Activation of the 'Stress Response' or fight or flight response

- A series of major hormonal and mediator induced altercations of metabolism aimed at rapid 
  mobilization of ENERGY when the host is threatened or ‘injured.’

- A genetically activated process never intended to persist long term as in a burn.

- Response overrides all the normal adaptive or protective responses to maintain different 
   energy while preserving the metabolic machinery (lean body mass)

What are the Major Metabolic Effects?

What Are The Major Metabolic Effects?

Click to Enlarge the Diagram

Having reviewed each of the basic component of the metabolic response to burn, we can put the process together in a schema which describes the entire process. The response to burn injury, in the absence of nutritional support, is described. No adaptive responses to preserve energy or lean mass are present.

A marked persistent increase in metyabolic rate (35-40 kcal/kg/day) is evident beginning several days after injury. The increased demands are in part related to the increase in body heat (a part of the stress response) and also the marked loss of heat from the burn wound until it is occluded.

As opposed to starvation, only a modest amount of fat is used for fuel despite the energy demand. In fact, the majority of fat which is converted to fatty acids for potential fuel is simply recycled back to fat, due to the hormone environment.

The energy is produced mainly by glucose through liver gluconeogenesis, using amino acids from the lean mass compartment. Amino acids are mainly converted with alanine which then is transformed into pyruvate then glucose. The gluconeogenesis exceeds cell needs thus amino acids are wasted. The process is driven by the glucose producing properties of the stress hormones.

Another amino acid from lean mass, glutamine is used by many organs plus the wound and soon becomes depleted as do antioxidants and micronutrients in the face of increased use and no replacement via nutrition.

The use of amino acids, for fuel, induces by the increased catabolic hormonal and mediator response leads to a rapid erosion of muscle and visceral protein and the resulting complications of lean mass loss. Endogenous anabolic activity is also decreased.

Click to Enlarge the Schema

Having described the fundamental problems, we will describe the specific metabolic factors responsible for the stress response. The hormonal response to injury is the most important component. There is a marked increase in the levels of the stress hormones: catechols, cortisol, and glucagon. These anti insulin hormones, especially glucagon drive the severe gluconeogenesis response leading to excess glucose production even with glucose replacement, at the expense of amino acids. The modest increase in insulin cannot neutralize this response. The decrease in growth hormone (anabolism) and increase in cortisol (catabolism) leads to a net catabolic stimulus.

Inflammatory mediators release post burn increase body temperature resulting in energy demands, which is a major problem with a burn as heat loss from the wound is increased. Direct cell damage from oxidants leads to tissue damage especially since antioxidants are decreased.