Burns

Introduction:

Burns are damage to the skin and body tissues caused by flames, heat, cold, fric-
tion, radiation (sunburn), chemicals, or electricity. Burns are generally divided into
three categories, depending on the damage. First-degree burns are those with
injury to the outer layer of skin called the epidermis. They will be red, and painful,
with some swelling. Asecond-degree burn is when the epidermis is burned, as well
as the next layer, the dermis. Severe pain, white and reddened areas, swelling, blis-
ters, and perhaps drainage will be seen. A third-degree burn goes through all the
layers of the skin and could involve underlying tissues. It is often painless due to
destruction of the nerves in the area. The area will look black (termed eschar)
and/or reddened. Many drugs may make the skin more sensitive to the sun, pro-
ducing the effect of a sunburn with little exposure. Common medications with this
effect include: amiodorone, carbamazepine, furosemide, naproxen, oral contra-
ceptives, piroxicam, quinidine, quinolones, sulfonamides, sulfonulureas, tetracy-
clines, and thiazides, among others.

PROGNOSIS
Prognosis depends on the severity of the burn plus the amount of surface area
involved. When large portions of the face, chest, hands, feet, genitalia, or joints
have sustained a large second- or third-degree burn, prompt medical attention is
necessary. Serious burns can lead to death. If smoke inhalation has occurred, or if
the nasal hairs are singed, or if quantities of soot are present around the face, assess
for adequacy of breathing and damage to the respiratory tract. CPR may need to be
started. Infants and elderly patients with burns require prompt medical attention.

SIGNS AND SYMPTOMS

• Redness, no break in skin—indicates a first-degree burn from damage to the
epidermis
• Deeper red, with clear fluid blisters—indicates a second-degree burn as the
epidermis and dermis are burned
• Charred black or dry white—indicates death of the tissue from the burn (third-
degree burn)

TREATMENT
The objective of burn treatment is to prevent infection, decrease inflammation and
pain, and promote healing of the areas. Treatment choices depend on the degree of
burn and the amount of body surface area that was burned. Any second-degree burn
greater than 5 to 10 percent of surface area and all third-degree burns belong in a
hospital, preferably within a specialized burn unit. All electrical burns and burns
of the ears, eyes, face, hands, feet, and perineum require hospital care, as do chem-
ical burns and burns in infants or the elderly.
• Check the area for any exposed electrical wires, if you are present on the scene.
• Use cold water to decrease the temperature of the area for a first-degree burn
or a small second-degree burn and to stop the burning.
• For chemical burns, ensure that all the chemical has been flushed away.
• For electrical burns, look for entrance and exit wounds.
• Cover the area with dry gauze.
• If the skin is broken (second-degree burn), use a topical antibiotic ointment such
as silvadene to prevent a secondary bacterial infection before applying the gauze.
• Administer pain medications (ibuprofen, acetaminophen) as needed.
• For third-degree burns, the eschar needs to be debrided (cut away) to allow
new tissue to grow.
• These wounds are often covered in moist sterile saline gauze, as new tissue
grows best in this environment. When the gauze dries; it adheres to the dead
tissue. The area is mechanically debrided when the gauze is removed.
• Oral antibiotics may be necessary.
• Administer pain medications (oxycodone, morphine) as needed, especially
before dressing changes that may be painful.
• Prevent heat loss due to large areas of tissue exposed from lack of skin
coverage.
• Maintain fluid levels since fluid loss is common from evaporation and
wound drainage.

NURSING DIAGNOSES

• Risk of fluid volume deficit
• Pain, discomfort
• Risk of altered body temperature

NURSING INTERVENTION

• Anticipate pain medication needs to make the patient more comfortable.
• Assist in range of motion to avoid contracture development due to pain with
movement.
• Encourage family visitation.
• Assist with activities of daily living.
• Isolation may be needed to protect the patient from bacteria, especially if a
large amount of skin is not intact.
• Teach the patient to look for signs and symptoms of infection: fever, increased
redness, increase in drainage, or change in color of drainage.

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.

Schizophrenia

Introduction:

The exact cause of schizophrenia is not known. There is a familial tendency to the
disease, and genes have been identified that are associated with the disease.
Dysfunction of the neurotransmitter dopamine seems to be partially responsible
for the development of the symptoms of psychosis associated with schizophrenia.
NMDA receptors may also be involved in the disease.

PROGNOSIS

Patients with schizophrenia typically need long-term medication to control symp-
toms. Medication compliance can be difficult for some patients, whether due to
accessibility of medications, side effects, symptoms of disease, or desire not to take
daily medication. Symptom recurrence is likely.

SIGNS AND SYMPTOMS

• Impairment in reality testing
• Flat affect
• Disorganized speech
• Disorganized thought process
• Unusual behavior
• Delusions
• Auditory hallucinations

TREATMENT

• Antipsychotic medications:
• clozapine
• aripiprazole
• ziprasidone
• loxapine
• risperidone
• olanzapine
• quetiapine
• thiothixene
• Psychotherapy.
• Behavioral therapy.

NURSING DIAGNOSIS

• Impaired environmental interpretation syndrome
• Disturbed thought process
• Disturbed auditory sensory perception

NURSING INTERVENTION

• Monitor medication intake.
• Discuss patient response to therapy.
• Discuss importance of medication compliance.
• Structured environment.

Bipolar Disorder

Patients suffering from mood disorders often have difficulty with interpersonal
interactions. Substance abuse occurs as patients attempt to self-medicate.

Introduction:

Some patients experience episodes of depression alternating with episodes of mania
or hypomania. These episodes may occur in a mixed or cyclic manner. There tends
to be a high comorbidity with substance abuse in these patients. Depressive
episodes tend to last longer than the manic episodes. During mania the patients are
overenthusiastic, elated, hyperactive, and often engage in activities that they later
regret. Others may be drawn to the patient during manic episodes due to their out-
going, engaging behavior. Later the patient’s behavior tends to alienate due to
mood swings, irritability, aggression, and grandiosity. There is a positive correla-
tion between creative behavior and mood disorders. During the manic phase, the
patient has grandiose ideas.

PROGNOSIS

Proper medication management is necessary to control the symptoms of bipolar
disorder. Initial diagnosis and treatment of depression without recognition of the
coexisting mania can lead to the onset of mania due to the antidepressant treat-
ment. It is important to treat both components of the disorder to effectively man-
age the patient. Ongoing treatment is often necessary to prevent the patient from
cycling into another manic or depressive episode. Some patients may have psy-
chotic symptoms as part of the disease process.

SIGNS AND SYMPTOMS

• Elation
• Hyperactivity
• Increased irritability
• Flight of ideas
• Grandiosity
• Diminished need for sleep
• Rapid speech
• Easily distracted
• Excessive spending
• Hypersexuality
• Episodes of depression
• The patient may stray from medication regimen because he or she feel weighed
down

TREATMENT

• Mood stabilizers:
• lithium
• valproic acid
• carbamazapine
• lamotrigine
• Antipsychotic medications:
• olanzapine
• risperidone
• aripiprazole
• Psychotherapy.
• Assess suicide risk.
• Antidepressants.

