Nutrition Flashcards
NUtritional assessment
Common in ICU
pre-existing or as result of illness
Hx - wt loss, changes in appetite, liver disease, DM, medicaitons
Exam -
- assess metabolic activity (temp, HR, BP, RR, LOC)
- hydration status
- muscle wasting
- signs of micro-nutrient deficiency
Ix -
- bedside - urine, ABG
- labs - electrolytes, albumin (chronic nutritional state), pre-albumin (acute nutritional state), transferrnin, coags, fat soluble vitamin levesl (DEKA), water soluble
- Special tests - anthropometric measurements (arm thickness, skin folds), indirect calorimetry, nitrogen balance
water soluble vitamins
thiamine zinc selenium B12 folate
Methods to assess resting energy expenditure
Predictive equations
- typically use gender, height, age and wt
- most simple - 25cal/kg/day
Reverse fick method
- uses PAC to determine oxygen consumption
- does not incorportate metabolic requirement of lungs
Indirect calorimetry
- O2 uptake and CO2 production are monitored using a specilised module on ventilator
- very expensive
Daily requirements
energy - 25kcal/kg Macronutrients - carbs 4g/kg - protein 1.5g/kg - fat 1g/kg
Water and electrlytes -
- water 30ml/kg
- Na 2mmol/kg
- K 1mmol/kg
- Ca/Mg/PO4 all 0.1mmol/kg
Vitamins
- water soluble
- fat soluble
- trace elements
Strategies to achieve nutritional goals in ICU
protocalised feeding minimizing interruptions use of prokinetics upright posture returning gasric residuals under 250mls use of post pyloric feeding supplementing inqdequate or poorly tolerated EN with some TPN
HOw to start TPN
assess daily metabolic requirements
establish indications for TPN
establish central access
supply macronutrients
- carb:fats 70:30 and additional protein 1.5-2g/kg/day
ensure regular contribution of trace elements, vitamins and micronutrients
ensure regular monitoring - BSL, U&E, Ca/Po4, LFTs
ensure good thromboprophylaxis
Ensure good monitoring of central line site
permissive underfeeding
provision of a reduced non-protein caloric target (around 40-60% of calculated total) hypothesing that lower non-protein calorie intake may be beneficial.
May be used as sole nutritional strategy.
Advantages of permissive underfeeding: - Avoids the disadvantages of full-volume enteral nutrition: Gastric distension Aspiration Diarrhoea/constipation Hyperglycaemia Excess insulin use Exposure to toxic prokinetics Need for NJ tubes, etc - Cheaper - Does not suppress the (possibly) constructive autophagy which may be required to recover from critical illness
trophic feeding
a small volume of balanced enteral nutrition insufficient for the patient’s nutritional needs but producing some positive gastrointestinal or systemic benefit
Advantages of trophic feeding:
- Improved feed tolerance (reduced gastric residual volumes)
- Maintenance of gastric and intestinal mucosal integrity
- Prevention of bacterial overgrowth and bacterial translocation
- Prevention of excessive protein catabolism (prevention of starvation)
- Evidence for trophic feeding:
EDEN trial (Rice et al, 2012)
5 days of <25% of their estimated requirements
No difference in any primary outcomes
Again, can be viewed as a demonstration of safety
Limitation: many patients were underfed with protein (0.6g/kg/day)
Pathophysiology of refeeding
With starvation, less carbohydrate becomes available
As the result of this, there is a switch to fatty acid and ketone based metabolism
This switch is in part mediated by a decrease in the insulin levels
Low oral intake also means decreased phosphate intake
However, there is a daily requirement for phosphate (for ATP synthesis)
This phosphate is not replenished by the poor oral intake
As a result, intracellular phosphate is depleted
Homeostatic mechanisms maintain a normal serum phosphate in spite of this
As carbohydrate is reintroduced, the secretion of insulin results in a large-scale uptake of phosphate into the tissues
As the intracellular phosphate is depeleted, there is nowhere to mobilise more phosphate from, and hypophosphataemia results.
Metabolic changes in starvation
Overall an adaptive hypometabolism whereby fat is used as the primary energy fuel and protein is relatively spared
Characterised by a switch from carbohydrate metabolism to fat metabolism, in the context of a hypometabolic state, with minimised catabolism.
Initially, stores of carbohydrate precursors (eg. glycogen) are depleted
Then, (in the first 24-48hrs) there is increased gluconeogenesis from amino acids and glycerol
Subsequently, ketogenesis takes over, and much of the body metabolic needs are met by ketone bodies and free fatty acids. This is the consequence of decreasing insulin levels, and relatively increased influence from catecholamines and cortisol.
Over prolonged starvation, protein catabolism begins, resulting in degradation of structurally important proteins, and organ system dysfunction
Metabolic changes seen in stressed state
Characterised by a mobilisation of available body fuels, and a hypermetabolic hypercatabolic state.
