Pranithi Hongsprabhas MD. Basic Clinical Nutrition.

77
Pranithi Hongsprabhas MD. Basic Clinical Nutrition

Transcript of Pranithi Hongsprabhas MD. Basic Clinical Nutrition.

Page 1: Pranithi Hongsprabhas MD. Basic Clinical Nutrition.

Pranithi Hongsprabhas MD.

Basic Clinical Nutrition

Page 2: Pranithi Hongsprabhas MD. Basic Clinical Nutrition.

Objective

E tiology of PEM Types/ prevalence of

malnutritionConsequences of

malnutritionHow to diagnose and assess

nutritional statusEffect of nutrition therapyNutrition for specific

diseases

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References

Shils M, Olson JA, Shike M, Modern Nutrition i n Health and Diseases. 2005

ASPEN manual of nutrition 2005ESPEN guideline for EN 2006ASPEN guideline 2009

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Malnutrition

State of nutrition in which a deficiency or excess (or imbalance) of energy, protein, and other nutrients caused measurable adverse effects on tissue/body form and function and clinical outcome

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Malnutrition

Over nutrition obesity dietary induced dyslipidemia

Under nutrition protein energy malnutrition specific nutrient deficiency

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Hospital Malnutrition

Incidence Community setting (common in chronically ill;

cancer, lungs etc.) Hospital setting: 30-60 % (10-25% are severe)

Progression Get worse in hospital

Effect on Health Diseases Prognosis Mortality

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Relationship Between Loss of Lean Mass and Degree of Mortality

LBM(% loss of total)

Complications (related to LBM loss

Associated mortality

10 Impaired immunity, increased infection

10

20 Decreased healing, weakness, infection

30

30 To weak to sit, pressure sore, pneumonia, no healing

50

40 Death usually from pneumonia

100

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Nutrient intake

Nutrient utilization

Medication

Difficult eating

Cytokines

Anorexia

Depression

dementia

Socioeconomic

Hypermetabolic State

Excessive activity

Malabsorption

Nutrient Loss

Physiologic Demand

Diseases and Conditions Predisposin g to Malnutrition

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Diseases and Conditions Predis posing to Malnutrition

Decreased intake Decreased absorption Increased losses Altered metabolism Increased requirement

Hensrud DD. Nutrition screening and assessment. Med Clin North Am 1999;83:1525-47

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10

20

30

40

I II III IV V

ExogenousGlycogenGluconeogenesis

Glu

cose

uti

lize

d (

g/h

ora

)

Ruderman NB. Annu Rev Med 1975;26:248

I II III IV V

GlucoseGlucose GlucoseGlucose, ketones

Fatty acid Glucose

Fuel for brain

LEGEND

Substrate Utilization in Starvation

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Simple Starvation: Marasmic Wasting

Response to t otal/partial cessati on of energy intake

Short term starvation (<72 hr) 72Prolonged starvation (> hr)

RMR, DIT, activity gluconeogenesis from aa, lactate tissue utilization of ketone, FFA

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Nitrogen excretion in Starvation

Long CL et al. JPEN 1979;3:452-456

010 20 30 40

Partial Starvation

Days

Nitr

ogen

Exc

retio

n (g

/day

)

12

8

44

Total Starvation

Normal Range

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Marasmus: Simple starvation

Decreased metaboli c rate

W WWWWW WWWW W WWWWW WW om fat and also LBM

W WWW WW WWWWW WW WWWWl

Bone and skin appearance

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Metabolic Response to Stress: Trauma/Sepsis

Time

Ener

gy E

xpen

ditu

re

Ebb PhaseEbb Phase Flow PhaseFlow Phase

Cutherbertson DP, et al. Adv Clin Chem 1969;12:1-55

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Metabolic Response to Stress: Protein Catabolism

Long CL, et al. JPEN 1979;3:452-456

10 20 30 40

28

24

20

16

12

8

4

0

Nitr

ogen

Exc

retio

n (g

/day

)