NURSING DIAGNOSIS

• Powerlessness
• Social isolation
• Risk for loneliness
• Altered sexuality patterns


NURSING INTERVENTION
• Monitor patient frequently when first admitted.
• Ask about suicidal ideation.
• Monitor medication intake.
• Discuss patient response to therapy.

Depression

Patients with depression have a persistent sense of sadness, more days than not,
often associated with somatic complaints. The medical work-ups for varied
physical complaints will be negative. Patients typically have a loss of interest in
normal activities and alterations in sleep and eating habits. Up to one-third of
patients will seek care from primary care providers. Patients can also present as
unkempt, dirty, withdrawn, and unwilling to engage in conversation. They see
life as a state of hopelessness. The patient’s depression must be treated seriously,
since it can lead to suicide. A patient’s request for help might be his or her last
recourse.

Introduction:

Several different theories exist involving the cause of depression. Genetic factors
may lead to changes in the normal functioning of neurotransmitters. Neurotrans-
mitters are released from one side of a synapse and land on a specific receptor
site on the other side of the synapse. When a balance is maintained between the
amount released and the amount needed to fill the receptor sites, normal function
continues. When there is an imbalance, the neurotransmission is altered. Develop-
mental factors can often be traced back to childhood. Personality disorders may
begin during school age or adolescence. Psychosocial stressors are another factor
linked to the development of depression. Major life changes such as the death of
a family member, unemployment, or moving away from family and friends may
lead to the onset of depression. A sense of sadness or grief is considered a normal
response to this type of loss and should resolve as the person progresses through
the normal stages of grieving. Depression, however, is not a normal response to loss.
A grieving person will have a sustained sense of self-esteem, whereas a person
with depression will have a sense of worthlessness.

PROGNOSIS
Proper treatment can help control the symptoms of depression. Adequate treatment
can cause remission of symptoms. It is not unusual for there to be a recurrence of
symptoms at some point in the future, even with appropriate treatment.


SIGNS AND SYMPTOMS
• Intense feeling of sadness
• Depressed mood
• Anhedonia (loss of interest in usual activities)
• Hopelessness or worthlessness
• Difficulty concentrating
• Indecision
• Changes in sleep (more or less than usual), eating (more or less than usual),
and activity (more or less than usual)
• Social withdrawal and isolation
• Decreased libido
• Thoughts of death
• Physical complaints include headache, malaise, decreased libido, and changes
in sleep, activity, and eating


TREATMENT
• Ask patient about suicidal thoughts.
• Ask patient about suicidal plan.
• Psychotherapy.
• Cognitive-behavioral therapy.
• Support groups.
• Antidepressant medications:
• SSRIs
• venlafaxine
• nefazodone
• bupropion
• mirtazapine
• tricyclics
• monoamine oxidase inhibitors
• Electroconvulsant therapy (ECT) in refractory cases.

NURSING DIAGNOSIS

• Hopelessness
• Risk for suicide
• Dysfunctional grieving
• Impaired social interaction
• Social isolation

NURSING INTERVENTION

• Monitor patient frequently when first admitted.
• One-to-one observation if patient is a suicidal risk.
• Develop a level of sensitivity and trust with the patient.
• Ask patient about suicidal ideation; do they have a plan, have they attempted
to carry out a plan.
• Monitor medication intake.
• Discuss patient response to therapy.
• Monitor vital signs; watch for elevation in blood pressure with some med-
ications.
• Monitor weight; some medications are associated with changes in weight.
• Monitor sleep; ask patient about restful sleep during the night, and difficulty
falling asleep.
• Disturbed self-esteem

Panic Disorder

Introduction:

Patients experience intermittent episodes that have a sudden onset and no pre-
dictable pattern, causing intense anxiety associated with pronounced physical symp-
toms. These episodes are short in duration and recurrent in nature. The disorder
tends to present before the age of 25, is twice as common in women as it is in men,
and tends to be familial. Some patients will choose to self-medicate with alcohol
in an attempt to escape the disease, diminish symptoms, or decrease the occur-
rence of the episodes. Others become dependent on tranquilizing medications.
Panic attacks can impede a person’s life and restrict activity, especially in antici-
pation of a panic attack.

PROGNOSIS

With proper treatment, the frequency and intensity of the episodes will decrease.
Some patients may not experience complete resolution of symptoms, even with
appropriate medications.

SIGNS AND SYMPTOMS

• Depersonalization, as if the symptoms are happening to someone else
• Sense of doom, fear of dying due to the intensity of the physical symptoms
• Fear of losing control due to the unpredictable nature of the episodes
• Worry about future attacks due to the unpredictable nature of the episodes
• Change in behavior due to anxiety about being in a place where an attack
might occur
• Palpitations, tachycardia, and chest pain
• Dyspnea
• Choking sensation
• Nausea
• Dizziness
• Diaphoresis
• Numbness

TREATMENT
• Cognitive-behavioral therapy.
• Relaxation therapy.
• Administer antidepressants:
• selective serotonin reuptake inhibitors
• tricyclics
• monoamine oxidase inhibitors
• Administer benzodiazepines as adjunctive treatment:
• clonazepam, alprazolam, lorazepam
• Provide reassurance to patient.

NURSING DIAGNOSIS

• Powerlessness
• Fear
• Social isolation

NURSING INTERVENTION

• Provide reassurance to patient.
• Reduce anxiety.
• Monitor vital signs.

Anxiety

Introduction:

Patients exhibit symptoms when an imbalance develops between the number of
open receptor sites and the number of available neurotransmitters. Neurotransmitters
are released from one side of a synapse and land on a specific receptor site across
the synapse. Asecond mechanism exists (a reuptake mechanism) to remove excess
neurotransmitters left within the space between where they are released and where
they fill the receptor sites. When there are insufficient neurotransmitters available
to fill the open neurotransmitter receptor sites, the patient develops symptoms.
Patients experience an uncontrollable feeling of anxiousness which is present more
days than not.
Symptom onset is typically in late teens through early thirties. Anxiety is more
common in women and in patients with a family history of anxiety.

PROGNOSIS
Without proper treatment the anxiety will continue, and symptoms may even
progress. The patient’s quality of life is adversely affected. Social functioning be-
comes impaired and in some cases the patient becomes more socially isolated.
Physical symptoms continue, at times necessitating visits to a primary care provider
or even the emergency room. With proper treatment, the symptoms are controlled,
neurotransmitter balance is restored, and remission is achieved. The symptoms will
typically recur at a later point, even when properly treated. It may be months or
years after a successful course of treatment before the symptoms recur. The treat-
ment that was effective in the past will typically be effective again in the future. A
longer treatment course is recommended for subsequent treatment cycles when
using SSRIs (selective serotonin reuptake inhibitors).