Under the influence of cortisol, cytokines and catecholamines the rates of protein catabolism, lipolysis glycogenolysis and gluconeogenesis are increased.
There is typically no ketosis, as there is a reasonably normal insulin response to the increase in circulating metabolic substrate. However, the insulin response is not completely coupled to the BSL, and hyperglycaemia results.
Hyperglycaemia, uraemia and hypoalbuminaemia may result.
List the consequences of underfeeding in the critically ill.
Impaired immune function Increased incidence of infection Weakness and fatigue Decreased ventilatory drive Prolonged mechanical ventilation Poor wound healing Muscle breakdown Depression and apathy Prolonged ICU and hospital stay
typical biochemical features of refeeding:
Hypophosphatemia
Hypomagnesemia
Hypokalemia
Less well known -
Thiamine depletion
Depletion of micronutrients (eg. selenium, copper and zinc)
Hypernatremia (with protein-dominant nutritional replacement)
Hyponatremia (with carbohydrate-dominant nutritional replacement)
major metabolic abnormalities seen in obesity
Insulin resistance and impaired glucose tolerance
Increased fatty acid mobilization and hyperlipidemia
Accelerated protein degradation
The proinflammatory state of obesity
The endocrine derangements due to an excess of fatty tissue
The increased resting metabolic rate of obesity
“Metabolic X syndrome” may exist: insulin resistance, hyperinsulinemia, hyperglycaemia, coronary artery disease, hypertension, and hyperlipidemia.
Define Cachexia
“A syndrome characterised by a loss of body weight and muscle tissue, which occurs in absence of starvation and is not associated with an adaptive decrease in catabolism.”
Predisposing factors for cachexia
Mechanisms not clearly understood
Exacerbating factors:
Catecholamine excess Corticosteroid use Immobility Hyperthyroidism Malabsorption Malnutrition Malignancy
Consequences of cachexia
Increased risk of death
Prolonged time on ventilator
Increased ICU and hospital length of stay
Increased risk of nosocomial infections
Poor wound healing
Malnutrition and nutritional deficiency syndromes
Cause and mechanism of cachexia
Causes and mechanisms:
Unclear mechanism; possible combination of the following:
Decreased circulating anabolic hormones (eg. androgens)
Increased circulating catabolic cytokines and hormones (eg. cortisol and catecholamines)
Pathologically increased nutrient demand by tissues:
Aggressively multiplying malignant tissue
Increased workload in pathological states, eg. respiratory effort in COPD
Pathologically decreased nutrient supply to tissues:
Chronically decreased cardiac output in cardiac cachexia
Chronic hypoxia in respiratory failure
metabolic and clinical problems associated with overfeeding
Hepatic steatosis
Hyperglycemia
Hyperlipidemia
Hypercarbia
Hyperosmolarity and hypertonic dehydration (in patients fed excess nitrogen who have impaired urine concentrating ability)
Azotemia (due to excess nitrogen intake)
Recommendations for immunonutrtion
The ASPEN guidelines make the following statements:
No evidence to recommend arginine
No evidence to recommend fish oil or antioxidants
No evidence to recommend ornithine ketoglutarate
No evidence to recommend zink supplements
Some evidence to support the use of glutamine (this recommendation has been downgraded since 2009)
Some evidence to support selenium
Lipid emulsion in TPN
one requires about 0.7-1.5g/kg/day of lipid emulsion via TPN
Side effects -
reticuloendothelial dysfunction, hypoxia, thrombophilia and hepatosteatosis
However - they are essential nutrients
Harris benedict equation - what it is, what it uses
Calculates basal metabolic rate
Weigh
Height
Age
Can be multiples by various factors depending on estimates of increased energy demand (eg heavy exercise x2)
Irten jones formula
Calculates energy expenditure in ventilated burns patients.
Different equations for ventilated vs spont breathing patients
Uses- Age Wt Gender And additional multipliers if burns and/or trauma present
Fusco formula
Estimates Energy requirements for obese patients
Frankenfeild fomula
Estimates energy requirements for patients with sepsis and trauma
Uses minute volume, Hb and a mulitiper for sepsis
What information can Indirect calorimetry provide
Resting energy expenditure
Respiratory quotient
Limitations of indirect calorimetry
Physical limitations
- innacurate gas concentration measurements
- innacurate volume measurements
Practical limitations
- it is a measure of metabolic fuel consumption, but we are actually interested in demand
- no proven clinical benefits
RQ for fats, carbs and protein
Fat 0.7
Carb 0.8
Protein 1
Main innacuracy of reverse Fock method
Underestimates total body energy expenditure as it neglects oxygen consumption from the lungs.
Underestimates by approx 88kcal/day
Much higher if energy expenditure from lung is massively increased eg ARDS