Days

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Metabolic Response to Stress

Fatty

Deposits

Liver &

Muscle

(glycogen)

Muscle

(amino acids)

Fatty

Acids

Glucose

Amino Acids

Endocrine Response

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Stress Starvation

Response to starvation and inflammation Days to weeks or months Depend on hormonal and cytokine control

Cytokine response C - atabolic (IL 1, IL-6, TNF-

) increased RMR decreased LBM increased protein breakdow

n

V ascular permeability

Hormonal response Aldosterone/ADH

salt/ water retention E pinephrine, glucago

n, cortisol lipolysis gluconeogenesis severe protein catabol

ism

Catabolic state cannot be reversed by nutrition alone: Nutritional ResistanceNutritional Resistance

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Stress Starvation

Kwashi or kor or hyp oal bumi nemi c mal n

ut r i t i on Low albumin level/ W

dema Loss of body protein

WWWWWWWWWW WWWWWW:

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Chronic Stress Starvation

- Mild moderate stres s + starvation

Develops in months

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Complication of Malnutrition

Reduced renal function: GFR and concentrating ability inability to handle Na load,

acid load polyuria

Liver: fatty liverCardiac functionGI: intestinal barrierAltered drug Pk

1989Perspect Crit Care ;21:

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Malnutrition Related Complication

Impaired immunity: CMI, chemotaxis, phagocytosis, complement

Slow wound healingM uscle atrophyC ompromised respiratory function: hypoxic v

entilatory drive, impaired resp muscle, VC, MV

LOS, treatment cost Mortality

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Risk of Malnutrition

Reilly J et al. JPEN 1988

7,902

18,896

26,359

4,979

11,174

6,858

0

5,000

10,000

15,000

20,000

25,000

30,000

Risk of Malnutri tion

No Risk of

Malnutri tion

Cos

t per

Pat

ient

(US

D)

Pneumonia Intestinal surgery Complication

Hospital cost

0 5 10 15 20

Severe

Mild

Normal

Hospital Stay

Nu

triti

ona

l sta

tus

Robinson et al. JPEN 1987

0

10

20

30

40

50

0 1 2 3 4 5 6 7 8 9

PEMnon-PEM

Months After HospitalizationAmerican Journal of Medicine (Cederholm T, Jägrén C, Hellström K. Outcome of Protein-Energy Malnutrition in Elderly Medical Patients, 1995;98:67-74)

% M

orta

lity

Cumulative mortality

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Characteristic Differentiating of Marasmus and Marasmic kwashiorkor

Marasmus -Develops over mo yr Low intake Usually emaciated Edema not prominent Usually normal albumi

n Lower mortality than k

washiorkor

Marasmic kwashiorkor Develops over weeks Usually from low intake a

nd stress Appear well nourished Edema is characteristic May be no wt loss Usually low serum protei

n Higher mortality

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How to Detect Patients at Risk?

Nutritional screening Identify the characteristics associated with

nutritional problems Identify patients at nutritional risk

Nutritional assessment Collect and evaluate clinical conditions, diet,

body composition and biochemical data, among others

Classify patients by nutritional state: well-nourished or malnourished

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Nutritional Screening

Involuntary increase or decrease in weight > 10% of usual weight over 6 months or > 5% of usual weight over 1 months

Inadequate oral intake

Barrocas et al. J Am Diet Assoc 1995: 95: 648

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Nutrition Screening Tool

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Nutritional Risk Screening

A) Body mass index 0 = greater than 20 1 = 18-20 2 = < 18

score

B) Has the patient unintentional loss BW over the past 3 months

0 = no 1 = a little up to 3 kg 2 = a lot more than 3 kg

score

C) Food intake- has this decrease over the last month prior to admission 0 = no 2 = yes

score

D)Stress factor/ severity of illness 0 = non 1 = moderate

2 = severe

score

Screening If score 0-2 No action If score 3-4 Monitor + review in a week/ food record chart If score > 5 refer to dietitic advice

