LIU POST

DEPARTMENT OF NUTRITION/DIETETIC INTERNSHIP

PATIENT MANAGEMENT REPORT (PMR)


Interns Name: Laryssa Grguric Date: 3/7/14
Rotation/Facility: Clinical/NUMC Preceptors Signature:


Part I:
A. Patient Information:

Initials: BMW Occupation: Retired (Previously dietitian) Admission Date: 3/3/14
Gender: F Socioeconomic Status: Middle Marital Status: Single
Age: 67 Residence (Home or LTC): LTC Ethnicity: African
American


B. Diagnosis: Lower GI Bleed s/p colonoscopy c! polyps removal


C. Medical Problem List: Pt. was brought into ED for vomiting and hematuria.

D. Medical/Social Hx:
ESRD+HD
PVD
B/L AKA (Dec 2013)
CAD s/p CABG
DM Type 2
HTN
CVA with L side hemiparalysis
Pressure ulcers: Stage III (sacral, 8 x 18 cm), Unstageable (ischium, 3 x 6 cm)

E. Physical/Anthropometric Data (if available):

Date: 3/6/14 Height: Actual ht 38
Prior to AKA: 64
UBW: n/a* %UBW: n/a*
Current Wt. 99.9# IBW (64) 120# +/- 10% %IBW: n/a* BMI, adj: 19.5
*Could not reach nursing home or daughter for more comprehensive history.

Note any findings from physical assessment: Pt. appears thin with some temporal wasting. Adjusted BMI
appears to be correct.




F. Pertinent Laboratory Data:
List
Normal
Values
Norm
( 12.1-
15.6 ) )
Hgb
Norm
(34-
45%)
Hct
Norm
(78-93) )

MCV
Norm
(3.5-5.0)

Alb.
Norm
( 8.4-
10.2)
Ca++
Norm
( 2.3-
4.3)
Phos
Norm
( 8-23 )

BUN
Norm
( 0.4-1
1.2)
Creat
Norm
(136-
144)
Na+
Norm
( 3.5-
5.0)
K+
Norm
( 70-
109)
Glucose
Norm
(1.3-
2.1 )
Mg+
3 3/5
Lab Value
6.9!

23.9! 103" 1.1! 7.3!
- 10
3.6"
145 3.8
125"
-
3/6
Lab Value
8.8! 28.8! 98.0" 1.1! 7.2!
-
6! 2.5"
140 4.0 82 -
3/7
Lab Value
9.3! 30.9! 101.0" 1.1! 7.4! 5.7"
8
3.4"
141 3.7
225" 1.4!

Additional Labs/Vitals:
FSBG, 80-120 mg/dL (3/6): 83, 80, 70!, 86, 110 (3/7) 215"
Serum Vit D25OH, 20-80 ng/mL: 11.6!, Serum Fe, 30-160: (3/7) 23!, TIBC, 240-450 (3/7):
22L, Ferritin, 12-150 ng/mL (3/7): 1525",
Vit B
12
, 210-911 pg/mL (3/7): >2000, Folate, 2.8-40 ng/mL (3/7): >20.0
BP (3/5): 118/67 (3/6): 123/66 (3/7): 129/73
GFR (3/5) 14 mL/min/1.73 m
2
, (3/6) 22 mL/min/1.73 m
2
, (3/7) 15 mL/min/1.73 m
2


Part II: Medical Problems, Laboratory Tests and Medications (address each of the three
areas (A-C) listed under guidelines; duplicate as many pages as necessary of this sheet)
Reference your medical text findings using APA (author, year, page number).

Summary of Medical Text Findings Comparison of Patient to Text
A. Pertinent Medical Problems: include
background of each disease from text
and include medical nutrition therapy
(MNT) for each; include kcal and
protein recommended if noted;
highlight information that can relate to
this patient.
C. Pertinent Medical Problems: include
how each disease is affecting patient;
what treatments patient is receiving;
therapeutic diet PTA and diet order in
hospital; how does the kcal/protein
recommended for each disease translate
for this patient? Do not complete an
assessment.
A. Chronic Kidney Disease /
End Stage Renal Disease + Hemodialysis

Also called Chronic Renal Failure. Chronic
Kidney Disease (CKD) is a progressive
deterioration of renal function (McMillan,
2011, p. 2442). CKD causes permanent
damage and eventually leads to end-stage
renal disease (ESRD) also known as CKD
Stage 5. It may result from any cause of renal
dysfunction but the most common is diabetic
nephropathy followed by hypertensive







Dx: ESRD +HD


Pt has hx of DM, HTN & PVD

nephroangiosclerosis (McMillan, 2011, p.
2442). Diabetic nephropathy is the leading
cause of ESRD (Escott-Stump, 2012, p. 861).
Metabolic syndrome is a large and growing
cause of renal damage (McMillan, 2011, p.
2442). About 23 million people have CKD c!
moderately or severely reduced glomerular
filtration rate (GFR) (Escott-Stump, 2012,
860). Fifty percent of patients with CKD
also have DM (Escott-Stump, 2012, p. 864).

Sx of CKD include: anorexia, nausea,
vomiting, stomatitis, dysguesia, nocturia,
lasstitude, fatigue, pruritus, decreased mental
acuity, muscle twitches, muscle cramps, water
retention, undernutrition, GI ulceration, GI
bleeds, peripheral neuropathies and seizures
(McMillan, 2011, p. 2442).

! renal function interferes c! the kidneys
ability to maintain fluid and electrolyte
homeostasis. The ability to concentrate urine
occurs early on in the disease and is followed
by ! in ability to excrete P, acid and K. Soon,
the ability to dilute urine is lost and urinary
volume does not differ c! " or ! fluid intake
(McMillan, 2011, p. 2443). Na+ and water
balance is maintained by " fractional excretion
of Na+ and normal fluid intake due to thirst.
Therefore, hypervolemia does not occur unless
dietary intake of Na+ or water is restrictive or
excessive (McMillan, 2011, p. 2443). K+
levels " when kidney failure becomes more
advanced. K-sparing diuretics, ACE
inhibitors, beta-blockers, NSAIDs,
cyclosporine, tacrolimus or angiotensin II
receptor blockers may " K in sooner in the
progression of disease (McMillan, 2011, p.
2443). Ca+, parathyroid hormone, vitamin
D metabolism and renal osteodystropy can
occur resulting in hypocalcemia,
hyperphosphatemia, " or ! bone turnover.
Osteopenia or osteomalacia may also occur
(McMillan, 2011, 2443).

