Download Case_Study_Pressure_Ulcer_Patient

Rachel Hudes
Benedictine University
Dietetic Internship Program
CASE STUDY ASSIGNMENT
NCP Step 1: Nutrition Assessment
Patient Profile
Practice Setting in which you are assessing
this patient/client
Age
Gender
Race
Relevant personal data (e.g. does not speak
English, marital status, lives in a nursing
home, SES etc.)
Symptoms/complaints
CURRENT Medical Conditions/Diagnoses
Hospital room at Saint Anthony Hospital;
general medical floor.
75 y/o
Male
Caucasian
Unable to communicate, resides in a
nursing home, single.
Dehydration, pressure ulcers, constipation.
Multiple contractures of the left
extremities, UTI, sepsis, pressure ulcers on
left ankle.
PAST Medical Conditions/Diagnoses
Medical Test(s) conducted or planned
Medical procedure(s) conducted or planned
Cerebrovascular accident, hypertension,
X-Ray
Anthropometric Data:
Indicator
Value for the patient/client
Height
Weight
Weight change
UBW
IBW
% IBW
BMI
Adjusted Body Weight (if
appropriate)
Patient Weight Goal
66 inches
167.8 lbs (76.3 kg)
None reported
n/a
142 lbs
118.2%
27.4
n/a
n/a
Food/Nutrition Related History
Food Allergies
None
Assessment of
patient/client value
Overweight
Chewing and/or Dental Problems
Swallowing Problems
Bowel Habits/Problems
Recent Changes in Eating Habits
Current Appetite
Food Preferences
Nutrient Malabsorption Problems?
N/V/D
Past Diet Prescriptions
Past Diet Instructions
Patient has difficulty chewing.
Patient has difficulty swallowing.
Currently is constipated.
Patient was placed on nutrition support.
Pt is on nutrition support. Appetite was not
assessed because of this and his inability to
communicate.
n/a
no
no
NPO, enteral tube feedings.
n/a
24 – Hour Recall- N/A (Pt is receiving enteral nutrition support)
Meal
Type of Food
Cooking Method
First Meal of Day
Snack
Second Meal of Day
Snack
Third Meal of Day
Snack
Portion
Food Recall Assessment- N/A
Analyze the recall using MyPyramid Guidelines
1. Analyze the recall using a computer nutrient analysis program of your choice.
2. Attach the computer analysis output to this assignment.
3. Explain the adequacy of the intake below in terms of macro and micro nutrients.
Nutrition Focused Physical Assessment
Physical Appearance
Patient is bedridden and immobile. Lies
with his elbows against the bed and head
back. Eyes were closed and patient was
not in a state to communicate. Appeared to
be resting comfortably. Pt was wearing
heal protectors.
Muscle and fat wasting
Swallowing function
Appetite
Affect (e.g. lethargic, sleeping, coma,
energetic, in pain, etc.)
He did not show signs of muscle wasting.
Poor swallowing function.
n/a
Sleeping.
LABORATORY DATA:
Laboratory Test:
Diet Order
Normal Values:
Height
Weight
Blood Pressure
120/80
Albumin
> 3.5 mg/dL
I&O
Glucose serum
65-110 mg/dL
BUN
Creatinine
BUN/Creatinine ratio
CRP
ESR
GFR
Calcium
Sodium
Potassium
Chloride
C02
Braden Score
6-20 mg/dL
0.61-1.30 mg/dL
0.60-20.00 mg/dL
<1
20 mm/hr
>59
8.6-10 mg/dL
136-145 mmol/l
3.5-5.1 mmol/l
98-115 mmol/l
23-29 mmol/l
23/23
Date:
4/6/2011
Values:
Date:
4/8/2011
Values:
Date:
Date:
4/20/2011
Values:
Values:
Tube feeding:
Jevity 1.2
80ml/hr with
300 ml flush
q 6hrs
Date:
Values:
Juven BID
66 inches
76.3 kg
105
34 H
.71
47.89 H
9.6 H
52 H
115
8.7
140
3.9
98-115
23
6/23 L
DISCUSSION of Laboratory Data
Instructions:
Discuss the relation of laboratory values to disease state and nutritional status.
Consider the following:
 What significance do the abnormal laboratory results have for this patient
( example: type anemia? type hyperlipidemia)?
 If the case is being completed during a rotation where minimal laboratory data is
available (such as WIC), provide a discussion regarding what labs would be
helpful in completing a more complete assessment of the patient/client.
The patient’s known abnormal labs include blood urea nitrogen (BUN),
BUN/Creatinine ratio, C-reactive protein (CRP), and erythrocyte sedimentation
rate (ESR).
ESR is a marker of inflammation within the body and the high level within this
patient may be related to the multiple contractures in his left extremities. The
constant tightness and lack of mobility, due to paralysis of this side of his body,
resulted in his joints stiffening up and leading to deformities, known as
contractures. Joint stiffness and deformity also can occur in people who have
severe arthritis, which is what ESR is used to screen for. Because this pt is
experiencing similar joint damage as to someone who has severe arthritis, it is
likely that this elevated lab is a marker of this pt’s multiple contractures.
CRP is elevated in this patient indicating that he is in a state of active
inflammation/has infection. This could reflect multiple problems that the patient is
experiencing. For example his three pressure ulcers, sepsis, and a urinary tract
infection (UTI).
BUN is elevated in this patient and not creatinine, which reflects his dehydration
status. This also caused his BUN/creatinine ratio to be elevated as well because of
his elevated BUN level. In a state of dehydration this happens because the body
decreases its urine output, leaving more urea in the body. Kidney function appears
to be normal because electrolytes and creatinine are all at normal levels.
This patient also has a Braden score of 6 which is very low and indicates that he is
at risk for developing pressure ulcers/more pressure ulcers.
Other important labs that should have been assessed with this pt are his
hemoglobin/hematocrit, albumin, prealbumin, total serum protein, and serum zinc
levels.
MEDICATIONS: 4/20/2011
Date:
Medication &Amount:
Desyrel: 150 mg via gastric
tube @ HS
Purpose or Function:
antidepressant
Celexa: 40 mg via gastric tube, antidepressant, SSRI
daily
Heparin: 5000 units via
anticoagulant
subcutaneous, BID
