Acute malnutrition

Metabolic response to starvation:

After 12 hours
- Insulin levels fall and glucagon rises
- Liver glycogen converted to glucose
- Muscle glycogen broken down into lactate, which is converted to glucose in the liver
After 24 hours
- De novo glucose production from non-carbohydrate precursors, predominately in the liver (breakdown of amino acids as a result of catabolism of skeletal muscle, up to 75g per day)
- Protein catabolism is readily reversed with administration of glucose
More prolonged fasting
- Reliance on fat oxidation to meet energy requirements (glycerol converted to glucose)
- Hepatic production of ketones from fatty acids, which is facilitated by low insulin levels
- After 48-72 hours, CNS may adapt to using ketone bodies as primary fuel source (keto-adaptation). This does not occur in sepsis and trauma, so protein is catabolised to provide gluconeogenic precursors.
- Once the body switches to using 'fat economy', the protein catabolism is reduced significantly
- Resting energy expenditure will also decrease, maybe mediated by a decline in conversion of T4 to T3
- Reduction in resting energy expenditure from about 25-30kcal/kg/day to 15-20kcal/kg/day

Development of a hypermetabolic state and increased protein breakdown
Increased counter-regulatory hormones (adrenaline, norad, cortisol, glucagon, growth hormone)
- Within a few minutes of beginning an operation, these hormones start rising
Increased energy requirement
Increased nitrogen requirement
Insulin resistance and glucose tolerance
Preferential oxidation of lipids
Increased gluconeogenesis and protein catabolism
Loss of adaptive ketogenesis
- Contrast this with simple starvation
Fluid retention with associated hypoalbuminaemia
No evidence that provision of high-energy intake would actually be helpful in this setting