SIGNS AND SYMPTOMS

• Fear, tension, apprehension due to alteration in neurotransmission
• Persistent worry
• Trouble concentrating
• Irritability and restlessness
• Tachycardia, palpitations, elevated blood pressure due to autonomic nervous
system stimulation
• Hyperventilation due to fear, elevated heart rate, and palpitations
• Sweating, tremors due to autonomic nervous system stimulation
• Sleep disturbance and fatigue due to alteration in neurotransmission
• Headache due to nervous system irritability and lack of sleep

TREATMENT

• Administer anxiolytics for acute management:
• Monitor for respiratory depression or decrease in blood pressure.
• Have benzodiazepine antagonist (flumazenil) on hand to reverse effect if
needed.
• Administer antidepressants:
• selective serotonin reuptake inhibitors—paroxetine
• selective serotonin and norepinephrine reuptake inhibitors—venlafaxine
• tricyclics
• Administer buspirone.
• Administer beta-blockers for symptom control.
• Psychotherapy.
• Cognitive-behavioral therapy.
• Relaxation techniques such as biofeedback.
• Desensitization—repeated exposures to graded doses of the object or situa-
tion that produces the anxiety.
• Group therapy.
• Family therapy.
• Emotive therapy.
• alprazolam, clonazepam, clorazepate, diazepam, lorazepam, oxazepam

NURSING DIAGNOSIS

• Sleep pattern disturbance
• Anxiety
• Fear
• Impaired social interaction
• Ineffective role performance

NURSING INTERVENTION

• Monitor medication intake.
• Discuss patient response to therapy.
• Monitor vital signs, watch for elevation in blood pressure with some
medications.
• Monitor weight; some medications are associated with changes in weight.
• Monitor sleep; ask patient about restful sleep during the night or difficulty
falling asleep.
• Teach patient to avoid alcohol intake with benzodiazepine use.

Mental Health

Alterations in mental health can be more difficult to diagnose because there is no
definitive laboratory test or radiological study with which to isolate the disorder.
Patients may initially seek treatment from primary care practitioners for a variety
of complaints: anxiety, insomnia, generalized aches, or other somatic complaints.
A thorough patient history should include past medical conditions, any prior
mental health conditions and their treatment course, current medications, social
history (including habits, work, exercise, and substance use), cultural background,
environmental factors, family history, and changes in libido, appetite, or sleep.
Physical examination focuses on the chief complaint from the patient’s point
of view and traces the progression of symptoms in a chronological order from
the time of onset. Mental status examination is completed focusing on the patient’s
appearance, activity and behavior, affect, mood, speech, content of thought, thought
process, cognition, judgment, and insight.
The majority of patients are cared for on an outpatient basis. Hospitalization
should be considered for those who:
• Are too sick to care for themselves.
• Present a serious threat to themselves or to others.
• Neglect to care for themselves.
• Are violent or have bizarre behavior.
• Have suicidal ideation.
• Have paranoid ideation.
• Have delusions.
• Have a marked impairment in judgment.
Patients with a coexisting mental health disorder are also admitted to a medical
surgical floor only if the medical condition warrants medical management. Caring
for the patient admitted with a medical or surgical condition does not preclude the
need to care for the patient’s depression or schizophrenia as well. Patients may also
develop medical conditions as a result of their mental health issues. Patients with
inadequate nutritional intake due to an eating disorder may have significant elec-
trolyte imbalances or cardiac dysfunction.

Ulcerative Colitis

Introduction:

An inflammatory disease of the large intestine that affects the mucosal layer begin-
ning in the rectum and colon and spreading into the adjacent tissue. There are ulcer-
ations in the mucosal layer of the intestinal wall, and inflammation and abscess
formation occur. Bloody diarrhea with mucous is the primary symptom. There are
periods of exacerbations and remissions. Symptom severity may vary from mild to
severe. The exact cause is unknown, but there is increased incidence in people with
northern European, North American, or Ashkenazi Jewish origins. The peak inci-
dences are from mid-teen to mid-twenties and again from mid-fifties to mid-sixties.

PROGNOSIS

Patients with ulcerative colitis may have an increase in symptoms with each flare-
up of the disease. Malabsorption of nutrients can cause weight loss and health
problems. Some patients will need surgery to resect the affected area of the large
intestine, resulting in a colostomy, ileal reservoir, ileoanal anastomosis, or ileoanal
reservoir. There is an increased risk of colon cancer in patients with ulcerative coli-
tis. The patient is also at risk for developing toxic megacolon or perforating the
area of ulceration.

SIGNS AND SYMPTOMS
• Weight loss
• Abdominal pain
• Chronic bloody diarrhea with pus due to ulceration
• Electrolyte imbalance due to diarrhea
• Tenesmus—spasms involving the anal sphincter; persistent desire to empty
bowel

TREATMENT
• Keep stool diary to identify irritating foods.
• Low-fiber, high-protein, high-calorie diet.
• Administer antidiarrheal medications:
• loperamide
• diphenoxylate hydrochloride and atropine
• Administer salicylate medications to reduce inflammation within the intes-
tinal mucosa:
• sulfasalazine
• mesalamine
• olsalazine
• balsalazide
• Administer corticosteroids during exacerbations to reduce inflammation:
• prednisone
• hydrocortisone
• NPO for bowel rest during exacerbations.
• Administer anticholinergics to reduce abdominal cramping and discomfort:
• dicyclomine
• Surgical resection of affected area of large intestine.

NURSING DIAGNOSES

• Acute pain
• Diarrhea
• Impaired skin integrity

NURSING INTERVENTION

• Monitor intake and output.
• Monitor stool output, frequency.
• Weigh patient regularly.
• Sitz bath.
• Vitamin A & D ointment or barrier cream applied to skin.
• Witch hazel to soothe sensitive skin.
• Monitor for toxic megacolon (distended and tender abdomen, fever, elevated
WBC, elevated pulse, distended colon).
• Teach home care for new ostomy patients or refer to enterostomal therapist
for education:
• Teach proper skin care of perianal area to avoid skin breakdown.
• Avoid fragranced products which can be irritating.
• Teach dietary modification, and which foods to avoid.
• Teach medication use, schedule, and side effects.
• Teach importance of follow-up care.
• Teach wound care for postoperative patients.
• Disturbed body image

Peptic Ulcer Disease (PUD)

Introduction:

An ulcer develops when there is erosion of a portion of the mucosal layer of either
the stomach or duodenum. The ulcer may occur within the stomach (gastric
ulcer), or the duodenum (duodenal ulcer). A break in the protective mucosal lin-
ing allows the acid within the stomach to make contact with the epithelial tissues.
Gastric ulcers favor the lesser curvature of the stomach. Duodenal ulcers tend to
be deeper, penetrating through the mucosa to the muscular layer. Helicobacter
pylori infection has been associated with duodenal ulcers. Stress ulcers are asso-
ciated with another acute medical condition or traumatic injury. As the body
attempts to heal from the other physical condition (for example, major surgery),
small areas of ischemia develop within the stomach or duodenum. The ischemic
areas then ulcerate.