Significant Nutritional Implications:
May cause constipation
Nausea, increased sweating, diarrhea
May cause constipation, subcutaneous and skin
necrosis
Aspirin: 325 mg via gastric
tube, daily
Analgesis, antipyretic,
antiarthritic, NSAID, to
prevent CVA or MI
May decrease iron and increase BUN
Tylenol: 650 mg via gastric
tube, q4-6hrsPRN
Omeprazole: 20 mg via
gastric tube, daily
Analgesic
Easy bruising, bleeding, nausea,vomitting
Antiulcer, antiGERD
May decrease calcium absorption and serum
vitamin B 12
Baclofen: 10 mg via gastric
tube, TID
Skeletal muscle relaxant,
antispasmodic
Used for brain injury
May cause constipation, increase urinary frequency
and increase glucose
Ensure hydration and vitamin C
Albuterol Sulfate: 0.083% via Antiasthma,
oral inhalation, q 6hrs pm
bronchodilator,
Sympathomimetic, beta 2
agonist
Diarrhea, indigestion, nausea, upper respiratory
infection, urinary tract infection
Abilify: 30 mg via gastric tube, Antipsycotic
HS
Stroke, akathisia (prolonged, abnormal muscle
spasms or contractions or a sense of restlessness or
need to move), increased blood sugar or diabetes,
low blood pressure, low white blood cell count,
seizures, nausea, vomiting, constipation
Nausea, vomiting, diarrhea, rash, headache, ringing
in the ears, decreased hearing
Minocycline: 100 mg via
gastric tube, q 12hrs X 7 days
Used to treat infections of
the skin, respiratory tract,
and urinary tract
Flagyl: 500 mg via gastric
Antibiotic: used to treat
tube, q 8hrs X 5 days
UTIs
Clistin: 110 mg via IV, daily X Antihistamine
4 days
Vitamin C: 500 mg via gastric Vitamin supplement
tube, BID
Ipratropium BR: 0.02%
Bronchiodilator
solution via nasal, q 6hrs pm
Naproxen: 375 mg via gastric Antiarthritic, analgesic,
tube, BID prn
NSAID
Apap: 160 mg/5 ml via gastric
tube, q 6hrs prn
Zosyn: 3.3 gm via IV, q 6hrs X
5 days
Zithromax: 500 mg via gastric
tube, daily X 5 days
Abdominal cramps, constipation, diarrhea, nausea,
upset stomach, vomiting
Decreased urination, rash
Can cause urinary retention, UTI, diarrhea,
nosebleeds
May cause UTI, increase bun, peripheral edema
Pain reliever and fever
reducer
Antibacterial used t o treat Diarrhea, constipation, nausea, fever, vomiting,
infection
urinary tract infection, rash
Antibacterial used to treat a Diarrhea, nausea, vomiting, upset stomach
variety of infections.
Infection of the urethra.
DISCUSSION of Medications
Instructions:
Discuss drug-nutrient interactions and side effects the medicines may cause that have
nutritional significance.
Consider the following:
 Include whether the patient exhibits any of these side effects.
 Discuss relevant relations of medications to disease symptom complaints.
The drugs that the patient is taking that have the most nutritional significance are
aspirin, desyrel, naproxen, flagyl, ipratropium BR, baclofen, and heparin. The
medications that may be either contributing to the patients constipation or making
it worse include the heparin, baclofen, and desyrel, The medications that may be
related to the patient’s increased BUN level and (urinary tract infection) UTI
include naproxen and ipratropium BR. The Heparin may also be negativily
effecting the patients skin integrity which is also vulnerable and experiencing
inflammation from pressure ulcers. In terms of Vitamin C, aspirin may cause a
decrease in the absorption of this nutrient but because of this he is receiving
additional vitamin C via his gastric tube to compensate for this. This is also
important because he may also be losing Vitamin C through wound fluid loss.
NCP Step 2: Nutrition Diagnosis
PATHOPHYSIOLOGY
CURRENT Medical Conditions/Diagnoses
List ALL current medical conditions and describe the pathophysiology of each. Add
additional rows as needed. Be sure to reference your findings. Diagrams may also be
helpful in explaining the pathophysiology of some diseases/conditions.
Pressure Ulcers:
A variety of factors contribute to putting someone at risk and causing
the development of pressure ulcers.
Pressure ulcers are areas of damage to the skin and underlying tissue
that usually occur over bony protrusions such as over the sacrum,
ischial tuberosities, trochanters, malleoli, and heels, primarily due to
on-going compression, moisture, friction, and/or shearing forces. The
chart above displays these primary/extrinsic factors as well as
secondary/intrinsic factors. These situations can lead to reduced blood
flow to the skin tissue which can eventually result in erosion, tissue
ischemia, and infarction. When blood carrying oxygen and nutrients
are not being utilized by skin tissue it can break open. Unrelieved
pressure of certain areas of the body due to lack of movement
Extrinsic Factors:
This image represents a person’s heal resting on a hard surface. The
arrow that is labeled with friction is showing how this force is opposite
of the direction of the shearing force, taking place between the skin of
the heel and the bone. Shearing forces are exerted parallel to the skin
and is generated by forces (friction) acting against it and moving in the
opposite direction.
Moisture also alters the resistance of the epidermis to extend forces by
softening the skin’s surface and reducing the tensile strength. Urine,
feces, perspiration and/or wound drainage may soften the skin, making
it more susceptible to pressure, shear and friction.
Friction is resistance to movement between the patient’s skin and the
external support surface. This force acts in a direction that is opposite
to patient movement. Abrasions of the epidermis and dermis occur as a
result of friction between the skin and the bed surface. Tissues, which
are attached to the bone, are compressed, obstructed and torn in both
shear and friction situations. Shearing and friction occur when the:
 patient slides in bed/chair

