Burn shock ( 燒燙傷休克 ) 馬偕紀念醫院整形重建外科 姚文騰醫師 2015/10/22

Transcription

1 Burn shock ( 燒燙傷休克 ) 馬偕紀念醫院整形重建外科 姚文騰醫師 2015/10/22

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3 重建階梯 Sheet STSG FTSG Mesh Meek Stamp

4 Meek

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6 Introduction Cutaneous thermal injury involving more than one-third of the total body surface area (TBSA) invariably results in the severe and unique derangements of cardiovascular function known as burn shock. Shock is an abnormal physiologic state in which tissue perfusion is insufficient to maintain adequate delivery of oxygen and nutrients and removal of cellular waste products.

7 Introduction Burn shock is a complex process of circulatory and microcirculatory dysfunction that is not easily or fully repaired by fluid resuscitation. Burn shock caused by Direct tissue injury Hypovolemia Release of multiple mediators of inflammation

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9 Introduction Subsequently, burn shock continues as a significant pathophysiologic state, even if hypovolemia is corrected. Inflammatory shock mediators, both local and systemic, that are implicated in the pathogenesis of burn shock. Histamine Serotonin Nitric oxide Oxygen free radicals Prostaglandin Thromboxane Tumor necrosis factor

10 Hypovolemia Burn injury causes extravasation of plasma into the burn wound. Hemodynamic changes similar to those that occur after hemorrhage. Decreased plasma volume Decreased cardiac output Decreased urine output Increased systemic vascular resistance with resultant reduced peripheral blood flow.

11 Hypovolemia An increase in hematocrit and hemoglobin concentration will often appear despite fluid resuscitation. The primary initial therapeutic goal is to promptly restore vascular volume and to preserve tissue perfusion in order to minimize tissue ischemia.

12 Hypovolemia Large volumes of resuscitation solutions are required to maintain vascular volume during the first several hours after an extensive burn. Despite fluid resuscitation normal blood volume is not restored until hours after large burns.

13 Normal microcirculatory fluid exchange Fluid transport across the microcirculatory wall in normal and pathological states is quantitatively described by the Landis Starling equation: Volume of fluid that crosses the microvasculature barrier (Jv) Capillary filtration coefficient (Kf) Capillary pressure (Pc) Interstitial hydrostatic pressure (Pif) Osmotic reflection coefficient (σ) Plasma colloid osmotic pressure (πp) Interstitial colloid osmotic pressure (πif)

14 The Landis-Starling equation

15 The Landis-Starling equation Edema occurs when the lymphatic drainage (JL) does not keep pace with the increased Jv.

16 Burn edema Edema develops when the rate by which fluid is filtered out of the microvessels exceeds the flow in the lymph vessels draining the same tissue mass.

17 Burn edema Edema formation often follows a biphasic pattern. An immediate and rapid increase in the water content of burn tissue is seen in the first hour after burn injury. A second and more gradual increase in fluid flux of both the burned skin and non-burned soft tissue occurs during the first hours after burn injury.

18 Burn edema Burn edema is unique in its rapidity compared to other types of edema, because it is only in burn edema that all of these variables change significantly in the direction required to increase fluid filtration. Edema formation in thermally injured skin is characterized by an extremely rapid onset. Tissue water content can double within the first hour after burn.

19 Burn edema

20 Non-burned tissue Generalized edema in soft tissues not directly injured is another characteristic of large cutaneous burns. Brouhard et al. reported increased water content in nonburned skin even after a 10% burn, with the peak edema occurring 12 hours post burn.

21 Non-burned tissue The sustained increase in water content and the elevated lymph flow of the non-burned tissue after the return of normal permeability is likely the result of the sustained hypoproteinemia. Several clinical and animal studies have established that maintaining higher levels of total plasma protein concentration can ameliorate the overall net fluid retention and edema.

22 Inflammatory mediators of burn injury A veritable cornucopia of local and circulating mediators are produced in the blood or released by cells after thermal injury. These mediators clearly play important but complex roles in the pathogenesis of edema and the cardiovascular abnormalities of burn injury.

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24 Inflammatory mediators of burn injury Histamine is released in large quantities from mast cells in burned skin immediately after injury. Histamine increase the leakage of fluid and protein from systemic micro vessels. Beneficial antihistamine treatment of human burn injury has not been demonstrated.

25 Edema and abdominal compartment syndrome Prompt and adequate fluid resuscitation has undoubtedly improved the outcome of burn-injured patients. Massive edema of burned and non-burned tissues continues to be a repercussion of large-volume fluid resuscitation.

26 Edema and abdominal compartment syndrome This trend of providing fluid in excess of the Parkland formula has been termed fluid creep. Over-resuscitation and its resulting edema are not without consequences. The problems of the over-resuscitated burn patient may include eye injuries due to elevated orbital pressures, pulmonary edema, the need for prolonged mechanical ventilation, or tracheostomy, graft failure or the need for fasciotomy of uninjured extremities due to massive edema.

27 Edema and abdominal compartment syndrome

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29 Abdominal compartment syndrome

30 Summary Thermal injury results in massive fluid shifts from the circulating plasma into the interstitial space, causing hypovolemia and swelling of the burned skin. Adequate resuscitation will prevent organ failure.

31 Thanks for your attention!