PROGNOSIS

The ulcerated areas may develop bleeding or may perforate. Depending on the
location of the ulceration, a vessel may become exposed to the effects of the stom-
ach acids. Damage to these vessels may result in significant bleeding. Perforation
of the ulcer can occur as the ulcer continues to erode more deeply into the tissue.
Perforation permits the contents of the stomach or duodenum to enter the peri-
toneum, leading to peritonitis, paralytic ileus, septicemia, and shock. This patient
will need emergency surgery due to a life-threatening condition.


SIGNS AND SYMPTOMS

• Sudden, sharp pain
• Tender, rigid, board-like abdomen
• Knee-chest position reduces pain
• Hypovolemic shock
• Weight changes
• Loss with gastric ulcer
• Gain with duodenal ulcer

TREATMENT
• Administer antacids
• Administer histamine-2 blockers:
• famotidine, ranitidine, nizatidine
• Administer proton pump inhibitors:
• omeprazole, lansoprazole, rabeprazole, esomeprazole, pantoprazole
• Administer mucosal barrier fortifiers:
• sucralfate
• Administer prostaglandin analogue:
• misoprostol
• Adjust diet.
• Treat H. pylori infection if present with combination therapy:
• Proton pump inhibitor plus clarithromycin plus amoxicillin or
• Proton pump inhibitor plus metronidazole plus clarithromycin or
• Bismuth subsalicylate plus metronidazole plus tetracycline.

NURSING DIAGNOSES

• Acute pain
• Risk for imbalanced nutrition: less than what body requires
• Risk for imbalanced nutrition: more than what body requires

NURSING INTERVENTION

• Monitor vital signs.
• Monitor intake and output.
• Assess abdomen for bowel sounds, tenderness, rigidity, rebound pain, guarding.
• Monitor stool for change in color, consistency, blood.
• Teach patient about home care:
• Diet modification to avoid acidic foods, caffeine, peppermint, alcohol.
• Eat more frequent, small meals.
• Avoid nonsteroidal anti-inflammatory medication.
• Stop smoking.

Peritonitis

Introduction:

Peritonitis is an acute inflammation of the peritoneum, which is the lining of the
abdominal cavity. Peritonitis may be primary or secondary to another disease
process. It typically occurs due to bacterial presence within the peritoneal space.
The bacteria may have passed from the gastrointestinal tract or the rupture of an
organ within the abdomen or pelvis. After the introduction of the bacteria into the
abdominal area, an inflammatory reaction occurs.

PROGNOSIS

It is a life-threatening disease process. Patients may develop septicemia from the
bacteria within the abdomen that enter the bloodstream.

SIGNS AND SYMPTOMS

• Fever
• Tachycardia
• Abdominal distention
• Abdominal pain—may be localized or generalized
• Rebound pain (pain when quickly removing pressure during palpation of
abdomen)
• Rigid abdomen
• Nausea, vomiting, loss of appetite
• Decreased bowel sounds
• Decreased urine output

TREATMENT
• Intravenous fluids.
• Administer broad-spectrum antibiotics.
• Surgical intervention may be necessary to correct cause of peritonitis.
• Pain management postoperatively.

NURSING DIAGNOSES

• Acute pain
• Impaired tissue integrity
• Impaired skin integrity

NURSING INTERVENTION
• Weigh daily.
• Monitor vital signs.
• Monitor intake and output.
• NPO to avoid irritation of intestinal tract, further stress on abdominal organs
• Position for comfort, head of bed elevated.
• Assess for return of bowel sounds postoperatively.
• Teach patient about home care:
• Pain management.
• Wound care, drains, etc.
• Monitor for signs of infection.

Pancreatitis

Introduction:

Pancreatitis is an inflammation of the pancreas which causes destructive cellular
changes. It may be an acute or a chronic process. Acute pancreatitis involves auto-
digestion of the pancreas by pancreatic enzymes and development of fibrosis. Blood
glucose control may be affected by the changes to the pancreas. Chronic pancreatitis
results from recurrent episodes of exacerbation, leading to fibrosis and a decrease in
pancreatic function. Presence of gallstones blocking a pancreatic duct, chronic use
of alcohol, post-abdominal trauma or surgery, or elevated cholesterol are associated
with an increased risk of pancreatitis.

PROGNOSIS

Acute pancreatitis may be life-threatening. Pleural effusion may develop as a com-
plication of acute pancreatitis; older patients have a greater risk of also developing
pneumonia. Disseminated intravascular coagulation is another complication that
may occur, affecting the body’s ability to clot due to depleted clotting factors in
the development of small thrombi.

SIGNS AND SYMPTOMS

• Epigastric pain due to inflammation and stretching of pancreatic duct
• Boring abdominal pain may radiate to back or left shoulder in acute pan-
creatitis
• Gnawing continuous abdominal pain with acute exacerbations in chronic
pancreatitis
• Patient in knee-chest position for comfort—reduces tension on abdomen
• Nausea and vomiting
• Bluish-gray discoloration of periumbilical area and abdomen (Cullen’s sign)
• Bluish-gray discoloration of flank areas (Turner’s sign)
• Ascites
• Weight loss
• Blood glucose elevation
• Fatigue

TREATMENT

• NPO during acute stage to reduce release of pancreatic enzymes.
• Intravenous fluids for hydration.
• Total parenteral nutrition.
• Administer vitamin supplementation.
• Pain management with narcotics during acute stage.
• Avoid morphine that may increase pain due to spasm of the sphincter of Oddi
at the opening to the small intestine from the common bile duct.
• Intravenous, patient-controlled analgesia or transdermal delivery preferable
to intramuscular.
• Acute:
• NG tube connected to suction if vomiting.
• Surgical intervention for abscess or pseudocyst.
• Chronic:
• Blood glucose control with insulin.
• Administer pancreatic enzymes with meals.
• Surgical intervention for pain control, abscess.

NURSING DIAGNOSES

• Acute pain
• Imbalanced nutrition: less than what body requires

NURSING INTERVENTION

• Assess vital signs for elevated temperature, elevated pulse, and changes in
blood pressure.
• Assess pain level.
• Monitor intake and output.
• Assess abdomen for bowel sounds, tenderness, masses, ascites.
• Monitor fingerstick blood glucose.
• Assess lung sounds for bilateral equality.
• Frequent oral care for NPO patients.
• Teach patient about home care:
• Avoid alcohol and caffeine.
• Bland, low-fat, high-protein, high-calorie, small, frequent meals.
• Use of blood glucose meter.
• Medication management, schedule, side effects.
• Plan rest periods until strength returns.