patient’s bed-head is elevated beyond 30 degrees (the most
common cause of shear injury)

patient is pulled across bed/chair as a result of incorrect manual
handling, causing friction between the skin and bed/chair’s
surface

patient is restless or has limb spasms, leading to friction between
the skin and the bed surface.
This image displays how pressure is transferred from the external
surface, through the layers of the skin, toward the underlying bone, as a
person sits. Skin, blood vessels, subcutaneous fat and muscle are
compressed between the bone (which acts as a counter pressure) and the
external surface.
This results in a cone, or pyramid shaped, pressure gradient. The apex
of the cone equates to the bony surface where tissue interface pressures
are highest. This leads to the intensity of pressure being up to five times
greater on deep tissues (muscles/bony surfaces) than that on the
epidermis.
Muscle tissue is more sensitive and less resistant to the pressure then the
skin and as a result, deep tissue necrosis often occurs first at the bony
interface as a result of this pressure. Pressure exerted at the bony
interface then emerges at a point in the surface of the skin. A small,
inflamed area, over a bony prominence, may indicate tissue breakdown
that is much deeper and wider than indicated at the surface of the skin.
Intrinsic Factors:
These factors contribute to the risk a person has for developing
pressure ulcers because they influence the skin’s supporting structure,
and/or lymphatic system. They are individual patient characteristics
that affect the ability of skin and soft tissue to withstand unrelieved
pressure, friction and shear forces. Therefore, identification of intrinsic
risk factors is important when assessing PU risk. They include
nutritional status, demographics, pain level, oxygen delivery system,
chronic illness, pain levels, and medications.
Nutritional status:
Poor nutrition has a significant role in PU development. Deficiencies
can result from either decreased intake or malabsorption. Research
indicates that the following factors increase the risk of developing a PU:

malnutrition

low levels of protein/albumin

recent weight loss or morbid obesity

specific deficiencies such as Vitamin C, iron, and zinc.
Demographics:
Individual characteristics that appear to be associated with increased
risk include:

> 65 years of age: this automatically puts the pt at risk for
depletion of lean body mass since this naturally occurs with age.
Older age also results in natural changes to the skin and body.
The skin of older adults is generally more fragile, thinner, less
elastic, and drier then the skin of young adults. Also new skin
cells are usually generated more slowly. All of these conditions
make their skin more vulnerable to damage

Male

Immobility

Caucasian

Multiple co-morbidities that may result in poor blood flow,
immobility, loss of senses.

Previous history of PU injury, including reperfusion injury and
those extending beyond the level of the dermis.
Once injured, the tensile strength of the skin and underlying soft tissues
are not restored to their original state and strength.
Oxygen delivery system:
Decreased supply of oxygen to the area under stress leads to increased
risk. Risk conditions include:
 respiratory disorders

cardiovascular impairment

smoking

autonomic dysfunction (as seen in spinal cord injury)

