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Case Study 1: Cedars-Sinai Medical Center

Description of Primary Disease and Nutrition Treatment​:


Encephalopathy is the gradual degradation of brain function, being categorized as a disease,
malfunction or damage to the brain. A common association of encephalopathy is hepatic encephalopathy,
in which mental status and abnormal neuromuscular function occur as a result of liver failure. When a
patient is in a coma, the Glasgow Coma Scale score is used as a reference of neurological responsiveness
of the individual, furthermore assessing their nutrient needs. While the cause for encephalopathy is
unknown, there has been research done to indicate that a possible contributor to the progression of
encephalopathy is ammonia hypothesis, synergistic neurotoxin hypothesis and false nuetotransmisster
hypothesis. To address the disease, the primary medical nutrition therapy is a reduction of ammonia,
comfort of living and assessment of swallowing to review if tube feeding would be needed. From a
nutritional viewpoint, encephalopathy yields concerns for pressure ulcer development, PO intake,
inability to swallow, need for tube feeding, weight loss, malnutrition and eventual hospice plan. These are
all scenarios that were drawn attention to in this Case Study.

Nutrition Therapy Suggestions for MD implemented by Dietetic Intern:


1. Suggest SLP for valuation of PO candidate
2. WOCN to evaluate stage of pressure ulcer
3. If safe for PO, consider the following supplementations for wound healing:
a. Multivitamin with minerals daily
b. Vitamin C 500 mg 2x daily for 10 days
c. Zinc Sulfate 220 mg daily for 10 days
d. Arginine 4.5 (1 pkt) 4x daily (total of 18 g arginine)
4. Monitor calibrated bed scale wt as able
5. Consider bowel regimen
6. Consider referral for Meal Time Mates.
7. Monitor calibrated bed scale wt as able
8. Consider BM regimen (per RN, MD put in an order for laxative)
9. If safe for PO, consider the following supplementations for wound healing:
- Multivitamin with minerals daily

Abstract​:
Encephalopathy is described as a disease, damage or malfunction of the brain. When addressing issues
pertinent to patients diagnosed with Encephalopathy, there is a main concern for the patient’s mental
status and furthermore, their ability to eat. The patient met with was a 70 year old male with progressive
encephalopathy after experiencing a stroke 3 months prior. The patient was unable to respond during each
meeting, initially pocketing food and medications provided, and limiting oral intake. Additionally, due to
the patient’s inability to move or be active, the patient developed a pressure ulcer that needed wound
healing recommendations. For a possible Stage 3, Stage 4, unstageable or deep tissue injury, I
recommended a Multivitamin, Vitamin C, Zinc Sulfate and Arginine as mentioned in the MD
recommendations box. Throughout the course of assessment, the patient experienced constipation, to
which it was recommended that the patient began a bowel regimen. This patient had loyal family
members that would visit everyday. Taking on the role of the RD, I built a relationship with the patient’s
family members, studied his case diligently and aspired to deliver the highest quality of care I could
provide as a Dietetic Intern. By the end of these assessments, there was planning by family and patient’s
personal wishes for hospice.
Nutrition Assessment​:
Initial Assessment:​ Clinical nutrition screen for pressure ulcer on sacrum, pending WOCN consult for
staging. Attempted to meet with patient at bedside, no family/ CG present. Per MD, patient has not eaten
since 3/30, has been pocketing food in mouth and not swallowing. Patient has been NPO since admission
(4/2). Pt meets criteria for severe malnutrition and wt loss.
Follow-Up​: Per WOCN nurse assessment (4/5), pt has CAPU evolving SDTI with partial thickness skin
breakdown on medial sacrum/coccyn. Recommendations provided above for wound healing. SLP
categorized pt as Mild Oropharyngeal suggesting a puree, nectar thick liquid diet; crushing medications
into puree. Pt was started on puree, nectar thick diet 4/5 PM. PO intake averages 83% per last 2 meals.
Since RD visit (4/5), no updated bed scale weight or BM documented. Will arrange for Nectar Thick
HCHP shake x1 daily to help meet nutrient needs.
Follow-Up​: ​Met pt at bedside, wife and CG present for nutrition education. Responding well to nectar
thick diet; increase in appetite AEB PO intake averaging 92% for last 3 meals. Per wife, pt has had an
increase in appetite, being more awake and responsive despite not talking.
Per MD, pt has shown improvement; has increased food intake being spoon fed by RN. Per RN, pt is a
good candidate for Meal Time Mates; referral made by Dietetic Student to Alicia.
Pt can nod his head yes or no, can grip hand, makes direct eye contact when being addressed and can
vocalize his own name.
PMHx​: Coronary artery disease; Dementia; Hyperlipidemia; Hypertension, Hyponatremia; Stage 3
Lymphoma s/p chemo 2015; S/P coronary artery stent placement
Cultural/ Religious hx​: No issues identified, pt admitted from assisted living facility
Food Intolerances/ allergies: No Known Allergies
Diet hx​: Per MD note, pt has not been eating since 3/30, has been pocketing food in mouth and not
swallowing.
Physical Appearance​: Mild fat loss around orbital region with slightly dark circles and hollow look. Mild
muscle loss in temporal region with hollowing temporal bone.
Patient met criteria for malnourishment
Anthropometrics​:
Height: 182.9 cm (6’0.01”)
Weight​: 67.1 kg (148#)
Weight Scale used​: Bed scale (4/2)
BMI​: 20.07
Desirable weight:​ 76.94 kg (170# at BMI of 23)
% Desirable weight​: 87%
Usual Weight:​ 171 to 182# (per wt hx)
% Usual Weight​: 81-87%
%Weight change:​ 14% loss in 5 months. Unknown

