Download Final Exam n250 Study Guide

This list is not a guarantee of final exam content. It is meant to help the student focus study time on important content, but may
not include all elements of final exam questions. The final exam is cumulative and the student is responsible for all material
covered in the course. Remember the emphasis is on assessment and nursing interventions.
50-60 Questions
2 hours
The following are the topics to be covered on the final and general areas of concentration:
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Med-Math calculations
dosage calculations
drip factor
flow rates
intake and output
Give amikacin 800 mg IVPB, now
Available: Amikacin 500 mg/2 ml
Set and solution: D W 150 ml minibag and a drop factor of 15 gtt/ml set
Instructions: Infuse over 60 min
5
a.
Drug dose?
b.
Flow rate?
I and O’s:
1 ounces = 30 ml
Any items that is liquid form at room temperature:
ex. pudding, jello, ice cream, ice

Intravenous Infusions and Blood Transfusions
care and assessment of IV sites and tubing
Complication
Finding
Treatment
Prevention
Infiltration
pallor, local swelling at the
site, decreased skin
temperature around the site,
damp dressing, slowed
infusion
• stop the infusion and remove the catheter.
• elevate the extremity.
• encourage active range of motion.
• apply warm compresses three to
four times/day.
• restart the infusion proximal to the
site or in anoth
• Carefully select site and catheter.
• secure the catheter.
phlebitis/
thrombophlebitis
edema; throbbing, burning,
or pain at the site; increased
skin
temperature; erythema; a red
line up the arm with a
palpable band
at the vein site; slowed
infusion
• promptly d/c the infusion and remove the catheter.
• elevate the extremity.
• apply warm compresses three to four times/day.
• restart the infusion proximal to the site or in another
extremity.
• Culture the site and catheter if drainage is
present.
• rotate sites at least every 72 hr.
• avoid the lower extremities.
• use hand hygiene.
• use surgical aseptic technique.
hematoma
ecchymosis at site
• do not apply alcohol.
• apply pressure after iv catheter removal.
• use warm compress and elevation after
bleeding stops.
• minimize tourniquet time.
• remove the tourniquet before
starting iv infusion.
• maintain pressure after iv
catheter removal.
Cellulitis
pain; warmth; edema;
induration; red streaking;
fever, chills, and malaise
• promptly d/c the infusion and
remove catheter.
• elevate the extremity.
• apply warm compresses three to
four times/day.
• Culture the site and cannula if drainage is
present.
• administer:
- antibiotics
- analgesics
- antipyretics
• rotate sites at least every 72 hr.
• avoid the lower extremities.
• use hand hygiene.
• use surgical aseptic technique.
fluid overload
distended neck veins,
increased BP, tachycardia,
SOB, crackles in the lungs,
edema
• stop infusion.
• raise the HOB
• assess vital signs.
• adjust rate as prescribed.
• administer diuretics if prescribed.
• use an infusion
pump.
• monitor i&o.
Catheter
embolus
missing catheter tip when
discontinued; severe pain at
the site with migration, or no
symptoms if no migration
• place the tourniquet high on the extremity to limit
venous flow.
• prepare for removal under x-ray or via surgery.
• save the catheter after removal to determine the cause
• do not reinsert the stylet into the
catheter.

steps in transfusion of blood and blood products
BEFORE DIFFUSION
During Infusion
Post infusion
1) The nurse will assess laboratory values.
Many institutions have specific guidelines for blood product transfusions
(e.g platelet count <20,000 or hemoglobin <6g/dL).
Hematocrit –
7) The nurse will administer the blood
product using the appropriate filtered tubing.
The filters remove aggregates and possible
contaminants.
• Obtain the pt's VS
upon completion of the
transfusion
• Dispose of the blood-
Females: 37%-47%
Increased: Fluid shift, dehydration
Decreased: Hemorrhage
Hemoglobin Females: 12-16 g/dL
Increased: Fluid shift, dehydration
Decreased: Hemorrhage
Potassium Females: 3.5-5.0 m/Eq/L or mmol/L
Increased: dehydration, acidosis
8) If dilution is necessary, dilute with normal
saline only.
Other IV solution will
destroy the blood product.
Infuse blood product at the prescribed rate.
Begin the infusion slowly
2) The nurse will verify the medical prescription.
Legally, a blood transfusion requires physician’s prescription. The
prescription will have the type of product, dose and
transfusion time.
3) The nurse will explain the procedure to the patient. The nurse will
assess the patient’s vital signs before beginning the transfusion and then
assess urine output, skin color, and history of transfusion reactions.
Assess whether or not the patient is able to handle the infusion. Gather
prior data about previous infusion allows a nurse to be aware of signs of
transfusion reaction.
4) The nurse will obtain venous access. Ideally, the nurse will use a
central catheter or at least a 20-gauge needle.
This prevents the cells from getting stuck.
5) The nurse will obtain blood products from a blood bank. Then
transfuse immediately.
Transfusion must occur ASAP once the blood product leave the blood
bank.
6) Two nurses must verify the patient by name and number, check blood
compatibility, and note expiration time. The nurse explains the
procedures to the patient.
This decreases the chance of ABO incompatibility reactions.
Remain w/pt for the first 15-30 min &
monitor:
- VS (then q1hr afterward). For older adult
pts, assess VS more frequently b/c changes in
pulse, B/P, & RR may indicate fluid overload
or may be the sole indicators of a transfusion
rxn. Older adult pts w/cardiac or renal
dysfunction are at an increased risk for heart
failure & fluid-volume excess when receiving
a blood transfusion.
- rate of infusion
- respiratory status
- sudden increase in anxiety
- breath sounds
- neck-vein distention
administration set
appropriately (biohazard
bags)
• Monitor blood values
as prescribed (CBC,
H+H; Hgb levels should
rise by ~1 g/dL w/each
unit transfused)
• Complete paperwork
& file in the appropriate
places
Document the pt's
response
Ask pt to report unusual sensations (like
chills, SOB, hives, or itching)
Notify the primary health care provider
immediately if any signs of a rxn occur
If there are no signs of a rxn, increase
transfusion rate to 1 unit in about 2 hrs
depending on pt's cardiac status
Complete the transfusion w/in a 2-4 hr time
frame to avoid bacterial growth.

know reactions and interventions for blood transfusions
When Given
How Supplied
How Given
Nursing Considerations
Whole Blood
To restore blood volume (to
maintain b/p). Excessive blood
loss caused by injury or
surgery. Hgb 6-10 g/dL,
depending on symptoms
450-500 mL
usually from
blood donors of
the same blood
type
Transfusions take 1 to 4
hours, depending on how
much blood and what
type is given, and no
special recovery time is
needed.
Most of the time whole blood is not used
because the patient's medical condition can
be treated with a blood component and too
much whole blood can raise a recipient's
blood pressure. High blood pressure can
have medical side effects
Packed RBCs
Most common
blood
component
given.
Given to replace cells lost due
to trauma, surgery or conditions
that destroy RBCs or impair
RBC maturation.
Anemia (Hgb 6-10 g/dL,
depending on symptoms)
Chronic renal failure
Supplied in 250ml
bags.
Infuse with special
tubing.
Given to patients with HGB < 8g/dL or who
are hypoxemic.
Actually a transplant of tissue.
Platelets
Given to pts with:
PLT counts < 10,000 mm3
or who have thrombocytopenia
or platelet dysfunction
(platelets < 20,000 or < 80,000)
and have active bleeding.
or are scheduled for an invasive
Packed in bags of
300ml from
pooled donors or
200ml from a
single donor.
Requires ABO
compatibility.
Infused over 15-30minute period.
Infuse with special
tubing.
Include on the labels:
• either: platelets, pooled, buffy coat
derived, leukocyte-depleted
or: platelets, apheresis, leucocyte-depleted;
• volume;
• blood component producer’s name;
• either: a unique pool or batch number
procedure.
Granulocytes
or: the donation number of all contributing
units
or: the donation number and, if subdivided,
the sub
batch number;
• the ABO group;
• the RhD group stated as positive or
negative;
• the expiry date;
• the blood pack lot number.
• store at 22˚C ± 2˚C with continuous gentle
agitation;
• always check the patient ⁄ component
compatibility ⁄ identity;
• inspect pack for signs of deterioration or
damage;
• risk of adverse reaction ⁄ infection.
For clients with infections.
Suspended in
400ml plasma.
Infuse in 45-60 minutes.
Take VS q15min throughout the transfusion.
Transfusion Reactions and Complications:
Febrile
30 min – 6 hr
after
transfusion
Cause
Manifestations
Occur most often in pts w/antiWBC antibodies, which can
develop after multiple
transfusions
Chills, tachycardia, fever, hypotension,
& tachypnea
Priority Nursing Action
1. D/C the transfusion
immediately.
2. Give antipyretics as
ordered.
3. Notify the physician.
4. KVO w/a NS
infusion.
Hemolytic
Onset may be
immediate
(acute- ) or
after
subsequent
units have
been
transfused
Blood type or Rh
incompatibility. When blood
containing antigens different
from the pt's own antigens is
infused, antigen-antibody
complexes are formed in
his/her blood. These complexes
destroy the transfused cells &
start inflammatory responses in
the blood vessel walls &
organs.
Mild: fever & chills
Life-threatening: disseminated
intravascular coagulation (DIC: a
pathological activation of coagulation
mechanisms → formation of small
blood clots inside the blood vessels
throughout the body. Small clots
consume coagulation proteins and
platelets, normal coagulation is
disrupted and abnormal bleeding occurs
from the skin (e.g. from sites where
blood samples were taken), the GI tract,
resp tract, and surgical wounds. The
small clots also disrupt normal blood
flow to organs (such as the kidneys),
which may malfunction as a result.
Occurs acutely but also on a slower,
chronic basis. Common in the critically
ill, and may participate in the
development of multiple organ failure
which may lead to death) & circulatory
collapse
Other manifestations:
– apprehension
– headache
– chest pain
1. D/C the transfusion
immediately. When the
transfusion is d/c, the
blood tubing must be
removed as well. Use
new tubing for the NS
infusion.
Treatment
Giving leukocytereduced blood or singledonor HLA-matched
platelets reduces the risk
for this type of rxn
WBC filters may be
used to trap WBCs &
prevent their infusion
into the pt
2. KVO w/NS, or
according to agency
protocol.
Replace donor blood w/
NS
Furosemide may be
administered to increase
renal blood flow.
Low-dose dopamine
may be considered to
improve renal blood
flow.
Maintain urine output at
30-100 mL/hr
3. Send the remaining
blood, a sample of the
client’s blood, and a
urine sample to the
laboratory.
To prevent a hemolytic
rxn, check the blood
type or Rh compatibility
with another RN before
transfusion.
4. Notify the physician
immediately.
5. Monitor VS.
6. Monitor fluid I&O.
– low back pain
– tachycardia
– tachypnea
– hypotension
– hemoglobinuria
– a sense of impending doom
Allergic
Mild: during
or up to 24 hr
after
transfusion
Mild:
sensitivity to infused plasma
proteins.
------------------------------Severe:
antibody-antigen reaction
Mild:
Flushing, itching, urticaria, bronchial
wheezing
--------------------------------Severe:
Dyspnea, chest pain, circulatory
collapse, cardiac arrest
Mild:
1. Stop/slow the
transfusion, depending
on agency protocol.
2. Notify the physician.
3. Administer
medication
(antihistamines) as
ordered.
------------------------Severe:
1. Stop the transfusion
2. KVO w/NS
3. Notify the physician
immediately.
Mild:
Administer
antihistamines.
Although the necessity
of stopping the
transfusion is unclear, in
more severe cases and in
uncertain cases, the
transfusion should be
stopped.
Pts w/a hx of allergy can
be given leukocytereduced or washed
RBCs in which the
WBCs & plasma have
been removed. This
procedure reduces the
possiblity of an allergic
rxn.
4. Monitor VS
Administer CPR if
needed.
5. Administer
medications and/or
oxygen as ordered.
Anaphylaxis
or -phylactic
Immediate
onset
Type I hypersensitivity
reaction (in this case, to whole
blood, cryoprecipitate, immune
serum globulin—all of which
is probably a result of direct
mast cell degranulation rather
than an IgE-mediated
hypersensitivity event)
Occurs systematically (affects
many organs) w/in secondsminutes of exposure to allergen
o
Wheezing, dyspnea, chest tightness,
cyanosis, & hypotension.
Stop the transfusion
immediately.
Maintain airway; give
O2 & IV fluids
Administer epinephrine,
antihistamines
(diphenhydramine),
corticosteroids, &
vasopressors.
Maintain intravascular
volume.
Administer epinephrine,
antihistamines
(diphenhydramine),
corticosteroids, &
vasopressors.
Chart 22-2 Emergency Care of the Pt w/ Anaphylaxis
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Immediately assess the respiratory status, airway, and oxygen saturation of pts who show any symptom of an allergic
reaction
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Call Rapid Response Team
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Ensure that intubation and tracheotomy equipment is ready
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Apply oxygen using a high-flow, non-rebreather mask at 40% to 60%
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Immediately discontinue the IV drug of a pt having an anaphylactic reaction to that drug. Do not discontinue the IV,
but change the IV tubing and hang normal saline.
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If the pt does not have an IV, start one immediately and run normal saline
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Be prepared to administer diphenhydramine (Benadryl) and epinephrine IV
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Diphenhydramine 25 mg to 50 mg IV push
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Epinephrine 1:1000 concentration, 0.3 to 0.5 mL IV push
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Repeat as needed every 10 to 15 min until the pt responds
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Keep the head of the bed elevated about 10 degrees of hypotension is present; if BP is normal, elevate the HOB to 45
degrees or higher to improve ventilation
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Raise the feet and legs
Stay w/ the pt
Reassure the pt that the appropriate interventions are being instituted
steps in transfusion of blood and blood products
know reactions and interventions for blood transfusions
~ focus on BLOOD. Packed RBCS, whole blood,
~ not cryoprecipitate, fresh frozen plasma
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Clients Having Surgery
pre-op assessment of high risk for intraoperative complication
o ~ what would keep pt from going to surgery
post-op complications
o ~ pt gets out of surgery,
o “RESTLESS”  THINK ABOUT HYPOXIA. Don’t assume… look for hypoxia. If not there, don’t put it there.
pre- and post-op pt teaching
o ~ know before surgery
o ~ during d/c
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Clients with Pain
assessment of pain
influences on pt perception of pain
o ~ culture
o ~ age  old people have potential to not feel pain (neuropathy)
o ~ liver, kidney
o ~ old people refuse pain meds – not wanting to admit – seem frail; want independence.
o ~ psychosocial - culture
pharmacological and non-pharmacological interventions
o ~ not pharm class. Don’t memorize but be familiar w/ opiates – assessment, giving meds.
Older Adult Pain
PREVALENCE OF PAIN
• Recognize that older adults are at great risk for undertreated pain.
• Consider the older adult at risk for the undertreatment of cancer pain because of inappropriate beliefs about pain sensitivity, tolerance, and ability to
take opioids.
Beliefs about pain:
• In addition to receiving less analgesia, older adults tend to report pain less often than do younger adults. These findings may be related to
beliefs and concerns about pain and the reporting of pain. Many older people hold these beliefs and concerns about pain:
• Pain is something that must be lived with.
• Expressing pain is unacceptable or is a sign of weakness.
• Reporting pain will result in being labeled as a "bad" patient.
• Nurses are too busy to listen to reports of pain.
• Pain signifies a serious illness or impending death.
• Nurses should be aware of the beliefs of older patients regarding pain management. Nurses and other caregivers often under-medicate
these patients and are sometimes reluctant to administer the prescribed analgesics.
ASSESSMENT
• Ask about present pain only.
• Use a standard scale, such as the numerical FACES rating scales.
• Explain the scale each time it is used.
• Use verbal descriptions such as "ache," "sore," and "hurt," rather than the word "pain."
-Use visual representations of pain measures rather than mental images of pain rating scales. Be sure that the patient is wearing glasses and hearing
aids if needed and available.
- Alter a written pain scale to include large lettering, adequate space between lines, nonglossy paper, and color for increased visualization.
-Provide adequate lighting and privacy to avoid distracting background noise.
CONSIDERATIONS FOR COGNITIVELY IMPAIRED PATIENTS
-Assess for nonverbal indicators of pain (facial expressions, grimacing, vocalizations, body movement, behavioral changes).
- Remember to "assume pain is present" (APP) in cognitively impaired patients with diseases and condition commonly associated with pain.
MANAGEMENT OF PAIN
-Use around-the-clock dosing of analgesics.
.-Consider an analgesic trial in a cognitively impaired patient
- Beware of adverse effects of acetaminophen (hepatotoxity, nephrotoxicity) and NSAIDs (Gl bleeding, nephrotoxicity).
- Start low and go slow with opioid dosing.
-Avoid the use of meperidine (Demorol), codeine, and propoxyphene (available in combination with acetaminophen, as Darvocet)
-Use methadone and tramadol with caution.
-Older adults and those with renal disease should not take meperidine because of the prolonged half-life of its drug metabolite, normeperidine.
-Use nondrug pain relief measures.
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pharmacological and non-pharmacological interventions
Non-pharmacological interventions:
Cutaneous stimulation: Pain relief is generally sustained only as long as the stimulation continues. Stimulation itself may aggravate preexisting pain or may produce new pain.
- heat/cold/pressure
-therapeutic touch, massage, vibration
-Transcutaneous electrical nerve stimulation (TENS) also known as percutaneous electrical nerve stimulation (PENS). *Not widely use but
older adults can benefit from this. It's safer and just as effective as medications.
Cognitive-behavior measures:
Distraction, imagery, hypnosis.
Other:
Acupuncture
Glucosamine for arthritis.
Nursing Interventions to Prevent Side Effects Opioids
Constipation
Nausea/vomiting
Sedation/confusion
Respiratory distress
. Assess previous bowel habits.
. Use measures to prevent this
problem because constipation is
the most common side effect (push
fluids, encourage activity, give
foods high in bulk and roughage).
. Keep a record of bowel
movements.
. Administer stool softeners and
stimulant laxatives.
. if ineffective, try suppository or
Fleet's enema.
Assess actual cause of
nausea.
Recognize that N/V may be
only an initial, temporary
side
effect for the first 24 to 48
hours because tolerance
seems to
develop quickly to this side
effect.
. Try an antiemetic
prophylactically before
administration, as
prescribed.
. Treat with
prochlorperazine
(Compazine) 5 mg orally
every
4 hours, as prescribed.
• Give metoclopramide
(Reglan) 10 mg before
meals and at
bedtime, or ondansetron
(Zofran) 4 mg IV.
• Assess actual cause of
sedation because the patient
may also
be on hypnotics and
antianxiety agents; eliminate
unnecessary sedating
medications
of Opioids
• Recall that tolerance to this
side effect generally occurs
after
2 to 3 days.
• Be aware that stimulants
such as caffeine may
counteract
opioid-induced sedation.
• Consider opioid rotation
using an equianalgesic chart.
• Be aware that clinically significant
respiratory depression is rarely seen in
patients with severe pain caused by cancer,
even when large doses of opioids are given.
• Recognize that pain and stress seem to
counteract the respiratory depression effects
of opioids.
• Recall that respiratory depression is usually
preceded by sedation.
• Monitor sedation level and respiratory
status frequently for the first 24 to 48 hours,
especially in opioid-naive patients.
• If increased sedation occurs, decrease
opioid dose and attempt to stimulate patient.
• Be aware that respiratory rate alone is not
indicative of respiratory status.
• If absolutely necessary in an unresponsive
patient, administer
naloxone (Narcan) 0.4 mg diluted in 10 mL
of normal saline; push 0.5 mL IV slowly for
2 minutes and observe the patient.
Management of Clients with Fluid & Electrolyte Imbalances

risk for (causes of) and assessment for fluid volume overload, deficiency
o ~ dehydration
o
o
o
o
o
o
Extracellular Fluid Volume Deficit: Dehydration

Average daily fluid intake 1500 to 2500 ml

Etiology

Lack of fluid intake

Excess fluid loss

Alteration in the fluid balance regulators
o Thirst
o Hormones
o Lymphatic system
o Kidneys
Excess Fluid Losses

Potential causes of excess fluid loss

Unmonitored use of diuretics

Severe vomiting and persistent diarrhea

Fever and diaphoresis

Gastrointestinal suction and fistula drainage

Blood loss and burns

Third spacing of fluids

Compensation for excess fluid loss

Interstitial fluid moves to restore volume

ADH & aldosterone increase, causing reabsorption of sodium, water

Baroreceptors are stimulated -> vasoconstriction & increased HR

Osmoreceptors signal thirst mechanism

When compensation fails, the individual experiences a fluid deficit
Types of Extracellular Fluid Volume Deficits

Hypertonic deficit

Water loss is greater than electrolyte loss

Increases the osmolarity of the remaining plasma, making it hypertonic or hyperosmolar

increased osmotic pressure that causes water to move from the ICF into the plasma and interstitial fluid
spaces

leads to cellular dehydration and shrinkage

also causes the plasma volume to increase to normal or greater than normal levels

Iso-osmolar or isotonic deficit

Water and electrolyte losses are equal

ECF osmolarity remains normal while volume is reduced

does not cause a shift of fluids between spaces, so intracellular fluid (ICF) volume remains normal.

Hypotonic deficit

Electrolyte loss is greater than fluid loss

The remaining fluid is dilute, with hyponatremia and hypokalemia causing skeletal muscle weakness.
Clinical Manifestations of a Fluid Deficit

Loss of body weight

Changes in intake and output

Changes in vital signs

Decrease in blood pressure (particularly orthostatic hypotension), central venous pressure (CVP), etc.

Increased heart rate and temperature

Other: dry mucous membranes, decreased skin turgor, etc.
Diagnostic Findings During a Fluid Deficit

Indicators of hemoconcentration

Osmolality above 295 mOsm/kg

Plasma sodium above 145mEq/L

Blood urea nitrogen above 25 mg/dl

Plasma glucose above 120 mg/dl

Hematocrit above 55%

Urine specific gravity above 1.030
Outcome Management of a Fluid Deficit

Fluid restoration

Oral or IV rehydration

Monitor for complications

Decreased cardiac output
o
o
o

Dysrhythmias

Electrolyte imbalances

Impaired mucous membranes

Correct the underlying problem

Nursing management

Assessments
o Vital signs
o Peripheral vein filling
o Intake, output, and daily weights
o Lab values
o Oral cavity
o Skin turgor

Restore fluids

Control underlying problem
Interventions for Fluid Deficits

Teach

Appropriate fluid replacement

Exercise with adequate fluid replacement
o Cool water before exercise
o 150 to 200 ml every 15 minutes during exercise

Do not decrease fluid intake for incontinence

Drink fluids even in the absence of thirst
Extracellular Fluid Volume Excess: Fluid Overload

Fluid overload or overhydration

Hypervolemia
o Excess fluids in the vascular system

Third-spacing
o Excess fluids in the interstitial spaces

Etiology

Simple overloading of fluids

Failure to excrete fluids
o Renal failure
o Edema
Types of Extracellular Fluid Volume Overload

Isotonic overhydration

AKA hypervolemia: caused by problems that arise from excessive fluid in ECF

isotonic fluids are ingested or retained, so that osmolarity remains normal

only the ECF compartment expands and fluid does not shift between the spaces

Hypotonic overhydration

AKA water intoxication

excess fluid is hypotonic to normal body fluids

the osmolarity of the ECF decreases and hydrostatic pressure increases

fluid moves into the intracellular space because of the decreased plasma osmotic pressure

all fluid spaces expand.

Hypertonic overhydration

rare, caused by an excessive sodium intake

hyperosmolarity of the plasma and interstitial compartments draws fluid from the intracellular fluid (ICF)
compartment

the ECF volume expands and the ICF volume contracts.
o
o
o
o

Clinical Manifestations of Fluid Excess

Respiratory and cardiovascular

Cough, dyspnea, crackles, pallor, etc.

Bounding pulse, elevated blood pressure (BP), CVP

Other

Peripheral edema

Weight gain

Confusion, seizure, coma
Diagnostic Findings During a Fluid Excess

Indicators of hemodilution

Osmolality less than 275 mOsm/kg

Sodium less than 135 mEq/L

Hematocrit less than 45%

Specific gravity less than 1.010

Blood urea nitrogen less than 8 mg/dl
Outcome Management of Fluid Excess

Restrict sodium

Restrict fluids

Promote urine output

Diuretics and digitalis

Improve myocardial function

Angiotensin-converting enzyme (ACE) inhibitors and beta-blockers

Nursing management

Assessments
o Vitals, lung sounds
o Edema
o Intake and output
o Lab values

Reduce sodium and fluid Intake

Mobilize fluids

Control underlying problem

patient teaching and nursing interventions for patients with fluid imbalances
o ~ if pt dehydrated, want to know if they have heart problems
 ~ CHF, renal failure…
 ~ assess electrolytes
o ~ Blood pressure – what fluid?
o ~ Pt teaching – weight gain/loss..