fever or other conditions that lead to increased skin or core body
temperature (every degree centigrade rise in temperature leads to
a 10% increased demand for oxygen)
Pain level:
Pain can decrease the amount of physical activity and movement of a
person.
Chronic Illness:
Certain conditions such as diabetes, renal impairment, and metastatic
cancer increase risk for developing pressure ulcers.
Medications:
Drugs that increase the risk of developing pressure ulcers include those
that decrease sensation, cause drowsiness which may result in less
movement, decrease inflammatory response, and decrease peripheral
blood pressure.
Dehydration:
Can occur when one is not being properly hydrated or is experiencing
an increase in fluid loss. When the body is deprived of water, fluid
volume decreases and the body works to retain water, which is why a
decrease in urination and elevated BUN levels are a marker of
dehydration.
Urinary Tract Infection:
Most are caused my bacterial infections and may occur due to poor
hygiene. Normally the bladder is coated with a variety of cationic
antimicrobial peptides such as defensins and cathelicidin, which disrupt
the integrity of bacterial cell walls. This helps to keep the urinary tract
sterile along with mannosylated proteins that interfere with the binding
of bacterium to the uroepithelium. When things such as urinary
catheter or trauma disturb the protective lining, bacteria can invade the
exposed epithelium by binding to it. As bacteria builds up they can
form structures that become more difficult for the immune system to
battle and antibiotics to treat.
Constipation:
The patient possesses several factors that may be contributing to his
constipation, such as dehydration, lack of mobility and physical activity,
and certain medications. During this state there is an increase in
colonic luminal pressure. During constipation, stool consistency lacks
sufficient water to make it easier to move through the colon.
Multiple Contractures of the left extremities:
This condition can happen when there is prolonged tightness and
immobility of a joint or muscle which leads to the deformity and
shortening of it. The joint will lock which is an irreversible situation
that only surgery can fix.
Sepsis:
Inflammatory Cascade:
Sepsis can occur from infection at body sites such as the lungs,
abdomen, soft tissue, urinary tract or as a result of primary blood
stream infection such as meningococcemia. Sepsis can be caused by the
signaling of mediators such as the out membrane component of either
gram negative or gram positive organisms or fungal, viral, or parasitic
components.
A family of transmembrane receptors are how these mediators produce
their signals. The production of proinflammatory cytokines such as
tumor necrosis factor and interkeukin 1 occur due to the activation of
nuclear factor-KB in the monocyte. This leads to the production of
toxic downstream mediators, including prostaglandins, leukotrienes,
platelet-activating factor, and phospholipase A2. Damage to the
endothelial lining, leading to increased capillary leakage is caused by
these mediators. These cytokines also lead to the production of
adhesion molecules on endothelial cells and neutrophils. Neutrophilic
endothelial interaction leads to further endothelial injury through the
release of the neutrophil components. Activated neutrophils release
nitric oxide, a potent vasodilator that then leads to septic shock.
Link between inflammation and coagulation:
IL-1 and TNF-α also have direct effects on the endothelial surface. As a
result of these inflammatory cytokines, tissue factor, the first step in the
extrinsic pathway of coagulation, is expressed on the surfaces of the
endothelium and of monocytes. Tissue factor leads to the production of
thrombin, which is a proinflammatory substance and results in fibrin
clots in the microvasculature. Fibrinolysis is also impaired during the
septic process due IL-1 and TNF-α causing the production of
plasminogen activator inhibitor-1. This is a potent inhibitor of
fibrinolysis which therefore reduces the break down of clots.
Proinflammatory cytokines, such as antithrombin and activated protein
C (ACP), also disrupts the body's naturally occurring modulators of
coagulation and inflammation. Protein C circulates as an inactive
zymogen but, in the presence of thrombin and the endothelial surfacebound protein thrombomodulin, is converted to the enzyme-activated
protein C. Studies have shown that proinflammatory cytokines can
shear thrombomodulin from the endothelial surface as well as lead to
downregulation of this molecule, thus preventing the activation of
protein C. APC and its cofactor protein S turn off thrombin production
by cleaving factors Va and VIIIa. APC also restores fibrinolytic
potential by inhibiting plasminogen activator inhibitor-1. In vitro
studies have revealed that APC has direct anti-inflammatory properties,
including inhibiting the production of proinflammatory cytokines by
LPS-stimulated monocytes, inhibiting leukocyte adhesion and rolling,
and inhibiting neutrophil accumulation.
Antithrombin is the second naturally occurring endothelial regulator
affected during sepsis. Antithrombin inhibits thrombin production at
multiple steps in the coagulation cascade as well as by binding and
inhibiting thrombin directly. Antithrombin, when bound to endothelial
cell surface glycosaminoglycans (GAGs), leads to the production of the
anti-inflammatory molecule prostacyclin (prostaglandin I2 [PGI2]).
Evidence exists that neutrophil elastase cleaves GAGs off the surface of
the endothelial lining, thus limiting the anti-inflammatory properties of
antithrombin
Immunoparalysis:
CD4 lymphocytes play a key role in the inflammatory response seen in
sepsis. Early in the sepsis process, these cells produce large amounts of
the proinflammatory mediators, including interferon gamma, TNF-α,
and IL-2. CD4 lymphocytes may evolve over time, whereby the CD4
lymphocytes produce anti-inflammatory cytokines, including IL-10, IL4, and IL-13. This is often driven by the release of stress hormones, such
as catecholamines and corticosteroids. These cytokines dampen the
immune response and can lead to the deactivation of monocytes.
Additionally, TNF released early can cause apoptosis of lymphocytes in
the gut, leading to further immunosuppression.
On-going inflammation and coagulation cardiovascular insufficiency
and multiple organ failure can occur and lead to death.
PAST Medical Conditions/Diagnoses
List ALL past medical conditions and describe the pathophysiology of each. Add
additional rows as needed. Be sure to reference your findings. Diagrams may also be
helpful in explaining the pathophysiology of some diseases/conditions.
Hypertension:
Lifestyle factors such as poor diet, limited physical activity, and
smoking can lead to this condition and result in disruption of healthy
physiological mechanisms that control blood pressure.
Inflammation can occur from consuming a diet that is high in sodium,
fat, processed foods, and is nutrient poor due to an increase in blood
acidity and free radicals. If this is prolonged, endothelial dysfunction
can occur and damage to the vascular walls, causing peripheral
resistance. The endothelial cells lose their ability to pump blood further
and more effectively throughout the vascular system. High blood
pressure results from this and in combination with the high levels of
