagnesemia is a lower-than-normal magnesium level in the blood. Low serum
levels of magnesium can be due to lack of sufficient intake or absorption (malnutri-
tion, vomiting, diarrhea, celiac disease, Crohn’s disease), excess excretion of mag-
nesium (renal loss, chronic alcohol intake, diuretic use, aminoglycoside antibiotics,
antineoplastics), or intracellular movement of magnesium (ascites, hyperglycemia,
insulin administration). The cell membranes become more excitable in the setting of
low magnesium levels. Patients may also have associated imbalances of potassium
and calcium.

PROGNOSIS
Correction of the magnesium level is necessary to return normal electrolyte bal-
ance to the patient. Correction or management of the underlying condition may be
necessary to correct the magnesium level. Nerve impulse transmission is increased
in patients with hypomagnesemia. As the magnesium level drops, the patient may
develop seizures or cardiac arrhythmias.

SIGNS AND SYMPTOMS
• Painful paresthesia (numbness and tingling)
• Hyperactive deep tendon reflexes—using a reflex hammer, strike tendon
at specific site to elicit response (patellar tendon, Achilles tendon, brachio-
radialis, bicep, or tricep)
• Muscle twitching
• Seizures due to irritability of nervous tissue in brain
• Confusion due to Central Nervous System (CNS) irritability
• Headaches
• Mood changes or irritability
• Decreased appetite, nausea, and constipation due to decreased gastrointestinal
motility
• Decreased bowel sounds and abdominal distention
• Arrhythmia, ectopic beats, ventricular arrhythmias
• Contraction of facial muscle after tapping facial nerve anterior to ear
(Chvostek’s sign) due to increased excitation of nerve and muscle cells if
concurrent hypocalcemia
• Carpal spasm after inflation of blood pressure cuff to upper arm—occludes
brachial artery and applies pressure to nerves (Trousseau’s sign) if concurrent
hypocalcemia

TREATMENT
• Administer magnesium sulfate intravenously to increase levels.
• Monitor deep tendon reflexes.
• Monitor cardiac rhythm.
• Increase magnesium in the patient’s diet.
• May need to correct calcium and potassium concurrently.

NURSING DIAGNOSES
• Impaired gas exchange
• Risk for injury
• Decreased cardiac output

NURSING INTERVENTION
• Monitor intake and output.
• Monitor vital signs for changes.
• Monitor cardiovascular status for changes in heart rhythm, pulse deficit.
• Explain to the patient:
• Eat whole grains, legumes, fish, and dark green leafy vegetables that are
high in magnesium.
• No laxatives.

Hyperkalemia

Introduction:

Hyperkalemia is an elevated level of potassium in the blood. Dietary intake is the
main source of potassium. Patients are at risk for hyperkalemia when there is exces-
sive ingestion of potassium-rich foods or salt substitutes, they are on medications
that cause potassium retention (ACE inhibitors, angiotensin receptor blockers,
potassium-sparing diuretics such as amiloride or spironolactone, NSAIDs, tri-
methoprim, pentamidine), or there is excess release of potassium from the cells
(hemolysis, acidosis, low insulin levels, beta blocker use, digoxin overdose,
succinylcholine, or rhabdomyolysis).

PROGNOSIS
As potassium levels rise, the risk of cardiac arrhythmias also increases. An extreme
elevation creates a medical emergency. Correction or management of the underly-
ing cause is necessary to help restore the electrolyte balance.

SIGNS AND SYMPTOMS

• Weakness and dizziness due to neuromuscular changes
• Abdominal distention
• Nausea, vomiting, diarrhea due to change in membrane potential on GI system
• Palpitations due to arrhythmias
• Arrhythmias due to changes in normal cardiac conduction
• Cardiac arrest

TREATMENT

The treatment choices will depend on the severity of the potassium elevation.
Decreasing further intake, enhancing renal excretion, and cellular uptake are all
goals of treatment.
• Monitor cardiac rhythm.
• Administer intravenous insulin and glucose to move potassium from extra-
cellular fluid to intracellular fluid.
• Administer calcium gluconate intravenously.
• Administer NaHCO3 to move potassium from extracellular fluid to intracel-
lular fluid.
• Administer diuretics to remove potassium from body.
• Administer kayexalate to remove potassium from body via GI tract.
• Monitor electrolyte levels.