Moderate acidosis and anemia are often






GFR (3/5) 14 mL/min/1.73 m
2
, (3/6) 22
mL/min/1.73 m
2
, (3/7) 15 mL/min/1.73 m
2










Pt admitted to NUMC for GI bleed





















Phos (3.7) 5.7, Ca+ (3/5) 7.3, (3/6) 7.2, (3/7)
7.4





evident. Anemia in CKD is normochromic-
normocytic: Hct 20-30% and is caused by !
erythropoietin. CKD pts may also be
deficient in Fe, folate, and vitamin B
12

(McMillan, 2011, p. 2443).

CKD is suspected when creatinine " but initial
steps include determining if renal insufficiency
is acute, chronic or acute superimposed on
chronic. Testing includes urinalysis,
electrolytes, BUN, creatinine, phosphate, Ca+
and CBC (McMillan, 2011, p. 2443).

Staging of CKD:
Stage 1: GFR ! 90 mL/min/1.73 m
2
(normal)
plus albuminuria or known structural or
hereditary renal disease
Stage 2: GFR 60-89 mL/min/1.73 m
2
Stage 3: GFR 30-59 mL/min/1.73 m
2
Stage 4: GFR 15-29 mL/min/1.73 m
2

Stage 5: GFR < 15 mL/min/1.73 m
2
(McMillan, 2011, p. 2443).

Progression of the disease is determined by
degree of proteinuria (McMillan, 2011, p.
2443). The kidney plays a role in regulation of
blood pressure (BP) through the renin-
angiotensin system (Escott-Stump, 2012, p.
860). HTN and other underlying disorders
are associated with more rapid progression
(McMillan, 2011, 2443). Weight loss and
anorexia are associated with mortality (Escott-
Stump, 2012, p. 860).

Hemodialysis (HD) is a type of renal
replacement therapy (RRT). RRT replaces
functions of the kidney. HD pumps a pts
anticoagulated blood into a dialyzer containing
2 fluid compartments in which the blood can
be filtered by concentration gradient technique.
Once the blood has been dialyzed, it is returned
to the pt. The immediate goal of HD is to
correct electrolyte and fluid imbalance while
also removing toxins. HD will also help to
prevent uremia, improve BP and optimize the
pts overall functional status (McMillan, 2011,



(3/7/14): Hgb 9.3!, Hct 30.9!, MCV 101" -
macrocytic anemia












GFR (3/5) 14 mL/min/1.73 m
2
, (3/6) 22
mL/min/1.73 m
2
, (3/7) 15 mL/min/1.73 m
2








Hx of HTN, CVA



















p. 2443). Other types of RRT are Continuous
Hemofiltration and Peritoneal Dialysis
(McMillian, 2011, p. 2449).

Annual mortality of those pts on HD is about
20%. Death is most often caused by
cardiovascular disease, then infection and
lastly withdrawal from HD tx (McMillian,
2011, p. 2449).

a. MNT for ESRD

A renal patient needs a detailed nutrition
assessment including Subjective Global
Assessment (SGA) to monitor physical
changes such as weight changes and changes in
muscle mass, diet history and gastrointestinal
symptoms. Fluid shifts related to edema may
cause difficulty in tracking weight losses
(Escott-Stump, 2012, p. 860).

Following a HTN diet, such as the DASH diet,
low in sodium c! regular exercise can help to
reduce BP to goal of <130 mm Hg systolic and
<80 mm Hg diastolic. Blood glucose should
be under control; aim for HbA1c " 7%. DM
pts may have to initiate carbohydrate counting.
All pts would benefit from and increase whole
grains, fruits and vegetables while limiting
processed foods (Escott-Stump, 2012, p. 869).

Renal pts undergoing HD must limit their
intake of phosphorus to 800-1200 mg/d and
total calcium to " 2000 mg/d (Escott-Stump,
2012, p. 876). Limit sodium to 2-4 g unless
there are large losses in dialysate or for losses
in vomiting/diarrhea (Escott-Stump, 2012, p.
877). Levels of potassium and phosphorus
should be monitored and diet should be
changed accordingly (Escott-Stump, 2012, p.
877). The goal for phosphorus is <5.5
mg/dL. This goal is met through dietary
adherence and use of phosphate binders
(Escott-Stump, 2012, p. 878).

Protein requirements for a HD pt, 50% from





































Phos 5.7 mg/dL" (borderline high for ESRD
pt)







high biologic value sources, are 1.2 g
protein/kg/day. Energy requirements for pts
<60 years of age: 35 kcal/kg. For pts " 60
years: 30-35 kcal/kg (Escott-Stump, 2012, p.
877).

Fluid restriction depends on output in the
dialysis pt. With # 1 L fluid output, 2 L of
fluid is needed daily. With <1 L fluid output,
1-1.5 L fluid is needed. If the pt is anuric, 1
L of fluid is needed for the day (Escott
Stump, 2012, p. 877). Fluid maximums
between dialysis sessions should be between 3-
5% of BW. Increased fluid intake can lead to
systemic and cardiac overload (Escott-Stump,
2012, p. 878).

B. Type 2 Diabetes Mellitus

Type 2 diabetes mellitus (T2DM) is marked by
inadequate insulin secretion. While insulin
levels are high in Type 2, peripheral insulin
resistance and " in hepatic glucose production
make insulin available inadequate to normalize
glucose level (Crandall, 2011, p. 867). T2DM
accounts for 90-95% of all DM cases; many
undiagnosed (Franz, 2012, p. 678). Risk
factors include genetic and environmental
factors, older age, obesity (particularly
intraabdominal), physical inactivity, prior hx of
gestational DM, race and ethnicity (Franz,
2012, p. 678).

