The document discusses malnutrition and its effects. It states that malnutrition is common in 30-60% of surgical patients, but often goes unrecognized. Patients who are malnourished have higher risks of complications and death. Both long-term and short-term malnutrition impact patient recovery. The aim of nutritional support is to identify at-risk patients and ensure their nutritional needs are met. The physiology section details the body's metabolic responses to starvation, including reliance on liver glycogen and gluconeogenesis from protein after 24 hours without food. It describes the increased breakdown of fat stores and production of ketones to reduce reliance on muscle protein. Starvation leads to adaptive reductions in energy expenditure. There remains a daily glucose requirement

1. Dr ismaaciil baarri

2. Nutrition and fluid therapy

3. INTRODUCTION
 Malnutrition is common. It occurs in about
30 per cent of surgical patients with
gastrointestinal disease and in up to 60 per
cent of those in whom hospital stay has
been prolonged because of postoperative
complications. It is frequently unrecognised
and consequently patients often do not
receive appropriate support.

4. There is a substantial body of
evidence to show that patients who
suffer starvation or have signs of
malnutrition have a higher risk of
complications and an increased
risk of death in comparison with
patients who have adequate
nutritional reserves

5. Long-standing protein–calorie
malnutrition is easy to recognise then
Short-term undernutrition, although
less easily recognised, frequently
occurs in association with critical
illness, major trauma, burns or
surgery, and also impacts on patient
recovery.

6. The aim of nutritional support is to
identify those patients at risk of
malnutrition and to ensure that
their nutritional requirements are
met by the most appropriate route
and in a way that minimises
complications.

7. PHYSIOLOGY
Metabolic response to starvation
After a short fast lasting 12 hours or
less, most food from the last meal
will have been absorbed. Plasma
insulin levels fall and glucagon
levels rise, which facilitates the
conversion of 200 g of liver
glycogen into glucose.

8. The liver, therefore, becomes an
organ of glucose production under
fasting conditions. Many organs,
including brain tissue, red and
white blood cells and the renal
medulla, can initially utilise only
glucose for their metabolic needs

9.  Additional stores of glycogen exist in
muscle (500 g), but these cannot be
utilised directly. Muscle glycogen is
broken down (glycogenolysis) and
converted to lactate, which is then
exported to the liver where it is
converted to glucose (Cori cycle).

10. With increasing duration of fasting
(>24 hours), glycogen stores are
depleted and glucose production from
non-carbohydrate precursors
(gluconeogenesis) takes place,
predominantly in the liver. Most of this
glucose is derived from the breakdown
of amino acids,

11. particularly glutamine and alanine as a
result of catabolism of skeletal muscle
(up to 75 g per day). This protein
catabolism in simple starvation is
readily reversed with the provision of
exogenous glucose. With more
prolonged fasting there is an
increased reliance on fat oxidation to
meet energy requirements.

12. Increased breakdown of fat stores
occurs, providing glycerol, which can
be converted to glucose, and fatty acids,
which can be used as a tissue fuel by
almost all of the body’s tissues. Hepatic
production of ketones from fatty acids
is facilitated by low insulin levels and,
after 48–72 hours of fasting,

13. the central nervous system may
adapt to using ketone bodies as
their primary fuel source. This
conversion to a ‘fat fuel economy’
reduces the need for muscle
breakdown by up to 55 g per day.

14. Another important adaptive response
to starvation is a significant reduction
in the resting energy expenditure,
possibly mediated by a decline in the
conversion of inactive thyroxine (T4)
to active tri-iodothyronine (T3 )

15. Despite these adaptive responses,
there remains an obligatory glucose
requirement of about 200 g per day,
even under conditions of prolonged
fasting

16. Metabolic response to starvation
■ Low plasma insulin
■ High plasma glucagon
■ Hepatic glycogenolysis
■ Protein catabolism
■ Hepatic gluconeogenesis

17. ■ Lipolysis: mobilisation of fat stores
(increased fat oxidation)– overall
decrease in protein and carbohydrate
oxidation
■ Adaptive ketogenesis
■ Reduction in resting energy
expenditure (from approximately 25–30
kcal/kg per day to 15–20 kcal/kg per day

18. Metabolic response to trauma and
sepsis
■ Increased counter-regulatory
hormones: adrenaline, noradrenaline,
cortisol, glucagon and growth hormone
■ Increased energy requirements (up to
40 kcal/kg per day)
■ Increased nitrogen requirements
■ Insulin resistance and glucose
intolerance

19. ■ Preferential oxidation of lipids
■ Increased gluconeogenesis and
protein catabolism
■ Loss of adaptive ketogenesis
■ Fluid retention with associated
hypoalbuminaemia

20. Any question
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