• Restrict potassium intake.
• Dialysis for severe elevations.

NURSING DIAGNOSIS
• Decreased cardiac output
• Risk for imbalanced fluid volume
• Activity intolerance
• Altered bowel elimination

NURSING INTERVENTIONS
• Monitor vital signs.
• Monitor cardiac rhythm.
• Monitor cardiovascular status for regularity of rhythm, rate, heart sounds, and
peripheral pulses.
• Monitor abdomen for bowel sounds, distention, and pain.
• Monitor intravenous site for redness, swelling, and pain.
• Teach patient about medications and diet:
• Avoid foods that are high in potassium.
• Avoid salt substitutes (most are potassium-based).

Hypokalemia

Introduction:

Hypokalemia is a lower-than-normal level of potassium in the blood. A balance
between the amount of potassium within the cell (intracellular) and outside the cell
(extracellular) is necessary. This allows the resting potential of the cell membrane
to be maintained. When there are low potassium levels, a greater-than-normal stim-
ulus is needed to depolarize the cell membrane. Many cells become more sluggish,
especially nerve cells. However, cardiac cells become more excitable. Fluid losses
due to diuretics or diarrhea, endocrine disorders (such as hyperthyroidism, hyper-aldosteronism), insufficient intake of potassium, and low magnesium levels can all
contribute to low potassium levels. Dietary intake is the main source of potassium,
so patients with poor nutritional intake or prolonged NPO status are also at risk for
hypokalemia.

PROGNOSIS
Low potassium levels may range from minor to life-threatening. The more abnor-
mal the level, the greater the chance the patient will develop a cardiac arrhythmia.
Correction or management of the underlying cause is necessary to help restore the
electrolyte balance.

SIGNS AND SYMPTOMS
• Muscle weakness due to need for greater stimulation of cell due to low potas-
sium level
• Muscle cramps
• Malaise and lethargy
• Decrease in deep tendon reflex response due to lack of response of nerve
tissue to normal stimuli
• Anorexia and constipation due to decrease in peristaltic activity
• Palpitations due to cardiac arrhythmias caused by excitability of cardiac muscle
• Rhabdomyolysis (destruction or degeneration of muscle tissue) in severe
hypokalemia
• Cardiac arrest in severe hypokalemia

TREATMENT
• Correct fluid imbalance.
• Stop or change medications that contribute to potassium loss, if possible (for
example, Loop diuretics).
• Encourage potassium-rich foods.
• Administer potassium supplements.
• Administer potassium in intravenous fluids:
• Avoid glucose in fluid which will shift potassium into cells.
• Potassium concentration of no more than 40 mEq/L in peripheral lines
• Monitor cardiac rhythm.

NURSING DIAGNOSIS
• Activity intolerance
• Decreased cardiac output
• Fatigue

NURSING INTERVENTIONS
• Monitor vital signs for change.
• Monitor cardiac system for rate, rhythm, and pulse deficit.
• Monitor intake and output.
• Monitor intravenous site for redness, swelling, warmth, and pain.
• Teach patient about medication and diet changes:
• Foods rich in potassium (bananas, tomatoes, orange juice)

Hypercalcemia

Introduction:

Hypercalcemia is an abnormally high amount of calcium in the blood. Excess
intake of calcium (such as supplements or antacids) or altered excretion of calcium
(such as in patients with renal failure or those taking thiazide diuretics) may cause
hypercalcemia. Patients may also develop elevated calcium levels with prolonged
immobility, glucocorticoid use, hyperthyroidism, hyperparathyroidism, lithium
use, dehydration, or malignancies with metastasis to the bone.

PROGNOSIS
Correction of the calcium level is necessary to control the signs and symptoms.
Correction or management of the underlying disorder is necessary to correct the
abnormal calcium level. High calcium levels cause altered excitability of heart, skele-
tal, and smooth muscle tissues of the gastrointestinal tract, and nervous tissues.

