NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
I. FLUID VOLUME DISTURBANCES
(Hypovolemia, Hypervolemia)
II. ELECTROLYTE IMBALANCES (Sodium,
Potassium, Calcium, Magnesium Imbalance,
Phosphorus, Chloride)
III. ACID–BASE DISTURBANCES (Metabolic
Acidosis, Metabolic Alkalosis, Respiratory
Acidosis, Respiratory Alkalosis , Mixed Acid–
Base Disorders)
IV. PARENTERAL FLUID THERAPY (Purpose,
Types of Intravenous Solutions, Nursing
Management of the Patient Receiving
Intravenous Therapy
V. KIDNEY DISORDERS (Chronic Kidney
Disease, Nephrotic Syndrome , Acute
Kidney Injury, End-Stage Kidney Disease or
Chronic Kidney Disease)
VI. RENAL REPLACEMENT THERAPIES
(Dialysis, Hemodialysis Dialyzers,
Continuous Renal Replacement Therapies,
Peritoneal Dialysis)
VII. INFECTIONS OF THE URINARY TRACT
(Lower Urinary Tract Infections)
ADULT VOIDING DYSFUNCTION (Urinary
VIII.
Incontinence, Urinary Retention, Neurogenic
Bladder)
FLUID VOLUME DISTURBANCES
HYPOVOLEMIA
 FVD, or hypovolemia, occurs when loss of ECF
(extracellular fluid) volume exceeds the intake of
fluid. It occurs when water and electrolytes are lost in
the same proportion as they exist in normal body
fluids, thus the ratio of serum electrolytes to water
remains the same. FVD should not be confused with
dehydration, which refers to loss of water alone, with
increased serum sodium levels. FVD may occur
alone or in combination with other imbalances.
Unless other imbalances are present concurrently,
serum electrolyte concentrations remain essentially
unchanged.
o Two distinct disorders:
 Volume Depletion
BSN 3A | PBL GROUP 1
 which describes the loss of sodium
from the extracellular space (i.e.,
intravascular and interstitial fluid) that
occurs during gastrointestinal
hemorrhage, vomiting, diarrhea, and
diuresis;
 Dehydration
 which refers to the loss of
intracellular water (and
total body water) that
ultimately causes cellular
desiccation and elevates
the plasma sodium
concentration and
osmolality.
ALTERATIONS IN HEALTH (DIAGNOSIS)
 Fluid volume deficit
CAUSES
 Commonly caused by dysfunction of various organs,
such as Congestive Heart Failure or Kidney
Failure.
 Rarely, neurological disorders, particularly those
affecting the hormones that regulate kidney
functioning can also cause hypovolemia.
 Dehydration, which may result from excessive water
evaporating from the skin in extreme heat or when
experiencing a fever. Dehydration can also result
from continuous vomiting or diarrhea without
sufficient fluid intake, usually associated with
infections that cause gastroenteritis.
 It may also result from excessive accumulation of
fluids within the interstitial space, between cells.
For instance, when an infection becomes severe,
sepsis can occur, which is a life-threatening condition
in which the individual's response to the infection
leads to organ dysfunction and systemic
inflammation.
 Other conditions that can cause fluids to exit blood
vessels include pancreatitis, pericarditis, burns,
and nutritional hypoalbuminemia.
 Sudden blood loss due to a trauma, like a motor
vehicle accident or a fall from a height. External or
internal bleeding may occur and, if not identified
quickly, can be life-threatening.
SIGNS & SYMPTOMS
Severity:
 Dizziness when standing.
 Dry skin and dry mouth.
 Feeling tired (fatigue) or weak.
 Muscle cramps.
 Unable to pee (urinate) or the color of your urine is
darker than normal.
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NCM112 LECTURE
MEDICAL-SURGICAL NURSING

FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS

Severe: your symptoms, especially if you get
dizzy when you’re upright, which is a
 Confusion. sign of hypovolemia.
 Difficulty breathing or fast breathing.
 Excessive sweating. CLINICAL MANIFESTATION
 Losing consciousness.
 Low blood pressure.
 Low body temperature.
 Pale skin tone or a blue tone to the skin and lips
(cyanosis).

COMPLICATIONS

 Hypoxia
 Hypovolemic Shock
 Dysrhythmias
 Acute Kidney Failure

PATHOPHYSIOLOGY

 FVD results from loss of body fluids and occurs more

rapidly when coupled with decreased fluid intake.
FVD can also develop with a prolonged period of
inadequate intake. Causes of FVD include abnormal
fluid losses, such as those resulting from vomiting,
diarrhea, GI suctioning, and sweating; decreased
intake, as in nausea or lack of access to fluids; and
third-space fluid shifts, or the movement of fluid from
the vascular system to other body spaces (e.g., with
edema formation in burns, ascites with liver
dysfunction). Additional causes include diabetes
insipidus (a decreased ability to concentrate urine
owing to a defect in the kidney tubules that interferes
with water reabsorption), adrenal insufficiency,
osmotic diuresis, hemorrhage, and coma.

ASSESSMENT AND DIAGNOSTIC FINDINGS

 LABORATORY TESTS
o Elevated Potassium and BUN
o Urine Specific Gravity
o Urine Sodium Concentration
o Creatinine
o Blood Test:
 CBC
 Chemistry Panels
o UTZ or Echocardiogram
 DIAGNOSTIC PROCEDURES
o Skin and Mucous Membrane
 During a physical exam, your provider
will examine your skin and the mucous
membranes in your mouth, tongue, and
nose for dryness, which is a sign of the
condition.
o Pulse, body temperature and blood pressure:
 Your provider will test your vitals while
you’re sitting and while you’re MEDICAL MANAGEMENT
standing to monitor changes. During
this process when you change your  Fluid Resuscitation
posture, your provider will examine o to increase the amount of fluid volume in your
body via fluid replacement (fluid resuscitation).

BSN 3A | PBL GROUP 1 2

NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
During this procedure, an IV (intravenous) tube
injects fluids into your vein
 Isotonic Electrolyte Solution (e.g.
lactated Ringer’s solution, 0.9%
sodium chloride) is frequently the first-
line choice to treat the hypotensive
patient with FVD because they expand
plasma volume
 Hypotonic electrolyte solution (e.g.,
0.45% sodium chloride) is often used to
provide both electrolytes and water for
renal excretion of metabolic wastes.
Note:
Shock can occur when the volume of fluid lost exceeds 25%
of the intravascular volume or when fluid loss is rapid.
 Oxygen Therapy
o to alleviate the adverse effects of hypoxemia
and tissue hypoxia
BSN 3A | PBL GROUP 1
 Accurate and Frequent assessment of I&O, weight,
vital signs, central venous pressure, level of
consciousness, breath sounds, and skin color
o should be performed to determine when
therapy should be slowed to avoid volume
overload. The rate of fluid administration is
based on the severity of loss and the
patient’s hemodynamic response to volume
replacement
 Fluid Challenge Test
o When is not excreting enough urine and to
determine whether the depressed renal
o Function is caused by reduced renal blood
flow secondary to FVD (prerenal azotemia)
or, more seriously, by acute tubular
necrosis from prolonged FVD
o During a fluid challenge test, volumes of
fluid are administered at specific rates and
intervals while the patient’s hemodynamic
response to this treatment is monitored (i.e.,
vital signs, breath sounds, orientation
status, central venous pressure, urine
output).
o An example of a typical fluid challenge test
involves administering 100 to 200 mL of
normal saline solution over 15 minutes. The
goal is to provide fluids rapidly enough to
attain adequate tissue perfusion without
compromising the cardiovascular system.
The response by a patient with FVD but
normal renal function is increased urine
output and an increase in blood pressure
and central venous pressure.
NURSING MANAGEMENT
 Monitors and measures fluid I&O at least every 8
hours, and sometimes hourly
o As FVD develops, body fluid losses exceed
fluid intake through excessive urination
(polyuria), diarrhea, vomiting, or other
mechanisms.
o Once FVD has developed, the kidneys
attempt to conserve body fluids, leading to
a urine output of less than 1 mL/kg/h in an
adult.
 Daily body weights monitored
o an acute loss of 0.5 kg (1 lb) represents a
fluid loss of approximately 500 mL (1L of
fluid weighs approximately 1 kg, or 2.2 lb)
(Crawford & Harris, 2011c).
 Vital Signs are closely monitored
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NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
o The nurse observes for a weak, rapid pulse
and orthostatic hypotension (i.e., a
decrease in systolic pressure exceeding 20
mm Hg when the patient moves from a lying
to a sitting position) (Weber & Kelley, 2010).
o A decrease in body temperature often
accompanies FVD, unless there is a
concurrent infection.
 Skin and tongue turgor are monitored on a regular
basis.
o In a healthy person, pinched skin
immediately returns to its normal position
when released (Weber & Kelley, 2010).
o This elastic property, referred to as turgor,
is partially dependent on interstitial fluid
volume. In a person with FVD, the skin
flattens more slowly after the pinch is
released.
o In a person with severe FVD, the skin may
remain elevated for many seconds.
o Tissue turgor is best measured by
pinching the skin over the sternum, inner
aspects of the thighs, or forehead. Tongue
turgor is not affected by age (see previous
Gerontologic Considerations), and
evaluating this may be more valid than
evaluating skin turgor. In a normal person,
the tongue has one longitudinal furrow.
o In the person with FVD, there are additional
longitudinal furrows and the tongue is
smaller because of fluid loss. The degree of
oral mucous membrane moisture is also
assessed; a dry mouth may indicate either
FVD or mouth breathing.
 Urine concentration is monitored by measuring the
urine specific gravity
o In a volume-depleted patient, the urine
specific gravity should be greater than
1.020, indicating healthy renal conservation
of fluid.
 Hemodynamic monitoring
o Mental function is eventually affected,
resulting in delirium in severe FVD as a
result of decreasing cerebral perfusion.
ALTERATIONS IN HEALTH (DIAGNOSIS)
Decreased peripheral perfusion can result
in cold extremities. In patients with relatively
normal cardiopulmonary function, a low
central venous pressure is indicative of
hypovolemia.
o Patients with acute cardiopulmonary
decompensation require more extensive
hemodynamic monitoring of pressures in
both sides of the heart to determine if
hypovolemia exists.
PREVENTION
 To prevent FVD, the nurse identifies patients at risk
and takes measures to minimize fluid losses. For
example, if the patient has diarrhea, measures
BSN 3A | PBL GROUP 1
should be implemented to control diarrhea and
replacement fluids administered. This includes
administering antidiarrheal medications and small
volumes of oral fluids at frequent intervals.
CORRECTING HYPOVOLEMIA
 When possible, oral fluids are administered to help
correct FVD, with consideration given to the patient’s
likes and dislikes. The type of fluid the patient has
lost is also considered, and fluids most likely to
replace the lost electrolytes are appropriate. If the
patient is reluctant to drink because of oral
discomfort, the nurse assists with frequent mouth
care and provides nonirritating fluids. The patient
may be offered small volumes of oral rehydration
solutions (e.g., Rehydralyte, Elete, Cytomax). These
solutions provide fluid, glucose, and electrolytes in
concentrations that are easily absorbed. If nausea is
present, an antiemetic may be needed before oral
fluid replacement can be tolerated. If the deficit
cannot be corrected by oral fluids, therapy may need
to be initiated by an alternative route (enteral or
parenteral) until adequate circulating blood volume
and renal perfusion are achieved. Isotonic fluids are
prescribed to increase ECF volume (Crawford &
Harris, 2011c).
HYPERVOLEMIA
 Hypervolemia is a medical condition when you have
too much fluid in your body, also described as having
excess water retention or fluid overload. Healthy
people have a certain amount of fluid in their bodies.
When you have too much excess fluid, it can cause
health complications such as swelling, high blood
pressure, heart problems, and more.
 Hypervolemia is common among people with chronic
kidney disease (CKD) and renal failure because their
kidneys aren't working to remove excess fluid as
healthy kidneys would. The good news is, once the
causes of your hypervolemia are understood, there
are treatments that can help control it.
 Fluid Volume Excess
CAUSES
 Kidney failure. Your kidneys are responsible for
removing excess fluid from your body. When your
kidneys aren’t working well, fluid can build up.
 Congestive heart failure. When your heart is not
pumping enough blood, your kidneys aren’t able to
work as well, leaving excess fluid in your body.
 Liver failure or cirrhosis. Your liver processes
nutrients and filters toxins. When your liver isn’t
working as it should, fluid can build up in your
abdomen.
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MEDICAL-SURGICAL NURSING

FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS

 Hormonal changes. Women may experience mild
fluid retention as a normal part of premenstrual
syndrome (PMS) or pregnancy. Excessive fluid
retention related to hormonal changes may be a sign
of high blood pressure and should be checked out by
a doctor.
 IV fluids. Receiving too much IV fluid, especially if
there are other health conditions present, can lead to
fluid overload and swelling.
 Salt (Sodium). Too much salt (sodium) in your body
causes hypervolemia. Salt is an essential mineral in
your body. Your body manages the amount of salt
you eat with water. If you eat food that contains too
much sodium, your body will use water to balance it
back to a normal level. This is why you might feel
thirsty after eating a lot of salty foods.
Note:
If you’re living with CKD: you may be at risk for
hypervolemia—especially in later stages as kidney function
declines. After a diagnosis of kidney failure, dialysis
treatments replace some kidney function to help to remove
excess fluid from your body and get you as close to your “dry
weight” as possible. Dry weight is your “ideal weight”—the
weight your care team determines you would be without the
excess fluid in your body.
factors can include heart failure, renal failure, and
cirrhosis of the liver. Another contributing factor is the
consumption of excessive amounts of table or other
sodium salts. Excessive administration of sodium-
containing fluids in a patient with impaired regulatory
mechanisms may predispose him or her to a serious
FVE as well
ASSESSMENT AND DIAGNOSTIC FINDINGS
 Laboratory data useful in diagnosing FVE include
BUN and hematocrit levels.
 In FVE, both of these values may be decreased
because of plasma dilution, low protein intake, and
anemia.
 In chronic renal failure, both serum osmolality and
the sodium level are decreased owing to excessive
retention of water.
 The urine sodium level is increased if the kidneys are
attempting to excrete excess volume.
 A chest x-ray may reveal pulmonary congestion.
Hypervolemia occurs when aldosterone is
chronically stimulated (i.e., cirrhosis, heart failure,
and nephrotic syndrome). Therefore, the urine
sodium level does not increase in these conditions.
MEDICAL MANAGEMENT

If you’ve never been diagnosed with CKD: your doctor may  Pharmacological Therapy
perform several tests to help determine the cause of your fluid o Diuretics
overload. You’ll probably be given a test to determine the  are prescribed when dietary restriction
amount of sodium in your blood. You’ll likely also get a urine of sodium alone is insufficient to reduce
test to help the doctor determine whether your hypervolemia edema by inhibiting the reabsorption of
is being caused by a kidney issue. Further testing for kidney sodium and water by the kidneys.
function can help your doctor decide which steps to take next.  The choice of diuretic is based on the
severity of the hypervolemic state, the
SIGNS & SYMPTOMS degree of impairment of renal function,
and the potency of the diuretic.
 Rapid weight gain  Thiazide diuretics
 Noticeable swelling (edema) in your arms, legs, and o block sodium
face reabsorption in the distal
 Swelling in your abdomen tubule, where only 5% to
 Cramping, headache, and stomach bloating 10% of filtered sodium is
 Shortness of breath reabsorbed.
 High blood pressure o Generally, thiazide
 Heart problems, including congestive heart failure diuretics, such as
hydrochlorothiazide
COMPLICATIONS (HydroDIURIL) or
chlorthalidone
 Pericarditis (Thalitone), are
 HF prescribed for mild to
 Delayed wound healing moderate hypervolemia
 Tissue Breakdown and loop diuretics for
 Decreased bowl function severe hypervolemia
(Karch, 2012).
PATHOPHYSIOLOGY  Loop diuretics
o such as furosemide
 FVE may be related to simple fluid overload or (Lasix), bumetanide
diminished function of the homeostatic mechanisms (Bumex), or torsemide
responsible for regulating fluid balance. Contributing (Demadex), can cause a