Teach
o
o
Appropriate fluid replacement
Exercise with adequate fluid replacement

Cool water before exercise

150-200 ml every 15 minutes during exercise
o Do not decrease fluid intake for incontinence
o Drink fluids even in the absence of thirst
A. fluid volume excess (overhydration) –pg. 182
 Monitor for indicators of increased fluid overload (bounding pulse, increasing neck vein distention, presence of crackles in lungs,
increasing peripheral edema, reduced urine output)
o Pulmonary edema can occur very quickly and lead to death
 Assess for skin breakdown esp. coccyx, elbows, hips, heels, nares, and ears (oxygen cannula) & turn patient every 2 hours
 Diuretics and digitalis to increase water and sodium excretion
 Restrict sodium intake in nutritional therapy
 Monitor I&O
 Take weight daily
o Fluid retention may not be visible but rapid weight gain is BEST indicator of fluid retention/overload
 Improve myocardial function (PPT)
o Angiotensin-converting enzyme (ACE) inhibitors and beta-blockers

Na+
B. fluid volume deficit (dehydration) –pg. 180
 Administer IV therapy, as prescribed
 Give fluids, as appropriate
 Promote oral intake (e.g. providing a drinking straw, offer fluids between meals, change ice water routinely), as appropriate
 Distribute the fluid intake over 25 hours, as appropriate
 Encourage significant other to assist patient with feedings, as appropriate
 Offer snacks (e.g. frequent drink and fresh fruits/fruit juice), as appropriate
Signs of decreased level
(hypo)
• Sodium less than 135
mEq/L
– Neurologic: headache,
confusion, etc.
Treatment of decrease
Signs of increased level (hyper)
Treatment of increase
• Medical and nursing
management
– Restore sodium
levels: replacement
• Early symptoms
–Polyuria, anorexia, weakness,
restlessness
• Late symptoms
 Medical/nursing outcome
mgmt
-replace fluid loss
-sodium restriction
K-
– Cardiovascular:
decreased BP,
tachycardia, thready
pulse, etc.
– Pulmonary: crackles,
dyspnea, etc.
– Gastrointestinal:
nausea, vomiting, etc.
– Other: dry skin and
mucous membranes
– Reduce sodium loss:
prevent vomiting and
diarrhea
– Restore sodium
balance
• Outcomes
– The nurse will
monitor sodium and
chloride levels and for
clinical
manifestations of
hyponatremia
– Confusion, seizures, coma,
tremors, muscle twitching,
rigid paralysis
• Cardiovascular
– Electrocardiogram
(ECG) changes,
dysrhythmias, arrest,
etc.
• Gastrointestinal
– Anorexia, abdominal
distention, etc.
• Musculoskeletal
– Weakness,
flabbiness, leg
cramps, etc.
• Neurologic
– Confusion,
convulsions, coma,
etc.
Restore potassium levels
• Potassium is given
intravenously for severe
hypokalemia.
• Maximum recommended
infusion rate is 5 to 10
mEq/hr.
• This rate is never to
exceed 20 mEq/hr under
any circumstances.
• Potassium is a severe
tissue irritant and is
never given by
intramuscular injection
or subcutaneous
injection.
Ongoing assessments
• Cardiopulmonary
–Hypotension, cardiac and
respiratory arrest due to
muscle paralysis
• Gastrointestinal
– Intestinal colic, diarrhea
• Musculoskeletal
– Paresthesias, muscle
irritability
Mg++  Myocardial irritability,
 Replacement
convulsions, etc.
Ca++ • Neuromuscular
• Medical/nursing
– Numbness and
management
tingling of hands, toes,
– Restore calcium
and lips
balance
– Facial twitching,
• Replacement
tetany, seizures (test
– Educate regarding
for Trousseau’s and
calcium-rich foods
Chvosteck’s signs)
– Move client with
• Cardiovascular
caution
– Hypotension,
– Careful assessments
dysrhythmias, weak
pulse
• Skeletal
– Spontaneous
fractures
ClPhos
 Cardiovascular
 Musculoskeletal (acute
muscle breakdown, or
rhabdomyolysis)
 CNS
 Restore phosphate
balance
 Muscle weakness, areflexia,
respiratory paralysis, sedation
• Urinary
– Polyuria related to an
osmotic diuresis
• Gastrointestinal
– Anorexia, constipation,
nausea, abdominal
distention
• Neuromuscular
– Fatigue, depression,
muscle weakness
 Outcomes
-the nurse will monitor
plasma sodium and chloride
levels and for clinical
manifestations of
hypernatremia
• Medical/nursing management
– Restore potassium
balance
• Administer fluids
and encourage
diuresis
• Utilize cation
exchange resin
(Kayexelate)
• Outcome
– The nurse will monitor
potassium levels and
report abnormal findings
and symptoms of
hyperkalemia
 IV hydration and diuretics
• Medical/nursing
management
– Restore calcium balance
• IV hydration and
diuretics
• Avoid calciumcontaining products
– Safety precautions
– Educate to avoid
calcium intake
 Problems caused by
 The management of
hyperphosphatemia center on
hyperphosphatemia entails
the hypocalcemia that results
the management of
when serum phosphate levels
hypocalcemia
increase
 Eliminate excess phosphate
 Early: tachycardia, palpitations
 Late: tetany, hyperreflexia
Direction of fluid
Isotonic fluid
 Isotonic fluids in the
vasculature will stay
there and will NOT
move
Hypotonic fluid
Water moves from
the IVS to ISC 
dilutes interstitial
fluid osmolarity
decreases  water
drawn into cells
Hypertonic fluid
 ~They draw water
into the vasculature

Uses (to treat what
problems)
• Fluids remain IVS &
expand volume.
– Hypotensive
– Hypovolemic
•
Cellular dehydration
– Dialysis
–
Diuretics
– DKA (high serum
glucose causes fluid
to move out of the
cells into the vascular
and interstitial
compartments).
• Stabilizing blood
pressure
• Increasing urine output
• Correcting hypotonic
hyponatremia and
decreasing edema
• ~For patients who have
vascular dehydration
Potential complications
•
•
Risk of fluid overloading exists.
– Left ventricular dysfunction,
history of CHF or hypertension.
Avoid volume hyper-expansion in
patients with intracranial pathology or
space occupying lesions.
• Caution
Sudden fluid shifts from IVS to cells
•
Cardiovascular collapse
•
Increased ICP in certain
patients.
These can be dangerous in the setting of
cell dehydration
Management of Clients with Acquired Immunodeficiency
Syndrome
spread of HIV
o ~who’s at risk? When? How?

Transmission
o Sexual: genital, anal, or oral sexual contact with exposure of mucous membranes to infected semen or vaginal secretions
o Parenteral: sharing of needles or equipment contaminated with infected blood or receiving contaminated blood products
o Perinatal: from the placenta, from contact with maternal blood and body fluids during birth, or from breast milk from an
infected mother to child
o Teach everyone about the transmission routes and ways to reduce their exposure (discussed next). Also stress that HIV is not
transmitted by casual contact in the home, school, or workplace. Sharing household utensils, towels and linens, and toilet
facilities does not transmit HIV. In addition, HIV is not spread by mosquitoes or other insects.
o Anal intercourse in which the semen depositor (inserting or active partner) is infected is a very risky sexual practice
regardless of whether the semen receiver (receiving partner) is male or female.
o Although there is less virus in seminal or vaginal fluids of people receiving HAART, the risk for transmission still exists
o
o


~ Need to have pt’s blood in contact w/ your blood system

~ Hollow bore needles. Inside the bore is where the blood can stay.

~ can get anti-retroviral drugs right away so it doesn’t have opportunity to replicate.

~ standard precautions – everyone assumed to have something that can cause harm to health care worker
Diagnostic testing
o Chart 21-6 Key Features AIDS

Immunologic Manifestations

• Low white blood cell counts:
o CD4+/CD8+ ratio < 2
o CD4+ count < 200/mm3

• Hypergammaglobulinemia

• Opportunistic infections

• Lymphadenopathy

• Fatigue

Integumentary Manifestations

• Dry skin

• Poor wound healing

• Skin lesions

• Night sweats

Respiratory Manifestations

• Cough

• Shortness of breath
Gastrointestinal Manifestations

• Diarrhea

• Weight loss

• Nausea and vomiting

Central Nervous System Manifestations

• Confusion

• Dementia

• Headache

• Fever

• Visual changes

• Memory loss

• Personality changes

• Pain

• Seizures
Test for HIV antibodies

~ may not be positive right after exposure b/c body hasn’t developed enough antibodies to get detected. Get tested
q6months
Home testing
Salivary and urine testing
Interpreting test results

Positive, negative, or indeterminate

~ positive – have enough antibodies for HIV

~ negative test doesn’t guarantee that they don’t have the virus

~ repeat testing important
HIV viral load testing

~ more direct but more expensive

~ detect how much virus is in blood

~ used for treatment, not diagnostic. We know pt is (+). Want to know how disease is progressing. If treatments
are working.

“Lower Limit” – want viral load to be undetectable. Not that there isn’t any virus in their body but we want very
small amount.
Laboratory Assessment

Lymphocyte counts ~ best indicator for viral infection

AIDS: < 3500 WBCs/mm3 (leukopenic); <1500 lymphocytes/mm3 (lymphopenic)

CD4/CD8 counts

~ CD4+ and viral count = inverse

Normal ratio of CD4+ to CD8+ is 2:1.

In HIV and AIDS, b/c of low number of CD4+ T-cells, the ratio is low.

Antibody tests

Enzyme-linked immunosorbent assay (ELISA)

Western blot, viral culture, viral load

 ELISA and Western blot tests antibodies to HIV

Quantitative RNA assays

p24 antigen assay  ways to see extent of the virus and extent of the effect on the immune system
Everyone who has AIDS has HIV infection; however, not everyone who has HIV infection has AIDS.
A diagnosis of AIDS requires that the person be HIV positive and have either a CD4+ T-cell count of less than 200
cells/mm3 or an opportunistic infection.

o
o
o
o
o
o
o
o


testing/diagnosis for HIV/AIDS
o ~ some tests for presence – HIV+
 ELISA, western blotter
 CD4+
o ~ how well treatment is working
 [viral load testing]
nursing interventions/patient teaching for clients with HIV/AIDS
o ~ not too much detail
Management of clients with Gastrointestinal Disorders

gastritis/reflux care & pt teaching
o ~ heartburn
o ~ not hiatal hernias

clinical manifestations and nursing care of peptic/duodenal ulcer disease
o ~ how to diagnose, sx, tx
o ~ gastric – lose weight
 Mucosal barrier
o ~ duodenal –
o *** difference b/t tx for two is so minor that don’t get caught up into details.
GERD




Assessment
Physical
o
o
Diagnostic
tests


Occurs as a result of the backward
flow (reflux) of GI contents into the
esophagus
Reflux produces sx by exposing the
esophageal mucosa to the irritating
effects of gastric or duodenal
contents, resulting in inflammation
A person w/ acute sx of
inflammation is often described as
having reflux esophagitis, which may
be mild or severe.
The degree of inflammation is r/t the
acid concentration of the refluxed
material, the # of reflux episodes,
and the length of time that the
esophagus is exposed to the irritant
Reflux esophagitis (excessive relaxation
of LES) –avoid fatty foods, caffeine,
chocolate, citrus, peppermint, etc.
Key features:
o Dyspepsia (heartburn)** main
symptom  substernal or
retrosternal burning sensation
that tends to move up and down
the chest in a wavelike fashion;
severe heartburn may radiate to
the neck or jaw or may be felt in
the back. It can resemble
angina…
o Regurgitation (may lead to
aspiration or bronchitis)
o Coughing, hoarseness, or
wheezing at night
o Water brash (hypersalivation)
o Dysphagia
o Odynophagia (painful
swallowing)
o Epigastric pain
o Belching and flatulence
o Nausea
o Pyrosis (retrosternal burning)
o Globus (feeling of something in
back of throat)
o Pharyngitis
o Dental caries (severe cases)
Most accurate method: 24-hour
ambulatory esophageal pH monitoring
EGD evaluating reflux esophagitis (biopsy
may be performed)
GASTRIC ULCER
Occurs when there is a break in the
mucosal barrier and HCl injures the
epithelium.
Gastric emptying is delayed, causing
regurgitation of duodenal contents.
Gastric ulcers are deep and
penetrating, and they usually occur on
the lesser curvature of the stomach
near the pylorus

DUODENAL ULCER
Chronic break in the duodenal
mucosa that extends through
the muscularis mucosa and
leaves a scar after healing.
Characterized by high gastric
acid secretion and is the most
common type of peptic ulcer
PUD is associated primarily w/ NSAIDs use and H. pylori
o
o
o
o
o
o
o
o
Epigastric tenderness (midline between umbilicus
and xyphoid process)
If perforation, rigid, board-like abdomen with
rebound tenderness ~peritonitis
Dyspepsia (indigestion) –discomfort in upper
abdomen (sharp, burning, gnawing)
Assess for fluid volume deficit (orthostatic
hypotension, dizziness)
H&H low due to bleeding
Stool specimen positive for occult
Testing methods for H. pylori
If perforation suspected, chest and abdominal x-ray

Esophageal manometry: motility testing
(not as common)
Treatment
Meds

Drug therapy: take before meals!
o Antacids: increase pH of gastric
content by deactivating pepsin
o Histamine receptors: decrease
gastric acid production (shortacting)
o Prokinetic drugs: increase
gastric emptying
o Proton pump inhibitors:
decreases gastric acid
production (long-acting)

Other

Nonsurgical management
o Most important role of nurse it pt
and family education and
ongoing mgmt.
o Nutritional therapy: eliminate
foods to decrease LES pressure:
chocolate, alcohol, fatty foods
(esp fried), caffeine, and
carbonated beverages, orange
juice, tomatoes –spicy or acidic
foods also, small portions, and
no bed time snacks (avoid
eating for 3 hrs (or more)
before bedtime)
o Right side lying position to
decrease effects of nighttime
episodes of reflux, sleep with 612 inch pillow
o Manage obesity, avoid heavy
lifting, straining, and working
over in bent-over position
Surgical management
o Laparoscopic Nissen
Fundoplication (LNF)
o Very small percentage require
anti-reflux surgery; manage
lifestyle to prevent GERD*


Complications




Increase risk for cancer with
prolonged GERD
Serious complications are
hemorrhage and aspiration
pneumonia
Dental decay
Associated w/ cardiac disease
o


Most accurate test is EGD** –direct visualization of ulcer
crater and allows H. testing biopsy
Acute pain; chronic pain
o Drug therapy

triple therapy including PPI, Prevacid, plus 2
antibiotics (PPI’s are drug of choice for pts with
acid-related disorders)

H2-receptor antagonists inhibit gastric acid
secretion

Prostaglandin analogues are effective in treating
duodenal ulcers

Antacids buffer gastric acid and prevent
formation of pepsin (1 hr before, and 2-3 hrs
after)

Sucralfate is mucosal barrier fortifier (protector)

~ don’t give levothyroxine
Acute pain; chronic pain
o Nutrition therapy

Management of nutrition is controversial

Eat bland diet with no caffeine
o CAM

Hypnosis and imagery, yoga (reduce stress and
anxiety)

Herbs and vitamins (slippery elm and
marshmallow root, quercetin, and licorice,
vitamin A, B, C, chamomile, ginger, dandelion,
cranberry) –heal inflamed tissues
Potential for GI bleeding
o Nonsurgical management

Emergency: upper GI bleeding (prevent
hypovolemic shock –ABC’s)

NG tube placement and lavage –lavage is
withdrawn until clear or light pink and without
clots (place client on left side)

Endoscopic therapy –for clients with active
bleeding, signed consent, NPO 6 hrs, do not
resume preprocedure diet until gag reflex
intact

Acid suppression –used to prevent rebleeding
Surgical management
o Not indicated unless medical therapy not working or they
develop PUD complication
o MIS via laparoscopy

Subtotal gastrectomy (partial stomach removal)

Pyloroplasty (open pylorus)

Vagotomy (vagus nerve cutting)

Hemorrhage – most serious
o Hematemesis (vomits bright red or coffee-ground
blood)
o Melena (occult blood in tarry stool)

Perforation, w/ the gastroduodenal contents emptying through
the anterior wall of the stomach or duodenum into the
peritoneal cavity
o Tender, rigid, and board-like (peritonitis)
o Surgical emergency and life threatening!

Pyloric obstruction – abd bloating, N/V

Intractable disease, which is characterized by lack of response
to conservative management and w/ symptoms that interfere
w/ ADLs

priority assessment of inflammatory and non-inflammatory GI problems

Pancreatitis*
ACUTE PANCREATITIS

Serious and, at times, life-threatening inflammatory
process of the pancreas caused by premature
activation of pancreatic enzymes and resulting in
autodigestion and fibrosis of the pancreas

The extent of the inflammation and tissue destruction
ranges from mild involvement, characterized by
edema and inflammation, to severe, necrotizing
hemorrhagic damage leading to diffusely bleeding
pancreatic tissue w/ fibrosis and tissue death

Many factors can cause injury to the pancreas:
o Biliary tract disease w/ gallstones
o Excessive alcohol ingestion [most frequent
cause]
o Postop trauma from surgical manipulation
after biliary tract, pancreatic, gastric, and
duodenal procedures
o External blunt trauma
o Metabolic disturbances
o Kidney failure or kidney transplant
o Drug toxicities, including opiates,
sulfonamides, thiazides, steroids, and oral
contraceptives
o Other medical diseases

In acute pancreatitis, four major pathophysiologic
processes occur: lipolysis, proteolysis, necrosis of
blood vessels, and inflammation
Assessment
Physical

Abdominal pain (most frequent symptom), including
sudden-onset pain in a midepigastric or LUQ location
w/ radiation to the back, aggravated by a fatty meal,
ingestion of a large amount of alcohol, or lying in the
CHRONIC PANCREATITIS

Progressive, destructive disease o the
pancreas w/ remissions and exacerbations

Inflammation and fibrosis of the tissue
contribute to pancreatic insufficiency and
diminished exocrine and endocrine function

Characterized by the loss of exocrine
function, which causes a decreased output of
enzymes and bicarbonate; loss of endocrine
unction results in diabetes mellitus
Chart 62-3 Key Features Chronic Pancreatitis

Intense abd pain (major clinical
manifestation) that is continuous and
burning or gnawing















Diagnostic
tests



Treatment
Meds



recumbent position; intense, boring, and continuous
and is worsened by lying in supine position.
E: Pain that worsens when lying supine and the
presence of jaundice are the only assessment findings
indicative of acute pancreatitis.
E: Pain associated with pancreatitis is usually located
in the mid-epigastric or upper left quadrant, and
jaundice is present.
E: Pain associated with acute pancreatitis usually has
an abrupt onset
E: Pain associated with pancreatitis usually lessens
with sitting up.
Weight loss, w/ N and V
Jaundice
Gray-blue discoloration of the abd and periumbilical
area (Cullen’s sign)
Gray-blue discoloration of the flanks (Turner’s sign)
Absent or decreased bowel sounds
Abd tenderness, rigidity, and guarding
Dull sound on abd percussion, indicating ascites
Elevated temp w/ tachycardia and decreased BP
Adventitious breath sounds, dyspnea, or orthopnea
Elevated serum amylase and lipase levels
Significant changes in VS may indicate shock.
Hypotension and tachycardia may result from
pancreatic hemorrhage, excessive fluid volume shifting,
or the toxic effects of abd sepsis from enzyme damage.
Observe LOC that may be r/t alcohol withdrawal,
hypoxia, or impending sepsis w/ shock.
Serum lipase , amylase , alkaline phosphatase ,
alanine aminotransferase (ALT) , bilirubin , WBC
, HGB, HCT, coagulation factors, Na+, Ca2+, Mg2+,
triglycerides, and albumin
~ Ca2+ and Mg2+ low
Imaging of the pancreas and gallbladder w/
ultrasound or CT scan



Opioids such as morphine or hydromorphone, often
w/ PCA device
Proton pump inhibitors or H2-histamine receptor
blockers to decrease gastric hydrochloric acid
production during fasting
Antibiotics for pts w/ acute necrotizing pancreatitis














Other




Relief of pain by assuming the fetal position or by
sitting upright and bending forward.
Diet therapy:
o Withhold foods and fluids in the acute
period; maintain hydration w/ IV fluids
o NG intubation to decrease gastric distention
and suppress pancreatic secretion
o Initiating nasojejunal enteral nutrition
o Assess frequently for presence of bowel
sounds
Comfort measures include:
o Side-lying position to decrease abd pain
o Avoiding oral stimulation while providing
measures to keep mucous membranes from
drying
~ NPO


Abd tenderness
Ascites
Possible LUQ mass (if pseudocyst or abscess
is present
Resp compromise manifested by adventitious
or diminished breath sounds, dyspnea, or
orthopnea
Steatorrhea; clay-colored stools
Weight loss
Jaundice
Dark urine
Polyuria, polydipsia, polyphagia (diabetes
mellitus)
~ Fatigue and muscle wasting
Elevated serum amylase, bilirubin, and
alkaline phosphatase
Identification of calcification of pancreatic
tissue in biopsy specimen
Opioid analgesia
Non-opioid analgesics
Pancreatic-enzyme replacement therapy
(PERT) is the standard of care to prevent
malnutrition, malabsorption, and excessive
weight loss
Insulin or oral hypoglycemic agents to control
diabetes
H2-histamine receptor antagonist or proton
pump inhibitor to decrease gastric aclid
Diet therapy includes: fasting to avoid
recurrent pain exacerbated by eating and
providing jejunal or TPN
Surgical management – not the primary
intervention
o Indicated for intractable pain,
incapacitating pain relapses, or
complications such as pseudocyst
and abscess
o I&D for abscesses or pseudocysts
o Laparoscopic cholecystectomy or
cholechotomy for underlying biliary
tract disease
o Sphincterotomy (incision of the
sphincter) for ibrosis
o Pancreatojejunostomy (pancreatic

Complications
E: Enzyme preparations should not be mixed with
foods containing protein because the enzymes will
dissolve the food into a watery substance.
duct is opened and anastomosed to
the jejunum, relieving obstruction)
to relieve pain and preserve
pancreatic tissue and fxn)
o Partial pancreatectomy, which may
be performed for advanced
pancreatitis or disabling pain
o Vagotomy w/ gastric antrectomy to
alter nerve stimulation and
decrease pancreatic secretion
Chart 62-5 Prevention of Exacerbations of Chronic
Pancreatitis

Avoid things that make your sx worse, such as
drinking caffeinated beverages

Avoid alcohol ingestion

Avoid nicotine

Eat bland, low-FAT, high-PRO, moderate-CHO
meals; avoid gastric stimulants, such as spices

Eat small meals and snacks high in calories

Take pancreatic enzymes that have be
prescribed for you w/ meals

Rest frequently; restrict your activity to one
floor until you regain your strength

E: Pancrelipase (Cotazym) is a pancreatic
enzyme used for enzyme replacement for
clients with chronic pancreatitis. To avoid
skin irritation and breakdown from residual
enzymes, the lips should be wiped.

Pseudocyst

Abscess
Table 62-3 Potential Complications of Acute Pancreatitis

Pancreatic infection (most common cause of death)

Hypovolemia

Hemorrhage

Acute renal failure

Paralytic ileus – peritoneal irritation and seepage of
pancreatic enzymes into the abd cavity

Hypovolemic or septic shock – shock results from
peripheral vasodilation form the released vasoactive
substances and the retroperitoneal loss of protein-rich
fluid form proteolytic digestion. Hypovolemia results
from decreased renal perfusion and acute renal
failure.

Pleural effusion

Acute resp distress syndrome (ARDS) – disruption of
the aveolar capillary membrane

Atelectasis

Pneumonia

Multi-organ system failure – caused by necrotizing
hemorrhagic pancreatitis

Disseminated intravascular coagulation (DIC) –
involves hypercoagulation of the blood, w/
consumption of clotting factors and development of
microthrombi

Diabetes mellitus

Appendicitis*
APPENDICITIS

Acute inflammation of the vermiform appendix, the small finger-like pouch attached to the cecum of the colon

Inflammation of the appendix can occur when the lumen of the appendix is obstructive

Inflammation leads to infection as bacteria invade the wall of the appendix

Most common cause of acute inflammation of RLQ of abd

Peak incidence is b/t 20 and 30 yrs; may occur at any age

Not common for older adults
Assessment
Physical

Abd pain originating in the epigastric or periumbilical area and shifting to the RLQ (McBurney’s point); pain may






Diagnostic
tests





Treatment
Meds
Other





Complications






not be localized
N/V
Anorexia after the initial diagnosis of pain
Urge to defecate or pass flatus
Muscle rigidity and rebound tenderness
Normal or slightly elevated temp
Abd pain that increase w/ cough or movement and is relieved by flexion of the right hip or knees suggests a
perforated appendix w/ peritonitis
~ pain before N/V
Increased WBC w/ possible increased segmented neutrophils – 10,000 to 18,000/mm3 w/ a “shift to the left”
(increased # of immature WBCs)
WBC elevation > 20,000/mm3 may indicate peritonitis
Ultrasound study may show presence of enlarged appendix
If sx are recurrent or prolonged, a CT scan can be used for diagnosis and may reveal the presence of a fecalith
Keep pt w/ suspected or known appendicitis on NPO to prepare for the possibility of emergency surgery and to avoid
making the inflammation worse
The pt w/ suspected appendicitis should NOT receive laxatives or enemas, which can cause perforation of the
appendix.
Heat should NEVER be applied to the abd b/c this may increase circulation to the appendix and result in increased
inflammation and perforation
Keep pt in semi-Fowler’s position so that abd drainage, if any, can be contained in the lower abd
Appendectomy may be performed as a traditional procedure through a small incision or, if not ruptured, by
means of laparoscopy
If the process occurs slowly, an abscess may develop
Rapid process may result in peritonitis
Perforated appendix w/ peritonitis
All complications of peritonitis are serious. Gangrene can occur w/in 24 to 36 hrs, is life threatening, and is one of
the most common indications for emergency surgery.
Perforation may develop w/in 24 hrs, but the risk rapidly rises after 48 hrs
Perforation is more common in older people, causing a higher mortality rate. The diagnosis of appendicitis is
difficult to establish in older adults b/c sx of pain and tenderness may not be as pronounced in this age-group,
resulting in tx delay and an increased risk for perforation, peritonitis, and death

Peritonitis*
PERITONITIS

Life-threatening, acute inflammation of the visceral/parietal peritoneum and endothelial lining of the abd cavity

Primary – acute bacterial infection that develops as a result of contamination of the peritoneum through the vascular system; rare

Secondary – bacterial invasion as a result of perforation or a penetrating wound, such as appendicitis, diverticulitis, peptic ulcer,
ascending genital infection, or a gunshot injury to the abd. Chemical peritonitis is the result of leakage of bile, pancreatic enzymes,
and gastric acid

Most often caused by contamination of the peritoneal cavity by bacteria or chemicals (secondary)
Assessment
Physical
Chart 60-1 Key Features Peritonitis

Rigid, boardlike abd (classic)

Abd pain (localized, poorly localized, or referred to the shoulder or chest)

Distended abd

N, anorexia, V

Diminishing BS

Inability to pass flatus or feces

Rebound tenderness in the abd

High fever

Tachycardia

Dehydration from high fever (poor skin turgor)

Decreased urine output

Hiccups

Possible compromise in resp status
Diagnostic

CBC: WBC elevated to 20,000/mm3 w/ high neutrophil count
tests

Blood culture – determine whether septicemia has occurred and to ID the causative organism

Serum electrolytes, BUN, creat

Abd x-rays or CT to determine presence of dilation, edema, and inflammation of the intestines
Treatment
Meds
Other
Complications






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



IV fluids and antibiotics
Pain management w/ IV analgesics, anticipate use of PCA pump
Keep pt NPO
Administer O2 as prescribed according to pt’s resp status
Surgical Management: may be necessary to ID and repair underlying cause of the peritonitis
o Focused on controlling the contamination, removing foreign material from the peritoneal cavity, and
draining fluids collections
o During surgery, the peritoneum is irrigated w/ antibiotic solution, and drainage catheters are inserted
o Exploratory laparotomy – usual approach to remove or repair inflamed or perforated organs
o Maintain the pt in semi-Fowler’s position to promote drainage of peritoneal contents into the lower region
of the abd cavity
o Monitor LOC, VS, resp status (RR and breath sounds), and I&O at least hourly immediately after surgery
Shock
Resp problems
Paralytic ileus
~ kidney failure
~ bacteremia, septicemia
Crohn’s vs. ulcerative colitis*
CROHN’S

