Demling R H, Kramer G C, Gunther R, Nerlich M
Surgery. 1984 May;95(5):593-602.
We studied the effect of a nonprotein colloid solution--namely low molecular weight dextran (LMWD)--on edema formation in burned and nonburned soft tissue and lung. Adult sheep with lung and bilateral flank lymph fistulas were given a unilateral 25% to 30% full-thickness burn under ketamine anesthesia and followed for 72 hours. Resuscitation (24-hour period) was performed with lactated Ringer solution (LR) (n = 9) or 10% LMWD in saline (n = 8) to restore baseline vascular pressures and cardiac output. Interstitial edema and microvascular protein permeability were monitored by lymph flow (QL) and lymph to plasma protein ratio, respectively. With LR, QL values in nonburned skin and lung were increased twofold to threefold in the first 24 hours, while with LMWD, values remained at baseline. The nonburn edema with LR was due to the burn-induced hypoproteinemia state. The prevention of this process with LMWD was due to the generation of a twofold to threefold increase in the plasma to interstitial colloid osmotic pressure (COP) gradient. Burn QL was increased fivefold in both groups despite a higher COP gradient with LMWD. Net fluid requirements for the first 24 hours were 75 and 35 ml/kg for animals treated with LR and LMWD, respectively. After cessation of dextran administration in the second 24 hours, the COP gradients for the two groups were equal but QL in nonburned skin and net fluid requirements now increased significantly in the LMWD group. The development of nonburn edema was believed to be due to the persistent hypoproteinemic state. We conclude that edema formation in nonburned tissues, which is due to hypoproteinemia, accounts for a substantial amount of the net fluid requirements after thermal injury. This process can be prevented by infusion of a nonprotein colloid as long as the COP gradient is increased. Edema in burned tissue appears to be unaffected by changes in COP.
我们研究了一种非蛋白胶体溶液——即低分子量右旋糖酐(LMWD)——对烧伤和未烧伤软组织及肺部水肿形成的影响。在氯胺酮麻醉下,对患有肺部及双侧胁腹淋巴瘘的成年绵羊进行单侧25%至30%的全层烧伤,并持续观察72小时。用乳酸林格液(LR)(n = 9)或10% LMWD生理盐水溶液(n = 8)进行复苏(24小时),以恢复基线血管压力和心输出量。分别通过淋巴流量(QL)和淋巴与血浆蛋白比率监测间质水肿和微血管蛋白通透性。使用LR时,未烧伤皮肤和肺部的QL值在最初24小时内增加了两倍至三倍,而使用LMWD时,该值保持在基线水平。LR导致的未烧伤水肿是由于烧伤引起的低蛋白血症状态。LMWD预防这一过程是由于血浆与间质胶体渗透压(COP)梯度增加了两倍至三倍。尽管LMWD的COP梯度较高,但两组烧伤后的QL均增加了五倍。接受LR和LMWD治疗的动物在最初24小时的净液体需求量分别为75和35 ml/kg。在第二个24小时停止给予右旋糖酐后,两组的COP梯度相等,但LMWD组未烧伤皮肤的QL和净液体需求量现在显著增加。未烧伤水肿的发展被认为是由于持续的低蛋白血症状态。我们得出结论,由于低蛋白血症导致的未烧伤组织水肿占热损伤后净液体需求量的很大一部分。只要COP梯度增加,通过输注非蛋白胶体就可以预防这一过程。烧伤组织中的水肿似乎不受COP变化的影响。