BSN 3A | PBL GROUP 1 5

NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
greater loss of both
sodium and water
because they block
sodium reabsorption in
the ascending limb of
Henle’s loop, where 20%
to 30% of filtered sodium
is normally reabsorbed.
 Electrolyte imbalances may result from the effect of
the diuretic. Hypokalemia can occur with all diuretics
except those that work in the last distal tubule of the
nephrons. Potassium supplements can be
prescribed to avoid this complication.
 Hyponatremia occurs with diuresis owing to
increased release of ADH secondary to a reduction
in circulating volume. Decreased magnesium levels
occur with the administration of loop and thiazide
diuretics due to decreased reabsorption and
increased excretion of magnesium by the kidney.
 High uric acid levels (hyperuricemia) can also occur
from increased reabsorption and decreased
excretion of uric acid by the kidneys
 Dialysis
o If renal function is so severely impaired that
pharmacologic agents cannot act efficiently,
other modalities are considered to remove
sodium and fluid from the body.
o Hemodialysis or peritoneal dialysis may be
used to remove nitrogenous wastes and
control potassium and acid–base balance,
and to remove sodium and fluid.
Continuous renal replacement therapy may
also be required.
 Nutritional Therapy
o Restriction of sodium.
 An average daily diet not restricted
in sodium contains 6 to 15 g of
salt, whereas low-sodium diets
can range from a mild restriction to
as little as 250 mg of sodium per
day, depending on the patient’s
needs.
 A mild sodium-restricted diet
allows only light salting of food
(about half the usual amount) in
cooking and at the table, and no
addition of salt to commercially
prepared foods that are already
seasoned
 Foods high in sodium must be
avoided. It is the sodium salt
(sodium chloride) rather than
sodium itself that contributes to
edema. Therefore, patients are
instructed to read food labels
carefully to determine salt content.
 About half of ingested sodium is in
the form of seasoning, seasoning
substitutes can play a major role in
BSN 3A | PBL GROUP 1
decreasing sodium intake. Lemon
juice, onions, and garlic are
excellent substitute flavorings,
although some patients prefer salt
substitutes. Most salt substitutes
contain potassium and must
therefore be used cautiously by
patients taking potassium-sparing
diuretics (e.g., spironolactone,
triamterene [Dyrenium], amiloride
[Midamor]). They should not be
used at all in conditions
associated with potassium
retention, such as advanced renal
disease. Salt substitutes
containing ammonium chloride
can be harmful to patients with
liver damage
 In some communities, drinking
water may contain too much
sodium for a sodium-restricted
diet. Depending on its source,
water may contain as little as 1 mg
or more than 1,500 mg of sodium
per quart. Patients may need to
use distilled water if the local water
supply is very high in sodium.
Bottled water can have a sodium
content that ranges from 0 to
1,200 mg/L; therefore, if sodium is
restricted, the label must be
carefully examined for sodium
content before purchasing and
drinking bottled water. Also,
patients on sodium-restricted diets
should be cautioned to avoid
water softeners that add sodium to
water in exchange for other ions,
such as calcium. Protein intake
may be increased in patients who
are malnourished or who have low
serum protein levels in an effort to
increase capillary oncotic
pressure and pull fluid out of the
tissues into vessels for excretion
by the kidneys.
NURSING MANAGEMENT
 Measures I&O at regular intervals to identify
excessive fluid retention
 Monitored weight daily and rapid weight gain is noted
o The patient is weighed daily, and rapid
weight gain is noted. An acute weight gain
of 1 kg (2.2 lb) is equivalent to a gain of
approximately 1 L of fluid
 Breath sounds are assessed at regular intervals in
at-risk patients, particularly if parenteral fluids are
being administered
 monitors the degree of edema in
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NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 the most dependent parts of the body, such as the
feet and ankles in ambulatory
 patients and the sacral region in patients confined to
bed
o Pitting edema is assessed by pressing a
finger into the affected part, creating a pit or
indentation that is evaluated on a scale of
1+ (minimal) to 4+ (severe).
o Peripheral edema is monitored by
measuring the circumference of the
extremity with a tape marked in millimeters
(Weber & Kelley, 2010).
PREVENTING HYPERVOLEMIA
 require sodium-restricted diets in some form, and
adherence to the prescribed diet is encouraged
 instructed to avoid over-the-counter (OTC)
medications without first checking with a health care
provider, because these substances may contain
sodium.
 If fluid retention persists despite adherence to a
prescribed diet, hidden sources of sodium, such as
the water supply or use of water softeners, should be
considered.
DETECTING AND CONTROLLING HYPERVOLEMIA
 Promote rest, restrict sodium intake, monitor
parenteral fluid therapy, and administer appropriate
medications.
 Regular rest periods may be beneficial because bed
rest favors the diuresis of fluid.
 Sodium and fluid restriction should be instituted as
indicated.
 Patients with FVE require diuretics, the patient’s
response to these agents is monitored.
 The rate of parenteral fluids and the patient’s
response to these fluids are also closely monitored
 If dyspnea or orthopnea is present, the patient is
placed in a semi-Fowler’s position to promote lung
expansion. The patient is turned and repositioned at
regular intervals because edematous tissue is more
prone to skin breakdown than normal tissue.
Note:
 conditions predisposing to FVE are likely to be
chronic, patients are taught to monitor their response
to therapy by documenting fluid I&O and body weight
changes. The importance of adhering to the
treatment regimen is emphasized.
EDUCATING PX ABOUT EDEMA
 gives special attention to edema when instructing the
patient with FVE. Edema can occur as a result of
increased capillary fluid pressure, decreased
capillary oncotic pressure, or increased interstitial
BSN 3A | PBL GROUP 1
oncotic pressure, causing expansion of the interstitial
fluid compartment
 Edema can be localized (e.g., in the ankle, as in
rheumatoid arthritis) or generalized (as in cardiac
and renal failure). Severe generalized edema is
called anasarca.
 Burns and infection are examples of conditions
associated with increased interstitial fluid volume.
 Obstruction to lymphatic outflow, a plasma albumin
level less than 1.5 to 2 g/dL, or a decrease in plasma
oncotic pressure contributes to increased interstitial
fluid volume.
 The kidneys retain sodium and water when there is
decreased ECF volume as a result of decreased
cardiac output from heart failure. A thorough
medication history is necessary to identify any
medications that could cause edema, such as
nonsteroidal anti-inflammatory drugs (NSAIDs),
estrogens, corticosteroids, and antihypertensive
agents.
o Ascites is a type of edema in which fluid
accumulates in the peritoneal cavity; it
results from nephrotic syndrome, cirrhosis,
and some malignant tumors. The patient
commonly reports shortness of breath and
a sense of pressure because of pressure on
the diaphragm.
 The goal of treatment is to preserve or restore the
circulating intravascular fluid volume. Thus, in
addition to treating the cause of the edema, other
treatments may include diuretic therapy, restriction of
fluids and sodium, elevation of the extremities,
application of anti-embolism stockings, paracentesis,
dialysis, and continuous renal replacement therapy
in cases of renal failure or life-threatening fluid
volume overload
ELECTROLYTE IMBALANCES
 An electrolyte imbalance occurs when certain
mineral levels in your blood get too high or too low.
 This imbalance may be a sign of a problem
like kidney disease.
 Electrolytes are minerals that give off an electrical
charge when they dissolve in fluids like blood and
urine. Our body makes electrolytes.
 Electrolytes in blood, tissue, urine and other body
fluids play a critical role in balancing body fluids,
regulating your heart rhythm and supporting nerve
and muscle function.
 Our kidneys and liver, as well as other organs and
tissue, continually move electrolytes in and out of
cells to adjust fluid levels within the compartments.
Certain health conditions can affect our body’s ability to
move and balance electrolytes. When fluid compartments
have too many or too few electrolytes, it can develop to an
electrolyte imbalance.
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MEDICAL-SURGICAL NURSING

FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS

COMPONENTS OF ELECTROLYTES COMPLICATIONS
 Sodium controls fluid levels and aids nerve and A significant electrolyte imbalance (either too high or too low)
muscle function. can cause serious, life-threatening problems. These
 Potassium supports heart, nerve and muscle
complications include:
functions. It also moves nutrients into cells and
waste products out of them while supporting your  Coma.
metabolism.  Seizures.
 Calcium helps blood vessels contract and expand  Sudden cardiac death (sudden cardiac arrest).
to stabilize blood pressure. It also secretes
hormones and enzymes (proteins) that help the
nervous system send messages. CLINICAL MANIFESTATIONS
 Chloride helps maintain healthy blood levels, blood
pressure and body fluids. Symptoms of an electrolyte imbalance vary depending on the
 Magnesium aids nerve and muscle function. It also severity and electrolyte type. A slight electrolyte imbalance
promotes the growth of healthy bones and teeth. may not cause noticeable changes. When problems occur,
 Phosphate supports the skeletal system, as well as
you may experience:
nerve and muscle function.
 Bicarbonate helps balance acids and basic alkaline  Confusion and irritability.
compounds (bases) in blood (pH balance).  Diarrhea or constipation.
Bicarbonate also helps move carbon dioxide (a  Fatigue.
waste product) through your bloodstream.  Headaches.
TYPES OF ELECTROLYTES  Irregular or fast heart rate (arrhythmia).
High electrolyte imbalances include:  Muscle cramps, muscle spasms or weakness.
 Nausea and vomiting.
 Sodium: Hypernatremia.  Numbness or tingling in limbs, fingers and toes.
 Potassium: Hyperkalemia.
 Calcium: Hypercalcemia.
 Chloride: Hyperchloremia. DIAGNOSTIC TEST
 Magnesium: Hypermagnesemia.
 Phosphate: Hyperphosphatemia. An electrolyte panel is a blood test that measures electrolyte
 Bicarbonate: Alkalosis (low alkaline base). levels. Healthcare providers often order an electrolyte panel
if you:

Low electrolytes or electrolyte deficiencies include:  Need blood tests for a routine physical exam.
 Are in the hospital.
 Sodium: Hyponatremia.  Have certain health conditions.
 Potassium: Hypokalemia.  Experience disease symptoms.
 Calcium: Hypocalcemia.
 Chloride: Hypochloremia.
 Magnesium: Hypomagnesemia. MEDICAL MANAGEMENT
 Phosphate: Hypophosphatemia.
 Bicarbonate: Acidosis (high acid levels).  Treatment depends on the specific electrolyte
RISK FACTORS imbalance and cause. Some imbalances will correct
without treatment.
Certain conditions can also throw off your body’s electrolyte  To treat dehydration, your provider may recommend
levels. You may be more likely to develop an electrolyte rehydrating with electrolyte drinks or an oral
imbalance if you have: rehydration salt (ORS) solution. Medical provider
can tell the correct amount of sugar, salt and water
 Burns. to make this solution at home. Or can buy ORS
 Cancer. packets at a drugstore.
 Cardiovascular disease, heart failure or high blood  Medical treatments for electrolyte imbalances
pressure. include:
 Dehydration due to not drinking enough liquids or  IV fluids like sodium chloride to rehydrate our
from excessive vomiting, diarrhea, sweating body.
(hyperhidrosis) or fever.  IV medicines to restore a healthy electrolyte
 Overhydration or water intoxication (drinking too balance.
much water).  Medications or supplements to replace lost
 Eating disorders. electrolytes.
 Kidney disease.  Hemodialysis to correct electrolyte imbalances
 Liver disease like cirrhosis. caused by kidney failure or severe kidney
 Substance use disorder. damage.
 Proper hydration can help our body maintain a
healthy level of electrolytes. It’s especially

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MEDICAL-SURGICAL NURSING

FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS

important to drink enough fluids if experience
prolonged diarrhea, vomiting or sweating.
The clinical presentation depends on the underlying etiology.
Symptoms may include:
ACID–BASE DISTURBANCES
ACUTE AND CHRONIC METABOLIC ACIDOSIS
(BASE BICARBONATE DEFICIT)
 The renal system is responsible for eliminating the
daily load of non-volatile acids, which is
approximately 70 millimoles per day. This daily load
comes primarily from anaerobic metabolism,
absorption of acids, and excretion of bases from the
GI system. Metabolic acidosis occurs when there is
an increase in the levels of new non-volatile acids
(e.g., lactic acid), renal loss of HCO3-, or ingestion of
toxic alcohols. Respiratory compensation occurs
very quickly (within minutes) and mitigates changes
in pH. In the acute period, metabolic disorders can
cause severe symptoms. Management is aimed at
correcting the underlying etiology.
 Metabolic acidosis is the process that results in the
gain of hydrogen ions (H+) or the loss of HCO3-. In
primary metabolic acidosis, arterial blood gas will
show:
 pH < 7.4
 HCO3- < 24 mEq/L
 Partial pressure of arterial CO2 (PCO2) < 40
mm Hg
PATHOPHYSIOLOGY
 Normal anion gap metabolic acidosis results from the
direct loss of bicarbonate, as in diarrhea, lower
intestinal fistulas, ureterostomies, use of diuretics,
early renal insufficiency, excessive administration of
chloride, and the administration of parenteral
nutrition without bicarbonate or
bicarbonateproducing solutes (e.g., lactate) (Emmett
& Szerlip, 2018).
 High anion gap metabolic acidosis occurs when
there is an excessive accumulation of acids. High
anion gap occurs in lactic acidosis, salicylate
poisoning (acetylsalicylic acid), renal failure,
methanol, ethylene or propylene glycol toxicity, DKA,
and ketoacidosis that occurs with starvation. The
high amount of hydrogen ions due to the acids
present are neutralized and buffered by HCO3−
causing the bicarbonate concentration to fall and
become exhausted. Other anions in the bloodstream
are called upon to neutralize the high acid in the
blood. In all of these instances, abnormally high
levels of anions are used to neutralize the H+, which
increases the anion above normal limits (high anion
gap) (Emmett & Szerlip, 2019).
CLINICAL MANIFESTATIONS
 Kussmaul respirations (slow, deep breathing)
 Diarrhea
 Ketoacidosis:
 Polyuria
 Polydipsia
 Epigastric pain
 Vomiting
 Renal failure:
 Nocturia
 Polyuria
 Pruritis
 Methanol poisoning: visual symptoms (photophobia,
scotomata, blindness)
 Salicylate overdose:
 Tinnitus
 Blurred vision
 Vertigo
ASSESSMENT AND DIAGNOSTIC FINDINGS
 ABG measurements are used in the diagnosis of
acid–base imbalances such as metabolic acidosis.
Expected ABG changes include a low bicarbonate
level (less than 22 mEq/L) and a low blood pH (less
than 7.35). The cardinal feature of metabolic acidosis
is a decrease in the serum bicarbonate level. In
conditions of acidosis there is elevated H+ and the
sodium–potassium cellular pump brings H+ into the
cells in place of K+. Therefore, high K+ accumulates
in the bloodstream in metabolic acidosis as a result
of the shift of potassium out of the cells (Theodore,
2019). Later, when the acidosis is corrected and pH
normalized, the cellular pump causes potassium to
move back into the cells and hypokalemia may
occur. Blood levels of potassium need to be closely
monitored. ECG monitoring is recommended as
changes of potassium in the bloodstream can cause
arrhythmias (Palmer & Clegg, 2016a).
 In metabolic acidosis, the lungs compensate for the
high H+ through hyperventilation to decrease the
CO2 level, which in turn reduces H+ (see carbonic
acid equation). Calculation of the anion gap is helpful
in determining the cause of metabolic acidosis.
There are certain conditions that cause high anion
gap metabolic acidosis and others that cause normal
anion gap metabolic acidosis

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MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
MEDICAL MANAGEMENT
 Treatment is directed at correcting the metabolic
imbalance. If the problem results from excessive
intake of chloride, treatment is aimed at eliminating
the source of the chloride. When necessary,
bicarbonate is given; however, the administration of
sodium bicarbonate during cardiac arrest can result
in paradoxical intracellular acidosis. Hyperkalemia
may occur with acidosis and hypokalemia with
reversal of the acidosis and subsequent movement
of potassium back into the cells. Therefore, the
serum potassium level is monitored closely, and
hypokalemia is corrected as acidosis is reversed
(Mount, 2017c)
 In chronic metabolic acidosis, low serum calcium
levels are treated before the chronic metabolic
acidosis is treated to avoid tetany resulting from an
increase in pH and a decrease in ionized calcium.
Alkalizing agents may be given. Treatment
modalities may also include hemodialysis or
peritoneal dialysis (Goltzman, 2019b)
ACUTE AND CHRONIC METABOLIC ALKALOSIS
(BASE BICARBONATE EXCESS)
 The renal system is responsible for eliminating the
daily load of non-volatile acids, which is
approximately 70 millimoles per day. This daily load
comes primarily from anaerobic metabolism,
absorption of acids, and excretion of base from the
GI system. Metabolic alkalosis develops when there
is an increase in serum HCO3- levels. Metabolic
alkalosis also occurs when there is an increased loss
of acid, either renally or through the upper GI tract
(e.g., vomiting), increased intake of HCO3-, or a
reduced ability to secrete HCO3- when needed.
Respiratory compensation occurs very quickly
BSN 3A | PBL GROUP 1
(within minutes) and mitigates changes in pH from
the primary metabolic disorder. Management is
aimed at correcting the underlying etiology.
 Metabolic alkalosis is the process that results in the
loss of hydrogen ions (H+) or the gain of HCO3-. In
primary metabolic alkalosis, arterial blood gas will
show:
 pH > 7.4
 Partial pressure of CO2 (PCO2) > 40 mm Hg
 HCO3- > 28 mEq/L
PATHOPHYSIOLOGY
 A common cause of metabolic alkalosis is severe
vomiting or gastric suction that causes loss of
stomach HCl (hydrogen and chloride ions). The
disorder also occurs in pyloric stenosis, in which only
gastric fluid is lost. Gastric fluid has an acid pH
(usually 1 to 3), and loss of this highly acidic fluid
pulls H+ ions from the bloodstream to replenish the
gastric acid. As a result, the bloodstream loses H+
ions and becomes alkalotic. Other situations
predisposing to metabolic alkalosis include those
associated with loss of potassium, such as diuretic
therapy that promotes excretion of potassium (e.g.,
thiazides, furosemide), and ACTH secretion (as in
hyperaldosteronism and Cushing’s syndrome)
(Emmett & Szerlip, 2017a; Norris, 2019).
 Hypokalemia produces alkalosis in two ways: (1)
when the bloodstream is low in K+, the nephrons
reabsorb K+ into the bloodstream and secrete H+
into the tubule fluid which is excreted in the urine and
(2) when the bloodstream is low in K+, intracellular
potassium moves out of the cells into the ECF, and
as potassium ions leave the cells, hydrogen ions
must enter to maintain electroneutrality (Mount,
2017c). Excessive alkali ingestion from antacids
containing bicarbonate or from the use of sodium
bicarbonate during cardiopulmonary resuscitation
can also cause metabolic alkalosis (Emmett &
Szerlip, 2017b).
 Chronic metabolic alkalosis can occur with long-term
diuretic therapy (thiazides or furosemide), villous
adenoma in the GI tract, external drainage of gastric
fluids, significant potassium depletion, cystic fibrosis,
and the chronic ingestion of milk and calcium
carbonate (Emmett & Szerlip, 2017b).
10
NCM112 LECTURE
MEDICAL-SURGICAL NURSING

FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS

CLINICAL MANIFESTATIONS - Licorice ingestion (glycyrrhizic acid)
- Liddle syndrome
- Bartter and Gitelman syndromes
o Severe hypokalemia (K+ < 2)
 Other tests:
 Basic metabolic panel (BMP):
o Allows assessment of HCO3-
o Important for managing electrolytes,
especially K+
 Arterial blood gas
The clinical presentation is dependent on the underlying  Testing relevant to the suspected underlying
etiology. Symptoms may include: etiology
 Vomiting
 BP abnormalities: MEDICAL MANAGEMENT
 Hypertension (primary mineralocorticoid
excess) Treatment is aimed at the underlying etiology.
 Hypotension (↓ effective circulating volume)  Attempt to improve renal HCO3- excretion to resolve
 Hypokalemia alkalosis:
 Hypocalcemia:  In patients without edema (true volume
depletion): volume repletion with isotonic
saline
 Tetany  In patients with ↓ effective circulating volume
 Chvostek sign: contraction of facial muscles (e.g., heart failure):
when the facial nerve is tapped o Potassium chloride
 Trousseau sign: carpopedal spasm with o K+-sparing diuretics (e.g., amiloride)
inflation of the BP cuff ​
 Changes in mental status/seizures o Avoid isotonic saline as it will worsen
symptoms without improving alkalosis.
 Findings consistent with a prerenal state:
 Congestive heart failure:  Correct electrolyte abnormalities, especially:
 K+
-Chest pain
 Cl-
-Dyspnea on exertion
-↑ Jugular venous distension  Na+ (through fluid management)
-Pulmonary edema(crackleson lung exam)  Consider dialysis in patients with CKD.
-Peripheral edema ACUTE AND CHRONIC RESPIRATORY ACIDOSIS
 Cirrhosis: (CARBONIC ACID EXCESS)
 Jaundice
 Ascites  The respiratory system is responsible for eliminating
 Hepatomegaly with/without splenomegaly the volatile acid carbon dioxide (CO2), which is
 Telangiectasias produced via aerobic metabolism. The body
produces approximately 15,000 mmol of CO2 daily,
DIAGNOSTIC FINDINGS
which is the majority of daily acid production; the
 The etiology of metabolic alkalosis is usually remainder of the daily acid load (only about 70 mmol
ascertainable from the history alone. Urine Cl- can of nonvolatile acids) is excreted through the kidneys.
be helpful in cases in which the patient is reluctant to In the setting of hypoventilation, this acid load is not
provide a full history (e.g., self-induced vomiting in adequately blown off, and respiratory acidosis
eating disorders) or for less common etiologies (e.g., occurs. Renal compensation occurs after 3–5 days,
Conn, Bartter, and Gitelman syndromes). as the kidneys attempt to increase the serum
bicarbonate levels. Patients are often asymptomatic,
 Urine chloride: or they may present with neuropsychiatric
 Urine Cl- < 20 mEq/L: body Cl- is also manifestations or mild dyspnea. Diagnosis is made
depleted, typically in volume depletion: with arterial blood gas measurement. Management
involves treating the underlying etiology, stabilizing
o Vomiting
the patient, and avoiding respiratory sedatives.
o Nasogastric suction
 Urine Cl- > 20 mEq/L: Body Cl- level is  Respiratory acidosis is the process that results in an
normal, typically in patients with volume accumulation of carbon dioxide (CO2) due to
expansion: abnormal gas exchange in the lungs. In primary
respiratory acidosis, the arterial blood gas will show:
o Mineralocorticoid excess:
- Cushing's syndrome (hypercortisolism)  pH < 7.35
-Conn syndrome (primary hyperaldosteronism)