Blood glucose (BG) levels " after eating,
especially after a meal " in carbohydrate. BG
levels take longer to return to normal post-
prandial (Crandall, 2011, p. 867). Obesity and
weight gain contribute to insulin resistance.
Adipose tissue " plasma levels of free fatty
acids and adipocytokines impairing glucose
transport and muscle glycogen synthase
activity (Crandall, 2011, p. 868).

Symptoms of DM during periods of
hyperglycemia include: frequent voiding of
urine, polyuria and polydipsia. Dehydration
Pt is 67 years old






Pt. on 1L FR PTA @ LTC Facility






































may occur. Weight loss, nausea, vomiting,
blurred vision and a predisposition to bacterial
or fungal infections may occur (Crandall,
2011, p. 868).

Complications can result from poorly managed
DM, primarily vascular complications, that
can result in retinopathy, nephropathy and
neuropathy. Microvascular disease also impairs
skin healing that can compromise skin
integrity. HTN and dyslipidemia are
commonly seen in patients with DM
(Crandall, 2011, p. 869). Screening for
complications related to DM should become
five years after diagnosis including food
examinations, funduscopic examinations, urine
testing for proteinuria and microalbuminuria
and measurement of creatinine and blood lipid
profiles (Crandall, 2011, p. 871).

DM is diagnosed by monitoring fasting plasma
glucose levels but sometimes, oral glucose
tolerance testing (OGTT) is performed. OGTT
is more sensitive but less convenient and
therefore often only reserved for diagnosing
gestational DM (Crandall, 2011, p. 871). A
random glucose test > 200 mg/dL may be
diagnostic but it may also be influenced by a
recent meal and must be confirmed by repeat
testing if no other symptoms are present.
Hemoglobin (Hb) A
1c
allows for a retrospective
look at glucose levels over the preceding 2-3
months. Urine glucose measurement is no
longer used (Crandall, 2011, p. 871).

Goals for glycemic control:
-BG 80-120 mg/dL during the day
-BG 100-140 mg/dL at bedtime
-HbA
1c
levels < 7% (Crandall, 2011, 872).

In the critically ill and hospitalized patients,
blood glucose levels should be ~110 mg/dL.
Pts in hospital will usually require IV
insulin (Escott-Stump, 2012, 548).

b. MNT for Type 2 DM




Hx of peripheral vascular disease, B/L AKA





























FSBG (3/6): 83, 80, 70!, 86, 110



(3/7) 215"
Pt is Rxd FS c! Humalog coverage at this time







MNT for T2DM requires an individualized
approach. There is no single diabetic diet
but a diet prescription based on individual
needs and goals (Escott-Stump, 2012, p. 521).
Pts should be educated on self-management via
diet and self-monitoring of blood glucose
(SMBG) (Franz, 2012, p. 684). Diet should be
reduced in calories and fat, carbohydrate
counting or exchange lists with simple meal
plans, physical activity and behavioral
strategies should be incorporated in treatment
(Franz, 2012, p. 684).

Total carbohydrate intake eaten regardless of
the source is the primary determinant of
postprandial glucose levels (Franz, 2012, p.
684). Carbohydrate should contribute to 45-
65% of total energy intake (Escott-Stump,
2012, p. 546). Consistency in carbohydrate
intake eaten at each mealtime or snack can help
to improve glycemic control either solely by
diet therapy, or in combination with glucose
lowering medications or insulin regimens
(Franz, 2012, p. 684). Carbohydrate counting
considers 15 g of carbohydrate to be 1 serving.
Exchange lists group foods into list depending
on their carbohydrate content. This method
utilizes symbols to identify foods high in fiber,
fat or sodium (Franz, 2012, p. 685). Protein
should contribute 15-20% of total calories if
renal function is normal. If the kidneys are
affected, protein restriction to 0.8-1.0 g/kg is
recommended (Escott-Stump, 2012, p. 546).
Fat can contribute 25-35% of total calories but
saturated fats should be restricted to 7-10%,
focusing on a higher intake of PUFAs and
MUFAs (Escott-Stump, 2012, p. 546). The
DASH diet principals are useful in planning a
DM diet plan, as it will help to manage HTN if
present and reduce NA+. Less than 2400 mg
Na+ is recommended (Escott-Stump, 2012, p.
546).

Testing pre-meal and post-meal glucose levels
can help pts to make adjustments to their meal





























Protein restricted not indicated for ESRD+HD.
















planning (Franz, 2012, p. 685). These diet
plans are portion controlled and can lead to
weight loss. Moderate weight loss of 5-10%
can ! hyperglycemia, dyslipidemia and
hypertension (Escott-Stump, 2012, p. 546).

C. Hypertension

Hypertension (HTN) is defined as sustained
SBP and DBP greater than 140 and 90 mm Hg
(Escott-Stump, 2012, p. 367). Pre-HTN is
defined as SBP between 120-139 mm Hg or
DBP b/w 80-89 mm Hg. Stage 1 HTN (140 to
159/90 to 99 mm hg) is the most prevalent
level seen in adults this population is most
likely to have MI or CVA (Raymond & Couch,
2012, p. 758). HTN risk increases with age
and therefore is prevalent in the elderly. HTN
doubles risk for heart attack, stroke, HF
(Escott-Stump, 2012, p. 367). Essential HTN
(HTN with unknown cause) is prevalent in 90-
95% of pt (Raymond & Couch, 2012, p. 758).

HTN is asymptomatic until complications
develop (Bakris, 2011, p. 2067). Sx of HTN
include frequent headaches, impaired vision,
sob, nosebleeds, chest pain, dizziness, failing
memory, snoring, sleep apnea and GI distress
(Escott-Stump, 2012, p. 367).

Sleep apnea, drug-related causes, CKD,
Cushings syndrome, steroid therapy,
pheochromocytoma, reno vascular disease can
cause high BP (Escott-Stump, 2012, p. 368).
Lifestyle choices such as poor diet, smoking,
physical inactivity, stress, obesity can
contribute to HTN. Secondary HTN is a result
of another disease, usually endocrine in nature
(Raymond & Couch, 2012, p. 758).

