Anda di halaman 1dari 83

Test 2/Unit 2/September 25, 2009

Fluids & Electrolytes/Accessory Organs


Chapter 44 pgs.1087-1133 Liver, pancreas & biliary tract problems
Chapter 16 pgs.289-290 Tunneled catheters
Chapter 17 pgs.315-341 Fluid, electrolyte & acid-base imbalances
Chapter 31 pgs.730-734 Blood transfusions
Chapter 40 pgs.965-968 Parenteral nutrition
FLUIDS AND ELECTROLYTES
INTRODUCTION
Fluid and electrolytes are an important foundational concept of the nursing curriculum. Every
course, throughout your program, will integrate the fluid and electrolyte information you learned
in nursing process. In this course you will add to your basic knowledge of fluid and electrolytes
by learning how these imbalances result is alterations effecting the GI/GU systems.
The unit starts with a fluid and electrolyte review. If you have trouble with any section of this
activity you should stop and revisit some of the basic information that was introduced to you in
nursing process. The fluid and electrolyte content from NUR 1021 has been uploaded into this
course so that you can easily review this information. The time you spend doing this review will
serve you well!
The next section of material, after the review, deals with body fluids. The distribution of body
fluids, fluid compartments, functions of body fluids, osmolality of body fluids and osmolarity of
solutions are discussed. Activities have been developed to aid you in learning this material.
The third section of this module is related to electrolytes. You will be responsible for six
electrolytes which are potassium, sodium, calcium, magnesium, phosphorus and chloride. Be
sure to focus in on their relation to human body functions, pathophysiology, clinical
manifestations and management. Also know normal serum levels and foods rich in these
electrolytes. Activities have been developed for portions of this section of material.
The fourth section of this unit deals with acid/base. Our body fluid must maintain a balance
between acidity and alkalinity for life to be maintained. Activities have been developed that will
assist you in the determination of acid/base imbalances including respiratory alkalosis and
acidosis; and metabolic alkalosis and acidosis.
Fluid/ Electrolyte and Acid/Base
Study Questions
1. What do these terms mean:

acidosis
active transport
aldosterone
alkalosis
angiotensin I and II
baroreceptor
compensation
diffusion
extracellular fluid (ECF)
hydrostatic pressure
hypertonic
hypotonic
hypovolemia
hypervolemia
interstitial fluid
intracellular fluid (ICF)
isotonic
oncotic pressure
osmolality
osmolarity
osmosis
osmotic pressure
2. What is the role of the pituitary gland in controlling fluid balance?
3. What is the role of aldosterone in controlling fluid balance?
4. What are the names of the body fluid compartments and how are interrelated?
5. What is the function of the kidney's in controlling extracellular fluids?
6. What are the signs and symptoms of hypovolemia?
7. What are the signs and symptoms of hypervolemia?
8. What are the routes that fluids leave the body and what organ is involved?
9. What is the effect that isotonic, hypotonic, and hypertonic have on serum osmolality?
10.Which IV fluids are isotonic, hypotonic and hypertonic.?
11.What are the indications for using isotonic, hypotonic and hypertonic solutions?
12.What is the normal serum osmolality and what is the meaning of high and low values?
13.What is the relationship between thirst and osmolality?
14.How is serum osmolality calculated?
15.What is the normal ranges for sodium, potassium, chloride, magnesium, calcium, and phosphorus?
16.What electrolyte is found primarily intracellular and what electrolyte is primarily found extracellular?
17.What is the physiologic functions of potassium, sodium, calcium, magnesium, phosphorus, and
chloride?
18.What are the common signs and symptoms of a patient with hypo/hyperkalemia, hypo/hypernatremia,
hypo/hypercalcemia, hypo/hypermagnesemia, hypo/hyperphosphatemia and hypo/hyperchloremia?
19.What is the common treatments used in the correction of hypo/hyperkalemia, hypo/hypernatremia,
hypo/hypercalcemia, hypo/hypermagnesium, hypo/hyperphosphatemia and hypo/hyperchloremia?
20.What common foods are high in potassium, sodium, calcium, magnesium, phosphorus, and chloride?
21.What is the interaction between hypokalemia and digitalis?
22.What are the normal ranges of pH, PaCO2, HCO3, and PaO2?
23.What are the steps in interpreting ABGs, including compensatory status?
24.What are the ways the lungs and kidneys compensate for acid/base imbalances?
25.What are the common causes of acid/base imbalance?
26. What are the common interventions done to correct acid/base imbalance?
Fluid/ Electrolyte and Acid/Base
Fluid Balance
The most abundant fluid in the body is water, which constitutes 60% of total body weight. Body
fluids are made of water and solutes (dissolved substances), such as electrolytes, nutrients and
waste products. Body fluids are found both inside and outside the cells.
The functions of body fluids are to:
• Transport nutrients, oxygen, carbon dioxide, waste products to and from the cells
• Act as a medium for chemical reactions
• Regulation of body temperature
• Provide insulation, lubrication. Cushion for the body and its cells
The body strives to maintain fluid balance thorough a variety of mechanisms including the fluid
intake and the body's output of fluid. These two should be approximately equal. For instance:
Intake:
• Oral fluids = 1200cc
• Water in food = 1000cc
• Water produces by metabolism = 300 cc
• Total = 2500cc
Output:
• Urine = 1500cc
• Feces = 200cc
• Insensible loss
• Perspiration = 300cc
• Respiration = 500cc
• Total = 2500cc
Fluid Compartments
The two major fluid compartments are the intracellular (all fluid inside the cells) and
extracellular (all fluid outside the cells). The extracellular compartment is further divided into
intravascular and interstitial compartments. A third smaller compartment is the transcellular
compartment. Fluid is able to more from one compartment to another. Water that is found in the
bones and other dense tissue cannot move form one area to another and is not considered a
compartment.
• Intracellular compartment
o Fluid inside the body cells
o Represents 2/3 of the body water
o Represents 42% of the body weight
• Extracellular compartment
o Fluid outside body cells
o Represents 1/3 of all body water
o Represents 15% of body weight
o Has 2 divisions
• Intravascular
o Fluid outside the cells within the circulatory system
o Represents 7.5% of body water
o 4.5% of body weight
• Interstitial fluid
o Fluid outside the cells and not in the circulatory system
o Represents 17.5% of body water
o Represents 10.5% of body weight
• Transcellular Space
o Small fluid compartment
o Consists of approximately 1L of fluid
o Fluid in this space is secreted and reabsorbed by epithelial cells
o If the fluid is not reabsorbed but lost, this can produce serious fluid and electrolyte
balances
o Includes:
 Fluid in the cerebrospinal space
 Fluid in the GI tract
 Fluid in the pleural, synovial, and peritoneal spaces
Other Factors Related to Fluid Balance
Fluid Spacing
This term describes the distribution of body water. Normally the ECF and the ICF are isotonic to
each other and no movement of water occurs. If a cell is surrounded by hypotonic fluid, water
moves into the cell, causing it to swell or burst. If a cell is surrounded by hypertonic fluid, water
moves out of the cell and the cell shrinks and may eventually die.
• First spacing
o Normal distribution of fluid in the ICF and ECF compartment
• Second Spacing
o Abnormal accumulation of interstitial fluid
o Edema
• Third spacing
o Fluid accumulation in areas that normally have no fluid or only minimal fluid
o Ascites
The term third spacing is used to describe extracellular fluid that has become trapped in a body
space as a result of a disease process or injury. Because this fluid has usually been lost from the
vascular compartment and is unavailable, it places the patient at risk for shock. Common sites of
this fluid to be trapped are the bowel, the pleural or pericardial spaces, or joints. Because this
fluid is still in the body, the usual means for assessment, such as intake/output imbalances or
weight changes, cannot detect this loss, and it may not be noted until an organ dysfunction
occurs.
Effective Circulating Blood Volume
• Plasma volume in addition to the blood cells circulating within the vessels
• Volume perfusing the tissues and sensed by the volume receptors
• Normally varies according to the ECF volume
• May be altered in certain clinical conditions where the volume between the interstitial fluid
and the ECBV shifts

Fluid/ Electrolyte and Acid/Base


Dynamics of Fluid and Electrolyte Movement
Fluids and electrolytes have the ability to move from compartment to compartment. There are
several factors that influence this movement: the substance that is shifting, the concentration of
the substance in the compartments, the type of membrane that surrounds the compartment and
various pressures.
Membranes:
• Cell membranes
o Separate cells from the interstitial fluid
o Selectively permeable: allows only certain molecules to move
 Oxygen
 Carbon dioxide
 Water
 Small water soluble molecules
o Proteins and other colloids cannot move thought this membrane
• Capillary membranes
o Separates the vascular compartment form the interstitial compartment
o Membrane has pores that allows certain molecules to pass through:
 Glucose
 Electrolytes
 Dissolved gases
 Water
Movement of Fluid
Osmosis
• Water moves through a membrane that allows water to move, but solutes may not.
• Water moves based on a concentration gradient.
• The water moves from an area of lower concentration of solutes to higher concentration.
Osmosis requires no outside energy source.
• Continues as long as the concentration remains unequal or the hydrostatic pressure
increases
• Main mechanism for movement of body fluid between the intracellular and
extracellular compartments
Movement of Molecules
Diffusion
• Molecules movement from an area of high concentration to an area of low concentration
• Movement stops when concentration becomes equal
• Molecules move between the intracellular and extracellular compartments in this way
• Requires no energy
Facilitated Diffusion
• Carrier substances aid molecules in crossing cell membranes
• Requires no energy
Active Transport
• Movement of molecules against a concentration gradient
• Requires energy
• Example: cells have a high concentration of K, extracellular compartments do not, in order
to maintain the concentration in the cell, active transport is used.
Movement of Fluid and Molecules
Filtration
• Movement occurs due to a pressure gradient rather than concentration.
• Water and solutes move
• Used to move water and solutes out of capillaries
• Mechanism used by kidneys and to move fluid and electrolytes into the interstitial space at
the arterial ends of capillaries
• Process will be discussed further later in this section under hydrostatic pressure
Influences on Fluid Movement
Tonicity
Tonicity refers to the effect on cells by the osmolality of fluid around them. Isotonic fluids have
the same osmolality as the inside of the cell. Fluids that are more concentrated than the fluid in
the cell are considered hypertonic . Fluids with less concentration than the fluid within the cells
are considered hypotonic .
• Isotonic solutions
o same amount of solute as the inside of the cell
o no net movement of water
• Hypertonic solutions
o more solute than found on the inside of the cell
o water moves from lesser concentration to greater
o water leaves the cell
o cell crenates (wrinkles and shrinks)
• Hypotonic solutions
o less solute than found on the inside of the cell
o water moves from lesser to greater concentration
o water moves into the cell
o cell becomes swollen and ruptures
Pressures that Influence Fluid Movement
Osmotic Pressure
This is the amount of pressure necessary to stop the flow of fluid from moving across the
semipermeable membrane. The concentration of solutes in solution determines the osmotic
pressure. It is measured in milliosmoles (mOsm).
Hydrostatic Pressure
This is the force exerted by a fluid against the walls that contain it. The pumping action of the
heart creates hydrostatic pressure in the vascular system. In the capillary, this pressure is high
on the arterial end and low at the venous end. Hydrostatic pressure is the major push that
moves fluid out of the vascular system at the capillary level. Although hydrostatic pressure
exists in tissues, it is a minimal pressure under normal conditions.
Oncotic Pressure
Oncotic pressure is also called colloidal osmotic pressure. In the body the plasma proteins,
particularly albumin, exert this pressure which serves as a source to pull or attract water.
Normally, proteins do not pass through the capillary pores because of their large size. Only a
small amount of protein is found in the interstitial space. This protein exerts a lower oncotic
pressure than found in the capillaries.
Fluid Movement in the Capillaries
There is normally movement between the capillaries and the interstitial tissue. The amount and
direction of this movement are determined by the interaction of:
• Capillary hydrostatic pressure
• Plasma oncotic pressure
• Interstitial hydrostatic pressure
• Interstitial oncotic pressure
Let's look at how these pressures facilitate this fluid movement.
Arterial End:
• The hydrostatic pressure (push out) in the arterial end of the capillary is about 40 mm Hg.
• The plasma oncotic pressure (pulling in) is 25 mm Hg and serves to keep fluid in the
capillary.
• The difference is 15 mm Hg. The pushing out pressure is higher than the pulling in
pressure. Because the pressure in the tissues is low, fluid moves out of the capillaries.
Venous End:
• The hydrostatic pressure (push out pressure) at the venous end of the capillary is about
10 mm Hg.
• The plasma oncotic pressure (pulling in) remains pretty constant at 25 mm Hg.
• Because the pulling in pressure is lower than the pushing out pressure, fluid is able to
move back into the capillary.
Fluid Shifts
Fluid may accumulate in the interstitial space if:
• The venous hydrostatic pressure is too high . Conditions such as congestive heart failure
cause venous congestion, raising the hydrostatic pressure in the veins. If becomes equal
to the oncotic pressure, fluid will not be pulled back into the capillary, causing fluid to
remain in the tissues, a condition known as edema.
• The plasma oncotic pressure is too low . Conditions, such as liver disease, cause a
decrease in proteins in the plasma, thus lowering oncotic pressure. The pulling in pressure
decreases and fluid remains in the tissues or edema.
• There is a rise in interstitial oncotic pressure . Normally this pressure is low, but injuries to
the vessel walls can cause proteins to leak into the tissues. The interstitial oncotic
pressure rises, pulling (or keeping) fluid in the tissues.
Fluid may shift into the plasma if:
• The plasma oncotic pressures increases . Administration of colloids solutions (protein
containing) or hypertonic solutions would cause fluid to be pulled from the tissues into the
capillary. These could be used as a treatment of edema.
• The tissue hydrostatic pressure is increased . By raising this pressure, fluid is forced back
into the capillary. Tissue hydrostatic pressure can be increased by placing elastic stockings
on the legs.

FLUIDS AND ELECTROLYTES


Nursing Assessment of Fluid and Electrolyte Balance
The nurse must be aware of common ways to assess fluid and electrolyte imbalances.
History:
• Question about diseases or conditions which frequently cause F & E imbalances
o Examples:
 Vomiting
 Diarrhea
 Renal diseases
 Liver diseases
 Congestive heart failure
o Use of drugs that can cause F & E imbalance
 Examples
 Diuretics
 Steroids
o Thirst
o Urination
Physical Findings:
• Vital signs
• Skin
• Jugular veins
• Level of consciousness
• Reflexes
• Thirst
• Weight
Calculation of Fluid Gains or Losses
One liter of water (1000 ml) weights 2.2 lbs (1 kg). Fluid gains or losses can be calculated using
this information. For example, a weight gain of 2 lbs within a few days may be an indication of
fluid retention of close to 1000 ml. of fluid. Conversely a loss of 2 lbs within a day or so may
indicate a loss of 1000 ml of fluid.

The most significant indicator of fluid gain or loss is a daily weight.


Measuring I & O
• Can be instituted without an order
• If patient is receiving IV fluids, the pat should be on I & O
• Notify patient
• Post sign
• Intake includes:
o All oral intake (or tube feedings)
o All IV intake
o Any fluids instilled into the body and not returned
• Output includes:
o Urine
o Emesis
o Liquid stool
o Drainage from wounds
o Drainage in suctioning devices
• Should be totaled each shift and balance calculated each 24 hours
• Balance is considered form the body's standpoint
o If patient takes in more than excretes, considered a positive balance
o Patient excretes more than intake, patient is in a negative balance

Common Abnormal Findings and their Significance


Parameter Finding Significance

Temperature Increased Fluid loss

Pulse Increased Fluid loss

x Weak Fluid loss

x Bounding Fluid excess

x Irregular K, Ca or Mg, imbalance

Respirations Increased Fluid loss

x Deep, rapid Alkalosis

x Slow, shallow Acidosis


BP Decreased Fluid loss

x Increased Fluid excess

Breath Sounds Crackles or dyspnea Fluid excess

Skin Condition Dry Fluid loss

Skin Turgor Nonelastic (tenting) Fluid loss

Edema If present Fluid excess

Tongue Furrowing Fluid loss

Mucus membranes Dry Fluid loss

Jugular Vein Distended (JVD) Fluid excess

Hand veins Increased filling time Fluid loss

x Increase time to empty Fluid excess

Level of consciousness Decreased Fluid excess or loss


Electrolyte imbalances

Restlessness Present Na excess


K loss

Confusion Present Fluid excess


Na or K loss,
Ca, Mg excess

Seizures Present Na imbalance


Ca loss

Reflexes Increased K loss


Ca excess

x Decreased Mg excess

Chovsteks' See calcium x

Trousseaeu See calcium x

Extremity Numbness, tingling Ca loss


K excess
FLUIDS AND ELECTROLYTES
Diagnositc Testing for Fluid and Electrolyte Imbalances
FLUID BALANCE
Osmolality and Osmolarity
• Osmolarity
o Amount of solute per liter of solution
o Reported in mOsm/L
• Osmolality
o Amount of solute per kilogram of water
o Measured in mOsm/kg
• Because body fluids are relatively dilute, these terms are often used interchangeably
• Typically the test performed to evaluate the concentrations of plasma and urine
• Approximately the same in the various body fluid spaces
• Can be used to determine the water balance of the body
• Normal plasma value of osmolality is between 275 and 295 mOsm/kg
o >295 mOsm/kg indicates that the concentration of a particular particle is too high,
or the water content is too low
 Water deficit
o <275 mOsm/kg indicates too low solute for the amount of water or too much water
for the amount of solute
 water excess
Specific Gravity
• Measures the amount of particles in the urine
• Normal value 1.010 - 1.020
• Increased value: urine is more concentrated, fluid loss
• Decreased value: urine is dilute, fluid excess
BUN
• Measures the urea nitrogen in the blood
• Used to evaluate renal function
• Is affected by hydration status
• Low BUN: Fluid excess dilutes the BUN.
• High BUN: Fluid loss concentrates the BUN.
• Many other factors affect this level, so evaluate it in conjunction with other findings
Hematocrit
• Measures the amount of RBC's versus the total blood volume
• Total blood volume is made of RBC's and plasma
• Amount of plasma is directly related to changes in fluid volume in the body
• High HCT: Fluid loss makes the number of RBC's higher
• Low HCT: Fluid excess makes the number of RBC's versus total volume seem low
• Many other factors affect this level, so use it in conjunction with other findings
Electrolyte Levels
These will be discussed with each imbalance.
Summary
Test (Normal) Value Significance

Osmolality (275-295 High (concentrated) Fluid loss


mOsm/kg)

x Low (dilute) Fluid excess

Specific Gravity (1.010 High (concentrated) Fluid loss


-1.020)

x Low (dilute) Fluid excess


BUN (10-20 mg/dl) High (concentrated) Fluid loss

x Low (dilute) Fluid excess

Hematocrit ( Male 42- High (concentrated) Fluid loss


52%, female 37-47%)

x Low ( dilute) Fluid excess

FLUIDS AND ELECTROLYTES


Calculating Serum Osmolality
Knowing the patient's fluid status is important to know and yet very easy to calculate.
You will need the patient's serum sodium level, plus the glucose and BUN.
Here are the formula's:
If the glucose is normal: osmolality = serum sodium X2
If the glucose is abnormal: Osmolality = (serum sodium X2) + (glucose/ 18) + (BUN/ 2.4)
Example: Na 120, BS = 100, BUN = 10
Glucose is normal
Osmolality: 120 X 2 = 240
(This patient is in fluid overload because the osmolality is less than 275)
Example: Na 120, BS = 126, BUN = 10
Glucose is abnormal
Osmolality: (120 X 2) + (126/ 18) + (10/ 2.4) = 251
(This patient is also in fluid overload)

FLUIDS AND ELECTROLYTES


Regulation of Water Balance
A number of regulatory mechanisms control water volume and osomlality.
Antidiuretic Hormone (ADH)
Tiny receptors called osmoreceptors, located in the hypothalamus, sense changes in the
concentration of the plasma (osmolality). If the plasma is too concentrated, the pituitary
releases ADH.
ADH, a hormone made in the hypothalamus is stored in the posterior pituitary. When it is
released in to the blood, it acts in the distal and collecting tubules of the kidneys. It signals the
kidneys to hold in the water and this increases the plasma vascular volume. When the
concentration is decreased the opposite happens. ADH is not released and kidneys eliminate the
excess fluid through the urine. Remember "When you got the "D" you don't pee!).
Thirst
One of the main regulators of fluid intake is the thirst mechanism. Thirst receptors, found in the
hypothalamus, sense an increase in osmolality (increased concentration) or a decrease in blood
pressure. Thirst is then stimulated and the patient takes in fluids. The patient who cannot
identify or act on this sensation is at risk for a fluid volume deficit.
Social situations and psychological states may affect fluid consumption. For example, anxiety
causes a dry mouth. This is the body's response from stimulation of the autonomic nervous
system. When in a social setting, individuals have something to drink even when not particularly
thirsty. In these cases the output will compensate for intake.
Pituitary Regulation
The hypothalamus stimulates the posterior pituitary to release ADH. Other factors that stimulate
ADH release are:
• Stress
• Nausea
• Nicotine
• Morphine
Disorders of ADH release can cause fluid balance problems. These disorders will be discussed in
further detail in the endocrine section of this course.
Alcohol inhibits the release of ADH. That is the reason an individual has increased urination after
several beers (or drinks). Although a cold beer may taste great when you are thirsty on an
extremely hot day, it is the quickest route to becoming dehydrated.
Aldosterone
A decrease in blood volume results in decreased perfusion of the kidneys. This decreased
perfusion stimulates the renin angiotension system. A chain of events then occurs that results in
vasoconstriction and the secretion of aldosterone by the adrenal cortex. Aldosterone causes the
conservation of sodium and water by the kidneys and the excretion of potassium.
Renal Regulation
The kidneys are the major organs responsible for regulating fluid volume and electrolytes.
Healthy kidneys either secrete or reabsorb water and electrolytes according to the body's intake
and needs. In the average adult, the kidney reabsorbs 99% of the filtrate and produces about
1.5 L of urine per day. If excess fluid or electrolytes are ingested, healthy kidneys are able to
excrete them.
Cardiac Regulation
Atrial natriuretic peptide (ANP) is a cardiac hormone found in the atria of the heart that is
released when atria are stretched by high blood volume or high BP. It works to lower blood
volume or BP by causing vasodilation of blood vessels and suppression of the renin-angiotensin
system. It also decreases aldosterone, which is released by the adrenal glands, causing
increased urinary excretion of sodium and water. ADH (anti-diuretic hormone), released by the
pituitary gland, causes increased urinary excretion of water. Lastly, ANP increases glomerular
filtration rate, increasing the rate of urine production and water excretion.
Gastrointestinal Regulation
Daily water intake and output are between 2000 – 3000 mls. An average person should take in
about 2500 ml of fluid each day, mostly through the GI tract. This intake includes fluids, water
created from food metabolism, and the water found in solid foods. The GI tract accounts for only
a small fluid loss in the feces.
Insensible Water Loss
Insensible water loss is unavoidable water loss. The body loses about 900 ml/day through the
lungs and skin. Changes in metabolism or body temperature can increase this insensible fluid
loss. Increases in the body temperature and increased exercise cause increases in metabolism.
Excessive sweating (sensible perspiration) caused by fever or high environmental temperatures
may lead to large losses of water and electrolytes.