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NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 PCO2 (partial pressure of carbon dioxide) >
45 mm Hg (i.e., hypercapnia)
PATHOPHYSIOLOGY
 Respiratory acidosis is due to inadequate excretion
of CO2 with inadequate ventilation, resulting in
elevated plasma CO2 concentrations and,
consequently, increased levels of carbonic acid. In
addition to an elevated PaCO2, inadequate
ventilation usually causes a decrease in PaO2. Acute
respiratory acidosis occurs in emergency situations,
such as acute pulmonary edema, aspiration of a
foreign object, atelectasis, pneumothorax, and
overdose of sedatives, as well as in nonemergent
situations, such as sleep apnea associated with
severe obesity, severe pneumonia, and acute
respiratory distress syndrome. Respiratory acidosis
commonly occurs in patients with severe chronic
obstructive pulmonary disease (COPD) when
patients acutely decompensate due to respiratory
infection or heart failure. Respiratory acidosis can
also occur in diseases that impair respiratory muscle
function and cause hypoventilation. These disorders
include severe scoliosis, muscular dystrophy,
multiple sclerosis, myasthenia gravis, and Guillain-
Barré syndrome (Feller-Kopman & Schwartzstein,
2017).
CLINICAL MANIFESTATIONS
 Clinical presentation of hypercapnia:
 Neurologic:
o Anxiety/paranoia
o Headaches
o Somnolence
o Delirium
o Coma
 Pulmonary: dyspnea (usually mild)
 Diagnosis: primarily with an arterial blood gas (ABG):
 Acute respiratory acidosis:
o pH < 7.35
o PaCO2 > 45 mm Hg
o Normal HCO3–
 Chronic respiratory acidosis (compensated):
o pH < 7.4 (low or near-normal)
o PaCO2 > 45 mm Hg
o HCO3– elevated
ASSESSMENT AND DIAGNOSTIC FINDINGS
 In respiratory acidosis, ABG analysis reveals a pH
less than 7.35, a PaCO2 greater than 45 mm Hg, and
variation in the bicarbonate level, depending on the
duration of the acute respiratory acidosis. When
compensation occurs over a prolonged period and
renal retention of bicarbonate has fully occurred, the
bicarbonate neutralizes the acidosis. Arterial pH is
within the lower limits of normal (e.g., pH 7.35).
Depending on the cause of respiratory acidosis,
BSN 3A | PBL GROUP 1
other diagnostic measures include monitoring of
serum electrolyte levels, chest x-ray for determining
respiratory infection or other disease, and a drug
screen if an overdose is suspected. ECG monitoring
is recommended to identify any cardiac involvement
as a result of COPD (Feller-Kopman &
Schwartzstein, 2017).
MEDICAL MANAGEMENT
 Assess the ABCs:
 Ensure that the airway is secure.
 Administer supplemental O2.
 Ventilatory support as needed
 Treat the underlying etiology; examples include:
 COPD exacerbation: bronchodilators and
corticosteroids
 Pneumonia in neuromuscular disorders:
antibiotics
 Avoid respiratory sedatives.
ACUTE AND CHRONIC RESPIRATORY ALKALOSIS
(CARBONIC ACID DEFICIT)
 The respiratory system is responsible for eliminating
the volatile acid carbon dioxide (CO2), which is
produced via aerobic metabolism. The body
produces approximately 15,000 mmol of CO2 daily,
which is the majority of daily acid production; the
remainder of the daily acid load (only about 70 mmol
of nonvolatile acids) is excreted through the kidneys.
When hyperventilation occurs, excess carbon
dioxide is blown off and respiratory alkalosis
​
 develops. The kidneys respond by decreasing serum
bicarbonate (HCO3–) through increased HCO3–
excretion or decreased excretion of H+. Patients
present with an increased respiratory rate, dyspnea,
light-headedness and potentially psychologic
symptoms. Diagnosis involves a thorough history, an
exam, and an arterial blood gas measurement.
Management focuses on addressing the underlying
abnormalities, stabilizing patients in acute distress,
and potentially a small dose of short-acting
benzodiazepines.
 Respiratory alkalosis refers to the process that
results in a decreased level of carbon dioxide (CO2)
within the blood.
PATHOPHYSIOLOGY
 Respiratory alkalosis is caused by hyperventilation,
which causes excessive loss or “blowing off” of CO2
and, hence, there is a decrease in the plasma
carbonic acid concentration (see carbonic acid
equation). Causes include extreme anxiety such as
panic disorder, hypoxemia, salicylate intoxication,
gram-negative sepsis, and inappropriate ventilator
settings.
12
NCM112 LECTURE
MEDICAL-SURGICAL NURSING

FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS

 Chronic respiratory alkalosis results from chronic MIXED ACID–BASE DISORDERS
hypocapnia which leads to decreased serum H+ ion,
resulting in alkalosis. Chronic hepatic insufficiency  Patients can simultaneously experience two or more
and cerebral tumors can cause chronic independent acid–base disorders. A normal pH in the
hyperventilation that leads to chronic respiratory presence of changes in the PaCO2 and plasma
alkalosis (Schwartzstein, Richards, Edlow, et al., HCO3− concentration immediately suggests a mixed
2018) disorder. An example of a mixed disorder is the
simultaneous occurrence of metabolic acidosis due
CLINICAL MANIFESTATIONS to lactic acid accumulation and respiratory acidosis
due to hypoventilation. Both of these disorders result
 Tachypnea in excessive acid accumulation in the bloodstream
 Dyspnea due to respiratory failure and cardiac arrest (Emmett
 Dizziness/light-headedness & Palmer, 2018b).
 Paresthesias (perioral, hands/feet) due to decreased
ionized calcium COMPENSATION
 Psychologic symptoms:
 Anxiety  Generally, the pulmonary and renal systems
 Fear compensate for each other to return the pH to
 Impending doom normal. In a single acid–base disorder, the system
 Highly variable presentation, based on underlying not causing the problem tries to compensate by
etiology; for example: returning the ratio of bicarbonate to carbonic acid to
 High-altitude illness: findings consistent with the normal 20:1. The lungs compensate for
pulmonary and/or cerebral edema metabolic disturbances by changing CO2 excretion;
 Sepsis: fever, hypotension, findings hypoventilation accumulates CO2, hyperventilation
consistent with originating infection (e.g., causes loss of CO2. The kidneys compensate for
cough or dysuria) respiratory disturbances by altering bicarbonate
 Pulmonary embolism: calf pain, unilateral reabsorption and H+ secretion (Norris, 2019;
lower-extremity edema Theodore, 2019).
 In respiratory acidosis, excess hydrogen in the blood
DIAGNOSTIC FINDINGS is excreted in the urine in exchange for bicarbonate
ions which are conserved. In respiratory alkalosis,
Diagnosing a respiratory alkalosis typically requires a the renal excretion of bicarbonate increases, and
thorough history and exam and an arterial blood gas hydrogen ions are retained. In metabolic acidosis,
measurement. the lungs compensate by increasing the ventilation
 Arterial blood gas: rate and the kidneys retain bicarbonate. In metabolic
 Acute respiratory alkalosis (uncompensated): alkalosis, the respiratory system compensates by
o pH > 7.45 decreasing ventilation to conserve CO2 and increase
o PaCO2 < 35 mm Hg the PaCO2, which in turn increases carbonic acid.
o Normal HCO3– Because the lungs respond to acid–base disorders
 Chronic respiratory alkalosis (compensated): within minutes, compensation for metabolic
imbalances occurs faster than renal compensation
o pH > 7.4 (slightly high or near-normal) for respiratory imbalances (Norris, 2019; Theodore,
o PaCO2 < 35 mm Hg 2019).
o HCO3– decreased
 Electrolytes: Abnormalities are common and may BLOOD GAS ANALYSIS
lead to complications.
 Basic metabolic panel  Blood gas analysis is often used to identify the
 Magnesium specific acid–base disturbance and the degree of
 Phosphate compensation that has occurred. The analysis is
 Chest X-ray: to rule out other causes of tachypnea usually based on an arterial blood sample; however,
if an arterial sample cannot be obtained, a mixed
MEDICAL MANAGEMENT venous sample may be used (Theodore, 2019).
Results of ABG analysis provide information about
 Assess and address the ABCs (airway, breathing, alveolar ventilation, oxygenation, and acid–base
and circulation) if patient is in acute distress.
balance. It is necessary to evaluate the
 Attempt to correct the underlying abnormality. concentrations of serum electrolytes (e.g., sodium,
 Small dose of short-acting benzodiazepine potassium, chloride) along with ABG data because
electrolytes are commonly affected by acid–base
imbalances. The health history, physical
examination, previous blood gas results, and serum

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NCM112 LECTURE
MEDICAL-SURGICAL NURSING

FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS

electrolytes should always be part of the assessment
used to determine the cause of the acid–base
disorder (Larkin & Zimmanck, 2015). Responding to
isolated sets of blood gas results without these data
can lead to serious errors in interpretation. Treatment
of the underlying condition usually corrects acid–
base disorders.

PARENTERAL FLUID THERAPY

 When patients cannot take oral fluid or oral feedings,

their status is termed NPO (nil per os), meaning
nothing by mouth.
 In patients who are NPO, parenteral fluid therapy,
also termed IV fluid therapy, is used to administer
fluids. IV fluid therapy can be initiated to replace
fluids in various clinical settings such as hospitals,
outpatient diagnostic and surgical settings, clinics,
and home health care. IV fluids can also be used to
administer medications and provide nutrients.

PURPOSE

 The choice of an IV solution depends on the purpose

of its administration. Generally, IV fluids are given to
achieve one or more of the following goals:

 To provide water, electrolytes, and nutrients to

meet daily requirements.
 To replace water and correct electrolyte
deficits.
 To administer medications and blood
products.