SIGNS AND SYMPTOMS
• Increased heart rate initially
• Bounding peripheral pulses
• Bradycardia later as electrical conduction is slowed
• Sinus arrest then cardiac arrest due to altered response of cardiac tissue to
normal stimuli
• Shallow respirations due to skeletal muscle weakness
• Muscle weakness due to changes in neuromuscular response to normal stimuli
• Cardiac arrhythmias
• Nausea and vomiting due to decrease in peristaltic activity
• Constipation due to decrease in peristaltic activity
• Dehydration
• Kidney stones form as excess calcium deposits in kidneys; may be excreted
in urine

TREATMENT
Medications are typically used to reduce calcium levels. When levels are highly
elevated or patients are having life-threatening problems, dialysis may also be uti-
lized to reduce calcium levels.
• Stop all calcium-containing medications (supplements, antacids).
• Monitor cardiac rhythm.
• Maintain intravenous access.
• Administer 0.9 percent normal saline solution to ensure adequate hydration
status; sodium aids in urinary excretion of calcium.
• Administer Loop diuretics to enhance the excretion of calcium:
• furosemide
• Administer plicamycin, a calcium binder, to lower calcium levels.
• Administer calcitonin, phosphorus, bisphosphonates (etidronate, pamidronate
—to inhibit calcium resorption from the bone).

NURSING DIAGNOSES

• Ineffective breathing pattern
• Decreased cardiac output
• Impaired urinary elimination

NURSING INTERVENTION
• Monitor vital signs for changes.
• Monitor cardiovascular status for irregularity of heart rhythm, pulse deficit.
• Monitor intake and output.
• Assess muscle strength—hand grips, foot pushes bilaterally for strength and
equality.
• Assess abdomen for bowel sounds, distention, and pain.
• Encourage mobilization, assist with ambulation if necessary to decrease bone
resorption due to immobility.
• Assist with range-of-motion exercises.
• Low-calcium diet to reduce intake.
• Strain urine for stones.
• Explain to patient:
• High calcium foods.
• Avoid calcium supplements.
• Avoid calcium-based antacids.
• Weight-bearing exercise is important to avoid bone resorption.

Hypocalcemia

Introduction:

Hypocalcemia is an abnormally low level of calcium in the blood. Decreased
levels of calcium may be due to inadequate intake or absorption (vitamin D defi-
ciency, malabsorption), excess loss (associated with burns, renal disease, diuretics,
or alcoholism), endocrine disorders (such as hypoparathyroidism), decreased serum
albumin, hyperphosphatemia, or sepsis.

PROGNOSIS
Identification and correction of the cause is necessary to return the patient to a nor-
mal fluid and electrolyte balance. As the calcium level becomes more abnormal,
the risk to the patient is greater. Seizures and cardiac arrhythmias may develop,
which may become life-threatening.

SIGNS AND SYMPTOMS

• Irritability
• Paresthesia of lips (circumoral) and extremities
• Muscle spasm and cramping
• Tetany—intermittent painful tonic spasms, usually involving the arms and legs
• Abdominal pain due to muscle cell cramping within the gastrointestinal tract
• Laryngospasm and stridor (abnormal high-pitched breathing sound) as air-
way becomes narrowed
• Seizures due to irritation of nervous system tissue
• Cardiac arrhythmias due to increased excitation of cardiac muscle cells
• Prolonged QT interval will predispose to ventricular arrhythmias
• Contraction of facial muscle after tapping facial nerve anterior to ear
(Chvostek’s sign) due to increased excitation of nerve and muscle cells
• Carpal spasm after inflation of blood pressure cuff to upper arm—occludes
brachial artery and applies pressure to nerves (Trousseau’s sign)

TREATMENT
• Maintain intravenous access.
• High calcium diet to replenish lost calcium.
• Administer vitamin D if patient has deficiency; helps with absorption of
calcium:
• ergocalciferol (vitamin D2)
• Administer calcium gluconate 10 percent IV (emergency treatment for seizure,
tetany, cardiac arrhythmia).
• Administer calcium chloride (emergency treatment).

NURSING DIAGNOSES

• Imbalanced nutrition: less than what body requires
• At risk for injury

NURSING INTERVENTION
• Monitor vital signs for changes.
• Monitor intake and output.
• Monitor neurologic status for change, irritability, and disorientation.
• Monitor cardiovascular status for changes, irregularity of heartbeat, pulse
deficit (difference between heartbeat and peripheral pulse checked at the
same time), and cardiac rhythm.
• Monitor for signs of hypercalcemia when administering medication (can over-
medicate with calcium):
• nausea
• vomiting
• anorexia
• Explain to the patient:
• Avoid dependence on laxatives—these medications can alter bowel pat-
terns, causing altered absorption and excess elimination of calcium and
other electrolytes.
• Avoid dependence or overuse of antacids—these medications cause excess
intake of calcium (or other electrolytes, depending on composition).