FLUIDS AND ELECTROLYTES


Hypovolemia (Fluid Volume Deficit)
Fluid deficits can result from and insufficient fluid intake or excessive loss or both. Depending on
the type of fluid lost, sometimes hypovolemia may be accompanied by electrolyte and acid-base
imbalances. An extreme fluid loss from the ECF may result in shock. When hypovolemia goes
untreated for a long period of time, it can result in acute renal failure. The cause is usually
abnormal losses from:
• Skin
o Excess sweating
• Gastrointestinal tract
o Vomiting
o Diarrhea
o GI suctioning
• Renal losses
o Diuretics
• Bleeding
• Decreased intake
o Altered thirst
o Inability to ingest fluid
• Third spacing
o Burns
o Trauma
(It is often hard to separate sodium effects and fluid problems, as sodium affects fluid volume.)
Clinical Manifestations
Mild Hypovolemia
• Anorexia
• Fatigue
• Weakness
Moderate Hypovolemia
• Orthostatic hypotension
• Tachycardia
• Decreased CVP
• Decreased urinary output
Severe Hypovolemia
• Supine hypotension
• Rapid, thready pulse
• Cool, clammy skin
• Oliguria
• Confusion, stupor, coma
Other findings
• Weight loss
• >2% mild deficivt
• >5% moderate
• >8% severe
• Slow hand vein filling
Diagnostic Tests
• BUN: elevated
• Hematocrit:
o Elevated with dehydration
o Decreased in the presence of bleeding

The hematocrit stays within normal ranges immediately following


an acute hemorrhage, but over a time from of several hours the
shift from the interstitial fluid to the plasma drops the
hematocrit.
• Serum electrolytes
o Varies depending on the type of fluid lost
o Hyponatremia occurs in most types of hypovolemia
• Urine Specific Gravity
o Increased
o Fixed in renal disease
Nursing Interventions
• Assess
o Vital signs (pay close attention to peripheral pulses)
o Assess for orthostatic hypotension
o Skin turgor, mucous membranes, tongue
o Flattened neck veins
o Neurological status
o Capillary refill
o Weight
• Monitor
o Body temperature
o CVP
o I&O
o Daily weights
• Monitor fluid replacement therapy
o The type of IV fluid replacement depends on the type of fluid lost and the severity
of the deficit
o Encourage oral fluids if permitted
(Discussion of intravenous fluid types is found in the section of Intravenous therapy
Be sure to review which types are hypertonic, isotonic, hypotonic).
FLUIDS AND ELECTROLYTES
Fluid Volume Excess
There are several types of fluid excess. An isotonic excess is known as hypervolemia and means
that the fluid excess is confined to the extracellular compartment. Both the extracellular and
intracellular compartments expand in hypotonic excess (also known as water intoxication).
Excess ingestion of hypertonic solutions results in expansion of the extracellular compartment
and a decrease in the intracellular compartment.
Excess fluid can result in congestive heart failure and pulmonary edema
Causes
• Disorders of ADH
• Abnormal renal function
• Extreme administration of intravenous fluids
• Interstial-to-plasma fluid shift
o Osmotic solutions
 Hypertonic saline
o Colloid solutions
 Albumin
• Fluid retention
o Heart failure
o Oliguric phase of renal failure
o Cirrhosis
o Excessive administration of glucocorticoids
• Administration of steroids
Clinical Manifestations
• Shortness of breath
• Orthopnea
• Increased BP
• Increased CVP
• Rales, rhonchi, wheezes
• Bounding pulses
• Ascites
• Distended neck veins
• Weight gain
• Edema
• Lethargy, confusion
Diagnostic Tests
• Hematocrit
o Decreased from hemodilution
• BUN
o Increased in renal failure
o Decreased in hypervolemia
• Serum Osmolality
o Decreased
• Urine Specific Gravity
o Decreased if the kidney is able to excrete the excess volume
o Fixed in renal failure
• Chest x-ray
Collaborative Care
• Diuretics: cause excretion of sodium and water
• Treat underlying cause
Nursing Interventions
• Daily weights
• I&O
• Assisting in identifying the cause
• Monitoring diuretic therapy
• Maintaining fluid (and sodium if warranted) restrictions
• Monitoring electrolytes
• Assessing
o For presence of edema (including dependent edema)
o Assessing neurological status
o Monitoring vital signs
 BP
o Cardiac Status
o Lung sounds
o Capillary refill
o Skin for pressure points
• Monitoring EKG changes
• Elevate edematous lower extremities (unless pulmonary edema or heart failure exists)
• Support edematous hands or arms on pillows
• Turn the client
• Teach clients about:
o Sodium containing foods (if this is pertinent to the cause of hypervolemia)
o Medications
o Fluid restrictions
o Weighing themselves daily
o Signs and symptoms of increased fluid volume
FLUIDS AND ELECTROLYTES
Edema
Edema is the palpable accumulation of fluid in the interstitial spaces. It can develop whenever a
change in the capillary hemodynamics takes place. These changes may cause an increase in the
formation of fluid in the interstitial space, or a decrease in the removal of fluid from the
interstitial space.
Edema can be localized or generalized. Localized edema is seen in disorders such as
thrombophlebitis with a venous obstruction. Generalized edema is seen in conditions such as
renal failure or cardiac failure. Another term for generalized edema is anasarca.
Causes
• Increased capillary hydrostatic pressure
• Increased capillary permeability
• Obstruction in lymphatic flow
• Decrease in plasma oncotic pressure
• Retention of sodium and water by the kidneys
Clinical Manifestations
• Fluid swelling in tissue areas
o Dependent
 Sacrum
 Ankles
 Feet
o Generalized
 Periorbital
 Rales (crackles)
Nursing Assessment
• Firmly push index finger into swollen area
o Maintain pressure for several seconds
o Withdraw finger
o If "pit" remains in area edema is present
• Record depth of edema
• Assist in identifying problem
• Assist in removal of excess fluid
• Monitor ordered diuretic therapy
• Maintain fluid and sodium restrictions as ordered
• Teach the client
o Diet
o Fluid restriction
o Medication
o Early signs of edema
o Use of supportive stockings
o Keeping extremities elevated
• FLUIDS AND ELECTROLYTES
Fluid Balance
Clinical Application
• Hospitalized patient's often have IV fluids infusing and it is the physician's responsibility to
select and order the appropriate IV solution. The bedside nurse, however, by
understanding basic concepts of bodily fluids, as well as principles of IV therapy, can
positively influence fluid balance outcomes. The chemical content, the tonicity of solution,
the compatibility with other solutions/additives and the potential complications or risk
factors needs be considered in ordering the best solution for the patient. Let's practice
applying theory to a clinical situation.
• Read the scenario below and decide:
1. The tonicity of the IV fluid (hypotonic, isotonic, hypertonic)
2. Which way will the fluid shift (IV fluid will go to the cells? Into the intravascular
space?)
3. Has the appropriate IV solution been ordered for the patient?

An 87 year-old-patient returns from the operating room following a colon resection and
creation of a colostomy. His BP is 100/60, P 92, R 20. The surgeon orders 1000 0.45%
saline at 150 cc/hr.
• As the nurse caring for this patient, would you question the IV order?
• ANSWER: Based on information related to solution osmolarity and its physiologic effect
on fluid shifts, you should question the order.
• RATIONAL : Cellular edema during and after surgery is common (due to IV fluids,
irrigation fluids, blood and blood products received intra-operatively). Post-operative
patients need a hypertonic infusion (D5.9NS or D5.45NS) to pull fluids out of the
intracellular fluid compartments and interstitial spaces into the vascular compartment.
This will decrease cellular edema and help maintain adequate urinary output and blood
pressure.
• If 0.45% saline (a hypotonic solution) is hung as ordered, fluid will shift out of
intravascular compartment into the intracellular compartment. The result of this will be a
further drop in blood pressure that may lead to circulatory collapse and death.

How did you do? If you experienced difficulty go back and re-read the notes on the key
concepts of osmolality, osmolarity, isotonic, hypertonic, and hypotonic fluids. Make sure
that you understand how fluids will shift between body compartments based on the the
type of IV solution given.
Fluid/ Electrolyte and Acid/Base
Non Electrolytes
The non-electrolytes are:
• Glucose
• Urea
• Creatinine
• Bilirubin
These substances are found in the fluid, but do not separate into ions when placed into solution.
They are measured by weight: milligrams per 100 ml of solution. This may be written as: mg/dl.
Because they are large molecules glucose and urea have the ability to pull fluid out of cells and
tissues. Urea may be used clinically as an "osmotic diuretic." When glucose levels are elevated
(hyperglycemia) fluid is pulled out of the cells and into the ECF. The kidneys eliminate the fluid
along with the excess glucose. The client dehydrates. This is known as an "osmotic diuresis."

Fluid/ Electrolyte and Acid/Base


Electrolytes
Electrolytes are substances that separate into electrically charged particles when placed in
water. Particles holding positive charges are called cations and negatively charged particles are
called anions.
Electrolytes all have different weights, so they are not usually measured in milligrams because it
would be difficult to make comparisons. They are measured in milliequivalents, which is a
measure of their chemical activity, thus allowing comparisons. 1 mEq of sodium has the same
chemical activity as 1 mEq of potassium although they have different weights.
In the ECF, the major cation is sodium and the major anion is chloride. Potassium is the major
cation of the ICF. The major anion of the ICF is phosphate. The sodium potassium pump (an
example of active transport) maintains the high concentration of sodium outside the cell and the
high concentration of potassium in the cell. Although the composition of electrolytes is not the
same between the compartments, the total number of the particles stays the same.
The function of electrolytes is to:
• Help regulate water balance
• Help regulate acid base balance
• Necessary for neuromuscular activity

Fluid/ Electrolyte and Acid/Base


Sodium
Sodium is the major extracellular cation and is responsible for maintaining the concentration and
fluid volume in the extracellular compartment. To coin a phrase: "Where goeth sodium there
goest water." For this reason, sodium and fluid problems often go together.
Sodium is responsible for maintaining blood pressure and electrical transmission of nerve
impulses. It also assists with the regulation of acid-base balance.
Ingestion of sodium in foods accounts for the major way sodium enters the body. Sodium loss
occurs in the urine, through sweat and in the feces. The kidneys regulate the sodium balance.
Aldosterone, the mineralcorticoid from the adrenal cortex is responsible for sodium reabsorption
by the kidneys.
The normal sodium level in the serum is 135-145 mEq/L.
Fluid/ Electrolyte and Acid/Base
Hyponatremia
(Na + <135 mEq/L)
Hyponatremia results from a loss of sodium containing fluids or from water excess without an
equal sodium gain. This condition causes hypo-osmolality and water shifts into the cells, causing
many of the signs and symptoms. If the decrease in sodium occurs slowly, the body adjusts and
the signs and symptoms do not become apparent until the NA is 125 mEq/L. Once the NA level
is 120 mEq, the neurological manifestations occur at a rapid rate.
Causes
Losses of sodium rich body fluids alone do not usually result in hyponatremia, as these fluids are
either isotonic or hypotonic.
• Sodium losses
o Gastrointestinal
 Diarrhea
 Vomiting
 Fistulas
 NG suction
o Renal
 Diuretics
 Adrenal insufficiency
 Renal disease
o Skin
 Burns
o Wound drainage
• Water Gain
o SIADH (Syndrome of Inappropriate ADH)
o CHF
o Excessive hypotonic fluids
o Primary polydipsia (a psychiatric disorder)
o Bladder irrigation with Na free solutions (during prostate surgery)
Clinical Manifestations of Fluid Gain with Sodium Deficit
• Early
o GI
 Anorexia
 Nausea and vomiting
 Abdominal cramping
 Diarrhea
• Neurological
o Seizures
o Confusion
o Stuporous
• Other manifestations depend on fluid balance
o If water excess, look for fluid overload
Diagnostic Tests
• Increased urinary specific gravity
• Na + < 135
• Serum Osmolality < 275 mOsm/kg
Collaborative Care
• Sodium Repalcement
• Mild Hyponatremia: dietary intake of high Na foods
• Severe: 3% Saline IV (100 cc may be given over several hours)
• If hypovolemic: Volume replacement with normal saline
• If water excess:
• Fluid restriction
• Diuretics
Nursing Interventions
• Be alert for patients who are at risk.
• Assist in identifying the underlying cause
• Daily weights
• Assess lung sounds
• Assess cardiovascular status
• Assess for peripheral edema
• Monitor administration of 3% NaCl (given slowly in small amounts using volume controller
IV)
• Use of sodium replacement tablets
• Teach client about foods and medications that contain sodium
• Monitor I & O
• Maintain fluid restrictions
• Monitor lab values
• Administer diuretics as ordered
o Assess Na + and K + levels prior to administration
• Safety
o Seizure precautions
• Teaching
o Symptoms of mild hyponatremia
o Importance of drinking fluids with sodium when participating in activities,
temperatures that cause heavy perspiration.
o Regular lab monitoring when taking drugs (diuretics) that lower Na levels

Fluid/ Electrolyte and Acid/Base


Hypernatremia
(Na + > 145 mEq/L)
Hypernatremia is defined as an elevated sodium level that may be caused by too much sodium
intake or too little fluid. This hyperosmolality causes fluid to move out of the cells causing
cellular dehydration.
Because sodium changes are closely linked with fluid movement, hypernatremia can occur with
normal fluid levels, fluid loss or fluid excess.
Causes
• Several clinical states produce hypernatremia through increased fluid losses:
o ADH deficiency (Diabetes insipidus)
o Concentrated hyperosmolar tube feedings
o Osmotic diuresis
o Insensible loss from high fevers
o Excessive sweating without adequate fluid replacement
• Increased sodium intake in excess of water intake can result in hypernatremia:
o Intravenous administration of sodium bicarbonate
o Increased intravenous administration of hypertonic saline
• Use of sodium containing medications
• Excessive oral intake of sodium (ingestion of seawater)
• Hyperaldosteronism
Clinical Manifestations
• Alterations in neuro function related to dehydration of brain cells:
o Intense thirst
o Restlessness
o Disorientation
o Lethargy
o Progression to coma
o WeaknessSeizures
o Increased excitability of nerves
o Muscle irritability
o Twitching
• Other signs and symptoms are related to fluid status
Diagnositc Tests
• Na+ >145
• Serum osmolality > 295 mOsm/kg
Collaborative Care
• Oral or IV fluid replacement
• Restriction of Na
• Diuretics are sometimes used
Nursing Interventions
• Assess the client for risk factors
• Monitor fluid and electrolytes
• Assist in identification and correction of the problem
• For increased fluid volume with sodium gain
o Assess LOC
o Initiate seizure precautions
o Assess for peripheral edema
o Assess lung sounds
o Maintain fluid restrictions as ordered
• For decreased fluid volume and increased sodium
o Assess LOC
o Establish seizure precautions
o Assess vital signs
o Assist in identification and correction of the problem
o Monitor ordered fluid replacement
• Daily weights
• Intake and Output
• Assess neurological status
• Skin assessment and care
o Skin turgor
o Mucous membranes
• Monitor Lab values
o Serum osmolality
• Administer diuretics as ordered
o Assess Na + and K + levels
• Assess lung sounds and cardiovascular status
• Low sodium diet
• Teach clients about foods and medications containing sodium
• Maintain fluid and sodium restrictions as ordered
o Maintain IV fluids as ordered
o Hypotonic fluids for decreased volume and increased sodium
• Safety precautions
• Low Sodium Diet
o Avoid high sodium foods
o Processed foods
 Lunch meats and cheese
 Canned foods
 Frozen entrees
o Olives, pickles
o Salted snack foods
o Seasonings with salt
 Mustard
 Soy sauce
 Ketchup
o Do not add salt to foods while cooking
o Limit milk products
Fluid/ Electrolyte and Acid/Base
Potassium
Potassium is the major cation of the intracellular fluid. The small amount of potassium in the ECF
is very important because the ECF potassium concentration is the main factor setting resting
membrane potential in most excitable cells. Changes in this level alter the excitability of muscle,
neurons, and other tissues including the beta cells of the Islets of Langerhans in the pancreas.
These cells release insulin. Potassium contributes to the cardiac rate and rhythm, transmission
and conduction of nerve impulses, skeletal muscle contraction and the function of smooth
muscle.
The body gets potassium mainly from oral ingestion of foods. The kidneys eliminate about 90%
of the potassium taken in by the body. This is important to remember when administering
potassium replacements to clients. Assessing renal function and output is of utmost importance.
Only a small amount is excreted through the feces, however, large amounts may be lost of GI
function is altered.
There is an inverse relationship between sodium and potassium reabsorption by the kidneys.
Factors causing sodium retention may be responsible for potassium loss in the urine. For
example, aldosterone caused Na and water retention, but loss of potassium.
It is also important that note that the body moves potassium (K) in and out of the cells as a
response to acid base imbalances. For instance, when the body becomes acidotic, too high a
hydrogen (H) ion level, the body will shift K out of the cells to move the H ions in the cells and
correct the acidosis. (H and K have the same charge) The patient then experiences a rise in the
serum K level. If the patient is alkalotic, the body will shift H ions out of the cell and K will then
shift into the cell. The H ions will help correct the alkalosis, but the serum K level becomes
lowered. This shifting of K and H can be used to as a treatment in hyperkalemia.
Because the range of serum potassium is very small, slight changes in the level are significant.
Normal K: 3.5-5 mEq/L
Tips on potassium administration
• Potassium should never be given as a bolus (this causes cardiac standstill)
• The maximum amount of KCL to be infused should not exceed 20 mEq/hr
• Never add more than 60 mEq of KCL to a liter of intravenous solution
• Always assess renal function prior to the administration of potassium
o Urinary output should be at least 0.5 ml per kg of body weight
o Assess BUN and creatinine
• When giving diuretics always check the potassium level (and don't forget to check the
sodium level too!)When giving potassium supplements for hypokalemia and the potassium
level is not returning to normal, check the magnesium levelIdentify the clients at risk for
potassium problems
• Dilute liquid oral forms of potassium
• Central lines should be used when rapid correction is necessary
Fluid/ Electrolyte and Acid/Base
Hypokalemia
(K+ < 3.5)
Hypokalemia may result from abnormal losses of potassium, a shift from the ECF to the ICF, or
rarely from a potassium-restricted diet. The most common causes are losses either from the GI
tract or through the kidneys. The use of diuretics enhances the renal loss of potassium.
Magnesium deficiencies can contribute to the loss of potassium. Metabolic alkalosis causes
potassium to leave the ECF and shift into the cells. This is the result of the decrease in hydrogen
ion.
Causes
• GI Losses
o Diarrhea
o Vomiting
o Fistulas
o NG suctioning
• Skin losses
o Diaphoresis
• Renal
o Dialysis
o Diuretics
• Hyperaldosteronism
• Magnesium depletion
• ECF to ICF shift
o Increased insulin
o Alkalosis
o Tissue repair
o Increased epinephrine (stress response)
A level < 2.5 causes serious disruption in cardiac functioning.
Clinical manifestations
• Many manifestations relate to decreased nerve transmission
o Fatigue
o Muscle weakness
o Leg cramps
o Decreased reflexes
o Nausea
o Vomiting
o Decreased bowel sounds
o Paralytic ileus
• Cardiac Alterations
o Weak irregular pulse
o ST segment depression
o Flattened T-wave
o Presence of a U-wave
o PVCs
o Bradycardia
Diagnostic Testing
• K level < 3.5 mEq/L
• Other electrolytes are checked, especially Mg
• Arterial blood gases to check acid base balance
• EKG to assess cardiac function
Collaborative Care
• Correct K levels
• Severe loss:
o Parenteral: see tips on first page of potassium
o IV piggyback: 10 or 20 mEq may be added to 100 cc given over 1 hour. An infusion
control device must be used. If 20 is given, should use central line.
• Moderate loss: Oral or IV (in bag) replacement
Nursing Interventions
• Identify cause
• Monitor EKG
• Administer medications as ordered:
o Administer potassium replacement as ordered
 Intravenous potassium (KCL)
 Oral potassium replacements
 Should always be diluted in juice or water
 Never give oral potassium directly into a PEG, PEGJ, or gastric feeding
tube; always dilute it first
• Monitor fluids and electrolytes
• Monitor I & O
• Teach clients at risk the signs and symptoms of hypokalemia
• Frequently assess IV sites
• Teach clients about foods high in potassium
• Fruits and their juices
o Citrus, melons, dried fruits
• Vegetables
o Greens, dark colored veggies
• Meats
• Milk products
• Salt substitute
Hypokalemia alters the resting membrane potential. This causes excitability in many
types of tissues. The most serious of the clinical problems are cardiac. The incidence of
potentially lethal ventricular dysrhythmias is increased in this electrolyte imbalance.
Clients taking digitalis will experience digitalis toxicity if the potassium is low.
Fluid/ Electrolyte and Acid/Base
Hyperkalemia
(K + > 5.0)
This is an excess of potassium in the ECF.
Causes
• Massive intake of potassium
• Impaired renal excretion
o Most common cause is renal failure
• Metabolic acidosis
o Shift of potassium from the ICF to the ECF
o Hyperglycemia of uncontrolled diabetes
• Clients with massive cell destruction (K from cells released)
o Burns
o Crushing injuries
• Adrenal insufficiency (Aldosterone deficient)
• Rapid transfusion of aged blood (K escapes from the cells)
• Catabolic state (potassium release from cells)
• Medications
o Potassium-sparing diuretics
o ACE inhibitors
Clinical Manifestations
• Most are the result of increased neuromuscular activity
o Irritability
o Anxiety
o Abdominal cramping; diarrhea
o Muscle tremors
o Parasthesias
• As the K level rises, muscle activity decreases
o Weakness of skeletal muscles
o Flaccid paralysis
o Eventually respiratory paralysis
• Cardiac function is altered
o Irregular pulse
o Cardiac standstill in sudden or severe hyperkalemia
o Tall, peaked T-wave on EKG
o Prolonged PR interval
o ST depression
o Ventricular fibrillation
Diagnostic Tests
• K > 5.0
• Mild hyperkalemia: 5-6.5
• Moderate: 6.5 - 8
• Severe > 8
• Note: A gradual rise is tolerated much better that a sudden rise. A sudden rise may cause
severe manifestations even though the level is not in the severe range.
• Other electrolytes are checked as they may affect the way the body reacts to the high K
• Blood gases: checking for acid base imbalance
• EKG to monitor cardiac effects
Collaborative care
• Object is to lower the K level
• Moderate to severe: short term management
• Shift K into the cells
o Dextrose (50%) and Regular Insulin IV (as glucose is forced into the cells, the K
follows)
o Sodium Bicarbonate: creates an alkalosis, causing the body to shift H out of the cell
and K will then shift into the cell.
• Protect cardiac function
o Calcium gluconate or calcium chloride IV (counteract the toxic effects of K on
cardiac function)
• Excrete potassium
o Diuretics
o Dialysis
• Mild or long term management
• Exchange K for another electrolyte
• Sodium polystryene sulfonate (Kayexalate); exchange K for Na in the bowel,
causing excretion of K thorough the gut. Using given with sorbitol which has a
laxative effect.
• Dialysis (if renal failure is the cause)
Nursing Interventions
• Eliminate oral and parenteral potassium
• Administer medications as ordered:
o Increase elimination of potassium (see collaborative care for drugs)
 Diuretics
 Dialysis
 IV glucose and insulin
 Kayexalate (ion-exchange resin)
• Increased fluid intake
• Monitor EKG
• Monitory fluid and electrolytes
• Check BUN, creatinine and urinary output on all clients receiving potassium
In cases where the elevation is not severe, often just withholding all forms of potassium,
increasing fluids, and administering diuretics is sufficient.