Hiatal Hernia

Introduction:

This is also known as a diaphragmatic hernia. A part of the stomach protrudes up
through the diaphragm near the esophagus into the chest. Patients may be asymp-
tomatic or have daily symptoms of gastroesophageal reflux disease (GERD). The
hernia may be a sliding hiatal hernia which allows movement of the upper portion
of the stomach including the lower esophageal sphincter up and down through
the diaphragm. These patients typically have symptoms of GERD. Another type
of hiatal hernia is a rolling hernia in which a portion of the stomach protrudes up
through the diaphragm, but the lower esophageal sphincter area remains below the
level of the diaphragm. These patients do not generally suffer from reflux.

PROGNOSIS

Lifestyle modifications may help control the symptoms of hiatal hernia. Some
patients who do not get adequate control of symptoms or are refractory to treat-
ment may need surgery to correct the movement through the diaphragm.

SIGNS AND SYMPTOMS

• Sliding hernia:
• Heartburn
• Difficulty swallowing (dysphagia)
• Burping (eructation)
• Chest pain
• Rolling hernia:
• Chest pain
• Shortness of breath after eating
• Feeling of fullness after eating

TREATMENT

• Administer antacids for patients with reflux symptoms:
• Maalox, Mylanta, Tums, Gaviscon
• Administer histamine type 2 (H2) blockers to reduce stomach acid:
• ranitidine, nizatidine, famotidine, cimetidine
• Administer proton pump inhibitors to reduce the production of acid:
• omeprazole, esomeprazole, pantoprazole, rabeprazole, lansoprazole
• Avoid lying down after eating.
• Modify eating schedule; small, frequent meals.
• Elevate head of bed.

NURSING DIAGNOSES

• Acute pain
• Chronic pain

NURSING INTERVENTION

• Monitor vital signs.
• Assess abdomen for distention, bowel sounds.
• Teach patient about lifestyle modifications:
• Medication management.
• Avoid clothing that is tight around the waist.
• Not to lie down after eating.
• Elevate head of bed.
• Avoid wearing clothing that is tight at waist.
• Avoid acidic foods (citrus, vinegar, tomato), peppermint, caffeine, alcohol.
• Stop smoking.
• Lose weight if overweight.

Hepatitis

Introduction:

Hepatitis is an inflammation of the liver cells. This is most commonly due to a
viral cause which may be either an acute illness or become chronic. The disease
may also be due to exposure to drugs or toxins.
Hepatitis A is transmitted via an oral route, often due to contaminated water or
poor sanitation when traveling; it is also transmitted in daycare settings and resi-
dential institutions. It can be prevented by vaccine.
Hepatitis B is transmitted via a percutaneous route, often due to sexual contact,
IV drug use, mother-to-neonate transmission or possibly blood transfusion. It can
be prevented by vaccine.
Hepatitis C is transmitted via a percutaneous route, often due to IV drug use or,
less commonly, sexual contact. There is currently no vaccine available.
Hepatitis D is transmitted via a percutaneous route and needs hepatitis B to
spread cell to cell. There is no vaccine available for hepatitis D.
Hepatitis E is transmitted via an oral route and is associated with water con-
tamination. There is no known chronic state of hepatitis E and no current vaccine
available.
Hepatitis G is transmitted via a percutaneous route and is associated with chronic
infection but not significant liver disease.
Exposure to medications (even at therapeutic doses), drugs, or chemicals can
also cause hepatitis. Onset is usually within the first couple of days of use, and may
be within the first couple of doses. Hepatotoxic substances include acetamino-
phen, carbon tetrachloride, benzenes, and valproic acid.


PROGNOSIS

Hepatitis may occur as an acute infection (viral type A, E) or become a chronic
state. The patient with chronic disease may be unaware of the illness until testing
of liver function shows abnormalities and further testing reveals presence of hep-
atitis. The chronic (viral type B, C) disease state creates the potential development
of progressive liver disease. Some patients with chronic disease will need liver
transplant. Recurrence rate post-transplant is high. Liver cancer may develop in
those with chronic disease states.

SIGNS AND SYMPTOMS

• Acute hepatitis:
• Malaise
• Nausea and vomiting
• Diarrhea or constipation
• Low-grade fever
• Dark urine due to change in liver function
• Jaundice due to liver compromise
• Tenderness in right upper quadrant of abdomen
• Hepatomegaly
• Arthritis, glomerulonephritis, polyarteritis nodosa in hepatitis B
• Chronic hepatitis:
• Asymptomatic with elevated liver enzymes
• Symptoms as acute hepatitis
• Cirrhosis due to altered liver function
• Ascites due to decrease in liver function, increased portal hypertension
• Bleeding from esophageal varices
• Encephalopathy due to diminished liver function
• Bleeding due to clotting disorders
• Enlargement of spleen


TREATMENT
• Avoid medications metabolized in the liver.
• Avoid alcohol.
• Remove or discontinue causative agent if drug-induced or toxic hepatitis.
• Intravenous hydration if vomiting during acute hepatitis.
• Activity as tolerated.
• High-calorie diet; breakfast is usually the best tolerated meal.
• Administer interferon or lamivudine for chronic hepatitis B.
• Administer interferon and ribavirin for hepatitis C.
• Administer prednisone in autoimmune hepatitis.
• Liver transplantation.

NURSING DIAGNOSES

• Fatigue
• Risk for injury
• Impaired tissue integrity

NURSING INTERVENTION

• Monitor vital signs.
• Assess abdomen for bowel sounds, tenderness, ascites.
• Plan appropriate rest for patient in acute phase.
• Monitor intake and output.
• Assess mental status for changes due to encephalopathy.
• Assist patient to:
• Plan palatable meals; remember that breakfast is generally the best toler-
ated meal.
• Avoid smoking areas—intolerance to smoking.

Gastritis

Introduction:

Gastritis is an inflammation of the stomach lining due to either erosion or atrophy.
Erosive causes include stresses such as physical illness or medications such as
nonsteroidal anti-inflammatory drugs (NSAIDs). Atrophic causes include a his-
tory of prior surgery (such as gastrectomy), pernicious anemia, alcohol use, or
Helicobacter pylori infection.

PROGNOSIS
Gastritis may cause changes within the cells of the stomach lining leading to mal-
nutrition, lymphoma, or gastric cancer. Hospitalized patients, especially in criti-
cal care settings, should have preventive medications to avoid the development
of gastritis.

SIGNS AND SYMPTOMS

• Nausea and vomiting
• Anorexia
• Epigastric area discomfort
• Epigastric tenderness on palpation due to gastric irritation
• Bleeding from irritation of the gastric mucosa
• Hematemesis—possible coffee ground emesis due to partial digestion of blood
• Melena—black, tarry stool

TREATMENT

• Administer antacids:
• Maalox, Mylanta, Tums, Gaviscon
• Administer sucralfate to protect gastric lining.
• Administer histamine 2 blockers:
• ranitidine, famotidine, nizatidine, cimetidine
• Administer proton pump inhibitors:
• omeprazole, esomeprazole, pantoprazole, rabeprazole, lansoprazole
• Eradicate Helicobacter pylori infection if present.
• Diet modification.
• Monitor hemoglobin and hematocrit.

