Basic Clinical Nutrition
Pranithi Hongsprabhas MD.
Objective
 Etiology of PEM
 Types/ prevalence of




malnutrition
Consequences of malnutrition
How to diagnose and assess
nutritional status
Effect of nutrition therapy
Nutrition for specific diseases
References
 Shils M, Olson JA, Shike M, Modern Nutrition in
Health and Diseases. 2005
 ASPEN manual of nutrition 2005
 ESPEN guideline for EN 2006
 ASPEN 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)
10
Complications (related to
LBM loss
Associated
mortality
Impaired immunity,
increased infection
10
20
Decreased healing,
weakness, infection
30
30
To weak to sit, pressure
sore, pneumonia, no
healing
Death usually from
50
40
100
Diseases and Conditions Predisposing to
Malnutrition
Hypermetabolic
State
Excessive activity
Difficult eating
Medication
Cytokines
Nutrient
intake
Nutrient utilization
Anorexia
Physiologic Demand
Depression
Nutrient Loss
dementia
Socioeconomic
Malabsorption
Diseases and Conditions Predisposing
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
Substrate Utilization in Starvation
Glucose utilized (g/hora)
I
II
IV
III
V
Exogenous
Glycogen
Gluconeogenesis
40
30
20
10
LEGEND
I
II
III
Fuel for
brain
Glucose
Glucose
Glucose
IV
Glucose,
ketones
V
Fatty acid
Glucose
Ruderman NB. Annu Rev Med 1975;26:248
Simple Starvation: Marasmic Wasting
Response to total/partial cessation
of energy intake
 Short
term starvation (<72 hr)
 Prolonged starvation (>72 hr)
 RMR, DIT, activity
 gluconeogenesis from aa, lactate
 tissue utilization of ketone, FFA
Nitrogen excretion in Starvation
Nitrogen Excretion (g/day)
12
Normal Range
8
Partial Starvation
4
Total Starvation
0
10
20
Days
Long CL et al. JPEN 1979;3:452-456
30
40
Marasmus: Simple starvation
 Decreased metabolic
rate
 Weight loss mainly from
fat and also LBM
 Normal albumin level
Bone and skin appearance
Metabolic Response to Stress: Trauma/Sepsis

Flow Phase
Energy Expenditure
Ebb Phase
Time
Cutherbertson DP, et al. Adv Clin Chem 1969;12:1-55
Metabolic Response to Stress: Protein
Catabolism
Nitrogen Excretion (g/day)
28
24
20
16
12
8
4
0
10
20
30
Days
Long CL, et al. JPEN 1979;3:452-456
40
Metabolic Response to Stress
Fatty Deposits
Endocrine
Response
Fatty Acids
Liver & Muscle
(glycogen)
Muscle (amino
acids)
Glucose
Amino Acids
Stress Starvation
 Response to starvation and inflammation
 Days to weeks or months
 Depend on hormonal and cytokine control
Cytokine response

Catabolic (IL-1, IL-6, TNF-)




increased RMR
decreased LBM
increased protein breakdown
Vascular permeability
Hormonal response

Aldosterone/ADH


salt/ water retention
Epinephrine, glucagon,
cortisol



lipolysis
gluconeogenesis
severe protein
catabolism
Catabolic state cannot be reversed by nutrition alone:
Nutritional Resistance
Stress Starvation
 Kwashiorkor or
hypoalbuminemic
malnutrition
 Low albumin level/
edema
 Loss of body protein:
functional change
Chronic Stress Starvation
 Mild -moderate stress
+ starvation
 Develops in months
Complication of Malnutrition
 Reduced renal function: 
GFR and concentrating
ability
inability to handle Na load, acid
load
 polyuria

 Liver: fatty liver
 Cardiac function
 GI: intestinal barrier
 Altered drug Pk
Perspect Crit Care 1989; 2:1
Malnutrition Related Complication
 Impaired immunity:

CMI, chemotaxis, phagocytosis, complement
 Slow wound healing
 Muscle atrophy
 Compromised respiratory function: hypoxic
ventilatory drive, impaired resp muscle, VC, MV
  LOS, treatment cost
  Mortality
Risk of Malnutrition
Hospital cost
Cumulative
mortality
26,359
Hospital Stay
50
(US D)
Cost per Patient
Mortality
%status
Nutritional
30,000
Ri sk of Mal nut r i t i on
18,896
PEM
40
25,000
Severe
No Ri sk of
non-PEM
20,000
30
Mal nut r i t i on
15,000
20
7,902
10,000
11,174
6,858
Mild
4,979
10
5,000
0 0
0
0
Normal
1
2
Pneumonia
3
4
5
Intestinal surgery
6
7
8
Complication
5
10
15
Months
After Hospitalization
9
20
Reilly
J et al. JPEN 1988
American Journal of Medicine (Cederholm T, Jägrén C, Hellström K. Outcome
of Protein-Energy
Malnutrition in
Robinson et al. JPEN 1987
Elderly Medical Patients, 1995;98:67-74)
Characteristic Differentiating of Marasmus and
Marasmic kwashiorkor
Marasmus
Marasmic kwashiorkor
 Develops over mo-yr
 Develops over weeks
 Low intake
 Usually from low intake and
 Usually emaciated
 Edema not prominent

 Usually normal albumin

 Lower mortality than

kwashiorkor


stress
Appear well nourished
Edema is characteristic
May be no wt loss
Usually low serum protein
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
University hospital Nottingham: A. Micklewright, S.P. Allison and Z. Stanga
Total score
Nutritional Assessment
 Clinical assessment
 Subjective
Global Assessment
 Body composition
 Biochemical data
 Functional assessment
Subjective Global Assessment
 History