Fluid/ Electrolyte and Acid/Base


Chloride
(98 – 106 mEq/L)
Chloride is an anion. It is usually lost along with sodium. The signs and symptoms are usually
related to sodium gains and losses. The basic functions of chloride are:
• Regulates extracellular fluid volume
• Works as a blood buffer – chloride shift (this is discussed in more detail in the section on
acid – base balance)
• Aids in digestion – required for the secretion of HCL (necessary for the activation of
protease, a digestive enzyme).
CHLORIDE DEFICIT
(Cl - < 98 mEq/L)
Causes
• Vomiting
• Diarrhea
• Suction
• Diuretics
• Interstitial fluid loss
• Adrenal insufficiency
CHLORIDE EXCESS (Cl - > 106 mEq/L)
• Related to sodium or potassium imbalances
• Excesses in cations
Fluid/ Electrolyte and Acid/Base
Calcium
The body has a large amount of calcium, about 98% of it is combined with phosphorous and
found in the bones and teeth. The rest of it is found in the extracellular compartment and is
found in 3 forms:
• Free or ionized (50%)
• Protein bound (50%)
• Complexed (as calcium phosphate, calcium citrate or calcium carbonate) (trace amount)
The calcium level is a combination of all three forms and is usually reported in mg/dl. The
normal level is 9-11 mg/dl.
The ionized form is responsible for most of the physiological effects of calcium which include:
• Nerve impulse transmission
• Muscle contraction
• Cardiac contraction
• Blood coagulation
The body acquires calcium from outside sources such as foods and Vitamin d is needed to absorb
it in the intestines. However most of the calcium is combined with phosphorus and is found in
the skeletal system. By the action of several hormonal activities this calcium can leave storage
and become active in the plasma. Phosphorous and calcium have an inverse relationship in the
plasma, as one rises, the other decreases.
Substances Promoting Calcium Balance
• Parathormone (PTH)
• Calcitonin
• Vitamin D
If the serum calcium level becomes too low, the parathyroid secretes more PTH), causing the
bones to release calcium (a process known as resorption), the intestines to absorb more calcium
and the kidneys to conserve calcium.
If the calcium level becomes too high, the thyroid secretes calcitonin. Calcitonin slows the
release of calcium by the bones, increases kidney excretion and reduces the intestinal absorption
of calcium.
Vitamin D helps calcium absorption in the GI tract.
Fluid/ Electrolyte and Acid/Base
Hypocalcemia
(Ca+ < 9 mg/dl)
Older women are particularly at risk for lowered calcium levels due to lower estrogen levels.
Other risk groups are older men and people who are lactose intolerant.
A decrease in ionized calcium results in the manifestations of hypocalcemia.
Causes
• Elevated phosphorus
o Chronic renal failure
o Administration of phosphorous
• Decreased PTH
o Primary hypoparathyroidism
o Surgical removal of the parathyroid
• Decreased absorption in the GI tract
o Vitamin D deficiency
o Intestinal diseases
• Magnesium deficiency
• Acute pancreatitis (excess enzymes break down more fats into fatty acids, which combine
with calcium)
• Drug Therapy
o Loop diuretics
• Alkalosis (decreases ionization of calcium)
• Administration of too much citrated blood (the citrate combines with calcium)
Clinical Manifestations
Stimulation of nerves and muscles
• Tetany (tonic muscle spasms)
• Hyperactive reflexes
• Laryngeal spasms
• Numbness and tingling of fingers, toes, feet and around the mouth
• Seizures
• Positive Trousseau's sign
• Positive Chvostek's sign
• EKG changes
o Elongated ST segment
o Prolonged QT interval
o Ventricular Tachycardia
Diagnostic Tests
• Serum Ca < 9 mg/dl
• Serum phosphate may be elevated
• Serum Mg: low Ca often associated with low Mg
• PTH: measures to assess function
• Trousseau's sign: inflate BP cuff to 20 mm Hg above SBP for 2 minutes, look for carpal
spasm
• Chvostek's sign: tap the facial nerve ( in front of the ear), look for twitching of facial
muscles
Collaborative Care
• Identify cause
• Administer calcium
• IV calcium (chloride or gluconate) if tetany or seizures present
o Make sure vein patient, can injure tissues if IV is infiltrated
o Give slowly (0.5 - 1cc/min), can cause bradycardia, cardiac arrest
• Oral calcium
Nursing Interventions
• Use of oral or intravenous calcium replacement
• Careful assessment of IV site
• Never administer calcium IM
• Identify clients at risk
o Head and neck surgery
o Thyroid surgery
o Massive transfusions
• Assess patients at risk for
o Cardiac and respiratory status
o Neuromuscular irritability
• Teaching
o Dietary sources of calcium
 Diary products are the best sources
o Post menopausal women should increase calcium intake
Fluid/ Electrolyte and Acid/Base
Hypercalcemia
(Ca + > 11 mg/dl
An excess of ionized calcium can have effects systemically.
Causes
• Increased resorption of calcium from bones
o Multiple myeloma (causes bones to mobilize Ca)
o Malignancies to the bone (causes bones to mobilize Ca)
o Immobility (lack of stress on bones)
o Hyperparathyroidism (increases PTH)
• Increased calcium intake
o Antacids with Ca
o Excess IV administration
• Decreased excretion
o Use of thiazide diuretics
• Acidosis (increase ionized Ca)
Clinical Manifestations

Decreased neuromuscular excitability


• Lethargy, weakness
• Depressed reflexes
• Memory deficits
• Confusion (may develop psychosis)
• Coma
• GI/GU effects
o Anorexia, nausea, vomiting
o Renal stones
• EKG changes
o Shortened ST segment
o Shortened QT interval
o Ventricular Dysrhythmias
o Increased effect of digitalis
Diagnostic Testing
• Serum Ca> 11mg/dl
• PTH
• ECG
Collaborative Care
• Identify cause
• Increase urinary excretion
• Increased IV fluid intake, saline or 1/2 saline
• Administer diuretics, especially loop diuretics
• If rapid reversal is needed, administer phosphorous IV
• Inhibit bone resorption
• Calcitionin
• Mithramycin (a cytotoxic antibiotic, used if other modalities are ineffective)
• Low calcium diet
Nursing Interventions
• I&O
• Monitor effects of diuretic treatments
• Monitor hydration with isotonic saline
• Increase fluid intake of client to 3000 – 4000 ml per day to help the kidneys excrete the
calcium
• Monitor calcium levels
• Encourage weight-bearing activities if possible
Fluid/ Electrolyte and Acid/Base
Phosphate
The majority of phosphorus in the body is combined with calcium and located in the teeth and
bones. Most of the rest of the phosphorous in the body is located inside the cells, Only 1% is
found in the extracellular compartment.
Functions of phosphorous in the body:
• Bone and teeth formation
• Nerve transmission
• Muscle function
• ATP production
• Formation of 2, DPG (an enzyme used in oxygen transport)
• Component of enzymes needed for protein, carbohydrate and fat metabolism
• Acid base balance
Phosphate is taken in through the gastrointestinal tract. So gastrointestinal problems such as
malabsorption syndromes will inhibit its absorption. The kidneys are the main method of
phosphorus excretion, so when the kidneys are not functioning properly there is impaired
elimination of phosphorus. Phosphorus has an inverse relationship to calcium.
The normal level is 2.8-4.5 mg/dl.
Fluid/ Electrolyte and Acid/Base
Hypophosphatemia
(PO 4 -3 < 2.8 mg/dl)
Causes
• Decreased intake or absorption
o Malabsorption syndromes
o Malnutiriton
o Parenteral nutrition with inadequate phosphorus replacement
• Increased intestinal loss
o Phosphate-binding antacids
• Respiratory alkalosis
• Hypercalcemia
Clinical Manifestations
• CNS difficulties
• Cardiac Dysrhythmias
• Muscle weakness
o Particularly respiratory muscles
• Hematological effects
Nursing Interventions
• Teaching regarding foods high in phosphorus
o Organ meats
o Nuts
o Milk products
• Monitoring replacement therapy
o Neutra Phos (oral therapy)
• Monitoring and assessing respiratory status
• Monitoring and assessing cardiac status
Fluid/ Electrolyte and Acid/Base
Hyperphosphatemia
(PO4 -3 > 4.5)
Causes
• Acute or chronic renal failure (most common cause)
• Chemotherapy for certain malignancies
• Excessive intake of dairy products
• Large doses of Vitamin D that increase absorption of phosphorus
• Excessive use of phosphate enemas
• Hypoparathyroidism
Clinical Manifestations
• Hypocalcemia
• Tetany
• Neuromuscular irritability
• Parathesias
• Calcium phosphate precipitate deposits in soft tissues
Nursing Interventions
• Identify underlying cause
• Maintain dietary restrictions
• Teach client about foods high in phosphorus
• Assess for signs of hypocalcemia
• Monitor renal function in clients with renal failure
• Use of phosphate binding agents
o Phos lo (calcium acetate) given with meals to bind with dietary PO4
Fluid/ Electrolyte and Acid/Base
Magnesium
About half of the body's magnesium is stored in the bone. Most of the rest of body's magnesium
is inside the cell, making magnesium the second major intracellular cation. A small amount is
found in the extracellular compartment.
Functions of Mg in the body
• Cellular enzyme activity
• Acts as a sedative on nerves and muscles by blocking or decreasing acetylcholine release
Patients who have a potassium and/or calcium imbalance often have a magnesium imbalance.
When potassium replacement does not correct hypokalemia , often the magnesium level is found
to be low. The magnesium level must be corrected before the potassium level will respond to
replacement therapy.
Diets that lack sufficient magnesium are thought to contribute to hypertension, cardiac
dysrhythmias, ischemic heart disease, and sudden cardiac death. The kidneys excrete
magnesium.
Fluid/ Electrolyte and Acid/Base
Hypomagnesemia
(Mg 2+ < 1.5 mEq/L)
Causes
• Decreased intake
o Long-term intravenous feedings without magnesium supplements
o Oral intake
• Intestinal losses
o Gastric suctioning
o Vomiting
o Diarrhea
• Impaired intestinal absorption
o Crohn's disease
o Celiac disease
• Increased renal excretion
o Drugs
o Hyperaldosteronism
o Diabetes (due to osmotic diuresis)

Clinical Manifestations
• May not be seen until the level is < 1 mEq/L
• Symptoms similar to hypocalcemia
• Confusion
• Hyperactive reflexes
• Seizures
• Possible cardiac dysrhythmias
Nursing Interventions
• Monitor electrolyte values
• Assess reflexes
• Monitor cardiac status
• Assess for signs of hypocalcemia
• Check potassium levels
• Initiate seizure precautions
• Identify individuals at risk
• Teach clients about foods high in magnesium
o Green leafy vegetables
o Milk
o Chocolate
o Citrus fruits
• Administer replacement
o IV Magnesium sulfate (MgSO4) infusion
o IM MgSO4
o Oral
 Slow mag
Fluid/ Electrolyte and Acid/Base
Hypermagnesemia
(Mg 2+ > 2.5 mEq/L)
Causes
• Increased intake
o Renal failure patient who ingest magnesium containing drugs (antacids or laxatives)
• Too rapid administration of intravenous magnesium sulfate
o Used as treatment of toxemia in pregnancy)
• Decreased output (renal disease)
• Adrenal insufficiency
Clinical Manifestations
• May not be seen until levels are over 4 mEq/L. Knee jerk reflex is lost when level is > 8,
and respiratory paralysis occurs at levels >10.
• Lethargy
• Drowsiness
• Nausea
• Vomiting
• Loss of DTRs (deep tendon reflexes)
• Respiratory weakness leading to arrest
• Cardiac dysrhythmias leading to arrest
Nursing Interventions
• Identify individuals at risk
o Renal clients
o Individuals receiving magnesium sulfate such as pregnant women suffering from
eclampsia
• Increasing fluids to promote renal excretion in the non-renal client
• Use of calcium gluconate to physiologically counteract the effects of the magnesium on
cardiac function
• Dialysis in renal impaired clients
• Teaching renal clients about foods and medications high in magnesium
• Fluid/ Electrolyte and Acid/Base
Acid-Base
• INTRODUCTION
• Acid-base balance means homeostatsis of the hydrogen ion concentration in body fluids.
Even a slight deviation in the hydrogen ion concentration causes pronounced changes in
the rate of chemical reactions. When hydrogen ion concentration deviates from normal,
survival is threatened.
• FUNDAMENTALS
• Acids release hydrogen ions and bases accept them; the number of hydrogen ions present
in a solution governs whether it is acid, alkali, or neutral. The normal pH value for the
body fluids is between pH 7.35 and 7.45. When the pH value of body fluids is below 7.35,
the condition is called acidosis, and when the pH is above 7.45, it is called alkalosis.
• Metabolism produces acidic products that lower the pH of the body fluids. Some examples
of these products include carbonic acid (the by-product of carbon dioxide), lactic acid
(product of anaerobic metabolism), phosphoric and sulfuric acid (product of protein
metabolism), and fatty acids (product of lipid metabolism).
• The major effect of acidosis is depression of the central nervous system. When the pH of
the blood falls below 7.35, the central nervous system malfunctions, and the individual
becomes disoriented and possibly comatose as the condition worsens.
• A major effect of alkalosis is hyperexcitability of the nervous system. Peripheral nerves
are affected first. Spasms and tetanic contractions as well as extreme nervousness or
convulsions result. Death can result of tetany of the respiratory muscles.
• Acidosis and alkalosis are categorized by the cause of the condition. Respiratory acidosis
or respiratory alkalosis results from abnormalities of the respiratory system. Metabolic
acidosis or metabolic alkalosis results from all causes other than abnormal respiratory
functions.
• RESPIRATORY ACIDOSIS
• Inadequate ventilation of lungs (hypoventilation) causes respiratory acidosis. The rate at
which carbon dioxide is eliminated from the body fluids through the lungs falls. The
increase in hydrogen ion concentration causes the pH of the body fluids to decrease. If the
pH of the body fluids fall below 7.35, symptoms of respiratory acidosis such as
restlessness, confusion, and tachycardia become apparent.
• The kidneys help compensate for failure of the lungs to prevent respiratory acidosis by
increasing the rate at which they secrete hydrogen ions and reabsorb bicarbonate ions. A
time period of 1 or 2 days is required for the kidney to become maximally functional. Thus
the kidneys are not effective if respiratory acidosis develops quickly (ex. Asthma attack),
but is effective if acidosis develops slowly (ex. Emphysema).
• RESPIRATORY ALKALOSIS
• Respiratory alkalosis results from hyperventilation of the lungs. This increases the rate at
which carbon dioxide is eliminated from the body fluids and results in a decrease
concentration of carbon dioxide in the body fluids. If the pH of body fluids increases above
7.45, symptoms of respiratory alkalosis such as dizziness, light-headness, muscle cramps,
paresthesia, and palpations will become apparent.
• The kidneys help to compensate for respiratory alkalosis by decreasing the rate of
hydrogen ion secretion into the urine and the rate of bicarbonate ion reabsorption. As
stated earlier, the kidneys need 1 or 2 days to be effective. The kidneys will not
compensate alkalosis that occurs in response to hyperventilation (triggered by emotions,
which usually begins quickly and subsides within minutes or hours). However, if alkalosis
results from staying at a high altitude over a 2 or 3 day period, the kidneys play a
significant role in helping to compensate.
• METABOLIC ACIDOSIS
• Metabolic acidosis results from all conditions that decrease the pH of the body fluids below
7.35, with the exception of respiratory related conditions. Some of these conditions might
include renal failure, diarrhea, and ketoacidosis caused by diabetes or prolonged
starvation. As hydrogen ions accumulate the reduced pH stimulates the respiratory center
and the patient will hyperventilate. During hyperventilation, carbon dioxide is eliminated
which helps maintain the pH within the normal range.
• METABOLIC ALKALOSIS
• Metabolic alkalosis results from all conditions that increase the pH of the body fluids above
7.45, with the exception of respiratory related conditions. Some of these conditions might
include vomiting, nasogastric suction, and hypokalemia. As hydrogen ions decrease in the
body fluids the increased pH causes the patient to hypoventilate. Reduced respirations
allow carbon dioxide to accumulate in the body fluids, which helps maintain the pH within
the normal range.
• For further information on acid/base see "Balancing act: Keeping blood pH in equilibrium"
an article by Frederick Tasota.
• Fluid/ Electrolyte and Acid/Base
Acid – Base Balance
• The body functions best when the pH is maintained within the normal range. The body
employs a variety of methods to equalize the production of acids or bases with the
excretion of acids or bases. This process is known as acid base balance. In order to
understand these processes, the nurse must first understand acids, bases and pH.
• The active substance in the majority of acids is the hydrogen ion (H + ), the more
hydrogen ions present, the more acidic the solution. The reverse is also true, the lower
the hydrogen ion concentration the less acidic (and more basic) the solution. By the strict
definition, an acid is a hydrogen ion donor, and a base is a hydrogen ion acceptor. This
means that a base will take a hydrogen ion away from an acid making the acid weaker.
These types of reactions usually cause the formation of a weak acid and a salt. (For the
chemical equation please refer to page 1375 in Taylor).
• The pH is the measure of the acidity or alkalinity (base) of a solution. The pH scale ranges
from 1 – 14, 7.0 is neutral. The lower the pH, the more acidic the solution, the higher the
pH, the more alkalotic the solution. Blood must stay within a very narrow pH range (7.35
– 7.45). The range of blood pH compatible with life is 6.8 – 7.8. Listed below are the pH's
of some body fluids.
• pH Values of Body Fluids
Fluid Value

Blood 7.35 – 7.45

Intracellular Fluid 6.9 – 7.2

Urine Averages about 6.0

Cerebrospinal Fluid 7.35 – 7.45 (notice that it is the same as


blood)