Regional enteritis, idiopathic inflammatory disease
that occurs anywhere in the GI tract but most
often affect the terminal ileum w/ patchy lesions
that extend through all bowel layers

Chronic nonspecific inflammation of the entire
intestinal tract occurs, and eventually deep fissure
and ulcerations develop and often extend through
all bowel layers, predisposing the pt to
development of bowel fistulas

Chronic pathologic changes include thickening of
the bowel wall, resulting in narrowing of the
bowel lumen and strictures
Assessment
Physical

Fever, abd pain (RLQ), loose stools
ULCERATIVE COLITIS

Creates widespread inflammation of mainly the
rectum and rectosigmoid colon but can extend to
the entire colon

Characterized by hyperemic intestinal mucosa
(increased blood flow) w/ resultant edema. In
more severe inflammation, the lining can bleed
and small erosions, or ulcers, occur. Abscesses
can form in these ulcerative areas and result in
tissue necrosis. Continued edema and mucosa
thickening can lead to a narrowed colon and
possibly a partial bowel obstruction

Stool typically contains blood and mucus








Diagnostic
tests

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




Treatment
Meds
Blood in stool
Periumbilical pain before and after BM
Weight loss (indicates serious nutritional
deficiencies)
Distention, masses, or visible peristalsis
Ulcerations or fissures of the perianal area
Bowel sounds diminished or absent in the
presence of severe inflammation
High-pitched or rushing sounds over the areas of
narrowed bowel loops
Diarrhea w/ steatorrhea (stool does not usually
contain blood but is fatty, frothy, foul-smelling)
Anemia – slow bleeding and poor nutrition
Low folic acid and cobalamin (vit B12 group)
serum levels b/c of malabsorption, further
contributing to anemia
Decreased albumin – amino acid malabsorption
and protein-losing enteropathy
C-reactive protein and ESR elevated – indicate
inflammation
WBCs in urine – infection (pyuria), caused by
uretal obstruction or an enterovesical (bowel to
bladder) fistula
Electrolyte losses, K+ and Mg2+ - if severe
diarrhea present
X-rays – show narrowing, ulcerations, strictures,
and fistulas
Abd ultrasound, CT scan
Biopsies obtained via colonoscopy may verify the
diagnosis



Aminosalicylates – anti-inflammation
Glucocorticoids – during exacerbation
Immunomodulatory therapy, used for pts w/
refractory disease

Metronidazole (Flagyl, Novonidazol) – fistulas
* bowel rest, TPN,


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
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

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
Other





Malnutrition: high-calorie, high-PRO, high-vitamin,
low-fiber meals; oral supplements such as Ensure
and Vivonex
Electrolyte therapy: F&E replacement by oral
liquids, nutrients, IV fluids
Impaired skin integrity results from fistula
formation: apply pouch, cover area w/ skin
barrier, clean and keep dry
Surgical Management: bowel rsn and anastomosis
w/ or w/o colon rsn
Stricturoplasy – for bowel strictures



Abd cramping, pain, and distention
Bloody diarrhea, tenesmus (unpleasant and
urgent sensation to defecate)
Lower abd colicky pain relieved w/ defecation
Low-grade fever, tachycardia
Malaise, anorexia, weight loss are common
Anemia occurs less often
Extraintestinal manifestations such as: migratory
polyarthritis, ankylosing spondylitis, and
erythema nodosum
Gallstones
Abnormal lab values: HCT, HGB, WBC, ESR, Creactive protein, and electrolytes
Results from most recent colonoscopy
Aminosalicylates – reduce inflammation
Glucocorticoids – during exacerbation
Anti-diarrheal drugs – symptomatic management
of diarrhea; given cautiously, b/c they can
precipitate colonic dilation and toxic megacolon
Immunomodulators – alter immune response and
are commonly given w/ glucocorticoids.
Inliximab (Remicade) or adalimumab (Humira)
may be given for refractory disease or for severe
complications such as toxic megacolon.
E: adalimumab (Humira) - The client should avoid
being around large crowds to avoid developing an
infection; The client should not take the
medication if he or she is allergic to certain
proteins.
Sulfasalazine (Azulfidine) is one of the primary
treatments for UC. It is thought to inhibit
prostaglandin synthesis and thereby to reduce
inflammation.
E: Lactose-containing foods are often poorly
tolerated and should be reduced or eliminated
from the diet of clients with UC.
E: Raw vegetables and high-fiber foods can cause
GI symptoms in clients with UC.
Diet therapy may include:
o NPO status for pt w/ severe sx
o TPN while NPO
o Elemental formulas, which are absorbed
in the upper bowel thereby minimizing
bowel sitmulation
o Avoiding high-fiber foods such a nuts
and fresh fruits or vegetables
Avoiding carbonated beverages, pepper,
nuts and corn, dried fruits, and smoking,
b/c these are common GI stimulants
that could cause discomfort
Complementary and alternative therapies used as
a supplement to traditional therapies may include
herbs such as flaxseed, selenium, vit C,
biofeedback, yoga, acupuncture, and Ayurveda
(combination of diet, herbs, and breathing
exercises)
Surgical procedures: total proctocolectomy w/
permanent ileostomy, total colectomy w/ a
continent ileostomy (Kock’s ileostomy) or ileal
reservoir, creation of ileoanal reservoir (aka
Resorative Proctocolectomy w/ Ileal Pouch Anal
Anastomosis (RPC-IPAA)
Intestinal perforation w/ peritonitis and fistula
formation
Toxic megacolon  Toxic megacolon is
characterized by an enlarged colon with fever,
leukocytosis, and tachycardia.
Hemorrhage
Increased risk for colon cancer
Malabsorption
Extraintestinal clinical manifestations
o


Complications








Malabsorption
Fistulas
Hemorrhage
Abscess formation
Bowel obstruction
Increased risk for cancer
Severe malnutrition
Diverticulitis vs diverticulosis*
DIVERTICULITIS

Inflammation of one or more diverticula, results
when the diverticulum retains undigested food,
which compromises the blood supply to that area
and facilitates bacterial invasion of the diverticular
sac, which may then perforate

A perforated diverticulum can progress to intraabd perforation w/ generalized peritonitis






DIVERTICULOSIS

Pouchlike herniations of the mucosa through the
muscular wall of any portion of the gut, but it
most commonly refers to diverticula of the colon

Can occur in any part of the intestine but most
common in sigmoid colon

High intraluminal pressure forces the formation
of a pouch in the weakened area of the mucosa,
commonly near blood vessels
Assessment
Physical







Diagnostic
tests







Treatment
Meds



Other




Abd pain that may begin as intermittent and may
progress to continuous
o pain may be localized to the LLQ and
increased w/ coughing, straining, or
lifting
o generalized abd pain is a sign of
perforation and peritonitis
Fever
N/V
Abd distention
Palpable, tender abd or rectal mass
Hypotension and dehydration occur if massive
bleeding occurs
Signs of septic shock occur if peritonitis has
occurred
Blood in stool (microscopic to larger amounts)
Elevated WBC, reduced HCT and HGB if bleeding
occurs
Flat plate x-ray to evaluate for free air and fluid
outside the GI tract
CT scan to diagnose abscess or thickening of
lumen caused by repeated inflammation and
injury
Serum electrolytes
I, O, and pt fluid status
If a NGT is used for gastric decompression or to
manage vomiting, check output for amount and
quality or color


broad-spectrum antibiotics such as metronidazole
(Flagyl) plus trimethoprim/sulfamethoxazole
(Bactrim, Septra), or ciprofloxacin (Cipro)
implement management for mild or moderate
pain; if pain is severe, use opioids
laxatives and enemas are not given, b/c they
increase intestinal motility
NGT inserted if N, V, or abd distention is severe
Recommend rest
Diet  AVOID FIBER
Surgical management: colon rsn w/ end-to-end
anastomosis or temporary or permanent
colostomy
Chart 60-6 Nursing Focus On The Older Adult
Diverticulitis
•
Provide antibiotics, analgesics, and anticholinergics as
prescribed. Observe older patients carefully for side
effects of these drugs, especially confusion (or
increased confusion), urinary retention or failure, and
orthostatic hypotension.
•
Do not give laxatives or enemas. Teach the patient and
the family about the importance of avoiding these
measures.
•
Encourage the patient to rest and to avoid activities
that may increase intra-abdominal pressure, such as
straining and bending.
•
While diverticulitis is active, provide a low-fiber diet.
When the inflammation resolves, provide a high-fiber
diet. Teach the patient and family about these diets and
when they are appropriate.
•
Because older patients do not always experience the


w/o inflammation, diverticula are asymptomatic
unless pain or bleeding develops, the condition
may go undiagnosed
intermittent pain in LLQ
history of constipation




Lab studies are not indicated
colonoscopy
barium enema (rectal)
upper GI tract series (small intestine)

Use a bulk-forming laxative such as psyllium
(Metamucil) to increase fecal size and consistency
if the recommended fiber requirements cannot be
tolerated

Eat diet high in cellulose and hemicellulose,
which are found in wheat bran, whole-grain
breads, and cereals. HIGH FIBER!
Foods containing seeds or indigestible material
that may block a diverticulum, such as nuts, corn,
popcorn, cucumbers, tomatoes, figs, and
strawberries, may be eliminated


Complications

typical pain or fever expected, observe carefully for
other signs of active disease, such as a sudden change
in mental status.
•
Perform frequent abdominal assessments to determine
distention and tenderness on palpation.
• Check stools for occult or frank bleeding.

Require emergent surgery:
o Rupture of the diverticulum w/
subsequent peritonitis
o Pelvic abscess
o Bowel obstruction
o Fistula
o Persistent fever or pain after 4 days of
medical tx
o Uncontrolled bleeding
colon cancer
o ~ who’s at risk? Older adults, ulcerative colitis, high fat, red meat
o ~ what do you do for colon cancer? Colectomy (take out portion of colon), may have colostomy [know concept, not
specific]
o ~ s/p colon cancer: complications/problems? Recurrence, imbalanced nutrition
 ~ think about time – 3 hrs? 1 days? 3 days?
 ~ what happens in colon? Water absorption. Be worried about F&E imbalance.
 ~ another complication  ADHESIONS  risk for obstruction
 ~ psychosocial – colostomy
COLON CANCER

Most CRCs are adenocarcinomas arising from the glandular epithelial tissue of the colon an develop as a multistep process,
resulting in loss of key tumor suppressor genes and activation of certain oncogenes that alter colonic mucosa cell division

Increased proliferation of the colonic mucosa first forms polyps that can transform into malignant tumors

Tumors occur in all areas of the colon and can spread by direct invasion and through the lymphatic and circulatory systems

Most common sites of metastasis: liver, lungs, brain, bones, and adrenal glands

E: Genetic testing is the only definitive way to determine whether the client has a predisposition to develop CRC. A higher incidence
of the disease has been noted in families who have a history; however, it is not the responsibility of the nurse to engage in genetic
counseling, and this client might not be predisposed to developing CRC.
Assessment
Physical

Rectal bleeding (most common manifestation)

Change in stool pattern or appearance

Cachexia (late sign) – (weight loss, muscle atrophy)

Guarding or abd distention (late sign)

Abd mass (late sign)
Diagnostic

Anemia (low HGB and HCT; stool positive for occult blood)
tests

Fecal occult blood test (FOBT) ~ avoid aspirin, vit C, and red meat 48hrs before stools specimen is collected to
avoid false positive

Carcinoembryonic antigen (CEA) blood test ~ elevated, but not specific to CRC

Colonoscopy ~ definitive test for diagnosis of colorectal cancer

CT or MRI of chest, abd, pelvis, lungs, or liver

E: Carcinoembryonic antigen may be elevated in many clients diagnosed with CRC.
Treatment
Meds

E: 5-FU cannot discriminate between cancer and healthy cells; therefore the side effects are diarrhea, mucositis,
leukopenia, mouth ulcers, and skin ulcers.

E: Cetuximab (Erbitux), a monoclonal antibody, may be given for advanced disease. This drug works by binding
to a protein (epidermal growth factor receptor) to slow cell growth.

E: Clients with advanced colorectal cancer and metastasis also receive drugs such as analgesics and antiemetics
for relief of symptoms, specifically pain and nausea.
Other

Non-surgical Management
o Radiation therapy: local or regional control of the disease; used postoperatively as a palliative measure
to reduce pain, hemorrhage, bowel obstruction, or metastasis
o Chemotherapy
o Targeted biotherapy – Bevacizumab (Avastin), Cetuximab (Erbitux)

Surgical Management
Colon rsn – bowel segment containing tumor is removed along w/ several inches of bowel beyond
tumor margin and regional lymph nodes, and an end-to-end anastomosis – open method or MIS
o Colectomy (colon removal) w/ temporary or permanent colostomy
o Abd peritoneal (A-P) rsn – sigmoid colon and rectum are removed, anus is closed, and a permanent
colostomy is formed
~ asc = liquid, transverse = pasty, desc = solid
Bowel perforation w/ peritonitis
Abscess
Fistula formation – to vagina or bladder
Frank hemorrhage – tumor may invade neighboring blood vessels and cause frank bleeding
Complete intestinal obstruction – tumors growing into bowel lumen can gradually obstruct and eventually block
intestine
o
Complications







GI obstruction
o ~ risk: previous GI surgery
BOWEL OBSTRUCTION

Can be partial or complete; intestinal contents accumulate at or above the obstruction

Mechanical obstruction  bowel is physically obstruction by disorders outside the intestine (adhesions or hernias) or blockages in
the lumen of the intestine (tumors, fecal impactions, and stricture)

Non-mechanical obstruction (paralytic or adynamic ileus)  peristalsis is decreased or absent, resulting in a slowing of the
movement or a backup of intestinal content caused by physiologic, neurogenic, or chemical imbalances: paralytic ileus is associated
w/ trauma, abd surgery, hypokalemia, MI, or vascular insufficiency

Strangulated obstruction  obstruction w/ compromised blood flow. SURGICAL EMERGENCY!
Assessment
Physical

E: A small bowel obstruction is characterized by upper or epigastric abdominal distention, metabolic alkalosis,
and a great amount of vomiting.

Chart 59-5 Key Features Small-Bowel and Large-Bowel Obstructions
o Small-Bowel Obstructions

Abd discomfort or pain possibly accompanied by visible peristaltic waves in upper and middle
abd

Upper or epigastric abd distention

N and early, profuse V (may contain fecal material)

Obstipation (no passage of stool)

Severe F&E imbalances

Metabolic alkalosis
o Large-Bowel Obstructions

Intermittent lower abd cramping

Lower abd distention

Minimal or no vomiting

Obstipation or ribbon-like stools

No major F&E imbalances

Metabolic acidosis (not always present)

Early  cramping - borborygmi (high-pitched BS) – intestine tries to push the mechanical obstruction forward

Later  BS absent, esp distal to the obstruction

Nonmechanical obstruction: pain described as constant, diffuse discomfort. Abd distention. Decreased BS in early
obstruction and absent BS in later stages. V of gastric contents and bile is frequent, but vomitus rarely has a foul
odor and is rarely profuse.
Diagnostic

Laboratory Assessment
tests
o WBC normal unless there is a strangulated obstruction in which case there may be leukocytosis
(increased WBCs)
o HGB, HCT, creat, and BUN often elevated, indicating dehydration
o Na+, Cl-, K+ reduced b/c of loss of F&E
o Elevation in serum amylase levels may be found w/ strangulating obstructions, which can damage the
pancreas
o High obstruction in small intestine have ABG values indicative of metabolic alkalosis
o Obstruction in large intestine may show values suggestive of metabolic acidosis

Imaging Assessment
o Flat-plate and upright abd x-rays and CT scan
o Distention w/ fluid and gas in small intestine w/ absence of gas in colon = obstruction in small intestine
o X-ray findings often normal when a strangulated obstruction exists in small intestine

Other
o Abd ultrasound to evaluate potential cause of obstruction
o Endoscopy (sigmoidoscopy or colonoscopy) to determine cause of obstruction, except when
perforation or complete obstruction is suspected
Treatment
Meds

Other




Complications





Pain management – opioid analgesics  withheld in diagnostic workup period so that clinical manifestations of
perforation or peritonitis are not masked
Broad-spectrum antibiotics if strangulation is suspected
Non-surgical Management
o NPO
o Semi-Fowler’s position helps alleviate pressure of abd distention on the chest
o Decompress GI tract by inserting or maintaining a gastric or intestinal tube, which can be inserted
nasally or orally
o Obstruction caused by fecal impaction resolves after disimpaction and enema
o Intussusception (telescoping of bowel) may result w/ hydrostatic pressure changes during a barium
enema or w/ manipulation under fluoroscopy
o Administer F&E replacement
o * changes from a colicky, intermittent pain to a constant discomfort can indicate perforation of the
intestine or peritonitis  ~ administer fluids…
Surgical Management
o Required for complete obstruction and for many cases of incomplete mechanical obstruction
o Exploratory laparotomy to locate obstruction and determine nature of the problem
o Examples of procedures:

lysis of adhesions

colon rsn w/ anastomosis for obstruction resulting from tumor or diverticulitis

embolectomy or thrombectomy for intestinal infarction

colon rsn and colostomy
Prevention of fecal impaction
o High fiber diet – raw vegetables, fruits, whole grain
o Drink adequate fluids esp water
o Do not routinely use laxatives –b/c it decreases abd muscle tone and contributes to atonic colon
o Exercise regularly
o Use natural foods to promote peristalsis like warm beverages and prune juice
o Take bulk forming products such as Metamucil to provide fiber
o Sit on toilet or bedtime commode
o Check stool for oozing, meaning obstruction
Absorption of F&E into the vascular space is compromised and can lead to reduced circulatory blood volume and
electrolyte imbalances
Hypovolemia
Perforation of intestine
Peritonitis
Sepsis, shock


Management of Clients with Musculoskeletal Disorders,
Trauma or Overuse
osteomyelitis causes and care
o ~ who’s at risk? What you do for it. Risk factors and treatment.
RA/OA
OSTEOARTHRITIS

Most common type of arthritis

Joint pain and loss of function characterized by progressive deterioration and loss of cartilage in the joints

Osteophytes

Synovitis

Subluxation
Assessment
Physical
Diagnostic
tests
Treatment
Meds
Other






Joint involvement
Heberden's nodes – DIP joints – painful and red
Bouchard’s nodes – PIP joints – “
Joint effusions – excess joint fluid
Atrophy of skeletal muscle – pain discourages movement of painful joints
Spine, esp L3-4 or C4-6 – radiating pain, stiffness, and muscle spasms in one or both extremities








Middle-aged or older women
Chronic joint pain and stiffness
Early: pain diminishes after rest and worsens after activity
Later: pain occurs w/ slight motion or even when at rest
Crepitus w/ ROM
Joint stiffness lasts <30 min after period of inactivity
ESR and high-sensitivity C-reactive protein (hsCRP) slightly elevated when secondary synovitis (synovial
inflammation) occurs
ESR tends to rise w/ age and infection



Analgesics
Glucosamine = decrease inflammation; careful w/ HTN, diabetics, anticoagulants
Chondroitin = increase/strengthen cartilage

Acetaminophen (Tylenol, Atasol) as the primary drug of choice because OA is not a primary anti-inflammatory
disorder.
NSAIDS
Opioids
Cortisone injection
Non-Surgical Management

Analgesics

Rest – local (immobilize unstable joint), systemic (nap), psychological

Positioning – position joints in their functional position

Thermal modalities – heat (decrease muscle tension), cold (numbing nerve endings and decreasing
secondary joint inflammation)

Weight control – less stress on weight-bearing joints, decrease pain, slow joint degeneration

Integrative therapies
Surgical Management

Total joint arthroplasty (TJA)









Total joint replacement (TJR)
Arthroscopy
Osteotomy
PP:
Sequestrectomy - Because bone cannot heal in the presence of necrotic tissue, a sequestrectomy may be
performed to débride the necrotic bone and allow revascularization of tissue. The excision of dead and
infected bone often results in a sizable cavity, or bone defect.

Bone grafts - The excision of dead and infected bone often results in a sizable cavity, or bone defect. The
use of bone grafts to repair bone defects is also widely used.

Bone segment transfers - When infected bone is extensively resected, reconstruction with
microvascular bone transfers may be done. Reserved for larger skeletal defects. Most common donor
sites are the patient's fibula and iliac crest.

Muscle flaps - The bone graft may have an attached muscle or skin flap, if necessary.

Amputation
Neurovascular (NV) assessments must be done frequently because the patient experiences increased swelling
after the surgical procedure. Elevate the affected extremity to increase venous return and thus control swelling.
~ fractures
~ DVT, VTE, PE


Complications


RHEUMATOID ARTHRITIS

One of the most common connective tissue diseases and the most destructive to the joints

Chronic, progressive, systemic inflammatory autoimmune disease affecting primarily the synovial joints

Autoantibodies (rheumatoid factors) formed that attack healthy tissue, especially synovium, causing inflammation

Affects synovial tissue of any organ or body system
Assessment
Physical
Early disease manifestations—joint stiffness, swelling, pain, fatigue, and generalized weakness and morning
stiffness

Late disease manifestations—as the disease worsens, the joints become progressively inflamed and quite painful

Frequent morning stiffness (gel phenomenon) which lasts for 45 min to several hours after awakening

PIP and MCP – slightly reddened, warm, stiff, swollen, tender or painful

Bilateral and symmetric

Migratory arthritis: migrating symptoms
Chart 20-7 Key Features The Patient with Rheumatoid Arthritis
Early Manifestations
Joint
• Inflammation
Systemic
• Low-grade fever
• Fatigue
• Weakness
• Anorexia
• Paresthesias
Late Manifestations
Joint
• Deformities (e.g., swan neck or ulnar deviation)
• Moderate to severe pain and morning stiffness
Systemic

Diagnostic
tests
Treatment
Meds
Other
Complications







• Osteoporosis
• Severe fatigue
• Anemia
• Weight loss
• Subcutaneous nodules
• Peripheral neuropathy
• Vasculitis
• Pericarditis
• Fibrotic lung disease
• Sjögren's syndrome (dry eyes/mouth/vagina)
• Renal disease
• Felty's syndrome (RA, hepatosplenomegaly, leukopenia)
rheumatoid factor (+) = rheumatoid disease
antinuclear antibody titer (+) = autoimmune disease
erythrocyte sedimentation rate  = inflammatory disease
serum complement
serum protein electrophoresis
serum immunoglobulins
Other diagnostic assessments—

x-ray – visualize joint changes an deformities

CT – may help determine presence and degree of cervical spine involvement

Arthrocentesis – monitor site for bleeding or leakage of synovial fluid. Notify physician.

bone scan – asses extent of joint involvement
NO GLUCOSAMINE OR CHONDROITIN

(1) Disease-modifying antirheumatic drugs – inflammation

(2) NSAIDs - inflammation

Biologic response modifiers

Other drugs:

Glucocorticoids

(3) Immunosuppressive agents

Gold therapy – don’t worry about this

Analgesic drugs
Non-pharmacologic Interventions

Adequate rest

Proper positioning

Ice and heat applications

Plasmapheresis

Gene therapy

Complementary and alternative therapies

Promotion of self-care

Carpal tunnel syndrome

Systemic Complications

Moderate to severe weight loss, fever, and extreme fatigue in late disease exacerbations

Subcutaneous nodules – ulnar surface of the arm, fingers, Achilles tendon

Vasculitis; periungal lesions – don’t worry about brown spots

Paresthesias – peripheral neuropathy associated w/ decreased circulation can cause foot drop and paresthesias

Respiratory complications: pleurisy, pneumonitis, diffuse interstitial fibrosis, and pulm HTN

Cardiac complications: pericarditis, myocarditis

Eye involvement: iritis, scleritis

Associated sydromes:
o Sjogren’s syndrome (dry eyes/mouth/vagina),
o Felty’s syndrome (RA, hepatosplenomegaly, leukopenia),
o Caplan’s syndrome (rheumatoid nodules in lungs and pneumoconiosis)

nursing management for patients with skin and skeletal traction
o ~ skin – boot, Velcro strap
o ~ skeletal – bone, infection issue
o
o
o
o
o
o
Traction




Application of a pulling force to the body to provide reduction, alignment, and rest at that site
Types of traction: skin, skeletal
Table 54-2 Types of Traction
Traction care:

Maintain correct balance between traction pull and countertraction force

Care of weights

Skin inspection

Pin care

Assessment of neurovascular status
Traction is the application of a pulling force to a part of the body to provide reduction, alignment, and rest. It is also used as a last
resort to decrease muscle spasm (thus relieving pain) and prevent or correct deformity and tissue damage. A patient in traction is
often hospitalized, but in some cases, home care is possible even for skeletal traction.
Skin traction involves the use of a Velcro boot (Buck's traction) (Fig. 54-5), belt, or halter, which is usually secured around the
affected leg.

The primary purpose: decrease painful muscle spasms that accompany hip fractures. The weight is used as a pulling
force and is limited to 5 to 10 pounds (2.3 to 4.5 kg) to prevent injury to the skin.
In skeletal traction, pins, wires, tongs (e.g., Crutchfield), or screws are surgically inserted directly into bone. These allow the use
of longer traction time and heavier weights—usually 15 to 30 pounds (6.8 to 13.6 kg). Skeletal traction aids in bone realignment.
Pin site care is an important part of nursing management to prevent infection.
The nurse may set up or assist in the setup of traction if specially educated. In larger or specialty hospitals or units, orthopedic
technicians or physician assistants often set up traction. Once traction is applied, maintain the correct balance between traction
pull and countertraction force.
Nursing Safety Priority Action Alert

When patients are in traction, weights usually are not removed without a prescription.

They should not be lifted manually or allowed to rest on the floor. Weights should be freely hanging at all times.

o
o
Teach this important point to UAP on the unit, to other personnel such as those in the radiology department, and to
visitors.

Inspect the skin at least every 8 hours for signs of irritation or inflammation. When possible, remove the belt or boot
that is used for skin traction every 8 hours to inspect under the device.
Check traction equipment frequently to ensure its proper functioning. Inspect all ropes, knots, and pulleys at least every 8 to 12
hours for loosening, fraying, and positioning. Check the weight for consistency with the health care provider's prescription.
Sometimes one of the weights is accidentally removed by a staff member or visitor who bumps into it. Replace the weights if
they are not correct, and notify the health care provider or orthopedic technician.
If the patient reports severe pain from muscle spasm, the weights may be too heavy or the patient may need realignment. Report
the pain to the health care provider if body realignment fails to reduce the discomfort. Assess neurovascular status of the affected
body part to detect circulatory compromise and tissue damage. The circulation is usually monitored every hour for the first 24
hours after traction is applied and every 4 hours thereafter.