Hypernatremia

Introduction:

Hypernatremia is an abnormally high amount of sodium in blood. Fluid volume
may be altered as a result of changes in the levels of sodium. Amild rise in sodium
levels causes tissue that is normally excitable to become more irritable—for exam-
ple, cardiac muscle. The osmolarity of extracellular fluid also increases as the
sodium level increases. This is in attempt to correct the sodium increase by bring-
ing more fluid from the cells into the extracellular area. These dehydrated, more
irritable cells have a decreased ability to respond to stimuli.
Causes may include insufficient water intake (patients who are NPO), insuffi-
cient sodium excretion due to hormone imbalance, renal failure, corticosteroids,
increased sodium intake or increased water loss due to fever, hyperventilation, in-
creased metabolism, and dehydration due to sweating, vomiting, or diarrhea.

PROGNOSIS
Identification and correction of the cause is necessary to return the patient to a
normal fluid and electrolyte balance. IV fluids are carefully monitored during this
treatment period to avoid overcorrection of the sodium level, causing hyponatremia.
If the sodium level is severely elevated, the patient may need hemodialysis. Hyper-
volemia associated with hypernatremia in some patients may cause heart failure
and pulmonary edema.


SIGNS AND SYMPTOMS
• Weight gain due to fluid retention
• Restlessness, irritability, and agitation due to increase in neural activity with
normal or low fluid volume
• Decreased level of consciousness due to decrease in neural activity with
hypervolemia
• Muscle twitching due to irregular muscle contractions
• Muscle weakness bilaterally
• Blood pressure increased—compare with normal for patient
• Decreased myocardial contractility, resulting in less effective pumping action
of heart muscle
• Distended neck veins in hypervolemic patients
• Less cardiac output, especially with hypovolemic patients
• Increased thirst in an attempt to increase fluid intake

TREATMENT

Hypotonic IV fluids are typically given to correct hypernatremic patients who are
volume-depleted. Diuretics are also used to help correct the sodium balance.
• Administer 0.225 percent sodium chloride, 0.33 percent sodium chloride, or
0.45 percent sodium chloride to correct fluid and sodium status.
• Administer diuretics to remove excess fluids and promote sodium loss:
• furosemide, bumetanide

NURSING DIAGNOSES
• Disturbed thought process
• Excess fluid volume
• Deficient fluid volume

NURSING INTERVENTION
• Monitor vital signs, check pulse rate and rhythm, check blood pressure, and
compare with prior.
• Weigh daily and compare.
• Record fluid intake and output to check balance of fluid.
• Monitor IV site for patency, signs of infiltration such as redness or induration.
• Consult with dietician.
• Explain to the patient:
• Restrict salt in the diet.
• Fluid intake restriction.
• Proper oral hygiene to avoid irritation due to fluid restriction.

Hyponatremia

Introduction:

Hyponatremia is an abnormally low amount of sodium in the blood. Low levels of
sodium may be due to loss of sodium from the body, movement of sodium from the
blood to other spaces, or dilution of sodium concentration within the plasma. Some
causes include increased excretion or abnormal excretion of sodium, water imbal-
ance, hormonal imbalance (such as excess ADH), ecstasy (methylenedioxymethy-
lamphetamine) use, hypothyroidism, renal failure, diuretics, diarrhea, vomiting, and
wound drainage.

PROGNOSIS

Identification and correction of the underlying cause is important in treatment of
hyponatremia. Water restriction of all patients with hyponatremia will help to pre-
vent further dilution of the plasma concentration of sodium. Seizure and death may
occur if the electrolyte imbalance is not identified and corrected.


SIGNS AND SYMPTOMS
• Hypotension, especially orthostatic (with position changes—from lying to
sitting) due to decrease in cardiac output in setting of hypovolemia
• Nausea
• Diarrhea due to increased gastrointestinal motility
• Increased bowel sounds due to increased gastrointestinal motility
• Malaise or excessive activity
• Muscle weakness
• Decreased deep tendon reflexes
• Personality changes due to cerebral edema and increased intracranial pressure
• Altered level of consciousness
• Seizure

TREATMENT

• Water restriction.
• Administer saline solution IV if patient has fluid deficit (hypovolemic).
• Furosemide if fluid-overloaded.
• Treat underlying cause to correct problem.

