🍔Gastro🍔 - Malnutrition & Nutrition Intervention Flashcards
What is the definition of malnutrition?
A state in which deficiency, excess or imbalance, of energy, protein or other nutrients, results in a measurable adverse effect on body composition, function and clinical outcome
What are the causes of malnutrition in hospitals?
Reduced intake
Maldigestion/malabsorption
Altered metabolism
What is meant by altered metabolism?
What are the reasons for reduced food intake in hospital?
Contraindicated
Disease related anorexia
Taste changes
Nil by mouth
Food options
Depression
Inactivity
Oral health
Fatigue
What are the causes of maldigestion/malabsorption?
Function
Length - reduced GI tract length
Losses - fluid, blood, through urine etc…
Drug-nutrient interactions
Give some context as to the impact of malnutrition
Surgery for perforated duodenal ulcer.
Postoperative mortality 10 x greater in those who had lost 20% bodyweight preoperatively, compared with those who had lost less
Malnutrition:
Direct cause 77 hospital deaths
Contributory factor 436 hospital deaths
What is the impact of malnutrition in a hospital setting?
Physical and functional decline
Poorer clinical outcomes
What are the indications that someone is malnourished?
BMI < 18.5 kg/m2
or
Unintentional weight loss >10 % past 3 - 6 / 12
or
BMI < 20 kg/m2 + unintentional weight loss > 5 % past 3 – 6 / 12
What are the indications that someone is at risk of malnutrition?
Have eaten little or nothing for > 5 days and / or are likely to eat little or nothing for the next 5 days or longer
or
Have a poor absorptive capacity, and / or have high nutrient losses and/or have increased nutritional needs from causes such as catabolism
What are the oral nutritional support options?
Fortification of meals and snacks
Altered meal patterns
Practical support
Oral nutritional supplements (ONS)
Tailored dietary counselling
What is artificial nutrition support?
Provision of enteral or parenteral nutrients to treat or prevent malnutrition
What is the superior form of artificial nutrition support?
Enteral nutrition (EN) is superior to parenteral nutrition (PN)
What is the overall aim of parenteral nutrition?
Where parenteral nutrition is used, the aim is to return to enteral → oral feeding as soon as (or where) clinically possible
What should be used if gastric feeding is possible?
Naso-gastric tube (NGT)
What should be used if gastric feeding is not possible?
Naso-duodenal tube (NDT)
or
Naso-jejunal tube (NJT)
When might gastric feeding not be possible?
Gastric outlet obstruction
Gastroparesis
Upper GI strictures or fistulas
High aspiration risk
What are the mechanical complications associated with enteral feeding?
Misplacement, blockage, buried bumper
What are the metabolic complications associated with enteral feeding?
Hyperglycaemia, deranged electrolytes
What are the GI complications associated with enteral feeding?
Aspiration, nasopharyngeal pain, laryngeal ulceration, vomiting, diarrhoea
What is an iatrogenic complication of enteral feeding?
Misplaced NGT
What is parenteral nutrition?
The delivery of nutrients, electrolytes and fluid directly into venous blood
What are the indications for parenteral nutrition support?
inadequate or unsafe oral and/or enteral nutritional intake
or
A non-functioning, inaccessible or perforated gastrointestinal tract
Where is parenteral nutrition support accessed?
Central venous catheter (CVC): tip at superior vena cava and right atrium
What are the mechanical complications with parenteral nutrition support?
Pneumo/haemothorax
Thrombosis/thrombus
Cardiac Arrythmias
Catheter related infections
What are the metabolic complications with parenteral nutrition support?
Deranged electrolytes
Hyperglycaemia
Abnormal liver enzymes
Oedema
Hypertriglyceridaemia
Outline albumin and its significance in acute inflammation
Albumin synthesised in the liver.
Hypoalbuminaemia = poor prognosis.
A negative acute phase protein = ↓ plasma albumin when ↑ inflammation
What is meant by a “negative acute phase protein?
A protein whose levels decrease during periods of inflammation, infection, or trauma
During inflammation, the liver shifts its protein production to prioritize acute phase reactants (positive acute phase proteins like CRP, fibrinogen, and haptoglobin).
Albumin production decreases because:
The liver reallocates resources to synthesizing proteins involved in the immune response
What causes the acute decrease of albumin synthesis?
Inflammatory stimulus → activation of monocytes & macrophages → release cytokines
Cytokines act on liver to stimulate synthesis of some proteins e.g. c-reactive protein, whilst downregulating production of others e.g. albumin
Is albumin a valid marker of malnutrition?
No
Albumin synthesis decrease is a response to inflammation - not a valid marker of nutrition status
What is refeeding syndrome (RFS)?
A group of biochemical shifts & clinical symptoms that can occur in the malnourished or starved individual on the reintroduction of oral, enteral or parenteral nutrition
What are the consequences of refeeding syndrome?
Arrhythmia, tachycardia, CHF → Cardiac arrest, sudden death
Respiratory depression
Encephalopathy, coma, seizures, rhabdomyolysis
Wernicke’s encephalopathy
Outline the pathogenesis of RFS
Prolonged fasting leads to depletion of electrolytes
The body shifts to fat and protein metabolism
Sudden carbohydrate intake causes a surge in insulin release - stimulates a huge intracellular shift of electrolytes
Leads to huge electrolyte disturbances
What are the electrolyte imbalances seen in RFS?
Hypophosphataemia → Weakness, confusion, seizures, heart failure
Hypokalaemia → Arrhythmias, muscle weakness, ileus
Hypomagnesaemia → Neuromuscular irritability, tetany, arrhythmias
How does RFS lead to Wernicke’s encephalopathy?
Thiamine deficiency → Increased glucose metabolism without sufficient thiamine can precipitate Wernicke’s encephalopathy
Who is at risk of developing RFS?
Very little/no food intake for >5 days
Who is at high risk of developing RFS?
1+ of the following:
BMI<16
Unintentional weight loss >15%
Very little/no nutrition >10days
Low K+, Mg2+, PO4 prior to feeding
2+ of the following:
BMI<18.5
Unintentional weight loss >10%
Very little/no nutrition >5days
PMHx alcohol abuse or drugs (insulin, chemo, antacids, diuretics)
Who is at extremely high risk of developing RFS?
BMI <14
Negligible intake >15days
What is the first step of management of RFS?
Administer thiamine 30 minutes before and for the first 10 days of feeding
How should patients be monitored to avoid development of RFS?
Correct and monitor electrolytes daily
Start 10-20kcal/kg
CHO 40-50% of energy
Micronutrients from onset of feeding
Monitor fluid shifts and minimise risk of fluid and Na+ overload
How is RFS treated?
Electrolyte Monitoring and Replacement
Phosphate:
Oral or IV phosphate supplements if levels drop <0.3 mmol/L.
Potassium:
Replace if <3.0 mmol/L to prevent arrhythmias.
Magnesium:
IV magnesium sulfate if <0.5 mmol/L or symptomatic#
most important is prevention