If left untreated, HTN can lead to stroke,
HF, renal failure, MI, accelerated bone loss,
increase risk of fracture and LT memory
problems (Escott-Stump, 2012, p. 367).

c. MNT for HTN
















Hx of CVA














BP (3/5): 118/67 WNL
(3/6): 123/66 (3/7): 129/73














For dietary tx of HTN, the DASH diet is
recommended. DASH is rich in fiber, includes
5-10 servings of fruit and vegetables a day and
non-fat dairy products. In comparison to BP
lowering medication, DASH significantly
reduced BP (Escott-Stump, 2012, p.368).
DASH can reduce SBP 8-44 mg Hg. Sodium
should be limited to 2300 mg/day. If target BP
is not reached, sodium can be further decreased
to 1600 mg/day. Reduction of sodium can
reduce SBP 2-8 mm Hg (Raymond & Couch,
2012, p. 762).

Fish oil rich in omega-3, antioxidants such as
vitamin C, folic acid, vitamin K, soy protein
and a Mediterranean style diet may also have a
positive effect in HTN tx (Escott-Stump, 2012,
p. 368). Including physical activity of 30
min/day on most days can reduce SBP by 4-9
mm Hg Reducing ETOH to 2 drinks/day for
men and 1 drink/day for women can reduce
SBP 2-4 mm Hg (Raymond & Couch, 2012, p.
762).

By following DASH and including an exercise
regime, weight management can be achieved
and possibly reduce SBP by 5-20 mm Hg
(Raymond & Couch, 2012, p. 762).

D. Pressure Ulcers (P/Us)

P/Us, formerly known as bedsores or decubitis
ulcers (Wellman & Kamp, 2012, p. 448) are
areas of necrosis and ulceration where tissues
are compressed between bony prominences
and a hard surface. They can result from
pressure solely or a combination of pressure,
friction or shearing forces (Collison, 2011, p.
736). Paralysis, incontinence and sensory
losses can also contribute to development of
P/Us (Wellman & Kamp, 2012, p. 448). P/Us
also develop due to lack of O
2
and nutrition
(Escott-Stump, 2012, 114). Prognosis for
early-stage P/Us is excellent, however, late-
stage ulcers pose risk of infection, nutritional














































stress and are difficult to heal (Collison, 2011,
p. 736).

P/Us are common among pts with protein-
energy malnutrition, in HIV infection,
pulmonary and cardiac cachexia. The risk of
P/Us increase by 74% with immobility, !
LBM and lowered immunity. Pts. are often
below their usual BW and have a less than
optimal PO intake that does not meet their
EEN (Escott-Stump, 2012, p. 114).

There are classification systems that describe
P/Us. There are four stages of P/U, which are
based on the depth of sore, and level of tissue
involvement (Wellman & Kamp, 2012, 448-9).
Stage III P/Us involve full thickness tissue
loss. Subcutaneous tissue is exposed, but
bone, tendon or muscle are not exposed
(Wellman & Kamp, 2012, p. 450).

d. MNT for P/Us

Main goals of P/U MNT are to correct protein-
energy malnutrition by providing a high-
quality protein diet. Protein recommendations
are 1.0-1.5 g/kg protein. If P/Us are deep or
have multiple sites, 1.5-2 g/kg protein may
be indicated. Kcal recommendations for
wound healing are 25-35 kcal/kg. These
recommendations will help heal current P/Us
and prevent further tissue breakdown. Energy
needs can be met by providing small,
frequent meals 4-6 times daily when PO
intake is not optimal (Escott-Stump, 2012, p.
116).

E. Cerebrovascular Accident

Cerebrovascular accident (CVA) is caused by
damage to portion of the brain due to loss of
blood caused by a clot, rupture or spasm.
Eighty percent of strokes are transient ischemic
attacks (TIA), which are brief episodes of
blood loss to the brain (Escott-Stump, 2012,
259). CVA is the third most common cause of



Pt may have been immobile PTA due to B/L
AKA









Stage III on sacrum. Unstageable P/U on
ischium.














Poor PO intake observed & reported by PCA,
potentially 2 to AMS.














death in the U.S. and the number one cause of
disability (Remig & Weeden, 2012, p. 933). In
2003, CVA cost the U.S. an estimated $51
billion in lost productivity and health care costs
(Remig & Weeden, 2012, p. 934). Modifiable
risk factors for CVA include hypertension,
smoking, obesity, coronary heart disease,
diabetes, physical inactivity and genetics
(Remig & Weeden, 2012, p. 934). Some
people may recover completely from their
CVA, but others may become disabled or die.
Unconsciousness, paralysis, sight, hearing,
speech and swallow difficulties may occur
depending on the location of brain involved
(Escott-Stump, 2012, p. 259).

e. MNT for CVA

Feeding difficulties caused by dysphagia
hinders MNT in CVA. Dysphagia is common
in stroke victims and contributes to
malnutrition, pulmonary infections, " hospital
stays and institutionalization (Remig &
Weeden, 2012, p. 935). Prevention of CVA by
diet and other lifestyle behavior changes is the
foundation in reducing risk of CVA (Remig &
Weeden, 2012, p. 934). A diet that has a high
intake of fruits and vegetables, fish and whole
grains may be protective against stroke
(Escott-Stump, 2012, 260). Use the DASH
Diet (Escott-Stump, 2012, p. 262).

Initially, the pt should remain NPO c! IV fluids
for 24-48 hours. If enteral nutrition (EN) is
indicated due to loss of consciousness, the bed
should be elevated to 30-45 to prevent
aspiration pneumonia (Escott-Stump, 2012, p.
261). Pts diet should then progress to liquids;
some pts may not have swallowing difficulty
with liquids (Escott-Stump, 2012, p. 261).
Progression to solid foods may require texture
modification due to dysphagia. Avoid foods
that can pose a choking hazard (Escott-Stump,
2012, p. 261).

