Theoretical Nutrition and Patient Assessment

T R Wilson

WHY IS NUTRITION IMPORTANT?

Prevalence Malnutrition in Hospital

• 30% Overtly malnourished• 8% Severely malnourished

• Screen all hospital admissions– Weigh (BMI) – Ask if they have lost weight– Ask when they last ate properly

MUST SCORING

Malnutrition and Surgical Complications

Morbidity Mortality0

10

20

30

40

50

60

70

80

Well NoursihedMalnourished

Perc

enta

ge P

atien

ts

ASSESSING PATIENTS

Who is at risk nutritional problems?

• Hospital patients (1/3)• Prolonged ITU stay• Prolonged fasting• Cancer patients• Crohn's Disease• Post (and Pre) bariatric surgery• Elderly• Chronic alcoholic abuse• Anorexia Nervosa

MUST Score

• Screening tool• 3 elements– BMI

• >20 = 0 18.5-20 = 1 <18.5 = 2

– % Weight loss last 3-6 months• <5% = 0 5-10% = 1 >10% = 2

– Acute disease effect• Acute illness, no nutritional intake ≥ 5 Days = 2

• Score from 0 to 6• 2 or more is high risk → dietician input

Assessment Nutritional Status

• Where has patient come from?– Long term history of nutritional problem– Risk factors– History of weight loss– History of inadequate intake

• Where is patient currently?– On going / current pathologies (cancer?)– Sepsis– Hydration/electrolyte status

• What you can do? – Where are you going?– What is likely course of their pathology– What is their likely nutritional intake in next 48 hours / week / longer?

Meeting Nutritional NeedsAssessment Provision Monitoring

Normally Nourished Ward Staff Catering Admission weightWeekly Weight

Under Nourished(BMI < 20)

(Weight loss >10%)

Ward StaffDieticians

Catering+/- Sip Feeds

Admission weightWeekly WeightIntake RecordsBiochemistry

Partial Intestinal Failure

(Functioning Gut)

Ward StaffDieticians+/- NST

Enteral Feed+/- Sip Feeds+/- CateringVia NG/NJ/PEG

Admission weightWeekly WeightIntake RecordsBiochemistryClinical (≥2x/week)

Intestinal Failure(Gut not

functioning)

NST Parenteral Nutrition+/- Enteral FeedVia CVP line

Daily Assessment(Clinical, fluid balance, biochem)Weight 2x/week

PATHOPHYSIOLOGY(WHAT GOES WRONG AND HOW TO FIX IT SAFELY)

Reductive Adaptation of Malnutrition

Reduced Intake

Reduced Mass Reduced Work

Altered Metabolism and Physiology

Altered Body Composition

Loss of Reserve

Brittle Metabolism

Loss Homeostasis

InfectionTraumaSmall bowel overgrowth

Excess Energy/ProteinAbnormal LossesSpecific Deficiency

Basal Metabolic Demand

• Mechanical Work– Cardiac Output/Ventilation/Movement

• Turnover Substances– Amino acids / Protein– Glucose / Glycogen– Fatty acids / TAG

• Transport across membranes– Substrates / Products– Electrolytes (Na/K pumps)

10%

20%

70%(67%)

Electrolyte Shifts• Down regulation of Na/K pumps• Leaking of K, Mg, PO4 out of cells– → High serum K/Mg/PO4– → Renal excretion – → Decreased body levels

• Leaking of Na into cells– → Low serum Na– → Renal conservation– → Increased body levels Na

• Fluid follows Na– → General fluid retention → Oedema– → Fluid shift into cells

Nutritional Oedema

• Impaired membrane function– Down regulation Na/K pumps– Free radical damage

• Salt and water retention– Impaired renal function– Potassium/phosphate depletion– Acid-base imbalance

• Hypoalbuminaemia– Decreased synthesis (minor long term)– Third space loss (SIRS, Sepsis, Membrane damage)

Problems of Na, Cl and Fluid excess• Left ventricular failure• Oedema• Skin breakdown• Hyperchloraemic acidosis• Ileus• Anastomotic and wound dehiscence• ↑ PN requirement• ↑ Length of Stay• ↑ Death

Loss Homeostasis

• Increased Toxins / Free radicals– Infection / Trauma– Iron (from RBC breakdown)– Small bowel overgrowth

• Reduced protection– Vitamins: B1, B2, B6, C, E, niacin, β carotene– Elements: Cu, Se, Zn, Mn– Other: Glutamine, Glycine, Cystine

• Electrolyte and fluid shifts• Decreased body stores – e.g. glycogen

Starvation

AA

Micronutrients

Enzyme

Co Enzyme

(e.g. Thiamine, Riboflavin, Pyridine, Iron, Zinc, Copper)Catabolism

AA

PN

PROTEIN

Refeeding

AA AA

Sepsis and malnutrition

• Malnourished → immunosuppression • May not mount typical immune response– Normal bloods– Hypothermia rather than temperature

• Refeeding / over feeding → further immunosuppression

• BEWARE THE DEADLY TRIAD– Low BMI– Hypoglycaemia– Hypothermia

Problems of over feeding / over enthusiastic early nutritional support

• Excess Nitrogen delivery– May produce toxic amino-acids– Drive ammonia and urea production– High renal solute load → contribute to Na retention

• Metabolic instability• Insulin resistance and hyperglycaemia• Liver dysfunction/diversion• Immunosuppression• Re-feeding syndrome

Refeeding Syndrome (definition)

• Potentially lethal• Occurs in malnourished patients undergoing

re-feeding• Can occur with any route of feeding • Results in severe electrolyte and fluid shifts• Associated with metabolic abnormalities• (Nearly 1% all hospital patients)

Refeeding Pathophysiology

Starvation• Protein catabolism• Gluconeogensis• ↑ Insulin resistance• ↓ soluble B vit levels• Down regulation cellular

pumps– Extracellular leakage

K/PO4/Mg– Excretion of K/PO4/Mg– Intracellular Na retention– Renal Na conservation

Refeeding• On going aa metabolism• ↑glucose metabolism• ↑Insulin• ↑ Thiamine utilisation• Reactivation cellular

pumps– Intracellular uptake

Na/PO4/Mg– Low serum levels

Specific refeeding problems

• Electrolyte disturbance– Weakness, seizures, arrhythmias, tetany,

paraesthesia• Heart failure / pulmonary oedema• Infection (CRP and WCC may not rise)• Hyper/hypoglycaemia– Risk of brain damage / Wernicke's

Avoiding all refeeding syndromes

• Start at appropriate low rate– 5 Kcal/Kg/Day in extreme cases– 10 Kcal/Kg/Day in severe cases– Half requirements 20/Day for less severe re-feeding

risk• Gradually increase over 4-7 days• Replace electrolytes aggressively• Vitamin supplementation (Thiamine)• Monitor observations