Wt 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 nourished
 Moderately malnourished or suspected
malnutrition
 Severely malnourished



Class A:

no change in BW, normal intake,

< 5 % wt loss, or > 5% wt loss but recent gain and improve appetite
Class B:

5-10% wt loss without recent stabilization or gain, poor dietary
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 height
 BMI = weight/ height2
 Triceps or subscapular
thickness of skin fold
 Mid-arm muscle
circumference and midarm muscle area
Anthropometric Measurement Limitation
 Fluid: overhydration, dehydration
 Technique: reproducibility
 Do not reflect variation in bone size, skin
compressibility
Creatinine Height Index
Correlates with lean body mass
 CHI
= actual 24-hr Cr excretion
expected Cr excretion
 estimated 18-20 kg muscle produce 1 g Cr
 expected Cr excretion


female
male
 interpretation
 > 80 %
 60-80%
 < 60%
18 mg/kg
23 mg/kg
0-mild depletion
moderate depletion
severe depletion
Creatinine Height Index/ Excretion
Factors affecting CHI reliability
 renal insufficiency
 rhabdomyolysis
 bed rest
 catabolic state
 incomplete collection
Laboratory Assessment: Visceral Protein
Reserve

Hepatic secretory protein
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
12-24 hr
160-350 mg/l
2-4 hr
0.10-0.40 mg/l
Prealbumin 54,980
RBP
21,000
Nutritional Assessment: Biochemical
Parameters
Serum albumin
Total lymphocyte count
Serum transferrin
Serum prealbumin
TIBC
Serum cholesterol
At risk level
< 3.5 g/dl
< 1500 cell/mm3
< 140 mg/dl
<17 mg/dl
<250 mg/dl
<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
catabolism
 Minimized nutritional
related complication


 Maintain nutritional
status/ prevent
malnutrition


malabsorption
unable to eat
critically illness
moderate hypercatabolic
state
 Improve clinical outcome



perioperative nutrition
nutrition in BMT
trauma
Estimated Energy Requirement
1. Requirement = BEE x AF x SF
Harris Benedict Equation
BEE m = 66+13.7 wt+5 ht-6.3 age
f = 655+9.6wt+17ht-4.7age
Activity factor = 1.2 (low), 1.3 ( moderate ) , 1.5 ( high )
Stress factor = mild 1-1.1, moderate 1.2-1.4, severe 1.5-2
2. Kcal/kg
25-30 kcal/kg/d
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 balance = N output - N intake
N output = UUN+UNUN+ misc
= UUN +(2-4) (g)
N intake = Protein intake(g)
6.25
Fat Requirement
 Essential fatty acid
 linoleic:
4% of total calorie
 linolenic: 0.2-0.4% of total calorie
 Source of energy : 9kcal/1g

20-35%
Mineral Requirement
Mineral
Requirement
Na /Cl
2-3
K
2-3
Mg
0.125-0.2
(meq/kg/d)
Ca
60
(meq/d)
PO4
60
(meq/d)
(meq/kg/d)
(meq/kg/d)
Vitamin Requirement/ Trace Element Requirement
According to RDA
Key Vitamins and Minerals
Vitamin A
Wound healing and tissue repair
Vitamin C
Collagen synthesis, wound healing
B Vitamins
Metabolism, carbohydrate utilization
Pyridoxine
Essential for protein synthesis
Zinc
Wound healing, immune function, protein synthesis
Vitamin E
Antioxidant
Folic Acid,
Iron, B12
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 Nutrition Support
 Unstable hemodynamics
 Severe fluid, electrolyte, acid- base disorder
(esp. PN)
 Uncontrolled infection
Enteral Nutrition: Contraindication
 Unstable condition: hemodynamics
 Intestinal obstruction
 Massive GI bleeding
 Intestinal ischemia
 Severe malabsorption, inflammation, severe
ileus
Contraindication of Nutrition Support
Unstable hemodynamics
 Severe fluid imbalance: overload or dehydration
 Severe electrolyte, acid- base disorder
 Uncontrolled sepsis
EN
PN
 Gut obstruction
 End stage malignancy:
EOL determined
 Massive GI bleeding
 Intestinal ischemia
 Severe malabsorption,
inflammation

Nutritional Support For A Patient At Risk Of
Malnourishment
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 ผูป
้ ่ วยที่ GI function ผิดปกติบางส่วน
 ผูป
้ ่ วยที่ GI tract failure
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: CRI
 Metabolic derangement/ re-feeding
syndrome
 Fluid/ electrolyte/ acid-base imbalance
 Overfeeding syndrome
 Liver complication
Infectious Complication
‘Catheter related infection’ (CRI)
 Tunnel site infection
 Hub contamination
 Infusate contamination
 Seeding 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+, PO43- 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 PO43- 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 patients
 Start 10 kcal/kg/d, gradually  within a week
 Before/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 day
 monitor and supplement oral, enteral, or intravenous K,
PO43- and Mg intake.



K+
PO43Mg2+
2-4 mmol/kg/day
0.3-0.6 mmol/kg/d
0.2 mmol/kg/d IV or 0.4 mmol/kg/d oral
Metabolic Complication to Overfeeding
 Hyperglycemia
 Hypertriglyceridemia
 Hypercapnia
 Fatty liver
 Hypophosphatemia,
hypomagnesemia, hypokalemia
Barton RG. Nutr Clin Pract 1994;9:127-139
Hepatobiliary Complication
Adults
Steatosis
 Steatohepatitis
 Cholestasis
 Biliary sludge
 Cholelithiasis

 Acalculous cholecystitis
 Fibrosis
 Micronodular 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