Bile 5.0 – 6.0

Gastric juice 1.0 – 2.0


•Acidosis occurs when the blood pH drops below 7.35. In this case the concentration of
the hydrogen ion is above normal. Alkalosis occurs when the blood pH increases to
values above 7.45. The hydrogen ion concentration is below normal, or the blood base
value (bicarbonate ion) may be above normal.
• The blood pH is examined through arterial blood bases (ABG's).
• Because body processes constantly produce acids, the body's regulatory mechanisms are
continually at work to maintain the pH in the normal range. If these regulatory
mechanisms are overwhelmed, acid base imbalances occur.
Fluid/ Electrolyte and Acid/Base
Regulation of Acid – Base Balance
The body controls acid – base balance in four ways (These are listed in order of their
occurrence):
• Buffer systems
• Lungs
• Cells
• Kidneys
Blood Buffers
These are chemicals that absorb or release hydrogen ions as needed in order to maintain the
arterial blood pH between 7.35 – 7.45. This ability, or buffer action, protects the body against
dangerous changes in the hydrogen ion concentration.
In the body, the major buffer method is the base bicarbonate (HCO 3 - )/carbonic acid (H 2
CO 3 ) mechanism. It is also the quickest acting. This mechanism controls the hydrogen ion
concentration of the body fluids by keeping a 20:1 ratio between the bicarbonate and carbonic
acid. An advantage of this buffer mechanism is that it can react instantaneously to the presence
of acid or alkaline increases. The disadvantage of the mechanism is that it cannot maintain this
action for a long period of time. The lungs assist by controlling carbon dioxide levels and the
kidneys assist by controlling bicarbonate levels.
Two other buffer systems are the phosphate system and the protein buffer system. These two
systems contain an acid-base component and will chemically join with a strong acid or base and
weaken its effect. Phosphate exerts its main effect in the cell and the renal tubules.
The protein buffers are seen inside the cells and within the plasma. The majority of protein
buffering is within the cells.
Lungs
The lungs act as the second mechanism to maintain acid – base balance in the body and exert
its effects within several hours. The respiratory system including the neurological breathing
control centers, controls the carbonic acid component of the buffer system. Weak carbonic acid
separates into carbon dioxide and water. If there is too much carbon dioxide, the lungs change
the rate and depth of respiration making breathing faster and deeper in order to rid the body of
excess carbon dioxide.
If the body becomes alkalotic, the body slows the respiratory rate in order to retain carbon
dioxide. This mechanism increases the carbonic acid level and counteracts the alkalosis.
Cells
The cells can take on or let go of excess hydrogen ions. With the potassium buffer system the
extra hydrogen ions leave the ECF and move into the cell. The potassium ions then move out
into the ECF. That is the reason that individuals with acidosis have elevated potassium level. In
alkalosis the opposite happens. The cells do this slowly and need at least 2 hours to control the
changes in the hydrogen ion concentration.
Kidneys
The renal system is the 4 th line of defense in acid – base regulation. The kidneys control the
bicarbonate in the bicarbonate/carbonic acid mechanism and the phosphate. They also excrete
lactic acid and all other acids except carbonic acid. To maintain compensation, the kidneys
change the rate of excretion of the hydrogen and bicarbonate ions in the body. When the pH is
acidotic, the kidneys keep the bicarbonate (base) and excrete the hydrogen ion. If the pH is
alkalotic, the kidneys excrete the bicarbonate and keep the hydrogen. The renal system is the
slowest of all the systems. It takes several hours to a few days for this system to correct acid –
base imbalances.
Fluid/ Electrolyte and Acid/Base
Acid – Base Imbalances
Normal functioning of the kidneys, lungs, cells, and brain is necessary for maintaining the body's
acid – base balance. Under normal conditions these organs adjust quickly and efficiently to the
changes in the hydrogen ion concentration. However if the body is exposed to extreme changes
in the balance or the regulating organs are diseased, the regulating organs may not be able to
control the situation and an imbalance can occur.
The two types of acid – base imbalances are acidosis and alkalosis. These two processes are
again broken down into metabolic and respiratory types. Respiratory acidosis and respiratory
alkalosis are caused by problems in the pulmonary system. If an imbalance is not directly
related to the pulmonary system, the acid – base imbalance is metabolic.
METABOLIC ACIDOSIS (Base Bicarbonate Deficit)
Causes
• Increased loss of bicarbonate
o Severe diarrhea
o Loss of biliary, pancreatic or lower bowel fluid
• Too much production of metabolic acids
o Diabetic acidosis
o Anaerobic metabolism in shock (increased production of lactic acid)
o Starvation
o Prolonged fasting
• TPN
• High ingestion of metabolic acids
o High fat intake, low CHO diets
o Salicylate toxicity
o Medications that increase the H + overload
• Renal disease
• Situations leading to an increase in serum potassium
o Compensatory chloride shift

Clinical Manifestations
• pH < 7.35
• HCO 3 - < 22 mEq/L
• Headache
• Confusion
• Drowsiness
• BP changes (may be decreased)
• Deep, rapid respirations
Nursing Interventions
• Assist in identifying the cause
• Monitor clients at risk
• Monitor electrolytes
o Potassium
o Chloride
• Monitor blood arterial blood gases
• If the pH < 7.2, sodium bicarbonate may be administered
o Very dependent on cause of problem
o Usually IV drip
o Must be given cautiously
• In diabetic ketoacidosis
o Insulin
o Fluids
o Assess blood glucose levels
METABOLIC ALKALOSIS (Base Bicarbonate Excess)
Causes
• Increased bicarbonate intake
o Baking soda (many older people take this as a treatment for "sour stomach")
• Loss of HCL acid
o Vomiting
o Gastric suctioning
• Renal loss
o Diuretic therapy
 Increased excretion of potassium and chloride
 Compensation by increasing bicarbonate
o Excess of aldosterone
o Hypercalcemia
• Massive blood transfusion
• Cystic fibrosis
• CHO refeeding after starvation
Clinical Manifestations
• Muscular weakness
• Neurological
o Hyporeflexia
o Apathy
o Confusion
o Flabby muscular responses
o Tingling of fingers
• pH > 7.45; HCO 3 - > 26 mEq/L
Nursing Interventions
• Assist in identifying the cause
• Identify the clients at risk
• Monitor electrolytes
• Monitor I & O
• Administration of KCL
o For clients with decreased potassium levels
• Adminstration of normal saline
o For clients with alkalosis caused by gastric losses
• Carbonic anhydrase inhibitors
o Diamox
o Used in clients who cannot be treated with rapid volume expansion
o Causes the kidneys to substantially increase the secretion of bicarbonate and
potassium (may be necessary to give potassium supplements if using this
medication)

RESPIRATORY ACIDOSIS (Carbonic Acid Excess)


Causes
• Conditions that increase retention of carbon dioxide
• Severe pneumonia
• Adult Respiratory Distress Syndrome
• Pneumothorax
• Smoke inhalation
• Upper airway obstruction
• Aspiration
• Laryngospasm
o Anaphylaxis
o Hypocalcemia
• Severe bronchospasm
• Prolonged acute asthma attack
• Depression of the central nervous system
• Massive pulmonary embolus
• Neuromuscular abnormalities affecting the respiratory system

Clinical Manifestations
• Dyspnea
• Restlessness
• Lethargy
• Confusion
• Coma
• Increased heart rate
• Diaphoresis
• Increased respiratory rate
• Increased intracranial pressure related to increased carbon dioxide levels
• Cyanosis
• pH < 7.35
• pCO 2 > 45 mmHg
Nursing Interventions
• Assist in identifying cause
• Identify clients at risk
• Support respiratory function
• Monitor blood gases
• Assess vital signs
• Administer medications
o Bronchodilators
• Promote gas exchange
o Position client to promote adequate gas exchange
o Remove secretions by encouraging client to cough or through suctioning
• Safety precautions
o Re-orient confused clients
o Keep bed in low position
o Keep call bell in reach

Respiratory Alkalosis (Carbonic Acid Deficit)


Causes
• Increased excretion of carbon dioxide
o Hyperventilation
 Anxiety
 Severe prolonged exercise
o High altitude
o Severe anemia
o Hypoxemia
o Fever
o Salicylates (early intoxication)
o Central nervous system disorders
 Intracerebral trauma
 Meningitis
 Encephalitis
Clinical Manifestations
• Lightheadedness
• Anxiety
• Parasthesias
• Extreme alkalosis
o Confusion
o Tetany
o Syncope
o Seizures

Nursing Interventions
• Assist in identifying the cause
• Identify clients at risk
• Monitor arterial blood gases
• Monitor electrolytes
• Monitor oxygen therapy as ordered
• Treatment of hyperventilation
o Encourage client to breath slowly
o Decrease anxiety
• Monitor vital signs
• Administer prescribed medications
• Monitor EKG
• Safety
Fluid/ Electrolyte and Acid/Base
Blood Gas Interpretation
When evaluating acid base imbalance, the nurse looks at three values in the arterial blood
gases, the pH, the pCO 2 , and the bicarbonate (HCO 3 ). This will provide a simple
interpretation of the blood gas, which is within the scope of this course. The concepts of
compensation and base excess are beyond the scope of this course and are examined in
subsequent courses where acid base balance will be studied in more detail.
Normal values:
pH 7.35 - 7.45

pCO 2 35 -45 mm Hg
HCO 3 22-26 mEq/L
When examining ABG's, not only the type of imbalance is noted, but also the origin (either
metabolic or respiratory) is also identified.
Steps in Interpretation
Write the values down in the following order: the pH is the first value, carbon dioxide (pCO2) is
second, then the bicarbonate (HCO3) third.
Examine the pH
• If between 7.35- 7.45, mark N (Normal) next to the pH
• If < 7.35, mark A (for acid)
• If > 7.45, mark B (for base).
Examine the CO 2 .
• Think if CO 2 as an acid, if you have too much, you become acidotic. If you don't have
enough, you become alkalotic (basic)
• CO 2 levels are controlled by the respiratory system, so imbalances here are respiratory
in origin.
• If between 35-45, mark N next to the CO 2
• If > 45, mark A .
• If < 35, mark B .
Examine the HCO 3
• Think of bicarbonate as a base, if you have too much, you become alkaltoic, if you have
too little, you become acidotic.
• HCO3 is controlled by the kidneys, so think of imbalances here as metabolic in origin.
• If between 22 - 26, mark N next to the HCO 3.
• If < 22, mark A
• If > 26, mark B
Look for a match! If there is an imbalance, you will be able to determine the imbalance and
which system caused it.
• If you have 2 A's, then an acidosis is present.
o One of the A's must be in the pH
o Is other A in the CO 2 ? If so, then the respiratory system is the origin
o Is other A in the HCO 3 , then the metabolic system is the origin
• If you have 2 B's then an alkalosis is present.
o One of the B's must be in the pH
o Is the other B in the CO 2 , then the respiratory system is the origin
o Is the other B in the HCO 3 , then the metabolic system is the origin.
• Example:
• pH = 7.32 A
• CO 2 = 48 A
• HCO 3 = 24 N
• What matches? pH and CO 2
• Interpretation: Respiratory acidosis
• Explanation:
• pH less than 7.35 = acidosis
• CO 2 higher than 45 = acidosis, system = respiratory
• HCO 3 is normal, metabolic system not involved.
• Match: pH and CO 2 , both acid. Origin: respiratory
Try your own:
1. pH = 7.48, CO 2 = 38, HCO 3 = 31

2. pH = 7.49, CO 2 = 29, HCO 3 = 26

3. pH = 7.29, CO 2 = 41, HCO 3 = 19


Answers:
1. Metabolic alkalosis :
• pH: 7.48 = B high, alkalosis
• CO 2 : 38 = N normal
• HCO 3 : 31 = B high, alkalosis, metabolic system
• Match: pH and HCO 3 , both alkalosis. System: metabolic
2. Respiratory alkalosis
• pH: 7.49 = B high, alkalosis
• CO 2 : 29 = B low, alkalosis respiratory system
• HCO 3 : 26 = N normal
• Match: pH and CO 2 , respiratory acidosis
3. Metabolic Acidosis
• pH: 7.29 = A low, acidosis
• CO 2 : 41 = N normal
• HCO 3 : 19 = A low, acidosis, metabolic system
• Match: pH and HCO 3 both acidosis, metabolic system

• FLUIDS AND ELECTROLYTES


ABG REVIEW
ARTERIAL BLOOD GAS INTERPRETATION
• STEP-BY-STEP
• Ph, PaCO2, and HCO3 are the only three values you will need from the aterial blood gas in order to
intrepret the acid-base status of your patient.
• Please note that the ABG does give you a lot more information than just acid-base. The paO2 level,
also found on the ABG, indicates the patient's oxygenation status. Based on this value you might
increase or decrease the amount of oxygen the patient is receiving.
• Write down pH, PaC02, and HCO3 values
pH 7.3 x

PaCO2 60 x

HCO3 24 x

Write "A" for acid, "B" for base or "N" for normal.
pH: < 7.4 = acid >7.4 = base
PaCO2: > 45 = acid <35 = base
HCO3: < 22 = acid >26 = base
Absolute normal = 7.4 (This is important to know when trying to determine compensation)
• Determine whether each value is acid, base, or normal

pH 7.3 A

PaCO2 60 A

HCO3 24 N
• If the ABG is normal the PaCO2 and HCO3 will be marked with an "N" and the pH will be between
7.35-7.45
• If the ABG is abnormal the pH and either the PaC02 OR the HCO3 will have the same letter. [match the
pH with CO2 or HCO3]
• If the ABG has compensated then the pH will be in the normal range but the PaCO2 and HCO3 will be
abnormal [this is discussed in-depth in step 5]
• Determine which letters that are the same
pH 7.3 A

PaCO2 60 A

HCO3 24 N
• In order to label the abnormality look at the two letters that are alike [the pH is matched up with either
the CO2 or HCO3]. If the 2 letters is an "A", then your patient is in acidosis. If the letters is a "B", then
your patient is in base or alkalosis.
• To decide if it is metabolic or respiratory, look again at the letter that matched with the ph. If the
matching letter is the CO2 then it is respiratory. If the matching letter if the HCO3 then it is metabolic.
• Label the underlying acid/base abnormality
• Will be one of four choices: metabolic acidosis,
• metabolic alkalosis, respiratory acidosis, respiratory alkalosis.
• The values in this example indicates respiratory acidosis
• Compensation can be a little "tricky". What you are actually looking to see is if the patient's kidneys or
lungs have "kicked" in to try to bring the pH back into the normal range (7.35-7.45)
• If the underlying problem has been determined to be respiratory acidosis or alkalosis, then you need to
look at the metabolic component (HCO3) of the ABG to see if compensation is taking place.
• If the underlying problem has been determined to be metabolic acidosis or alkalosis, then you need to
look at the respiratory component (PaCO2) of the ABG to see if compensation is taking place.
• With compensation there are 3 scenarios that may occur:
• There is no compensation
Example: The patient is in a respiratory acidosis. The opposite system (metabolic) will be in a normal
range of 22-26. In other words, the kidneys are not compensating by retaining bicarbonate and making
the blood more alkalotic to off- set the acidosis. If the kidneys were trying to compensate then the
HCO3 level would be higher than normal indicating the retention of bicarbonate.
• Partial compensation
Example: The patient is still in respiratory acidosis. Several days have gone by and now the kidneys
have had time to start to correct the acidosis by excreting hydrogen and retaining bicarbonate. The
HCO3 level will now be outside the normal range of 22-26. It will be above 26 because the blood is
becoming more alkalotic. This is considered partial compensation (AKA "compensating") because the
pH is NOT within the normal range and the compensation process has not been completed.
• Fully compensated
Example: The patient that had been in respiratory acidosis 4 days earlier now has a pH that is within
the normal range of 7.35-7.45. The kidneys have been working hard retaining bicarbonate and
excreting hydrogen and it's finally paid off. In this blood gas you will see at normal pH, but the CO2 and
HCO3 will be abnormal. From this we can tell that the patient is in full compensation (*normal pH). We
know, for this patient because we've been tracking his ABG's for several days, that his underlying
problem was respiratory acidosis with a metabolic compensation.
• What if you had a patient that you had not been tracking? Then you would need to decide what the
underlying problem originally was before the compensation took place. Remember to follow the same
steps with this one exception. When you look at the pH (it will be within normal limits) you still must
label it as acid or base. This is where you use 7.4 as the absolute normal. If it's below 7.4 then the pH
is on the acidic side (even though it's in the normal range) and you would place an "A" next to it. If it's
above 7.4 then the pH is on the base side (even though it's in the normal range) and you would place a
"B" next to it. Continue labeling the other components (CO2 and HCO3) so you can match the letters.
This will give you your underlying problem and you will then know which system compensated for the
problem.
• To assess for compensation, determine whether the other variable is moving in the
opposite direction.
• Possible interpretations:
• Fully compensated (pH within normal range)
• Partial compensation (also stated as compensating)
• Because HCO3, in the example, is within the normal range (22 to 26), no compensation
is occurrin. (If compensation were present, the HCO3 value would be greater that 26 and
you would have marked it with a B for base.)
• FLUIDS AND ELECTROLYTES
Intravenous Therapy: Principles and Practice
• I. Purpose and Indications
• A. Purpose
1. Maintain or restore fluid and electrolyte balance
2. Correct Acid-Base deficits
3. Replenish lost fluids or blood volume
4. Provide alternative routes for administration of medications and/or nutrients
• B. Indications - as a medication and/or treatment for:
1. Fluids and Electrolyte imbalances
2. Administration of additives (Drugs)
3. Temporary by-pass of the G.I. system
4. Nutritional support therapy (additional calories etc.)
5. Establishment of "life-line" in critical situations
6. Re-establishment of homeostasis and regulatory functions
• C. Types of IV Therapy
1. Continuous - large volume infusion over extended period of time with
or without additives
2. Intermittent - specific volume/additives without continuous infusion of
solution (via saline lock)
• II. Client Preparation
• A. Client should be prepared for therapy in order to enhance cooperation and
reduce risk factors
1. Purpose of therapy
2. Venipuncture procedure
3. Signs and symptoms that need to be reported [burning, redness, swelling,
warmth]
4. Importance of compliance with I.V. management principles
5. Nursing management (monitoring) of I.V. therapy
• III. Classifications of I.V. Solutions
• A. Major Types of Solutions
1. Water Solutions - to provide hydration and establish renal function
EX: Dextrose 5% in water (D5W)
• 2. Balanced Solutions - to treat and/or correct electrolyte imbalances
EX: Lactated Ringers (LR)
• 3. Therapeutic Solutions - to provide calories, electrolytes, and fluid to clients
unable to take in food over a long period of time
EX: TPN (Total Parenteral Nutrition)
May also be referred to as Nutritional Support Therapy
• B. Factors used to select I.V. Solutions
1. Chemical content
2. Tonicity of solution
3. Compatibility with other solutions/additives and therapy
4. Potential complications/risk factors
• C. Tonicity of Solutions
- Body fluids are mostly isotonic but may be altered when IV solutions are
added
- In response, body will attempt to maintain homeostasis by adjusting
internal environment
- Changes are based on osmosis and diffusion principles
• 1. Isotonic - solutions having the same osmolality as serum and/or other
body fluids.
Isotonic solutions do not alter the serum osmolality or change the structure
of cells.
• Indications: Hypotension caused by hypovolemia
EX: Normal Saline (.9%NS); Lactated Ringers (LR); D5W
• 2. Hypotonic - solutions having a lower osmotic pressure than that of body
fluids
(serum).
Solutions pull fluid inside the cell, causing cell to expand (Hemolysis)
• Indications: Diarrhea; dehydration; establishing of renal function
EX: 0.45% NS
• 3. Hypertonic - solutions having a higher osmotic pressure than that of body
fluids (serum).
Solutions pull fluid from inside the cell to surrounding fluid, causing the cell
to shrink (Crenation).
• Indications: Reduction of post-operative edema; stabilize blood pressure;
maintain urinary output.
EX: D5 0.9%NS; D5 0.45%NS, D10W; D20W (TPN); D5 LR; Dextran;
Albumin
Note: Dextran and Albumin are considered plasma volume expanders for
blood plasma replacement therapy
• D. Availability of IV Solutions
• 1. Preparation
-Premixed by manufacturer under sterile conditions (commercial solutions)
or created by IV pharmacist (additive therapy)
• 2. Volume
-Volumes include 50cc (ml); 100cc (ml); 250cc (ml); 500cc (ml); 1000cc
(ml)
-Drug additives can be added to any amount of solution as long as
compatibility exists. Amount and type will depend on
(1) desired therapeutic effect; (2) drug manufacturer's recommendations;
(3) risk factors
• EX: Antibiotics 50-100 cc volume
KCL 500 - 1000cc volume
KVO 250 - 500cc volume
• General Rule: Smallest volume to deliver additives safely without
complications or loss of drug concentration or stability
• IV. Nursing Management of IV Therapy
• A. IV Infusion sites and indications
• 1. Peripheral
• a) Routine
• 2. Central Access (Central lines)
• b) Special needs
• B. IV Flow Rates and Calculations
• 1. Flow Rates
-Each tubing has a drip chamber that delivers a specific drop factor
(gtts/ml).
Standard (macro) flow rates include:
10 gtts/ml
15 gtts/ml
20 gtts/ml
The tubing package will let you know that the drop factor is for that tubing
• -Tubing also comes with a microdrip chamber that delivers 60 gtts/ml
(Universal)
• -The flow rate will be determined by three factors:
• a) Total volume to be infused (TVBI)
• b) Time (in minutes)
• c) Drop factor of tubing (or pump)
• 2. IV Calculation Formulas:
• a) Formula for calculating standard flow rates:


• b) Formula for calculating an IV via infusion pump
-Flow is in cc/hr
-Delivery factor - 100cc/hr (for most pumps)
-EX: 100 cc to run over 1/2 hour on pump


