Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
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
x Decreased Mg excess
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."
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
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)
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
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
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
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.
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.
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
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.
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.
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.
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:
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
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.
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]
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)