Total score

University hospital Nottingham: A. Micklewright, S.P. Allison and Z. Stanga

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Nutritional Assessment

Clinical assessment Subjective Global Assessment

Body compositionBiochemical dataFunctional assessment

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Subjective Global Assessment

History W t change Changes in dietary intake Gastrointestinal symptoms Functional capacity Link between disease and nutritional requirement

PE focused on nutritional aspects degree of fat loss muscle wasting edema/ ascites clinical signs of nutritional deficiency

Detsky AS, et al. JPEN 1987; 11: 8-15.

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SGA

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SGA: Classification

Well nourishedModerately malnourished or suspected

malnutritionSeverely malnourished

Class A: no change in BW, normal intake, < 5 % wt loss, or > 5% wt loss but recent gain and improve app

etite Class B:

- 510%wt l oss wi thout recent stabi l i zati onor gai n, poor di et ary intake and mild loss of subcutaneous tissue

Class C: ongoing wt loss of > 10% with severe subcutaneous tissue loss

and muscle wasting often with edema

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General: Muscle Wasting

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Hair

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Flaky paint dermatosis: protein deficiency

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Essential fatty acid deficiency syndromes (EFADs)

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Zinc deficiency

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Pellagra

•dermatitis

•dementia

•diarrhea

•death

niacin deficiency

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Perifollicular Petechia: Vitamin C deficiency

Vitamin K deficiency

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Nutritional Assessment Body Composition Parameter

Weight and heightBMI = weight/ height2

Triceps or subscapular thickness of skin fold

Mid-arm muscle circumference and mid-arm muscle area

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Anthropometric MeasurementLimitation

Fluid: overhydration, dehydration Technique: reproducibility Do not reflect variation in bone size, skin com

pressibility

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Creatinine Height Index

Correlates with lean body massCHI = - actual 24 hr Cr excretion expected Cr excretion - estimated 18 20 kg muscle produce 1 g Cr expected Cr excretion

female 18 mg/kg male 23 mg/kg

interpretation 80> % - 0 mi l d depl et i on -60 80% W WWWWWWW WWWWWWWWW < 60% sever e depl et i on

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Creatinine Height Index/ Excretion

Factors affecting CHI reliability renal insufficiencyrhabdomyolysis bed rest catabolic state incomplete collection

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Laboratory Assessment: Visceral Pro tein Reserve

Protein MW T 1/2 Normal range

Albumin 65,000 18-20 d 3.5-5.5 g/dl

TFN 76,000 7-10 d 1.6-3.6 g/l

Prealbumin 54,980 12-24 hr 160-350 mg/l

RBP 21,000 2-4 hr 0.10-0.40 mg/l

Hepatic secretory protein

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Nutritional Assessment: Biochemical Parameters

At risk level

Serum albumin < 3.5 g/dl

Total lymphocyte count < 1500 cell/mm3

Serum transferrin < 140 mg/dl

Serum prealbumin <17 mg/dl

TIBC <250 g/dl

Serum cholesterol <150 mg/dl

Heymsfield SB, et al. In: Modern Nutrition in Health and Disease. Phiadelphia, PA: Lea& Febiger; 1994: 812-41.

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Nutrition Support

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Nutritional Support:Indication

- NPO > 10 14 day PEM or at nutritional risk

Inadequate oral intake Maldigestion, malabsorption Nutrient loss fistula, dialysis, drainage Hypercatabolic state: sepsis, burn, multiple

trauma Perioperative severely malnorished

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Nutrition Aim/ Goal

Improve nutritional depletion malnourished/ low cat

abolism Maintain nutritional s

tatus/ prevent malnutrition malabsorption unable to eat

Minimized nutritional re lated complication

critically illness moderate hypercatabolic

state Improve clinical outcom

e perioperative nutrition nutrition in BMT trauma

Page 50: Pranithi Hongsprabhas MD. Basic Clinical Nutrition.