Wt Readings from Last 15 Encounters:


04/02/18 67.1 kg (148#)

10/23/17 77.8 kg (171#)

10/10/17 78.2 kg (172# 4.8 oz)

04/27/17 82.6 kg (182#)

04/21/17 82.3 kg (181# 6.4 oz)

01/26/17 78 kg (172#)

01/26/17 77.8 kg (171# 9.6 oz)

I/O​: +1051.8 for the last 24 hours


Skin​: Pressure ulcer on medial sacrum (possible stage 3, 4 SDTI, Unstageable (WOCN to Stage));
impaired skin integrity on right elbow/ arm (intact)
Edema:​ none documented
Labs​: Glucose 149; Na 144; K+ 3.2; Cl- 108; Cr 0.7
Meds​: IV Dextrose Saline, Continuous; KCl 10 mEq/100 mL (completed 4/4)
GI​: No BM during admission

Estimated Needs Based on 148# (67.1 kg) bed scale (as of 4/2):
1873 to 2123 kcals (Mifflin RMR 1441 x 1.3 + 250 kcals for wt gain)
101 to 134 g protein (1.5 to 2 g/kg)
~2000 ml fluids (~1 ml/ kcal)

Nutrition Diagnosis
Dx​: Acute toxic/ Metabolic Encephalopathy (improving), Alzheimer’s Dementia
PES:​ Increased nutrient (Energy, Protein, Vit/Min) needs related to increased physiological
demands as evidence by Possible Stage #, Stage 4, SDTI, Unstageable pressure ulcer and severe
malnutrition
Nutrition Intervention
Interventions​:
1. Coordination of Care: Nutrition care plan communicated with team; discussed with RN, Loida.
See recommendations box at top of note.
2. Nutrition Education: Pt not appropriate for nutrition education at this time d/t AMS. RD to
continue to follow for discharge planning needs as needed.
Nutrition discharge planning needs: to be determined. ​Eventual planning for hospice.
Nutrition Monitoring and Evaluation
Monitor/ Evaluate​:
1. NPO diet <2 days. New goal.
2. Weight maintenance/ gain towards IBW. New goal.
3. No further skin breakdown. New goal.
4. BM 1-3 every 1-3 days. New goal.
Nutrition priority level is 3; RD to follow up within 5 days.