sodium and increased water retention due to high sodium content.
Normally high blood pressure signals the parasympathetic system to
inhibit the systems responsible for increasing blood pressure. The
parasympathetic system works to decrease blood pressure, stimulate
vasodilation, and excrete sodium. Nitric oxide and natriuretic peptide
are involved in doing this. Because endothelial damage results in the
decreased production and effect of nitric oxide, vasodilatation of the
arteries declines along with sodium excretion, and high blood pressure is
prolonged within the body. The continuation of high sodium levels
within the body cause high blood pressure because of the signal to
continue to reabsorb water in order to dilute the blood, which increases
blood volume. Increased blood volume = increased blood pressure.
Two of the major systems, when activated, that cause an increase in
blood pressure are the rennin-angiotensin-aldosterone system and the
sympathetic systems because they work to retain sodium and water.
When these systems become hyperactive, hypertension can result.
This diagram displays how the rennin-angiotensin-aldosterone system
functions. It is normally activated when blood pressure falls. If
hyperactive, the kidney will over produce the hormone rennin which
will participate in its normal function of converting angiotensinogen to
angiotensin 1. Angiotenson-converting enzyme then converts
angiotensin 1 to angiotensin 2. Angiotensin 2 is a hormone with
powerful effects on blood pressure. It stimulates the adrenal gland to
secrete aldosterone, which is another hormone that stimulates the
kidneys to reabsorb sodium and water, causing an increase in blood
volume. Angiotensin 2 also stimulates vasoconstriction at the same time
blood volume is increased, which further increases blood pressure.
Normally the kidneys regulate blood pressure by controlling the
extracellular fluid (ECF) volume. The major cation in the ECF is
sodium. The Kidneys control how much is excreted from the body,
which in a healthy individual, is enough to maintain homeostasis and
fluid volume. This results in normal blood pressure levels. When a diet
high in sodium is consumed, this may disrupt the balance of sodium
within the ECF because the level of intake becomes much greater than
the output and excretion by the kidneys. When this occurs over a
prolonged period of time, vasoconstriction, which decreases the space
between the walls of arteries, continue to increase the amount of sodium
retained. The systolic pressure will also increase with high sodium
intake because the heart is going to pump harder in order to pump the
sodium rich blood fast through the body and into the kidneys for
excretion. The heart muscle can become over-worked and artery walls
can lose elasticity from this process which makes it harder for
vasodilatation to occur and increases resistance to blood flow. The lack
of accommodation to the high systolic pressure can cause damage
arteries
Vasoconstriction can also be enhanced by lack of exercise because of the
decreased stimulation of vasodilatation. Exercise promotes
vasodilatation because the rate that oxygen is transported to tissues is
increased because of the need for more oxygen during exercise. In order
for blood to deliver oxygen and nutrients to tissue of the body to utilize
and produce energy during this active state, the vasoconstriction of
arteries is stimulate in order for blood to move through them efficiently.
High blood pressure also results from an increase and prolonged
sympathetic activity. This system works by secreting norepinephrin
which is a vasoconstrictor of arteries, increasing peripheral resistance
and high blood pressure.
Leukocytosis:
White blood cell maturation and release into the circulation are
influenced by colony-stimulating factors, interleukins, tumor necrosis
factor, and complement components. Within the bone marrow there
are white blood cells that are undergoing maturation and those who are
mature and in storage. Their release is stimulated by infection or
inflammation and the number that circulates can increase by 2-3fold
within a couple of hours. This increase is indicative of how the bone
marrow responds to infection or inflammation. The white blood cells
released called leukocytes are divided into two classes: one pool of cells
circulates freely and the second pool is deposited along the margins of
blood vessel walls. Cytokines, growth factors, and adhesion molecules
control the amount of white blood cells released into the free circulation
from the bone marrow, the rate of consumption of cells into the tissues,
and the rate of marginating cells out of blood vessels into the tissues.
Severe leukocytosis is common in those who have had stroke due to
occlusion and ischemia.
Cerebral Vascular Accident (CVA):
Endothelial cells line the innermost layer of the blood vessel and releases
nitric oxide. Nitric oxide is produced by healthy endothelial cells and it
works to relax and dilate blood vessels. It also helps to prevent
monocytes from sticking under the endothelial wall within the artery.
The is important when one has atherosclerosis because diet change that
results in lowering blood pressure and stimulating the release of nitric
oxide can decrease their build up within the blood vessel walls and
therefore, stabilize it. The blood vessel is also made up of the media
which is the middle layer, containing smooth muscle cells. It also
contains collagen which provides structure to the blood vessel, elastin
which provides elasticity, and the smooth muscle which relaxes when
nitric oxide is present.
A stroke can result from having prolonged hypertension throughout life
along with a high fat diet, which can result in blood clot formation that
blocks blood flow in an artery that feeds the brain, preventing oxygen
and nutrient transportation to the brain. This occurs due to damage of
the endothelial cells and artery walls. The damage can lead to
atherosclerosis which further causes decrease in elasticity, constriction
of blood flow, and thrombus formation. During an ischemic stroke,
which happens in about 80% of stroke victims, a thrombus (blood clot)
or embolus occludes a cerebral artery, causing hypoxia and neuronal
injury.
An irreversible neuronal injury occurs when cerebral blood flow (CBF)
is very low for longer than 30-60 minutes. Normal CBF is 50-55
ml/100gm/min. If the CBF drops below 18, electrical activity pauses. If
the CBF dips below 10, neuronal metabolism stops. The chart above
displays the pathway of injury due to lack of fuel to the brain. Due to a
lack of fuel and oxygen being transported to the brain cells,
excitotoxicity occurs. This results from an over-reaction of the
neurotransmitters; primarily glutamate and aspartate. An energy
dependant process clears glutamate and aspartate from the synaptic
terminals which increases the concentration of both in the extracellular
spaces due to membrane pump failure. This occurs in an energy
depleted state which causes the receptors, N-methy1-D-asapartate
(NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxanole propionate
to stimulate the opening of calcium channels. This then leads to calcium
building up/ influx in the intracellular space. Intracellular calcium is
responsible for activating the destructive enzymes (proteases, lipases,
and endonucleases) which allow the release of the cytokines and
inflammatory mediators. T he most prominent cytokine include
interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and IL-6.
Shortly after the ischemic attack, leukocytes are recruited to the
ischemic areas. The leukocytes end up contributing to the damage as
well as aid in improving it. Their beneficial effects include activating
vasoactive substances such as nitric acid, oxygen free radicals, and
arachidonic acid metabolites (cytokines). These same cellular mediators
also cause vasoconstriction, increased permeability, increased platelet
aggregation, increased leukocyte adherence to the endothelial wall, and
immunoregulation.
Endothelial cells react to hypoxia by swelling which causes mechanical
plugging by erythrocytes, leukocytes, and platelets in the ischemic area.
This interrupts the vasoactive effects of nitric acid and endothelial
peptides and leukocyte adherence to the endothelial wall is promoted.
The degree and duration of decreased CBF determines the severity of
the ischemic injury. Before neuronal death there is a window of
opportunity for a reverse in blood flow abnormalities within the brain,
called ischemic penumbra. This situation is characterized as having a
CBF between 10 and 18. Perfusion/blood flow must be reestablished
before 3-6 hours of ischemia or before the CBF drops to 10. After 3-6
hours of ischemia, irreversible damage occurs to the capillary
endothelium. The blood-brain barrier becomes dysfunctional and serum
proteins and water leak into the interstitial space. This damages the
plasma membrane and coagulation necrosis occurs.
Hypoxia:
Due to an embolism or thrombus, hypoxia can occur. This results from
the occlusion of a blood vessel resulting in the blockage of blood flow
and oxygen. Hypoxia can from as a result of atherosclerosis. In blood
vessels that are experiencing atherosclerosis, blood clots can result in an
embolism which is when the blood clot breaks off and travels through
the cardiovascular system and ends up blocking a smaller vessel because
it is too big to move through it.
When there are high levels of LDL present in the circulatory system it
can get oxidized which creates injury by burrowing into the artery wall.
High blood pressure contributes to this injury because of the damage it
can cause to endothelial cells within the vessel wall.
In response to the injury, the immune system recruits white blood cells
and platelets which turn into marcophages in the artery wall. The
macrophages are responsible for getting rid of the LDL-cholesterol but
they can build up in the artery. When they become stuffed with LDLcholesterol they form a fatty streak which visibly starts the
atherosclerosis process. If this remains ongoing throughout the years,
more cholesterol, connective and elastic tissue, calcium, and cell debris
accumulate and turn the fatty streak into plaque. As the artery tries to
heal itself, smooth muscle cells migrate in to cover the plaque, forming a
fibrous cap around it. Macrophages kill the smooth muscle cells within
the media, within the blood vessel, and release enzymes that break down
the fibrous cap. The cap ruptures which causes more inflammation,
causing a blood clot because the body thinks it is an emergency. The
blood clot can lead to hypoxia if it occludes an artery.
Medical Conditions/Diagnoses INTER-RELATIONSHIPS
Describe the inter relationship of the patient/clients disease states.
The use of a diagram is encouraged, but the diagram must be accompanied by a
narrative explanation. Be sure to reference your findings..
HTN: the pt’s history of HTN may have contributed to his weakened
blood vessels. The damage caused by this led to the compromised
ability for blood to carry oxygen and nutrients to tissues in his body.
Tissues deprived of nutrients and oxygen is a cause of pressure ulcers
and also contributed to his past CVA.
Hypoxia: when tissue is deprived of oxygen. Direct cause of a pressure
ulcer formation because of the occlusion of a blood vessel. This
situation is what may have been cause by prolonged hypertension
and/or other lifestyle factors. For example, eating a high-fat diet and
getting little physical activity throughout life, may have caused
constriction of his blood vessels and possible plaque formation, leading
to blood clot formation.
The chart above is a general representation of what the pt’s past CVA
led to.
CVA with Hemiplegia: led to paralysis of the left side of the pt’s body
because of brain cell necrosis and loss of nerve function. The CVA
caused injury to the right side of the brain since he is experiencing
paralysis on the left. This caused the patient to be confined to his bed
and unable to change positions. Decreased mental awareness also
decreased his ability to take care of himself and prevent pressure ulcers.
This condition contributed to the development of multiple contractures
and inability for anyone to move joints of the lower extremities. A
combination of immobility, loss of lean body mass comprising muscle
and skin – as well as challenges to the immune system increase the risk
of pressure ulcers by 74%. (8) This patient has experienced all of these
factors due to being 75 y/o, being immobile, and having inflammation
and infection.
The UTI may have resulted from the patient being incontinent after his
CVA, which caused him to lose all sensation on one side of his body. If
the pt is incontinent, it is known that problems with bladder control can
greatly increase the risk of pressure sores because the skin may be
frequently moist, making it more susceptible to pressure, friction, and
break down, especially while the pt is already immobile.
Sepsis: Sepsis could have occurred by bacteria entering the blood
stream through the broken skin from his pressure ulcers or may have
been the result of his urinary tract infection, where the build of bacteria
entered his blood stream. Sepsis further increases the pt’s nutritional
and energy demands because it is a severe infection, causing
inflammation and may interfere with ability for wounds to heal and
organs to function normally, if protein stores are depleted due to
cytokine release and increased demands. This could lead to the
formation of more wounds and complications if aggressive nutritional
therapy is not administered, along with other medically appropriate
actions.
Dehydration: This may be contributing to a disruption in the wound
healing process, maintaining healthy skin, and preventing tissue break
down, since adequate hydration is needed for this and for bodily
reactions to occur. This could also be contributing to the constipation
the patient is suffering from. If his wounds have been releasing fluid,
this would increase his fluid needs depending on the amount of
drainage. In this patient dehydration was possibly caused by his
current state of sepsis, not being properly hydrated, or experiencing an
increase in fluid loss, possibly from his wound. The patient’s tube
feeding alone did not provide him with enough water to meet his needs,
so if water flushes were not performed at his nursing home as ordered,
this could have resulted in the patient becoming dehydrated.
Assessment of Nutrition Needs
Calories: 1900-2100 kcals
Show your work:
(30-35 kcals/kg)
30 X 76.3 = 2290 kcals
35 X 76.3 = 2670 kcals
(nutrition care manual)
Rationale for calorie level:
The patient is not malnourished and has a BMI that classifies him as being
overweight. He is also 75 years old and because of this he is experiencing a decline
in lean body mass. I would not want restrict or determine his calorie needs based on