Estimated Energy Requirement

1. Requirement = BEE x AF x SF

Activity factor = 12 13 15. (low), . ( moderate ) , . ( high )

Stress factor = - - 111 1214 1mild . , moderate . . , severe .

-52

2. Kcal/kg

-2530 kcal/kg/d

Harris Benedict EquationBEE m = 66+13.7 wt+5 ht-6.3 age

f = 655+9.6wt+17ht-4.7age

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Protein Requirement

Population Rates(g/kg/d)normal/unstress .8

postoperative* 1.1-1.5

septic 1.2-1.5

multiple trauma 1.8

burned 1.5-4.0

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Nitrogen Balance

N output = UUN+UNUN+ misc

- = UUN +(2 4) (g) N intake = Protein intake(g)

625.

N balance = N output - N intake

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Fat Requirement

Essential fatty acid linoleic: 4% of total calorie - linolenic: 0.2 0.4% of total calorie

Source of energy : 9 /1kcal g -20 35%

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Mineral Requirement

Mineral RequirementNa /Cl 2-3 (meq/kg/d)

K 2-3 (meq/kg/d)

Mg 0.125-0.2 (meq/kg/d)

Ca 60 (meq/d)

PO4 60 (meq/d)

Vitamin Requirement/ Trace Element Requirement According to RDA

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Key Vitamins and Minerals

Vitamin A

Vitamin C

B Vitamins

Pyridoxine

Zinc

Vitamin E

Folic Acid,Iron, B12

Wound healing and tissue repair

Collagen synthesis, wound healing

Metabolism, carbohydrate utilization

Essential for protein synthesis

Wound healing, immune function, protein synthesis

Antioxidant

Required for synthesis and replacement of red blood cells

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How is Nutritional Support Prescribed?

Average nutritional prescription should include 25-35 kcal/kg/day total energy, 0.8-1.5 g protein (0.13-0.24 g

nitrogen)/kg/day, 30-35 ml fluid/kg, electrolytes, minerals, micronutrients, and

fiber

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Contraindication of NutritionSupport

Unstable hemodynamics - Severe fluid, electrolyte, acid base dis

order (esp. PN) Uncontrolled infection

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Enteral Nutrition: Contraindication

Unstable condition: hemodynamics Intestinal obstruction Massive GI bleeding Intestinal ischemia Severe malabsorption, inflammation,

severe ileus

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ENENGut obstruction Massive GI bleeding Intestinal ischemia Severe malabsorption,

inflammation

PNPN End stage malignancy:

EOL determined

Unstable hemodynamics Severe fluid imbalance: overload or dehydration Severe - electrolyte, acid base disorder Uncontrolled sepsis

Contraindication of Nutrition Support

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Nutritional Support For A Patient At Risk Of Malnourishment

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ผู้��ป่�วยกิ�นเองได้�ผู้��ป่�วยกิ�นเองได้�น�อยผู้��ป่�วยกิ�นเองได้�น�อยมากิหรื�อกิ�นเองไม�ได้�แต่� GI

function ย�งป่กิต่�ผู้��ป่�วยที่�� GI function ผู้�ด้ป่กิต่�บางส่�วนผู้��ป่�วยที่�� GI tract failure

Page 63: Pranithi Hongsprabhas MD. Basic Clinical Nutrition.

Nutrition Support

Oral diet Soft Regular

For specific disease Diabetic diet High protein diet Renal diet Low sodium diet Low fat diet

Oral supplement

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Artificial Nutrition Support

Enteral tube feeding Naso/Orogastric gastrostomy Enteric:

nasojejunostomy, jejunostomy

Parenteral nutrition PPN TPN

Page 65: Pranithi Hongsprabhas MD. Basic Clinical Nutrition.