Energy needs for CVA victims will vary
















Pt has hx of CVA; this diet TX is not indicated
at this time (indicated immediately following
CVA)



























depending on activity level from 25-45
kcal/kg. Protein needs will also vary from 1.2-
1.5 g/kg depending on weight and lean body
mass status (Escott-Stump, 2012, p. 261).
Saturated fats in the diet should be limited to
<10% of total calories. Saturated fats in the
diet can be replaced with monounsaturated fat
sources and " omega-3s from dietary sources
such as fish. Dietary cholesterol should be
limited to <300 mg/day (Escott-Stump, 2012,
p. 261). Fluid needs should be given as
tolerated (30-35 mL/day) (Escott-Stump, 2012,
p. 262).

F. Peripheral Artery Disease

Peripheral artery disease (PAD) can affect the
arteries, veins or lymph vessels. The most
common type of PVD is peripheral artery
disease (PAD). Prevalence increases with age.
In population of pts 70 years or older, 20% are
affected by PAD. Non-Hispanic blacks and
Mexican Americans are more affected than
other race or ethnic groups. Individuals
with PAD have a 6-7x greater risk of heart
attack or CVA (Escott-Stump, 2012, p. 377).
Other risk factors include HTN, DM,
dyslipidemia, cigarette smoking and obesity
(Hallett, 2012, p. 2218). Artery occlusion
occurs from a clot or plaque formation that can
lead to pain, numbness or tingling in the lower
extremities. In others, difficult ambulation,
gangrene and potential amputation may
occur (Escott-Stump, 2012, p. 377).
Amputation is indicated for uncontrolled
infection, unrelenting rest pain and progressive
gangrene (Hallett, 2012, p. 2220).

Causes of PAD include smoking, arterial
embolism, obesity, DM, renal insufficiency,
poor circulation, atherosclerosis, dyslipidemia
and HTN (Escott-Stump, 2012, p. 377).

f. MNT for PAD

Pts will benefit from aggressive risk factor





























Pt underwent B/L AKA in Dec 2013.
















modifications such as smoking cessation,
control of DM, dyslipidemia and HTN.
Exercise for 35-50 minutes 3-4x a week can "
symptom-free walking and improve quality of
life (Hallett, 2012, p. 2219).

Goals of MNT in PAD are to decrease
cardiovascular risk to reduce complications
such as angina, HF, MI, CVA, renal failure,
ulcerative disease and gangrene (Escott-Stump,
2012, p. 378). Pts who are overweight or
obese should undergo weight management
therapy using a low calorie diet high in fiber
(Escott-Stump, 2012, p. 378).

Serum vitamin D levels may be low and
should be corrected via supplementation.
Diet should also be high in vitamin E. Monitor
serum tHcy levels. If tHcy levels are elevated,
" folic acid, riboflavin, vitamin B
6
and B
12
. If
warfarin is used, monitor vitamin K foods and
avoid: dong quai, fenugreek, feverfew,
excessive garlic, ginger, ginkogo or ginseng
(Escott-Stump, 2012, p. 379).

G. Coronary Artery Disease/Atherosclerosis
s/p Coronary Artery Bypass Graft

Coronary Artery Disease (CAD) involves the
narrowing of small vessels that provide oxygen
to the heart also known as artheroscerosis.
Narrowing occurs due to accumulation of
plaque caused by an inflammation response.
Monocytes migrate to tissues and become
marcrophages that then ingest oxidized
cholesterol and become foam cells and then
progress to fatty streaks in vessels (Raymond
& Couch, 2012, p. 743). Risk factors for CAD
include high levels of low-density lipoprotein
(LDL) cholesterol, HTN, age, DM, GFR <60
mL/min, smoking, physical inactivity and poor
diet (Raymond & Couch, 2012, p. 748).

In the coronary arteries, CAD may cause
angina, MI and sudden death. In cerebral
arteries it can cause CVA and transient












Serum Vit D25OH: 11.6!; pt. likely on
calcitriol (could not confirm with HD unit)
































ischemic attacks (TIA). In peripheral
circulation, it can cause intermittent walking
impairment, limb ischemia and gangrene
(Raymond & Couch, 2012, p. 743).

Coronary Artery Bypass Graft (CABG)
surgery involves an artery from the chest being
used to redirect blood flow around a diseased
or damaged vessel. Generally, a candidate pt
for CABG has two or more occluded arteries
(Raymond & Couch, 2012, p. 758). CABG
surgeries are decreasing in popularity and
usage due to an increased rate of percutaneous
coronary intervention (PCI) procedures, which
are done while the pt is asymptomatic. PCI
uses a catheter with a balloon that, when
inflated, breaks down plaque deposits in the
artery affected (Raymond & Couch, 2012, p.
757).

g. MNT for CAD

Therapeutic Lifestyle Changes (TLC) is
helpful for preventing Coronary Heart Disease
(CHD) (Raymond & Couch, 2012, p. 753), a
result of CAD (Coronary Heart Disease
Coronary Artery Disease, 2013) and reducing
cardiovascular disease (CVD). These
guidelines in conjunction with the Dietary
Approaches to Stop Hypertension Diet
(DASH), which increases fruits, vegetables,
whole grains, lean meats and non-fat dairy
products (while decreasing processed foods)
are helpful in prevention and treatment
(Raymond & Couch, 2012, p. 753). Risk
factor reduction has been shown to reduce
CAD in persons of all ages. Many coronary
events can be prevented with a heart healthy
diet, regular exercise and ! use of tobacco
along with compliance to lipid and HTN drug
therapy (Raymond & Couch, 2012, p. 747).

Dietary Pattern for TLC:
Total fat should be restricted to 25-35% of
total calories. Saturated fat should contribute
>7% of calories and trans fatty acids should be
B/L AKA likely 2 to prolonged and serious
infection.












































kept as close to zero as possible. Therefore,
only lean meats, poultry and fish should be
included in the diet. Protein in this dietary
pattern attributes to 15% of total calories.
Polyunsaturated fats (PUFAs) and
monounsaturated fats (MUFAs) can help to
lower triglycerides and LDL while raising
HDL should contribute 10% and 20% of
calories respectively. Carbohydrates, mostly
fiber rich whole grain, should contribute to 50-
60% of the diet. Guidelines recommend 2 g of
fiber daily. Cholesterol is restricted to 200
mg/daily. Desirable body weight should be
obtained and further weight loss should be
prevented. The guidelines also recommend
moderate physical activity daily (Raymond &
Couch, 2012, p. 753).
