• B. Pre-infusion and Initiation Phase
• 1. Assessment of client (physiological)
• 2. Selection of site (peripheral) and appropriate catheter
• 3. Performance of venipuncture (this skill be be taught in ortho/neuro)
• 4. Documentation of procedure (site, catheter size, date, and client
response)
• C. Maintenance Phase
• 1. Monitoring activities (solution, tubing, site)
• 2. Observation for S/S of complications
a) Infiltration
b) Phlebitis
c) Fluid overload
d) Bleeding
e) Infection
• 3. Documentation of Infusion
a) Intake
b) Clients response
c) Site observation
• 4. Termination Phase
a) Removal of catheter
b) Post observation of site
c) Documentation (site, date, time, client response)
• V. Nursing Process and IV Therapy
• A. Assessment (Subjective; Objective)
• 1. Pre-infusion Phase
2. Maintenance Phase
• B. Nursing Diagnoses (General)
• - Fluid Volume (Excess/Deficit) R/T.....
- Potential for Infection R/T.....
- Potential for Injury R/T....
- Impaired Mobility R/T......
-Alteration in Comfort R/T.....
-Sleep Pattern Disturbances R/T....
• C. Plan/Implementation
• -Nursing actions related to safe management and desired therapeutic response
related to IV therapy
• D. Evaluation
• -Client outcome (response) to therapy
1) Subjective
2) Objective
• VI. Legal Aspects of IV Therapy
• A. Licensed Personnel (RN/LPN)
• -Standards of practice within the community according to State Board
of Nursing and Professional Specialty Association
(Intravenous Nurses Society - INS)
1) Venipuncture (after a formal class)
2) Maintenance / monitoring activities
3) Additives and IV push medications
4) Termination
Fluid/ Electrolyte and Acid/Base
Central Lines
Central Venous Access Devices (CVAD)
A central line is a special intravenous line which is inserted through the chest and threaded into
one of the large veins that lie close to the heart (diagram 1)

(diagram 1)
A central line is used for:
• Gaining emergency IV access when the usual IV access into an arm vein is not possible
• Monitoring central venous pressure during major surgery or after severe trauma or illness
• Giving fluids, blood products , chemotherapy, hyperalimentation, and other medications
• Drawing blood samples
• Administering long-term IV therapy
The central line is inserted under sterile conditions. The skin is cleansed, and a local anesthetic is
injected to make the area numb. A health care professional (physician or specially trained nurse)
advances the line until it reaches the large vein in the chest. The catheter is then sutured in
place and a sterile dressing applied. A chest x-ray will be done right away after catheter
insertion to confirm proper placement. The line should not be used until the x-ray is done. A
central line can usually stay in place for up to 4 weeks.
Catheter Types
Nontunneled (or percutaneous) central catheters: (single or multi-lumen)
These are the most commonly used CVAD. The physician can insert this catheter at the bedside,
in the operating room, or in the emergency department. They are suitable for short-term use
and for all types of IV therapy.
(diagram 2)

(diagram 3)
The triple lumen CVP (diagram 3) has 3 lumens varying in size and recommended useage. The
proximal lumen (white port) is an 18 gauge and is the longest pigtail. It should be used if blood
samples, medications or blood administration is required. The middle lumen is blue, 18 gauge,
and is the medium pigtail. It should be used for hyperalimentation (or capped for future hyperal
use) and medications (only is hyperalimentation is not used or anticipated). The third lumen is
called the distal lumen. It is brown, 16 gauge, and is the shortest pigtail. It should be used for
C.V.P. monitoring, blood administration, high volume or viscous fluids, colloids and medications.
Peripherally inserted central catheters (PICCs)
These are useful for patients needing intermediate-length therapy. They can remain in place 3 to
12 months. They are inserted in the cephalic or basilic vein at the antecubital fossa or 3 inches
above or below it. The catheter tip is then is advanced into the superior vena cava or subclavian
vein.. This is the only central device that can be inserted by a specially prepared RN. They may
be used in patients receiving all types of IV therapy, including long-term TPN.
(diagram 4)

(diagram 5)
Points to remember regarding CVC and PICC lines:
• Always access the system under aseptic conditions.
• Use sterile equipment
• Use electronic infusion device for infusions
• Always prep cap with alcohol before each use.
• Never re-use injection cap; change cap minimum of once a week.
• Clamp catheter prior to disconnecting or tubing change.
• Secure connections with tape.
• Any lumen not being used will be routinely flushed Q8h with heparinized saline (follow
hospital policy or refer to diagram 10)
• Always maintain positive pressure when flushing by withdrawing the needle while injecting
the last 0.5cc to prevent reflux of blood into the catheter and possibly clotting catheter
(note: if using a needless system, slowly close the slide clamp during the last 0.5cc of the
injection).
• Use SASH method for administering intermittent medications through a heparin-locked
lumen.
S - 2 cc NS before each IVPB medication
A - Any IVPB medication
S - 2cc NS after each IVPB medication
H - Heparinized saline
• CVC dressing change: You will need to check your hospital policy regarding what kind of
dressing is used on CVC sites as well as protocol for when the dressing changes should
occur. If a transparent dressing is used then often it will be changed every week. If a
gauze dressing is used it will probably be changed every 48 hours. If the dressing is
damp, soiled, or loose, then it needs to be changed regardless of when it was changed
last.
CVC Site Care/ Dressing Change
• Obtain CVC dressing kit
• Take off old dressing. Inspect the site for signs and symptoms of infection.
• Aseptically clean the catheter site with alcohol first [to remove Staphylococcus
epidermidis, the most common cause of catheter-related sepsis] working outward from
the insertion site using moderate friction on the skin to remove dirt.
• After the alcohol dries on the skin, clean the site with betadine or chloraprep-To remove
Candida, another cause of infection. Do not use alcohol to remove the betadine as it's
antimicrobial action is released over time.
• Apply biopatch if protocol, then dressing.
• Document

Tunneled catheters: ( Hickman/Broviac, Groshong)


These catheters may remain in place for many years (sometimes 10 years or more). It is
surgically implanted in subcutaneous tissue, and the access end exits the body on the anterior
chest, usually above the nipples. They can be used for most IV therapies, including long-term
TPN.
(diagram 6: Groshong Catheter)

The Groshong catheter works when pressure is applied to it. When a liquid (medications,
nutritional supplements, saline, blood) is introduced into the catheter lumen, the positive
pressure pushes the valve open outward letting the liquid enter the bloodstream. When negative
pressure (suction) is applied (usually by a syringe), it causes the valve to open inward allowing
blood to flow through the catheter into the syringe (diagram 6).
Points to remember regarding Groshong:
• Routine clamping of the catheter outside the body is not needed.
• Change injection caps every 7 days (or about 18 needle insertions), when the cap has
been removed for any reason, and any time the cap appears damaged
• Heparin is not needed to keep the catheter open.
• Flush line with 0.9% saline per hospital policy
• Teach patient to flush at home with 0.9% saline following the guidelines below:
5cc after each use of the catheter (except for blood withdrawal)
5cc every 7 days when the catheter is not in use
10 cc after putting in or taking out blood
Implanted Ports: (Port-A-Cath or InfusaPort)
A long-term vascular access which consists of a catheter attached to a plastic or metal reservoir
with a rubber top that is surgically implanted on the chest wall. A physician must insert the
device. There is no external catheter and accessing the port requires a needle stick, which can
be done by the nurse. A needle, which is bent at a 45 degree angle, called the Huber needle is
used (diagram 9). When not in use, the port must be accessed every 4 to 6 weeks, and flushed
with heparin to maintain patency (refer to diagram 10).
(diagram 7)

(diagram 8)
A straight needle is used for blood sampling and bolus injections.

(diagram 9)
A 90 degree needle (Huber needle) is preferred for infusions because it is easier to stabilize and
more comfortable for the patient. Never bend a straight needle because that will occlude it.
(diagram 10)
Complications
Sepsis
Catheter-related sepsis is the most common life-threatening complication of CVADs. Below are a
list of factors that may increase the risk of this sepsis:
• Poor insertion technique: Failing to maintain a sterile field or prepare the skin properly.
• Multiple-lumen catheters: A larger-gauge introducer is needed to insert the catheter and
result is greater trauma at the insertion site. Also, a catheter with multiple lumens is
handled more often increasing the opportunity for microorganisms to enter the line.
• A jugular or femoral insertion site: A jugular site is difficult to keep immobilized and to
keep the dressing on. Both sites are close to areas (mouth and groin) with larger number
or microorganisms to enter the line.
• Long-term catheterization: The length of therapy is a factor. Risk for contamination is
considered cumulative and increases with time.
• Contaminated dressing changes. Failing to maintain a sterile field.
• Poor patient health : Critical illness, immunosuppression, diabetes, and hypercoagulability
will put the patient at risk for catheter-related sepsis.
Catheter Sepsis: Signs and Symptoms
• Redness
• Tenderness
• Purulent drainage at insertion site
• Fever spikes
• Malaise
Air Embolism
A bolus of air in the bloodstream can travel to the lungs, heart or brain causing brain damage or
death. The signs and symptoms to watch out for include: respiratory distress, increased heart
rate, cyanosis, thready pulse, hypotension and a sudden change in level of consciousness. If you
suspect air embolism, clamp the catheter, turn patient to left side, put the head down with feet
elevated if possible, and administer oxygen. To reduce the risk of air embolism, have the patient
perform the Valsalva's maneuver (will increase intrathoracic pressure) during catheter insertion,
removal, and during tubing or cap changes.
Venous Thrombosis
A thrombi can result from an improperly placed CVAD as well as improper insertion technique.
You will need to assess for a thrombus if the IV solution will not infuse by gravity or the pump
indicates occlusion. In the beginning you may see swelling in the patient's hand on the side
where the central lines was inserted. If untreated the swelling will progress up the arm, into the
patient's chest and neck. A thrombus can also occlude blood return to the head. In this case you
may see the patient's face become swollen and flushed. If you see any of these signs, stop the
infusion and call the physician. The patient may need anticoagulants and may need thromolytic
therapy (i.e. clot busters).
Phlebitis
Inflammation of the vein is mostly associated with PICC lines. Signs and symptoms include:
pain, redness, problems with infusion of solution, and a red streak may be seen along the vein
path. Removal of the catheter is necessary if the symptoms continue.
CVC Removal
Non-tunneled catheters and PICC lines may be removed by clinicians (check hospital policy). The
patient must be lying down during catheter removal. Instruct the patient to perform valsalva
maneuver while the catheter is withdrawn to prevent air embolism. If the patient is unconscious,
withdraw the catheter during expiration. After catheter removal, apply direct pressure at the site
for 10 to 15 minutes depending on the size of the catheter. Apply pressure dressing with sterile
gauze and tape.

FLUIDS AND ELECTROLYTES


Parenteral Nutrition
AKA Hyperalimentation
TPN (total parenteral nutrition) is a hypertonic nutrient solution administered through a
large central vein. It is usually indicated for patients whose GI tract is not functioning and who
won't be able to eat for 5 to 10 days or longer. Conditions that may leads to this disruption in
eating include:
• Crohn's disease
• Ulcerative colitis
• Bowel obstruction
• Severe diarrhea or vomiting
• AIDS
• Severe pancreatitis
• Those undergoing chemotherapy, radiation, or bone marrow transplant
• Hypermetabolic patients (sepsis, trauma, burns, major surgery)
Others signs that may indicate a need for TPN are:
• Albumin less than 3gm/dl
• Prealbumin below 10 mg/dl
• A drop in body weight of 10% or more when compared to pre-illness weight
• Weight that's less than 86% of what's considered ideal for the patient.

Protein ( Total protein: 6.4-8.3 g/dl or 64-83 g/L (SI units) Albumin (normal: 3.5-5.0 g/dl or
35-50 g/L (SI units)
Recall that proteins are the most significant component contributing to the osmotic pressure with
the vascular space. The osmotic pressure keeps fluid within the vascular space, minimizing
extravasation of fluid. Albumin and globulin constitute most of the protein within the body and
are measured in the total protein. Malnourished patients, especially after surgery, have a greatly
decreased level of serum proteins.
Prealbumin (normal 15-36 mg/dl or 150-360 mg/L (SI units).
Prealbumin is one of the major plasma proteins. It's half-life is 1.9 days compared to 21-days for
albumin. Because prealbumin has a short half-life, it is a sensitive indicator of any change
affecting protein synthesis and catabolism. For this reason, prealbumin is frequently ordered to
monitor the effectiveness of total parenteral nutrition (TPN). Serum albumin levels less than
10.7 mg/dl indicate severe nutritional deficiency.

TPN is not for everyone. Patients which have determined that they do not wish aggressive
therapy, or patients with untreatable end-stage disease, should not be consider as candidates
for TPN therapy.
Getting Started
The physician is responsible for inserting the central venous catheter that is used to deliver the
TPN. A large vein, such as the superior vena cava, or sometimes the femoral vein, will be the
site of choice. For patients, where it is anticipated that TPN may be needed longer than 4-6
weeks, indwelling catheters such as the Hickman or Groshong and other implanted venous
access devices may be used. Another alternative may be the peripherally inserted central
catheter (PICC), which can be inserted by a specially trained RN. Radiography must be done to
verify proper catheter position prior to giving TPN.
Nursing Responsibilities
Once placement is verified, the nurse must check the physician's orders against the bag to verify
the patient's name, room number and the solution's ingredients, additives and expiration date
before beginning the infusion. Remember that each TPN bag has been specifically prepared for
each patient based upon the individuals condition and labs. Patient's receiving the wrong
solution can cause serious complications, including electrolyte imbalances;
Other nursing considerations that you will need to be aware of include:
• Prior to hanging the bag checked for leaks, foreign matter, discoloration, or separation of
fluids in the bag.
• An IV control device (pump) must be used to infuse the solution.
• Do not speed up or slow down TPN (if TPN has been off, check glucose and re-start at the
same rate)
• The TPN line cannot be used for any other purpose other than TPN and lipid administration
(No antibiotics or blood products etc.) [Risk for infection is greater in TPN lines because
the high dextrose concentration encourages bacterial growth].
• Must use an in-line filter on TPN tubing to collect particulate matter.
• TPN bag may not hang longer than 24 hours.
• If TPN bag runs dry and the next TPN bag is not ready, hang 10% dextrose and watch for
signs of hypoglycemia.
• Accu-checks are done AC and HS with a sliding scale for insulin coverage (this will be
ordered by physician).
• TPN bags are numbered. Be sure that bags are hung sequentially as ingredients may vary
from bag to bag.
• Document intake and output as well as body weight.
• V.S. should be taken every 4 hours (elevations can be the first sign of catheter-related
sepsis.
• Perform site care and dressing to central line per hospital policy (usually 3x/week; either
a dry sterile dressing or a transparent semipermeable dressing is used) using aseptic
technique.
• Provide frequent oral care if patient is NPO.
TPN Formula
Most hospitals have pre-printed TPN forms (click here to see a sample form) to aid the physician
in ordering everything that is pertinent to the patient receiving hyperalimentation. The major
components-protein (amino acids), carbohydrates (dextrose) and fats (lipid) along with trace
elements, electrolytes, minerals, and vitamins must all be ordered by the physician. Other
medications that may be added include regular insulin, H2 antagonists such as cimetidine
(Tagamet) or ranitidine (Zantac). Labs that are required to properly monitor the patient's
response to TPN include blood glucose, electrolytes, proteins, liver and renal function tests.
Complications
Below is a chart adapted from Nursing96 (April) that lists common problems with parenteral
nutrition and how to correct the problem.
Complication Signs and Symptoms Interventions
Metabolic Hepatic Elevated serum aspartate • Reduce total
Problems dysfunction aminotransferase caloric intake
(SGOT/SGPT), alkaline and dextrose,
phosphatase, and making up
bilirubin levels lost calories
by
administering
a lipid
emulsion.
• Change to
cyclical
infusion (TPN
that infuses
over 10-16
hours per
day)
• Use specific
hepatic
formulations
only if the
patient has
encephalopat
hy
• Reduce total
caloric and
Heightened oxygen
dextrose
consumption,and
xx Hypercapnia intake, and
increased carbon dioxide
balance
production
dextrose and
fat calories
• Restrict
dextrose
intake by
decreasing
either the
Fatigue, restlessness, rate of
confusion, anxiety, infusion or
weakness, polyuria, the dextrose
xxx Hyperglycemia dehydration, elevated concentration
serum glucose levels; in • Compensate
severe hyperglycemia, for caloric
delirium or coma loss by
administering
a lipid
emulsion
• Begin insulin
therapy
x Hyperosmolarity Confusion, lethargy, • Discontinue
x seizures, hyperosmolar dextrose
nonketotic syndrome, infusion
hyperglycemia, • Administer
dehydration, glycosuria regular
insulin and
0.45% or
0.9% sodium
chloride
solution to
rehydrate the
patient. Give
electrolyte
replacement
(potassium,
magnesium,
or calcium) as
ordered
Paresthesia, muscle • Adjust
cramps, tetany, ECG calcium and
x Hypocalcemia
changes (such as phosphate
prolonged QT interval) supplements
• Increase
dextrose
Tachycardia, sweating,
intake
Hypoglycemia shaking, irritability after
• Adjust
the infusion has stopped
exogenous
insulin intake
Muscle weakness,
paralysis, paresthesia,
arrhythmia's, ECG • Increase
Hypokalemia changes (such as potassium
depressed ST segment supplements
and flat or inverted T
waves)
Tingling around the
• Increase
mouth, paresthesia in
Hypomagnesemia magnesium
fingers, mental changes,
supplements
hyperreflexia, nausea
• Adjust
Irritability, weakness,
phosphate
Hypophosphatemia paresthesia, coma,
and calcium
dyspnea
supplements
Dermatitis, alopecia,
apathy, depression, taste • Increase zinc
Hypozincemia
changes, confusion, poor supplements
wound healing, diarrhea
Elevated serum chloride
• Increase
and potassium levels,
acetate and
reduced serum
decrease
bicarbonate level,
Metabolic acidosis chloride in
decreased arterial pH,
parenteral
decreased or normal
nutrition
PaCo2, hypotension,
solution
arrhythmias
Metabolic alkalosis Diminished serum • Decrease
chloride and potassium acetate and
levels, elevated serum increase
bicarbonate level, chloride in
increased arterial pH, parenteral
increased or normal nutrition
PaCo2, tetany, seizures,
changes in level of
solution
consciousness,
arrhythmias
• Start TPN at a
slow rate
(aprox 1000
calories per
24 hours) and
Occurs within first 24-48 gradually
of TPN initiation; increase rate
Refeeding respiratory depression, • Monitor
x
Syndrome lethargy, confusion, serum
weakness, electrolytes
cardiopulmonary arrest closely for
first 2 days;
adjust
electrolytes
on correct
imbalances
• Attempt to
aspirate the
clot
• If
unsuccessful,
instill
Interrupted flow rate, urokinase into
Mechanical
Clotted catheter resistance to flushing and central line as
Problems
blood aspiration ordered to
clear catheter
lumen
• Prepare for
catheter
replacement
as necessary
• Apply a
padded
hemostat
above the
Cracked or broken
x Fluid leaking from tubing break to
tubing
prevent air
from entering
the line, then
replace tubing
Nausea, headache, • Check the
x Too-rapid infusion
lethargy infusion pump
Other Air embolism Apprehension, chest pain, • Clamp
Problems tachycardia, hypotension, catheter
cyanosis, seizures, loss of • Place the
consciousness, cardiac patient in a
arrest left lateral
trendelenburg
position
• Administer
oxygen as
ordered
• Begin CPR if
cardiac arrest
occurs
• Notify the
physician
immediately
• When the
catheter is
removed,
cover the
insertion site
with a
dressing
(occlusive, if
the patient
has a central
line) for 24 to
48 hours
• Stop the
infusion
• Treat the area
according to
the protocol
appropriate
for the drug
that
Swelling and pain around
Extravasation extravasated
the insertion site
• Assess the
patient for
cardiopulmon
ary
abnormalities
; a chest x-ray
may be
needed
• Remove the
catheter
• Apply a warm,
moist
compress to
Pain, tenderness,
Phlebitis the area
redness, warmth
• Elevate the
extremity if
possible (ex:
arm if PICC
line)
Pneumothorax and Dyspnea, chest pain, • Assist with
chest tube
insertion and
cyanosis, decreased
hydrothorax connect to
breath sounds
suction as
ordered
• Remove the
catheter and
send the tip
Red and swollen catheter
for culture
site, chills, fever,
Sepsis • Obtain blood
leukocytosis, backache,
cultures
hypotension
• Administered
antibiotic as
ordered
• Leave the
catheter in
place;
removing the
catheter could
cause an
embolism
• Apply warm,
moist
compresses
to the
insertion site
Erythema and edema at and elevate
the insertion site; the affected
ipsilateral swelling of the extremity
arm, neck, face, and • Monitor
x Thrombosis
upper chest; pain at the airway
insertion site and along patency
the vein; • Establish
malaise;fever;tachycardia another I.V.
access
• Administer
anticoagulant
therapy as
ordered
through the
new I.V.
access
• Administer
thrombolytic
therapy as
ordered
Weaning TPN