NURSING DIAGNOSES

• Risk for imbalanced nutrition: less than what body requires
• Risk for imbalanced fluid volume

NURSING INTERVENTION

• Monitor vital signs.
• Monitor intake and output.
• Monitor stool for occult blood.
• Assess abdomen for bowel sounds, tenderness.
• Teach patient about:
• Diet restrictions: avoid alcohol, caffeine, acidic foods.
• Medications.
• The need to avoid smoking.
• The need to avoid NSAIDs.
• Nausea

Gastrointestinal Bleed

Introduction:

Bleeding from the gastrointestinal tract may cause significant blood loss. The bleed-
ing may be from either the upper or lower gastrointestinal tract. Upper gastrointesti-
nal bleeds are commonly from ulcers, esophageal varices, neoplasms, arteriovenous
malformations, Mallory-Weiss tears secondary to vomiting, or anticoagulant use.
Lower gastrointestinal bleeds are commonly due to fissure formation, rectal trauma,
colitis, polyps, colon cancer, diverticulitis, vasculitis, or ulcerations.

PROGNOSIS

The amount and speed of blood loss coupled with the patient’s age and co-
morbidities account for the prognosis. The greater the loss of blood, the harder it
is for the system to overcome the stress. Multiple transfusions to replace the lost
blood increase the patient’s risk for a reaction. Patients with blood-clotting disor-
ders have a greater risk of a significant bleed. Patients may go into shock if the
amount of blood loss is great, as they become hemodynamically unstable.

SIGNS AND SYMPTOMS

• Hematemesis—vomiting of blood (red, maroon, coffee ground)
• Melena—black, tarry stool
• Hematochezia—red or maroon blood rectally
• Orthostatic changes—drop in BP of at least 10 mmHg with position changes
• Tachycardia as body attempts to circulate lesser blood volume
• Pallor due to decrease in circulating blood volume
• Lightheadedness

TREATMENT
• Maintain IV access.
• Administer isotonic fluids like normal saline.
• Monitor serial hemoglobin and hematocrit levels.
• Type and cross match for 3 to 6 units depending on amount of blood loss.
• Transfuse packed RBCs, type-specific when possible (type O negative when
type-specific unavailable—no time to get results back from lab yet).
• May need to administer albumin or fresh frozen plasma, depending on amount
of units transfused and comorbidities such as cirrhosis or clotting disorders.
• Endoscopic procedures to treat ulcer topically, with injectable or laser treatment.
• Esophageal varices may be treated by tamponade with Blakemore-Sengstaken
tube.
• Surgery indicated when bleeding uncontrolled.

NURSING DIAGNOSES

• Deficient fluid volume
• Decreased cardiac output

NURSING INTERVENTION

• Monitor vital signs for changes—drop in BP, increase in pulse or respiration.
• Monitor intake and output.
• Replace volume lost.
• Monitor abdomen for bowel sounds, tenderness, distention.
• Maintain large bore IV (14- to 18-gauge) access.
• Assess IV site for signs of redness or swelling.
• Monitor lab results—drop in lab values may lag behind blood loss.
• Monitor during blood transfusion as per institution protocol for checking
blood unit, patient identity, frequency of vital signs, and documentation
• Anxiety

Gastroesophageal Reflux Disease (GERD)

Introduction:

The reflux of stomach acid and contents into the esophagus. This typically causes
symptoms because the lining of the esophagus is not protected against the acid that
is normally found only in the stomach. The pain that is produced is often referred to
as heartburn, or may be mistaken for cardiac pain. The pain may also be referred
to the back. The pain occurs more frequently in men, people who are obese, smok-
ers, and those who use alcohol or medications that lower the muscle tone of the
lower esophageal sphincter. The pain due to acid refluxing into the esophagus is
worse after eating or when lying down. Patients with a hiatal hernia may also
experience reflux due to the increased pressure that exists from a portion of the
stomach protruding upward through the diaphragm.

PROGNOSIS
Control of symptoms is possible through lifestyle modification and use of med-
ications to reduce acid production within the stomach. There has been no correla-
tion shown between the severity of patient symptoms and the degree of damage
being done to the tissue of the esophagus. Patients with ongoing symptoms should
have an upper endoscopy to allow for visualization and biopsy of the area to mon-
itor for the possibility of cancer of the esophagus developing due to long-term
reflux. Barrett’s esophagus is a premalignant condition of the esophagus that
occurs due to reflux, where cellular changes have occurred and the patient needs
to be monitored for progression to a malignant cell type. Some patients may
develop trouble with swallowing due to the development of scarring from long-
term exposure to acid. These patients may develop strictures over time. Procedures
can be performed to help stretch the lumen of the esophagus to aid in swallowing.

SIGNS AND SYMPTOMS
• Epigastric burning, worse after eating
• Heartburn
• Burping (eructation) or flatulence
• Sour taste in mouth, often worse in the morning
• Nausea
• Bloating
• Cough due to reflux high in the esophagus
• Hoarseness or change in voice

TREATMENT
• Administer antacids to neutralize acid; these medications act quickly:
• Maalox, Mylanta, Tums, Gaviscon
• Administer H2 (histamine type 2) blockers to decrease the production of acid:
• ranitidine, famotidine, nizatidine, cimetidine
• Administer proton pump inhibitors to reduce the production of acid:
• omeprazole, esomeprazole, pantoprazole, rabeprazole, lansoprazole
• Have patient eat six small meals rather than three large ones to reduce intra-
abdominal pressure.
• Surgery or endoscopic procedures may be performed to prevent the reflux
from occurring.

NURSING DIAGNOSES

• Risk for imbalanced nutrition: less than what body requires
• Risk for imbalanced nutrition: more than what body requires
• Acute pain
• Chronic pain

NURSING INTERVENTION

• Monitor vital signs.
• Assess abdomen for distention, bowel sounds.
• Teach about medication management.
• Teach patient about lifestyle modifications:
• Not to lie down after eating.
• Elevate head of bed.
• Avoid wearing clothing that is tight at waist.
• Avoid acidic foods (citrus, vinegar, tomato), peppermint, caffeine, alcohol.
• Stop smoking.
• Lose weight if overweight

Gastroenteritis

Introduction:

An acute inflammation of the gastric and intestinal mucosa which is most com-
monly due to bacterial, viral, protozoal, or parasitic infection. It may also be caused
by irritation due to chemical or toxin exposure or allergic response. Viral exposure
is more likely in winter; bacterial exposure is more common in summer when
food-borne illness exposure is likely.

PROGNOSIS

Symptoms may be self-limiting or may need prescription medication to resolve the
illness. Older or debilitated patients may have more severe symptoms or require
hospitalization due to dehydration.