References Used to Prepare Case Study


1. Vogel T, Dali-Youcef N, Kaltenbach G, Andres E. Homocysteine, vitamin B-12, folate and
cognitive functions: a systematic and critical review of the literature. Int J Clin Pract. Jul
2009;63(7):1061-1067.
2. Morris MS, Selhub J, Jacques PF. Vitamin B-12 and folate
3. status in relation to decline in scores on the mini-mental state examination in the framingham
heart study. J Am Geriatr Soc. Aug 2012;60(8):1457-1464.
4. McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of
Alzheimer’s disease: report of the NINCDS-ADRDA Work Group under the auspices of
Department of Health and Human Services Task Force on Alzheimer’s Disease. Neurology. Jul
1984;34(7):939-944.
5. Nutrition and Dementia: ​https://www.alz.co.uk/sites/default/files/pdfs/nutrition-and-dementia.pdf
6. Litchford, Bacon, Dondero, & Thompson. (2001). Use of arginine and glutamine supplements to
enhance wound healing in a long-term care (LTC) resident. Journal of the American Dietetic
Association, 101(9), A-49.
7. Bozkırlı, B., Gündoğdu, R., Ersoy, E., Lortlar, N., Yıldırım, Z., Temel, H., . . . Karakaya, J.
(2015). Pilot Experimental Study on the Effect of Arginine, Glutamine, and β-Hydroxy
β-Methylbutyrate on Secondary Wound Healing. Journal of Parenteral and Enteral Nutrition,
39(5), 591-597.
8. Previous studies have found that nutritional formulas, supplemented with arginine, zinc, and
antioxidants, speed wound healing. (2014). Nutrition Health Review, (112), 20.
9. Gottschlich, M. M., DeLegge, M. H., & Guenter, P. (2007). ​The A.S.P.E.N. nutrition support core
curriculum: A case-based approach: The adult patient. Silver Spring, MD: American Society for
Parenteral and Enteral Nutrition.
10. Mueller, C., McClave, S., & Kuhn, J. M. (2012). ​The A.S.P.E.N. Adult Nutrition Support Core
Curriculum: Complications of Enteral Nutrition. Silver Spring, MD: American Society for
Parenteral and Enteral Nutrition.
11. H​olmes, S. (2003). Undernutrition in hospital patients. ​Nursing Standard (through 2013), ​17(19),
45-52; quiz 54-5.
12. Grover, Z., & Ee, L. (2009). Protein Energy Malnutrition. ​Pediatric Clinics of North America,
56(5), 1055-1068.
13. Nutrition Care Manual: ​https://www.nutritioncaremanual.org/?err=NLI
14. World Health Organization. Dementia: a public health priority. Geneva 2012.
15. Addison T. Anemia: disease of the suprarenal capsules. Lond Med Gaz. 1849;43:517.
16. Garcia A, Zanibbi K. Homocysteine and cognitive function in elderly people. CMAJ. Oct 12
2004;171(8):897-904.
17. Clarke R, Grimley Evans J, Schneede J, et al. Vitamin B12 and folate deficiency in later life. Age
and ageing. Jan 2004;33(1):34- 41.
18. O’Leary F, Allman-Farinelli M, Samman S. Vitamin B(1)(2)
19. status, cognitive decline and dementia: a systematic review of prospective cohort studies. The
British journal of nutrition. Dec 14 2012;108 (11):1948-1961.
20. Morris MS. The Role of B Vitamins in Preventing and Treating Cognitive Impairment and
Decline. Adv Nutr. Nov 2012;3(6):801- 812.
21. Hinterberger M, Fischer P. Folate and Alzheimer: when time matters. Journal of Neural
Transmission. Jan 2013;120(1):211-224.
22. Nelms, M. N., Sucher, K., Lacey, K., Habash, D., Nelms, G. R., Hansen-Petrik, M., . . . Wong, J.
(2016). ​Nutrition therapy and pathophysiology. Boston, MA: Cengage Learning.
Case Study 2: Cedars Sinai Medical Center

Description of Primary Disease and Nutrition Treatment:


ALS (Amyotrophic Lateral Sclerosis) is a progressive neurological disease that causes destruction of the
motor neurons of the nervous system, resulting in muscle weakness, twitching, and atrophy. The cause
and progression of ALS is unknown although research indicates that there may be a correlation with
genetics for about 10% of cases (Lacey, 2016). The condition itself is multifactorial, having contributions
from genetics, biology and environment. Although there has been attention drawn to the neurological
disease with references such as Lou Gehrig's disease and the water bucket challenge, there is still no
known cure. Conclusively, the primary nutrition therapy for ALS is controlling symptoms as much as
possible, attending to nutrient needs and attentively evaluating swallowing ability. With the progression
of ALS, patients are anticipated to lose voluntary functions including swallowing, breathing, talking and
movement of extremities.