Interventions include:

Emergency care: assess for respiratory distress, bleeding and head injury

Nonsurgical management: closed reduction and immobilization with a bandage, splint, cast, or traction
post op care and assessment after musculoskeletal surgery (hips, knees, fracture)
Management of Clients with Peripheral & Central Nervous
System Disorders


assessment & care of pts with spinal cord injury
o ~ complications?
 Incontinence,
 paralysis (skin, move regularly, CONTRACTURES, ROM), ***Alignment***
 respiratory – what kind of movement do you expect pt to have
 bowel care b/c they can’t go on their own.
 Need muscles of peristalsis to move bowel out of colon. Incontinence…
 Psychosocial – depression, ROLE conflict
 KNOW DIFF B/T AUTONOMIC DYSREFLEXIA AND SPINAL SHOCK
 Spinal shock – right after surgery. SWELLING  48-72 hrs??
 Nutrition – physically not putting food in mouth, depression, metabolic needs
MS/ALS/ MG/Guillain-Barré – priority care, meds, interventions
o ~ which one does this pt have? (assessment)
o ~ safety issues r/t diseases?
o ~ how to prevent complications that will kill pt
o ~ distinguish
o ~ psychosocial issues
First priority: ABC
After the airway is established, assess the patient’s breathing pattern.
Spinal nerve (C3-5) innervate the phrenic nerve, which controls the diaphragm.
A significant head injury, pneumothorax, hemothorax, and fracture may also cause respiratory distress.
C2 injury are common in older who fell from a low height.
Assessing motor function in Spinal cord injury:
-To assess C4-5, apply downward pressure while the patient shrugs his or her shoulders upward.
-To assess C5-6, apply resistance while the patient pulls up his or her arms.
-To assess C7, apply resistance while the patient straightens his or her flexed arms.
-To assess C8, make sure the patient is able to grasp an object and form a fist.
-To assess L2-4, apply resistance while the patient lifts his or her legs from the bed.
-To assess L5, apply resistance while the patient dorsiflexes his or her feet.
-To assess SI, apply resistance while the patient plantar flexes his or her feet.
The Patient with a Spinal Cord Injury intervention
Airway Management: Facilitation of patency of air passages.
Positioning: Neurologic: Achievement of optimal, appropriate body
alignment for the patient experiencing or at risk for spinal cord injury or
vertebral irritability.
• Position patient to maximize ventilation potential.
• Identify patient requiring actual/potential airway insertion.
• Insert oral or nasopharyngeal airway, as appropriate.
• Perform chest physical therapy, as appropriate.
• Remove secretions by encouraging coughing or by suctioning.
• Encourage slow, deep breathing; turning; and coughing.
• Instruct how to cough effectively.
• Assist with incentive spirometer, as appropriate.
• Auscultate breath sounds, noting areas of decreased or absent
ventilation and presence of adventitious sounds.
• Perform endotracheal or nasotracheal suctioning, as appropriate.
• Administer humidified air or oxygen, as appropriate.
• Regulate fluid intake to optimize fluid balance.
• Position to alleviate dyspnea.
• Monitor respiratory and oxygenation status, as appropriate.
• Immobilize or support the affected body part, as appropriate.
• Place in the designated therapeutic position.
• Maintain proper body alignment.
• Position with head and neck in alignment.
. Turn using the log roll technique.
• Apply an orthosis collar.
• Instruct on orthosis collar care, as needed.
• Apply and maintain a splinting or bracing device.
. Monitor skin integrity under bracing device/orthosis collar.
• Instruct on pin site care, as needed.
• Monitor traction pin insertion site.
• Perform traction/orthosis device pin insertion site care.
• Monitor traction device setup.
Spinal shock, also called spinal shock syndrome, occurs immediately as a concussion response to the injury. The patient has flaccid paralysis and
loss of reflex activity below the level of the lesion. It often lasts less than 48 hours but may continue for several weeks. Muscle spasticity begins in
patients with cervical or high thoracic injuries when spinal shock is resolved.




Spinal shock, also called spinal shock syndrome, occurs immediately as the cord’s response to the injury.
The patient has complete but temporary loss of motor, sensory, reflex, and autonomic function
Often lasts less than 48 hours but may continue for several weeks.
Several manifestations include:

absence of tactile sensation

absence of reflexes*

flaccid paralysis (inability to move) of all voluntary muscles*

hypoesthesia (decreased sensation)

hyperesthesia (increased sensation)

bladder incontinence

parasthesia or dull pain.
Autonomic dysreflexia
Symptoms
Emergency intervention
• Sudden onset of severe, throbbing headache
• Severe, rapidly occurring hypertension
• Bradycardia
• Flushing above level of lesion (face and
chest)
• Pale extremities below level of lesion
• Nasal stuffiness
• Sweating
• Nausea
• Blurred vision
• Piloerection (goosebumps)
• Feeling of apprehension
-Place patient in sitting position (first priority!).
-Page/notify health care provider.
- Loosen tight clothing on the patient.
-Assess for and treat the cause.
-Check the urinary catheter tubing (if present) for kinks or obstruction.
-If a urinary catheter is not present, check for bladder distention and catheterize immediately if
indicated.
-Place anesthetic ointment on tip of catheter before insertion
-Check the patient for fecal impaction; if present, disimpact immediately using anesthetic ointment.
-Check the room temperature to ensure that it is not too cool or drafty.
-Monitor blood pressures every 10 to 15 minutes.
-Give nitrates or hydralazine (Apresoline, Novo-Hylazin*) as prescribed.
Disease
Brief
pathophysiology/etiology
Manifestations
GuillainBarre
Syndrome
is an acute inflammatory Motor Manifestations:
demyelinating
• Ascending symmetric muscle
polyneuropathy (AIDP)
weakness → flaccid paralysis
that affects the peripheral
without muscle atrophy
nervous system, causing
• Decreased or absent deep
motor weakness and sensory
tendon reflexes (DTRs)
abnormalities. It is an
• Respiratory compromise
uncommon disorder,
(dyspnea, diminished breath
affecting both genders
sounds, decreased tidal volume
equally and peaking after age and vital capacity) and
55 years. As a result of
respiratory failure
demyelination (destruction of • Loss of bowel and bladder
the myelin sheath) of the
control (less common)
peripheral nerves,
• Ataxia
progressive motor weakness
and sensory abnormalities
Sensory Manifestations
occur. Symptoms typically
•Paresthesias
begin in the legs and spread
• Pain (cramping)
to the arms and upper body.
This is referred to as an
Progression
Nursing interventions
Progression of GBS
changes depending on
the variant of the
disease. The three
different types of
GBS are:
(1) ascending,
(2) pure motor
(3) descending.
- Managing the airway and
respiratory status.
- Monitor the ABG values
- keep emergency airway equipment
supplies at easy access.
- managing cardiac function
- pain management.
- improving mobility and preventing
effects of immobility.
- Tx – plasmapheresis
The ascending
affects the nervous
system functionality
(paresthesias) from
the feet rising up to
the head.
The pure motor
presents itself and
follows the same path
PP:
Ineffective breathing pattern
interventions:
- chest physiotherapy
- IS
- O2
- monitor ABG and vital capacity
- keep equipment for endotracheal
intubation at the bedside
ascending paralysis.
Cranial Nerve Manifestations
Paralysis can increase in
• Facial weakness
intensity until the muscles
•Dysphagia
cannot be used at all and the
• Diplopia
patient is almost totally
• Difficulty speaking
immobile. As a result, some
patients require mechanical Autonomic Manifestations
ventilation because of weak
• Labile (~easily altered) blood
or paralyzed respiratory
pressure
muscles. Healing occurs in
• Cardiac dysrhythmias
reverse; the neurons affected
•Tachycardia
last are the first to recover.
GBS is the result of a variety
PP:
of related immune-mediated
* muscle weakness and P have
pathologic processes. The
abrupt onset; cause remains
immune system starts to
obscure
destroy the myelin sheath
* cerebral function or pupillary
that surrounds the axons of
signs are NOT affected
the peripheral nerves or
* the most common clinical
attacks the axons themselves.
pattern is that the immune
Segmental demyelination
system starts to destroy the
(the destruction of myelin
myelin sheath surrounding the
between the nodes of
axons.
Ranvier) is the major
* weakness and paresthesia
pathologic finding in GBS.
begin in LE and progress upward
This destruction affects the
toward trunk, arms, and cranial
transmission of impulses
nerves in ascending GBS
from node to node by
slowing it down. Also, the
***COGNITIVE STATUS
brain receives fewer sensory
NOT AFFECTED.
signals, affecting the patient's
ability to feel textures, heat,
***REVERSIBLE
and pain. On the other hand,
the brain may receive altered
~ weakness. Takes naps a lot.
signals that cause the tingling
or “crawling-skin” sensation
many patients report.
*
as the ascending GBS
however this version
is absent of sensory
manifestations.
Descending GBS
starts in the face of
the patient usually
affecting the jaw
muscles making its
way downward. This
type can be more life
threatening due to the
fact that it affects
respiratory function
soon in the disease
process.
Interventions for cardiac
dysfunction:
- can affect both the sympathetic and
parasympathetic systems
- client placed on cardiac monitor
b/c of risk for arrhythmias
- HTN treated w/ beta blocker or
nitroprusside
- IV fluids for hypotension; client
placed in supine position
- atropine may be used for
bradycardia
Drug Therapy
- plasmapheresis (remove
immune complexes and then
give blood back) or IV
immunoglobulin
- plasma exchange
- IV immunoglobulin
- NO corticosteroids
EVOLVE
* has three acute stages
* demyelination of peripheral
neurons
* affect resp status and
muscle function
Myasthenia
Gravis (MG)
“gravity”
is an acquired autoimmune
disease characterized by
fatigue and weakness
primarily in muscles
innervated by the cranial
nerves, as well as in skeletal
and respiratory muscles. This
autoimmune disease of the
neuromuscular junction may
take many forms—from mild
Motor Manifestations
• Progressive muscle weakness
(proximal) that usually improves
with rest
• Poor posture
• Ocular palsies
• Ptosis
• Weak or incomplete eye
closure
• Diplopia
The onset of MG is
usually insidious.
This starts with a
rapid onset of fatigue.
In more severe cases
all muscle groups are
affected, in most all
cases some facial
component is always
affected.
- Provide respiratory support
- promote mobility with pt doing as
much as possible.
- Rx therapy:
anticholinesterases and
immunosuppressants
- Teach the patient and family to
monitor for these two types of crises:
- Myasthenic crisis—an
exacerbation (flare-up or worsening)
disturbances of the ocular
muscles to a rapidly
developing, generalized
weakness that may lead to
death from respiratory
failure. It has remissions and
exacerbations (worsening or
“flare-ups”). Although MG
can present at any age, it is
less commonly seen in the
United States than GuillainBarré syndrome. The
incidence is equal between
men and women.
MG is caused by an
autoantibody attack on the
acetylcholine receptors
(AChRs) in the muscle end
plate membranes. As a result,
nerve impulses are not
transmitted to the skeletal
muscle at the neuromuscular
junction and the muscles
cannot contract.
EVOLVE
* autoimmune disease w/
ocular symptoms
* characterized by
exacerbations and
remissions
* affect resp status and
muscle function
* should not take OTC
drugs w/o checking w/
health care provider
Amyotrophic
Lateral
Sclerosis
(ALS)
Lou Gehrig’s
disease
Patho:
-adult onset upper and
lower motor neuron
disease.
-characterized by progressive
weakness, muscle wasting
and spasticity eventually
leading to paralysis
PP:
There is loss of anterior horn
cells, so that patients present
with progressive weakness
that proceeds to paralysis
from neurogenic muscular
atrophy. Because of the loss
• Respiratory compromise
Sensory Manifestations
• Muscle achiness
• Paresthesias
• Decreased sense of smell and
taste
*** assess muscle strength in
FACE & NECK!
*** biggest concern is
AIRWAY b/c problem
swallowing (dysphagia)
*** diplopia, trouble focusing
b/c decrease control of muscles
that move eyes.
*** associated w/ thymus.
Thymectomy.
*** like MS, worse w/ exertion
and exercise. Schedule rest
periods.
***Eye muscles, speech ability
and patterns.
* AChR – Tensilon Testing.
Diagnostic Test
~ Tensilon Test 
vagus nervous
system decreases
HR (vagal
response, then you
are positively
diagnosed w/ MG.
Tensilon test we
administer
cholinergic agent to
see if you have
positive response
to cholinergic
agent. If you have
positive test, you
are positive for MG.
of the myasthenic symptoms caused
by not enough anticholinesterase
drug
- Tx- maintaining adequate
respiratory function.
*** give the meds
Characteristics:
Increase P and resp
Rise in BP
Anoxia
Cyanosis
Bowel and bladder incontinence
Decreased urine output
Absence of cough and swallow
reflex
- Cholinergic crisis—an acute
exacerbation of muscle weakness
caused by too many
anticholinesterase drugs
- Tx- immunosuppression with
corticosteroids.
***Hold the meds
Characteristics:
N/V
Diarrhea
Abd cramps
Blurred vision
Pallor
Facial muscle twitching
Pupillary miosis
hypotension
PP:
- cholinesterase-inhibitor drugs
- immunosuppressants
- corticosteroids for
immunosuppression
- plasmapheresis
PP:
Early symptoms:
-fatigue while talking,
-tongue atrophy
-dysphagia
-weakness of the hands and arms
-fasciculations
-nasal quality of speech
Dysarthria
Drooling
PP:
- no known cure, no treatment, no
preventive measures
- Riluzole, only drug approved by
FDA to extend survival time
(monitor kidney)
- exercise and mobility program
- management of swallowing
difficulties
- respiratory support
PNS
- SKIN
- feeding tube
- DVT
Pt cannot move!
****DOESN’T AFFECT
MENTAL STATUS
DIFFERENTIATES ALS AND
of anterior horn cells, the
anterior (ventral) spinal
motor nerve roots
demonstrate atrophy
M.S.
no cognitive involvement.
You know everything going on
but you can’t speak… 
Motor neurons are
SCARRED
Later, muscles of respirations.
Riluzole – 50 mg bid on an empty
stomach. Monitor for liver toxicity.
Inability to walk.
All b/c of weakness.
Hyporeflexivity – twitching.
Fasciculations.
Speech b/c inability to use
muscles necessary.
Senses and cognition will
remain.
No specific test. Usually follow a
viral infection and onset of GBS
but we don’t really know. Acts
much like MS in which in
demyelinates the sheaths.
Multiple
Sclerosis
(MS)
“myelin
sheaths”
Patho:
autoimmune disease.
characterized by an
inflammatory response that
results in diffuse random or
patchy areas of plaque in the
white matter (axons). In
Particularly it affects optic
nerves, pyramidal tracts,
posterior columns, brainstem
nuclei, and periventricular
region of brain. Myelin
sheath damaged and its
thickness reduced
(demyelinated). Slows down
electrochemical transmission
of impulses between the
brain and spinal cord. Can
lead to complete blockage
over time.
Etiology:
cause unknown. thought to
be d/t viral, immunologic,
and genetic (first-degree) and
environmental etiologic
factors. Pre disposition
determined by antigens
(HLA DR2 and DQ6). tends
to affect family members,
especially siblings.
Things that exacerbate
Ability to move
increased fatigue and stiffness of
the extremities particularly in the
legs, continuous sensitivity to
temperature, flexor spasm at
night, increased or hyperactive
deep tendon reflexes , clonus,
positive Babinski’s reflex, absent
abdominal reflexes, gait
unsteady because of weakness
Cerebellar:
intention tremor (tremor when
performing an activity),
dysmetria (inability to direct or
limit movement),
dysdiadochokinesia (inability to
stop one motor impulse and use
another, clumsy motor
movements, loss of balance, poor
coordination
Cranial nerves and brainstem
tinnitus (ringing in both ears),
vertigo (dizziness), hearing loss,
facial weakness and dysphagia,
dysarthria ( slurred speech)
Vision:
blurred vision, diplopia (double
vision), decreased visual acuity,
scotomas (changes in peripheral
vison, scotomas (changes in
Chronic and
progressive disease
with no cure.
Symptoms progress
in severity over time.
Initial symptoms so
vague that most of the
time goes unnoticed
for years. disease
does not affect life
expectancy.
monitor effects on immune system,
prevent exacerbations, manage
symptoms, improve function.
requires collaborative care.
The onset is usually
between 20-40 years
of age, and occurs
twice as often in
women.
-immunosupressive agents to reduce
the frequency of relapses
-antispasmodics to treat muscle
spasticity
-immunodulators to prevent relaspse
-anticonvulsants for paresthesia
-stool softeners for constipation
-anticholinergics for bladder
dysfunction
-beta-blockers for tremors
4 types:
relapsing-remitting
MS (RRMS)
-most common
-mild to moderate,
depends on the
degree of disability
-symptoms develop
and resolve in a few
weeks to months
-patient returns to
baseline
primary progressive
Drug therapy:
one or more of:
-interferon beta
-natalizumab
-glatirame
Promoting mobility and managing
symptoms
-team with PT
-include ROM, stretching, and
strengthening
Health teaching
-promote community resources and
respite services for patient and
family
relapse:
-viruses and infectious agents
-living in a cold climate
-physical injury
-emotional stress
-pregnancy
-fatigue
-overexertion
-temperature extremes
-hot shower/bath
peripheral vision), nystagmus
(involuntary, rapid eye
movement)
Sensory:
hypalgesia (diminished
sensitivity to pain), paresthesia,
facial pain, decreased
temperature perception,
numbness tingling, burning,
crawling sensations
If demyelination has occurred:
-bowel and bladder dysfunctions
-alterations in sexuality
-flexic bladder
-frequency
-urgency
-nocturia
PP:
Common physical assessment
- key feature is muscle weakness
and spasticity
Findings include:
- flexor spasms at night
- intention tremor
- dysmetria
- blurred vision, diplopia,
decreased visual acuity
- tinnitus, vertigo
- hypalgesia, numbness, tingling
or burning
- bowel and bladder dysfunction
- Cognitive changes come later
in the disease
*** assess mental status
MS (PPMS)
-steady and gradual
neurological
deterioration without
remission of
symptoms
-progressive
disability with no
acute attacks
-usually 40-60 yrs old
during onset
secondary
progressive MS
(SPMS)
-begins with
relapsing-remitting
course
-later becomes
rapidly progressive
-functioning
continues to decline
with no clear times of
remission
progressiverelapsing (PRMS)
-frequent relapses
with some partial
recovery, but never
back to baseling
-progressive and
cumulative symptoms
and deterioration
occur over several
years
-avoid overexertion , stress,
extremes in temperature, humidity,
people with upper respiratory tract
infections
-explain all medications upon
discharge
-how to differentiate side effects
from adverse or allergic reactions
-devices to promote ADL’s
-include information about bowl and
bladder management, skin care,
nutrition, and positioning techniques
-importance of adequate rst
-engage in regular social activities
-coping strategies
**** quality of life.
ADLs. #1 goal.
Longer, better functioning life.
Helping support immune system.
Management of clients with Functional and Structural Cardiac
Disorders

clinical manifestations associated with selected structural abnormalities of the heart (valves and cardiomegaly)
VALVULAR
DISORDERS
(General)
includes mitral stenosis (valve
thickening by fibrosis and
calcification), mitral regurgitation
(prevents valve from closing
Mitral stenosis- fatigue, dyspnea
on exertion, orthopnea, neck
vein distention, pitting edema,
afib, paroxysmal nocturnal
Nonsurgical management focus on drug
therapy & rest (~don’t wanna overwork
heart to reduce risk of HF)
-monitor ECG for development of irregular
ENDOCARDITIS

completely during systole which
allows for backflow of blood),
mitral prolapse ( valvular leaflets
enlarge and prolapse into left
atrium), aortic stenosis (orifice
narrows and obstructs left
ventricular outflow and the
resistance leads to ventricular
hypertrophy, and aortic
regurgitation ( valve leaflets don’t
close properly during diastole
which allows backflow from aorta
back into L ventricle..
dyspnea, hemoptysis,
hepatomegaly, apical diastolic
murmur
Mitral regurg.- fatigue, dyspnea
on exertion, orthopnea, neck
vein distention, pitting edema,
afib, palpitations, high-pitched
holosystolic murmur
Mitral Prolapse- atypical chest
pain, dizziness, syncope,
palpitations, atrial tachycardia,
ventricular tach., systolic click
Aortic stenosis- dyspnea on
exertion, angina, syncope on
exertion, orthopnea, paroxysmal
nocturnal dyspnea, harsh
systolic crescendo decrescendo
murmur
Aortic regurg.- fatigue, dyspnea,
orthopnea, paroxysmal
nocturnal dyspnea, angina,
sinus tach, blowing decrescendo
diastolic murmur
heart rhythm and notify doctor if one
develops.
-a balance of rest and exercise is needed
to prevent skeletal muscle atrophy and
fatigue.
-Surgery such as valvuloplasty (opens
stenosis valve) may be needed and it is
the nurses priority afterwards to observe
for bleeding from the catheter insertion
site and institute post-angiogram
precautions.
-assess for signs of regurgitant valve by
monitoring heart sounds, CO, and heart
rhythm.
-observe for signs of systemic emboli
(~**thromboemboli: give anticoagulants)
~prophylactic antibiotics (prevent
infection)
~cardiac diet (low salt diet to decrease
volume and decrease pressure)
~diuretics to decrease fluid volume
(monitor F&E for imbalance)
refers to a microbial infection
involving the
endocardium. Occurs primarily in
patients who abuse IV drugs,
have had valve replacements,
have experienced systemic
infection or have natural cardiac
defects. With Cardiac defect,
blood may flow rapidly from a
high pressure area to a low
pressure zonem eroding section
of the endocardium. Platelets and
fibrin adhere to the denuded
endocardium, forming a
vegetative lesion. For
bacteremia, bacteria becomes
trapped in the low pressure
sinkhole and are deposited in the
vegetation. Additional platelets
and fibrin are deposited, which
causes the vegetative lesions to
grow. The endocardium and
valve are destroyed. Valvular
insufficiency may result when the
lesions interfere with normal
alignment of the valve. if
vegetations become so large that
blood flow through the valve is
obstructed the valve appears
stenotic and then likely to
embolize.
almost all endocarditis develop
heart mumurs. heart failure is
the most common cause of
ineffective endocarditis. Assess
for right sided HF (as evidenced
by peripheral edema weight gain
and anorexia) and left sided as
evidenced by fatigue shortness
of breath, and crackles on
auscultation of breath sounds).
-fever associated with chills
night sweats, malaise, and
fatigue
-anorexia and weight loss
-cardiac murmur
-development of heart failure
-evidence of systemic
embolization
-petechiae
-splinter hemorrhages
-oslers nodes ( on palms and
soles of feet)
-janesways lesions (flate
reddened macules on hands
and feet)
care of the patients with endocarditis
usually includes antimicrobials, rest
balanced with activity, and supportive
therapy for HF. if not successful then
surgery is required.
antimicrobials are the main treatment with
the choice of drug depending on the
specific organism involved.
because vegetative surround and protect
the offending microorganisms an
appropriate drug must be given in a
sufficiently high dose to ensure
its destruction. Most are given 4-6 weeks.
balance the patients activities with
adequate rest. consistently
use appropriate aseptic technique to
protect the patient from contact with
potential infective organisms.
Group Study
o mitral stenosis – under 45, rheumatic fever

physical manifestations of and assessment of pts with CHF
o Left ventricular failure is associated with decreased cardiac output and elevated pulmonary venous pressure. It may appear
clinically as:
•
Weakness
•
Fatigue
•
Dizziness
•
Acute confusion
•
Pulmonary congestion
•
Breathlessness
•
Oliguria (scant urine output)
o The pulse may be tachycardic, or it may alternate in strength (pulsus alternans). Take the apical pulse for a full minute, noting
any irregularity in heart rhythm. An irregular heart rhythm resulting from premature atrial contractions (PACs), premature
ventricular contractions (PVCs), or atrial fibrillation (AF) is common in HF
o Chart 37-1 Key Features Left-Sided Heart Failure
•
DECREASED CARDIAC OUTPUT

Fatigue

Weakness

Oliguria during the day (nocturia at night)

Angina

Confusion, restlessness

Dizziness

Tachycardia, palpitations

Pallor

Weak peripheral pulses

Cool extremities
•
PULMONARY CONGESTION


Hacking cough, worse at night

Dyspnea/breathlessness

Crackles or wheezes in lungs

Frothy, pink-tinged sputum

Tachypnea - respiratory rate typically exceeds 20 breaths/min.

S3/S4 summation gallop - often the first sign of HF
o Laboratory Assessment
•
Electrolyte imbalance may occur from complications of HF or as side effects of drug therapy, especially diuretic
therapy. Regular evaluations of a patient's serum electrolytes, including sodium, potassium, magnesium, calcium, and
chloride, are essential.
•
Any impairment of renal function resulting from inadequate perfusion causes elevated blood urea nitrogen and serum
creatinine and decreased creatinine clearance levels.
•
Hemoglobin and hematocrit tests should be performed to identify HF resulting from anemia.
•
If the patient has fluid volume excess, the hematocrit levels may be low as a result of hemodilution.
•
B-type natriuretic peptide (BNP) is used for diagnosing HF (in particular, diastolic HF) in patients with acute
dyspnea. As discussed earlier, it is part of the body's response to decreased cardiac output from either left or right
ventricular dysfunction. An increase in BNP, in conjunction with history and physical, best differentiates between the
dyspnea of HF and that associated with lung dysfunction (Wexler et al., 2009). However, patients with renal disease
may also have elevated BNP levels (Chen et al., 2010).
•
Urinalysis may reveal proteinuria and high specific gravity.
•
Microalbuminuria is an early indicator of decreased compliance of the heart and occurs before the BNP rises. It serves
as an “early warning detector” that lets the health care provider know that the heart is experiencing early signs of
decreased compliance, long before symptoms occur.
•
Arterial blood gas (ABG) values often reveal hypoxemia (low blood oxygen level) because oxygen does not diffuse
easily through fluid-filled alveoli. Respiratory alkalosis may occur because of hyperventilation; respiratory acidosis
may occur because of carbon dioxide retention. Metabolic acidosis may indicate an accumulation of lactic acid.
•
CXR  heart enlarged (cardiomegaly), representing hypertrophy or dilation
•
Echocardiography is considered the best tool in diagnosing heart failure.