As a general rule TPN will be discontinued once the patient is taking between 50% and 60% of
his calories by mouth. It is important that the patient's dietary intake be documented as a
percentage. For example, instead of saying that the patient "eat well", it is better to state that
the patient eat 90% of his hamburger. Due to the hypertonicity of the IV fluid and the potential
for hypoglycemia, TPN must be discontinued slowly. Weaning usually takes place over 24 to 48
hours but can be completed in 4 to 6 hours if the patient receives sufficient oral or I.V.
carbohydrates.
Peripheral parenteral nutrition (PPN) is used for patients who are able to
take oral feeding but not enough to meet nutritional levels. A
combination of lipid emulsion and an amino acid-dextrose solution is used.
Intralipids
(Lipid Emulsions)
Lipid emulsions are thick emulsions that supply the patient with essential fatty acids as well as
calories. They are needed for cell wall integrity and for the absorption of fat soluble vitamins.
Patients with known allergies to eggs or soy, disturbances with normal fat metabolism, severe
liver disease, or acute pancreatitis should not receive intralipids.
Below are some specific points that you will want to remember about intralipids:
• Normally a milky consistency
• Can be given through a central venous catheter or through a peripheral line
• Piggyback to TPN/PPN at closest port to patient
• Normally hung once a day and infused over 8 hours (note: there is a "3-in-1 system" in
which lipids are mixed with amino acids and dextrose in one container and these are
infused over a 24-hour period of time)
• Comes in glass bottles and requires "vented" tubing
• Do not administer through a filter
• Does not need to be refrigerated
• Do not add anything to the bottle
• Observe for adverse reaction and stop the infusion immediately if any symptoms occur
(i.e. chills, fever, dyspnea, cyanosis, flushing, diaphoresis, dizziness, headache)
• Monitor liver function studies
Blood Transfusions
Transfusions of blood products can be for acute or chronic conditions. Either way, it is not
without risks.
1. Indications
o Blood loss – due to hemorrhage, burns, injuries
o Anemia
o Shock
o Maintain O2 transport
o Promote homeostasis
o Fight infections
b
2. Types of blood products
3.
o Whole blood - rarely used; large volume causes circulatory overload
o PRBC's – whole blood minus plasma. Increases the O2 carrying capacity of blood
o Platelets – pooled from several different individuals; used to treat
thrombocytopenia
o FFP – a frozen and thawed portion of plasma with clotting factors. Used to treat
deficiencies (ex. To reverse Coumadin)
o Cryoprecipitate – another portion of plasma used to treat deficiency of clotting
factors, fibrinogen, factor VII (hemophilia)
o Albumin – Commercially prepared plasma; doesn't transmit hepatitis, no cross-
match necessary. Used to treat hypovolemia.
o WBC's – replaces WBC's during sepsis, cancer etc.
j
4. Lab Indices
o H&H
o Platelet count
o WBC
o Individual clotting factors
j
5. Type and Cross Match
o Must be done prior to transfusion and every 48 hours if additional blood products is
to be given
o ABO group system
j
BLOOD TYPE COMPATIBLE DONOR
GROUPS
Type A A and O
Type B B and O
Type AB (universal recipient) A, B, AB, O
Type O (universal donor) O
o Rh system – positive or negative. Never give positive to a negative
6. Modes of Transfusion Therapy
o Indirect transfusion
o Anonymous volunteer donor
o Designated donor
• Autotransfusion
o Patient donates blood ahead of time to himself
o Patient receives his own blood back during or after procedure after it has
been filtered and prepared
6. Refusal of blood transfusion
• Any patient who is competent can refuse blood transfusion.
• Jehovah Witnesses – religion that prohibits receiving a blood transfusion
• Most institutions require a signed consent for blood transfusions
7. Transfusion reactions – Baseline Assessment Imperative
• Hemolytic transfusion reactions
o usually seen early in transfusion (first 15 minutes)
o usually due to ABO incompatibility
o usually due to nursing, clerical error (not checking patient armband, lab slip
error)
o CAN BE FATAL!!!
o signs/symptoms
 burning at IV site
 facial flushing
 fever
 chills
 nausea
 temperature up to 104 degrees
 chest pain
 rapid labored breathing
 headache
 low back pain
 shock
o treatment
 stop transfusion (severity depends on how much blood patient
receives)
 notify MD
 maintain IV access with NS
 treat shock (administer O2, fluids, epinephrine)
 monitor urine for blood (hemoglobinuria), renal failure
 follow hospital protocol for transfusion reaction – send blood, urine
etc.
• Allergic reaction
o allergic reaction to something in donor blood
o if patient has known sensitivity, may premedicate with tylenol, benadryl,
steroid
o may need washed cells
o signs/symptoms
 hives (uticaria)
 pruritis
 facial and/or glottal edema
 anaphylaxis
o treatment
 stop transfusion
 notify MD
 maintain IV access with NS
 treat symptoms
.
8. Other complications
• circulatory overload – may need to decrease IVF during transfusion, administer
diuretics, monitor CVP, BP, pulse, JVD, assess breath sounds for crackles
• infection –
o most infections transmitted by transfusions are viral in origin.
o can receive infection through blood (hepatitis, malaria, etc.) or by improper
handling of blood by staff.
o HIV – now with donor education, donor screening, HIV antibody testing – this
is rare
o hepatitis is most common transmitted disease
o blood is screened for HIV, hepatitis B,C, D, human T-cell leukemia, tropical
spastic paraparesis, syphilis
• air embolism –
o use basic nursing skills to expel air from line.
o if patient becomes SOB, has CP, cyanosis - consider air embolism.
o place patient in trendelenberg and on his left side.
o call MD
• hypothermia –
o a. if blood is given too fast and is not warmed, can become
hypothermia
o never warm blood in microwave (use an accepted blood warmer
9. Transfusion Procedure
• Use a large gauge catheter to start IV line
• Use a Y-type administration set that has an in-line filter (most tubing boxes
will indicate "Blood tubing")
• Use only 0.9% normal saline solution with blood
• Follow agency protocol in obtaining blood products from blood bank
• Identify blood product and client with another licensed nurse (some hospitals
allow an RN and LPN to check blood, other hospitals require two RN's..check your
hospital policy)
• Take baseline vital signs, begin transfusion and monitor for transfusion
reactions.
• Document administration of blood in the nurse's notes.
• When infusion complete, depending on the hospital, you may return blood
bag (sometimes tubing) to blood bank. Alternative is to discard blood bag and
tubing into a red bag.

Accessory Organs
Structure and Function

The accessory organs that are covered in this section include the liver, gallbladder and
pancreas. Use any A & P text to review the anatomy and physiology as well as the basic
functions of each of these organs. This information will be integrated throughout this section
and will provide the foundation on which pathophysiological changes associated with each
disease will be based.
Specific objectives have not been written for this section but instead will be incorporated into the
appropriate disease as indicated.
Viral Hepatitis
Viral hepatitis is a bigger threat that most of us realize. Did you know that it's easier to catch than human
immundeficiency virus (HIV)? Experts are saying that millions of people throughout the world are infected and do not
even know it.
There are five types of viral hepatitis from A to E. For this course you will be responsible for A, B, and C only. When
reading the information in your med-surg book these are the key points you want to be sure you understand:
1. Definition of hepatitis
2. Know the differences in A, B, and C with regard to:
o mode of transmission
o source of infection
o periods of infectivity
o complications
3. Know how to differentiate active, previous and chronic carrier states as it applies to Hepatitis A, B and C utilizing
appropriate laboratory values
4. Understand how to prevent Hepatitis A, B, and C
5. Know the post-exposure management of A, B, and C
6. List the clinical manifestations seen in the preicteric, icteric, and posticteric phases of hepatitis.
7. Know the common diet and activity orders seen in hepatitis patients.
8. Know how health care providers should protect themselves when caring for patients with Hepatitis.

Gastrointestinal Accessory Organs


Viral Hepatitis
Viral hepatitis is an inflammation of the liver. Currently there are six virus (A,B,C,D, E, and G)
and the likelihood of identifying more are great. For this course you will only be responsible for
A, B, and C.
The hepatitis A (HAV) virus is transmitted through the fecal-oral route. Small outbreaks are
caused by fecal contamination of food or drinking water. Hepatitis A will often be found in
crowded conditions, in individuals with poor personal hygiene or infected food handlers. We've
had several incidences in Fort Lauderdale where an outbreak of hepatitis A has been traced back
to one individual working in a restaurant. You might remember the boat that was converted to a
seafood restaurant called the Ancient Mariner. For years it was located on the New River Canal
behind the courthouse. They had a hugh outbreaks of hepatitis A which was traced back to the
salad bar and if my memory serves me correctly, one waiter. They did manage to re-open but
then another outbreak occurred. The publicity from the second outbreak ultimately resulted in
this very profitable establishment shutting down and the boat being sunk in the ocean.
The incubation period for hepatitis A is about 15 to 50 days. It's important to know that these
people are infectious two or more weeks before the onset of symptoms and up to one week after
the onset of jaundice [virus is found in the stool] . As the stools are becoming negative, a
serum sample will show the presence of Igm, which indicates acute infection. The infected
individual will often have only mild symptoms that they describe as "flu-like".
Once the patient has had hepatitis A they will develop life-long immunity and do not become
carrier's as can be found in other forms of hepatitis. If a person is going into an area that puts
them at high risk for contacting hepatitis, such as traveling to an under developed country, they
can receive the vaccine havrix to prevent them from contracting the disease.
Hepatitis B (HBV) is a virus that has received alot of attention. Do you remember the country
western singers The Judd Sisters? The mother, before becoming a well-known singer, use to be
an ICU nurse who contacted hepatitis B. She ultimately had to stop touring due to the long-term
effects of the hepatitis B virus. Dialysis nurses are considered to be at higher risk for contracting
the disease because of their daily exposure to blood. Luckily this risk has gone down over the
years since the development of the hepatitis B vaccinations.
An individual can get this virus through percutaneous means such as IV drug use or an
accidental needlestick. It is also found in individuals with high-risk lifestyles such as male
homosexuals who practice anal intercourse or heterosexuals with multiple partners. Other
methods of transmission include infectious blood, blood products, other body fluids [semen,
vaginal secretions, saliva], and perinatal. It is equally important to know that this virus is not
found in urine, feces, milk, tears, or sweat.
The incubation period for hepatitis B is about 45 to 180 days. These people are infectious before
they themselves have symptoms [they will be infecting others without even realizing it]. This
infectious period will continue and can last as long as 4 to 6 months. A percentage [6-10%] of
hepatitis B patients will become chronic carries and will be infectious for their lifetime. Carrier
states can be determined by drawing a hepatitis profile. A +HbsAg [hepatitis b surface antigen]
found in the serum of a patient with hepatitis B, 6 to 12 months after contracting the disease,
indicates a carrier state.
Hepatitis C (HCV) is the most common chronic bloodborne infection and the leading reason for
liver transplantation in the United States (Johnsen, C. [1999, June 1] Hepatitis C: The shadow
epidemic. Nursing spectrum) . Risk factors that lead to hepatitis C infection include IV drug use,
transfusions, hemodialysis and occupational exposure. The risk due to multiple sex partners and
perinatal exposure is still unclear but it is generally believed to play a role in the transmission of
hepatitis C.
The incubation period is aprox. 14-180 days. The period of infectivity begins 1-2 weeks before
symptoms and continues during the clinical course. If patient becomes a carrier, then they will
remain infectious indefinitely.
The pathogenesis of hepatitis results in widespread inflammation of liver tissue. The liver will
become necrotic, scar, and the kupffer cells become enlarged [kupffer cells line the liver and
are responsible for filtering bacteria and other foreign proteins out of the blood]. The
inflammatory process also causes bile duct injury and obstructive jaundice. The liver does have
the unique ability to regenerate and will resume normal appearance and function if there is no
complications.
Some of the systemic effects include rash, angioedema [acute, painless, swelling of short
duration involving the face, lips, hands, feet and genitalia], arthritis, fever, malaise,
glomerulonephritis and vasculitis [inflammation of blood vessels] .
A term that is associated with hepatitis is "icter" meaning pertaining to jaundice or "icterus"
meaning jaundice. If you will recall jaundice is a yellow discoloration of the skin, mucous
membranes, and sclera of the eyes. It is caused by large amounts of bilirubin in the blood.
[Review: Bilirubin is the yellow-orange pigment of bile that is formed when the hemoglobin in a
red blood cell is broken down at the end of it's normal life span of 120 days. It is first water-
insoluable and unconjungated and must travel to the liver via the bloodstream where it becomes
water-soluable and conjugated. It is then excreted into the bile. In a healthy person aprox. 250
mg of bilirubin is produced daily and the majority is excreted in the stool. This is what gives
stool is characteristic brown color]
Hepatitis is divided into three phases. These include the preicteric, icteric , and posticteric
phases. The preicteric phase lasts about 1 to 21 days and precedes the appearance of
jaundice. These patients suffer from severe anorexia and will say they find food "repugnant"
[this is caused by a toxin produced by the diseased liver]. Along with the anorexia will
come nausea and vomiting, weight loss, right upper quadrant discomfort, fever [low grade],
arthralgias [joint pain], urticaria [skin eruptions, wheels {caused by vasodilatation of
the dermis} , hepatomegaly [enlarged liver], and sometimes splenomegaly [enlarged
spleen].
The icteric phase lasts from 2 to 4 weeks and is characterized by jaundice. The patient may
have dark colored urine due to excess bilirubin being excreted by the kidney's. Light colored
stools is the result of conjugated bilirubin's inability to flow out of the liver because of
obstruction or swelling of bile ducts. These patients will also itch due to the accumulation of bile
salts under the skin. They will continue to have hepatomegaly.
The posticteric phase lasts aprox. 2-4 weeks. The onset of this phase coincides with the
disappearance of jaundice. Usually the patient is very fatigued. In fact, this is their major
complaint during this time. The splenomegaly will start to subside but the liver will remain
enlarged for several more weeks.
A diagnostic test that will be done are the LFTs (liver function tests) which will probably be
elevated. There is a article entitled Clarifying the complexity of Liver Function Tests written by L.
Siconolfi. This is an excellent article that you might want to review.
Another lab that will be ordered is the serologic test which is the hepatitis profile. You may find
the profile hard to interpret and this is somewhat related to the fact that different reference labs
report the findings in different ways. Once you start working and you get use to the reports for
your hospital it won't be so confusing. To hear a brief explanation of how to intrepretate a
hepatitis profile (hepatitis A) click here (hepatitis B) click here . I do want to give you some
frame of reference as to what you should be looking for when you look at these reports.
First of all, they will report on all types of hepatitis unless the requisition specifically states a
certain hepatitis. Let's be sure you understand the abbreviations. Example Anti-HBcIgM: Anti =
antibody, H=hepatitis, B=B (type of hepatitis), c=core, IgM = acute infection. Example HBsAg:
H=hepatitis, B=B, s=surface Ag=antigen
Are you getting the hang of this?
For hepatitis A two results can basically come back. A positive anti-HAV IgM signifies an acute
infection or a positive anti-HAV IgG indicates a previous infection and the patient has life-time
immunity.
The profile for hepatitis B is more complicated. First of all you must realize that hepatitis B has 3
distinct antigens.
1. HBsAg (hepatitis B surface antigen)
2. HBcAg (hepatitis B core antigen) [Alot of people make the mistake of thinking that the
small c represents hepatitis C. This is a mistake, it stands for core]
3. HBeAg (hepatitis B e-antigen) [The e does not stand for anything like in the above where
"s" stood for surface; I've asked several doctors what it stands for and none of them have
any ideas why it labeled "e"]
If the report comes back +HbsAg this could indicate either a current infection or it will be
because the patient is a chronic carrier.
If the report comes back + AntiHBs (antibody to surface antigen) [Remember that antibodies
are good unless the patient has HIV] then this would indicate immunity to hepatitis B. This is the
marker that will be looked at if you have under gone the Hepatitis B vaccination series to
determine if you have developed antibodies.
If the report comes back + HBeAg (hepatitis B e antigen) then this patient is highly infective.
If the report comes back + AntiHBe (antibody to e antigen) this indicates this patient is less
infected than when he had +HBeAg. [e is used to determine the degree of infectivity]
Hepatitis C serologic test uses the presence of antibodies to help with the diagnose. What's
interesting about this is that there is not one test that can differentiate between acute and
chronic infection. A positive Anti-HCV is a marker for acute or chronic infection. To be called a
chronic infection then the patient will have to have a positive hepatitis C antibody test, and
elevated liver enzymes (AST/ALT) that persists for more than six months. The other way in
which to diagnose chronic hepatitis C is to do a liver biopsy which will show evidence of hepatitis
in spite of the fact that ALT and AST levels are normal.
Besides the LFTs and serologic testing, other tests that may be ordered include :
1. alkaline phosphatase: will show some elevation [indicative of impaired excretory function
of the liver]
2. serum proteins: normal or increased [if increased this is reflective of impaired clearance
by liver]
3. serum albumin: normal or decreased [due to liver damage]
4. serum bilirubin (total): will be increased [due to hepatocullular damage]
5. urinary bilirubin: increased [due to conjugated hyperbilirubinemia]
6. urinary urobilinogen: increased [due to diminished reabsorption of urobilinogen]
7. prothrombin time: prolonged [decreased production of prothrombin by liver]

The treatment for hepatitis is non-specific. It will usually include rest in order to decrease the
metabolic demands on the liver and promote regeneration. Isolation of the patient is longer
required. If the patient has hepatitis A and is incontinent of stool or is poorly compliant in the
area of personal hygiene, then a private room may be necessary. It is extremely important that
gloves are worn and good handwashing is done.
The pharmacological management is usually supportive therapy. The patient will receive an
antiemetic if nausea is a problem. Immune globulin (IG) provides temporary passive immunity
for 6-8 weeks. IG is effective for hepatitis A if given up to 2 weeks after exposure [remember
that if the exposed person has anti-HAV {antibodies} IG is not necessary] . IG is also
recommended for people who have been in close contact and have been exposed to hepatitis A.
Exposure may have come from close proximity in a household {to someone who has hepatitis
A}, daycare centers, travelers to foreign countries to name a few.
Hepatitis B Immune Globulin (HBIG) provides temporary passive immunity. It is recommended
for post-exposure prophylaxis in the case of needlestick, mucous membrane contact or sexual
exposure. This medication is very expensive because it is prepared from plasma donors with
high titers of antiHBs.
The dietary management of hepatitis includes low fat [fats are poorly tolerated because of
decreased bile production] , small frequent meals, carbonated beverages, and an emphasis on
breakfast as this is the time that anorexia is lowest. If anorexia or N/V is severe, the patient
may need IV glucose and/or tube feedings.
Just a reminder that immunizations are available for hepatitis A (Havrix) which was already
mentioned. Day care workers, institutional residents, and military personnel are example of
people who should receive this vaccine. Also, there is a vaccine for hepatitis B. If you have not
received your series of three injections, you have passed up the most effective method of
preventing HBV infection. As an employee of a hospital, you will be asked to sign a release if you
choose not to take part in hepatitis B vaccination program. It is usually offered free, and has
very few side-effects. Infants now receive hepatitis B as part of their routine immunization
schedule and children entering kindergarten and 7th grade must be immunized. The drug is
recombivax HB or engerix-B which is given I.M. in the deltoid. The first shot is given followed by
a second shot one month after the first and the third shot is given about six months after the
first. These injections should result in anti-HBs titers of 10 mIU/ml or greater.
Gastrointestinal Accessory Organs
Viral Hepatitis

Guide to Three Types of Viral Hepatitis


Hepatitis A virus Hepatitis C virus
z Hepatitis B virus (HBV)
(HAV) (HCV)
Mode of Fecal-to-oral route Sexual contact; blood-to- Blood-to-blood
transmission primarily; poor blood contact; perinatal contact;
sanitation and (at birth);contaiminated contaminated
blood
water contribute to
products;risks not
the risk; many
well defined for
outbreaks are blood products;
sexual or perinatal
traced to infected occupational risks from
transmission;
food handlers; needlesticks and other
occupational risks
intimate contact blood exposures
to health care
within households;
professionals are
sexual contact
similar to HBV
14 to 180 days
Incubation 15 to 50 days 45 to 180 days (average:
(average: 40 to 60
period (average 60 to 90 days)
days)
Most infectious Begins one to two
during two weeks Begins before symptoms, weeks before
before onset of appear and persists for symptoms appear;
illness; in most four to six months after continues
Infectiousness
cases, unlikely to acute illness; persists for throughout clinical
be infectious after the lifetime of chronic course and
first week of carriers indefinitely in
jaundice chronic carriers
HBsAg (indicates current
or chronic infection)
HBeAg (a marker for
increased infectivity)
Anti-HAV IgM
Anti-HBc (a marker for
(indicates current Anti-HCV (a
infection at some time)
Laboratory infection) marker for
Anti-HBe (a marker for
tests Anti-HAV IgG infection with HCV
decreased infectivity)
(indicates past, virus)
Anti-HBs (a markers for
resolved infection)
immunity and the
antibody produces in
response to the HBV
vaccine)
Immune globulin
In the unimmunized
with two weeks of The value of
person exposed, give HBV
exposure; if given immune globulin is
Postexposure vaccine and high titer
early in incubation unclear; no other
management immune globulin (HBIG)
period, it has 80% treatment is
to reduce the risk of HBV
to 90% presently available
infection
effectiveness
With acute HBV infection, Chronic carrier
death from fulminate state in as many
Rare, but can be
hepatitis is possible; up to as 50% of those
fatal if fulminant
10% become chronic infected via blood
hepatitis develops;
Complications carriers and may be at transfusions or IV
protracted
risk for cirrhosis, liver drug abuse;
cholestasis can
cancer, and death; anyone chronic liver
occur
with HBV is at risk for HDV disease; cirrhosis;
infection liver cancer; death
Prognosis Good; generally Good; generally, a full Chronic carrier
full recovery; no recovery, except for rate high;
chronic carrier generally, a full
chronic carriers
state recovery in others
Handwashing prior
HBV vaccine for all infants,
to food
health care professionals, Screening donated
preparation;
and others at risk; blood; avoidance
proper personal
condom use; screening of blood-to-blood
hygiene;
donated blood; devices to exposure for at
environmental
minimize to health care risk individuals
sanitation
professionals (such as and health care
Prevention measures; food
needless IV access professionals
and water
devices); personal withthe same
sanitation;
protective devices for measures as for
immune globulin
health care professionals HBV
for travelers into
(such as aprons, eye and Note: There is no
areas where HAV
mucous membrane HCV vaccine
is common; HAV
protection, gloves, gowns)
vaccine (Havrix)

Gastrointestinal Accessory Organs


Viral Hepatitis
Definitions of Terms
Hepatitis B Virus Infection
Term Definition
HBV The hepatitis B virus is the agent that causes hepatitis B virus
infection (formerly called serum hepatitis).
HBsAg The hepatitis B surface antigen (formerly called Australia antigen or
hepatitis-associated antigen) is found on the surface of the virus.
HBsAg, detected in serum 30 to 60 days after HBV exposure, persists
for variable periods.
Anti- Antibody to HBsAg is associated with long-term protection against
HBs reinfection and, in most persons, persists for many years after natural
infection. Anti-HBs is also produced as an immune response to
hepatitis B vaccine or is passively transferred when HBIG is
administered. Anti-HBs is currently measured by radioimmunoassay
(RIA) or enzyme-linked immunosorbent assay (ELISA).
HBeAg The core of the virus contains hepatitis B e antigen, which is
associated with HBV replication, high concentrations of HBV in serum,
and high infectivity of serum.
Anti- Antibody to HBeAg is produced in most HBV infections and is
HBe associated with low infectivity of serum.
HBcAg The core of the virus contains the hepatitis B core antigen, which is
distinct form HBsAg. There is no commercial test to detect HBcAg.
When you see a small c as above, do not confuse this with the
hepatitis "c" virus. The c in this case is referring to the core
Anti- Antibody to HBcAg is produced in all HBV infections; it indicates
HBc infection at some undefined time and persists indefinitely.
IgM IgM class antibody to HBcAg indicates recent infection with HBV and is
anti-
positive for approximately 6 months after infection
HBc
HBsAg Through serologic testing, a person is confirmed as an HBsAg carrier
carrier when (1) HBsAg is detected on at least two tests at least 6 months
apart or (2) the results of a single serum specimen as HBsAg-positive
and IgM anti-HBc-negative. Carriers may be asymptomatic and
unaware that they are HBV-infected. Because they carry HBsAg in
their blood, they are capable of infecting others.
HBIG Hepatitis B immune globulin is a preparation obtained from the blood
plasma from donor pools selected for a high antibody content of anti-
HBs. In some situations, HBIG is administered with hepatitis B
vaccine to provide additional protection against HBV infection.