Part II: continued

Summary of Medical Text Findings Comparison of Patient to Text
b. Medications: list medication,
indication, effect of food and drug
interactions relative to nutrition: factors
that can affect nutrition
intake/GI/vitamins, minerals and labs.
Reference
c. Medications: how is medication
affecting patient? Is patient
experiencing any side effects?
1. Low Dose Aspirin (81 mg)
Analgesic. NSAID. To prevent CVA or MI.
Platelet aggregation inhibitor. Insure adequate
fluid intake. " foods high in Vit C & Folate c!
LT dose. Avoid or limit products that affect
coagulation (garlic, ginger, etc.) Limit caffeine
to ! GI effects. Avoid alcohol. Caution c!
diabetes. May cause anorexia. N/V.
(Pronsky, 2012, p. 44).

2. Humalog/insulin lispro
Antidiabetic, hypoglycemic. Use c! diabetic
meal plan to balance carbohydrate c! doses. "













wt. Avoid ETOH. Large wt. gain " insulin
needs. ! Glucose, ! HbA1
c,
! K, ! Mg, ! P
(Pronsky, 2012, p. 167).

3. Protonix
Proton pump inhibitor (PPI). Antiulcer,
antigerd, antisecretory. May ! absorption of
Fe. ! absorption of B
12
. Ca supplement may
be advised. May cause diarrhea (Pronsky,
2012, p. 260).
(3/7) Mg 1.4!




TIBC (3/7): 22 !
VitB
12
WNL

Summary of Medical Text Findings Comparison of Patient to Text
d. Laboratory Tests: key tests and their
implications relative to patients
medical problems; include reasons for
increase and decrease for each lab.
Reference
e. Laboratory Tests: assess patients
laboratory values; refer to chart on first
page or use values from your facility;
note if any medications are affecting
lab values.
1. Mean Corpusal Volume: Norm (78-93)
! with megaloblastic anemia due to Fol or Vit
B12 def, liver disease, reticulocytosis,
myelofibrosis
Spurious with cold agglutinins.
" with Fe def anemia, hereditary,
spherocytosis, thalassemia minor, sideroblastic
anemia, Pyr-responsive anemia, lead poisoning
(Pronsky, 2012, p. 349).

2. Hemoglobin: Norm (12.1-15.6 g/dL)
# c! severe burns, polycythemia, shock
" c! anemia, blood loss, hemolysis, leukemia,
hyperthyroidism, cirrhosis, over hydration
(Pronsky, 2012, p. 346).

3. Hematocrit: Norm (34-45%)
# c! dehydration, polycythemia, CHF,
thalassemia, COPD, dehydration.
" c! anemia (<30), hyperthyroidism, cirrhosis,
many systemic diseases (eg. Leukemia, Lupus,
Hodgkins disease), HIV/AIDS (Pronsky,
2012, p. 346).

4. Albumin: Norm (3.5-5.0 g/dL)
# c! dehydration
" c! edema, hepatic disease, malabsorption,
diarrhea, burns, eclampsia, ESRD,
MCV (3/5) 103" (3/6) 98.0" (3/7) 101.0"

Anemia Panel:
TIBC (3/7): 22!, Ferritin (3/7): 1525"
VitB12 (3/7): >2000, Folate (3/7): >20.0
r/o vit b12/folate def
Anemia ! due to erythropoiten due to kidney
disease


Hgb (3/5) 6.9!, (3/6) 8.8!, (3/7) 9.3!

GI bleed, surgical wound sites, needle sticks





Hct (3/5) 23.9!, (3/6) 28.8! (3/7) 30.9!






Alb 1.1!


malnutrition, low pro intake, stress, over-
hydration, cancer (Pronsky, 2012, p. 340).

5. Calcium (Ca): Norm (8.4-10.2 mg/dL)
# c! cancer, hyperparathyroidism, adrenal
insufficiency, hyperthyroidism, Pagets
disease, prolonged immobilization, excessive
Vit D or Ca intake, LT use of thiazide
diuretics, respiratory acidosis, milk-alkali,
Chronic renal failure, granulomatous disease
" c! hypoaluminemia, elevated phosphorus,
alkalosis, diarrhea, hypoparathyroidism, sprue,
osteomalacia, malabsorption, diarrhea, acute
pancreatitis, hypomagnesemia, starvation,
steroid use, vit D def (Pronsky, 2012, p. 342).

6. Phosphorus: Norm (2.3-4.3 mg/dL)
! c! ESRD, hypocalcemia, hypervitaminosis
D, bone tumors, Addisons,
hypoparathyroidism, acromegaly, sickle cell
anemia
" c! hyperparathyroidism, alcoholism,
hypovitaminosis D, rickets or osteomalacia,
hyperinsulinism, acute gout, overuse of P
binders, Cushings syndrome, salicylate
poisoning, DM, alcoholism (Pronsky, 2012, p.
350).

7. Blood urea nitrogen: Norm (8-23
mg/dL)
# (azotemia) c! renal failure (> 50 = serious
impairment), shock, dehydration, infection,
DM, chronic gout, excessive pro
intake/catabolism, MI
" c! hepatic failure, malnutrition,
malabsorption, overhydration (excessive IV
fluids), pregnancy, SIADH (Pronsky, 2012, p.
342).

8. Creatinine: Norm (0.4-1.2 mg/dL)
# c! acute & chronic renal disease, muscle
damage, hyperthyroidism, muscle mass,
starvation, diabetic acidosis, high meat intake,
gigantism, acromegaly.
" c! pregnancy (Pronsky, 2012, p. 344).

H/o poor PO intake PTA; continued at NUMC.







Alb consistently 1.1 !




Phos (3/7): 5.7"

Ca+: (3/5) 7.2!, (3/6) 7.3 !, (3/7) 7.4 !
Corrected Ca+ (albumin 1.1) =
(3/5) 9.5 !, (3/6) 9.6 !, (3/7) 9.7!












BUN (3/6) 6!

Pt has evidence of muscle wasting.





