Pathophysiology (burns).

What happens to K+ during the emergent phase?

A K+ shift develops initially because injured cells and hemolyzed RBCs release K+ into the circulation.

Why is a burn patient at a greater risk for infection?

The inflammatory cytokine cascade, triggered by tissue damage, impairs the function of lymphocytes, monocytes, and neutrophils.

What is the normal insensible loss?

The normal insensible loss of 30 to 50 mL/hr is increased in the severely burned patient.

What does a patient with a burn injury generally have an elevated Hct?

An elevated hematocrit is commonly caused by hemo-concentration resulting from fluid loss. After fluid balance has been restored, dilution causes the hematocrit levels to drop.

As the capillary walls become more permeable in a burn patient what happens?

As permeability increases that causes water, sodium, and plasma proteins (especially albumin) to move into the interstitial spaces and other surrounding tissue.

Inflammation and Healing

Burn injury to tissues and vessels causes coagulation necrosis. Neutrophils and monocytes accumulate at the site of injury.

Toward the end of the emergent phase, what happens to the capillary membrane permeability?

Capillary membrane permeability is restored if fluid replacement is adequate. Fluid loss and edema formation end.

What are clinical signs of hypovolemic shock?

Decreased (BP) and increased HR.

How are (WBCs) affected with a burn injury?

Defects occur in the function of white blood cells (WBCs).

What are examples of third spacing in a burn injury?

Exudate and blister formation, as well as edema in non-burned areas.

For the healing process when do the fibroblasts and newly formed collagen fibrils appear?

Fibroblasts and newly formed collagen fibrils appear and begin wound repair within the first 6 to 12 hours after injury.

What is second spacing?

Fluid accumulation in the interstitium.

What is third spacing?

Fluid also moves to areas that normally have minimal to no fluid, a phenomenon termed third spacing.

What is the greatest initial threat to a patient with a major burn?

Hypovolemic shock (Fig. 25-5).

What are other sources of fluid loss?

Insensible losses by evaporation from large, denuded body surfaces and the respiratory system.

Toward the end of the emergent phase what else happens?

Interstitial fluid gradually returns to the vascular space (Fig. 25-7). Diuresis occurs, and the urine has a low specific gravity.

If hypovolemic shock is not corrected what may happen?

Irreversible shock and death may result.

The circulatory system is also affected by what in a burn patient?

It is affected by the hemolysis of RBCs from circulating factors (ex: oxygen free radicals) released at the time of the burn, as well as by the direct insult of the burn injury.

Emergent phase (Na+, K+ shifts).

Major electrolyte shifts of Na+ and K+ also occur during this phase.

What causes hypovolemic shock in a burn patient? And how soon can it begin?

Massive shift of fluids out of the blood vessels as a result of increased capillary permeability and it can begin as early as 20 minutes post burn.

What happens to Na+ during the emergent phase?

Sodium rapidly moves to the interstitial spaces and remains there until edema formation ceases (Fig. 25-7).

Immunologic Changes.

The body's immune system is challenged when a burn injury occurs.

What happens to the colloidal osmotic pressure with a burn injury?

The colloidal osmotic pressure decreases with progressive loss of protein from the vascular space. This results in more fluid shifting out of the vascular space into the interstitial spaces (Fig. 25-6).

Skin barrier in a burn injury.

The skin barrier to invading organisms is destroyed, bone marrow depression occurs, and circulating levels of immunoglobulins are decreased.

What is intravascular volume depletion?

This is the net result of the fluid shifts and losses.

What also causes an additional loss of circulating RBCs?

Thrombosis in the capillaries of burned tissue.