his BMI because his body is in a state of stress and inflammation due to skin
breakdown and pressure ulcers. This would cause an increase in his metabolic rate.
I chose 30 because this level will prevent over feeding the patient, will help to
maintain his weight, and meet his metabolic needs. Along with other nutrients given
to him, the kcals provided should help to provide enough energy to the patient in
order for him to utilize additional nutrients given to him for wound healing. It is
also important to maintain his weight because the loss of weight in the form of fat
and muscle results in less cushioning between bones and a bed.
Protein: 115-150 grams
Show your work:
1.5-2 grams/kg)
1.5 X 76.3 = 115 grams
2 X 76.3 = 152 grams
Rationale for calorie level:
He is naturally experiencing a decline in lean body mass due to older age. He also is
experiencing skin breakdown from pressure ulcers, causing inflammation and
stress. This condition increases his need for protein to promote the fibroblastic
response, collagen synthesis, and the wound remodeling processes. I also figured his
protein needs based on him having sepsis which would further increase his
metabolic needs.
Other pertinent macronutrient levels:
Show your work:
Rationale for calorie level:
Other pertinent micronutrient levels:
Show your work:
Vitamin C: 500-1000 mg/day
Arginine: 14 g/day
Glutamine: 14 g/day
Rationale for calorie level:
Preservation of skin tissue, strengthening of tissue resistance, and promoting tissue
repair. Research has shown the benefits of maintaining adequate levels of these
nutrients in those with pressure ulcers or who are at risk.
Arganine: Appears to favorably influence pressure ulcer healing by affecting
microvascular and perfusion changes, enhancing collagen production via proline synthesis.
(8) One study showed that giving an oral nutrition supplement with this nutrient at 9 g per
day and 21 grams of protein total significantly improved the rate of pressure ulcer healing.
The 14 grams per day of arginine and the 14 grams of glutamine almost just about equal the
28 grams of total protein given by the oral nutritional supplement in the study. (21 grams
pro + 9 grams Arginine = 30 grams total Pro)
Glutamine: This amino acid serves as an energy source and for proliferation by
inflammatory cells within the wound. It has been shown to maintain mucosal integrity and
reduce infection rates. In recent research, it has been included in nutrient mixtures, also
containing HMB and arginine. (14 gm glutamine, 14 gm arginine, 2 gm HMB) This
mixture showed to be effective in promoting wound healing.
Vitamin C: One study showed that giving an oral nutrition supplement made up of a
combination of 500 mg Vitamin C, arginine, and zinc, significantly improved the rate of
pressure ulcer healing 2.5 fold in PU pts. Because the pt may be experiencing fluid loss
from wound drainage, he may also be losing vitamin C since it is water soluble. To be safe I
would want to provide 500 -100 mg/day to compensate for any losses. Since the UL is 2g
this would be considered safe.
Fluid
Show your work:
35 mL/kg
35 X 76.3 = 2670.5 mL
Rationale for calorie level:
The patient does not show any symptoms of kidney problems because electrolytes
are all within normal limits, along with creatinine. BUN and BUN/creatinine ratio
are likely elevated due to the dehydration the patients is experiencing. Due to the
state of stress this patient is experiencing and inflammation due to pressure ulcers I
recommend 35 mL/kg of body weight. He may have increased needs because of
fluid loss from his wounds, older age, and an increase in protein being given.
Which of the following domains is the patient/client presenting with :
DOMAIN
INTAKE
Energy Balance
Oral or Nutrition Support
Intake
Fluid Intake
Check () if patient
presents with this
characteristic
Y
If checked, explain
evidence to support this
decision
Patient was admitted to the
hospital with dehydration
and constipation. His BUN
and BUN/creatinine ratio
also indicate dehydration.
Bioactive Substance Intake
Nutrient Intake
Y
Three pressure ulcers on the
patient’s body. Lack of
nutrients may be
contributing to their
formation and lack of
healing.
CLINICAL
Functional
Y
Biochemical
Y
Paralysis of the left side of
the body caused by past
CVA, affecting the right
side of the brain.
Elevated CRP, BUN,
BUN/creatinine ratio, and
ESR levels.
Weight
BEHAVIORAL-ENVIRONMENTAL
Knowledge and Beliefs
Physical Activity &
Y
Function
The patient is immobile and
bedridden because of
multiple contractures and
paralysis of his left side.
Food Safety and Access
What is the Nutrition Diagnosis for this client/patient?
Diagnosis or
Etiology
Problem
Increased
Related to
Wounds
nutrient needs
(Protein,
Vitamin A,
Zinc)
Inadequate
Related to
dehydration
fluid intake
Related to
Related to
Signs and/or
Symptoms
Stage 1, 2, and
4 pressure
ulcers.
High BUN and
BUN/Creatinine
ratio and
constipation.
NCP Step 3: Nutrition Intervention:
Nutrition Prescription (Diet Order)
Indicate the diet changes and progression since patient’s admission to present
Date
Diet Prescription/Order
4/09/2011
Enteral Tube Feeding: Jevity 1.2 @
80ml/hr X 18hrs with 300 ml H20 q 6.
4/13/2011
Enteral Tube Feeding: Jevity 1.2 @
80ml/hr X 18hrs with 300 ml H20 q 6.
4/20/2011
Juven BID
Enteral Tube Feeding: Jevity 1.2 @
80ml/hr X 18hrs with 300 ml H20 q 6.
Juven BID
Discussion of Diet Order(s)
Consider:
 Rationale & indications for current diet order
 Do you agree with the order? Discuss why or why not.
 Would any other dietary modifications be realistic and appropriate? Discuss why
or why not.
In the nursing home this patient was receiving enteral nutrition support. Nutrition
support in the form of enteral nutrition was chosen as an intervention previously
because of lack of neurological and swallowing function, and inability to feed
himself, due to his past CVA. He was receiving Jevity 1.2 @ 80mL/hr X 8hrs with
300ml h20 flushes q 6hrs. This tube feeding was providing the patient with a daily
intake of 1728 kcals, 80 grams of protein, and 2366 mL of water. Along with his
first assessment, the RD recommended that the Dr. order Juven BID for this patient
in order to promote wound healing along with keeping his current tube feeding that
was provided at his nursing home.
I do not agree with his current diet order of Jevity 1.2 @ 80mL/hr X 18 hours
because after calculating his calorie and protein needs, this rate does not them.
Malnutrition has been found to delay pressure ulcer healing and increase the risk of
developing chronic pressure ulcers. Because this patient was not receiving enough
enteral formula to meet his needs, this could have contributed to the advancement in
the formation of his pressure ulcers. I also calculated how much protein and
calories he was getting from the Juven BID which still did not add enough extra
calories and protein to meet his daily needs. With the calories from the Juven and
the tube feeding (TF), he was receiving 1868 kcals and 95 grams of protein per day.
Since he is tolerating the 80mL/hr, I would recommend advancing it to 100mL/hr X
18 hours because this plus the Juven BID would supply him with 2300 kcals and 111
grams of protein, which would be sufficient. At 100mL/hr X 18hrs he would be
receiving a total of 1800 mL/day of Jevity 1.2. Because he is dehydrated, fluid losses
from his wounds are unkown, and he is getting an increase in protein, I would leave