Creat (3/5) 3.6", (3/6) 2.5", (3/7) 3.4"




Na+ WNL


9. Sodium (Na): Norm (136-144 mEq/L)
# (hypernatremia) c! dehydration & low fluid
intake, diabetes insipidus, Cushings
syndrome, coma, primary aldosteronism.
" (hyponatremia) c! edema, severe burns,
severe diarrhea/vomiting, diuretics, SIADH,
water intoxication, Addisons disease, severe
nephritis, starvation, hyperglycemia,
malabsorption, AIDS (Pronsky, 2012, p. 352).

10. Potassium (K): Norm (3.5-5.0 mEq/L)
# (hyperkalemia) c! renal failure, tissue
damage, acidosis, Addisons, uncontrolled
DM, internal hemorrhage, overuse of K suppl,
acute AIDS.
" (hypokalemia) with GI loss, IV fluid with
without K suppl, alcohol abuse, malabsorption,
malnutrition, diarrhea, vomiting, chronic stress
or fever, K depleting diuretic, steroid, estrogen
use, hepatic disease with ascites, excessive
licorice intake, renal disease (Pronsky, 2012, p.
351).

11. Glucose: Norm (70-109 mg/dL)
# DM, Cushings syndrome, Thi def,
acromegaly, gigantism, chronic hepatic
dysfunction, severe infections,
hyperthyroidism, pancreatitis, chronic hepatic
disease, prolonged physical inactivity,
chronic hepatic disease, chronic malnutrition,
K def drugs (eg corticosteroids), high dose,
antihypertensives, cyclosporine)
" c! insulin overdose, islet-cell carcinoma,
bacterial sepsis, hypothyroidism, Addisons
disease, extensive liver disease, glycogen
storage disease, alcohol abuse, starvation,
vigorous exercise, pancreatitis, oral
hypoglycemic drugs (Pronsky, 2012, p. 345).

12. Magnesium (Mg): Norm (1.3-2.1
mEq/L):
# c! renal failure, diabetic acidosis,
hypothyroidism, Addisons, dehydration,
overuse of Mg supplement or antacid.
" c! chronic diarrhea, alcoholism, pancreatitis,
renal disease, hepatic cirrhosis, toxemia of












K+ WNL













Glu (3/5) 125", (3/6) 82, (3/7) 225"















Mg (3/7) 1.7 !



pregnancy, hyperthyroidism, malabsorption,
ulcerative colitis, K-depleting diuretics,
malnutrition (Pronsky, 2012, p. 348).

13. Ferritin: Norm (F: 12-150, M: 30-320
ng/mL)
# c! inflammatory diseases, chronic renal
disease, malignancy, hepatitis, Fe overload,
hemochromatosis
" c! Fe def anemia (Pronsky, 2012, p. 344).

14. Folic Acid: Norm (2.8-40 ng/mL)
" with megaloblastic or hemolytic anemia,
malnutrition, folate antagonist drug (eg.
Anticonvulsant, methotrexate, oral
contraceptives), malabsorption (eg. Sprue,
celiac disease), alcoholic hepatic disease,
hyperthyroidism, vit C def, dialysis, febrile
states, pregnancy, cancer (Pronsky, 2012, p.
345).

15. Vitamin B12: Norm (210-91 pg/mL)
! (> 1100 pg/mL) with hepatic disease, some
leukemias, cancer (especially with hepatic
metastasis), pregnancy, oral contraceptives
" (< 100 pg/mL) with pernicious anemia,
malabsorption syndromes, primary
hypothyroidism, " gastric mucosa (eg.
gasterectomy or stomach cancer), vegetarian
diet, achlorhydria (Pronsky, 2012, p. 354).

16. Serum Iron (Fe): Norm (F: 30-160, M:
50-170 g/dL)
" c $ excessive Fe intake, hemolytic anemias,
hepatic disease, estrogen use, hemochromatosis
c $ Fe def anemia, chronic diseases, infections,
hepatic disease, surgery, MI (Pronsky, 2012,
347).

17. Creatine clearance GFR: Norm (M: 85-
125, F: 75-115 mL/min)
# in acromegaly and burns
" in CHF, glomerular disease, eclampsia,
gout, multiple myeloma (Pronsky, 2012, 344).




Ferritin (3/7): 1525"





Folate (3/7): >20.0 "








VitB12 (3/7): >2000"







Fe (3/7) 23 !






GFR (3/5) 14 mL/min/1.73 m
2
, (3/6) 22
mL/min/1.73 m
2
, (3/7) 15 mL/min/1.73 m
2





Part III: Nutrition History:

PTA pt received carbohydrate controlled, low sodium and low potassium meals at LTC facility.

Pt currently NPO pending more GI surgery (endoscopy)

Part IV: Nutrition Care Process: Assessment, Diagnosis, Intervention, Monitoring and
Evaluation (ADIME)

S: Pt came into the hospital with what was thought to be vaginal bleeding or possible hematuria
and vomiting. Under further evaluation, rectal bleeding was found. PTA she was able to eat
solid meals and followed a regular consistency diet at the LTC facility. Pt has noticeable
temporal wasting. At this time, unable to obtain further information from family or nursing
facility at this time no answer when telephoned. Pt is also non-verbal at this time. SLP did a
swallow evaluation and determined that puree consistency foods were not well tolerated by pt
and recommended initiation of TF.

O: 67 y/o %. Dx: Lower GI bleed. PMH: ESRD+HD, PVD, B/L AKA, CAD s/p CABG, DM,
HTN, CVA. Rx: Baby aspirin, Humalog, Protonix. Ht: prior to AKA 64. Wt: 45.3 kg.
Adjusted BMI 2 to AKA 19.5. Diet Rx: 1800 kcal, 2 g Na+, 2 g K+. Labs: (3/7/14) Hbg 9.3 !,
Hct 30.9!, MCV 101.0", Alb 1.1!, Ca++ 7.4!, Phos 5.7", BUN 8 WNL, Creat 3.4", Na+ 141
WNL, K+ 3.7 WNL, Glu 225", Mg 1.4!, GFR 15.