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NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 IV solutions contain dextrose and/or electrolytes
mixed in various proportions with water. Pure,
electrolyte-free water can never be given by IV
because it rapidly enters RBCs and causes them to
rupture
TYPES OF INTRAVENOUS SOLUTIONS
 IV solutions are categorized as isotonic, hypotonic,
or hypertonic, according to whether their total
osmolality is the same as, less than, or greater than
that of blood, respectively.
 Electrolyte solutions are considered isotonic if the
total electrolyte content (anions + cations) is between
250 and 375 mEq/L, hypotonic if the total electrolyte
content is less than 250 mEq/L, and hypertonic if the
total electrolyte content is greater than 375 mEq/L.
ISOTONIC FLUIDS
 Fluids that are classified as isotonic have a total
osmolality close to that of the ECF and do not cause
cells to shrink or swell.
 When isotonic fluids are administered they expand
the ECF volume.
 An isotonic solution is a crystalloid solution (water
containing soluble mineral salts).
 Plasma is a colloidal solution. A colloidal solution is
a mixture of fluid containing insoluble large particles,
such as proteins.
 Colloidal solutions exert oncotic pressure;
crystalloids do not exert oncotic pressure
Note: It is important for the nurse to recognize that in
blood loss, 3 L of isotonic fluid (crystalloid solution)
is needed to replace 1 L of
blood (colloidal solution).
 Isotonic fluids expand the water volume in the
intravascular space, patients with heart failure or
hypertension who receive isotonic solutions should
be carefully monitored for signs of fluid overload.
D5W
 A solution of D5W is unique in that it may be both
isotonic and hypotonic.
 It is essential to consider this action of D5W,
especially if the patient is at risk for increased
intracranial pressure.
 During fluid resuscitation, this solution should not be
used because hyperglycemia can result.
 Therefore, D5W is used mainly to supply water and
to correct an increased serum osmolality.
 About 1 L of D5W provides less than 170 kcal and is
a minor source of the body’s daily caloric
requirements.
BSN 3A | PBL GROUP 1
NORMAL SALINE SOLUTION
 Normal saline (0.9% sodium chloride) solution
contains water, sodium, and chloride.
 Because the osmolality is entirely contributed by
electrolytes, the solution remains within the ECF and
expands the intravascular volume.
 For this reason, normal saline solution is often used
to correct an extracellular volume deficit but is not
identical to ECF.
 It is used with administration of blood transfusions
and to replace large sodium losses, such as in burn
injuries.
 It should not be used in heart failure, pulmonary
edema, renal impairment, or sodium retention.
 Normal saline does not supply calories.
OTHER ISOTONIC SOLUTION
 Several other solutions contain ions in addition to
sodium and chloride and are somewhat similar to the
ECF in composition.
 Lactated Ringer’s solution contains potassium and
calcium in addition to sodium chloride.
 It is used to correct dehydration, blood loss, and
sodium depletion and to replace GI losses.
HYPOTONIC SOLUTIONS
 One purpose of hypotonic solution is to replace fluid,
because it is hypotonic compared with plasma.
 Another purpose of hypotonic solution is to provide
free water. At times, hypotonic sodium solutions are
used to treat hypernatremia and other hyperosmolar
conditions.
 Half-strength saline (0.45% sodium chloride) solution
is frequently used.
 Patients with any type of cardiac implantable
electronic device need to be screened to determine
if they can safely undergo MRI.
 The nurse should educate the patient regarding what
to expect during and after the procedure.
 The patient should be prepared to lie on a cold, hard
table that slides into an enclosed small tube.
 The nurse should inform the patient that they will
hear noises, including periodic banging and popping
sounds.
 Patients with claustrophobia may be prescribed a
sedative prior to the procedure.
 Patients should be instructed to close their eyes
before entering the tube, and to keep them closed,
as this may decrease claustrophobic symptoms.
HYPERTONIC FLUIDS
 Hypertonic fluids include 3% NaCl and IV mannitol.
15
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 If a patient is sodium depleted, a hypertonic sodium
IV solution might be used.
 If a patient is experiencing acute cerebral edema, IV
mannitol is often used
 Hypertonic solutions pull water from the interstitial
and intracellular compartments into the bloodstream.
These solutions draw water out of intracellular
compartments causing cellular dehydration.
 Normal saline and lactated Ringer’s solution are
considered isotonic solutions. When 5% dextrose
(D5W) is added to normal saline solution or lactated
Ringer’s solution, the total osmolality exceeds that of
the ECF.
 Saline solutions are also available in osmolar
concentrations greater than that of the ECF.
 These solutions draw water from the ICF to the ECF
and cause cells to shrink.
 As a result, these solutions must be given cautiously
and usually only when the serum osmolality has
decreased to dangerously low levels.
 Hypertonic solutions exert an osmotic pressure
greater than that of the ECF.
OTHER INTRAVENOUS THERAPIES
 When the patient is unable to tolerate food,
nutritional requirements are often met using the IV
route.
 Solutions may include high concentrations of glucose
(such as 50% dextrose in water), protein, or fat to
meet nutritional requirements.
 Many medications are also delivered by the IV route,
either by continuous infusion or by intermittent bolus
directly into the vein.
 Because IV medications enter the circulation rapidly,
administration by this route is potentially hazardous
Note: The nurse must assess the patient for a history
of allergic reactions to medications. Although
obtaining drug allergy information is important when
administering any medication,
It is especially critical with IV administration, because
the medication is delivered directly into the
bloodstream. This can trigger an immediate
hypersensitivity reaction.
NURSING MANAGEMENT OF THE PATIENT RECEIVING
INTRAVENOUS THERAPY
 In many settings, the ability to perform venipuncture
to gain access to the venous system for
administering fluids and medication is an expected
nursing skill.
 This responsibility includes selecting the appropriate
venipuncture site and type of cannula and being
proficient in the technique of vein entry.
BSN 3A | PBL GROUP 1
FLUID OVERLOAD
 Overloading the circulatory system with excessive IV
fluids causes increased blood pressure and central
venous pressure.
 Signs and symptoms of fluid overload include moist
crackles on auscultation of the lungs, cough,
restlessness, distended neck veins, edema, weight
gain, dyspnea, and rapid, shallow respirations.
 Its treatment includes decreasing the IV rate,
monitoring vital signs frequently, assessing breath
sounds, and placing the patient in a high Fowler
position.
 The primary provider is contacted immediately. This
complication can be avoided by using an infusion
pump and by carefully monitoring all infusions.
AIR EMBOLISM
 It is most often associated with cannulation of central
veins and directly related to the size of the embolus
and the rate of entry.
 Air entering into central veins gets to the right
ventricle, where it lodges against the pulmonary
valve and blocks the flow of blood from the ventricle
into the pulmonary arteries.
 Treatment calls for immediately clamping the
cannula and replacing a leaking or open infusion
system, placing the patient on the left side in the
Trendelenburg position, assessing vital signs and
breath sounds, and administering oxygen.
 Air embolism can be prevented by using locking
adapters on all lines, filling all tubing completely with
solution, and using an air detection alarm on an IV
infusion pump.
PHLEBITIS
 Phlebitis, or inflammation of a vein, can be
categorized as chemical, mechanical, or bacterial;
however, two or more of these types of irritation often
occur simultaneously.
 Phlebitis can be prevented by using aseptic
technique during insertion, using the appropriate
size cannula or needle for th vein, considering the
composition of fluids and medications when
selecting a site, observing the site hourly for any
complications, anchoring the cannula or needle well,
and changing the IV site according to agency policy
and procedures.
THROMBOPHLEBITIS
 Thrombophlebitis refers to the presence of a clot plus
inflammation in the vein.
 Treatment includes discontinuing the IV infusion;
applying a cold compress first to decrease the flow
16
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
of blood, followed by a warm compress; elevating the
extremity; and restarting the line in the opposite
extremity.
 If the patient has signs and symptoms of
thrombophlebitis, the IV line should not be flushed
(although flushing may be indicated in the absence
of phlebitis to ensure cannula patency and to prevent
mixing of incompatible medications and solutions).
HEMATOMA
 Hematoma results when blood leaks into tissues
surrounding the IV insertion site.
 Leakage can result if the vein wall is perforated
during venipuncture, the needle slips out of the vein,
a cannula is too large for the vessel, or insufficient
pressure is applied to the site after removal of the
needle or cannula.
 Treatment includes removing the needle or cannula
and applying light pressure with a sterile, dry
dressing; applying ice for 24 hours to the site to avoid
extension of the hematoma; elevating the extremity
to maximize venous return, if tolerated; assessing
the extremity for any circulatory, neurologic, or motor
dysfunction; and restarting the line in the other
extremity if indicated.
CLOTTING AND OBSTRUCTION
 Blood clots may form in the IV line as a result of
kinked IV tubing, a very slow infusion rate, an empty
IV bag, or failure to flush the IV line after intermittent
medication or solution administrations.
 If blood clots in the IV line, the infusion must be
discontinued and restarted in another site with a new
cannula and administration set.
 The tubing should not be irrigated or milked. Neither
the infusion rate nor the solution container should be
raised, and the clot should not be aspirated from the
tubing.
 Clotting of the needle or cannula may be prevented
by not allowing the IV solution bag to run dry, taping
the tubing to prevent kinking and maintain patency,
maintaining an adequate flow rate, and flushing the
line after intermittent medication or other solution
administration.
KIDNEY DISORDERS
CHRONIC KIDNEY DISEASE
 Chronic kidney disease (CKD) is a long-term
condition in which the kidneys are damaged and
cannot filter blood as effectively as they should. This
leads to a build-up of waste and fluid in the body,
which can cause a range of symptoms and
complications over time. CKD is typically diagnosed
BSN 3A | PBL GROUP 1
based on measures of kidney function and urine
tests, and it is classified into stages based on the
level of kidney damage and the degree of reduction
in the glomerular filtration rate (GFR). The condition
can be caused by a variety of factors, including
diabetes, high blood pressure, and certain genetic or
autoimmune disorders. Treatment may include
medications, lifestyle changes, and in severe cases,
dialysis or kidney transplantation.
PATHOPHYSIOLOGY
 Chronic kidney disease (CKD) is a progressive and
irreversible deterioration in renal function, with the
loss of nephrons, the functional unit of the kidney,
over time. The pathophysiology of CKD involves
complex interactions between different factors,
including genetic, environmental, and metabolic
factors. The most common causes of CKD are
diabetes and hypertension, which can lead to
damage to the small blood vessels and the nephrons
in the kidneys. Other causes include
glomerulonephritis, polycystic kidney disease, and
obstructive uropathy. As the nephrons are damaged,
the kidneys' ability to filter waste products and
excess fluid from the blood is reduced, leading to a
build-up of toxic substances in the body. This can
cause a variety of symptoms, including fatigue,
weakness, nausea, and fluid retention. In addition to
the loss of renal function, CKD can also lead to a
number of other complications, including anemia,
bone disease, and cardiovascular disease. These
complications are thought to be related to a
combination of factors, including inflammation,
oxidative stress, and altered hormone levels. Overall,
CKD is a complex and multifactorial condition that
requires ongoing management and monitoring to
prevent further kidney damage and to manage its
associated complications.
RISK FACTORS
 Diabetes: Diabetes is the leading cause of CKD.
High blood sugar levels can damage blood vessels
in the kidneys, making them less effective at filtering
waste.
 High blood pressure: High blood pressure damages
the blood vessels in the kidneys and can lead to
CKD.
 Family history of kidney disease: If you have a family
history of kidney disease, you may be at increased
risk of developing CKD.
 Age: The risk of CKD increases as you get older.
 Smoking: Smoking damages blood vessels
throughout the body, including those in the kidneys,
and can increase the risk of CKD.
 Obesity: Being overweight or obese can increase the
risk of CKD.
17
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 Cardiovascular disease: People with cardiovascular
disease are at increased risk of developing CKD.
 Certain ethnic groups: African Americans, Native
Americans, and Hispanics are at higher risk of
developing CKD than other ethnic groups.
 Prolonged use of certain medications: Some
medications, such as nonsteroidal anti-inflammatory
drugs (NSAIDs), can damage the kidneys if used for
long periods.
CLINICAL MANIFESTATIONS
 Fatigue and weakness: As the kidneys become less
effective at removing waste products, toxins can
build up in the body, causing fatigue and weakness.
 Fluid retention: The kidneys play a key role in
regulating the body's fluid balance. As they become
damaged, fluid can build up in the body, leading to
swelling in the legs, ankles, feet, and face.
 High blood pressure: The kidneys are also involved
in regulating blood pressure. When they are
damaged, blood pressure can rise.
 Decreased urine output: As CKD progresses, the
kidneys may produce less urine or stop producing
urine altogether.
 Changes in urine: Urine may be foamy or contain
blood or protein as a result of kidney damage.
 Anemia: The kidneys produce a hormone called
erythropoietin that stimulates the production of red
blood cells. As the kidneys become damaged, they
produce less erythropoietin, leading to anemia.
 Bone disease: CKD can lead to bone disease
because the kidneys are involved in regulating
calcium and phosphorus levels in the body.
 Itching: Build-up of waste products in the blood can
cause skin itching.
 Nausea and vomiting: As toxins build up in the body,
it can cause nausea and vomiting.
 Shortness of breath: As fluid builds up in the lungs, it
can cause shortness of breath.
ASSESSMENT AND DIAGNOSTIC FINDINGS
 Medical history: A complete medical history is
important in the diagnosis of CKD. Risk factors for
CKD, such as diabetes, high blood pressure, family
history of kidney disease, and previous kidney
infections or diseases, will be assessed.
 Physical examination: A physical examination will be
conducted to check for signs of kidney disease, such
as high blood pressure, swelling in the legs or ankles,
and anemia.
 Blood tests: Blood tests, such as a complete blood
count (CBC), serum creatinine, and blood urea
nitrogen (BUN), will be conducted to measure the
levels of waste products in the blood. An abnormal
result could indicate kidney damage or disease.
 Urine tests: Urine tests, such as a urinalysis and
urine albumin-to-creatinine ratio (ACR), will be
BSN 3A | PBL GROUP 1
conducted to check for protein or blood in the urine,
which can be a sign of kidney damage.
 Imaging tests: Imaging tests, such as an ultrasound,
CT scan, or MRI, may be conducted to check the size
and shape of the kidneys and to detect any
abnormalities or blockages.
 Kidney biopsy: A kidney biopsy may be performed to
obtain a sample of kidney tissue for analysis if the
cause of CKD is uncertain.
MANAGEMENT AND TREATMENT
 Medications: Medications may be prescribed to treat
conditions that can cause kidney damage, such as
high blood pressure, diabetes, and high cholesterol.
Medications may also be used to control symptoms
associated with CKD, such as anemia and bone
disease.
 Dietary changes: A diet low in sodium, protein, and
phosphorus can help reduce the workload on the
kidneys and prevent further damage. It is also
important to consume enough calories to maintain a
healthy weight and to limit the intake of fluids.
 Blood pressure control: High blood pressure is a
common complication of CKD and can worsen
kidney damage. Controlling blood pressure through
medication, lifestyle changes, and regular monitoring
is essential to prevent further damage.
 Blood sugar control: For people with diabetes,
maintaining tight control of blood sugar levels is
essential to prevent or slow the progression of CKD.
 Regular monitoring: Regular check-ups with a
healthcare provider are important to monitor kidney
function and to adjust treatment plans as needed.
 Dialysis: In advanced stages of CKD, when the
kidneys are no longer able to function properly,
dialysis may be necessary to filter waste products
from the blood.
 Kidney transplant: For some people with advanced
CKD, a kidney transplant may be an option. This
involves surgically implanting a healthy kidney from
a donor.
NURSING INTERVENTIONS
 Monitor and manage fluid and electrolyte balance:
CKD can affect the body's ability to regulate fluid and
electrolyte levels, leading to imbalances. Nurses
should monitor the patient's fluid intake and output,
assess for signs of fluid overload or dehydration, and
administer IV fluids and medications as needed to
maintain electrolyte balance.
 Control blood pressure: High blood pressure is a
common complication of CKD and can further
damage the kidneys. Nurses should monitor blood
pressure regularly and administer antihypertensive
medications as prescribed.
18
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 Administer medications as prescribed: Patients with
CKD may require medications to manage symptoms,
control blood pressure, and reduce the risk of
complications. Nurses should ensure that patients
are taking their medications as prescribed and
monitor for any adverse reactions.
 Monitor and manage nutrition: Patients with CKD
may have specific dietary needs, such as limiting
protein, phosphorus, and potassium intake. Nurses
should work with a registered dietician to develop a
nutrition plan that meets the patient's needs and
provide education on how to manage their diet.
 Manage anemia: CKD can lead to anemia, which can
cause fatigue and weakness. Nurses should monitor
the patient's hemoglobin levels and administer
erythropoietin-stimulating agents or iron
supplements as prescribed.
 Educate patients on self-care: Patients with CKD
need to be involved in their care and understand how
to manage their condition. Nurses should provide
education on self-care, such as monitoring blood
pressure, managing medications, and following a
renal diet.
 Monitor and manage dialysis: Patients with
advanced CKD may require dialysis to filter waste
and excess fluid from the blood. Nurses should
monitor the patient during dialysis and assess for any
complications, such as infection or hypotension.
 Assess and manage complications: CKD can lead to
a variety of complications, such as cardiovascular
disease, anemia, and bone disease. Nurses should
assess for these complications and implement
appropriate interventions to manage them.
NEPHROTIC SYNDROME
 Nephrotic syndrome is a condition characterized by
high levels of protein in the urine (proteinuria), low
levels of protein in the blood, swelling (edema), and
high levels of cholesterol and triglycerides. It is
usually caused by damage to the tiny blood vessels
in the kidneys, which can lead to the loss of large
amounts of protein in the urine. The condition can be
caused by a variety of underlying health problems,
such as diabetes, lupus, and certain infections or
medications. Nephrotic syndrome is typically treated
with medications that help reduce proteinuria and
inflammation, as well as other supportive measures
such as dietary changes and rest.
PATHOPHYSIOLOGY
 The pathophysiology of nephrotic syndrome involves
damage to the glomeruli, which are tiny blood
vessels in the kidneys responsible for filtering waste
products and excess fluid from the blood. This
damage may be due to various causes, such as
immune system disorders, infections, medications,
BSN 3A | PBL GROUP 1
and underlying medical conditions such as diabetes
and lupus. When the glomeruli are damaged, they
become more permeable to protein, allowing protein
to leak out of the blood and into the urine. This results
in decreased levels of protein in the blood, leading to
a drop in the oncotic pressure (the pressure that
keeps fluid inside the blood vessels) and the
development of edema. The liver responds to the low
protein levels by producing more proteins, including
cholesterol and triglycerides, leading to their
increased levels in the blood. In addition to
proteinuria, other common features of nephrotic
syndrome include hypoalbuminemia (low levels of
the protein albumin in the blood), hyperlipidaemia
(high levels of lipids such as cholesterol and
triglycerides in the blood), and edema. Treatment of
nephrotic syndrome depends on the underlying
cause and may include medications to control blood
pressure, reduce proteinuria, and prevent
complications such as infections and blood clots.
RISK FACTORS
 Primary glomerular disease: This is the most
common cause of nephrotic syndrome, and it occurs
when the small blood vessels in the kidneys become
inflamed and damaged. The primary glomerular
diseases that can lead to nephrotic syndrome include
minimal change disease, focal segmental
glomerulosclerosis (FSGS), and membranous
nephropathy.
 Secondary glomerular disease: This is a less
common cause of nephrotic syndrome, and it occurs
as a result of an underlying medical condition such
as diabetes, lupus, or amyloidosis.
 Infections: Certain infections, such as hepatitis B and
C, HIV, and malaria, can increase the risk of
developing nephrotic syndrome.
 Medications: Some medications, such as
nonsteroidal anti-inflammatory drugs (NSAIDs),
antibiotics, and ACE inhibitors, can increase the risk
of developing nephrotic syndrome.
 Genetic factors: Certain genetic mutations can
increase the risk of developing nephrotic syndrome,
such as mutations in the NPHS1, NPHS2, and WT1
genes.
 Age: Nephrotic syndrome is more common in
children than in adults.
 Gender: Boys are more likely to develop nephrotic
syndrome than girls.
 Race and ethnicity: Nephrotic syndrome is more
common in people of African American, Hispanic,
and Asian descent than in Caucasians.
CLINICAL MANIFESTATIONS
 Edema: One of the most common clinical
manifestations of nephrotic syndrome is edema or
swelling. It usually starts in the lower extremities,
19
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
such as the ankles and feet, and can spread to other
parts of the body, including the face and abdomen.
 Proteinuria: Nephrotic syndrome is also
characterized by proteinuria, which means that large
amounts of protein are excreted in the urine. This
results in foamy urine and can lead to low protein
levels in the blood.
 Hypoalbuminemia: As a result of proteinuria, the
level of albumin, a protein made by the liver that
helps to maintain the fluid balance in the body,
decreases in the blood, leading to hypoalbuminemia.
 Hyperlipidaemia: Nephrotic syndrome can also
cause an increase in the level of lipids, such as
cholesterol and triglycerides, in the blood.
 Fatigue and weakness: Due to the loss of protein in
the urine, the body may not have enough protein to
maintain muscle mass, leading to fatigue and
weakness.
 Decreased urine output: In some cases, nephrotic
syndrome can lead to decreased urine output or
oliguria.
 Increased risk of infections: As a result of decreased
levels of immunoglobulin’s in the blood, patients with
nephrotic syndrome are at an increased risk of
developing infections.
ASSESSMENT AND DIAGNOSTIC FINDINGS
 Medical history: The healthcare provider will ask
about the patient's medical history, including any
past or present kidney problems, infections, or other
medical conditions.
 Physical exam: The healthcare provider will perform
a physical exam to look for signs of swelling,
particularly in the legs, feet, and ankles. They will
also listen to the patient's lungs and heart to check
for signs of fluid buildup.
 Urine tests: Urine tests are done to measure the
amount of protein in the urine. A 24-hour urine
collection may be done to get an accurate
measurement of protein excretion.
 Blood tests: Blood tests are done to measure the
level of protein, cholesterol, and triglycerides in the
blood. Blood tests may also be done to check for
kidney function and to look for signs of infections or
other medical conditions.
 Kidney biopsy: A kidney biopsy is a procedure in
which a small piece of kidney tissue is removed and
examined under a microscope to look for signs of
damage or disease.
 Imaging tests: Imaging tests such as ultrasound, CT
scan, or MRI may be done to check for signs of
kidney damage or to look for other possible causes
of the patient's symptoms.
MANAGEMENT AND TREATMENT
 is a rapid loss of renal function due to damage to the
 Medications: The mainstay of treatment for nephrotic
syndrome is medication. The most commonly used
BSN 3A | PBL GROUP 1
drugs are corticosteroids, such as prednisone, which
help reduce inflammation and decrease proteinuria.
Other medications that may be used include
diuretics, ACE inhibitors, and angiotensin receptor
blockers.
 Dietary changes: Dietary changes, such as reducing
salt intake, may be recommended to help control
edema and hypertension, which are common
complications of nephrotic syndrome.
 Immunosuppressive therapy: If the underlying cause
of nephrotic syndrome is an autoimmune disorder,
such as lupus or vasculitis, immunosuppressive
therapy may be prescribed to suppress the immune
system and reduce inflammation.
 Plasmapheresis: In some cases, plasmapheresis, a
procedure in which the plasma is removed from the
blood and replaced with a protein solution, may be
recommended to remove excess antibodies and
other proteins from the blood.
 Kidney transplant: If nephrotic syndrome is caused
by irreversible kidney damage, a kidney transplant
may be the best option for treatment.
NURSING INTERVENTIONS
 Monitor fluid and electrolyte balance: Monitor the
patient's intake and output, assess the patient's fluid
status, and monitor for signs of electrolyte
imbalances such as hyperkalemia and hyponatremia.
 Administer medications: Administer medications as
ordered by the healthcare provider, such as diuretics
to manage edema, angiotensin-converting enzyme
(ACE) inhibitors to lower blood pressure, and