NURSING DIAGNOSES
• Deficient fluid volume
• Excess fluid volume
• Risk for disturbed thought processes
• Decreased cardiac output

NURSING INTERVENTION
• Record fluid intake and output to monitor fluid status.
• Monitor vital signs.
• Weigh patient daily.
• Monitor for signs of dehydration: decreased skin turgor (elasticity), dry
mucous membranes, decreased sweating, neurologic changes.
• Appropriate oral hygiene for dry mucous membranes.
• Proper skin care is especially important if the patient is experiencing diarrhea
or dehydration.
• Explain to the patient fluid restriction and dietary modifications.
• Increase sodium in diet appropriately, considering comorbidities.

How Fluids and Electrolytes Work

Fluids in the body are found in three basic places: within the cells (intracellular),
outside the cells (extracellular), and within the tissue spaces (interstitial space or
third space). A balance should be maintained to keep concentrations of both fluids
and electrolytes in the proper areas for normal function. The cell walls are semi-
permeable to allow for movement (diffusion) of molecules. This helps to maintain
osmotic pressure.
Edema occurs when too much fluid enters the interstitial space. Peripheral
edema usually collects in subcutaneous areas. The higher hydrostatic pressure in
the vessel causes fluids to move into the interstitial areas which have lower pres-
sure, allowing the fluid to build up.
Normal osmolarity of plasma is 270 to 300 mOsm/L. Isotonic or normotonic flu-
ids have similar concentrations. This prevents fluids from shifting into spaces they
do not belong. Hypertonic solutions have a concentration greater than 300 mOsm/L
and exert a greater pressure, which pulls water from the isotonic area to the hyper-
tonic solution in an attempt to equalize the osmolarity. Hypotonic solutions have a concentration of less than 270 mOsm/L and exert less pressure, which allows water
to be pulled from the hypotonic area into the isotonic area.
HORMONAL REGULATION OF FLUIDS AND ELECTROLYTES
Aldosterone is secreted by the adrenal cortex in response to sodium changes. Where
sodium goes, water follows. Aldosterone signals the tubules within the nephrons
in the kidneys to reabsorb sodium and therefore water. This increases blood osmo-
larity. Aldosterone also aids in control of potassium levels.
Renin is secreted by the kidneys in responses to changes in sodium or fluid vol-
ume. In the circulation, renin acts on a plasma protein called renin substrate (also
called angiotensinogen), converting it to angiotensin I. In the pulmonary circula-
tion, angiotensin-converting enzyme converts angiotensin I to angiotensin II. This
causes vascular constriction and aldosterone secretion.
Antidiuretic hormone (ADH) is produced in the brain and stored in the poste-
rior pituitary. It is released when there is a change in the osmolarity of the blood.
ADH acts on the renal tubules, causing them to reabsob more water, which de-
creases blood osmolarity. When the osmolarity gets too low, the release of ADH is
not needed and the water is excreted in the urine.
Natriuretic peptides are secreted in response to increases in blood volume and
blood pressure. When atrial natriuretic peptide (ANP) and brain natriuretic peptide
(BNP) are secreted, kidney reabsorption of sodium is inhibited and the glomerular fil-
tration rate is increased. Blood osmolarity is decreased and urine output is increased.

ACID BASE BALANCE
Maintaining acid-base balance will keep the pH level within the normal range of
7.35 to 7.45. The lungs and the kidneys are integral in maintaining the normal
acid-base balance. The body constantly monitors the pH level and makes adjust-
ments in an attempt to correct any abnormalities. pHCO3 is regulated by the kid-
neys. pCO2 is regulated by the lungs. If the patient develops acidosis there will be
a low pH and either a drop in pHCO3 (metabolic) or a rise in pCO2 (respiratory).
If the patient develops alkalosis there will be an increase in pH and either an
increase in pHCO3 (metabolic) or a drop in pCO2 (respiratory). In an attempt to
maintain as normal an internal environment as possible, the body will attempt
to compensate for the changes that are occurring. The lungs are able to correct
much more rapidly than the kidneys.