Cardiac valvular changes, pericardial effusion, chamber enlargement, and ventricular hypertrophy can be
diagnosed using this noninvasive technique. The test can also be used to determine ejection fraction.
o ~ Interventions:
•
Vavluloplasty - Open stenosis valve
o Chart 37-2 Key Features Right-Sided Heart Failure
•
Systemic Congestion

Jugular (neck vein) distention

Enlarged liver and spleen

Anorexia and nausea

Dependent edema (legs and sacrum)

Distended abdomen

Swollen hands and fingers

Polyuria at night

Weight gain

Increased blood pressure (from excess volume) or decreased blood pressure (from failure)
o TABLE 37-1 COMMON CAUSES AND RISK FACTORS FOR HEART FAILURE
•
Hypertension
•
Coronary artery disease
•
Cardiomyopathy
•
Substance abuse (alcohol and illicit/prescribed drugs)
•
Valvular disease
•
Congenital defects
•
Cardiac infections and inflammations
•
Dysrhythmias
•
Diabetes mellitus
•
Smoking/tobacco use
•
Family history
•
Obesity
•
Severe lung disease
•
Sleep apnea
•
Hyperkinetic conditions (e.g., hyperthyroidism)
nursing interventions and patient teaching for patients with CHF
o Chart 37-4 Home Care Assessment The Patient with Heart Failure
•
Assess for signs of heart failure, including:

Changes in vital signs (heart rate >100 beats/min at rest, new atrial fibrillation, blood pressure <90 or >150
systolic)

o
o
o
Indications of poor tissue perfusion:
o Fatigue
o Angina
o Activity intolerance
o Changes in mental status
o Pallor or cyanosis
o Cool extremities

Indications of congestion:
o Presence of cough or dyspnea
o Weight gain
o Jugular venous distention and peripheral edema
•
Assess functional ability, including:

Performance of ADLs

Mobility and ambulation (review frequency and duration of walking, development of symptoms, and pulse
rate)

Cognitive ability

Assess nutritional status, including:

Food and fluid intake

Intake of sodium-rich foods

Alcohol consumption

Skin turgor

Assess home environment, including:

Safety hazards, especially related to oxygen therapy

Structural barriers affecting functional ability

Social support (family, home health services)

Assess the patient's adherence and understanding of illness and its treatment, including:

Signs and symptoms to report to health care provider

Dosages, effects, and side or toxic effects of medications

When to report for laboratory and health care provider visits

Ability to accurately weigh self on scale

Presence of advance directive

Use of home oxygen, if appropriate
•
Assess patient and caregiver coping skills
TABLE 37-4 HEART FAILURE SELF-MANAGEMENT HEALTH TEACHING (MAWDS)
•
Medications:

•Take medications as prescribed, and do not run out.

•Know the purpose and side effects of each drug.

•Avoid NSAIDs to prevent sodium and fluid retention.
•
Activity:

•Stay as active as possible, but don't overdo it. - When exercise is indicated, teach the patient to begin
walking 200 to 400 feet per day. At home the patient should try to walk at least three times a week and
should slowly increase the amount of time walked over several months.

•Know your limits.

•Be able to carry on a conversation while exercising.
•
Weight:

•Weigh each day at the same time on the same scale to monitor for fluid retention.
•
Diet:

•Limit daily sodium intake to 2 to 3 grams as prescribed.

•Limit daily fluid intake to 2 liters.
•
Symptoms:

•Note any new or worsening symptoms, and notify the health care provider immediately.
Nursing Safety Priority Action Alert
•
Per the HF Core Measure for discharge instructions, teach the patient and caregiver to immediately report to the health
care provider the occurrence of any of these symptoms, which could indicate worsening or recurrent heart failure:
•
•Rapid weight gain (3 lb in a week or 1 to 2 lb overnight)
•
•Decrease in exercise tolerance lasting 2 to 3 days
•
•Cold symptoms (cough) lasting more than 3 to 5 days
•
•Excessive awakening at night to urinate - nocturia
•
•Development of dyspnea or angina at rest or worsening angina
•
•Increased swelling in the feet, ankles, or hands
Chart 37-5 Patient and Family Education: Preparing for Self-Management Beta Blocker/Digoxin Therapy
•
• Establish same time of day to take this medication every day.
•
• Continue taking this medication unless your health care provider tells you to stop.
•
• Do not take digoxin at the same time as antacids or cathartics (laxatives).
•
•
•
•
o
o

• Take your pulse rate before taking each dose of digoxin. Notify your health care provider of a change in pulse rate
(60 to 100 beats/min is normal) or rhythm, as well as increasing fatigue, muscle weakness, confusion, or loss of
appetite (signs of digoxin toxicity).
• If you forget to take a dose, it may be delayed a few hours. However, if you do not remember it until the next day,
you should take only your usual daily dose.
• Report for scheduled laboratory tests (e.g., potassium and digoxin levels).
• If potassium supplements are prescribed, continue the dose until told to stop by your health care provider.
The priority problems for patients with heart failure (HF) include:
•
1. Impaired Gas Exchange related to ventilation/perfusion imbalance
•
2. Decreased Cardiac Output related to altered contractility, preload, and afterload
•
3. Fatigue and weakness related to hypoxemia
•
4. Potential for pulmonary edema related to left-sided HF
diagnostic studies used to assess clients with cardiac disorders
o valves

o Cardiomyopathy - subacute or chronic disease of cardiac muscle, and the cause may be unknown

Etiologies:

ETOH

Hypertension

CAD

idiopathic

Heart enlarged, muscle thickens and stiffens

Weaken the ability to pump blood

TYPES:

Dilated - DCM involves extensive damage to the myofibrils and interference with myocardial metabolism.
Ventricular wall thickness is normal, but both ventricles are dilated (left ventricle is usually worse) and
systolic function is impaired. Causes may include alcohol abuse, chemotherapy, infection, inflammation, and
poor nutrition. Decreased CO from inadequate pumping of the heart causes the patient to experience dyspnea
on exertion (DOE), decreased exercise capacity, fatigue, and palpitations.
o Most common
o Stasis in the ventricles
o Treat like CHF
o Inotropics
o Diuretics
o Antidysrhythmics
o Rest
o Signs and symptoms

Fatigue and weakness

HF (left side)

Dysarhythmias or heart block

Systemic or pulmonary emboli

S3 and S4 gallops

Moderate to severe cardiomegaly
o Treatment

Symptomatic treatment of HF

Vasodilators

Control of dysrhythmias

Surgery: heart transplant


o
Hypertropic - asymmetric ventricular hypertrophy and disarray of the myocardial fibers. Left ventricular
hypertrophy leads to a stiff left ventricle, which results in diastolic filling abnormalities. Obstruction in the
left ventricular outflow tract is seen in most patients with HCM. In about half of patients, HCM is transmitted
as a single-gene autosomal dominant trait
o Usually under age 30
o Sudden death in professional athletes
o Hank Gathers
o Reggie Lewis
Restrictive - characterized by stiff ventricles that restrict filling during diastole. Symptoms are similar to left
or right heart failure (HF) or both. The disease can be primary or caused by endocardial or myocardial
disease such as sarcoidosis or amyloidosis. The prognosis for this type of cardiomyopathy is poor.
o Infiltrative process
o Fibrosis & thickening
o Inpaired diastolic stretch
o Ventricular stretch

cardiac infections

infective endocarditis
o Assess the patient's cardiovascular status. Almost all patients with infective endocarditis develop
murmurs. Carefully auscultate the precordium, noting and documenting any new murmurs (usually
regurgitant in nature) or any changes in the intensity or quality of an old murmur. An S3 or S4 heart
sound also may be heard.
o Heart failure (HF) is the most common complication of infective endocarditis. Assess for rightsided HF (as evidenced by peripheral edema, weight gain, and anorexia) and left-sided HF (as
evidenced by fatigue, shortness of breath, and crackles on auscultation of breath sounds). See
discussion of HF earlier in this chapter.
o Arterial embolization is a major complication in up to half of patients with infective endocarditis.
Fragments of vegetation break loose and travel randomly through the circulation. When the left
side of the heart is involved, vegetation fragments are carried to the spleen, kidneys, GI tract, brain,
and extremities. When the right side of the heart is involved, emboli enter the pulmonary
circulation.
o Splenic infarction with sudden abdominal pain and radiation to the left shoulder can also occur.
When performing an abdominal assessment, note rebound tenderness on palpation. The classic pain
described with renal infarction is flank pain that radiates to the groin and is accompanied by
hematuria (red blood cells in the urine) or pyuria (white blood cells in the urine). Mesenteric
emboli cause diffuse abdominal pain, often after eating, and abdominal distention.
o The most reliable criteria for diagnosing endocarditis include positive blood cultures, a new
regurgitant murmur, and evidence of endocardial involvement by echocardiography.
o


A positive blood culture is a prime diagnostic test. Both aerobic and anaerobic specimens are
obtained for culture. Some slow-growing organisms may take 3 weeks and require a specialized
medium to isolate. Low hemoglobin and hematocrit levels may also be present.

Chart 37-8 Key Features Infective Endocarditis

• Fever associated with chills, night sweats, malaise, and fatigue

• Anorexia and weight loss

• Cardiac murmur (newly developed or change in existing)

• Development of heart failure

• Evidence of systemic embolization

• Petechiae

• Splinter hemorrhages

• Osler's nodes (on palms of hands and soles of feet)

• Janeway's lesions (flat, reddened maculae on hands and feet)

• Positive blood cultures

Interventions:
o Antimicrobials – main treatment; 4-6 weeks; STREP.
o Rest, balanced with activity
o Supportive therapy for heart failure
o Anticoagulants
o Surgical management

•Removing the infected valve (either biologic or prosthetic)

•Repairing or removing congenital shunts

•Repairing injured valves and chordae tendineae

•Draining abscesses in the heart
Rheumatic Carditis (AKA Rheumatic heart disease

Rheumatic carditis, also called rheumatic endocarditis, is a sensitivity response that develops after an upper
respiratory tract infection with group A beta-hemolytic streptococci

~ mitral valve stenosis

Rheumatic carditis is one of the major indicators of rheumatic fever. The common manifestations are:
o
•Tachycardia
o
•Cardiomegaly (enlarged heart)
o
•Development of a new murmur or a change in an existing murmur
o • Pericardial friction rub
o • Precordial pain
o • Electrocardiogram (ECG) changes (prolonged PR interval)
o • Indications of heart failure (HF)
o • Evidence of an existing streptococcal infection

Primary prevention is extremely important. Teach all patients to remind their health care providers to provide
appropriate antibiotic therapy if they develop the indications of streptococcal pharyngitis:
o
•Moderate to high fever
o
•Abrupt onset of a sore throat
o
•Reddened throat with exudate
o
•Enlarged and tender lymph nodes

Penicillin is the antibiotic of choice for treatment. Erythromycin (Eryc, Erythromid ) is the alternative for
penicillin-sensitive patients.
Pericarditis

Chart 37-9 Best Practice for Patient Safety & Quality Care - Care of the Patient with Pericarditis
o
•Assess the nature of the patient's chest discomfort. (Pericardial pain is typically substernal. It is
worse on inspiration and decreases when the patient leans forward.)
o
•Auscultate for a pericardial friction rub.
o
•Assist the patient to a position of comfort.
o
•Provide anti-inflammatory agents as prescribed.
o
•Explain that anti-inflammatory agents usually decrease the pain within 48 hours.
o
•Avoid the administration of aspirin and anticoagulants because these may increase the
possibility of tamponade.
o
•Auscultate the blood pressure carefully to detect paradoxical blood pressure (pulsus paradoxus),
a sign of tamponade:
o
•Palpate the blood pressure, and inflate the cuff above the systolic pressure.
o
•Deflate the cuff gradually, and note when sounds are first audible on expiration.
o
•Identify when sounds are also audible on inspiration.
o
•Subtract the inspiratory pressure from the expiratory pressure to determine the amount of
pulsus paradoxus (>10 mm Hg is an indication of tamponade).
o
•Inspect for other indications of tamponade, including jugular venous distention with clear lungs,
muffled heart sounds, and decreased cardiac output.
o
•Notify the physician if tamponade is suspected.
Acute pericarditis is most commonly associated with:
o
•Infective organisms (bacteria, viruses, or fungi) (usually respiratory)
o
•Post–myocardial infarction (MI) syndrome (Dressler's syndrome)
o
•Post-pericardiotomy syndrome
o
•Acute exacerbations of systemic connective tissue disease

Chronic constrictive pericarditis occurs when chronic pericardial inflammation causes a fibrous thickening of
the pericardium. It is caused by tuberculosis, radiation therapy, trauma, renal failure, or metastatic cancer. In
chronic constrictive pericarditis, the pericardium becomes rigid, preventing adequate filling of the ventricles
and eventually resulting in cardiac failure.

Assessment
o Assessment findings for patients with acute pericarditis include substernal precordial pain that
radiates to the left side of the neck, the shoulder, or the back. Pain is classically grating and
oppressive and is aggravated by breathing (mainly on inspiration), coughing, and swallowing. The
pain is worse when the patient is in the supine position and may be relieved by sitting up and
leaning forward. Ask specific questions to evaluate chest discomfort to differentiate it from the pain
associated with an acute MI (see Chapter 40).
o A pericardial friction rub may be heard with the diaphragm of the stethoscope positioned at the left
lower sternal border. This scratchy, high-pitched sound is produced when the inflamed, roughened
pericardial layers create friction as their surfaces rub together.
o Patients with acute pericarditis may have an elevated white blood cell count and usually have a
fever. Therefore blood culture and sensitivity may be analyzed in the laboratory. The ECG usually
shows ST-T spiking with the onset of inflammation, which returns to baseline with treatment.
Atrial fibrillation is also common. Echocardiograms may be used to determine a pericardial
effusion.
o Patients with chronic constrictive pericarditis have signs of right-sided HF, elevated systemic
venous pressure with jugular distention, hepatic engorgement, and dependent edema. Exertional
fatigue and dyspnea are common complications. Thickening of the pericardium is seen on
echocardiography or a computed tomography (CT) scan.

Interventions
o The focus of collaborative management is to relieve pain and treat the cause of pericarditis before
severe complications occur.
o NSAIDS for pain
CAD - broad term that includes chronic stable angina and acute coronary syndromes. It affects the arteries that provide blood,
oxygen, and nutrients to the myocardium. When blood flow through the coronary arteries is partially or completely blocked,
ischemia and infarction of the myocardium may result. Ischemia occurs when insufficient oxygen is supplied to meet the
requirements of the myocardium. Infarction (necrosis, or cell death) occurs when severe ischemia is prolonged and decreased
perfusion causes irreversible damage to tissue.

Cardiovascular Disease

Leading single cause of death

Risk Factors
o Nonmodifiable

Age, gender, family history, ethnic background,

Age is the most important risk factor for developing CAD in women. - When they are
older than 40 years, women are more likely than men to die within 1 year after their MI
o Modifiable - diet, exercise, smoking

•Elevated serum lipid levels

•Tobacco use

•Limited physical activity

•Hypertension

•Diabetes mellitus

•Obesity

•Excessive alcohol

•Stress
o Chart 40-1 Patient and Family Education: Preparing for Self-Management
o Prevention of Coronary Artery Disease
o Smoking

• If you smoke, quit.

• If you don't smoke, don't start.
o Diet

• Consume sufficient calories for your body to include:

•Less than 7% from saturated fats

•Avoiding trans fatty acids

• Limit your cholesterol intake to less than 200 mg/day.

• Limit your sodium intake as specified by your health care provider.

o
o


Cholesterol

• Have your lipid levels checked regularly.

• If your cholesterol and LDL levels are elevated, follow your health care provider's
advice.
o Physical Activity

• If you are middle-aged or older or have a history of medical problems, check with
your health care provider before starting an exercise program.

• Appropriate exercise should be enjoyable, burn 400 calories per session, and sustain a
heart rate of 120 to 150 beats/min, depending on your age.

• Exercise periods should be at least 20 to 30 minutes long with 10-minute warm-up
and 5-minute cool-down periods.

• If you cannot exercise moderately three to five times each week, walk daily for 30
minutes at a comfortable pace.

• If you cannot walk 30 minutes daily, walk any distance you can (e.g., park farther
away from a site than necessary; use the stairs, not the elevator, to go one floor up or two
floors down).

Diabetes

• Manage your diabetes with your health care provider.
o Blood Pressure

• Have your blood pressure checked regularly.

• If your blood pressure is elevated, follow your health care provider's advice.

• Continue to monitor your blood pressure at regular intervals.
o Obesity

• Avoid severely restrictive or fad diets.

• Restrict intake of saturated fats, simple sugars, and cholesterol-rich foods.

• Increase your physical activity.
o Reducing Elevated Serum Lipid Levels

• 130-159 mg/dL—borderline high

• 160-189 mg/dL—high

• ≥190 mg/dL—very high

The desired LDL level in patients who are at high risk or have existing CAD is less than
70 mg/dL.

For patients at low or moderate risk, LDL should also be substantially less than 100
mg/dL (AHA, 2010).

HDL cholesterol levels should be above 40 mg/dL, although this recommendation may
soon be changed to a higher level.

The recommended triglyceride level is

less than 135 mg/dL in women

150 mg/dL in men (Pagana & Pagana, 2010).

Approaches to decrease lipids are focused on diet, exercise, and drug therapy that lowers
cholesterol and triglyceride levels. Teach patients with elevated lipid levels to:

•Reduce intake of saturated fats to less than 7% of total calories

•Avoid trans fatty acids

•Consume less than 200 mg per day of cholesterol

•Participate in daily physical activity

•Manage weight

Contributing Risk Factors
Stable Angina Pectoris - chest discomfort that occurs with moderate to prolonged exertion in a pattern that is familiar
to the patient. The frequency, duration, and intensity of symptoms remain the same over several months. CSA results in
only slight limitation of activity and is usually associated with a fixed atherosclerotic plaque. It is usually relieved by
nitroglycerin or rest and often is managed with drug therapy. Rarely does CSA require aggressive treatment.

~ exertion, exercise

Relieved by rest

Nitroglycerin sublingual

Stable – fine

Unstable – relieved by rest

Unrelieved by rest or nitroglycerin for 15, go to ER
Acute Coronary Syndromes - unstable angina or an acute myocardial infarction

atherosclerotic plaque in the coronary artery ruptures, resulting in platelet aggregation (“clumping”),
thrombus (clot) formation, and vasoconstriction (Fig. 40-1). The amount of disruption of the atherosclerotic
plaque determines the degree of coronary artery obstruction (blockage) and the specific disease process. The
artery has to have at least 40% plaque accumulation before it starts to block blood flow.

Unstable angina (the most commonly used term) is chest pain or discomfort that occurs at rest or with
exertion and causes severe activity limitation. An increase in the number of attacks and in the intensity of the
pressure indicates unstable angina. The pressure may last longer than 15 minutes or may be poorly relieved
by rest or nitroglycerin. Unstable angina describes a variety of disorders, including new-onset angina, variant
(Prinzmetal's) angina, and pre-infarction angina. Patients with unstable angina will present with ST changes
on a 12-lead ECG but will not have changes in troponin or creatine kinase (CK) levels.


Ischemia
Infarction – troponin (up to 21 days?, if there is damage), CKMB (first 24 hrs, last 3 days, how much damage),
myoglobin

Acute MI: Sudden loss of blood supply to an area of the heart causing permanent heart damage or death

Most serious acute coronary syndrome

Occurs when myocardial tissue is abruptly and severely deprived of oxygen

Dynamic process that does not occur instantly but evolves over several hours

***EKG changes associated w/ MI – T wave inversion, ST elevation, abnormal Q wave are all EKG
results that you will see w/ pt w/ MI!!!


o
o
Outcome Management: Interventional Therapy
o Reduce risk factors
o Antiplatelet aggregation therapies
o Restore blood supply – PTCA
o Coronary atherectomy
o Stent placement
o Cardiac surgery
o Laser revascularization ~ break up plaque

heart failure ^

PVD - arterial, venous

Peripheral Vascular Disease

Disorders that alter the natural flow of blood through the arteries and veins of the peripheral circulation

Manifestation of systemic atherosclerosis: a chronic condition in which partial or total arterial occlusion
deprives the lower extremities of oxygen and nutrients

Arterial

Physical Assessment (Arterial)
o Intermittent claudication
o Pain that occurs even while at rest; numbness and burning
o Hair loss and dry, scaly, mottled skin and thickened toenails
o Arterial ulcers

Management
o Nonsurgical

Exercise

Positioning

Promoting vasodilation

Drug therapy

Angioplasty
o Surgical



Arterial bypass
Amputation
Venous Insufficiency
o Result of prolonged venous hypertension, stretching veins and damaging valves
o Stasis dermatitis, stasis ulcers
o Management of edema
o Management of venous stasis ulcers
o Drug therapy
o Surgical management

Varicose Veins
o Distended, protruding veins that appear darkened and tortuous
o Collaborative management includes:

Elastic stockings

Elevation of extremities

Sclerotherapy

Surgical removal of veins

Radio frequency energy to heat the veins
Chart 38-5 Home Care Assessment The Patient with Peripheral Vascular Disease
Assess tissue perfusion to affected extremity(ies), including:
•Distal circulation, sensation, and motion
•Presence of pain, pallor, paresthesias, pulselessness, paralysis, poikilothermy (coolness)
•Ankle-brachial index
Assess adherence to therapeutic regimen, including:
•Following foot care instructions
•Quitting smoking
•Maintaining dietary restrictions
•Participating in exercise regimen
•Avoiding exposure to cold and constrictive clothing
Assess ability to manage wound care and prevent further injury, including:
•Use of compression stockings or compression pumps as directed
•Use of various dressing materials
•Signs and symptoms to report to nurse
Assess coping ability of patient and family members.
Assess home environment, including:
•Safety hazards, especially related to falls
Chart 38-6 Patient and Family Education: Preparing for Self-Management Foot Care for the Patient with Peripheral Vascular Disease
• Keep your feet clean by washing them with a mild soap in room-temperature water.
• Keep your feet dry, especially the ankles and between the toes.
• Avoid injury to your feet and ankles. Wear comfortable, well-fitting shoes. Never go without shoes.
• Keep your toenails clean and filed. Have someone cut them if you cannot see them clearly. Cut your toenails straight across.
• To prevent dry, cracked skin, apply a lubricating lotion to your feet.
• Prevent exposure to extreme heat or cold. Never use a heating pad on your feet.
• Avoid constricting garments.
• If a problem develops, see a podiatrist or physician.
• Avoid extended pressure on your feet or ankles, such as occurs when you lean against something.
o
o
5 Million Lives – Seven Key Interventions



1. Left ventricular systolic (LVS) heart function assessment (CMS,JCAHO,ACC,AHA)
2. ACE inhibitor or ARB at discharge for CHF patients with systolic dysfunction (LVEF<40)
(CMS,JCAHO,ACC,AHA)
3. Anticoagulant at discharge for CHF patients with chronic/recurrent atrial fibrillation (ACC,AHA)




o
o
4. Influenza immunization (ACIP)
5. Pneumococcal immunization (ACIP)
6. Smoking cessation counseling (CMS,JCAHO,ACC,AHA)
7. Discharge instructions that address all of the following: activity level, diet, discharge medications, follow-up
appointments, weight monitoring, and what to do if symptoms worsen (CMS,JCAHO,ACC,AHA)

Tips for Transition Planning
o Focus on discharge at admission
o Use a discharge checklist with nurse-patient/family/caregiver face time

Assure health literacy; use teach back to insure understanding; test using “Ask-Me-3”

Reconcile medications; use teach back to ensure understanding of purpose, regimen, and
side effects

Provide real-time information transfer to next provider(s)

Speak with emergency contact for high risk patients

Schedule follow-up phone calls to patient/family to occur within 48 hours and physician
visit within one week for average risk patients

Schedule, before patient leaves, follow-up visit (home or office) for high risk patients to
occur within 48 hours after discharge
The Six Interventions AMI

Interventions in the ACC clinical guidelines & measured by JCAHO and CMS

1. Early administration of aspirin

2. Aspirin at discharge

3. Beta-blocker at discharge

4. ACE-inhibitor or angiotensin receptor blockers (ARB) at discharge for patients with systolic dysfunction

5. Timely initiation of reperfusion (thrombolysis or percutaneous intervention)

6. Smoking cessation counseling
Heart attack 6 steps:

The 100,000 Lives Campaign asked hospitals to implement the following six interventions:

1) Deploy Rapid Response Teams at the first sign of patient decline.

2) Deliver reliable, evidence-based care for acute myocardial infarction to prevent deaths from heart attack.

3) Prevent adverse drug events by implementing medication reconciliation.

4) Prevent central line infections by implementing a series of scientifically grounded steps.

5) Prevent surgical site infections by reliably delivering the correct preoperative antibiotics at the proper time.

6) Prevent ventilator-associated pneumonia by implementing a series of interdependent, scientifically grounded steps.

Management of Clients with Cancer
characteristics of normal cells and cancer cells.
o ~ 2 slide chart… don’t just memorize; what does this contribute to?
 Normal adhere; cancer don’t adhere. r/t to metastasis – can break off.
 Normal apoptosis; cancer don’t have time clock. Contributes to tumor growth.
Normal
Have limited cell division
Undergo apoptosis (programmed cell death)
Show specific morphology
Have a small nuclear-cytoplasmic ratio
Perform specific differentiated functions
Adhere tightly together
Non-migratory
Grow in an orderly and well-regulated manner
Contact inhibited
Euploid w/ 23 pairs of chromosomes
Cancer
Have rapid or continuous cell division
Do not respond to signals for apoptosis
Show anaplastic morphology
Have a large nuclear-cytoplasmic ratio
Lose some or all differentiated functions
Adhere loosely together
Able to migrate through embryonic cells
Grow by invasion
Are aneuploidy (> or < 23 chromosomes)



Side effects of cancer treatment – radiation vs. chemotherapy
o ~ radiation –
o ~ brachytherapy…
o ~ who gets it, side effects, nursing care
o ~ no surgery!
radiation therapy as a treatment for neoplastic disorders, its potential side effects, and nursing care.
chemotherapy as a treatment modality for neoplastic disorders, its side effects, and nursing care.
o
Radiation – types, pt care, side effects
Types

External beam – beam comes from outside and targets particular tissue

Brachytherapy – “short” or “close” therapy - radiation source comes into direct,
continuous contact w/ the tumor tissues for a specific period of time
o Ex) Radioactive iodine

Side Effects site dependent – in head and neck can cause permanent facial hair;
destroy salivary glands

Long-term sequelae
Patient

Consider time, distance and shielding (little time, far away, use shield like iron
Care
vest)

Teach accurate objective facts to help client cope. (be realistic)

Do not remove markings. (allows radiation in right place each time)

Administer skin care. (protect, cover, moisturize) no lotion before RT

Do not use lotions or ointments.

o
Brachytherapy: With all types of brachytherapy, the radiation source is within
the patient. Therefore the patient emits radiation for a period of time and is a
hazard to others
Side

Vary according to treatment site and is dependent on the total absorbed dose
Effects
o Local skin changes and hair loss
o Altered taste sensations (head and neck)
o Fatigue related to increased energy demands
o Inflammatory responses that cause tissue fibrosis and scarring
o Avoid direct exposure of the skin to the sun.
o Care for xerostomia (dry mouth).
o Bone exposed to radiation is more vulnerable to fracture.
Chemotherapy – types, pt care, side effects
Types
 Antimetabolites
 Antitumor antibodies
 Alkylating agents
 Antimitotic agents
 Topoisomerase inhibitors
 Miscellaneous chemotherapeutic agents
 Combination chemotherapy [check Table 24-2 categories]
Patient
Care



Side
Effects









Administration
 Verification of agent, dose, schedule
 Safe preparation, handling, and disposal
Routes of administration
 Intravenous, regional, oral, etc.
Adverse reactions
 Hypersensitivity reaction and extravasation
Safe preparation, handling, and disposal
Myelosuppression (Neutropenia, Thrombocytopenia, Anemia) -- leading to
infection, anemia, bleeding ~ decreasing immune system. Monitor CBC.
Nausea and vomiting ~ irritation of meds to GI tissues
Mucositis in the entire gastrointestinal tract
Diarrhea/ Constipation
Fatigue
Alopecia or hair loss
Fertility problems
~ extravasation, PPE, fluids b/c vomiting and bleeding, peripheral neuropathy,
memory… (?)