SIGNS AND SYMPTOMS

• Nausea and vomiting due to gastric irritation
• Diarrhea—watery, soft, may be mixed with mucous or blood
• Abdominal pain due to intestinal irritation
• Abdominal distention
• Fever due to infection
• Anorexia due to gastric irritation
• Malaise due to infection
• Headache due to viral illness
• Signs of dehydration—dry, flushed skin and mucous membranes, decreased
urine output, tachycardia, poor skin turgor, orthostatic blood pressure changes

TREATMENT

• Monitor intake and output.
• Replace fluids lost.
• Administer antiemetic medication for symptom relief:
• prochlorperazine
• trimethobenzamide
• Administer antidiarrheal medications for symptom relief:
• loperamide
• diphenoxylate
• kaolin-pectin
• bismuth subsalicylate
• Need to allow organism one way out of gastrointestinal system (either anti-
emetic or antidiarrheal, not both).
• ciprofloxacin
• metronidazole
• Intravenous fluids to correct dehydration.
emetic or antidiarrheal, not both).

NURSING DIAGNOSES

• Risk for imbalanced nutrition: less than what body requires
• Deficient fluid volume
• Altered bowel elimination
• Diarrhea
• Fatigue

NURSING INTERVENTION

• Monitor vital signs for changes.
• Monitor intake and output.
• Replace fluids lost.
• Assess skin and mucous membranes for signs of dehydration.
• Assess abdomen for bowel sounds, tenderness

Diverticulitis Disease

Introduction:

Small out-pouchings called diverticula develop along the intestinal tract. Diverti-
culosis is the condition of having these diverticula. Any part of the large or small
intestine may be involved. The area of the intestinal tract that most commonly
develops diverticula is the lower portion of the large intestine. Certain types of
undigested foods can become trapped in the pouches of the intestine. Bacteria mul-
tiply in the area, causing further inflammation. Diverticulitis is an inflammation of
at least one of the diverticula. Diets that have a low fiber content, seeds, or nuts
have been implicated in the development of diverticulitis. Perforation of the diver-
ticula is possible when they are inflamed.

PROGNOSIS

Inflammation in diverticulitis increases the risk of perforation of the intestine.
Peritonitis will develop from bacterial contamination after perforation of a diver-
ticula. Bleeding from the intestinal mucosa in the area of inflammation can also
occur. The presence of diverticula and repeated periods of inflammation may allow
development of fistula formation from the diverticula to other areas within the
abdomen, such as the intestine or bladder. Patients needing surgery may have a
colostomy postoperatively. Depending on the location of the diverticulitis and the
reason for the surgery, the colostomy may be reversible after healing has occurred.


SIGNS AND SYMPTOMS

• Asymptomatic in diverticulosis
• Change in bowel habits
• Bloating, increased gas
• Abdominal pain most often in the left lower quadrant with diverticulitis
• Rectal bleeding due to inflammation with diverticulitis
• Fever with diverticulitis
• Nausea, vomiting
• Tachycardia due to fever
• Peritonitis if diverticula ruptures

TREATMENT

• Administer antibiotics:
• ciprofloxacin
• metronidazole
• trimethoprim-sulfamethoxazole
• Administer adequate intravenous hydration.
• Manage pain as needed.
• NPO or clear liquids (depending on order) during acute inflammation to rest
intestinal tract.
• Surgical intervention to correct perforation of diverticula, abscess formal-
tion, bowel obstruction, fistula formation.
• NG tube postoperatively.

NURSING DIAGNOSES

• Acute pain
• Altered bowel elimination
• Disturbed body image

NURSING INTERVENTION

• Monitor vital signs for fever, increased heart rate, and decreased blood pressure.
• Assess abdomen for distention, presence of bowel sounds.
• Monitor intake and output.
• Postoperatively check:
• Stoma at colostomy site
• Wound site for drainage or signs of infection
• Peripheral circulation, swelling due to increased risk of clot formation
• Teach patients:
• Eat low-residue foods during flare-ups.
• Eat high-fiber diet when asymptomatic, fresh fruits and vegetables, whole
wheat breads, bran cereals.
• Avoid laxatives and enemas due to increased irritation and intra-abdominal
pressure.
• Avoid lifting during exacerbation.
• Avoid eating nuts and seeds.

Cirrhosis Prognosis Sign and Symptoms

Introduction

Injury to the cellular structure of the liver causes fibrosis due to chronic inflamma-
tion and necrotic changes, resulting in cirrhosis. There are nodular changes to the
liver. The bile ducts and blood vessels through the liver may become blocked due
to both the nodular changes and fibrosis. These changes to the liver cause enlarge-
ment of the organ and change in texture. There is increased pressure within the
portal vein. This causes resistance to blood flow throughout the venous system in
the liver and also backs up venous blood to the spleen, causing enlargement of this
organ also. Damage to the liver may be reversible if the cause if identified early and
removed. The most common causes of cirrhosis include chronic alcohol use, liver
damage secondary to exposure to drugs or toxins, viral hepatitis (especially hepati-
tis B, hepatitis C, and hepatitis D in those already infected with hepatitis B), fatty
liver (steatohepatitis), autoimmune hepatitis, cystic fibrosis, metabolic disorders
(excess iron storage—hemachromatosis), or genetic causes.

PROGNOSIS

As cirrhosis progresses, the patient may develop encephalopathy and coma. Early
signs and symptoms of encephalopathy include altered level of consciousness,
neuromuscular changes, and elevated serum ammonia levels.

SIGNS AND SYMPTOMS
• Initially asymptomatic
• Weakness, fatigue due to chronic disease
• Muscle cramps
• Weight loss
• Anorexia
• Nausea with possible vomiting
• Ascites—the accumulation of fluid within the abdominal cavity due to por-
tal hypertension
• Abdominal pain
• Portal hypertension
• Pruritus (itching)
• Ecchymosis (bruises) or petechiae (small, pinpoint, round, reddish purple
marks)
• Coagulation defects due to problems with vitamin K absorption, causing
problems with production of clotting factors
• Amenorrhea
• Impotence due to inactivity of hormones
• Gynecomastia
• Jaundice due to problems with excretion of bilirubin
• Hepatomegaly (enlarged liver) in over one-half of the patients

TREATMENT

• Low-sodium diet; adequate calorie intake.
• Restrict fluid intake if hyponatremic (low serum sodium) or fluid overloaded.
• Restrict alcohol intake to prevent further damage.
• Administer vitamin supplements—folate, thiamine, multivitamin.
• Administer diuretics to reduce excess fluids:
• furosemide
• spironolactone
• Paracentesis to remove ascitic fluid.
• Monitor electrolytes for imbalance.
• Monitor coagulation profile (PT, PTT, INR).
• Administer lactulose to promote removal of ammonia in the gut.
• Administer antibiotics to destroy the normal GI flora which decreases pro-
tein breakdown and the rate of ammonia production:
• neomycin sulfate
• metronidazole
• Shunt placement:
• Peritoneovenous—moves ascitic fluid from abdomen to superior vena
cava.
• Portocaval—diverts venous blood flow from liver to decrease portal and
esophageal pressures.
• Transjugular intrahepatic portal systemic—nonsurgical procedure per-
formed in interventional radiology—sheath placed into jugular and hepatic
vein; needle threaded through sheath and pushed into portal vein through
the liver; balloon enlarges the tract and stent maintains.
• Gastric lavage.
• Esophagogastgric balloon tamponade for control of bleeding from esophageal
varices.
• Administer blood products as needed for patients with bleeding esophageal
varices.
• Sclerotherapy for esophageal variceal bleeding.