his water flushes at 300 mL q 6 hours which would provide him with a total of 2658
mL/day. His renal function also appears to be good as evidenced by his electrolyte
levels which are within normal limits and does not have chronic heart failure which
further implies the safety of increasing the fluid given for this specific pt..
I agree with the order of Juven because of the nutrient mixture it provides as well as
additional calories for protein which help to meet the energy needs of the patient.
The specific nutrients within it have been shown to improve and promote wound
healing when given in combination. They include: calcium beta-hydroxy-betamethylbutyrate, arginine, glutamine.
(ADA Nutrition Care Manual)
Nutrition Intervention Plan
Consider the Types of Interventions for this patient/client...
 Food and/or Nutrient Delivery
 Nutrition Education
 Nutrition Counseling
 Referral to other disciplines will in current setting
 Referral to other disciplines/services post D/C.
Identify each of the short and long term specific nutrition and wellness education needs.
Be very specific and very comprehensive. Based on perceived level of current
motivation, determine the specific educational goals. Of these goals, which is the most
important goal, and why? Also, discuss how you determined the patient’s motivational
level, and identify any obstacles which may interfere with diet compliance (i.e. finances,
disability, lack of family support, etc.)
Nutrition Intervention(s)
Intervention #1
1. Provide Juven BID and increase
Goal(s)
pt’s tube feeding by 10 ml in
To see an improvement in and to heal
order to meet his needs.
the pt’s stage 4, 2, and 1 pressure ulcers.
2. Speaking to the pt’s nursing
This is important in order to decrease
home about additional nutrition
the inflammation cause by these which
therapy and educating them on
in turn may produce further medical
its importance and the goal of
and organ problems.
promoting pressure ulcer healing
and avoiding further skin
damage.
Problem
Intervention #2
Increased nutrient and fluid needs for
Goal(s)
wound healing.
Informing the patient’s nursing home of
the patient’s recent order for Juven BID
and explaining the importance of this in
order to encourage their compliance
since the patient is fully dependent on
nursing home care.
Etiology
Related to pressure ulcers.
Signs/Symptoms
Elevated CRP (9.6), BUN (34) and stage
4, 2, 1 pressure ulcers.
Nutrition Prescription
Current order:
Jevity 1.2 @ 80 ml/hr/18hrs w/ 300mL
H20 flushes q 6hrs
Your Recommendation:
Other wound healing and preventative
techniques should also be discussed, such
as an individual rotation schedule and
change in position of the patient.
Intervention #3
Goal(s)
Jevity 1.2 @ 100 ml/hr/18hrs w/ 300mL
H20 flushes q 6hrs
Which goal is the priority at this time?
1. Getting the pt properly hydrated
and correcting his dehydration.
2. Maintaining the patient’s weight
and nutritional status because he
is in a very stressful state and
would decline further if his body
was not receiving adequate
nutrition, energy, and fluid to
help with the healing process and
his immune system.
If instruction was given, who did you
instruct?
What instructional materials did you
use? Where they effective? Why or why
not?
If patient has been education, what is
their motivation/compliance level at this
time?
Does the patient have any barriers to
compliance to the interventions?
n
n/a
n/a
n/a – education was inappropriate for
this patient.
NCP Step 4: Monitoring and Evaluation
Health Care Outcomes
Based on your Nutrition Intervention indicate below what outcome measurements you
will use to monitor progress and success of the interventions.
Intervention
Juven BID
Health & Disease
Outcomes
Increasing the
rate of healing
pressure ulcers.
Increase to
Prevention of
Jevity 1.2 @
additional
100mL/hr/18hrs chronic
Cost Outcomes
Patient
Outcomes
Less money spent Increased skin
on wound and
integrity and rate
medical care.
of wound
healing.
Prevention of
complication
associated with
non-healing
wound.
Less hospital
Nutritional status
trips and medical and weight
costs on trying to maintained.
illness/meeting
nutritional needs
and increasing
hydration.
Monitoring and Evaluation
Question to Consider
What indices are you using to determine
success of your intervention?
Did the intervention work? Explain
If the intervention is not working, indicate
what follow up action you took.
What are the causes of initial interventions
that did not work?
How will you monitor success of your
follow up interventions?
treat further
complications
developed from
not receiving
adequate
nutrition.
Prevention of
quicker decrease
of LBM.
Adequate
hydration to
promote wound
healing.
Answer/Reflection
Wound healing status and
normalization of his lab values
(CRP and BUN especially)
The patient was discharged so his
dehydration and UTI may have
been resolved and/or managed via
medications and medical nutrition
therapy.
N/A – patient was discharged.
N/A- there was no proof of recent
intervention not working.
I would contact the patient’s
nursing home to follow up with
how he is doing and the status on
his pressure ulcers. If they
continue to not heal it may indicate
the need for the pt to undergo
testing for cancer. At this point
the patient is not a candidate for
surgery because of his current
medical state, so managing his
wounds and making sure his
nursing home is complying with
order is crucial in order to
promote healing and prevent
further complications that may
develop as a result of non-healing
wounds.
DOCUMENTATION
Attach all initial and follow up notes for this patient/client to this report. Be sure to
delete any data that may identify the patient such as name or room number.
References
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•
•
•
•
•
•
•
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Dorner B, Posthauer ME, Thomas D.(2009)The Role of Nutrition in Pressure Ulcer Prevention and
Treatment: National Pressure Ulcer Advisory Panel White Paper. Nutrition White Paper. 1-15.
Doley J. (2010) Nutrition Management of Pressure Ulcers. Nutrition in Clinical Practice, (25), 50-60.
Desneves KJ, Todorovic BE, Cassar A, Crowe TC. (2005) Treatment with supplementary arginine,
vitamin C, and zinc in patients with pressure ulcers: A randomized controlled trial. Clinical Nutrition,
(24), 979-987.
University of Washington. Taking Care of Pressure Sores.
http://www.sci.washington.edu/info/pamphlets/pressure_sores.asp.
Mahan KL, Escott-Stump K. (2008) Krause’s Food & Nutrition Therapy: 12th Edition. Saunders
Elsevier. St. Louis, MO. 287-295.
Victorian Government Health Information. (2008) Pressure Ulcer Basics.
http://www.health.vic.gov.au/pressureulcers/pu_basics/module1/topic2/page9.htm
American Dietetic Association. ADA Evidence Analysis Library.
American Association for Clinical Chemistry. (2001-2011) ESR. Lab Tests Online.
http://www.labtestsonline.org
Version.pdfhttp://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/infectiousdisease/sepsis/#s0020
American Dietetic Association. Pressure Ulcers. Nutrition Care Manual.
Lizaka S, Sanada H, Nakagami G, Sekine R, Koyanagi H, Konya C, Sugama J. (2010) Estimation of
protein loss from wound fluid in older patients with severe pressure ulcers. J. Nutrition, (26), 890-895.\
Shah S. Foundation for Education and Research in Neurological Emergencies.
http://www.uic.edu/com/ferne/pdf/pathophys0501.pdf.