[[ 招待講演３："REVIEW OF COLLOIDS IN FLUID RESUSCITATION OF BURN PATIENTS" ]]
招待講演３："Review of Colloids in Fluid Resuscitation of Burn Patients"
Dennis C. Gore, M.D. 司会：八木 義弘(浦安市川市民病院) |
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To maintain intravascular volume after severe injury, Iarge quantities of fluids high in sodium content are required. Traditionally, the adequacy of this resuscitation is indexed by a urine output of greater than 0.5 ml/kg/h. Yet this amount of intravenous fluid often results in extreme elevations in total body sodium and water content creating tremendous tissue edema. To minimize tissue edema, many clinicians supplement their crystalloid fluid resuscitation with colloids. Theoretically, colloid infusions reduce tissue edema by augmenting intravascular colloid oncotic pressure, thus by Starling's equilibrium, more fluid is retained within the intravascular space. Several studies have confirmed that colloid solutions can replenish intravascular volume in a third the amount required for an isotonic crystalloid solution. With this justification, colloids have been used extensively in the acute resuscitation of burn patients as a means of maintaining intravascular volume while minimizing tissue edema. This attempt to reduce tissue edema was considered extremely important for patients with pulmonary insufficiency, most commonly smoke inhalation, where it was hoped that colloid fluid resuscitation could replenish and maintain intravascular volume without exacerbating the hypoxemia associated with pulmonary edema. Furthermore, the liver responds to severe traumatic stress by increasing the production of acute phase proteins while greatly reducing the production of albumin. The net effect is a precipitous fall in plasma albumin levels in burn patients. Many clinicians theorized that the liver could simply synthesize and excrete only so much protein, thus, albumin production was sacrificed in order to augment production of acute phase proteins. Thus, many physicians assumed that normalizing a patient's plasma albumin concentration with exogenous supplementation would be beneficial in maintaining intravascular homeostasis. Despite these several theoretical advantages, growing scientific evidence both laboratory and clinical, has now clearly demonstrated numerous detrimental effects when colloids are given to burn patients. It appears that tissue edema results not only from cellular swelling, but also from an increase in interstitial fluid volume related to a loss of endothelial integrity. Thus, colloids appear to leak into the interstitium through defects in the capillary membranes following severe injury. Well controlled studies investigating both hemorrhagic and burn shock have recently shown that colloids given for resuscitation actually increase interstitial colloid oncotic pressure. The net effect is a prolongation and exacerbation of tissue edema. Furthermore, several clinical studies have demonstrated that colloid supplementation in burn patients substantially reduces the glomerular filtration rate thus inhibiting and delaying the diuresis and natriuresis that should naturally accompany adequate fluid resuscitation. With these new findings strongly suggesting that the fall in plasma albumin concentration in critically injured patients is advantageous especially in regards to improved renal filtration, several authors now speculate that the decrease in hepatic albumin synthesis that accompanies traumatic injury may be an appropriate adaptive response. To replete a patient's albumin simply counteracts this appropriate response to injury and may be detrimental.
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