Gastrointestinal Accessory Organs


Viral Hepatitis
Serologic Markers

The following table is a summary of some important serologic markers that occur during acute
and chronic HBV infection. The graphs are illustrations of how these serologic markers appear,
disappear, or persist during acute or chronic HBV infection.

Marker Acute Chronic Indication


HBsAg (hepatitis B surface antigen) identified can be person is
in serum identified infectious
30 to 60 in
days after
blood
exposure
to HBV
peaks
when
symptoms
appear
disappears
when
symptoms
abate
HBeAg (hepatitis B confirmed is positive viral
e antigen) the same early in replication
time as infection high
HBsAg is more infectivity
infection likely to be
negative
after
longer
infection
IgM anti-HBc (IgM class antibody to confirmed disappears acute or
hepatitis B core antigen [HBcAg]) 2 months 6 months recent
after after infection
exposure exposure
to HBV to HBV
present in
high titers
disappears
3 to 6
months
later
Anti-HBc (antibody to HBcAg) initially persists earlier
consists of indefinitely infection at
IgM some
antibody unspecified
after 6 time
months,
consists of
IgG
persists
indefinitely
Anti-HBs (antibody to HBsAg) appears does not immunity to
last, develop HBV, either
usually 6 from past
to 8 infection or
months in response
after to vaccine
exposure
lasts
indefinitely
Cirrhosis of the Liver
Cirrhosis of the liver is a disease that is prevalent in today's society and therefore you will probably care for patients with
this diagnosis. It is a very complex disorder that will challenge your ability to see the "interconnectiveness" of the body
systems. It does have a stigma attached because the primary cause of cirrhosis is related to alcoholism. Members of the
medical community often apply their personal views to these patients and have an attitude that "they brought this on
themselves".
There are four types of cirrhosis but you are primarily responsible for Alcoholic Cirrhosis. When reading the information
in your med/surg book these are the points you want to be sure you understand:

1. Know the most common type of cirrhosis


2. List the major systemic clinical manifestations of cirrhosis of the liver (hint: use figure 41-5 as a guide)
3. Define and understand the cause of the two kinds of skin lesions commonly found in cirrhosis
4. Know the laboratory results which will be expected in a patient with cirrhosis with regard to: folic acid, serum
bilirubin, albumin, total protein, potassium, platelets, prothrombin time [PT], WBC, RBC
5. Describe how portal hypertension, hypoalbuminemia and hyperaldosteronism leads to ascites, a advanced
development found in cirrhosis
6. Describe the difference(s) between a LaVeen and Denver shunt
7. Describe the mechanism that causes hepatitic encephalopathy
8. Know the relationship between ammonia and hepatic encephalopathy
9. Be able to list the foods that patient's with hepatic encephalopathy should avoid
10.Know the purpose for administering neomycin and cephulac
11.Understand the relationship of portal hypertension and esophageal varices
12.Understand the 2 balloons of the Sengstaken-Blakemore Tube with regard to purpose, maintenance and safety
issues
13.Understand the purpose and side-effects of vasopressin therapy
14.Know the name of the surgical shunts used to treat portal hypertension as will as the pros/cons of each procedure

Gastrointestinal Accessory Organs


Viral Hepatitis
Cirrhosis of the Liver
Brief Overview
PATHOPHYSIOLOGY
Cirrhosis of the liver is the result of a degeneration and destruction of liver cells which are
replaced with scar tissue. The liver cells attempt to regenerate and in the process cause the
liver lobules to become irregular in size and shape with impaired vascular flow.
ETIOLOGY
There are four types of cirrhosis but only Alcoholic Cirrhosis (formerly known as Laennec's) is
featured in this section. You will have read about Postnecrotic Cirrhosis in conjunction with
hepatitis, since it is a complication of that disease.
MANIFESTATIONS
1. Early
• GI symptoms such as anorexia, dyspepsia, gas, N/V, changes in bowel habits [These
are often due to liver's altered metabolism of CHO, fats & proteins]
• Abdominal pain which is dull & heavy in RUQ or epigastrium [Pain is due to swelling &
stretching of liver capsule and spasm of the biliary ducts]
• Fever, lassitude, slight weight loss, enlarged liver & spleen. [Note: as disease progresses,
liver shrinks and becomes nodular]
2. Late (Usually due to liver failure and portal hypertension)
• Jaundice [Due to derangement of liver cells & compression of bile ducts by connective
tissue overgrowth; unable to excrete bilirubin]
• Severe pruritis [Due to accumulation of bile salts]
• Skin lesions: Spider angiomas & palmar erythema [Due to the liver's inability to
metabolize steroids ie. estrogen]
• Hematological problems: thrombocytopenia, leukopenia, anemia & coagulation disorders
[Due to spenomegaly from backup of blood from the portal vein into the spleen]

1. Anemia [Due to overactivity of enlarged spleen, poor diet, poor absorption of folic
acid and blood loss from bleeding esophageal varices]
2. Coagulation defects: bleeding tendencies, purpura, petechiae, easy bruising,
bleeding gums, increased menstrual bleeding [Due to the inability of liver to
produce prothrombin and other clotting factors]
• Endocrine disturbances: a) gynecomastia, loss of pubic hair, testicular atrophy,
impotence, amenorrhea {younger women}, vaginal bleeding {older women} [Due to
liver's inability to inactivate estrogen and testerone] ; b) hyperaldosteronism [due to
liver's failure to metabolize aldosterone adequately]
• Peripheral neuropathy [Due to dietary deficiency of thiamin, folic acid and B12]

COMPLICATIONS
Complications that are often seen in cirrhosis are a result of portal hypertension. This
hypertension results from obstruction of NORMAL blood flow through the portal system
[Remember that structural changes as the result of cirrhosis causes compression /destruction of
portal and hepatic veins].
Below are a summary of the 3 biggest complications found in cirrhosis:
1. Varices: collateral circulation [ie blood goes around the liver not through it] develops to
decrease portal pressure. Collateral channels form in the lower esophagus, anterior abdominal
wall, peritoneum and rectum. Varicosities
[weakened vessels] develop in area's where collateral and systemic circulation communicate.
Patients end up with esophageal and gastric varices, caput medusae and hemorrhoids.
• Esophageal Varices: collateral vessels contain little elastic tissue and are fragile.
Increased pressure is poorly tolerated and the veins become distended and bleed
easily. Alcohol ingestion, poorly chewed food and acid regurgitation can cause
rupture and bleeding. Any activities that increase intraabdominal pressure (N/V,
straining, coughing & sneezing) puts the patient at greater risk for bleeding
esophageal varices. Patient may present with melena or hematemesis
2. Ascites: accumulation of serous fluid in the peritoneal or abdominal cavity. There are several
causes that contribute to this state:
• Increased pressure causes proteins and water to leak into the peritoneal cavity [the
lymph system cannot drain off excess protein and water..the osmotic pressure of the
proteins pulls additional fluid which leads to abdominal distention and weight gain]
• Hypoalbuminemia [liver unable to synthesize albumin which results in decreased
colloidal osmotic pressure in the portal vein]
• Hyperaldosteronism [Aldosterone not metabolized by the cells which results in
sodium reabsorption by renal tubules; increased sodium reabsorption leads to
increased levels of ADH and more water is retained; renin-angiotensin system is
activated due to renal vasoconstriction from decreased circulation {edema causes
decrease intravascular volume} ; sodium and water retained which leads to increased
hydrostatic pressure..ascites formation continues!
• Signs and Symptoms: weight gain, everted umbilicus (if severe ascites), and
abdominal striae w/ distended abdominal wall veins.
3. Hepatic Encephalopathy: Blood is shunted past liver via collateral circulation and prevents
liver from converting ammonia to urea. Large amounts of NH3 (nitrous ammonia) circulates in
the blood stream and crosses the blood-brain barrier producing toxic manifestations
[REMEMBER: Ammonia is the product of protein breakdown by bacteria in the intestine.
Normally ammonia goes to the liver and is converted to urea and excreted by the kidneys]
DIAGNOSTIC STUDIES
Please read the corresponding section in your med/surg book. Be sure to understand the
nursing care r/t a liver biopsy.
Therapeutic Management
Rest: To allow time for recovery of some liver cells
Ascites: I/O, daily weights, abdominal girth, salt poor albumin {maintains intravascular volume
and adequate u/o by increasing plasma colloid osmotic pressure}, diuretic therapy, low sodium
diet, paracentesis and surgical shunts [LeVeen, Denver]
Hepatic encephalopathy: reduction of ammonia formation by restricting proteins, sterilization of
the intestines with antibiotics [neomycin], and lactulose therapy.
Esophageal varices: Teaching {no ETOH, ASA, irritating food}; treat upper respiratory infections
quickly to control sneezing etc.; If bleeding {medical emergency} airway, vasopressin therapy
w/ nitroglycerin and sodium nipride to decrease the side effects of angina or MI, cardiac
arrhythmia's, and difficulty urinating that sometimes are seen with vasopressin therapy; balloon
tamponade {Sengstaken-Blakemoore} ; portacaval and distal splenorenal shunts.

Sengstaken-Blakemoore Tube
The sengstaken-blakemoore tube controls bleeding esophageal varices by mechanically
compressing the area that's bleeding. This brand of tube is only one of several on the market
but is the one most often used. Use the picture in your med-surg book to get a visual of how this
tube looks. It has 2 balloons (gastric and esophageal) and 3 lumens (one to inflate the gastric
balloon, one to inflate the esophageal balloon and the third is for gastric aspiration). Patient's
that need this type of device will always be in an ICU setting. Below are some key points related
to this tube:
1. Balloons are checked for patency prior to MD insertion
2. The deflated tube is inserted via the nose into the stomach. ALL LUMENS MUST BE
LABELED.
3. The GASTRIC balloon is inflated with 150 to 300ml air and tube is retracted until
resistance is felt. The purpose of the gastric balloon is to ANCHOR the tube and to apply
pressure to gastric varices. THIS LUMEN SHOULD NEVER BE DEFLATED UNLESS YOU
ARE DISCONTINUING THE TUBE! IF THIS TUBE BECOMES DEFLATED, THE
ESOPHAGEAL BALLOON WILL MIGRATE UPWARD AND OCCLUDE THE AIRWAY.
THIS IS IMPORTANT!!
4. The esophageal balloon is inflated between 25 to 40 mmHg. The purpose is to put
pressure on the bleeding esophageal varice. This tube may be deflated (if ordered by he
physician) every 8-12 hours to avoid necrosis. This is only done with an MD order
because as soon as you release pressure to the varice you stand a great risk of bleeding
again. The doctor will not allow you to release pressure if the bleeding is not under
control. If you are allowed to release pressure BE SURE THAT YOU RELEASE THE
ESOPHAGEAL BALLOON (NOT THE GASTRIC); THIS IS WHY YOU MUST LABEL THE
BALLOONS CORRECTLY!
5. The third lumen is used for gastric suction. The physician may order lavages (either room
temperature or iced). You need to know there is great controversy over this in the
literature. The premise behind "iced" lavages is that the cold saline will vasocontrict the
bleeding blood vessels that the saline comes in contact with. Research (limited research)
has shown that iced saline actually interferes with the body's natural clotting mechanisms
and therefore should not be done. You will see both sides in the books and you will still
see physician's ordering iced lavages. Either way, you insert saline (apox. 50-75cc) into
the gastric port of the SB tube. You will let it "sit" there in the stomach for aprox. 15-30
seconds and then withdraw it. You immediately repeat the procedure over and over again
until you see the bleeding slowing down or the doctor decides to try something else. {You
will see variations to the amounts and times I just gave you...need to use your
judgement...if your patient is actively bleeding you need to be quick}.
6. Keep the HOB elevated at all times
7. Mouth care frequently
8. Oral and pharyngeal suctioning (patient unable to swallow)
9. WATCH FOR esophageal rupture: patient will c/o sudden back pain or abdominal pain; BP
will drop, pulse will increase. CALL MD STAT
10. WATCH FOR regurgitation & aspiration of gastric contents
11. WATCH FOR occlusion of airway. Scissors should always be at bedside for
emergency deflation (don't fool around with a syringe! CUT the balloons and remove the
tube!)
Gastrointestinal Accessory Organs
Cirrhosis of the Liver
Complication: Ascites
Ascites is an accumulation of serous fluid in the peritoneal or abdominal cavity.

Source: www.medicouncilalcol.demon.co.uk/ handbook/ima...


The causes can be attributed to:
• Increased pressure causes proteins and water to leak into the peritoneal cavity
o Lymph system cannot drain off excess protein and water
o Osmotic pressure of the proteins pulls additional fluid which leads to abdominal distention and
weight gain
• Hypoalbuminenia
o Liver is unable to synthesize albumin which results in decreased colloidal osmotic pressure in
the portal vein
• Hyperaldosteronism
o Aldosterone is not metabolized by the cells which results in sodium reabsorption by renal
tubules
o Increased sodium reabsorption leads to increased levels of ADH and more water is retained
o Renin-angiotensin system is activated due to renal vasconstriction from decreased circulation
 Edema causes decreased intravascular volume
o Sodium and water retained which leads to increased hydrostatic pressure
o Ascites formation continues
Signs and Symptoms
• Weight gain
• Everted umbilicus (if severe ascites)
• Abdominal striae with distended abdominal wall veins
Treatment
• I/O
• Daily weights
• abdominal girth
• Salt poor albumin
• Abdominal girth
• Salt poor albumin
• Maintains intravascular volume and adequate u/o
o Increases plasma colloid osmotic pressure
• Diuretic therapy
• Low sodium diet
• Paracentesis
• Surgical shunts (LeVeen, Denver)
Gastrointestinal Accessory Organs
Cirrhosis of the Liver
Manifestations - Early
• GI symptoms - Due to altered metabolism of CHO, fats, and proteins
o Anorexia
o Dyspepsia
o Gas
o Nausea/vomiting
o Changes in bowel habits
• Abdominal pain - Due to swelling and stretching of liver capsule and spasms of biliary ducts
o Dull and heavy
o Found in RUQ or epigastrium
• Fever
• Lassitude
• Slight weight loss
• Enlarged liver and spleen
o As disease progresses, liver shrinks and becomes nodular
Primary liver cancer is a rare form of cancer accounting for about 2% of cancers in North America. You book devotes
very little space to this topic and so we will skim through this section. After reading you should know these key facts:
1. Rationale as to why the liver is a common metastatic site
2. Prognosis r/t cance of the liver
3. Difinition of AFP and it's significance
4. Treatment options r/t cancer of the liver

Gastrointestinal Accessory Organs


Viral Hepatitis
Liver Cancer
Brief Overview
Liver cancer that originates in the liver's parenchymal cells or intrahepatic bile ducts is
considered primary liver cancer . It is a very aggressive cancer that is difficult to detect and
treat. It is usually fatal within 6 months of diagnosis.
Metastatic liver cancer is 20X more common that primary due to the liver's rich extensive blood
supply. Metastasis often occurs from melanoma or cancers of the gastrointestinal tract, lung
and breast.
Signs and Symptoms
• epigastric and RUQ pain
• fatigue
• anorexia
• weight loss
• fever
• jaundice
• dependent or peripheral edema [r/t low plasma albumin levels]
• itching [r/t jaundice]
• orthopnea and dyspnea [r/t ascites]
• tender, enlarged liver
• venous hum
Diagnostic Tests
• LFTs (liver function tests)
• Alpha-fetoprotein (elevated w/ primary malignancy and disappear if cancer is eliminated)
• Liver biopsy confirms the diagnosis
Treatment
• Rarely resectable
• Transplantation (if not metastasized)
• Radiation (note: liver has a low tolerance for radiation so this is of limited value)
• Chemotherapy
Interventions
• Analgesics
• Ascites (measure abdominal girth, daily weight, restrict sodium, fluids and proteins, I/O,
elevate legs)
• Monitor for SOB
• Fever (sponge baths, ASA suppositories, antibiotics if prescribed) [note: do not give
acetaminophen {Tylenol} because liver cannot metabolize it]
• Skin care (antipruritics to prevent itching)
• Monitor of encephalopathy (check ammonia level, vs, neuro status)
• Transhepatic catheter [used to relieve obstructive jaundice] : irrigate as prescribed
• Chemotherapy/radiation: monitor of n/v, anemia, thrombocytopenia, nuetropenia, and
hair loss
Gastrointestinal Accessory Organs
Viral Hepatitis

Liver Transplantation
Transplanted organs (of all types) has become a successful treatment option for a large number
for patients. The University of Miami is the hospital that serves this area by assisting in the
process of organ procurement. Due to time constraints this course does not focus on this
material in great detail. After reading the book, you should understand these key points:
1. Know the major indicators for liver transplantation in adults
2. Understand the major complication of liver transplantation and the nurses role in
preventing it.
3. Know the pharmacological management for liver recipients

Pancreatitis
Pancreatitis is an inflammation of the pancreas and can become a life-threatening emergency as the pancreas literally
digests itself. There are two types of pancreatitis, acute and chronic. Chronic pancreatitis is further divided into two
subtypes which are chronic obstructive pancreatitis and chronic calcifying pancreatitis. You will be responsible for acute
and chronic calcifying aka alcohol-induced pancreatitis.
Your book does a through job discussing this disease. Be sure that you get these key points from your reading:
1. Know the location of the pancreas
2. Understand the exocrine [including the primary pancreatic enzyme] and endocrine functions of the pancreas
3. Know the definition of acute pancreatitis
4. Know the 2 most common causes of acute pancreatitis
5. Know the main clinical manifestation of acute pancreatitis and some of its characteristics
6. Know what Gray Turner's sign, Cullen's sign, Chvostek's sign and Trousseau's sign are and why they appear.
7. Know the 2 most common diagnostic tests used for acute pancreatitis
8. Know the common complications, including s/s, and treatment of acute pancreatitis
9. Understand why a patient will be NPO and may have NGT
10. Know the drug of choice for pain relief for pancreatitis
11. Know the definition of chronic pancreatitis
12. Know how the pain in chronic pancreatitis differs from acute
13. Define the term steatorrhea and understand why it occurs
14. Understand the purpose and procedure of the secretin stimulation test
15. Know the nursing interventions related to giving pancreatic enzymes
16. Understand the purpose of the Ransom's Clinical Indicators.
Gastrointestinal Accessory Organs
Viral Hepatitis

