Odland Rick, Schmidt Andrew H, Hunter Brian, Kidder Lou, Bechtold Joan E, Linzie Bradley M, Pedowitz Robert A, Hargens Alan R
Department of Otolaryngology, Hennepin County Medical Center, Minneapolis, MN 55415, USA.
J Orthop Trauma. 2005 Apr;19(4):267-75. doi: 10.1097/01.bot.0000155308.20133.71.
To demonstrate the efficacy of compartment syndrome ultrafiltration for the treatment of acute compartment syndrome in an animal model. Our hypothesis is the removal of interstitial fluid will result in a reduction of intramuscular pressure compared with untreated controls in a model of bilateral induced compartment syndrome.
Controlled experimental model.
Animal research facility.
PATIENTS/PARTICIPANTS: Three pairs of porcine hindlimbs.
Acute compartment syndrome was created in the pig hindlimb by infusion of saline to maintain the intramuscular pressure 30 mm Hg greater than the animal's mean arterial pressure for 8 hours. After a 2-hour reperfusion interval, ultrafiltration (removal of fluid through 1 mm diameter porous catheters, connected to -500 mm Hg suction) was commenced in 1 limb only and continued for 9.5 hours.
Intramuscular pressure, ultrafiltrate volume, ultrafiltrate and serum levels of creatine kinase and lactate dehydrogenase, histologic measurement of extracellular and intracellular edema, as well as the degree of cellular necrosis.
Intramuscular pressure tended to be lower on the treated side at the end of the treatment period [treated leg: 9.3 +/- 4.0 mm Hg (+/- SE), control leg: 19.3 +/- 1.4 mm Hg, P = 0.03]. Analysis of ultrafiltrate fluid showed that levels of creatine kinase and lactate dehydrogenase were elevated compared with serum levels. Creatine kinase levels in serum were measured at 4150 +/- 780 U/L, whereas ultrafiltrate levels of creatine kinase were 28,700 +/- 17,700 U/L (+/- SE) (P = 0.1). Lactate dehydrogenase was measured at 1950 +/- 180 U/L in serum, but markedly elevated in ultrafiltrate [160,000 +/- 88,900 U/L (+/- SE), P = 0.05]. Quantification of cellular and interstitial dimensions showed no difference in control and experimental limbs. Quantification of the degree of muscle necrosis revealed 6.1 +/- 2.7% necrosis in the treated limb compared to 11.3 +/- 1.6% necrosis in the control group (P = 0.02, df = 2, 1-tailed paired t test).
This pilot study demonstrates the feasibility of tissue ultrafiltration for reduction of intramuscular pressure in this porcine model. Further studies are underway. Compartment syndrome ultrafiltration may be useful prophylactically in patients at risk for acute compartment syndrome. Sampling of interstitial fluid and frequent measurement of intramuscular pressure may allow earlier diagnosis and treatment of acute compartment syndrome, whereas the reduction of tissue pressure by compartment syndrome ultrafiltration may prevent acute compartment syndrome from occurring. Additionally, compartment syndrome ultrafiltration will not hinder the ability of clinicians to use the clinical examination and pressure monitoring as the gold standard.
在动物模型中证明骨筋膜室综合征超滤治疗急性骨筋膜室综合征的疗效。我们的假设是,在双侧诱导性骨筋膜室综合征模型中,与未治疗的对照组相比,去除间质液将导致肌肉内压力降低。
对照实验模型。
动物研究设施。
患者/参与者:三对猪后肢。
通过输注生理盐水使猪后肢产生急性骨筋膜室综合征,将肌肉内压力维持在比动物平均动脉压高30 mmHg的水平达8小时。在2小时的再灌注间隔后,仅对1条肢体开始超滤(通过连接到-500 mmHg负压吸引的直径1 mm的多孔导管去除液体),并持续9.5小时。
肌肉内压力、超滤液量、超滤液及血清中肌酸激酶和乳酸脱氢酶水平、细胞外和细胞内水肿的组织学测量以及细胞坏死程度。
在治疗期结束时,治疗侧的肌肉内压力趋于较低[治疗腿:9.3±4.0 mmHg(±标准误),对照腿:19.3±1.4 mmHg,P = 0.03]。对超滤液的分析表明,与血清水平相比,肌酸激酶和乳酸脱氢酶水平升高。血清中肌酸激酶水平测得为4150±780 U/L,而超滤液中肌酸激酶水平为28700±17700 U/L(±标准误)(P = 0.1)。血清中乳酸脱氢酶测得为1950±180 U/L,但在超滤液中显著升高[160000±88900 U/L(±标准误),P = 0.05]。细胞和间质尺寸的量化显示,对照肢体和实验肢体无差异。肌肉坏死程度的量化显示,治疗肢体的坏死率为6.1±2.7%,而对照组为11.3±1.6%(P = 0.02,自由度=2,单尾配对t检验)。
这项初步研究证明了在该猪模型中组织超滤降低肌肉内压力的可行性。进一步的研究正在进行中。骨筋膜室综合征超滤在有急性骨筋膜室综合征风险的患者中可能具有预防性作用。间质液采样和频繁测量肌肉内压力可能有助于急性骨筋膜室综合征的早期诊断和治疗,而通过骨筋膜室综合征超滤降低组织压力可能预防急性骨筋膜室综合征的发生。此外,骨筋膜室综合征超滤不会妨碍临床医生将临床检查和压力监测作为金标准的应用能力。