immunosuppressant medications to manage
inflammation.
 Monitor vital signs: Monitor the patient's blood
pressure, pulse rate, and respiratory rate regularly,
as hypertension is a common complication of
nephrotic syndrome.
 Assess for edema: Assess the patient for edema,
particularly in the face, legs, and feet. Measure and
document the circumference of affected body parts,
and monitor the patient's weight daily.
 Promote skin integrity: Keep the skin clean and dry,
and apply moisturizing lotion to prevent cracking and
dryness.
 Provide education: Educate the patient on the
importance of adhering to medication regimens,
following a low-sodium diet, and monitoring their fluid
intake.
 Monitor laboratory values: Monitor the patient's
laboratory values, such as serum albumin levels,
serum creatinine levels, and urine output, and report
any abnormalities to the healthcare provider.
ACUTE KIDNEY INJURY
kidneys.
20
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 Depending on the duration and severity of AKI, a wide
range of potentially life-threatening metabolic
complications can occur, including metabolic acidosis as
well as fluid and electrolyte imbalances.
 problem seen in patients who are hospitalized and those
in outpatient settings.
 The term acute kidney injury has replaced the term acute
renal failure because it better describes this syndrome,
in both those who require RRT and also in those patients
who experience minor changes in renal function.
NOTE: A widely accepted criterion for AKI is a 50% or greater
increase in serum creatinine above baseline (normal
creatinine is less than 1 mg/dL) (The Acute Dialysis Quality
Initiative, 2004). Urine volume may be normal, or changes
may occur including nonoliguria (greater than 800 mL/day),
oliguria (less than 400 mL/day or 0.5 mL/kg/h over 6 hours),
or anuria (less than 50 mL/day) (Odom, 2017).
PATHOPHYSIOLOGY
 Although the exact cause of AKI and oliguria is not
always recognized, many people suffer from them.
There is sometimes a specific underlying cause.
Some of the risk factors may be reversible if they are
detected and treated early before kidney function is
compromised. Hypovolemia, hypotension, reduced
cardiac output and heart failure, obstruction of the
kidney or lower urinary tract by tumor, blood clot, or
kidney stone, and bilateral obstruction of the renal
arteries or veins are all examples of conditions that
reduce blood flow to the kidney and impair kidney
function. Increased BUN and creatinine levels,
oliguria, and other symptoms may be reversed if
these diseases are treated and rectified before the
kidneys are irreparably damaged. Although renal
stones are not a prevalent cause of AKI, they do
occur on occasion. AKI risk may be increased.
Some inherited stone disorders, primary struvite
stones, as well as infection-related urolithiasis.
Urinary tract anatomic and functional abnormalities,
as well as spinal cord damage, may occur
and induce recurring obstructions as well as crystal-
specific injury to tubular epithelial cells and
interstitial renal cells (Odom, 2017).
CLASSIFICATIONS OF ACUTE KIDNEY INJURY
 Classification criteria for AKI include assessment of
three grades of severity and two outcome-level
classifications. This 5-point system is known as the
RIFLE classification system. RIFLE stands for risk,
injury, failure, loss, and ESKD (Bellomo et al., 2004).
Risk, injury, and failure are considered grades of
AKI severity, whereas loss and ESKD are
considered outcomes of loss that require some form
of RRT, at least temporarily (Bellomo et al., 2004).
BSN 3A | PBL GROUP 1
CATEGORIES OF ACUTE KIDNEY INJURY
 PRERENAL - hypoperfusion of kidney; occurs in
60% to 70% of cases, is the result of impaired blood
flow that leads to hypoperfusion of the kidney
commonly caused by volume depletion (burns,
hemorrhage, GI losses), hypotension (sepsis,
shock), and obstruction of renal vessels, ultimately
leading to a decrease in the GFR (Odom, 2017).
 INTRARENAL - actual damage to kidney tissue; the
result of actual parenchymal damage to the
glomeruli or kidney tubules.
 Acute tubular necrosis (ATN), or AKI in which
there is damage to the kidney tubules, is the most
common type of intrinsic AKI. Characteristics of
ATN are intratubular obstruction, tubular back leak
(abnormal reabsorption of filtrate and decreased
urine flow through the tubule), vasoconstriction, and
changes in glomerular permeability. These
processes result in a decrease of GFR, progressive
azotemia, and fluid and electrolyte imbalances.
CKD, diabetes, heart failure, hypertension, and
cirrhosis can contribute to ATN.
 POSTRENAL - obstruction to urine flow; usually
results from obstruction distal to the kidney by
conditions such as renal calculi, strictures, blood
clots, benign prostatic hyperplasia, malignancies,
and pregnancy. Pressure rises in the kidney
tubules, and eventually the GFR decreases.
PHASES OF ACUTE KIDNEY INJURY
 INITIATION - begins with the initial insult and ends
when oliguria develops.
 OLIGURIA - is accompanied by an increase in the
serum concentration of substances usually excreted
by the kidneys (urea, creatinine, uric acid, organic
acids, phosphorus, and the intracellular cations
[potassium and magnesium]). In this phase, uremic
symptoms first appear and life-threatening
conditions such as hyperkalemia develop.
 DIURESIS - is marked by a gradual increase in urine
output, which signals that glomerular filtration has
started to recover. Laboratory values stabilize and
eventually decrease. Although the volume of urinary
21
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
output may reach normal or elevated levels, renal
function may still be markedly abnormal since the
filtration of urea and creatinine has not yet
commenced.
 Because uremic symptoms may still be present, the
need for expert medical and nursing management
continues. The patient must be observed closely for
dehydration during this phase; if dehydration occurs,
the uremic symptoms are likely to increase and an
elevated serum BUN and creatinine will be noted.
 RECOVERY - signals the improvement of renal
function and may take 3 to 12 months. Laboratory
values return to the patient’s normal level. Although
a permanent 1% to 3% reduction in the GFR may
occur, it is not clinically significant. However, in those
patients with preexisting CKD, an episode of AKI
may necessitate beginning CRRT.
CLINICAL MANIFESTATIONS
 The patient may appear critically ill and lethargic.
Central nervous system signs and symptoms include
drowsiness, headache, muscle twitching, and
seizures. Table 48-3 summarizes common clinical
characteristics in all three categories of AKI.
ASSESSMENT AND DIAGNOSTIC FINDINGS
 Assessment of the patient with AKI includes
evaluation for changes in the urine, diagnostic tests
that evaluate the kidney contour, and a variety of
laboratory values.
 ULTRASONOGRAPHY - a critical component of the
evaluation of patients with kidney disease.
 SONOGRAM OR NONCONTRAST CT SCAN - may
show evidence of anatomic changes.
 SERUM CREATININE LEVELS - useful in
monitoring kidney function and disease progression
and increase with glomerular damage.
BSN 3A | PBL GROUP 1
PREVENTION
 Continually assess renal function (urine output, laboratory
values) when appropriate.
 Monitor central venous and arterial pressures and hourly
urine output of patients who are critically ill to detect the
onset of kidney dysfunction as early as possible.
 Pay special attention to wounds, burns, and other
precursors of sepsis.
 Prevent and treat infections promptly. Infections can
produce progressive kidney damage.
 Prevent and treat hypotensive shock promptly with blood
and fluid replacement.
 Provide adequate hydration to patients at risk for
dehydration, including:
 Before, during, and after surgery
 Patients undergoing intensive diagnostic studies
requiring fluid restriction and contrast agents (e.g.,
barium enema, IV pyelograms), especially older
patients who may have marginal renal reserve or
CKD.
 Patients with neoplastic disorders or disorders of
metabolism (e.g., gout) and those receiving
chemotherapy with potential tumor lysis syndrome
Patients with skeletal muscle injuries (e.g., crush
injuries, compartment syndrome).
 Patients with heat-induced illnesses (e.g., heat
stroke, heat exhaustion).
 To prevent infections from ascending in the urinary tract,
give meticulous care to patients with indwelling catheters.
Remove catheters as soon as possible.
 To prevent toxic drug effects, closely monitor dosage,
duration of use, and blood levels of all medications
metabolized or excreted by the kidneys.
MEDICAL MANAGEMENT
Treatment is aimed at replacing renal function temporarily to
minimize potentially lethal complications and reduce potential
causes of increased kidney injury with the goal of minimizing
long-term loss of renal function. Management includes
eliminating the underlying cause; maintaining fluid balance;
avoiding fluid excesses; and, when indicated, providing RRT.
Prerenal azotemia is treated by optimizing renal perfusion,
whereas postrenal failure is treated by relieving the
obstruction. Intrarenal or intrinsic azotemia is treated with
supportive therapy, with removal of causative agents,
aggressive management of pre- and postrenal failure, and
avoidance of associated risk factors.
 HEMODIALYSIS - a procedure that circulates the
patient’s blood through an artificial kidney [dialyzer]
to remove waste products and excess fluid.
 PERITONEAL DIALYSIS - a procedure that uses the
patient’s peritoneal membrane (the lining of the
peritoneal cavity) as the semipermeable membrane
to exchange fluid and solutes.
22
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 CONTINOUS RENAL REPLACEMENT THERAPY -
methods used to replace normal kidney function by
circulating the patient’s blood through a hemofilter.
PHARMACOLOGIC THERAPY
 SODIUM POLYSTYRENE SULFONATE - treats
elevated potassium levels by exchanging sodium
ions for potassium ions in the intestinal tract.
 IV DEXTROSE 50%, INSULIN, AND CALCIUM
REPLACEMENT - may be given to shift potassium
back into the cells.
NURSING MANAGEMENT
 The nurse monitors for complications, participates in
emergency treatment of fluid and electrolyte imbalances,
assesses the patient’s progress and response to
treatment, and provides physical and emotional support.
 The nurse keeps family members informed about the
patient’s condition, helps them understand the treatments,
and provides psychological support.
 The nurse continues to provide nursing care indicated for
the primary disorder (e.g., burns, shock, trauma,
obstruction of the urinary tract).
 The nurse monitors the patient’s serum electrolyte levels
and physical indicators of these complications during all
phases of the disorder.
 The nurse monitors fluid status by paying careful attention
to fluid intake (IV medications should be given in the
smallest volume possible), urine output, apparent edema,
distention of the jugular veins, alterations in heart sounds
and breath sounds, and increasing difficulty in breathing.
 The nurse takes steps to reduce the patient’s metabolic
rate. Fever and infection, both of which increase the
metabolic rate and catabolism, are prevented and treated
promptly; blood, urine and wound cultures are ordered as
indicated.
 Attention is given to pulmonary function, and the patient is
assisted to turn, cough, and take deep breaths frequently
to prevent atelectasis and respiratory tract infection.
Drowsiness and lethargy may prevent the patient from
moving and turning without encouragement and
assistance.
 Asepsis is essential with invasive lines and catheters to
minimize the risk of infection and increased metabolism.
An indwelling urinary catheter is avoided whenever
possible due to the high risk of UTI associated with its use,
but may be required to provide ongoing data required to
accurately monitor fluid I&O.
END-STAGE KIDNEY DISEASE OR CHRONIC KIDNEY
DISEASE
 When a patient has sustained enough kidney damage
to require RRT on a permanent basis, the patient has
moved into the fifth or final stage of CKD, also referred
to as ESKD.
BSN 3A | PBL GROUP 1
PATHOPHYSIOLOGY
 As renal function declines, the end products of protein
metabolism (normally excreted in urine) accumulate
in the blood. Uremia develops and adversely affects
every system in the body. The greater the buildup of
waste products, the more pronounced the symptoms.
The rate of decline in renal function and progression
of ESKD is related to the underlying disorder, the
urinary excretion of protein, and the presence of
hypertension. The disease tends to progress more
rapidly in patients who excrete significant amounts of
protein or have elevated blood pressure than in those
without these conditions (Mahaffey, 2017).
CLINICAL MANIFESTATIONS
 Cardiovascular Disease
 Peripheral Neuropathy
 Severe pain and discomfort
 Restless leg and burning feet
ASSESSMENT AND DIAGNOSTIC FINDINGS
 GLOMERULAR FILTRATION RATE - As the GFR
decreases (due to nonfunctioning glomeruli), the
creatinine clearance decreases, whereas the serum
creatinine and BUN levels increase. Serum creatinine
is a more sensitive indicator of renal function than
BUN. The BUN is affected not only by kidney disease
but also by protein intake in the diet, catabolism
(tissue and RBC breakdown), parenteral nutrition, and
medications such as corticosteroids.
 SODIUM AND WATER RETENTION - The kidney
cannot concentrate or dilute the urine normally in
ESKD. Appropriate responses by the kidney to
changes in the daily intake of water and electrolytes,
therefore, do not occur. Some patients retain sodium
and water, increasing the risk for edema, heart failure,
and hypertension. Hypertension may also result from
activation of the renin–angiotensin–aldosterone axis
and the concomitant increased aldosterone secretion.
Other patients have a tendency to lose sodium and
run the risk of developing hypotension and
hypovolemia. Vomiting and diarrhea may cause water
depletion, which may worsen the uremic state.
 ACIDOSIS METABOLIC - acidosis occurs in ESKD
because the kidneys are unable to excrete increased
loads of acid. Decreased acid secretion results from
the inability of the kidney tubules to excrete ammonia
(NH3 −) and to reabsorb sodium bicarbonate (HCO3
−). There is also decreased excretion of phosphorus
and other organic acids.
 ANEMIA - Anemia develops as a result of inadequate
erythropoietin production, the shortened lifespan of
RBCs, nutritional deficiencies, and the patient’s
tendency to bleed, particularly from the GI tract.
Erythropoietin, a substance normally produced by the
kidneys, stimulates bone marrow to produce RBCs. In
ESKD, erythropoietin production decreases and
23
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
profound anemia results, producing fatigue, angina,
and shortness of breath (Evans, 2017).
 CALCIUM AND PHOSPHORUS IMBALANCE -
Another abnormality seen in ESKD is a disorder in
calcium and phosphorus metabolism. Serum calcium
and phosphate levels have a reciprocal relationship in
the body: As one increases, the other decreases. With
a decrease in filtration through the glomerulus of the
kidney, there is an increase in the serum phosphorus
level and a reciprocal or corresponding decrease in
the serum calcium level. The decreased serum
calcium level causes increased secretion of
parathormone from the parathyroid glands. However,
in kidney disease, the body cannot respond normally
to the increased secretion of parathormone. As a
result, calcium leaves the bone, often producing bone
changes and bone disease as well as calcification of
major blood vessels in the body. In addition, the active
metabolite of vitamin D (1,25-
dihydroxycholecalciferol) normally manufactured by
the kidney decreases as kidney disease progresses
(Brooks, 2017).
COMPLICATIONS
 ANEMIA due to decreased erythropoietin production,
decreased RBC lifespan, bleeding in the GI tract from
irritating toxins and ulcer formation, and blood loss in
the dialysis circuit and dialyzer after HD has been
completed.
 BONE DISEASE AND METASTATIC AND
VASCULAR CALCIFICATIONS due to retention of
phosphorus, low serum calcium levels, and abnormal
vitamin D metabolism.
 HYPERKALEMIA due to decreased excretion,
metabolic acidosis, catabolism, and excessive
potassium intake from diet, medications, or IV
solutions.
 HYPERTENSION due to sodium and water retention
and malfunction of the renin–angiotensin–aldosterone
system.
 PERICARDITIS, PERICARDIAL EFFUSION, AND
PERICARDIAL TAMPONADE due to retention of
uremic waste products and inadequate dialysis.
MEDICAL MANAGEMENT
 The goal of management is to maintain kidney
function and homeostasis for as long as possible.
Management is accomplished primarily with
medications and diet therapy, although dialysis may
also be needed to decrease the level of uremic waste
products in the blood and to control electrolyte
balance. The close collaboration of a renal dietitian is
essential in dietary therapy.
 DIALYSIS The patient with increasing symptoms of
kidney disease is referred to a dialysis and
transplantation center early during progressive kidney
disease. Dialysis is usually initiated when the patient
BSN 3A | PBL GROUP 1
cannot maintain a reasonable quality of life with
conservative treatment.
PHARMACOLOGIC THERAPY
 CALCIUM AND PHOSPHORUS BINDERS -
Hyperphosphatemia and hypocalcemia are treated
with medications that bind dietary phosphorus in the
GI tract. Binders such as calcium carbonate or
calcium acetate are prescribed, but there is a risk of
hypercalcemia. This medication binds dietary
phosphorus in the intestinal tract; one to four tablets
are given with the first bite of food to be effective.
 ANTIHYPERTENSIVE AND CARDIOVASCULAR
AGENTS - Hypertension is managed by intravascular
volume control and a variety of antihypertensive
agents. Heart failure and pulmonary edema may also
require treatment with fluid restriction, low-sodium
diets, diuretic agents, inotropic agents, and dialysis.
The metabolic acidosis of ESKD usually produces no
symptoms and requires no treatment. However,
sodium bicarbonate supplements or dialysis may be
needed to correct the acidosis if it causes symptoms.
 ERYTHROPOIETIN - Anemia associated with ESKD
is treated with erythrocyte-stimulating agents
(recombinant human erythropoietin).
NURSING MANAGEMENT
 Nursing care is directed toward assessing fluid status
and identifying potential sources of imbalance,
working with a renal dietitian to implement a dietary
program to ensure proper nutritional intake within the
limits of the treatment regimen, and engaging the
patient by encouraging increased self-care and
greater independence. It is extremely important to
provide explanations and information to the patient
and family concerning ESKD, treatment options, and
potential complications. A great deal of emotional
support is needed by the patient and family because
of the numerous changes experienced. A social
worker is also a vital part of the interprofessional care
at the dialysis center. Specific interventions, along
with rationale and evaluation criteria, are presented in
more detail in the plan of nursing care for the patient
with ESKD.
RENAL REPLACEMENT THERAPIES
 Renal replacement therapy is a term used to
encompass life-supporting treatments for renal
failure. Renal replacement therapy replaces
nonendocrine kidney function in patients with renal
failure. Techniques include intermittent
hemodialysis, continuous hemofiltration and
hemodialysis, and peritoneal dialysis. All modalities
exchange solute and remove fluid from the blood,
using dialysis and filtration across permeable
membranes.
24
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 Dialysis and filtration can be done intermittently or
continuously. Continuous therapy is used exclusively
for acute renal failure; benefits over intermittent
therapy are improved tolerability as a result of slower
removal of solute and water.
DIALYSIS
 Dialysis is a treatment for individuals whose kidneys
are failing. When you have kidney failure, your
kidneys don’t filter blood the way they should.
Dialysis does the work of your kidneys.
WHO NEEDS DIALYSIS
 People who have kidney failure end- stage
renal disease (ESRD)
 Injuries and conditions like high blood
pressure, diabetes and lupus can damage
kidneys, leading to kidneydisease.
TWO TYPES OF DIALYSIS
 Hemodialysis
 Peritoneal Dialysis
HEMODIALYSIS
 With hemodialysis, a machine removes blood
from your body, filters it through a dialyzer
(artificial kidney) and returns thecleaned blood
to your body. This 3- to 5-hour process may
take place in a hospitalor a dialysis center three
times a week.
 You can also do hemodialysis at home. You
may need at-home treatments four to seven
times per week for fewer hourseach session.
PERITONEAL DIALYSIS
 With peritoneal dialysis, tiny blood vessels
inside the abdominal lining (peritoneum) filter
blood through the aid of a dialysis solution. This
solution is a type of cleansing liquid that
contains water, salt, and other additives.
Two ways to do this treatment:
 Automated peritoneal dialysis uses amachine
called a cycler.
 Continuous ambulatory
peritoneal dialysis (CAPD) takes place
manually.
NURSING RESPONSIBILITIES: HOSPITALIZED PATIENT
 Protecting the vascular access
 Precautions during, I.V therapy
 Monitoring symptoms of uremia
BSN 3A | PBL GROUP 1
 Detecting cardiac and respiratory
Complications
 Controlling electrolyte levels and Diet
 Managing discomfort and pain
 Monitoring BP
 Preventing infection
 Caring for the catheter site
 Administering medications
 Providing psychological support -pt andfamily
PRESCRIPTION MANAGEMENT
 Understand your medications
 Keep your medications organized
 Stick with your treatment plan
 Take all the medication you were prescribed.
 Tell your doctor if you’re having side effects.
 Check with your doctor first before you stop taking
your medication.
 Ask your doctor if your prescription needs to be
refilled.
ACTIVITY RESTRICTION WHILE ON DIALYSIS
 Limit exercise or certain physical activities when the
abdomen fills with dialysis solution. Otherwise,
exercise is typically OK for people on dialysis.
 You should ask your provider about participating in
specific activities or sports.
NOTE: Dialysis only replaces part of your kidney function.
Hemodialysis and peritoneal dialysis allow people with
kidney failure to feel better and continue doing the things
they enjoy, but neither replaces all the jobs that healthy
kidneys do.
HEMODIALYSIS DIALYZERS
HEMODIALYSIS
 It is used for patients who are acutely ill and require
short-term dialysis for days to weeks until kidney
function resumes, as in patients with AKI, and for
patients with advanced CKD and ESKD who
require long-term or permanentRRT.
 Prevents death but does not cure kidney disease
and does not compensate for the loss of endocrine
or metabolic activities of the kidneys.
 The objectives of HD are to extract toxic
nitrogenous substances from the blood and to
remove excess fluid.
DIALYZERS
 Also referred to as an artificial kidney.
 Hollow-fiber devices containing thousands oftiny
capillary tubes that carry the blood through the
artificial kidney.
 Dialyzers have undergone many technologic
changes in performance and biocompatibility.
25
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
VASCULAR ACCESS
 Access to the patient’s vascular system must be
established to allow blood to be removed,
cleansed, and returned to the patient’s vascular
system at the rapid rates of 300 and 500 mL/min.
Several types of access can be surgically created
or placed during procedures performed in
interventional radiology suites or at the bedside.
VASCULAR ACCESS DEVICES
 Immediate access to the patient’s circulation for
acute HD is achieved by inserting a double- lumen,
noncuffed, large-bore catheter into the right or left
internal jugular or femoral vein of either leg by the
physician, nurse practitioner, or physician
assistant.
 This method of vascular access involves some risk
(e.g., hematoma, bleeding, pneumothorax,
infection, thrombosis of the vein, inadequate flow).
 The catheter is removed when no longer needed.
ARTERIOVENUS FISTULA
 The preferred method of permanent vascular
access for dialysis.
 This is created surgically (usually in theforearm)
by anastomosing (joining) an artery to a vein,
either side to side or end to side.
 Needles are inserted into the vessel to obtain
blood flow which is adequate to pass through the
dialyzer.
 The patient is encouraged to perform hand
exercise.
ARTERIOVENUS GRAFT
 Can be created by subcutaneously interposing a
biologic, semi biologic, or synthetic graft material
between an artery and vein.
 Patients with compromised vascular systems
(e.g., from diabetes) often require a graft because
their native vessels may not be suitable for
creation of an AVF.
 Stenosis, infection, and thrombosis are the most
common complications of this access.
COMPLICATIONS
 Although HD can prolong life, it does not alter the
natural course of the underlying CKD, nor does it
completely replace kidney function. The CKD
complications previously discussed will continue to
worsen and require treatment.
 Many people undergoing HD experience major
sleep problems that further complicate their overall
health status. Early-morning or late-afternoon
dialysis may bea risk factor for developing sleep
disturbances.
BSN 3A | PBL GROUP 1
 Other complications of dialysis may include the
following:
o Episodes of shortness of breath
o Hypotension
o Painful muscle cramping
o Exsanguination
o Arrhythmias
o Air embolism
o Chest pain
o Dialysis disequilibrium
NURSING MANAGEMENT
 The nurse in the dialysis unit has an important
role in monitoring, supporting, assessing, and
educating the patient.
PHARMACOLOGICAL THERAPY
 Many medications are removed from the blood
during HD.
 Medications that are water soluble are readily
removed during HD treatment, and those that are fat
soluble or adhere to other substances (like albumin)
are not dialyzed out very well.
 Patients undergoing HD who require medications
(e.g., cardiac glycosides, antibiotic agents,
antiarrhythmic medications, antihypertensive
agents) are monitored closelyto ensure that blood
and tissue levels of these medications are
maintained without toxic accumulation.
 Many medications that are taken once daily should
be administered after the dialysistreatment.
NUTRITIONAL AND FLUID THERAPY
 Diet is important for patients on HD.
 Restriction of fluid is also part of the dietary
prescription because fluid accumulation may
occur, leading to fluid volume excess, heart failure,
and pulmonary edema.
 With the initiation of HD, the patient usually
requires some restriction of dietary sodium,
potassium, phosphorus, and fluid intake.
 The goal for patients on HD is to keep their
interdialytic (between dialysis treatments) weight
gain less than 4% of their estimated dryweight
(Gonyea, 2017).
MEETING PSYCHOLOGICAL NEEDS
 Patients requiring long-term HD, as theyengage in
psychosocial adaptation, tend to feelmired in a
cyclical routine (Lin, Han, & Pan, 2015).
 The regimented lifestyle that frequents dialysis
treatments and restrictions in food and fluid intake
impose can be demoralizing to the patient and
family.
 Dialysis alters the lifestyle of the patient and
family.
26
NCM112 LECTURE
MEDICAL-SURGICAL NURSING

FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS

 The nurse needs to give the patient and family the
opportunity to express feelings of anger and
concern about the limitations that the disease and
treatment impose, possible financial problems,
and job insecurity.
PROMOTING HOME, COMMUNITY-BASED, AND
TRANSITIONAL CARE
 High-quality transitional care is especially
important for older adults with multiple chronic
conditions and complex therapeutic regimens, as
well as for their family caregiver.
 Communication about prognosis and patientgoals by
a dedicated team with time and expertise leads to
decision making, clarity of the care plan, and
consistent follow-through.
EDUCATING PATIENTS ABOUT SELF-CARE
 Preparing a patient for HD is essential.
 Assessment helps identify the learning needs of the
patient and family members.
 The diagnosis of ESKD and the need for dialysis
is a big adjustment for the patient and family.
 Many patients with ESKD have clinical
depression, and chronic uremia contributes to a
shortened attention span, a decreased level of
concentration, and altered perception.
 The nurse needs to convey a nonjudgmental
attitude to enable the patient and family to discuss
options and their feelings about those options.
HOME HEMODIALYSIS
 Most patients who undergo HD do so in an
outpatient setting, but home HD is an option for
some.
 Home HD requires a highly motivated patient who
is willing to take responsibility for the
procedure and can adjust each treatment to meet
the body’s changing needs.
 The health care team never forces a patient to use
home HD, because this treatment requires
changes in the home and family.
 The patient undergoing home HD and the
caregiver assisting that patient must be trained to
prepare, operate, and disassemble the dialysis
machine; maintain and clean the equipment;
administer medications (e.g., heparin) into the
machine lines; and handle emergency problems
(HD dialyzer rupture, electrical or mechanical
problems, hypotension, shock, and seizures)
(Harwood & Dominski, 2017).
 Before home HD is initiated, the home
environment, household and community
resources, and ability and willingness of the
patient and family to carry out this treatment are
assessed.
functional status, and quality of life (Browne &
Johnstone, 2017).
 Many patients with CKD can resume relatively
normal lives, doing the things that are important to
them: traveling, exercising, working, or actively
participating in family activities.
 Outcome goals for renal rehabilitation include
employment for those able to work, improved
physical functioning of all patients, improved
understanding about adaptation and options for living
well, increased control over the effects of kidney
disease and dialysis, and resumption of activities
enjoyed before dialysis.
CONTINUOUS RENAL REPLACEMENT THERAPY
 CRRT is a method used to replace normalkidney
function in patients who are hemodynamically
unstable by circulating thepatient’s blood through a
hemofilter and returning it to the patient.
 Continuous renal replacement therapy (CRRT)is a
method of slower, continuous dialysis to allow solute
and fluid homeostasis. There are different
techniques of CRRT that aredistinguished by their
method of solute removal,each detailed below. The
choice of CRRT is primarily based on provider
preference insteadof specific patient characteristics
or outcome data. This activity details the principles,
indications, and complications of CRRT, and it
discusses when to consider initiating CRRT andwhen
to discontinue it. It highlights the role of the inter-
professional team in managing patients on CRRT.
 CRRT may be indicated for patients with acute or
chronic kidney disease who are too clinicallyunstable
for traditional HD, for patients with fluid overload
secondary to oliguric (low urine output) kidney
disease, and for patients whose kidneys cannot
handle their acutely high metabolic or nutritional
needs. Some forms of CRRT may not require dialysis
machines or dialysis personnel to carry out the
procedures and can be initiated quickly in the critical-
care unit. The methods are similar, as they require
access to the circulation and blood to pass through
an artificial filter. A hemofilter (an extremely porous
blood filter containing a semipermeable membrane)
is used in all types.
SEVERAL TYPES OF CRRT
 These are available and widely used incritical-
care units.

CONTINUING AND TRANSITIONAL CARE

 The health care team’s goal in treating patients with

CKD is to maximize their vocational potential,

BSN 3A | PBL GROUP 1 27

NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 Devices for administering continuous renal
replacement therapy (CRRT) offer an integrated
fluid warmer for the heating of infusion and
dialysate fluids, a weighing or volumetric
measuring system to reduce the possibility of
error in assessing fluid balance, and a battery
backup that allows treatments to continue when
the patient is moved.
 The involvement of specialists external to
conventional intensive care staff with expertise
in critically ill patients is not a new practice. The
following is a list of external groups involved in
the interprofessional management of patients
on CRRT:
o Respiratory care practitioners
o Nutritional support team
o Clinical pharmacology
o Diagnostic and interventional radiology
o Cardiology
o Rehabilitation and physiotherapy
COMPLICATIONS
 As with every procedure, CRRT has risks, and these
should be communicated to the patient or family
when considering initiation. Firstly, the risks
associated with intravascular lines include
hemorrhage, AV fistula, infection, or thrombosis.
The risks of the therapy itself include electrolyte
disturbances, clearance of trace elements or
antibiotics, hypothermia, and hypotension.
 Although hypotension should occur less commonly
than in IHD, hypotension may occur if the net
ultrafiltration rate exceeds the intravascular filling
Your child will be connected to the CRRT machine thewhole
rate. Monitoring of electrolytes and acid-base
time. The machine is run by specially trained nurses in the
statusshould be done every 6 to 12 hours when
ICU.
starting CRRT. If remaining stable after the first 24
to 48 hours, the interval may be increased to 12 to
24 hours. The exception, as discussed above, is
when using citrate as regional anticoagulation
because this requires frequent monitoring of
ionized calcium levels.
 The removal of medications during CRRT is
variable, and so it is advised to check the dose of
required drugs when on CRRT. This practice is
critical when it comesto administering antibiotics, as
the troughconcentrations of these medications will
determine their bacteriocidal or bacteriostatic
effectiveness. Most affected are water-soluble
antimicrobials, aminoglycosides, and beta-lactam
antibiotics. Many patients who meet indications for
CRRT will do so because of sepsis, meaning that
appropriate antibioticdosage is vital.
 CRRT will result in amino acid, micronutrient, and
water-soluble vitamin loss. Patients are also often in
asubstantial negative nitrogen balance. Appropriate
caloric and protein intake with supplementation of
water-soluble vitamins should be ensured.
 Finally, the risks associated with the extracorporeal
circuit include hypersensitivity to the circuit, air
BSN 3A | PBL GROUP 1
embolization, and blood loss that occurs with the
filter or circuit changes.
HOW CRRT WORKS?
 CRRT does some of the work normally done by
healthy kidneys. It gently filters and cleans your
child’s blood by removing waste products and extra
fluid. This keeps chemicals and electrolytes, like
potassium and phosphorus, in your child’s blood
balanced. CRRT does not actually improve your
child’s kidney function, but instead it keeps
everything in line in your child’s body until the
kidneys recover function.
 A central venous catheter (CVC) is placed in one of
your child’s large veins. This is usually in the neck or
groin.
 The CVC is connected to a machine that circulates
some of your child’s blood in a loop outside the body.
After the blood has been filtered and cleaned, it is
sent back into the body. Nationwide Children’s
Hospital uses 2 types of machines for CRRT:
PrisMax™ and Aquadex®.
BEFORE CRRT
 Placement of the dialysis catheter (CVC) is a sterile
procedure. It is done by an intensive care unit (ICU)
doctor or a radiology doctor skilled in catheter
placement. The doctor placing the catheter will
decideif the parents may stay during the procedure.
DURING CRRT
 The machine works best if your child doesn’t move
a lot. They may be given medicines, called
sedatives, to keep them still so the CRRT goes
smoothly.
 There are situations when your child will be taken
off(disconnected) from the CRRT machine. These
include:
 If they need to have a test or a procedure. The
machine will be restarted afterward.
 Routine change of the tubing and filter to keep the
system operating well. This only requires a short
time off the machine.
 Sometimes small blood clots get in the filter and
tubing and stop the machine from working well. A
nurse will change the tubing and filter if this
happens.
 The machine’s alarm may go off during CRRT.
Most of the alarms are not because of an
emergency. They are usually meant to alert the
nurse(s) to changesolution bags. The machine may
also alarm to let the nurse know to change your
child’s position or check the catheter to help the
treatment run smoothly.
28
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
AFTER CRRT
 As your child gets better, the team may try some
time off CRRT. This is to see how well your child’s
kidneys work. If kidney support is still needed,
CRRT may need to be restarted, or they may be
changed to a less frequent type of dialysis called
hemodialysis. This is done for shorter periods of
time (3 to 5 days perweek).
 If you have questions about your child’s kidney
functionor the CRRT treatment, please talk to your
child’s kidney doctor (nephrologist).
PERITONEAL DIALYSIS
Peritoneal dialysis (PD) is one type of dialysis treatment for
kidney failure. It uses a fluid that you put in your belly and
then remove to clean your blood. It can be done at home.
 The goals of PD are to remove toxic substances and
metabolic wastes and to reestablish normal fluid and
electrolyte balance.
 PD may be the treatment of choice for patients with
kidney disease who are unable or unwilling to
undergo HD or kidney transplantation.
 Patients with diabetes or cardiovascular disease,
many older patients, and those who may be at risk
for adverse effects of systemic heparin are likely
candidates for PD.
 Severe hypertension, heart failure, and pulmonary
edema not responsive to usual treatment regimens
have been successfully treated with PD.
In PD, the peritoneal membrane that covers the abdominal
organs and lines the abdominal wall serves as the
semipermeable membrane. Sterile dialysate fluid, containing
dextrose and electrolytes, is introduced into the peritoneal
cavity through an abdominal catheter at established intervals.
Once the sterile solution is in the peritoneal cavity, uremic
toxins such as urea and creatinine begin to be cleared from
the blood.
PROCEDURE
Preparing the Patient
 Assess the patient’s physical and psychological
status, mental status, previous experience with
dialysis, and understanding of and familiarity with the
procedure.
 The nurse and surgeon or interventional radiologist
or nephrologist explains the procedure to the patient.
 The nurse assists the provider in obtaining signed
consent for insertion of the catheter. Baseline vital
signs, weight, and serum electrolyte levels are
recorded.
 The patient is instructed to empty the bladder and
bowel to reduce the risk of puncture of internal
organs during the insertion procedure.
 A prophylactic antibiotic agent will be given to
prevent infection.
BSN 3A | PBL GROUP 1
 The peritoneal catheter can be inserted in
interventional radiology, in the operating room, or,
rarely, at the bedside.
Preparing the Equipment
 The nurse consults with the physician to determine
the concentration of dialysate to be used and the
medications to be added.
o Heparin may be added to prevent fibrin
formation and resultant occlusion of the
peritoneal catheter.
o Potassium chloride may be prescribed to
prevent hypokalemia.
o Antibiotic agents may be added to treat
peritonitis (inflammation of the peritoneal
membrane) caused by infection.
o Insulin is rarely added to PD fluid due to
widespread use of subcutaneous insulin
pumps and sliding scales.
 In a hospital setting, to prevent contamination, a
pharmacist generally adds all medications to the
dialysate bags in the pharmacy under a laminar flow
hood.
 In the home setting, the nurse instructs the patient or
family on how to aseptically add medications to PD
fluid.
 The dialysate is warmed to body temperature to
prevent patient discomfort and abdominal pain and
to dilate the vessels of the peritoneum to increase
urea clearance.
 Immediately before initiating dialysis, using aseptic
technique, the nurse assembles the dialysate with
attached tubing and drainage bag.
 All PD dialysate fluid, tubing, and drainage bags are
manufactured as closed systems and no spiking of
solution is needed.
 The tubing is primed with the prepared dialysate to
prevent air from entering the catheter and peritoneal
cavity, which would cause abdominal discomfort and
interfere with instillation and drainage of the fluid.
Inserting the Catheter
 The peritoneal catheter is inserted in the operating
room or radiology suite to maintain surgical asepsis
and minimize the risk of contamination.
 Catheters for long-term use are usually soft and
flexible and made of silicone with a radiopaque strip
to permit visualization on x-ray.
 These catheters have three sections:
o an intraperitoneal section, with numerous
openings and an open tip to allow dialysate
to flow freely.
o a subcutaneous section that passes from
the peritoneal membrane and tunnels
through muscle and subcutaneous fat to the
skin.
29
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
o an external section for connection to the
manufacturer specific transfer set which
then connects to the dialysate tubing with
attached dialysate.
 Most adult catheters have 2 cuffs made of Dacron
polyester.
 The cuffs stabilize the catheter, limit movement,
prevent leaks, and provide a barrier against
microorganisms.
 One cuff is placed just distal to the peritoneum, and
the other cuff is placed subcutaneously. The
subcutaneous tunnel (5 to 10 cm long) further
protects against bacterial infection.
Performing the Exchange
All types of PD involve a series of exchanges or cycles. An
exchange is the entire cycle including drainage of the effluent
(fluid), instillation of the dialysate, and dwell. This cycle is
repeated throughout the course of the dialysis.
 The dialysate is infused by gravity into the peritoneal
cavity. A period of about 10 minutes is usually
required to infuse 2 to 3 L of fluid.
 A sterile cap is applied to the transfer set and the
patient can perform ADLs.
 The prescribed dwell, or equilibration time, allows
diffusion and osmosis to occur.
 At the end of the prescribed dwell, the patient
performs hand hygiene, dons a mask, removes the
sterile cap, unclamps the transfer set, and the
solution drains from the peritoneal cavity by gravity
through a closed system.
 Drainage is usually completed in 20 to 30 minutes.
 The drainage fluid is normally colorless or straw-
colored and should not be cloudy. Bloody or pink-
colored drainage may be seen in the first few
exchanges after insertion of a new catheter, but
should not occur after that time.
The number of cycles or exchanges and their frequency are
prescribed based on monthly laboratory values and the
presence of uremic symptoms.
The exchanges can be performed manually during the waking
hours by the patient (continuous ambulatory peritoneal
dialysis [CAPD]) or via the use of a PD machine (cycler) that
automatically performs exchanges, usually while the patient is
sleeping at night (continuous cycling peritoneal dialysis
[CCPD]).
COMPLICATIONS
Most complications of PD are often minor; however, several,
if unattended, can have serious consequences.
ACUTE COMPLICATIONS
 Peritonitis: is the most common and serious
complication of PD.
BSN 3A | PBL GROUP 1
o The first sign of peritonitis is cloudy
dialysate effluent. Diffuse abdominal pain
and rebound tenderness often occur later.
Hypotension and other signs of shock may
also occur with advancing infection.
o The patient with peritonitis may be treated
as an inpatient or outpatient (most
common), depending on the severity of the
infection and the patient’s clinical status.
o Antibiotic therapy continues for 14 to 21
days.
o During an episode of peritonitis, the patient
loses large amounts of protein through the
peritoneal membrane due to inflammation
and increased permeability.
o Attention must be given to educating the
patient to detect and promptly seek
treatment for peritonitis.
 Leakage: leakage of dialysate through the catheter
site may occur even after a healing period.
o Usually, the leak stops spontaneously when
dialysis is withheld for several days, giving
the tissue the opportunity to heal around the
catheter cuffs and to seal the insertion
tunnel.
o It is important to reduce factors that might
delay healing, such as undue abdominal
muscle activity (bending, lifting over 5 lb)
and straining during bowel movements.
o In many cases, leakage can be avoided by
using small volumes (500 mL) of dialysate,
gradually increasing the volume up to 2000
to 3000 mL.
 Bleeding: Bleeding is also common during the first
few exchanges after a new catheter insertion
because some blood enters the abdominal cavity
following insertion. The bleeding most often clears up
after several exchanges.
o Most often, bleeding stops in 1 to 2 days
and requires no specific intervention.
o More frequent exchanges and the addition
of heparin to the dialysate during this time
may be necessary to prevent blood clots
from obstructing the catheter.
LONG-TERM COMPLICATIONS
 Hypertriglyceridemia, likely due to the use of glucose
containing dialysate, is common in patients on long-
term PD.
 Other complications that may occur with long-term
PD include abdominal hernias (incisional, inguinal,
diaphragmatic, and umbilical), likely resulting from
continuously increased intra-abdominal pressure.
The persistently elevated intra-abdominal pressure
also aggravates symptoms of hiatal hernia and
hemorrhoids.
30
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 Mechanical problems occasionally occur and may
interfere with instillation or drainage of the dialysate.
Formation of clots and fibrin in the peritoneal
catheter and constipation are factors that may
contribute to these problems.
APPROACHES
ACUTE INTERMITTENT PERITONEAL DIALYSIS
 Indications for acute intermittent PD, a variation of
PD, include uremic signs and symptoms (nausea,
vomiting, fatigue, altered mental status), fluid
overload, acidosis, and hyperkalemia.
 Exchange times range from 30 minutes to 2 hours.
 Acute intermittent PD is not indicated for long-term
patient management, but for specific situations such
as patients who are referred late in the course of
CKD (CKD stage 5) and require immediate dialysis.
 The nurse uses a flow sheet on paper or within the
electronic health record to document each exchange
and records vital signs, dialysate concentration,
medications added, exchange volume, dwell time,
dialysate fluid balance for each exchange (fluid lost
or gained), and cumulative fluid balance.
 The nurse also carefully assesses skin turgor and
mucous membranes to evaluate fluid status and
monitor the patient for edema. Daily weight is the
most accurate indicator of fluid volume status
 The nurse must ensure that the PD catheter remains
secure and that the dressing remains dry and is
changed on a routine basis.
 The patient and family are educated about the
procedure and are kept informed about progress
(fluid loss, weight loss, laboratory values).
CONTINUOUS AMBULATORY PERITONEAL DIALYSIS
(CAPD)
 This works on the same principles as other forms of
PD: diffusion and osmosis. Less extreme fluctuations
in the patient’s laboratory values occur with CAPD
than with intermittent PD or HD because the dialysis
is constantly in progress. The serum electrolyte
levels often remain in the normal range
Procedure
 The patient performs exchanges four or five times a
day, 24 hours a day, 7 days a week, at intervals
scheduled throughout the day.
 A closed Y-shaped system is most commonly used.
 To perform an exchange, the patient (or person
doing the exchange) washes their hands, dons a
mask, and then removes the cap from the transfer
set while maintaining sterility.
 The open end of the “Y” set is connected to the end
of the transferset and the dialysate is drained into the
attached empty sterile bag (effluent) (over about 20
to 30 minutes). Then the attached dialysate is
infused, the patient clamps off the transfer set and
BSN 3A | PBL GROUP 1
the tubing set, disconnects the tubing set, and
applies a new sterile cap to the transfer set, making
it a closed system.
Complications
 To reduce the risk of peritonitis, the patient (and all
caregivers) must use meticulous aseptic care to
avoid contaminating the catheter, fluid, or tubing and
to avoid accidentally disconnecting the catheter from
the tubing.
 Whenever a connection or disconnection is made,
hand hygiene must be performed and a mask worn
by anyone within 6 ft of the area to avoid
contamination with airborne bacteria.
 Excess manipulation should be avoided, and
meticulous care of the catheter exit site is provided
using a standardized protocol.
 At home, a patient is taught to use clean technique
for exit site care.
 In the hospital, due to the increased risk of infection,
sterile technique is employed by the nurse and
patient.
CONTINUOUS CYCLIC PERITONEAL DIALYSIS
 It uses a machine called a cycler to provide the fluid
exchanges. It is programmed to deliver an
established amount of PD solution that will dwell in
the peritoneal cavity for a programmed period of time
before it drains from the peritoneal cavity via gravity.
 CCPD may combine overnight intermittent PD with a
prolonged dwell time during the day.
 Every evening, the patient connects the peritoneal
catheter to tubing on the cycler machine, usually just
before the patient goes to sleep for the night.
Because the machine is very quiet, the patient can
sleep, and the extra-long tubing allows the patient to
move and turn normally.
 In the morning, the patient disconnects from the
cycler. This process is done every day to achieve the
effects of dialysis required.
 CCPD has a lower infection rate than other forms of
PD because there are fewer opportunities for
contamination with bag changes and tubing
disconnections.
 It also allows the patient to be free from exchanges
throughout the day, making it possible to engage in
work and activities of daily living more freely.
NURSING MANAGEMENT
MEETING PSYCHOSOCIAL NEEDS
 Patients who elect to do PD may experience altered
body image because of the presence of the
abdominal catheter, bag, tubing, and cycler. The
nurse may arrange for the patient to talk with other
patients who have adapted well to PD.
31
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 Patients undergoing PD may also experience altered
sexuality patterns and sexual dysfunction. The
patient and partner may be reluctant to engage in
sexual activities, partly because of the catheter being
psychologically “in the way” of sexual performance.
 Questions by the nurse about concerns related to
sexuality and sexual function often provide the
patient with a welcome opportunity to discuss these
issues and a first step toward assisting in their
resolution
PROMOTING HOME, COMMUNITY-BASED, AND
TRANSITIONAL CARE
 Patients are educated as inpatients or outpatients to
perform PD once their condition is medically stable.
Education generally takes 5 days to 2 weeks.
 Patients are taught according to their own learning
ability and knowledge level and only as much at one
time as they can handle without feeling
uncomfortable or becoming saturated.
 Because of protein loss with PD, the patient is
instructed to eat a highprotein (1.2 to 1.3g/kg/day),
low phosphorus, nutritious diet (NKF KDOQI, 2000).
 The patient is also encouraged to increase their daily
fiber intake to help prevent constipation, which can
impede the flow of dialysate into or out of the
peritoneal cavity.
 Patients may gain 3 to 5 lb within a month of initiating
PD, so they may be asked to limit their carbohydrate
intake to avoid weight gain.
 Potassium and fluid restrictions are not usually
necessary. Patients commonly lose at least 1 to 2 L
of fluid over and above the volume of dialysate
infused into the abdomen during a 24-hour period,
permitting a moderate fluid intake.
CONTINUING AND TRANSITIONAL CARE
 Follow-up care through phone calls, visits to the
dialysis clinic, outpatient department, and continuing
home care assists patients in the transition to home
and promotes their active participation in their own
health care.
 Patients often check with the nurse to see if they are
making the correct choices about dialysate or control
of blood pressure, or simply to discuss a problem.
 If a referral is made for home care, the home health
nurse assesses the home environment and suggests
modifications to accommodate the equipment and
facilities needed to carry out PD.
 The nurse assesses the patient’s and family’s
understanding of PD and evaluates their technique
in performing PD.
 Assessments include checking for changes related
to kidney disease; any complications such as
peritonitis; medication management; and treatment
related problems such as heart failure, inadequate
drainage, and weight gain or loss.
BSN 3A | PBL GROUP 1
 The nurse continues to reinforce and clarify
education about PD and ESKD and assesses the
patient’s and family’s progress in coping with the
procedure.
INFECTIONS OF THE URINARY TRACT
 caused by pathogenic microorganisms in the
urinary tract
 NORMAL URINARY TRACT: sterile above urethra
 Classified by location
 LOWER URINARY TRACT: bladder & structures
below bladder
 UPPER URINARY TRACT: kidneys & ureters
 second most common infection in the body
 CATHETER-ASSOCIATED URINARY TRACT
INFECTIONS (CAUTI): hospital acquired infection
o associated with indwelling urinary
catheters.
o UTI that occurs while the patient had an
indwelling urinary catheter in place for
more than 2 calendar days on the day that
the infection was detected.
LOWER URINARY TRACT INFECTION
 Bladder & structures below the bladde
 Bladder: sterile
 Mechanisms that protects the sterility of the
bladder:
o physical barrier of the urethra assists in
keeping bacteria away from the bladder
o antibacterial enzymes and antibodies
o antiadherent effects mediated by the
mucosal cells of the bladder
 LOWER UTIs include:
o BACTERIAL CYSTITIS: inflammation of
urinary bladder
o BACTERIAL PROSTATITIS: inflammation
of prostate gland
o BACTERIAL URETHRITIS: inflammation
of the urethra
PATHOPHYSIOLOGY
 For infection to occur, bacteria must gain access to
the bladder, attach to and colonize the epithelium of
the urinary tract to avoid being washed out with
voiding, evade host defense mechanisms, and
initiate inflammation. Many UTIs result from fecal
organisms ascending from the perineum to the
urethra and the bladder and then adhering to the
mucosal surfaces.
RISK FACTORS
 Female gender
 Diabetes
 Pregnancy
 Neurologic disorders
32
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 Gout
 Altered states caused by incomplete emptying of
the bladder and urinary stasis
 Decreased natural host defenses or
immunosuppression
 Inability or failure to empty the bladder completely
 Inflammation or abrasion of the urethral mucosa
 Instrumentation of the urinary tract (e.g.,
catheterization, cystoscopic procedures)
 Obstructed urinary flow caused by:
o Congenital abnormalities
o Urethral strictures
o Contracture of the bladder neck
o Bladder tumors
o Calculi (stones) in the ureters or kidneys
o Compression of the ureters
BACTERIAL INVASION OF THE URINARY TRACT
 Bacterial removal: due to increased normal slow
shedding of bladder epithelial cells
 Glycosaminoglycan (GAG): hydrophilic protein;
attracts water forming a water barrier that serves as
defensive layer between bladder & urine
 Urinary immunoglobulin A (IgA): provides barrier to
bacteria
REFLUX
 URETHROVESICAL REFLUX: obstruction of free-
flowing urine
o Backward flow of urine from urethra to the
bladder
o COUGHING, SNEEZING, OR
STRAINING: the bladder pressure
increases, which may force urine from the
bladder into the urethra
o caused by dysfunction of the bladder neck
or urethra
o When the ureterovesical valve is impaired
by congenital causes or ureteral
abnormalities, the bacteria may reach the
kidneys and eventually destroy them
 URETHROVESICAL ANGLE AND URETHRAL
CLOSURE PRESSURE: altered w/ menopause
(increased infection in postmenopausal women)
UROPATHOGENIC BACTERIA
 BACTERIURIA: presence of bacteria in the urine.
 a clean-catch midstream urine specimen is the
measure used to establish bacteriuria.
ROUTES OF INFECTION
 3 ways:
o Transurethral route (ascending infection)
o Bloodstream (hematogenous spread)
o Fistula from the intestine (direct extension)
 TRANSURETHRAL: most common route of
infection
BSN 3A | PBL GROUP 1
o bacteria (often from fecal contamination)
colonize the periurethral area and
subsequently enter the bladder by means
of the urethra
 increased incidence of UTI to those who engage in
penile-vaginal intercourse
o due to short urethra
CLINICAL MANIFESTATIONS
UNCOMPLICATED UTI
 burning on urination
 urinary frequency (more than every 3 hrs)
 urinary urgency
 nocturia
 incontinence
 suprapubic or pelvic pain
 hematuria
 back pain
COMPLICATED UTI
 asymptomatic bacteriuria to gram-negative sepsis
with shock
GERONTOLOGIC CONSIDERATIONS
 Bacteriuria increases with age and disability
 women are affected more frequently than men
 In older adults, structural abnormalities secondary
to decreased bladder tone, neurogenic bladder
(dysfunctional bladder) secondary to stroke, or
autonomic neuropathy of diabetes may prevent
complete emptying of the bladder and increase the
risk of UTI
 ABSENCE OF ESTROGEN: postmenopausal
women are susceptible to colonization & increased
adherence of bacteria to vagina & urethra
o Oral or topical estrogen has been used
 incidence of bacteriuria also increases in men with
confusion, dementia, or bowel or bladder
incontinence.
 BACTERIAL PROSTATITIS: common cause of
recurrent UTI in older males
o Resection of prostate gland (management)
FACTORS THAT CONTRIBUTE TO UTI IN OLDER
ADULTS
 Cognitive impairment
 Frequent use of antimicrobial agents
 High incidence of multiple chronic medical
conditions
 Immune compromised
 Immobility and incomplete emptying of bladder
 Low fluid intake and excessive fluid loss
 Obstructed flow of urine (e.g., urethral strictures,
neoplasms, clogged
 indwelling catheter)
33
NCM112 LECTURE
MEDICAL-SURGICAL NURSING

FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS

 Poor hygiene practices CELLULAR STUDIES

 Escherichia coli: most common seen in OLDER  Pyuria: WBC in urine

patients in COMMUNITY or HOSPITAL o Seen with renal calculi, interstitial nephritis
 Proteus, Klebsiella, Pseudomonas, or & renal tuberculosis
Staphylococcus: seen in px w/ INDWELLING
CATHETERS OTHER STUDIES
 Enterococcus: seen in px who are
PREVIOUSLY TREATED w/ ANTIBIOTICS  multiple-test dipstick often includes testing for
WBCs, known as the leukocyte esterase test, and
nitrite testing
SIGNS & SYMPTOMS IN POSTMENOPAUSAL WOMEN &  X-ray images, computed tomography (CT) scan,
OLDER ADULTS ultrasonography, and kidney scans are useful
diagnostic tools.
 Malaise  CT SCAN: detect pyelonephritis or abscesses
 Nocturia  ULTRASONOGRAPHY & KIDNEY SCANS:
 Urinary incontinence detecting obstruction, abscesses, tumors, and cysts
 Complain of foul-smelling urine
 Burning, urgency, & fever MEDICAL MANAGEMENT
 ONSET OF UTI: delirium & incontinence
DRUG CLASSES GENERIC MAJOR
ASSESSMENT AND DIAGNOSTIC FINDINGS NAME INDICATIONS
Anti-infective, Nitrofurantoin UTI
 Bacterial colony counts urinary tract Cephalexin Genitourinary
 Cellular studies Bactericidal Infection
 Urine culture Cephalosporin Cefadroxil UTI
 UNCOMPLICATED UTI: strain of bacteria Fluoroquinolone Ciprofloxacin UTI
determines antibiotic of choice Ofloxacin Pyelonephritis
Norfloxacin
URINE CULTURES Gatifloxacin
Fluoroquinolone levofloxacin Uncomplicated
 useful for documenting a UTI and identifying the UTI
specific organism present. Penicillin ampicillin UTI—not
 INFECTION: colony count >100,000 CFU/ml amoxicillin commonly used
alone due to
 GROUPS OF PATIENTS SHOULD HAVE URINE
Escherichia coli
CULTURES OBTAINED WHEN BACTERIURIA IS resistance
PRESENT Pyelonephritis
o All children UTI—not
o All men (because of the likelihood of commonly used
structural or functional alone due to E.
o abnormalities) coli resistance
o Patients who have been recently Trimethoprim– Co-trimoxazole UTI
hospitalized or who live in longterm care sulfamethoxazole Pyelonephritis
facilities combination
o Patients who have undergone recent Urinary analgesic Phenazopyridine For relief of
instrumentation (including catheterization) agen burning, pain,
of the urinary tract and other
o Patients with diabetes symptoms
o Patients with prolonged or persistent associated with
symptoms UTI
o Patients with three or more UTIs in the
previous year
o Women who are postmenopausal NURSING MANAGEMENT
o Women who are pregnant
o Women who are sexually active  To relieve pain:
o Women who have new sexual partners o Antispasmodic agents: relieving bladder
o Women with a history of compromised irritability and pain
immune function or renal o Analgesic agents and the application of
o Problem heat to the perineum help relieve pain and
spasm