Pancreatitis
Brief Overview
Acute Pancreatitis
This is an acute, inflammatory process of the pancreas associated with the escape of activated
pancreatic enzymes into the pancreas and surrounding tissue causing necrosis and hemorrhage.
Causes
There are many causes of pancreatitis but Alcoholism and Gallbladder Disease is the two most
common.
Pathophysiology
When pancreas is functioning normally, the digestive enzymes do not begin working until they
reach the duodenum.
Pancreatitis involves the pancreas autodigesting or in other words "it eats itself"! The reasons
why this occurs are as follows:
1. Reflux of bile from the duodenum or obstruction of the pancreatic duct due to gallstones
may be responsible for activation of digestive enzymes while still in the pancreas. [may
become impacted at the ampulla of vater]
2. Obstruction of bile ducts raises pressure in these ducts, blocking pancreatic duct outflow.
3. Contents of duodenum (with activated pancreatic enzymes) back up into the pancreatic
duct.
4. Excess hydrochloric acid (could be caused by alcohol intake) causes spasms of the
sphincter of Oddi and the ampulla of Vater, obstructing pancreatic fluid flow.
Clinical Manifestations
• abdominal pain (LUQ or mid-epigastrium, radiates to back [due to retroperitoneal location
of pancreas] , sudden onset, severe, deep, piercing, aggravated by eating, not relieved by
vomiting)
• N/V
• fever
• leukocytosis
• hypovolemia (will see related hypotension, tachycardia)
• jaundice
• abdominal tenderness, distention [r/t ascites}
• bowel sounds may be decreased or absent
• greenish, yellow-brown discoloration of abdominal wall [due to intravascular damage from
circulating trypsin]
• Gray Turner's Sign
• Cullen's Sign [Both of these signs results from seepage of blood-stained exudate from the
pancreas]
• Chvostek's Sign
• Trousseau's Sign [Both of these signs are result of low calcium levels]

Diagnostic Studies
1. Serum Amylase [The hallmark of acute pancreatitis. An abnormal rise in the serum level of
amylase {>200u/L} occurs within 12 hours of the onset of the disease. Because it is rapidly
cleared by the kidneys, levels will return to normal within 48 to 72 hours. ]
2. Serum Lipase [Lipase is only produced in the pancreas, so elevated serum levels are specific
to pathologic pancreatic conditions. Normal findings are 0-130 units/L. Levels will rise after the
first 48 hours and remain elevated for 5 to 7 days. Persistent elevation sometimes indicates
pseudocyst formation.]
3. Urinary Amylase [There is an increase for several days beyond the levels of serum amylase.
Large quantities of amylase in the urine reflect transient inhibition of renal tubule reabsorption of
amylase. Orange-red urine may reflect extensive tissue damage of pancreatic necrosis. A timed
2 hr collection is more dependable than a randomly collected urine specimen.]
4. Abdominal x-ray [Checks for free air from perforation or abscess formation; if ascites is
present may see "ground glass" appearance which is characteristic of intraabdominal fluids.]
5. Ultrasound [Will detect abscess or cyst formation, identify gallstones, distended CBDs
(common bile duct), and masses]
6. Serum glucose [elevated from lack of insulin because of pancreatic destruction and sepsis]
7. Blood urea nitrogen (BUN) [Rises because of dehydration, catabolism, "third spacing" of
fluids, bleeding, and impaired renal clearance.]
8. Elevated triglycerides
Complications
• Pseudocysts [cavity that surrounds the pancreas that is filled with necrotic products
{plasma, enzymes, inflammatory exudate}; S/S: abd. pain, n/v, anorexia, palpable
epigastric mass; Treatment: may resolve in few weeks or internal drainage will be
necessary]
• Abscess [cavity within the pancreas; S/S: upper abd. pain, fever, leukocytosis;
Treatment: surgical drainage
• Tetany [results from hypocalcemia; Treatment: Calcium Gluconate]
• Hypovolemic Shock [occurs from hemorrhage or fluid shifts into the abdomen; Treatment:
Vasopressors, blood products, volume expanders (dextran or albumin)]
• Renal Failure [ a complication of hypovolemia; Monitor: I/O, urine SG, BUN/creatinine,
K+]
• Respiratory Failure [results from shallow breathing and hypoventilation r/t abdominal
pain. At high risk for pneumonia and atelectasis; Treatment: Oxygen, ABGs and
pulmonary toilet]
• Diabetes Mellitus [Monitor: blood sugar levels and urine for ketones]
General Treatment
1. NPO (if vomiting or abd. distention will have NGT) [Suppresses pancreatic secretions]
2. Pain medication (Demerol is drug of choice) [NO morphine sulfate-causes spasms in sphincter
of Oddi]
3. Antispasmodics [Bentyl, ProBanthine]
4. Positioning (HOB elevated 45 degrees, sitting up, or fetal position)
5. Bedrest w/ quiet environment [will minimize stimulation of gastric secretions]
6. H2 Histamine Antagonist (Zantac) [will reduce HCL secretion]
7. Stool chart (frequency, color, odor and consistency) [steatorrhea is undigested fat r/t
impaired fat and protein metabolism]
8. Patient teaching: [Trying to prevent chronic pancreatitis]
• avoid alcohol and smoking
• avoid stressful situations
• avoid dieting and binge eating
• suggest low fat, high carbohydrate, high protein diet
• instruct on s/s of diabetes mellitus and steatorrhea [signals destruction of pancreatic
tissue]

Chronic Pancreatitis
A progressive destruction of the pancreas with fibrotic replacement of pancreatic tissue.
Eventually chronic pancreatitis progresses to the point that both exocrine and endocrine
functions of the pancreas are impaired.
While chronic pancreatitis is classified as one of two types, it is the chronic calcifying pancreatitis
that is the most common. It is also called alcohol-induced pancreatitis because the metabolic
abnormalities are due to direct toxic effects of alcohol.
Clinical Manifestations
• abdominal pain (LUQ; heavy, gnawing, burning, cramp like; not relived with food or
antacids)
• weight loss
• constipation
• dark urine
• steatorrhea
Diagnostic Tests
• increased serum amylase
• increased serum bilirubin
• increased alkaline phoshatase
• + secretin stimulation test [most useful test in diagnosing chronic pancreatitis] (+ for
pancreatitis if there is a reduced volume of secretions and reduced bicarbonate
concentration)
• fecal fat determination [indicative of maldigestion]
• increased blood sugar
Treatment
1. Diet (bland, low fat, high carbohydrates and protein); No alcohol.
2. Medications (antacids and anticholingergics to decrease HCL acid; pancreatic enzymes {give
with meals and snacks}; bile salts {to facilitate absorption of fat-soluble vitamins}; insulin or
hypoglycemic drugs {if diabetes develops}).
Ransom's Criteria
Using the clinical indicators below the mortality rate associated with pancreatitis can be
predicted:
Signs on admission
• >55 years of age
• WBC >16,000 mm3
• Serum glucose >200mg/dl
• Serum lactate dehydrogenase >350 units/liter
• Aspartate aminotransferase >250 units/liter
Signs during first 48 hours
• Fall in hematocrit >10%
• Blood urea nitrogen rise >5 mg/dl
• Serum calcium <8 mg/dl
• Base deficit >4 mEq/liter
• Estimated fluid sequestration >6 liters
• PaO2 < 60mmHg
Relation to Morbidity/Mortality
• 2 or fewer signs: 1% mortality
• 3 signs: severe pancreatitis
• 3-4 signs: 15% mortality
• 5-6 signs: 40% mortality
• More that 6 signs: 100% mortality
Gastrointestinal Accessory Organs
Pancreatitis: Acute
Causes and Pathophysiology
Acute:
• This is an acute, inflammatory process of the pancreas associated with the escape of activated
pancreatic enzymes into the pancreas and surrounding tissue causing necrosis and hemorrhage.
• There are many causes of pancreatitis, including alcohol consumption, gallbladder disease,
medications, biliary tract disease,pancreatic cysts and/or tumors and trauma.
Pathophysiology:
• When the pancreas is functioning normally, the digestive enzymes do not begin working until they
reach the duodenum. Pancreatitis involves the pancreas autodigesting or in other words "it eats itself."
• Autodigestion occurs because:
o Reflux of bile from the duodenum or obstruction of the pancreatic duct due to gallstones may be
responsible for activation of digestive enzymes while still in the pancreas
o May become impacted as the ampulla of vater
o Obstruction of bile ducts raises pressure in these ducts, blocking pancreatic duct outflow.
o Contents of duodenum with activated pancreatic enzymes, back up into the pancreatic duct.
o Excess hydrochloric acid, which may be caused by alcohol intake, causes spasms of the
sphincter of Oddi and the ampulla of vater, obstructing pancreatic fluid flow.
Diagram showing the pancreas, liver, duodenum, and stomach. The gall bladder and bile ducts are shown in
green, the portal vein and tributaries in blue, and the abdominal aorta and branches in red.

Gastrointestinal Accessory Organs


Pancreatitis - Chronic
Chronic Pancreatitis
• Chronic pancreatitis is a progressive destruction of the pancreas with fibrotic replacement of pancreatic
tissue.
• Eventually chronic pancreatitis progresses to the point that both exocrine and endocrine functions of
the pancreas are impaired.
• The disease is irreversible
• While chronic pancreatitis is classified as one of two types, it is the chronic calcifying pancreatitis that is
the most common. It is alcohol-induced pancreatitis because the metabolic abnormalities are due to the
direct toxic effects of alcohol.
• Signs and symptoms, diagnostic tests and treatment of chronic pancreatitis are the same as acute
pancreatitis with the following modifications:
Signs and Symptoms
• As the disease progresses patient will develop:
o Steatorrhea (fatty stools)
o Greasy stools/oil droplets
o Dark colored urine
o Glucose intolerance (islet cell destruction decreases insulin secretion)
o Weight loss
Diagnostic Tests
• + Secretin test
o Most useful test in diagnosing chronic pancreatitis
 + for pancreatitis if there is a reduced volume of secretions and reduced bicarbonate
concentration (< 0- mEq/L)
o Requires insertion of double-lumen nasogastric tube (one for gastric aspirate; one for duodenal
aspirate)
• Fecal fat determination - indicative of maldigestion
Treatment
• Allow the patient to eat a bland, low fat, high carbohydrate and protein diet without alcohol
consumption.
• Medications:
o Pancreatic enzymes - give with meals and snacks
o Bile salts - to facilitate absorption of fat-soluble vitamins
o Insulin or oral hypoglycemic drugs - if diabetes develops
Gastrointestinal Accessory Organs
Pancreatitis - Complications
• Pseudocysts - cavity that surrounds the pancreas that is filled with necrotic products (plasma, enzymes,
inflammatory exudates); Signs and symptoms: abdominal pain, nausea/vomiting, anorexia, palpable
epigastric mass.
o Treatment: May resolve in few weeks or internal drainage will be necessary.
• Abscess - cavity within the pancreas; Signs and symptoms: upper abdominal pain, fever, leukocytosis
o Treatment: Surgical drainage
• Tetany - results from hypocalcemia
o Treatment: Calcium Gluconate
• Hypovolemic Shock - occurs from hemorrhage or fluid shifts into the abdomen
o Treatment: Vasopressors, blood products, volume expanders like dextran or albumin
• Renal Failure - a complication of hypovolemia
o Monitor: I/O, urine specific gravity, blood urea nitrogen/Creatinine, potassium
• Respiratory problems - results from shallow breathing and hypoventilation r/t abdominal pain. At high
risk for pneumonia, atelectasis, pleural effusion, ARDS (Adults Respiratory Distress Syndrome).
o Treatment: Oxygen, arterial blood gases and pulmonary toilet
• Diabetes Mellitus
o Monitor: Blood sugar levels and urine for ketones
Gastrointestinal Accessory Organs
Diagnostic Studies

Serum Amylase
• Important: Hallmark of acute pancreatitis.
• An abnormal rise in the serum level of amylase > 200u/Liter occurs within 12 hours of the onset of the
disease.
• Peak levels are usually reached in 24 hours.
• Because it is rapidly cleared by the kidneys, levels will return to normal within 48 to 72 hours despite
continued symptoms.
Serum Lipase
• Lipase is only produced in the pancreas, so elevated serum levels are specific to pathologic pancreatic
conditions.
• Normal findings are 0-130 units/Liter.
• Levels will rise after the first 48 hours and remain elevated for 5 to 7 days.
• Persistent elevation sometimes indicates pseudocyst formation.
Urinary Amylase
• There is an increase for several days beyond the levels of serum amylase.
• Large quantities of amylase in the urine reflect transient inhibition of renal tubule reabsorption of
amylase.
• Orange-red urine may reflect extensive tissue damage of pancreatic necrosis.
• A timed 2 hour collection is more dependable than a randomly collected urine specimen.
Abdominal X-Ray
• Checks for free air from perforation or abscess formation.
• If ascites is present may see "ground glass" appearance which is characteristic of intraabdominal fluids.
Ultrasound
• Detects abscess or cyst formation.
• Identifies gallstones, distended common bile duct, and masses.
Blood Tests
• Elevations of serum glucose, bilirubin, alkaline phosphatase, cholesterol and triglycerides
• Due to lack of insulin because of pancreatic destruction and sepsis.
• Decreases of serum albumin, calcium, sodium, magnesium and sometimes potassium.
• Often due to vomiting.
Blood urea nitrogen (BUN)
• Rises because of dehydration, catabolism, "third spacing" of fluids, bleeding, and impaired renal
clearance.
Endoscopic Retrograde Cholangiopancreatography (ERCP)
• Can identify ductal system abnormalities and can differentiate pancreatitis from other disorders such as
pancreatic cancer.
Example of endoscope used in ERCP:

ERCP 2 (1) Stone viewed during ERCP:


Gastrointestinal Accessory Organs
General Treatment
• Important: Patient will be NPO - this will suppress pancreatic secretions (if vomiting or abdominal
distention will have NGT)
• Pain medication – Demerol or Dilaudid
• Important: No morphine sulfate - causes spasms of sphincter of Oddi
Demerol should only be ordered for acute pain management (surgical patients). Demerol is not ordered
for long term pain management due to the build up of the toxic metabolite, normeperidine, that is a
central nervous system irritant and can cause seizures.
• Medications include
o H2 histamine antagonists (Zantac) – will reduce HCL secretion
o Antacids
o Electrolytes replacement, if values are low
o Insulin
o Antispasmodics - Bentyl, ProBanthine
• Positioning - HOB elevated 45 degrees, sitting up, or fetal position.
• Bedrest with a quiet environment - will minimize stimulation of gastric secretions.
• Stool chart - frequency, color, odor and consistency.
o Steatorrhea is undigested fat related to impaired fat and protein metabolism.
• Protective skin barrier creams – to prevent excoriation and skin breakdown due to steatorrhea.
• Partial parenteral nutrition (PPN) or total parenteral nutrition (TPN) as well as IV fluids – prevent weight
loss and dehydration
o Weigh patient – every other day. Report weight loss of 2 lbs. or greater to physician.
• Supplemental oxygen and respiratory treatments to maintain SpO2 saturation > 93%. – impaired gas
exchange can result from pleural effusion.
• Deep breathing and coughing along with incentive spirometry – to prevent atelectasis
Gastrointestinal Accessory Organs
Pancreatitis

Patient Education
• Abstain from alcohol and smoking
• Avoid stressful situations – provide adequate rest
• Avoid dieting and binge eating
• Suggest low fat, high carbohydrate, high protein diet
• Educate on prescribed medications
• Instruct on signs and symptoms of diabetes mellitus and steatorrhea; these signal destruction of
pancreatic tissue.
• Advise patient to seek medical care:
o Acute pain
o Shortness of breath
o Nausea and vomiting
o Low grade temperature
o Steatorrhea
o Signs and symptoms of diabetes mellitus occur.
Gastrointestinal Accessory Organs
Pancreatitis

Signs and Symptoms


• Important: Predominate Symptom: Intense abdominal pain in the left upper quadrant or mid-
epigastrium, radiates to back (due to retroperitoneal location of pancreas), sudden onset, severe, deep,
piercing, aggravated by eating, not relieved by vomiting
• Nausea and vomiting, weight loss
• Fever
• Leukocytosis
• Hypovolemia, will see related hypotension, tachycardia
• Jaundice
• Abdominal tenderness, distention related to ascites, rigidity, guarding
• Bowel sounds may be decreased or absent
• Greenish, yellow-brown discoloration of abdominal wall due to intravascular damage from circulating
trypsin.
Gray Turner's Sign (bluish flank discoloration):

Cullen's Sign (bluish periumbilical discoloration):


Both of these signs results from seepage of blood-stained exudate from the pancreas. Occurs in
extensive hemorrhagic necrosis of the pancreas.

Chvostek's Sign

Contraction of facial muscles in response to a light tap over the facial nerve in front of the ear.

Trousseau's Sign

A carpal spasm induced by inflating a blood pressure cuff above the systolic pressure for a few minutes.

Both of these signs are the result of low calcium levels


Pancreatic Cancer
Pancreatic cancer is probably one of the most devastating diagnosis a patient can receive. The fact that the cancer has
usually metastasized to other organs and tissues at the time of discovery means that treatment options are very limited.
The prognosis is very grim with only a 3% survival rate at five years of diagnosis and it is not unusual for patients to
survive less than 6 months from the confirmation of the disease.
Your book has aprox. 1 page on this material and I have not provided any further information on this topic. The key points
have been listed below:
1. Know the population where pancreatic cancer commonly occurs
2. Know the risk factors associated with this disease
3. Know the symptoms associated with pancreatic cancer
4. Know which lab is specific for pancreatic cancer
5. Know the best diagnostic test for pancreatic cancer
6. Know the surgical procedure most commonly associated with this disease
Gallbladder Disease

Who thinks about their gallbladder and what it does? Hardly anyone, unless their gallbladder is causing problems. The
gallbladder stores bile, a fluid produced by the liver that breaks down the fats in the foods that's eaten and aids in
digestion. Usually bile moves smoothly from the gallbladder into the digestive system. But if gallstones form, the flow of
bile may be blocked, resulting in pain and complications. Every year more than 500,000 people in the United States
undergo gallbladder surgery, most often because of stones. The cholecystectomy is one of the safest and most most
successful kinds of surgery. The new laparoscopic cholecystectomy is becoming increasingly popular and is sometimes
being done as an outpatient procedure. After reading this section in your book be sure that you understand these key
points:
1. Know the definition of cholelithiasis, cholecystitis and cholecystectomy
2. Understand what factors predisposes individuals to gallstone formation
3. Know which substance most commonly results in the formation of a gallstone
4. Understand why fatty foods cause pain in patients with gallbladder disease
5. Know the definition of steatorrhea and why it occurs in cholelithiasis
6. Understand the relationship of bilirubin and the clay-colored stools found in cholelithiasis
7. Know the differences between an oral cholecystography and a IV cholangiogram
8. Know which test is the best means of diagnosing gallstones
9. Know the consequences of a patient having a cholecystectomy (ie patients will ask you "How can I live without
my gallbladder")
10.Understand when and why a patient will return from OR with a T-tube
11.Know the expected amount and color of t-tube drainage during the first post-op day
12.Know the differences between a laparoscopic cholecystectomy and an open procedure cholecystectomy
Gastrointestinal Accessory Organs
Viral Hepatitis
Disorders of the Gallbladder

Cholelithiasis
Definition
Formation of stones within the gallbladder or bilary duct system. Gallstones are hardened
cholesterol and are more common than other types of stones called pigment stones.
Predisposition
People who are more prone to getting gallstones include:
• women who have had several pregnancies
• overweight people
• people who eat a lot of dairy products, animal fats and fried foods
Location of the stones
• remain in the gallbladder
• migrate to the cystic duct
• migrate to the common bile duct
Clinical Manifestations
• right-sided abdominal pain, n/v, intolerance to fatty foods
• steatorrha
• jaundice
• clay-colored stools
• dark foamy urine
[all related to the stone blocking the passage of bile and bilirubin from reaching the duodenum]
Cholecystitis
Definition
Inflammation of the gallbladder associated with stones, fasting, weight fluctuations and
neoplasms.
Clinical Manifestations
• fever
• elevated WBC count
• elevated serum bilirubin
• elevated alkaline phosphatase
• abdominal muscle guarding w/ rebound tenderness and rigidity [seen in chronic
cholecystitis due to perforation that results in peritonitis]

Diagnostic Tests (pertains to both diseases)


• gallbladder ultrasound [90-95% accurate]
• oral cholecystography aka GB series [preprocedure: 12 hours before study give patient a
fat free meal and iodine tablets]
• IV cholangiogram [check allergies to contrast dye]
• percutaneous transhepatic cholangiography [contrast material introduced directly though
skin into liver; patient sedated, local anesthetic]
• CBC
• serum amylase and lipase
• serum bilirubin [elevated direct or unconjugated bilirubin = obstruction of biliary duct
system; elevated indirect on conjugated bilirubin = hepatic damage]
Pharmacology
• UDCA (ursodeoxycholic acid)
o drug that dissolves stones under 20mm
o monitor for diarrhea
o monitor hepatic enzymes
• Chenodiol
o decreases the amount of cholesterol in bile [stone becomes more soluable]
• Questran [helps pruritis (itching) due to obstructive jaundice]

Diet
• low fat [foods such as whole milk, cream, butter, fried foods, rich pantries, gravies and
nuts will cause the gallbadder to contract]

Surgery
The type of surgery will depend on the location of the stone. If the stone is within the
gallbladder then a cholecystectomy (removal of the gallbladder) will be performed. If the stone
is within the ducts then a choleystectomy with common bile duct exploration will be done. If a
common bile exploration is done then the patient will return to the floor with a small rubber t-
shaped tube, the T-tube, to drain bile out of the duct for several days after the surgery.
There are currently two approaches to gallbadder removal. An open method means that the
physician will make a incision, usually under the right rib margin or near the abdominal midline.
The second method is the laparoscopic surgery which usually leads to a shorter hospital stay and
recovery period. In this method the physician will perform surgery through 4 small incisions.
The abdomen is inflated with carbon dioxide through one incision that allows the doctor to see
and move easily within the body. The second incision will be used for the laparoscope which is
the instrument that has a light and camera that allows the doctor to view the procedure on a
large screen. The third incision is for the instruments that will remove the gallbladder and the
fourth (in the umbilicus)