Nutrition Therapy Suggestions for MD implemented by Dietetic Intern:


1. Nutren 1.5 kcal, 250 ml bolus 5x daily as ordered, while in the hospital
2. TF at home: Consider Jevity 1.5 or equivalent, 1 can (~250 ml) 5x daily administered as bolus feeds
in G-Tube
3. Free water flushes 200 ml 5x daily in between bolus feeds

Abstract:
Amyotrophic Lateral Sclerosis is a neurological disease that results in the destruction of motor neurons of
the nervous system, resulting in the loss of movement of extremities, swallowing, talking and breathing.
With no cure available for the disease, the main nutrition therapy for ALS is to address the patient’s needs
and comfort as the disease progresses. Meeting with a 74 year old male with ALS, the patient was
assessed with dysphagia that prevented the patient from oral food intake. Anticipating a life expectancy of
3 to 5 years after diagnosis, Cedars-Sinai Medical Center holds a standard of care that incorporates
modern day research into addressing the specific nutrient requirements of ALS patients. Incorporating the
staging of the progression of ALS with Mifflin St. Jeor’s recommended estimated energy needs, the ​ALS
Functional Rating Scale is referred to assess energy recommendations.

From a nutritional standpoint, the textures of foods are crucial to address swallowing inability and
formula specific to the patient’s inability for daily living. Conducting a follow-up, the patient’s ALS
progressed to a state where tube feeding is required. Tube feeding regimen was recommended
accordingly, explained to wife and caregiver and explained to medical staff. To provide the utmost
nutrition therapy while inpatient, it was recommended that the patient be on Nutren 1.5 with 250 ml bolus
feeds 5 x daily. When making the transition for home tube feeding, basing my research of availability and
financial feasibility, it was recommended that Jevity 1.5 or equivalent is to be administer in 250 ml bolus
feeds, 5 x daily. Conclusively, the patient was admitted primarily for tube feeding placement and was
quickly discharged upon completion of placement. For routine check ups on ALS progression, the patient
keeps in close contact with medical staff and team.

Nutrition Assessment:
RD consult received for TF. 74 yo M with ALS admitted for dysphagia. Met pt at bedside s/p EGD PEG;
wife present. Pt has had ongoing wt loss with progressive dysphagia d/t inability to tolerate puree and
thickened liquids diet. Wife was provided with nutrition education regarding TF and different modes of
TF. Suggest high fiber formula to assist with pt's bowel motility/ constipation. Current TF order by MD
meets nutrient demands but lacks fiber. For home, suggest high fiber formula.
Diet history​: Puree, thick liquids
Physical Appearance​: pt on bi-pap support
Anthropometrics​:
​Height​: 182.9 cm (6' 0.01")
​Weight​: 72.6 kg (160 lb)
​BMI ​(Calculated): 21.69
Desirable Weight: 178#
% Desirable Weight: 90%
Usual Weight: 176# (~4 months ago)
%Usual Weight: 91%
%Weight change​: 9% loss in 4 months. Unintentional
Wt Readings from Last 15 Encounters:
05/09/18 72.6 kg (160 lb)
03/21/18 76.7 kg (169 lb 3.2 oz)
01/24/18 79.8 kg (176 lb)
01/10/18 80 kg (176 lb 6.4 oz)
12/13/17 83.9 kg (185 lb)
09/06/17 81.9 kg (180 lb 9.6 oz)
06/07/17 80.2 kg (176 lb 12.8 oz)
03/08/17 85.8 kg (189 lb 3.2 oz)
11/30/16 86.6 kg (191 lb)
09/14/16 88 kg (194 lb)
06/01/16 86.7 kg (191 lb 3.2 oz)
03/02/16 90 kg (198 lb 6.4 oz)
12/02/15 90.3 kg (199 lb)
09/02/15 88.9 kg (196 lb)
08/21/15 88.3 kg (194 lb 9.6 oz)
Skin:​ No Pressure Ulcer documented.
Impaired Skin Integrity-Wound Right Posterior Leg
Edema​: none documented
GI​: No BM within last 24 hours; none since 5/6. Upon admission, experienced episodes of emesis and
nausea. None documented since admission.
Oral Enteral or Parenteral Intake:
Current diet Rx​: Lowfat clear liquids