BSN 3A | PBL GROUP 1 34

NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
o Encouraged to drink liberal amounts of
fluids (water and cranberry juice are the
best choices) to promote renal blood flow
and to flush the bacteria from the urinary
tract
o Coffee, tea, citrus, spices, colas, alcohol
should be avoided
o Void every 2 to 3 hours
PREVENTING RECURRENT UTI
 HYGIENE
o Shower rather than bathe in the tub
because bacteria in the bathwater may
enter the urethra.
o Clean the perineum and urethral meatus
from front to back after each bowel
movement. This will help reduce
concentrations of pathogens at the urethral
opening and, in women, the vaginal
opening.
 FLUID INTAKE
o Drink liberal amounts of fluids daily to flush
out bacteria. It may be helpful to include at
least one glass of cranberry juice per day.
o Avoid coffee, tea, colas, alcohol, and other
fluids that are urinary tract irritants.
 VOIDING HABITS
o Void every 2 to 3 hours during the day,
and completely empty the bladder. This
prevents overdistention of the bladder and
compromised blood supply to the bladder
wall. Both predispose the patient to urinary
tract infection. Precautions expressly for
women include voiding immediately after
penile-vaginal intercourse.
 INTERVENTIONS
o Take medication exactly as prescribed.
Special timing of administration may be
required.
o Keep in mind that if bacteria continue to
appear in the urine, long-term antimicrobial
therapy may be required to prevent
colonization of the periurethral area and
recurrence of infection.
o For recurrent infection, consider daily
consumption of cranberry juice or
capsules.
o If prescribed, test urine for presence of
bacteria following manufacturer’s and
health care provider’s instructions.
o Notify the primary provider if fever occurs
or if signs and symptoms persist.
o Consult the primary provider regularly for
follow-up.
UPPER URINARY TRACT INFECTIONS
 Upper UTIs are much less common than those in the
lower urinary tract.
BSN 3A | PBL GROUP 1
 Acute pyelonephritis and chronic pyelonephritis
are thought to be the most likely type, with interstitial
nephritis (inflammation of the kidney) and kidney
abscesses also a potential cause.
 Upper UTIs are a common cause of urosepsis.
 Pyelonephritis is a bacterial infection of the renal
pelvis, tubules, and interstitial tissue of one or both
kidneys. Causes involve either the upward spread of
bacteria from the bladder or spread from systemic
sources reaching the kidney via the bloodstream.
ACUTE PYELONEPHRITIS
 usually leads to enlargement of the kidneys with
interstitial infiltrations of inflammatory cells.
 Abscesses may be noted on or within the renal
capsule and at the corticomedullary junction.
 Eventually, atrophy and destruction of tubules and
the glomeruli may result.
CLINICAL MANIFESTATIONS
– Chills
– Fever
– Leukocytosis
– Bacteriuria
– Pyuria
– Low back pain
– Flank pain
– Nausea and vomiting
– Headache
– Malaise
– Painful urination
– Lower urinary tract involvement, such as urgency
and frequency, are common.
ASSESSMENT AND DIAGNOSTIC FINDINGS
– Ultrasound study or a CT scan may be performed
to locate an obstruction in the urinary tract.
– An IV pyelogram may be indicated if functional and
structural renal abnormalities are suspected.
– Radionuclide imaging with gallium citrate and
indium-111 (111In)–labeled WBCs may be useful to
identify sites of infection that may not be visualized
on CT scan or ultrasound.
– Urine culture and sensitivity tests are performed
to determine the causative organism so that
appropriate antimicrobial agents can be prescribed.
MEDICAL MANAGEMENT
– Patients with acute uncomplicated pyelonephritis are
most often treated on an outpatient basis if they are
not exhibiting acute symptoms of sepsis,
dehydration, nausea, or vomiting.
– For outpatients, a 2-week course of antibiotic agents
is recommended because renal parenchymal
disease is more difficult to eradicate than mucosal
bladder infections. Commonly prescribed agents
35
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
include many of the same medications prescribed for
the treatment of UTIs.
– Following acute pyelonephritis treatment, the patient
may develop a chronic or recurring symptomless
infection persisting for months or years. After the
initial antibiotic regimen, the patient may need
antibiotic therapy for up to 6 weeks if a relapse
occurs.
– A follow-up urine culture is obtained 2 weeks after
completion of antibiotic therapy to document clearing
of the infection.
– Hydration with oral or parenteral fluids is essential in
all patients with UTIs when there is adequate kidney
function. Hydration helps facilitate “flushing” of the
urinary tract and reduces pain and discomfort.
CHRONIC PYELONEPHRITIS
— Repeated bouts of acute pyelonephritis may lead to
chronic pyelonephritis.
— When pyelonephritis becomes chronic, the kidneys
become scarred, contracted, and nonfunctioning.
— Chronic pyelonephritis is a cause of chronic kidney
disease that can result in the need for renal
replacement therapy (RRT) such as transplantation
or dialysis.
CLINICAL MANIFESTATIONS
– No symptoms of infection unless an acute
exacerbation occurs.
– Fatigue
– Headache
– Poor appetite
– Polyuria
– Excessive thirst
– Weight loss.
– Persistent and recurring infection may produce
progressive scarring of the kidney, resulting in
chronic kidney disease.
ASSESSMENT AND DIAGNOSTIC FINDINGS
– The extent of the disease is assessed by an IV
urogram.
– Measurements of creatinine clearance, blood urea
nitrogen, and creatinine levels.
COMPLICATIONS
– End-stage kidney disease (from progressive loss of
nephrons secondary to chronic inflammation and
scarring).
– Hypertension
– Formation of renal calculi (from chronic infection with
urea-splitting organisms).
MEDICAL MANAGEMENT
– Bacteria, if detected in the urine, are eradicated if
possible.
BSN 3A | PBL GROUP 1
– Long-term use of prophylactic antimicrobial therapy
may help limit recurrence of infections and kidney
scarring.
– Impaired kidney function alters the excretion of
antimicrobial agents and necessitates careful
monitoring of kidney function, especially if the
medications are potentially toxic to the kidneys.
NURSING MANAGEMENT
– The patient may require hospitalization or may be
treated as an outpatient.
– When the patient requires hospitalization, fluid intake
and output are carefully measured and recorded.
Unless contraindicated, 3 to 4 L of fluids per day is
encouraged to dilute the urine.
– Decrease burning on urination
– Prevent dehydration
– The nurse assesses the patient’s temperature every
4 hours and administers antipyretic and antibiotic
agents as prescribed.
ADULT VOIDING DYSFUNCTION
URINARY INCONTINENCE
 sudden, intense urge to urinate followed by an
involuntary loss of urine
 unintentional passing of urine
 loss of bladder control
TYPES/SYMPTOMS OF URINARY INCONTINENCE
1. Stress Incontinence: urine leaks out at times when
bladder is under pressure (e.g. coughing or laughing)
2. Urge Incontinence: urine leaks as an intense or
sudden urge to pee
3. Overflow Incontinence (chronic urinary
retention): unable to fully empty the bladder. There
is an obstruction or blockage in the bladder.
4. Total Incontinence: bladder cannot pass urine at all
CAUSES OF URINARY INCONTINENCES
 Pregnancy or vaginal birth
 Obesity
 Family history
 Increasing age
 Urinary tract infection (UTI)
 Constipation
 Enlarged prostate
 Neurological disorders (can interfere with nerve
signals involved in bladder control)
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NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
TREATMENT
NON-SURGICAL
1. Lifestyle changes (losing weight, cutting down on
caffeine or alcohol)
2. Pelvic floor exercises (strengthening pelvic floor
muscles by squeezing them)
3. Bladder training (learning ways to wait longer
between needing to urinate and passing urine)
SURGICAL
1. Sling procedure - used to reduce pressure on the
bladder or strengthen the muscles that control
urination
2. Enlarging the bladder or implanting a device that
stimulates the nerve that controls the detrusor
muscles.
PREVENTION
 Maintain a healthy weight
 Practice pelvic floor exercises
 Avoid bladder irritants (such as caffeine, alcohol,
acidic foods).
 Eat more fiber, which can prevent constipation
URINARY RETENTION
 Urinary retention is the inability to empty the bladder
completely during attempts to void.
 Chronic urine retention often leads to overflow
incontinence
 In a healthy adult younger than 60 years, complete
bladder emptying should occur with each voiding,
with no residual.
 In adults older than 60 years, 50 to 100 mL of
residual urine may remain after each voiding
because of the decreased contractility of the detrusor
muscle.
 Urinary retention can occur postoperatively in any
patient, particularly if the surgery affected the
perineal or anal regions and resulted in reflex spasm
of the sphincters.
 General anesthesia reduces bladder muscle
innervation and suppresses the urge to void,
impeding bladder emptying.
PATHOPHYSIOLOGY
 Urinary retention may result from diabetes, prostatic
enlargement, urethral pathology (infection, tumor,
calculus), trauma (pelvic injuries), pregnancy, or
neurologic disorders (e.g., stroke, spinal cord injury,
multiple sclerosis, Parkinson’s disease).
 Some medications cause urinary retention either by
inhibiting bladder contractility or by increasing
bladder outlet resistance
ASSESSMENT AND DIAGNOSTIC FINDINGS
BSN 3A | PBL GROUP 1
 What was the time of the last voiding, and how much
urine was voided?
 Is the patient voiding small amounts of urine
frequently?
 Is the patient dribbling urine?
 Does the patient complain of pain or discomfort in the
lower abdomen? (Discomfort may be relatively mild
if the bladder distends slowly.)
 Is the pelvic area rounded and swollen (could
indicate urine retention and a distended bladder)?
 Does percussion of the suprapubic region elicit
dullness (possibly indicating urine retention and a
distended bladder)?
 Are other indicators of urinary retention present, such
as restlessness and agitation?
 Does a postvoid bladder ultrasound test reveal
residual urine?
 The patient may verbalize an awareness of bladder
fullness and a sensation of incomplete bladder
emptying.
 Signs and symptoms of UTI (hematuria, urgency,
frequency, and nocturia) may be present.
 A series of urodynamic studies may be performed to
identify the type of bladder dysfunction and to aid in
determining appropriate treatment.
 A voiding diary can be used to provide a written
record of the amount of urine voided and the
frequency of voiding.
 Postvoid residual urine may be assessed by using
either straight catheterization or an ultrasound
bladder scanner is considered diagnostic of urinary
retention.
 Normally, residual urine amounts to no more than 50
mL in the middle-aged adult and less than 50 to 100
mL in the older adult
COMPLICATIONS
 The retention of urine can lead to chronic infections
that, if unresolved, predispose the patient to renal
calculi (urolithiasis or nephrolithiasis), pyelonephritis,
sepsis, or hydronephrosis.
 Urine leakage can lead to perineal skin breakdown,
especially if regular hygiene measures are
neglected.
NURSING MANAGEMENT
 Strategies are instituted to prevent overdistention of
the bladder and to treat infection or correct
obstruction.
 The nurse explains to the patient why normal voiding
is not occurring and monitors urine output closely.
 The nurse also provides reassurance about the
temporary nature of retention and successful
management strategies.
 Promoting Urinary Elimination [Nursing measures to
encourage normal voiding patterns include providing
privacy, ensuring an environment and body position
conducive to voiding, and assisting the patient with
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NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
the use of the bathroom or bedside commode, rather
than a bedpan, to provide a more natural setting for
voiding.]
 If his condition allows, the male patient may stand
beside the bed to use the urinal; most men find this
position more comfortable and natural.
 applying warmth to relax the sphincters (e.g., sitz
baths, warm compresses to the perineum, showers),
giving the patient hot caffeine-free beverage and
offering encouragement and reassurance.
 Simple trigger techniques, such as turning on the
water faucet while the patient is trying to void, may
also be used. Other examples of trigger techniques
are stroking the abdomen or inner thighs, tapping
above the pubic area, and dipping the patient’s
hands in warm water.
 After surgery or childbirth, prescribed analgesic
agents should be given because pain in the perineal
area can make voiding difficult.
 When the patient cannot void, bladder scanning is
used to assess for distention, then straight
catheterization (as prescribed) is used to prevent
overdistention of the bladder
 In the case of prostatic obstruction, attempts at
catheterization (by the urologist) may not be
successful, requiring insertion of a suprapubic
catheter (catheter inserted through a small
abdominal incision into the bladder)
 After urinary drainage is restored, bladder retraining
is initiated for the patient who cannot void
spontaneously.
 Promoting Home, Community-Based, and
Transitional Care
 modifications to the home environment can provide
simple and effective ways to assist in treating urinary
incontinence and retention. For example, the patient
may need to remove obstacles, such as throw rugs
or other objects, to provide easy, safe access to the
bathroom.
 Other modifications that the nurse may recommend
include installing support bars in the bathroom;
placing a bedside commode, bedpan, or urinal within
easy reach; leaving lights on in the bedroom and
bathroom; and wearing clothing that is easy to
remove quickly.
NEUROGENIC BLADDER
 Neurogenic bladder is a dysfunction that results from
a disorder or dysfunction of the nervous system and
leads to urinary incontinence.
 It may be caused by spinal cord injury, spinal tumor,
herniated vertebral disc, multiple sclerosis,
congenital disorders (spina bifida or
myelomeningocele), infection, or complications of
diabetes
PATHOPHYSIOLOGY
BSN 3A | PBL GROUP 1
 The two types of neurogenic bladder are spastic (or
reflex) bladder and flaccid bladder.
 Spastic bladder is the more common type and is
caused by any spinal cord lesion above the voiding
reflex arc (upper motor neuron lesion). The result is
a loss of conscious sensation and cerebral motor
control.
 A spastic bladder empties on reflex, with minimal or
no controlling influence to regulate its activity.
 Flaccid bladder is caused by a lower motor neuron
lesion, commonly resulting from trauma. This form of
neurogenic bladder is also increasingly being
recognized in patients with diabetes.
 The bladder continues to fill and becomes greatly
distended, and overflow incontinence occurs.
 The bladder muscle does not contract forcefully at
any time. Because sensory loss may accompany a
flaccid bladder, the patient feels no discomfort.
ASSESSMENT AND DIAGNOSTIC FINDINGS
 Evaluation for neurogenic bladder involves
measurement of fluid intake, urine output, and
residual urine volume; urinalysis; and assessment of
sensory awareness of bladder fullness and degree of
motor control. Comprehensive urodynamic studies
are also performed.
COMPLICATIONS
 The most common complication of neurogenic
bladder is infection resulting from urinary stasis and
catheterization.
 Other complications include renal calculi, impaired
skin integrity, and urinary incontinence or retention.
MEDICAL MANAGEMENT
 Several long-term objectives appropriate for all types
of neurogenic bladders include preventing
overdistention of the bladder, emptying the bladder
regularly and completely, maintaining urine sterility
with no stone formation, and maintaining adequate
bladder capacity with no reflux.
 Specific interventions include continuous,
intermittent, or self-catheterization (discussed later in
this chapter); the use of an external condomtype
catheter; a diet low in calcium (to prevent calculi);
and encouragement of mobility and ambulation.
 A liberal fluid intake is encouraged to reduce the
urinary bacterial count, reduce stasis, decrease the
 concentration of calcium in the urine, and minimize
the precipitation of urinary crystals and subsequent
stone formation.
 A bladder retraining program may be effective in
treating a spastic bladder or urine retention.
 The use of a timed, or habit, voiding schedule may
be established.
 To further enhance emptying of a flaccid bladder, the
patient may be taught to “double void.” After each
38
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
voiding, the patient is instructed to remain on the
toilet, relax for 1 to 2 minutes, and then attempt to
void again in an effort to further empty the bladder
PHARMACOLOGIC THERAPY
 Parasympathomimetic medications, such as
bethanechol, may help to increase the contraction of
the detrusor muscle.
SURGICAL MANAGEMENT
 Surgery may be carried out to correct bladder neck
contractures or vesicoureteral reflux, or to perform a
urinary diversion procedure.
URINARY CATHETERS
 When urine cannot be eliminated naturally and must
be drained artificially, catheters may be inserted
directly into the bladder, the ureter, or the renal pelvis
Catheterization is performed to achieve the following:
 Assist with postoperative drainage in urologic and
other surgeries
 Provide a means to monitor accurate urine output in
patients who are critically ill
 Promote urinary drainage in patients with neurogenic
bladder dysfunction, urine retention, or at end-of-life
care
 Prevent urinary leakage in patients with stage III to
IV pressure injuries
 Relieve urinary tract obstruction
NOTE: An indwelling urinary catheter should be placed only if
necessary because catheterization commonly leads to
CAUTI.
INDWELLING CATHETERS
 Use strict aseptic technique during insertion of the
smallest catheter possible
 Secure the catheter to prevent movement
 Frequently inspect urine color, odor, and consistency
 Perform daily perineal care with soap and water
Maintain a closed system
 Follow the manufacturer’s instructions when using
the catheter port to obtain urine specimens
Discontinue use as soon as feasible
SUPRAPUBIC CATHETERS
 Suprapubic catheterization allows bladder drainage
by inserting a catheter or tube into the bladder
through a suprapubic (above the pubis) incision or
puncture
 The catheter or suprapubic drainage tube is then
threaded into the bladder and secured with sutures
BSN 3A | PBL GROUP 1
or tape, and the area around the catheter is covered
with a sterile dressing.
 The catheter is connected to a sterile closed
drainage system, and the tubing is secured to
prevent tension on the catheter. This may be a
temporary measure to divert the flow of urine from
the urethra when the urethral route is impassable
(because of injuries, strictures, prostatic obstruction),
after gynecologic or other abdominal surgery when
bladder dysfunction is likely to occur, and
occasionally after pelvic fractures.
 A permanent indwelling suprapubic catheter may be
needed in the patient who is incontinent following a
spinal cord injury
 Suprapubic bladder drainage may be maintained
continuously for several weeks.
 When the patient’s ability to void is to be tested, the
catheter is clamped for 4 hours, during which time
the patient attempts to void.
 After the patient voids, the catheter is unclamped,
and the residual urine is measured. If the amount of
residual urine is less than 100 mL on two separate
occasions (morning and evening), the catheter is
usually removed.
 if the patient complains of pain or discomfort, the
suprapubic catheter is usually left in place until the
patient can void successfully
 Patients can usually void sooner after surgery than
those with urethral catheters, and they may be more
comfortable.
 The catheter allows greater mobility, permits
measurement of residual urine without urethral
instrumentation, and presents less risk of bladder
infection.
 The suprapubic catheter is removed when it is no
longer required, and a sterile dressing is placed over
the site.
 The patient requires liberal amounts of fluid to
prevent encrustation around the catheter.
 Other potential problems include the formation of
bladder stones, acute and chronic infections, and
problems collecting urine.
 A wound-ostomy continence (WOC) nurse may be
consulted to assist the patient and family in selecting
the most suitable urine collection system and to
educate them about its use and care.
NURSING MANAGEMENT
 Assessing the Patient and the System: Patients at
high risk for CAUTI need to be identified and
monitored carefully.
 They are observed for signs and symptoms of
CAUTI: cloudy malodorous urine, hematuria, fever,
chills, anorexia, and malaise. Any drainage and
excoriation in the area around the urethral orifice is
noted. Urine cultures provide the most accurate
means of assessing a patient for infection.
PREVENTING INFECTION
39
NCM112 LECTURE
MEDICAL-SURGICAL NURSING
FLUID DISTRUBANCES, ELECTROLYTE IMBALANCES, RENAL AND KIDNEY DISORDERS
 Certain principles of care are essential to prevent
infection in patients with a closed urinary drainage
system
 Avoid contamination of the drainage spout. A
receptacle in which to empty the bag is provided for
each patient. Avoid routine catheter changes.
 The catheter is changed only to correct problems
such as leakage, blockage, or encrustations. Avoid
unnecessary handling or manipulation of the
catheter by the patient or staff.
 Carry out hand hygiene before and after handling
the catheter, tubing, or drainage bag.
 Ensure a free flow of urine to prevent infection.
Improper drainage occurs when the tubing is
kinked or twisted, allowing pools of urine to collect
in the tubing loops.
 Evaluate the benefit of placing an indwelling urinary
catheter versus the risk of the patient developing a
catheter-associated urinary tract infection (CAUTI).
 If the collection bag must be raised above the level
of the patient’s bladder, clamp the drainage tube.
This prevents backflow of contaminated urine into
the patient’s bladder from the bag.
 Monitor the patient’s voiding when the catheter is
removed. The patient must void within 8 hours; if
unable to void, the patient may require
catheterization with a straight catheter.
 Never disconnect the tubing to obtain urine
samples, to irrigate the catheter, or to ambulate or
transport the patient.
 Never irrigate the catheter routinely. If the patient is
prone to obstruction from clots or large amounts of
sediment, use a three-way system with continuous
irrigation. Never leave the catheter in place longer
than is necessary to decrease the risk of CAUTI.
Obtain a urine specimen for culture at the first sign
of infection.
 To prevent contamination of the closed system,
never disconnect the tubing. The drainage bag
must never touch the floor.
 The bag and collecting tubing are changed if
contamination occurs, if urine flow becomes
obstructed, or if tubing junctions start to leak at the
connections.
 To reduce the risk of bacterial proliferation, empty
the collection bag at least every 8 hours through
the drainage spout—more frequently if there is a
large volume of urine.
 Use scrupulous aseptic technique during insertion
of the catheter. Use a preassembled, sterile, closed
urinary drainage system of the smallest catheter
size possible to minimize trauma.
 Wash the perineal area with soap and water at
least twice a day; avoid a to-and-fro motion of the
catheter.
 Dry the area well, but avoid applying powder
because it may irritate the perineum
BSN 3A | PBL GROUP 1
RETRAINING THE BLADDER WHEN AN INDWELLING,
 urinary catheter is in place, the detrusor muscle
does not actively contract the bladder wall to
stimulate emptying because urine is continuously
draining from the bladder. As a result, the detrusor
may not immediately respond to bladder filling
when the catheter is removed, resulting in either
urine retention or urinary incontinence. This
condition, known as postcatheterization detrusor
instability, can be managed with bladder retraining
 Immediately after the indwelling catheter is
removed, the patient is placed on a timed voiding
schedule, usually every 2 to 3 hours.
 At the given time interval, the patient is instructed
to void. The bladder is then scanned using a
portable ultrasonic bladder scanner, and if the
bladder has not emptied completely, straight
catheterization may be performed
 After a few days, as the nerve endings in the
bladder wall become resensitized to the bladder
filling and emptying, bladder function usually
returns to normal. If the patient has had an
indwelling catheter in place for an extended period
(e.g., greater than 1 month), bladder retraining will
take longer; in some cases, function may never
return to normal, and long-term intermittent
catheterization may become necessary.
ASSISTING WITH INTERMITTENT SELF-
CATHETERIZATION.
 Intermittent self-catheterization provides periodic
drainage of urine from the bladder.
 By promoting drainage and eliminating excessive
residual urine, intermittent catheterization protects
the kidneys, reduces the incidence of UTIs, and
improves continence.
 It is the treatment of choice in some patients with
spinal cord injury and other neurologic disorders,
such as multiple sclerosis, when the ability to
empty the bladder is impaired. Self-catheterization
promotes independence, results in few
complications, and enhances self-esteem and
quality of life.
40