Management of Clients with Respiratory Disorders
hypoxemia and hypoxia symptoms and treatment
tracheostomy care
o ~ not types
o ~ assessing for: cuff pressure, WEANING off a trach. The steps.
o
Care


o

Weaning





Chart 30-3 Best Practice for Patient Safety & Quality Care Tracheostomy Care

1 Assemble the necessary equipment.

2 Wash hands. Maintain Standard Precautions.

3 Suction the tracheostomy tube if necessary.

4 Remove old dressings and excess secretions.

5 Set up a sterile field.

6 Remove and clean the inner cannula. Use half-strength hydrogen peroxide to clean the cannula and sterile
saline to rinse it. If the inner cannula is disposable, remove the cannula and replace it with a new one.

7 Clean the stoma site and then the tracheostomy plate with half-strength hydrogen peroxide followed by
sterile saline. Ensure that none of the solutions enters the tracheostomy.

8 Change tracheostomy ties if they are soiled. Secure new ties in place before removing soiled ones to
prevent accidental decannulation. If a knot is needed, tie a square knot that is visible on the side of the neck.
One or two fingers should be able to be placed between the tie tape and the neck.

9 Wash hands.

10 Document the type and amount of secretions and the general condition of the stoma and surrounding skin.
Document the patient's response to the procedure and any teaching or learning that occurred.
Chart 30-4 Focused Assessment The Patient with a Tracheostomy

• Note the quality, pattern, and rate of breathing:

•Within patient's baseline?

Tachypnea can indicate hypoxia.

Dyspnea can indicate secretions in the airway.

• Assess for any cyanosis, especially around the lips, which could indicate hypoxia.

• Check the patient's pulse oximetry reading.

• If oxygen is prescribed, is the patient receiving the correct amount, with the correct equipment and
humidification?

• Assess the tracheostomy site:

•Note the color, consistency, and amount of secretions in the tube or externally.

•If the tracheostomy is sutured in place, is there any redness, swelling, or drainage from suture sites?

•If the tracheostomy is secured with ties, what is the condition of the ties? Are they moist with secretions
or perspiration? Are the secretions dried on the ties? Is the tie secure?

•Assess the condition of the skin around the tracheostomy and neck. Be sure to check underneath the
neck for secretions that may have drained to the back. Check for any skin breakdown related to pressure from
the ties or related to excess secretions.

•Assess behind the faceplate for the size of the space between the outer cannula and the patient's tissue.
Are any secretions collected in this area?

• If the tube is cuffed, check cuff pressure.

• Auscultate the lungs.

• Are a second (emergency) tracheostomy tube and obturator available?
Weaning is a gradual decrease in the tube size and ultimate removal of the tube.
Cuff is deflated as soon as the patient can manage secretions and does not need assisted ventilation.
Change from a cuffed to an uncuffed tube.
Size of tube is decreased by capping; use a smaller fenestrated tube.
Tracheostomy button has a potential danger of getting dislodged.

Button maintains stoma patency and assists spontaneous breathing.
types of tracheostomies
System
FiO2 Delivered
When Used
Nasal Cannula
24%-40% at 1-6 L/min
Chronic lung disease and for
any pt needing long-term O2
therapy
Simple
Facemask
40%-60% at 5-8 L/min;
flow rate must be sat at
least at 5 L/min to flush
mask of CO2
Nursing Responsibilities
- ensure that prongs are in the nares properly
- provide water-soluble jelly to nares PRN
- assess the patency of the nostrils
- assess the pt for changes in resp rate and depth
- be sure mask fits securely over nose and mouth
- assess skin and provide skin care to the area covered by the
mask
- monitor the pt closely for risk of aspiration
Partial
Rebreather
Mask
- provide emotional support to the pt who feels claustrophobic
- make sure that the reservoir does not twist or kink, which
results in a deflated bag
- adjust the flow rate to keep the reservoir bag inflated
60%-75% at 6-11
L/min, a liter flow rate
high enough to
maintain reservoir bag
two-thirds full during
inspiration and
expiration
80%-95% at liter flow
to maintain reservoir
bag two-thirds full
NonRebreather
Mask
Venturi mask
(venti mask)
45%-50% w/ flow rates
as recommended by the
manufacturer, usually
4-10 L/min; provides
high humidity
Pt w/ chronic lung disease
b/c it delivers a more
precise O2 concentration
Aerosol mask,
face tent,
tracheostomy
collar
24%-100% w/ flow
rates of at least 10
L/min; provides high
humidity
Face tent: facial trauma or
burns
Aerosol mask: high humidity
needed after extubation or
upper airway surgery or for
thick secretions
Tracheostomy collar: high
humidity and the desired O2
to the pt w/ tracheostomy
T-piece
24%-100% w/ flow
rates of at least 10
L/min; provides high
humidity
Noninvasive
Positive
Pressure
Ventilation
CPAP
Can deliver O2 or may
just use room air
Transtracheal
Oxygen
Delivery
Long-term method of
delivering O2 directly
into the lungs
Home Oxygen
Therapy
Concentrated from
room air and is
delivered at more than
90%

- interventions as for partial rebreather mask; this pt requires
close monitoring
- make sure that valves and rubber flaps are patent, functional,
and not stuck. Remove mucus or saliva
- closely assess the pt on increased FiO2 via non-rebreather
mask. Intubation is the only way to provide more precise FiO2
- provide constant surveillance to ensure an accurate flow rate
for the specific FiO2
- keep the orifice for the Venturi adaptor open and uncovered
- provide a mask that fits snugly and tubing that is free of kinks
- assess the pt for dry mucous membranes
- change to a nasal cannula during mealtime
- assess that aerosol mist escapes from the vents of the delivery
system during inspiration and expiration
- empty condensation from the tubing
- empty condensation from the tubing
- keep the exhalation port open and uncovered
- position the T-piece so that it does not pull on the
tracheostomy or endotracheal tube
- make sure the humidifier creates enough mist. A mist should
be seen during inspiration and expiration
Those w/ atelectasis after
surgery or cardiac-induced
pulm edema; sleep apnea
More cosmetically
acceptable
Least expensive, does not
need to be filled.
Nurse or RT teaches the pt about the equipment needed for
home O2 therapy, including the O2 source, delivery devices,
humidity sources, and safety aspects of using and maintaining
the equipment
No smoking. Candles, gas burners, and fireplaces (or other open
flames) are not to be used in the same room that O2 is being
used.
suctioning techniques and complications
o
Suctioning

Chart 30-2 Suctioning the Artificial Airway

1 Assess the need for suctioning (routine unnecessary suctioning causes mucosal damage, bleeding, and
bronchospasm).

2 Wash hands. Don protective eyewear. Maintain Standard Precautions.

3 Explain to the patient that sensations such as shortness of breath and coughing are to be expected but that
any discomfort will be very brief.










o Complications
Complication and
description
Tracheomalacia: constant
pressure exerted by the cuff
causes tracheal dilation and
erosion of cartilage
Tracheal stenosis:
narrowed tracheal lumen is
due to scar formation from
irritation of tracheal
mucosa by the cuff
Tracheoesophageal fistula
(TEF): excessive cuff
pressure causes erosion of
the posterior wall of the
trachea. A hole is created
b/t the trachea and the
anterior esophagus. the pt
at highest risk also has a NG
tube present
4 Check the suction source. Occlude the suction source, and adjust the pressure dial to between 80 and
120 mm Hg to prevent hypoxemia and trauma to the mucosa.
5 Set up a sterile field.
6 Preoxygenate the patient with 100% oxygen for 30 seconds to 3 minutes (at least three hyperinflations) to
prevent hypoxemia. Keep hyperinflations synchronized with inhalation.
7 Quickly insert the suction catheter until resistance is met. Do not apply suction during insertion.
8 Withdraw the catheter 0.4 to 0.8 inch (1 to 2 cm), and begin to apply suction. Use a twirling motion of the
catheter during withdrawal. Never suction longer than 10 to 15 seconds.
9 Hyperoxygenate for 1 to 5 minutes or until the patient's baseline heart rate and oxygen saturation are within
normal limits.
10 Repeat as needed for up to three total suction passes.
11 Suction mouth as needed, and provide mouth care.
12 Wash hands.
13 Describe secretions, and document patient's responses.
Manifestations
Management
Prevention
- an increased amount of air is
required in the cuff to maintain
the seal
- a larger tracheostomy tube is
required to prevent an air leak at
the stoma
- food particles are seen in
tracheal secretions
- pt does not receive the set tidal
volume on the ventilator
- stenosis is usually seen after the
cuff is deflated or the
tracheostomy tube is removed
- pt has increased coughing,
inability to expectorate
secretions, or difficulty in
breathing or talking
No special management is
needed unless bleeding
occurs
- use an uncuffed tube ASAP
- monitor cuff pressure and
air volumes closely, and
detect changes
Similar to tracheomalacia:
- food particles are seen in
tracheal secretions
- an increased amount of air is
required in the cuff to maintain
the seal
- increased coughing and choking
while eating
- does not receive the set tidal
volume on the ventilator
- manually administer O2
by mask to prevent
hypoxemia
- use small, soft feeding
tube instead of NG tube
for tube feedings. A
gastrostomy or
jejunostomy may be
performed by the
physician
- monitor the pt w/ a NG
closely; assess for TEF
and aspiration
- remove trach tube
immediately
- apply direct pressure to
the innominate artery at
the stoma site
- prepare the pt for
immediate repair surgery
Keep cuff pressure 14-20
mmHg
Tracheal dilation or
surgical intervention is
used
- prevent pulling of and
traction on the tracheostomy
tube
- properly secure the tube in
the midline position
- maintain proper cuff
pressure
- minimize oronasal
intubation time
- maintain cuff pressure
- intor the amount of air
needed for inflation, and
detect changes. Progress to a
deflated cuff or cuffless tube
ASAP
Trachea-innominate artery
- trach tube pulsates in
- correct the tube size, length,
fistula: a malpositioned
synchrony w/ heartbeat
and midline position
tube causes its distal tip to
- heavy bleeding from stoma
- prevent pulling or tugging
push against the lateral
- life-threatening complication
on trach tube
wall of the tracheostomy.
- immediately notify
Continued pressure causes
physician of the pulsating
necrosis and erosion of the
tube
innominate artery. This is
a medical emergency.

Possible complications assessment:
o Tube obstruction

Difficulty breathing; noisy respirations; difficulty inserting a suction catheter; thick, dry secretions; and
unexplained peak pressures (if a mechanical ventilator is in use). Assess the patient at least hourly for tube
patency.

o
o
o
o
o
Prevent obstruction by helping the patient cough and deep breathe, providing inner cannula care, humidifying the
oxygen source, and suctioning.

If tube obstruction occurs as a result of cuff prolapse over the end of the tracheostomy tube, the physician or
advanced practice nurse repositions or replaces the tube.
Tube dislodgment—accidental decannulation

This problem can be prevented by securing the tube in place. This action reduces movement and traction on the
tube from oxygen or ventilator tubing or accidental pulling by the patient. Tube dislodgment in the first 72 hours
after surgery is an emergency because the tracheostomy tract has not matured and replacement is difficult. The
tube may end up in the subcutaneous tissue instead of in the trachea.

If the tube is dislodged on an immature tracheostomy, ventilate the patient using a manual resuscitation bag and
facemask while another nurse calls the Rapid Response Team.
Pneumothorax

(air in the chest cavity) can develop during the tracheotomy procedure if the chest cavity is entered. When
pneumothorax occurs during tracheotomy, it usually does so at the apex of the lung. Chest x-rays after placement
are used to assess for pneumothorax.
Subcutaneous emphysema

occurs when there is an opening or tear in the trachea and air escapes into fresh tissue planes of the neck. Air can
also progress throughout the chest and other tissues into the face. Inspect and palpate for air under the skin around
the new tracheostomy.

* crepitus
Bleeding

constant oozing is abnormal. Wrap gauze around the tube and pack gauze gently into the wound to apply pressure
to the bleeding sites. Sterile technique
Infection

In the hospital, use sterile technique to prevent infection during suctioning and tracheostomy care. Assess the
stoma site at least once per shift for purulent drainage, redness, pain, or swelling. Tracheostomy dressings may be
used to keep the stoma clean and dry.

These dressings resemble a 4 × 4 gauze pad with an area removed to fit around the tube. If tracheostomy dressings
are not available, fold standard sterile 4 × 4s to fit around the tube. Do not cut the dressing because small bits of
gauze could then be aspirated through the tube. Change these dressings often because moist dressings provide a
medium for bacterial growth. Careful wound care prevents most local infections.

Management of Clients with Endocrine Disorders
hypo/hyper thyroid
o ~ diagnosis
o ~ lab values [increased/decreased] beyond TSH, T3, T4  antibodies!!!
o ~ interventions
o ~ s/sx
HYPOTHYROID
•
Myxedema ~ mucous and fluid
•
Causes
•
Primary
•
Pituitary gland
•
Hypothalamus
•
Older
•
Females – 30-60 yrs
Assessment
Physical
Chart 66-6 Key Features Hypothyroidism

Skin Manifestations
o
• Cool, pale or yellowish, dry, coarse, scaly skin
o
• Thick, brittle nails
o
• Dry, coarse, brittle hair
o
• Decreased hair growth, with loss of eyebrow hair
o
• Poor wound healing

Pulmonary Manifestations
o Hypoventilation
o Pleural effusion
o Dyspnea

Cardiovascular Manifestations [DECREASED]
o
• Bradycardia
o
• Dysrhythmias
o
• Enlarged heart
o
• Decreased activity tolerance
o
• Hypotension

Metabolic Manifestations
o
• Decreased basal metabolic rate
o
• Decreased body temperature
o
• Cold intolerance

Musculoskeletal Manifestations
o
• Muscle aches and pains
o
• Delayed contraction and relaxation of muscles

Neurologic Manifestations
o
• Slowing of intellectual functions:

•Slowness or slurring of speech

•Impaired memory

•Inattentiveness
o
• Lethargy or somnolence
o
• Confusion
o
• Hearing loss
o
• Paresthesia (numbness and tingling) of the extremities
o
• Decreased tendon reflexes

Psychological/Emotional Manifestations
o • Apathy
o • Depression – most common reason for seeking medical attention
o • Paranoia
o • Withdrawal

Gastrointestinal Manifestations
o
• Anorexia
o
• Weight gain
o
• Constipation
o
• Abdominal distention

Reproductive Manifestations
o Women

• Changes in menses (amenorrhea or prolonged menstrual periods)


o

• Anovulation
• Decreased libido
Men

• Decreased libido

• Impotence
Other Manifestations
o
• Periorbital edema
o
• Facial puffiness
o
• Nonpitting edema of the hands and feet
o
• Hoarseness
o
• Goiter (enlarged thyroid gland)
o
• Thick tongue
o
• Increased sensitivity to opioids and tranquilizers
o
• Weakness, fatigue
o
• Decreased urine output
o
• Anemia
o
• Easy bruising
o
• Iron deficiency
o
• Folate deficiency
o
• Vitamin B12 deficiency
Diagnostic
tests


Treatment
Meds
Other

T3/T4 - DECREASED
TSH - INCREASED
Lifelong thyroid hormone replacement: levothyroxine sodium (Synthroid, T4) – start at lowest dose
o Weight loss indicates a need for a decreased dose
o If the client is gaining weight and continues to feel tired, that is an indication that the dose may need to
be increased.
Chart 66-7 Best Practice For Patient Safety & Quality Care - Emergency Care of the Patient During Myxedema
Coma
• Maintain a patent airway.
• Replace fluids with IV normal or hypertonic saline, as prescribed.
• Give levothyroxine sodium IV as prescribed.
Complications
• Give glucose IV as prescribed.
• Give corticosteroids as prescribed.
• Check the patient's temperature hourly.
• Monitor blood pressure hourly.
• Cover the patient with warm blankets. – b/c cold intolerance
• Monitor for changes in mental status.
• Turn every 2 hours.
• Institute Aspiration Precautions.

Myxedema coma = overall metabolism slows to the point that cardiac and resp arrest can occur
o Coma
o Respiratory failure
o Hypotension
o Hyponatremia
o Hypothermia
o Hypoglycemia

Myxedema coma can lead to shock, organ damage, and death. Assess the patient with hypothyroidism at least
every 8 hours for changes that indicate increasing severity, especially changes in mental status, and report these
promptly to the health care provider

~ hyperthyroidism (with hormone replacement therapy)
HYPERTHYROID – THYROTOXICOSIS
•
Etiology
•
Graves Disease (autoimmune)
•
Excess TSH from pituitary
•
Neoplasms
•
Thyroiditis
•
Excessive thyroid replacement
Assessment
Physical
Chart 66-1 Key Features Hyperthyroidism

Skin Manifestations
o • Diaphoresis (excessive sweating)
o • Fine, soft, silky body hair
o • Smooth, warm, moist skin
o • Thinning of scalp hair
o ~ pretibial myxedema – dry waxy swelling in front of tibia

Neurologic Manifestations
o • Blurred or double vision
o • Eye fatigue
o • Corneal ulcers or infections
o • Increased tears
o • Injected (red) conjunctiva
o • Photophobia
o • Eyelid retraction, eyelid lag* [Graves’ disease only]
o • Globe lag* [Graves’ disease only]
o • Hyperactive deep tendon reflexes
o • Tremors
o • Insomnia

Metabolic Manifestations
o • Increased basal metabolic rate
o • Heat intolerance
o • Low-grade fever
o • Fatigue

Psychological/Emotional Manifestations
o • Decreased attention span
o • Restlessness
o • Irritability
o • Emotional lability
o • Manic behavior

Reproductive Manifestations
o • Amenorrhea
o • Decreased menstrual flow
o • Increased libido

Other Manifestations





o • Goiter
o • Wide-eyed or startled appearance (exophthalmos)* [Graves’ disease only]
o • Decreased total white blood cell count
o • Enlarged spleen
Pulmonary Manifestations
o • Shortness of breath with or without exertion
o • Rapid, shallow respirations
o • Decreased vital capacity
Cardiovascular Manifestations
o • Shortness of breath with or without exertion
o • Rapid, shallow respirations
o • Decreased vital capacity
GI Manifestations
o • Weight loss
o • Increased appetite
o • Increased stools
o • Hypoproteinemia
Musculoskeletal Manifestations
o
• Muscle weakness
o
• Muscle wasting
Serum antibodies – positive = Graves
TSH ~ used to guide treatment, not T3/T4 - DECREASED
T3 & T4 INCREASED
Uptake tests
Suppression tests

Thyroid scan evaluates the position, size, and functioning of the thyroid gland.
•
Anti-Thyroid meds
•
Tapazole
•
PTU
Beta adrenergic blockers
Radioactive iodine
Thyroidectomy
•
Preoperative Meds
•
PTU (propylthiouracil) or Tapazole - Block T3 & T4 production by inhibiting thyroid binding
of iodide and by preventing the conversion of T4 to T3
•
Assess for liver problems for PTU
•
Dark urine may indicate liver toxicity or failure. The client must notify the
provider immediately.
•
Methimazole needs to be taken every 8 hours for an extended period of time. Levels
of T3 and T4 will be followed and dosages adjusted as levels fall.
•
Methimazole is an iodine preparation that decreases blood flow through the thyroid
gland. This action reduces the production and release of thyroid hormone. The client
should see some effects within 2 weeks; however, it may take several more weeks
before metabolism
•
The client should avoid large crowds and people who are ill. Propylthiouracil
reduces blood cell counts and the immune response, which increases the risk for
infection. The client does not, however, need to remain completely at home.
•
The client must notify the provider of weight gain because this may indicate
hypothyroidism. A lower drug dose may be required.
•
SSKI or Lugol’s Solution - Decrease vascularity of the thyroid gland
•
Iodine preparations – short term therapy before surgery
•
Decrease blood flow through the thyroid gland, reducing the production and release
of thyroid hormone
•
Lopressor - Block adrenergic effects of hyperthyroidism
•
relieve diaphoresis, anxiety, tachycardia, and palpitations but do not inhibit thyroid
hormone production
Thyroidectomy
o Post-Operative

Respiratory Distress

Mucous, laryngeal edema

Vocal cord paralysis




Diagnostic
tests
Treatment
Meds
Other
•
•
•
Complications




Humidify air

Trach tray, suction available

Hemorrhage

Check behind neck

Expect ~50 ml drainage in first 24 hours

Verify proper functioning of drain

~ check H&H; lethargy, pale, pulse ox go down, make sure dressing not too tight

Hypocalcemia

Tetany

+ Chvostek’s sign

+ Trousseau’s sign

Calcium Gluconate at the bedside

~ early: tingling around fingers and mouth, small muscle twitching, numbness

Thyroid Storm

Tachycardia, HTN, Hyperthermia

Reduce fever

Anticipate a beta blocker

PTU

~ temperature change (early), increase HR (early), sweating, HTN, hyperactive BS,
diarrhea

~ late: seizures, coma

Chart 66-5 Best Practice For Patient Safety & Quality Care Emergency Care of
the Patient During Thyroid Storm
o Maintain a patent airway and adequate ventilation.
o Give antithyroid drugs as prescribed: methimazole (Tapazole), up to 60 mg
daily; propylthiouracil (PTU, Propyl-Thyracil ), 300 to 900 mg daily.
o Administer sodium iodide solution, 2 g IV daily as prescribed.
o Give propranolol (Inderal, Detensol ), 1 to 3 mg IV as prescribed. Give
slowly over 3 minutes. The patient should be connected to a cardiac
monitor, and a central venous pressure catheter should be in place.
o Give glucocorticoids as prescribed: hydrocortisone, 100 to 500 mg IV daily;
prednisone, 4 to 60 mg IV daily; or dexamethasone, 2 mg IM every 6 hours.
o Monitor continually for cardiac dysrhythmias.
o Monitor vital signs every 30 minutes.
o Provide comfort measures, including a cooling blanket.
o Give non-salicylate antipyretics as prescribed.
o Correct dehydration with normal saline infusions.
o Apply cooling blanket or ice packs to reduce fever.
Nonsurgical Management
o Monitor apical pulse, BP, temp q4h

Increase in temp may indicate thyroid storm

Immediately report temp increase of even one degree Fahrenheit
o Reduce stimulation
o Promote comfort
Cushing’s/ Addison’s
o ~ adrenal gland
o ~ meds – esp cortisol, glucocorticoids, steroids (steroids most pharm info you’ll need)


ADDISON’S DISEASE (Adrenal Insufficiency)

Highest levels of ACTH is after sleep b/c of regeneration
Assessment
Physical

Adrenal Crisis: Clinical Signs
o Thorough history essential to look for cause
o Symptoms of hypovolemia
o Fluid and electrolyte imbalances
o Postural hypotension
o Change level of consciousness
o Hyperkalemia
o Fatigue, weakness
o Gastrointestinal complaints
o Decreased renal perfusion and decreased urine output
o Skin changes (hyperpigmentation)
o Decreased libido
o Hyperkalemia, hyponatremia, hypotension, hypoglycemia, shock
o Sex, salt, sugar, skin

Sex – decreased libido

Salt – hyponatremia; decreased volume

Sugar – decreased glucose – decreased ability to respond to stress

Skin – hyperpigmentation
Diagnostic
tests
Chart 65-8 Key Features Adrenal Insufficiency
Neuromuscular Manifestations
• Muscle weakness
• Fatigue
• Joint/muscle pain
Gastrointestinal Manifestations
• Anorexia
• Nausea, vomiting
• Abdominal pain
• Bowel changes (constipation/diarrhea)
• Weight loss
• Salt craving
Skin Manifestations
• Vitiligo
• Hyperpigmentation
Cardiovascular Manifestations
• Anemia
• Hypotension
• Hyponatremia
• Hyperkalemia
• Hypercalcemia
•
Laboratory values
•
Hyponatremia
•
Hyperkalemia
•
Azotemia (elevated BUN)
•
Hypoglycemia
•
Low plasma cortisol levels and urinary metabolites
•
ACTH (cosyntropin) stimulation test
•
Give ACTH, doesn’t respond – adrenal gland!
•
If cortisol levels don’t go up very much, we know problem is w/ adrenal gland.
•
Give ACTH, cortisol levels rise, then problem is hypothalamus or pituitary.
Treatment
Meds
•
•
•
•
Cortisol and aldosterone deficiencies are corrected by replacement therapy.
Hydrocortisone corrects glucocorticoid deficiency (Chart 65-10).
Oral cortisol replacement regimens vary.
The most common drug used for this purpose is prednisone.
o Generally, divided doses are given, with two-thirds given in the morning and one-third in the late
afternoon to mimic the normal release of this hormone.
Other
•
•
•
•
Nursing interventions focus on promoting fluid balance, monitoring for fluid deficit, and preventing
hypoglycemia.
Weigh the patient daily, and record intake and output.
Assess vital signs every 1 to 4 hours, depending on the patient's condition and the presence of dysrhythmias or
postural hypotension.
Monitor laboratory values to identify hemoconcentration (e.g., increased hematocrit or BUN).
Chart 65-7 Best Practice For Patient Safety & Quality Care Emergency Care of the Patient with Acute Adrenal
Insufficiency
Hormone Replacement
• Start rapid infusion of normal saline or dextrose 5% in normal saline.
• Initial dose of hydrocortisone sodium succinate (Solu-Cortef) is 100 to 300 mg or dexamethasone 4 to 12 mg
as an IV bolus.
• Infuse additional 100 mg of hydrocortisone sodium succinate by continuous IV drip over the next 8 hours.
• Give hydrocortisone 50 mg IM concomitantly every 12 hours.
• Initiate an H2 histamine blocker (e.g., ranitidine) IV for ulcer prevention.
Hyperkalemia Management
• Administer insulin (20 to 50 units) with dextrose (20 to 50 mg) in normal saline to shift potassium into cells.
• Administer potassium binding and excreting resin (e.g., Kayexalate).
• Give loop or thiazide diuretics.
• Avoid potassium-sparing diuretics, as prescribed.
• Initiate potassium restriction.
• Monitor intake and output.
• Monitor heart rate, rhythm, and ECG for manifestations of hyperkalemia (slow heart rate; heart block; tall,
peaked T waves; fibrillation; asystole).
Hypoglycemia Management
• Administer IV glucose, as prescribed.
• Administer glucagon, as needed and prescribed.
• Maintain IV access.
• Monitor blood glucose level hourly.
Complications
CUSHING’S DISEASE (HYPERCORTISOLISM)
•
Excessive secretion of cortisol from the adrenal cortex – problem in adrenal cortex, anterior pituitary gland, or hypothalamus
•
Cushing’s disease is a condition in which the anterior pituitary gland releases too much adrenocorticotropic hormone (ACTH).
Oversecretion of ACTH can result from a pituitary adenoma, an adrenal adenoma, or drug therapy with corticosteroids (aka
glucocorticoids) for another health problem)
•
Adrenal Cortex Disorder
•
Hyperaldosteronism
•
Primary hyperaldosteronism (rare)
•
Secondary hyperaldosteronism
•
Cushing’s Syndrome
•
Pheochromocytoma – tumor on adrenal medulla
Assessment
Physical