Estimated Needs ​based on 160# (72.7 kg) admit weight (as of 5/9):
Harris Benedict Equation for basal energy expenditure (BEE): 1480 kcal
ALS Functional Rating Scale-6 score (speech, handwriting, dressing/hygiene, turning in bed,
walking, dyspnea) total: 5
Calculated daily energy expenditure with ALS population specific predictive formula: 1592 kcal to
maintain weight; >1842 kcals (weight gain plus 250 kcal)
Protein goal: 1 g/kg: 73 g
Fluids: at least 1842 ml/D (1 ml/kg)

Labs reviewed:​ Na 133 (low); BUN 3 (low); Lipase 575 (high)


Meds reviewed:​ lactated ringers continuous; zofran; pantoprazole (protonix)
Nutrition Diagnosis
Dx​: Dysphagia
PES​: Difficulty swallowing related to ALS progression as evidenced by TF (G-tube) placement.
Nutrition Intervention
Interventions​:
1. Coordination of care: Nutrition care plan communicated with team. See recommendations box at top of
note.
2. Nutrition Education: explained rationale for tube feeding to wife/CG. CG receptive to education and
nutrition plan; expect good compliance. RD to continue to follow for discharge planning needs as needed.
Nutrition discharge planning needs: bolus GT feeds for home.
Nutrition Monitoring and Evaluation
Monitor/Evaluate​:
1. Nutrition support to meet +/-10% of energy and protein goals. New goal.
2. Lab: WNL (POC gluc < 180, Chemistries WNL). New goal.
3. GI: 1-3BM Q1-3 days (or 500mL max daily). New goal.
4. Residuals < 200 ml; abdomen non- distended, no abdominal pain. New goal.
Nutrition priority level is 3; RD to follow up within 5 days.

References Used to Prepare Case Study


1. Salvioni, C., Stanich, P., Almeida, C., Oliveira, A., Dos Santos Salvioni, C., &
BulleOliveira, P. (2014). Nutritional care in motor neuronedisease/amyotrophic lateral
sclerosis. ​Arquivos De Neuro-Psiquiatria,72(2), 157-163.
2. Wills, Hubbard, Macklin, Glass, Tandan, Simpson, . . . Cudkowicz. (2014). Hypercaloric
enteral nutrition in patients with amyotrophic lateral sclerosis: A randomised,
double-blind, placebo-controlled phase 2 trial. ​The Lancet,383(9934), 2065-2072.
3. Nieves, J., Gennings, C., Factor-Litvak, P., Hupf, J., Singleton, J., Sharf, V., . . .
Mitsumoto, H. (2016). Association Between Dietary Intake and Function in Amyotrophic
Lateral Sclerosis. ​JAMA Neurology,73(12), 1425-1432.
4. Kasarskis, Edward J., Mendiondo, Marta S., Matthews, Dwight E., Mitsumoto, Hiroshi,
Tandan, Rup, Simmons, Zachary, . . . Kryscio, Richard J. (2014). Estimating daily energy
expenditure in individuals with amyotrophic lateral sclerosis. ​American Journal of
Clinical Nutrition,99(4), 792-803.
5. Price, S., & Wilson, L. (1986). ​Pathophysiology: Clinical concepts of disease
processes(3rd ed.). New York: McGraw-Hill.
6. Nahikian-Nelms, M. (2011). ​Nutrition therapy and pathophysiology(2nd ed.). Belmont,
CA: Wadsworth, Cengage Learning.
7. Mahan, LK, Escott-Stump, S, Raymond, J. (2011) Krause’s Food and the Nutrition Care
Process (13th edition). Saunders.
8. Nelms, M. N., Sucher, K., Lacey, K., Habash, D., Nelms, G. R., Hansen-Petrik, M., . . .
Wong, J. (2016). ​Nutrition therapy and pathophysiology. Boston, MA: Cengage
Learning.

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