Pranithi Hongsprabhas MD. Basic Clinical Nutrition.
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Transcript of Pranithi Hongsprabhas MD. Basic Clinical Nutrition.
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
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
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
Malnutrition
Over nutrition obesity dietary induced dyslipidemia
Under nutrition protein energy malnutrition specific nutrient deficiency
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
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
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
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
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
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
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
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
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
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
Metabolic Response to Stress
Fatty
Deposits
Liver &
Muscle
(glycogen)
Muscle
(amino acids)
Fatty
Acids
Glucose
Amino Acids
Endocrine Response
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
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:
Chronic Stress Starvation
- Mild moderate stres s + starvation
Develops in months
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:
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
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
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
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
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
Nutrition Screening Tool
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
Nutritional Assessment
Clinical assessment Subjective Global Assessment
Body compositionBiochemical dataFunctional assessment
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.
SGA
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
General: Muscle Wasting
Hair
Flaky paint dermatosis: protein deficiency
Essential fatty acid deficiency syndromes (EFADs)
Zinc deficiency
Pellagra
•dermatitis
•dementia
•diarrhea
•death
niacin deficiency
Perifollicular Petechia: Vitamin C deficiency
Vitamin K deficiency
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
Anthropometric MeasurementLimitation
Fluid: overhydration, dehydration Technique: reproducibility Do not reflect variation in bone size, skin com
pressibility
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
Creatinine Height Index/ Excretion
Factors affecting CHI reliability renal insufficiencyrhabdomyolysis bed rest catabolic state incomplete collection
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
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.
Nutrition Support
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
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
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
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
Nitrogen Balance
N output = UUN+UNUN+ misc
- = UUN +(2 4) (g) N intake = Protein intake(g)
625.
N balance = N output - N intake
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%
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
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
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
Contraindication of NutritionSupport
Unstable hemodynamics - Severe fluid, electrolyte, acid base dis
order (esp. PN) Uncontrolled infection
Enteral Nutrition: Contraindication
Unstable condition: hemodynamics Intestinal obstruction Massive GI bleeding Intestinal ischemia Severe malabsorption, inflammation,
severe ileus
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
Nutritional Support For A Patient At Risk Of Malnourishment
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Nutrition Support
Oral diet Soft Regular
For specific disease Diabetic diet High protein diet Renal diet Low sodium diet Low fat diet
Oral supplement
Artificial Nutrition Support
Enteral tube feeding Naso/Orogastric gastrostomy Enteric:
nasojejunostomy, jejunostomy
Parenteral nutrition PPN TPN
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
Monitoring of EN
Assessment of GI tolerance Abdominal discomfort
(fullness, cramping, pain)
Nausea and vomiting Abdominal distention Bowel sound Stool pattern
Diarrhea constipation
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
Parenteral Nutrition (PN)
PPN, TPN Indication
GI tract failure Inadequate EN
Contraindication Unstable condition Uncontrolled serious condition Terminal stage conditions (EOL determined)
Complication of PN
Line sepsis: CRIM - etabolic derangement/ re feeding sy
ndrome WWWW -WWWW WWWWWWWWW/ / Overfeeding syndromeLiver complication
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
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
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
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
Metabolic Complication to Overfeeding
HyperglycemiaHypertriglyceridemiaHypercapniaFatty liverHypophosphatemia,
hypomagnesemia, hypokalemia
Barton RG. Nutr Clin Pract 1994;9:127-139
Hepatobiliary Complication
AdultsSteatosisSteatohepatitisCholestasisBiliary sludgeCholelithiasisAcalculous cholecystitisFibrosisMicronodular cirrhosis
Nutrition Monitoring
For nutrition response Monitoring of complication
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