Key Features
•
Elevated plasma cortisol levels
•
Weight gain
•
Truncal obesity
•
“Moon face”
•
Extremity muscle wasting
•
Loss of bone density
•
Hypertension
•
Hyperglycemia
•
Purple striae
•
Acne
•
Thin, easily damaged skin
•
Hyperpigmentation
•
PP – Hyperaldosteronism: Clinical Signs
•
Thorough history essential to look for cause
•
Hypertension
•
Hypokalemia
•
Weight gain and fatty deposits
•
Slow wound healing
•
Glucose intolerance that may lead to diabetes
Fatigue and muscle weakness
Depression, anxiety and irritability; loss of emotional control
For Women:
•
Hirsutism (increased hair growth)
•
Irregular or absent menstrual periods
•
For Men:
•
Decreased libido,
•
Decreased fertility
•
Erectile dysfunction
•
Other signs and symptoms include:
•
Striae on the abdomen, thighs, breasts and arms
•
Thinning, fragile skin that bruises easily
•
Acne
•
Headache
•
Bone loss, leading to fractures over time
Chart 65-11 Key Features Hypercortisolism (Cushing’s Disease/Syndrome)
•
General Appearance
•
• Fat redistribution:
•
Moon face
•
Buffalo hump
•
Truncal obesity
•
• Weight gain
•
Skin Manifestations
•
• Thinning skin (“paper-like” appearance, especially on the back of the hands)
•
• Striae
•
• Increased pigmentation (with ectopic or pituitary production of ACTH)
•
Cardiovascular Manifestations
•
• Hypertension
•
• Increased risk for thromboembolic events
•
• Frequent dependent edema
•
• Capillary fragility:
•
Bruising
•
Petechiae
•
Immune System Manifestations (b/c high levels of corticosteroids kill lymphocytes and shrink organs
containing lymphocytes, such as liver, spleen, and lymph nodes)
•
• Increased risk for infection
•
• Decreased immune function:
•
•Decreased circulating lymphocytes
•
•Decreased production of immunoglobulins (antibodies)
•
• Decreased inflammatory responses:
•
Decreased eosinophil count
•
Slight increase in neutrophil count but activity is reduced
•
• Decreased production of proinflammatory cytokines, histamine, and prostaglandins
•
• Manifestations of infection/inflammation may be masked
•
Musculoskeletal Manifestations
•
• Muscle atrophy (most apparent in extremities)
•
• Osteoporosis (bone density loss)
•
Pathologic fractures
•
Decreased height with vertebral collapse
•
Aseptic necrosis of the femur head
•
Slow or poor healing of bone fractures
ACTH
o Pituitary Cushing’s disease: ACTH elevated
o Adrenal Cushing’s disease or when Cushing’s syndrome results from chronic steroid use: ACTH low
Increased blood glucose!
Decreased lymphocyte
Increased sodium
Decreased serum calcium level
Decreased potassium level
•
•
•
•
Diagnostic
tests
•
•
•
•
•
•
Treatment
Meds
•
•
Fluid overload
o Administer drugs to interfere w/ ACTH production or adrenal hormone synthesis: aminoglutethimide
(Elipten, Cytadren), Metyrapone (Metopirone), Cyproheptadine (Periactin), Mitotane (Lysodren)
Risk for injury
Other
•
•
•
Complications


•
Risk for infection
•
~ restrict fluid, glucocorticoid inhibitors
Fluid overload
o Pt safety includes preventing fluid overload becoming worse pulmonary edema and heart failure
o Watch for signs of overload: increased pulse quality, increase neck vein distention, presence of crackles in
lungs, increase peripheral edema, reduce UO) –checked every 2 hours
o Pulmonary edema can occur quickly and can lead to DEATH
o Assess skin pressure areas and changed position every 2 hrs
o Drug therapy that interferes with ACTH production or adrenal hormone synthesis for temporary relief
o Nutrition may involve both fluid and sodium restriction
o Monitor I&O and daily weight
o Check urine specific gravity (<1.005 may indicate fluid overload)
o Radiation therapy for pituitary adenomas
o Surgery for removal of pituitary gland or partial or complete removal of adrenal gland
Risk for injury – risk for skin breakdown, bone fractures, and GI bleeding
-Use soft toothbrush and an electric shaver
-Caution using adhesive tape
-Exert pressure over site of venipuntures to prevent bleeding and bruising
-Use drawsheets
-Milk, cheese, yogurt, and green leafy and root vegetables add calcium and promote bone density
-Monitor for GI bleeding
-Antacids to protect GI mucosa
-H2 receptor to prevent formation of hydrochloric acid
Risk for infection
-Thorough handwashing*
-Hypercortisolism may not show manifestations of infection
-Monitor CBC with differential WBC and absolute neutrophil count (ANC)
-Assess for temperature elevation of even 0.5 F (or 0.5 C) above baseline –significant!
•
-Pulmonary hygiene every 2-4 hrs
Potential for acute adrenal insufficiency
Cortisol replacement therapy
o Chart 65-12 Patient And Family Education: Preparing For Self-Management Cortisol Replacement Therapy
o
• Take your medication in divided doses—the first dose in the morning and the second dose between 4 and 6 pm.
o
• Take your medication with meals or snacks.
o
• Weigh yourself daily.
o
• Increase your dosage as directed for increased physical stress or severe emotional stress, including surgery,
dental work, influenza, fever, pregnancy, and family problems.
o
• Never skip a dose of medication. If you have persistent vomiting or severe diarrhea and cannot take your
medication by mouth for 24 to 36 hours, call your physician. If you cannot reach your physician, go to the nearest
emergency department. You may need an injection to take the place of your usual oral medication.
o
• Always wear your medical alert bracelet or necklace.
o
• Make regular visits for health care follow-up.
o
• Learn how to give yourself an intramuscular injection of hydrocortisone.
Be aware of lab values
Management of Clients with Renal/Urinary Disorders

Polycystic kidney disease
POLYCYSTIC KIDNEY DISEASE

Inherited disorder

Fluid-filled cysts develop in nephrons - develop anywhere in the nephron as a result of abnormal kidney cell division.

Assessment
Physical






Diagnostic
tests






Treatment
Meds



Chart 70-1 Key features Polycystic Kidney Disease
o Abdominal or flank pain – pain often first manifestations

Dull, aching  increased kidney size w/ distention or by infection w/in cyst

Sharp, intermittent  cyst ruptures or stone is present

When a cyst ruptures, the patient may have bright red or cola-colored urine.
o Hypertension – r/t kidney ischemia from the enlarging cysts. As the vessels are compressed and blood
flow to the kidneys decreases, the renin-angiotensin system is activated, raising blood pressure.
o Increased abdominal girth – distended abd
o Constipation
o Bloody or cloudy urine
o Kidney stones
Infection is suspected if the urine is cloudy or foul smelling or if there is dysuria (pain on urination).
Nocturia (the need to urinate excessively at night) is an early manifestation and occurs because of decreased
urine concentrating ability.
As kidney function further declines, the patient has increasing hypertension, edema, and uremic manifestations
such as anorexia, nausea, vomiting, pruritus, and fatigue
Because berry aneurysms often occur in patients with PKD, a severe headache with or without neurologic or
vision changes requires attention.
Psychosocial: While obtaining the family history, listen carefully for spoken and unspoken feelings of anger,
resentment, futility, sadness, or anxiety.
Urinalysis shows proteinuria (protein in the urine) once the glomeruli are involved.
Hematuria (blood in the urine) may be gross or microscopic.
Bacteria in the urine indicate infection, usually in the cysts. Obtain a urine sample for culture and sensitivity
testing when there is evidence of infection.
As kidney function declines, serum creatinine and blood urea nitrogen (BUN) levels rise. With decreasing kidney
function, creatinine clearance decreases.
Changes in kidney handling of sodium may cause either sodium losses or sodium retention.
Diagnostic studies include:
o Renal sonography, computed tomography (CT), and magnetic resonance imaging (MRI).
o Small cysts are detected by sonography, CT, or MRI.
o Renal sonography shows evidence of PKD, with minimal risk.
Managing Pain
o NSAIDs are used cautiously because of their tendency to reduce kidney blood flow. Aspirin-containing
compounds are avoided to reduce the risk for bleeding.
o If cyst infection causes discomfort, antibiotics such as trimethoprim/sulfamethoxazole (Bactrim, Septra,
Trimpex) or ciprofloxacin (Cipro) are prescribed.

Monitor the serum creatinine levels because antibiotic therapy can be nephrotoxic.
Preventing Constipation
o Advise him or her about the use of stool softeners and bulk agents, including the careful use of laxatives,
to prevent chronic constipation.
Controlling Hypertension and Preventing End-Stage Kidney Disease
o Antihypertensive agents:

Angiotensin-converting enzyme (ACE) inhibitors - may help control the cell growth aspects of
PKD and reduce microalbuminuria

Calcium channel blockers

Beta blockers

Vasodilators (see Chapter 38)
o Diuretics
Other


Assessment
Physical

Control of hypertension is a top priority because proper treatment can disrupt the process that leads to further
kidney damage

Managing Pain
o Apply dry heat to the abdomen or flank to promote comfort when kidney cysts are infected.
o When pain is severe, cysts can be reduced by needle aspiration and drainage; however, they usually
refill.

Preventing Constipation
o Teach the patient who has adequate urine output how to prevent constipation by maintaining adequate
fluid intake, increasing dietary fiber when fluid intake is more than 2500 mL/24 hr, and exercising
regularly.

Controlling Hypertension and Preventing End-Stage Kidney Disease
o When kidney impairment results in decreased urine concentration with nocturia and low urine specific
gravity, urge the patient to drink at least 2 L of fluid per day to prevent dehydration, which can further
reduce kidney function.
o Restricting sodium intake may help control blood pressure.

Chart 70-2 Patient And Family Education: Preparing for Self-Management Polycystic Kidney Disease
o Measure and record your blood pressure daily, and notify your health care provider for consistent
changes in blood pressure.
o Take your temperature if you suspect you have a fever.
o Weigh yourself every day at the same time of day and with the same amount of clothing; notify your
physician or nurse if you have a sudden weight gain.
o Limit your intake of salt to help control your blood pressure.
o Notify your physician or nurse if your urine smells foul or has blood in it.
o Notify your physician or nurse if you have a headache that does not go away or if you have visual
disturbances.
o Monitor bowel movements to prevent constipation.
Complications

HTN

cerebral aneurysms (outpouching and thinning of an artery wall) is higher in patients with PKD

Heart valve problems (e.g., mitral valve prolapse), left ventricular hypertrophy, and colonic diverticula also are
common in patients with PKD.

Hydronephrosis, hydroureter
HYDRONEPHROSIS, HYDROURETER

Hydronephrosis  the kidney enlarges as urine collects in the renal pelvis and kidney tissue. Obstruction w/in the pelvis or
ureteropelvic junction results in renal pelvic distention, and extensive damage to the vasculature and renal tubules can result.

Hydroureter (enlargement of the ureter)  the obstruction of the ureter at the point of the iliac vessel crossing or the
ureterovesical entry. Dilation of the ureter occurs at the point proximal to the obstruction as urine accumulates.

Urethral stricture  the obstruction is very low in the urinary tract, causing bladder distention before hydroureter and
hydronephrosis

Causes of hydronephrosis or hydroureter include tumors, stones, trauma, structural defects, and fibrosis.

Urethral stricture occurs from chronic inflammation

Obtain a history from the patient, focusing on known kidney or urologic disorders. A history of childhood urinary
tract problems may indicate previously undiagnosed structural defects.
Ask about his or her usual pattern of urination, especially amount, frequency, color, clarity, and odor. Ask about
recent flank or abdominal pain.



Diagnostic
tests







Treatment
Meds
Other



Chills, fever, and malaise may be present with a urinary tract infection (UTI).
Inspect each flank to identify asymmetry, which may occur with a kidney mass
Gently palpate the abdomen to locate areas of tenderness.
o Palpate and percuss the bladder to detect distention, or use a bedside bladder scanner. Gentle pressure
on the abdomen may cause urine leakage, which reflects a full bladder and possible obstruction.
Urinalysis may show bacteria or white blood cells if infection is present.
When urinary tract obstruction is prolonged, microscopic examination may show tubular epithelial cells.
Blood chemistries are normal unless glomerular filtration decreases.
Blood creatinine and blood urea nitrogen (BUN) levels increase with a reduced glomerular filtration rate (GFR).
Serum electrolyte levels may be altered with elevated blood levels of potassium, phosphorus, and calcium along
with a metabolic acidosis (bicarbonate deficit).
IV urography shows ureteral or renal pelvis dilation.
Urinary outflow obstruction can be seen with sonography (renal echography) or computed tomography (CT).
Urinary retention and potential for infection are the primary problems.
Failure to treat the cause of obstruction leads to infection and end-stage kidney disease.
Radiologic Interventions
o When a stricture is causing hydronephrosis and cannot be corrected with urologic procedures, a
nephrostomy is performed. This procedure diverts urine externally and prevents further damage to the
kidney.
o After nephrostomy, notify the physician immediately when the drainage decreases or stops, drainage
becomes cloudy or foul-smelling, the nephrostomy site leaks blood or urine, or the patient has back
pain.
Complications

Pyelonephritis
PYELONEPHRITIS
 Bacterial infection in the kidney and renal pelvis (upper urinary tract)
 Acute pyelonephritis is the active bacterial infection
 Chronic pyelonephritis results from repeated or continued upper urinary tract infections or the effects of such infections.
 Often occurs with a urinary tract defect, obstruction, or, most commonly, when urine refluxes from the bladder back into
the ureters.

Assessment
Physical



Increased risk: pregnancy, DM, and chronic renal calculi
Key features include:
◦
Fever, chills, tachycardia, and tachypnea
◦
Flank, back, or loin pain
◦
Abdominal discomfort
◦
Turning, nausea and vomiting, urgency, frequency, nocturia
◦
General malaise or fatigue
Chart 70-3 Key Features Acute Pyelonephritis
• Fever
• Chills
• Tachycardia and tachypnea
• Flank, back, or loin pain

Diagnostic
tests
Treatment
Meds
Other
• Tender costovertebral angle (CVA)
• Abdominal, often colicky, discomfort
• Nausea and vomiting
• General malaise or fatigue
• Burning, urgency, or frequency of urination
• Nocturia
• Recent cystitis or treatment for urinary tract infection (UTI)
Chart 70-4 Key Features Chronic Pyelonephritis
• Hypertension
• Inability to conserve sodium
• Decreased urine concentrating ability, resulting in nocturia
• Tendency to develop hyperkalemia and acidosis

Urinalysis shows a positive leukocyte esterase and nitrite dipstick test and the presence of white blood cells and
bacteria.

Blood cultures are obtained for specific organisms. Other blood tests include the C-reactive protein and
erythrocyte sedimentation rate to determine the presence of inflammation.

An x-ray of the kidneys, ureters, and bladder (KUB) and IV urography are performed to diagnose stones or
obstructions.

A cystourethrogram is indicated for some patients.


Broad spectrum antibiotics
Nutrition therapy involves ensuring that the patient's nutritional intake has adequate calories from all food
groups for healing to occur. Fluid intake is recommended at 2 L/day unless another health problem requires
fluid restriction.

Surgical Procedures:
o Pyelolithotomy (removal of a stone from the renal pelvis)
o Nephrectomy (removal of a kidney)
o Ureteral diversion or reimplantation of the ureter to restore the bladder drainage mechanism)

Maintain sufficient perfusion to the kidneys to prevent acute (hypotensive) or chronic (hypertensive) kidney
injury

Maintain sufficient fluid intake to promote urine output greater than 1 mL/kg/hr

Assess for signs of acute kidney injury such as increasing BUN or CREAT level or decreased urinary output
Complications

Abscess formation

Septicemia

Glomerulonephritis/nephrotic syndrome
GLOMERULONEPHRITIS/NEPHRITIC SYNDROME (ACUTE)
GLOMERULONEPHRITIS/NEPHRITIC SYNDROME
(CHRONIC)

Glomerulonephritis may be caused by problems with the body's
immune system. Damage to the glomeruli causes blood and protein to

Develops over 20 to 30 years or even longer
be lost in the urine.

Changes in the kidney tissue result from
hypertension, infections and inflammation, or

The condition may develop quickly, and kidney function is lost within
weeks or months
poor blood flow to the kidneys.

Onset of symptoms is about 10 days from the time of infection.

Chronic glomerulonephritis always leads to
end-stage kidney disease
Assessment
Physical

Common symptoms

Mild proteinuria and hematuria, hypertension,
o Blood in the urine (dark, rust-colored, or
fatigue, and occasional edema are often the
brown urine)
only manifestations.
o Foamy urine (due to excess protein in the

Ask about other health problems, including
urine)
systemic diseases, kidney or urologic disorders,
o Swelling (edema) of the face, eyes, ankles,
infectious diseases (e.g., streptococcal
feet, legs, or abdomen
infections), and recent exposures to infections.

Fluid overload and circulatory congestion (which

Ask about changes in urine color, odor, or
may accompany the sodium and fluid retention
clarity and whether dysuria or incontinence
occurring with acute GN)
has occurred.

Ask about any difficulty in breathing or shortness

Nocturia also is a common symptom.
of breath.

Assess for systemic circulatory overload.

Assess for crackles in the lung fields, an S3 heart

Auscultate lung fields for crackles, observe the
sound (gallop rhythm), and neck vein distention.
respiratory rate and depth, and measure blood

Dysuria, Oliguria
pressure and weight.

Fluid retention – check weight

Auscultate the heart for rate, rhythm, and the
presence of an S3 heart sound.

Mild to moderate HTN as a result of Na+ and fluid
retention

Inspect the neck veins for venous engorgement,
and check for edema of the foot and ankle, on

Fatigue, a lack of energy, anorexia, nausea, and/or






vomiting if uremia from severe kidney impairment
The less common manifestations of acute GN are
more likely to occur in older adults. Circulatory
congestion often is present, causing acute GN to be
easily confused with congestive heart failure.
Nausea, vomiting, or anorexia indicates that
uremia is present.
TABLE 70-1 PRIMARY GLOMERULAR DISEASES
AND SYNDROMES
o Acute glomerulonephritis
o Rapidly progressive glomerulonephritis
(RPGN)
o Chronic glomerulonephritis
o Nephrotic syndrome
o Persistent, vague urinary abnormalities
with few or no symptoms
TABLE 70-2 SECONDARY GLOMERULAR
DISEASES AND SYNDROMES
o Systemic lupus erythematosus (SLE)
o Schönlein-Henoch purpura
o Goodpasture's syndrome
o Systemic necrotizing vasculitis
o Wegener's granulomatosis
o Periarteritis nodosa (also called
polyarteritis nodosa)
o Amyloidosis
o Diabetic glomerulopathy
o HIV-associated nephropathy
o Alport's syndrome
o Multiple myeloma
o Viral hepatitis B
o Viral hepatitis C
o Cirrhosis
o Sickle-cell disease
o Nonstreptococcal postinfectious acute
glomerulonephritis
o Infective endocarditis
o Hemolytic-uremic syndrome
o Thrombotic thrombocytopenic purpura
TABLE 70-3 INFECTIOUS CAUSES OF ACUTE
GLOMERULONEPHRITIS
o Group A beta-hemolytic Streptococcus
o Staphylococcal or gram-negative
bacteremia or sepsis
o Pneumococcal, Mycoplasma, or Klebsiella
pneumonia
o Syphilis
o Visceral abscesses
o Infective endocarditis
o Hepatitis B
o Infectious mononucleosis
o Measles
o Mumps
o Rocky Mountain spotted fever
o Cytomegalovirus infection
o Histoplasmosis
o Toxoplasmosis
o Varicella
o Chlamydia psittaci infection
o Coxsackievirus infection
o Any bacterial, parasitic, fungal, or viral
infection (potentially)
Most causes of acute GN are infectious (Table 70-3)
or are related to other systemic diseases



the shin, and over the sacrum.
Assess for uremic symptoms, such as slurred
speech, ataxia, tremors, or asterixis (flapping
tremor of the fingers or the inability to
maintain a fixed posture with the arms
extended and wrists hyperextended).
Inspect skin for a yellowish color, texture,
bruises, rashes, or eruptions.
Ask about itching, and document areas of
dryness or any excoriation from scratching.
Diagnostic tests









Treatment
Meds

Other





Urinalysis shows red blood cells (hematuria) and
protein (proteinuria).
The glomerular filtration rate (GFR) decreased to
50 mL/min.
BUN are usually increased.
The older patient may have a greater decline in
GFR.
The protein excretion rate for patients with acute
GN may be increased from 500 mg to 3 g/24 hr in
most patients.
Serum albumin levels are decreased because of the
protein lost in the urine and because of fluid
retention causing dilution.
Specimens from the blood, skin, or throat are
obtained for culture, if indicated.
Other serologic tests include antistreptolysin-O
titers, C3 complement levels, cryoglobulins
(immunoglobulin G [IgG]), antinuclear antibodies
(ANAs), and circulating immune complexes.
A kidney biopsy provides a precise diagnosis of the
condition, assists in determining the prognosis,
and helps outline treatment

Penicillin, erythromycin, or azithromycin is
prescribed for GN caused by streptococcal
infection.
For patients with fluid overload, hypertension, and
edema, diuretics and a sodium and water
restriction are prescribed.
Antihypertensive drugs may be needed to control
hypertension (see Chapter 38).
The usual fluid allowance is equal to the 24-hour
urine output plus 500 to 600 mL.
Patients with oliguria usually have increased
serum levels of potassium and blood urea nitrogen
(BUN).
Potassium and protein intake may be restricted to
prevent hyperkalemia and uremia as a result of the
elevated BUN.

Drug therapy to control the problems from
uremia.

Diet changes, fluid intake sufficient to prevent
reduced blood flow volume to the kidneys, and
Eventually, the patient requires dialysis or
transplantation to prevent death from uremia.
Sodium restriction
Water restriction
Diuretics
Protein restriction – til they’re not losing
protein in urine














Urine output decreases, but the urine appears
normal unless a urinary tract infection (UTI)
also is present.
Urinalysis shows protein, usually less than 2 g
in a 24-hour collection. The specific gravity is
fixed at a constant level of dilution (around
1.010). Red blood cells and casts may be in the
urine.
GFR low.
The serum creatinine level is elevated, usually
greater than 6 mg/dL but may be as high as 30
mg/dL or more.
The BUN is increased, often as high as 100 to
200 mg/dL.
Sodium retention is common, but dilution of
the plasma from excess fluid can result in a
falsely normal serum sodium level (135 to 145
mEq/L) or a low sodium level (less than 135
mEq/L).
When oliguria develops, potassium is not
excreted and hyperkalemia occurs when levels
exceed 5.4 mEq/L.
Hyperphosphatemia, hypocalcemia
Acidosis
The kidneys are abnormally small on x-ray and
on IV urography and when measured by
sonography or computed tomography (CT).
Complications

Nephrotic Syndrome
NEPHROTIC SYNDROME
 Condition of increased glomerular permeability that allows larger molecules to pass through the membrane into the urine and then
be excreted.
 Severe loss of protein into the urine, edema formation, and decreased plasma albumin levels.
 Most common cause of glomerular membrane changes  an immune or inflammatory process.
 Defects in glomerular filtration can also occur as a result of genetic defects of the glomerular filtering system, such as Fabry disease.
 Altered liver activity may occur with nephrotic syndrome, resulting in increased lipid production and hyperlipidemia.
Assessment
Physical

Chart 70-5 Key Features Nephrotic Syndrome
Sudden onset of these manifestations:
o
•Massive proteinuria (> 3.5 g protein in 24 hrs)
o
•Hypoalbuminemia (< 3 g/dL)
o
•Edema (especially facial and periorbital)
o
•Lipiduria
o
•Hyperlipidemia
o
•Increased coagulation
o
Diagnostic
tests
Treatment
Meds
Other
◦
◦
◦
◦
◦