A: PES: Malnutrition in the context of chronic disease related to DM, ESRD and GI bleeding
evidenced by muscle loss indicated by temporal wasting and prominent clavicles, pt inability to
eat sufficiently to meet energy and protein needs secondary to altered mental status, history of
poor PO intake >50%, ! BUN and pressure ulcers.

Calorie needs 30-35 kcal/kg using IBW of 54.5 kg (secondary to amputation) ~1630-1900
kcal/day. Protein needs secondary to stage 2 pressure ulcer and HD 1.5-2 g/kg using IBW of
54.5 kg 56-109 g/day. Fluid needs limited to 1L/day secondary to ESRD and anuria. Dietary
phos limited to 800-1200 mg/day with biochemical lab value goal of <5.5 mg/dL. Ca+ should be
limited to >2 g and Na+ is limited to 2-4 g/day. No current diet observed to comment on actual
intake. Pt is at high nutritional complexity due to multiple co-morbidities including ESRD+HD,
malnutrition and altered mental status resulting in poor PO intake. Subjective global assessment
reveals temporal wasting and prominent clavicle indicating loss of muscle mass, but no edema is
evident at this time.

! H&H and " MCV indicate megaloblastic anemia but Vit B
12
and Folate levels indicate good
stores. " Ferritin expected for pt on HD. Pt has ! serum Fe with coupled with ! H&H can
indicate Fe deficiency anemia likely secondary to decreased renal function ! EPO. " phos, "
creat, " ferritin and ! serum Fe all likely secondary to ESRD+HD.


Part IV: Nutrition Care Process continued (Intervention, Monitoring and Evaluation)

Measurable Goals of Nutrition Care Specific Plans (Intervention):

Goal 1:
" H&H and Serum Fe to WNL
Plan 1:
Recommend Epogen and Fe supplements

Goal 2:
Maintain current wt; ! muscle wasting
Plan 2:
" kcal and protein to meet estimated
energy needs (~1630-1900 kcal, 56-109 g
prot)
o Due to ! cognitive awareness and
poor PO intake, recommend
initiation of TF:
Recommend Nepro @ 40 mL/hr (960 mL
total/24 hrs) providing 1728 kcal, 78 g
protein with 100% delivery.
Nepro indicated for pt as it is carb steady,
low in K and calorically dense indicated for
fluid restriction. Nepro provides 778 mL
H
2
0 with this Rx addl H
2
0 flush 222
mL/d ~56 mL q 6h)
Progress pt to PO intake as feasible (when
AMS resolves and SLP clears initiation of
PO diet)

Goal 3:
" wound healing
! pressure ulcer occurrence and heal current
ulcers (stage 3 on sacral, unstageable ulcer on
ischium)

Plan 3:
Provide Vit C @ 500 mg/d, ZnSO
4
120 mg q o
d (lower dose indicated secondary to kidney
function)

Goal 4:
" Serum Vit D 25OH level to WNL

Plan 4:
Recommend replenishment dose of Vit D:
50,000 mg for 5 days. Continue Vit D
supplementation @ 2000 IU/day afterwards.


References

Coronary Artery Disease Coronary Heart Disease. 2013. American Heart Association.
Retrieved from:
http://www.heart.org/HEARTORG/Conditions/More/MyHeartandStrokeNews/Coronary-
Artery-Disease---Coronary-Heart-Disease_UCM_436416_Article.jsp.

Collison, D. W. (2011). Pressure ulcers. In R. S. Porter & J.L. Kaplan (Ed.) The Merck
Manual. (19
th
ed., pp. 736, 738). Whitehouse Station, NJ: Merck Sharp & Dohme Corp.
Crandall, J. P. (2011). Diabetes mellitus and disorders of carbohydrate metabolism. In R. S.
Porter & J. L. Kaplan (Ed.), The Merck Manual. (19
th
ed., pp. 867, 868, 869, 871).
Whitehouse Station, NJ: Merck Sharp & Dohme Corp.
Escott-Stump, S. (2012) Nutrition and diagnosis-related care. (6
th
ed., pp. 114, 116, 259, 260,
261, 262, 367, 377, 378, 379, 521, 546, 548, 860, 861, 864, 869, 876, 877, 878)
Baltimore: Lippincott Williams & Wilkins.
Franz, M. J. (2012). Medical nutrition therapy for diabetes mellitus and hypoglycemia of
nondiabetic origin. In Y. Alexopoulous (Ed.), Krauses Food and the Nutrition Care
Process (13 ed., pp. 678, 684, 685). St. Louis, MO: Elsevier.
Hallett, J. W. (2011). Peripheral arterial disorders. In R. S. Porter & J. L. Kaplan (Ed.), The
Merck Manual. (19
th
ed., pp. 2218, 2219, 2220). Whitehouse Station, NJ: Merck Sharp
& Dohme Corp.
McMillan, J. I. (2011). Renal failure. In R. S. Porter & J. L. Kaplan (Ed.), The Merck Manual.
(19
th
ed., pp. 2442, 2443, 2449). Whitehouse Station, NJ: Merck Sharp & Dohme Corp.
Pronsky, M. Z. & Crowe, S. J. (2012). Food medication interactions. (16 ed., pp. 44, 167, 260,
340, 342, 343, 344, 345, 346, 347, 348, 349, 350, 351, 352, 354) Birchrunville, PA:
Food-Medication Interactions.
Raymond, J. L. & Couch, S. C. (2012). Medical nutrition therapy for cardiovascular disease. In
Y. Alexopoulous (Ed.), Krauses Food and the Nutrition Care Process (13 ed., pp. 743,
747, 753, 757, 758, 762). St. Louis, MO: Elsevier.
Remig, V. M. & Weeden, A. (2012). Medical nutrition therapy for neurologic disorders. In Y.
Alexopoulous (Ed.), Krauses Food and the Nutrition Care Process (13 ed., pp. 933, 934,
935).
Wellman, N. S. & Kamp, B. J. (2012). Nutrition in aging. In Y. Alexopoulous (Ed.), Krauses
Food and the Nutrition Care Process (13 ed., pp. 448, 449). St. Louis, MO: Elsevier.