NURSING DIAGNOSES

• Ineffective breathing pattern
• Excess fluid volume
• Risk for infection

NURSING INTERVENTION

• Monitor intake and output.
• Monitor vital signs.
• Weigh patient daily.
• Measure abdominal girth—making sure to measure at level of umbilicus for
consistency; marks are typically made at sides of abdomen to align tape meas-
ure on subsequent days.
• Assess peripheral edema.
• Assess heart and lung sounds for excess fluid.
• Elevate head of bed 30 degrees or greater to ease breathing.
• Elevate feet to decrease peripheral edema.
• Monitor for signs of bleeding or bruising.
• Monitor level of consciousness, orientation, recent and remote memory, be-
havior, mood, and affect.

Cholecystitis

Introduction:

An inflammation of the gallbladder, often accompanied by the formation of gall-
stones (cholelithiasis), is cholecystitis. The inflammation may be either acute or
chronic in nature. In an acute cholecystitis, the blood flow to the gallbladder may
become compromised which in turn will cause problems with the normal filling and
emptying of the gallbladder. A stone may block the cystic duct which will result in
bile becoming trapped within the gallbladder due to inflammation around the stone
within the duct. Blood flow to the inflamed area will be minimized, localized
edema develops, the gallbladder distends due to retained bile, and ischemic changes
will occur within the wall of the gallbladder. Chronic cholecystitis occurs when
there have been recurrent episodes of blockage of the cystic duct, usually due to
stones. There is chronic inflammation. The gallbladder is often contracted, which
leads to problems with storing and moving the bile. Patients may develop jaundice
due to back-up of bile or obstructive jaundice. They will exhibit a yellowish tone to
skin and mucous membranes. If patients have a naturally dark pigmentation to their
skin, check palms and soles. Icterus is the yellow color change seen in the sclera
(white) of the eye.
There is increased risk for gallbladder inflammation and development of gall-
stones with increasing age, being female or overweight, having a family history of
gallbladder disease, people on rapid weight loss diets, and during pregnancy.

PROGNOSIS

The ischemic changes of the gallbladder wall increase the risk of perforation of the
organ or development of gangrene. Peritonitis is a potential risk in patients if a sig-
nificant area of gallbladder perforates or there is associated infection or abscess
that spreads. A small percentage of patients will develop cancer of the gallbladder.
There is increased surgical risk for older patients or patients with comorbidities.

SIGNS AND SYMPTOMS

• Upper abdominal, epigastric, or right upper quadrant abdominal pain which
may radiate to right shoulder
• Right upper quadrant (RUQ) pain increases with palpation of right upper
abdomen during inspiration (Murphy’s sign) causing the patient to stop tak-
ing deep breaths
• Nausea and vomiting, especially following fatty foods
• Loss of appetite
• Fever
• Increased air in intestinal tract (eructation, flatulence)
• Pruritis (itching) of skin due to build-up of bile salts
• Clay-colored stools due to lack of urobilinogen in gut (normally converted
from bilirubin which was blocked with bile flow)
• Jaundice—yellowish skin and mucous membrane discoloration
• Icterus—yellowish discoloration of sclera (white of eye)
• Dark, foamy urine as kidneys attempt to clear out bilirubin

TREATMENT

• Low-fat diet.
• Intravenous fluid replacement for vomiting.
• Administer antiemetics for control of nausea and vomiting:
• prochlorperazine
• trimethobenzamide
• Replace fat-soluble vitamins (A, D, E, K) as needed.
• Administer analgesics for adequate pain control:
• avoid morphine (may cause spasm of sphincter of Oddi, increasing pain).
• Administer antibiotics for acute symptoms.
• Placement of stent into gallbladder if the patient is not a candidate for surgery.
• Ultrasound-guided aspiration of gallbladder.
• Surgical removal of gallbladder:
• Laparoscopic cholecystectomy
• Open cholecystectomy

NURSING DIAGNOSES

• Acute pain
• Chronic pain
• Risk for imbalanced nutrition: less than what body requires
• Nausea

NURSING INTERVENTION

• Monitor vital signs for changes in temperature, pulse rate, respiratory rate,
and blood pressure.
• Assess abdomen for bowel sounds, distention, and tenderness.
• Assess pain level for adequate pain control.
• Assess postoperative wound for drainage, signs of infection.
• Monitor T-tube drainage in postoperative open cholecystectomy patients;
empty and record at least every 8 hours.
• Advance diet to low-fat diet postoperatively as tolerated.
• meperidine

Appendicitis

Introduction:

Inflammation of the vermiform appendix (a blind pouch located near the ileocecal
valve in the right lower quadrant of the abdomen) is known as appendicitis. It may
be due to obstruction from stool. The mucosal lining of the appendix continues to
secrete fluid, which will increase the pressure within the lumen of appendix, caus-
ing a restriction of the blood supply to the appendix. This decrease in blood sup-
ply may result in gangrene or perforation as the pressure continues to build. Pain
localizes at McBurney’s point, located midway between the umbilicus and right
anterior iliac crest. Appendicitis may occur at any age, but the peak occurrence is
from the teenage years to 30.

PROGNOSIS

Rupture of the appendix is more likely to occur in acute appendicitis within the
first 36 to 48 hours. Symptoms of peritonitis (inflammation of the peritoneum—
the membrane lining the abdominal cavity) may occur as a complication of appen-
dicitis. Rapid diagnosis and surgical intervention are necessary to avoid rupture of
the appendix.

SIGNS AND SYMPTOMS

• Rigidity of the abdomen (abdomen feels more firm when palpating)
• Fever due to infection
• Nausea, vomiting, loss of appetite
• Right lower quadrant pain that improves with flexing the right hip suggests
perforation

TREATMENT

• Surgical removal of the appendix—appendectomy (may be done via laparo-
scopy or open laparotomy).
• NPO—nothing by mouth to avoid further irritation of the intestinal area, and
prep for surgery.
• Intravenous fluids until diet resumed.
• Pain medications after surgery as needed; pain medication is used cautiously
preoperatively to maintain awareness of increase in pain due to possible rup-
ture of appendix.
• Antibiotics postoperatively if needed.

NURSING DIAGNOSES

• Acute pain
• Hyperthermia
• Nausea

NURSING INTERVENTION

• Monitor vital signs for fever, increased heart rate, respiratory rate, and decrease
in blood pressure.
• Assess pain level for changes.
• Monitor surgical site for appearance of wound, drainage.
• Monitor abdomen for distention, presence of bowel sounds.
• Monitor intake and output.
• Monitor bowel function.