•Reduced kidney function
Immunosuppressive agents (corticosteroids) ~ b/c immune related disorder
Angiotensin-converting enzyme inhibitors (to keep BP down and decrease protein lost in the urine)
Heparin (may reduce urine protein loss and improve kidney function)
Diet changes (low salt )
Mild diuretics (control edema and hypertension)
ONLY RENAL DISORDER IN WHICH YOU INCREASE PROTEIN IN PT! [PROTEIN REPLACEMENT]
If the glomerular filtration rate (GFR) is normal, dietary intake of complete proteins is needed.
If the GFR is decreased, dietary protein intake must be decreased.
Complications

risks for renal failure
o Causes of Renal Failure

Unrecognized acute renal failure

Diabetes

Trauma

Chronic Med Use

Anomalies ~ structural problems

Genetics ~ polycystic disease, genetic disorders
DISEASE
Assessment
Physical
ACUTE
◦
Sudden onset
◦
Reversible
◦
AKI (formerly known as acute renal failure), is a
rapid decrease in kidney fxn leading to the
accumulation of metabolic wastes in the body
◦
Can result from:
◦
conditions that reduce blood flow or O2
to the kidneys (prerenal failure);
◦
damage to the glomeruli, interstitial
tissue, or tubules (intrarenal or intrinsic
renal failure);
◦
obstruction of urine flow (postrenal
failure).
CHRONIC - also known as End Stage Renal Disease (ESRD)
◦
End Stage Kidney Disease (ESKD)
◦
Insidious, chronic
◦
Irreversible
◦
Requires dialysis for survival
Chart 71-1 Key Features Acute Kidney Injury
Chart 71-6 Key Features Severe Chronic Kidney Disease
Prerenal Azotemia
• Hypotension
• Tachycardia
• Decreased cardiac output
• Decreased central venous pressure
• Decreased urine output
• Lethargy
Intrarenal (Intrinsic) AKI and Postrenal Azotemia
• Renal manifestations:
•Oliguria or anuria
•Increased urine specific gravity
Cardiac manifestations:
•Hypertension
•Tachycardia
•Jugular venous distention
•Increased central venous pressure
•ECG changes: tall T waves
Respiratory manifestations:
•Shortness of breath
•Orthopnea
•Crackles
•Pulmonary edema
•Friction rub
Gastrointestinal manifestations:
•Anorexia
•Nausea
•Vomiting
•Flank pain
Neurologic manifestations:
•Lethargy
•Headache
•Tremors
•Confusion
General manifestations:
•Generalized edema
•Weight gain
Neurologic Manifestations
• Lethargy and daytime drowsiness
• Inability to concentrate or decreased attention span
• Seizures
• Coma
• Slurred speech
• Asterixis (jerky movements or “flapping” of the hands)
• Tremors, twitching, or jerky movements
• Myoclonus
• Ataxia (alteration in gait)
• Paresthesias
Cardiovascular Manifestations
• Cardiomyopathy
• Hypertension
• Peripheral edema
• Heart failure
• Uremic pericarditis
• Pericardial effusion
• Pericardial friction rub
• Cardiac tamponade
Respiratory Manifestations
• Uremic halitosis
• Tachypnea
• Deep sighing, yawning
• Kussmaul respirations
• Uremic pneumonitis
• Shortness of breath
• Pulmonary edema
• Pleural effusion
• Depressed cough reflex
• Crackles
Hematologic Manifestations
• Anemia (fatigue, pallor, lethargy, weakness, SOB,
dizziness)
• Abnormal bleeding and bruising (brusing, petechiae,
purpura, MM bleeding in nose or gums, intestinal [melena])
Gastrointestinal Manifestations
• Anorexia
• Nausea
• Vomiting
• Metallic taste in the mouth
• Changes in taste acuity and sensation
• Uremic colitis (diarrhea)
• Constipation
• Uremic gastritis (possible GI bleeding)
• Uremic fetor (breath odor)
• Stomatitis
Urinary Manifestations
• Polyuria, nocturia (early)
• Oliguria, anuria (later)
• Proteinuria
• Hematuria
• Diluted, straw-colored appearance (early)
• Concentrated and cloudy appearance (later)
Integumentary Manifestations - UREMIA
• Decreased skin turgor
• Yellow-gray pallor
• Dry skin
• Pruritus
• Ecchymosis
• Purpura
• Soft-tissue calcifications
• Uremic frost (late, premorbid)
Musculoskeletal Manifestations
Diagnostic
tests






Similar to those occurring in chronic kidney
disease (CKD) (Chart 71-2)
Rising BUN and serum creatinine levels and
abnormal blood electrolyte values.
Patients with AKI, however, usually do not have
the anemia associated with CKD unless there is
hemorrhagic blood loss or unless blood urea
levels are high enough to break (lyse) red blood
cells.
X-rays help determine the cause of AKI. An
abdominal x-ray is used to check the size of the
kidneys. Enlarged kidneys, possibly due to
obstruction, may result from hydronephrosis. Xrays may show stones obstructing the renal
pelvis, ureters, or bladder.
Renal ultrasonography useful in the diagnosis of
urinary tract obstruction. Dilation of the renal
calyces and collecting ducts, as well as stones, can
be detected.
CT scans without contrast dye can identify
obstruction or tumors.
• Muscle weakness and cramping
• Bone pain
• Pathologic fractures
• Renal osteodystrophy
Reproductive Manifestations
• Decreased fertility
• Infrequent or absent menses
• Decreased libido
• Impotence
How is CKD Diagnosed?
 Astute clinician
 Sees the big picture
 Knows who is at risk
 Advocates for the patient
 Collaborates with the team








Treatment
Meds




Other
In the early stages of CKD, urinalysis may show
excessive protein, glucose, red blood cells (RBCs),
white blood cells (WBCs), and decreased or fixed
specific gravity.
Urine osmolarity is usually decreased.
GFR
24 creatinine clearance
As CKD progresses, the urine output decreases
dramatically.
In severe CKD, measurements of the serum
creatinine and BUN levels may be used to
determine the presence and degree of uremia.
Serum creatinine levels may increase gradually
over a period of years, reaching levels of 15 to 30
mg/dL or more, depending on the patient's
muscle mass.
BUN levels are directly related to dietary protein
intake.
Prerenal azotemia  fluid challenges and
diuretics are often used to promote kidney blood
flow. Diuretics such as furosemide (Lasix) also
may be prescribed along with a fluid bolus.
If oliguric kidney injury is diagnosed, the fluid
challenges and diuretics are d/c.
Patients often require central venous pressure
(CVP) monitoring or measurement of pulmonary
arterial pressure by means of a pulmonary artery
catheter for accurate evaluation of their
hemodynamic status. They also require constant
nursing supervision for assessment of the
response to fluid and drug therapy. Carefully
monitor for signs of possible fluid overload.
Calcium channel blockers may be used to treat
AKI resulting from nephrotoxic acute tubular
necrosis (ATN)  prevent the movement of
calcium into the kidney cells, maintain kidney cell
integrity, and improve the glomerular filtration
rate (GFR) by improving kidney blood flow.
Chart 71-7 Best Practice for Patient Safety & Quality
Care - Managing Fluid Volume
•Weigh the patient daily at the same time each day, using
the same scale, with the patient wearing the same amount
and type of clothing, and graph the results.
•Observe the weight graph for trends (1 liter of water
weighs 1 kilogram).
•Accurately measure all fluid intake and output.
•Teach the patient and family about the need to keep
fluid intake within prescribed restricted amounts and to
ensure that the prescribed daily amount is evenly
distributed throughout the 24 hours.
•Monitor for these manifestations of fluid overload at
least every 4 hours:
•Decreased urine output
•Rapid, bounding pulse
•Rapid, shallow respirations
•Presence of dependent edema
•Auscultation of crackles or wheezes
•Presence of distended neck veins in a sitting position
•Decreased oxygen saturation
•Elevated blood pressure
•Narrowed pulse pressure
•Assess level of consciousness and degree of cognition.
•Ask about the presence of headache or blurred vision.
Nursing Considerations
 Infection
 Monitor drug levels
 Alterations in nutrition
◦
Limit protein, sodium, and potassium
 Potential injury (mentation changes from uremia,
electrolyte changes, acidosis)
 Monitor electrolytes
 Fatigue and weakness
 Monitor ECG changes
 Neurological assessment
 Preparation for dialysis
 Monitor hematocrit and hemoglobin
 Assist with ADL’s
 Administration of epogen
 Impaired skin integrity
~ Prioritize: Meds  diet  EKG  HCT/HGB
Treatment of Hyperkalemia
 Dialysis
 Cation Exchange Resin
◦
Kayexalate ~ rid of excess K+
 Shift intracellularly
◦
Glucose and insulin
◦
Alkali (sodium bicarbonate)
◦
Antagonize cellular membrane effect
◦
Calcium gluconate for membrane
stabilizing effect
Complications

Systemic Manifestations – End Stage Renal Disease
o Neurological  confusion, lethargy, decreased level of consciousness, stupor
Gastrointestinal  nausea, vomiting, anorexia, distention, constipation, or diarrhea
Respiratory  crackles, pulmonary edema, pleural effusion, risk for infection
Cardiovascular  tachycardia, dysrhythmias, rub, pericarditis, increased blood pressure
Integumentary  dry skin, pruritus, edema, bruising, pallor, uremic frost
Fluid/Electrolyte Imbalances

Hyperkalemia: low excretion

Hyponatremia: fluid retention

Hypocalcemia: low excretion of phosphorus

Hyperphosphatemia
o Hematological???
Patient teaching for renal failure pts – including diet and meds
o Chart 71-5 Patient and Family Education: Preparing for Self-Management Prevention of Kidney and Urinary Problems

Be alert to the general appearance of your urine. Note any changes in its color, clarity, or odor.

Changes in the frequency or volume of urine passage occur with changes in fluid intake. More frequent or infrequent
voiding not associated with changes in fluid intake may signal potential problems.

Any discomfort or distress with the passage of urine is not normal. Pain, burning, urgency, aching, or difficulty with
initiating urine flow or complete bladder emptying is of some concern.

The kidneys need 1 to 2 quarts of fluid a day to flush out your body wastes. Water is the ideal flushing agent.

Reduce your intake of carbonated soft drinks.

Changes in kidney function are often silent for many years. Periodically ask your health care provider to measure your
kidney function with a blood test (serum creatinine) and a urinalysis.

If you have a history of kidney disease, diabetes mellitus, hypertension (high blood pressure), or a family history of
kidney disease, you should know your serum creatinine level and your 24-hour creatinine clearance. At least one
checkup per year that includes laboratory blood and urine testing of kidney function is recommended.

If you are identified as having decreased kidney function, ask about whether any prescribed drug, diet, diagnostic test,
or therapeutic procedure will present a risk to your current kidney function. Check out all nonprescription drugs with
your physician or pharmacist before using them.
o Health Promotion and Maintenance

The health-promotion activities to prevent or delay the onset of CKD focus on controlling the diseases that lead to its
development, such as diabetes and hypertension.

Identifying patients who have these disorders at an early stage is critical to CKD prevention.

Teach patients to adhere to drug and diet regimens and engage in regular physical activity to prevent the blood vessel
changes that lead to kidney damage.

Instruct patients with diabetes to keep their blood glucose levels within the prescribed range.

Teach patients with hypertension that drug therapy is not a cure and must be continued along with lifestyle changes.

Urge patients with diabetes or hypertension to have yearly testing for microalbuminuria.

Teach everyone treated for an infection anywhere in the kidney/urinary system to take all antibiotics as prescribed.

Urge everyone to drink at least 3 L of water daily unless a health problem requires fluid restriction.

Caution people who use over-the-counter NSAIDs to avoid abusing these drugs because they reduce blood flow to the
kidney and their long-term use reduces kidney function
Hemodialysis
o what should you do as nurse about medications

Hemodialysis Nursing Care

Many drugs, such as antibiotics, are dialyzable (i.e., can be partially removed from the blood during dialysis)
and should not be administered just before or during dialysis.

Vasoactive drugs can cause hypotension during HD and may also be held until after treatment.

Coordinate with the physician to assess the patient's drug regimen and determine which drugs should be held
until after HD treatment.

Table 71-12 lists common dialyzable and vasoactive drugs that should be given after rather than before HD.
o *Post hemodialysis symptoms

Post-Dialysis Care

Closely monitor the patient immediately and for several hours after dialysis for any side effects from the
treatment.

Common problems include hypotension, headache, nausea, malaise, vomiting, dizziness, and muscle
cramps.

Obtain vital signs and weight for comparison with pre-dialysis measurements.

Blood pressure and weight are expected to be reduced as a result of fluid removal.

Hypotension may require rehydration with IV fluids, such as normal saline.

The patient's temperature may also be elevated because the dialysis machine warms the blood slightly.

If he or she has a fever, sepsis may be present and a blood sample is needed for culture and sensitivity.

The heparin required during HD increases the clotting time, which increases the risk for excessive bleeding.
All invasive procedures must be avoided for 4 to 6 hours after dialysis. Continually monitor the patient for
hemorrhage during and for 1 hour after dialysis
o *Dialysis disequlibrium syndrome

Complications of Hemodialysis – disequilibrium syndrome and viral infections
o
o
o
o
o







Dialysis disequilibrium syndrome may develop during HD or after HD has been completed.
The cause appears to be the rapid decrease in fluid volume and blood urea nitrogen (BUN) levels during HD.
The change in urea levels can cause cerebral edema and increased intracranial pressure.
Neurologic symptoms can result (e.g., headache, nausea, vomiting, restlessness, decreased level of
consciousness, seizures, coma, or death).

The problem may be PREVENTED by starting HD for short periods with low blood flows so that rapid
changes in plasma composition are avoided.

***Assess for and document symptoms of disequilibrium syndrome (headache, nausea, vomiting,
restlessness, decreased level of consciousness, seizures, coma) during and after HD, because early
recognition and treatment with anticonvulsants and barbiturates may prevent a life-threatening situation.
o Chart 71-9 Best Practice for Patient Safety & Quality Care Caring for the Patient Undergoing Hemodialysis

Weigh the patient before and after dialysis.

Know the patient's dry weight.

Discuss with the health care provider whether any of the patient's drugs should be withheld until after dialysis.

Be aware of events that occurred during previous dialysis treatments.

Measure blood pressure, pulse, respirations, and temperature.

Assess for symptoms of orthostatic hypotension.

Assess the vascular access site.

Observe for bleeding.

Assess the patient's level of consciousness.

Assess for headache, nausea, and vomiting.
o Hemodialysis Nursing Care (PP)

Drugs

Post-dialysis assess for hypotension, headache, nausea, malaise, vomiting, dizziness, and muscle cramps or bleeding

Dialysis disequilibrium syndrome
Complications:
o Thrombosis or stenosis
o Infection – most serious are hepatitis and HIV
o Aneurysm formation
o Ischemia
o Heart failure
o

Chart 71-8 Best Practice for Patient Safety & Quality Care Caring for the Patient with an Arteriovenous Fistula or
Arteriovenous Graft
•
Do not take blood pressure readings using the extremity in which the vascular access is placed.
•
Do not perform venipunctures or start an IV line in the extremity in which the vascular access is placed.
•
Palpate for thrills and auscultate for bruits every 4 hours while the patient is awake.
•
Assess the patient's distal pulses and circulation in the arm with the access.
•
Elevate the affected extremity postoperatively.
•
Encourage routine range-of-motion exercises.
•
Check for bleeding at needle insertion sites.
•
Assess for manifestations of infection at needle sites.
•
Instruct the patient not to carry heavy objects or anything that compresses the extremity in which the vascular access is
placed.
•
Instruct the patient not to sleep with his or her body weight on top of the extremity in which the vascular access is placed.
Nursing Considerations (PP)
o Planning for dialysis
o
o
o


Medications

Meals

Activities

Procedures
Dialysis nurse relies on accurate nursing data

Determines “dry weight”

Blood pressure baseline

Lab values

Other considerations
Patient requires close surveillance post-dialysis
Procedure is exhausting
Peritoneal dialysis

How it’s done

Procedure
•
Each PD exchange process consists of three phases: fill, dwell, and drain.
•
A siliconized rubber (Silastic) catheter is surgically placed into the abdominal cavity for infusion of
dialysate (Fig. 71-10).
•
Usually 1 to 2 L of dialysate is infused by gravity (fill) into the peritoneal space over a 10- to 20minute period, according to the patient's tolerance.
•
The fluid stays (dwells) in the cavity for a specified time prescribed by the physician.
•
The fluid then flows out of the body (drains) by gravity into a drainage bag.
•
The peritoneal outflow contains the dialysate and the excess water, electrolytes, and nitrogen-based
waste products.
•
The dialyzing fluid is called peritoneal effluent on outflow.
•
The three phases of the process (infusion, or “fill”; dwell; and outflow, or drain) make up one PD
exchange.
•
The number and frequency of PD exchanges are prescribed by the physician, depending on
manifestations and laboratory data.
•
The more hypertonic the solution, the greater the osmotic pressure (pulling pressure) for water
filtration and fluid removal from the patient during an exchange.

Dialysate Additives
•
Heparin may be added to the dialysate to prevent clotting of the catheter or tubing. Usually
intraperitoneal (IP) heparin is needed only after new catheter placement or if peritonitis occurs. IP
heparin is not absorbed systemically and does not affect blood clotting.
•
Other agents that may be given in the dialysate include potassium and antibiotics. Commercially
prepared dialysate does not contain potassium. Some patients need potassium added to the dialysate
to prevent hypokalemia. Antibiotics may be given by the IP route when peritonitis is present or
suspected. Potassium and antibiotics are not mixed in the same dialysate bag because interactions
may reduce the antibiotic effect.

Nursing care before, during, after

Potential complications
o Peritoneal Dialysis (PP)

Uses the peritoneal membrane as filter

Less efficient

High risk of peritonitis

Procedure involves siliconized rubber catheter placed into the abdominal cavity for infusion of dialysate.

Types of peritoneal dialysis:
Continuous
ambulatory peritoneal
dialysis (CAPD)
Performed by the
patient with the
infusion of four 2-L
exchanges of dialysate
into the peritoneal
cavity.
Each time, the dialysate
remains for 4 to 8 hours,
and these exchanges
occur 7 days a week
(Fig. 71-11 through 7113).
Automated peritoneal dialysis
Intermittent
peritoneal dialysis
Continuous-cycle
peritoneal dialysis
May be used in the acute care setting, the outpatient dialysis
center, or the patient's home.
APD uses a cycling machine for dialysate inflow, dwell, and
outflow according to preset times and volumes.
A warming chamber for dialysate is part of the machine (Fig.
71-14).
The functions are programmed for the patient's specific needs.
A typical prescription calls for 30-minute exchanges
(10/10/10 for inflow, dwell, and outflow) for a period of 8 to
10 hours.
The machines have many safety monitors and alarms and are
relatively simple to learn to use (Fig. 71-15).
Combines osmotic
pressure gradients
with true dialysis.
Form of automated
dialysis that uses an
automated cycling
machine.
The patient usually
requires exchanges
of 2 L of dialysate at
30- to 60-minute
intervals, allowing 15
to 20 minutes of
drain time.
For most patients, 30
Exchanges occur at
night while the patient
sleeps.
The final exchange of
the night is left to
dwell through the day
and is drained the next
During the dwell period,
the patient can use a
continuous connect
system or a disconnect
system.


Advantages
Permits in-home dialysis while the patient sleeps, allowing
him or her to be dialysis-free during waking hours. The
incidence of peritonitis is reduced with APD because fewer
connections and disconnections are needed. Also, APD can be
used to deliver larger volumes of dialysis solution for patients
who need higher clearances.
to 40 exchanges of 2
L three times weekly
are needed.
IPD treatments can
be automated or
manual.
evening as the process
is repeated.
Advantages
Permits 24-hour
dialysis, as in CAPD,
but the sterile catheter
system is opened less
often.
Complications of Peritoneal Dialysis (PP)

Peritonitis – most common cause is connection site contamination; use meticulous sterile technique when
caring for PD catheter and when hooking up or clamping off dialysate bags
•
Manifestations: cloudy dialysate outflow (effluent), fever, abdominal tenderness, abdominal pain,
general malaise, nausea, and vomiting.
•
Cloudy or opaque effluent is the earliest sign of peritonitis. Examine all effluent for color and
clarity to detect peritonitis early. When peritonitis is suspected, send a specimen of the dialysate
outflow for culture and sensitivity study, Gram stain, and cell count to identify the infecting
organism.

Pain - during the inflow of dialysate is common when patients are first started on PD therapy.
•
Usually this pain no longer occurs after a week or two of PD.
•
Cold dialysate increases discomfort. Warm the dialysate bags before instillation by using a heating
pad to wrap the bag or by using the warming chamber of the automated cycling machine.
[Microwave ovens are not recommended for the warming of dialysate.]

Exit site and tunnel infections - should be clean, dry, and without pain or inflammation.
•
can lead to peritonitis, catheter failure, and hospitalization.
•
Dialysate leakage and pulling or twisting of the catheter increase the risk for ESIs.

Poor dialysate flow - usually related to constipation.
•
To prevent constipation, a bowel preparation is prescribed before placement of the PD.
•
An enema before starting PD may also prevent flow problems.
•
Teach patients to eat a high-fiber diet and use stool softeners to prevent constipation.
•
Other causes of flow difficulty include kinked or clamped connection tubing, the patient's position,
fibrin clot formation, and catheter displacement.
•
Ensure that the drainage bag is lower than the patient's abdomen to enhance gravity drainage.
•
Turning the patient to the other side or ensuring that he or she is in good body alignment may help.
•
Having the patient in a supine low-Fowler's position reduces abdominal pressure.
•
Increased abdominal pressure from sitting or standing or from coughing contributes to leakage at
the PD catheter site.
•
Fibrin clot formation may occur after PD catheter placement or with peritonitis.
•
Milking the tubing may dislodge the fibrin clot and improve flow.
•
An x-ray is needed to identify PD catheter placement. If displacement has occurred, the physician
repositions the PD catheter.


Dialysate leakage - seen as clear fluid coming from the catheter exit site
•
Leakage occurs more often in obese patients, those with diabetes, older adults, and those on longterm steroid therapy.
•
During periods of catheter leak, patients may require hemodialysis (HD) support.

Other complications - include bleeding, which is expected when the catheter is first placed, and bowel
perforation, which is serious.
•
When PD is first started, the outflow may be bloody or blood tinged.  This condition normally
clears within a week or two.
•
After PD is well-established, the effluent should be clear and light yellow.
•
Observe for and document any change in the color of the outflow.

Brown-colored effluent occurs with a bowel perforation.

If the outflow is the same color as urine and has the same glucose level, a bladder
perforation is probable.

Cloudy or opaque effluent indicates infection.
Nursing Care During Peritoneal Dialysis (PP)

Before treating, evaluate baseline vital signs, weight, and laboratory tests.

Continually monitor the patient for respiratory distress, pain, and discomfort.

- Check the dressing around the catheter exit site every 30 minutes for wetness during the procedure.

Monitor prescribed dwell time, and initiate outflow.

Observe the outflow amount and pattern of fluid.
Chart 71-10 Best Practice for Patient Safety & Quality Care Caring for the Patient with a Peritoneal Dialysis Catheter

Mask yourself and your patient. Wash your hands.

Put on sterile gloves. Remove the old dressing. Remove the contaminated gloves.

Assess the area for signs of infection, such as swelling, redness, or discharge around the catheter site.

Use aseptic technique:
o Open the sterile field on a flat surface, and place two precut 4 × 4–inch gauze pads on the field.
o Place three cotton swabs soaked in povidone-iodine on the field. Put on sterile gloves.

Use cotton swabs to clean around the catheter site. Use a circular motion starting from the insertion site and moving away toward the
abdomen. Repeat with all three swabs.

Apply precut gauze pads over the catheter site. Tape only the edges of the gauze pads.
TABLE 71-9 A COMPARISON OF HEMODIALYSIS AND PERITONEAL DIALYSIS AS RENAL REPLACEMENT THERAPY
OPTIONS
Hemodialysis
Peritoneal Dialysis
Advantages
More efficient clearance
Easy access
Short tie needed for tx
Few hemodynamic complications
Complications
Disequilibrium syndrome
Protein loss
Muscle cramps
Peritonitis ~ HIGH RISK
Hemorrhage
Hyperglycemia
Air embolus
Respiratory distress
Hemodynamic changes (hypotension, anemia)
Bowel perforation
Cardiac dysrhythmias
Infection
Infection
Contraindications
Hemodynamic instability
Extensive peritoneal adhesions
Peritoneal fibrosis
Recent abdominal surgery
Access
Vascular access route
Intra-abdominal catheter
Procedure
Complex
Simple
Specially trained RN required
Training less complex than for hemodialysis
Nursing Implications
Vascular access care
Abdominal catheter care
Restrict Diet
More flexible diet
LAB TESTS

GFR
o
o
The glomerular filtration rate (GFR) is used as an indicator of kidney function and as a guide to safe levels of protein intake.
A patient with a severely reduced GFR who is not undergoing dialysis is usually permitted 0.55 to 0.60 g of protein per kilogram
of body weight (e.g., 40 g of protein daily for a 150-pound [about 70-kg] adult). If protein is lost in the urine, protein is added to


the diet in amounts equal to that lost in the urine. Protein requirements are calculated based on actual body weight (corrected for
edema), not ideal body weight.
o Best measure of CKD
Creatinine
o Adult
o
Female: 0.5-1.1 mg/dL or 44-97 μmol/L (SI units)
o
Male: 0.6-1.2 mg/dL or 53-106 μmol/L (SI units)
o Elderly: decrease in muscle mass may cause decreased values
o This test measures the amount of creatinine in the blood.
o Creatinine is a catabolic product of creatine phosphate, which is used in skeletal muscle contraction. The daily production of
creatine, and subsequently creatinine, depends on muscle mass, which fluctuates very little. Creatinine, as with blood urea
nitrogen (BUN, see p. 993), is excreted entirely by the kidneys and therefore is directly proportional to renal excretory function.
Thus, with normal renal excretory function, the serum creatinine level should remain constant and normal.
o Besides dehydration, only such renal disorders as glomerulonephritis, pyelonephritis, acute tubular necrosis, and urinary
obstruction will cause abnormal elevations in creatinine. There are slight increases in creatinine levels after meals, especially
after ingestion of large quantities of meat. Furthermore, there may be some diurnal variation in creatinine—nadir at 7 AM and
peak at 7 PM.
o The serum creatinine test, as with BUN, is used to diagnose impaired renal function. Unlike BUN, however, the creatinine level
is affected very little by hepatic function. The creatinine test is used as an approximation of glomerular filtration rate (GFR).
The serum creatinine level has much the same significance as the BUN level but tends to rise later. Therefore, elevations in
creatinine suggest chronicity of the disease process. In general, a doubling of creatinine suggests a 50% reduction in GFR. The
creatinine level is interpreted in conjunction with the BUN test. These tests are referred to as renal function studies. The
BUN/creatinine ratio is a good measurement of kidney and liver function. The normal adult range is 6-25, with 15.5 being the
optimal adult value for this ratio.
BUN
o Adult: 10-20 mg/dL or 3.6-7.1 mmol/L (SI units)
o Elderly: may be slightly higher than those of adult
o The BUN measures the amount of urea nitrogen in the blood.
o Urea is formed in the liver as the end product of protein metabolism. During ingestion, protein is broken down into amino acids.
In the liver these amino acids are catabolized, and free ammonia is formed. The ammonia is combined to form urea, which is then
deposited into the blood and transported to the kidneys for excretion. Therefore, BUN is directly related to the metabolic function
of the liver and the excretory function of the kidney. It serves as an index of the function of these organs. Patients who have
elevated BUN levels are said to have azotemia.
o Nearly all renal diseases cause inadequate excretion of urea, which causes the blood concentration to rise above normal. If the
disease is unilateral, however, the unaffected kidney can compensate for the diseased kidney, and BUN may not become
elevated.
o BUN also increases in conditions other than primary renal disease. For example, when excess amounts of protein are available
for hepatic catabolism (from a high-protein diet or gastrointestinal [GI] bleeding), large quantities of urea are made.
o BUN levels also may vary according to the state of hydration, with increased levels seen in dehydration and decreased levels seen
in overhydration.
o Finally, one must be aware that the synthesis of urea depends on the liver. Patients with severe primary liver disease will have a
decreased BUN. With combined liver and renal disease (as in hepatorenal syndrome), BUN can be normal not because renal
excretory function is good but because poor hepatic functioning has resulted in decreased formation of urea.
DISEASE
Assessment
Physical
Diagnostic
tests
Treatment
Meds
Other
Complications