Common Complications: ETF

Mechanical Irritation or infection Tube displacement Aspiration Tube clogging

Gastrointestinal Nausea Vomiting Abdominal distention Diarrhea Constipation

Metabolic Dehydration Hyperglycemia Elevated serum electrolytes Low serum electrolytes

Mizock BA. J Crit Illness 1993;8:1116-1127, American Gastroenterological Association. Gastroenterol 1995;108:1280-1301, ottlieb K, Iber F. J Crit Illness 1991;6:817-824

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Monitoring of EN

Assessment of GI tolerance Abdominal discomfort

(fullness, cramping, pain)

Nausea and vomiting Abdominal distention Bowel sound Stool pattern

Diarrhea constipation

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Monitoring of EN

Aspiration precaution Tube feeding residual:

Gastric residual volume (GRV)

Head lift ≥ 30o

Aspiration detection Clinical signs and

symptoms CXR

Hydration status Assessment of

hydration status Physical exam I/O

Determine fluid requirement 30-35 ml/kg/d Extra fluid

Assessment of nutrition intake Caloric count

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Parenteral Nutrition (PN)

PPN, TPN Indication

GI tract failure Inadequate EN

Contraindication Unstable condition Uncontrolled serious condition Terminal stage conditions (EOL determined)

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Complication of PN

Line sepsis: CRIM - etabolic derangement/ re feeding sy

ndrome WWWW -WWWW WWWWWWWWW/ / Overfeeding syndromeLiver complication

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Infectious Complication ‘Catheter related infection’ (CRI)

T unnel site infectionH ub contaminationI nfusate contaminationW eeding of other site of infection

Guideline for prevention of intravascular device-related infection.Infectious control and hospital epidemiology 1996;17(7):438-473

Page 71: Pranithi Hongsprabhas MD. Basic Clinical Nutrition.

Refeeding Syndrome (Nutrition Recovery Syndrome)

Metabolic complication occurs when nutritional support given to severely malnourished

Electrolyte abnormalities Hypo K+, Mg2+, PO4

3- from intracellular shift Weakness Respiratory failure arrhythmia

Na/fluid retention from Insulin/Glucagon ratio (antinatriuresis) Refeeding edema, Fluid overload

Metabolic thiamin demand Substrate shift: from FA to glu VCO2/O2

and work of breathing

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Risk For Refeeding Syndrome

≥ 1 BMI <16 Unintentional weight loss >15% in 3-6 months ≥ 10 days with little or no nutritional intake Low Mg2+, K+, or PO4

3- before feeding≥ 2

BMI <18.5 Unintentional weight loss >15% in 3-6 months ≥ 5 days with little or no nutritional intake Alcohol misuse, chronic diuretic, antacid, insulin

use, or chemotherapy

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How To Prevent and Management of Refeeding Syndrome

In high risk patientsStart 10 kcal/kg/d, gradually within a weekBefore/during of 1st 10 d of feeding

oral thiamin 200-300 mg/day +1-2 vitamin B co strong tablets 3 times/d or IV

vitamin B +balanced multivitamin and mineral supplement each

daymonitor and supplement oral, enteral, or

intravenous K, PO43- and Mg intake.

K+ 2-4 mmol/kg/day PO4

3- 0.3-0.6 mmol/kg/d Mg2+ 0.2 mmol/kg/d IV or 0.4 mmol/kg/d oral

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Metabolic Complication to Overfeeding

HyperglycemiaHypertriglyceridemiaHypercapniaFatty liverHypophosphatemia,

hypomagnesemia, hypokalemia

Barton RG. Nutr Clin Pract 1994;9:127-139

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Hepatobiliary Complication

AdultsSteatosisSteatohepatitisCholestasisBiliary sludgeCholelithiasisAcalculous cholecystitisFibrosisMicronodular cirrhosis

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Nutrition Monitoring

For nutrition response Monitoring of complication

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Monitoring

•Vital signs, body weight •Fluid intake and output •Electrolytes, glucose, BUN/Cr, Ca, P, Mg•24-hour total urinary urea nitrogen•Estimated nutrient intake (all

administration routes)•Liver enzymes