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June 20, 2014

Adequate protein intake for recovery from injury and schock

by Helene van den Berg

Nutritional status is extremely important in wound healing. Maintenance of anabolism and controlling catabolism is critical to optimize the healing process. Increased protein intake is required to keep up with catabolic losses and allow wound healing anabolic activity. Protein as a micronutrient, is inappropriately used for fuel after injury, so intake needs to be increased to allow for protein synthesis. Supplementation with GLUTAMINE improves wound healing and immunity and decrease trauma and burn-induced mortality.

After injuries, shock, trauma, burns, pancreatitis and sepsis, the resulting hypermetabolism and catabolism can cause malnutrition. The goal of clinical nutrition is to modify the stress response below the extreme, positively influence recovery and give optimum nutrition support with amino acids. After a variety of injuries mentioned above, patients develop a systemic inflammatory response, which is beneficial if it resolves as the patient recovers. If this inflammatory response is exaggerated or perpetuated, severe disturbances in protein metabolism may arise. The resulting hypermetabolism and catabolism can cause acute protein malnutrition, with impairment in immune function and multiple organ dysfunction, like acute renal failure.

The HYPERMETABOLISM of the stressed patient is due to increases in muscle proteolysis (breakdown of muscle), enhanced glucose production (hepatic ureagenesis) and increased usage of fat. The whole body of injured and septic patients show increased protein CATABOLISM with a slight increase in protein synthesis, leading to a negative nitrogen balance. Patients with severe burns, has an 8 times higher negative nitrogen balance and in those with severe injuries it is 6 times higher than normal.

Infusion with an adequate amount of amino acids, partially improves the synthesis rate, but the extent of protein catabolism is insensitive to intravenous nutrition.

The metabolic rate and nitrogen are related to the extent of injury. The infusion of a combination of cortisol, epinephrine and glucagon, could increase the glycemia (seen in stress conditions), thermogenesis and N loss.

When starvation accompanies injury and critical illness, protein sparing and reduction of energy expenditure, do not occur. Instead lean body mass is catabolised as an energy source, to meet the increased energy needs, resulting in loss of body defenses, increase in morbidity and mortality. In critically ill patients, up to 20% of body proteins are lost within 3 weeks; 70% of this protein loss is from skeletal muscle.

Estimations of nitrogen loss can be obtained from urine urea nitrogen (UUN) and approximate nonurinary nitrogen losses.

The patient whose problem is primarily partial starvation, can be put into a positive nitrogen balance with good nutritional support. The strongly catabolic patient can only achieve a positive nitrogen balance by nutritional intervention, until the peak of the catabolic drive has passed!. Provision of a protein intake of up to 1.5 g/kg/day can improve the nitrogen balance – going above that level, only increase the rate of protein synthesis and breakdown, without improving the nitrogen balance.

With critical illness or endocrine diseases (lean tissue wasting over long periods), muscle tissue and whole-body protein turnover, are depressed. Therefore the aim should be to increase muscle protein synthesis, rather than decrease muscle protein breakdown.

One of the most typical features of the response to trauma and infection is, a uniform reduction of 50% of free muscular glutamine associated with negative nitrogen balance. During catabolic stress, peripheral glutamine stores are rapidly diminished and shunted toward visceral organs as a fuel source. Therefore glutamine is considered essential for catabolic stress. Glutamine should be added to a standard enteral formula in burn and trauma ICU patients.

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