腹腔间隔室综合征动物模型的构建特点

背景：腹腔间隔室综合征导致多器官功能损害的具体机制尚不十分清楚,为深入研究其发病机制及病理生理过程,需要合适的动物模型。 目的：就腹腔间隔室综合征动物模型的制备过程中可能遇到的相关问题进行讨论,包括制备模型的标准、方法、动物的选择及监测腹压的方式。 方法：由第一作者检索PubMed数据及CNKI数据库1990/2011有关腹腔间隔室综合征及腹腔高压及相关动物模型方面的文献。 结果与结论：一个成功的腹腔间隔室综合征动物模型最好能保持腹腔压力的稳定,并能持续一定的时间,同时尽可能少的影响实验结果。所以无论选择腹腔灌注气体还是灌注液体模型的测量腹腔内压并维持压力的稳定是关键。腹腔灌注液体模型无法动态监测腹压,且压力波动较大,与之相比腹腔灌注气体模型测压较为方便,若使用电子供气系统动态监测则更为理想。生理模型是前瞻性的实验,但现有的生理模型有待改进。     

烧伤后肢体筋膜间室综合征防治

目的探讨烧伤后肢体筋膜间室综合征的发生原因和预防措施。方法回顾性分析5例烧伤后发生下筋膜间室综合征病例的临床表现及形成原因，在测定30例整形患者小腿筋膜间室压力的基础上，对42例严重烧伤患者的小腿进行了压力测定和探查性深筋膜切开，观察小腿肌肉的状态，总结烧伤面积和小腿筋膜间室压力与筋膜间室综合征之间的关系，提出了有关早期切开深筋膜的指征。结果5例发生肢体筋膜间室综合征患者均未切开深筋膜，其中2例小腿截肢。在探查性切开深筋膜的42例患者中，面积越大，筋膜间室压力越高，当筋膜间室压力超过25cm H2O以上时有出现肢体筋膜间室综合征的倾向。结论深筋膜与烧伤后肢体筋膜间室综合征的发生有密切关系，重视早期切开深筋膜能较好地预防筋膜间室综合征的发生。     

恶性腹水源性腹腔间隔室综合征行早期腹腔减压治疗中患者心率、血压和呼吸变化规律的临床观察

目的 探讨恶性腹水源性腹腔间隔室综合征(MAACS)行早期置管减压治疗过程中,腹水引流量与心率、血压、呼吸变化的关系。方法 采用回顾性横断面调查,分析2012年6月—2017年6月山西大同大学附属医院肿瘤外科22例MAACS患者的临床资料。其中男13例、女9例,年龄45～74(56.44±4.46)岁。肝癌6例,胃癌2例,结肠癌1例,直肠癌2例,胰腺癌1例,胆管癌1例,卵巢癌6例,宫颈癌2例,癌性腹水未找到原发灶1例;其中合并腹腔内转移癌6例。患者均行早期腹腔减压治疗,在腹腔引流减压过程中,测量记录腹水引流前、每引流500 mL及引流完毕时腹腔压力,并同步监测患者心率、血压、呼吸的变化情况,采用简单线性回归分析腹腔引流量与心率、血压、呼吸的相关性。结果 22例患者均顺利完成腹腔置管减压治疗,腹水减压引流时间3~6(4.32±0.54)h。引流腹水量4 000～6 900(5 260±610)mL。在腹腔引流减压过程中,与腹水引流前比较:引流量≥1 500 mL时,腹腔压力下降、呼吸次数减少,差异均有统计学意义(P值均＜0.05);从流量≥1 000 mL时,各观察点心率下降,差异均有统计学意义(P值均＜0.05)。简单线性回归分析显示,随着腹腔引流量的逐渐增加,腹腔引流量与心率、呼吸有相关性(r=0.952、0.888, P值均＜0.05)。线性回归分析得回归方程为:＾Y_心率=-0.004 57 X_{腹腔引流量(mL)} + 119.0,＾Y_呼吸=-0.003 43 X_{腹腔引流量(mL)} +35.8。减压治疗后24 h内,19例心率、血压、呼吸平稳;3例出现血压下降,心率再次增加,其中2例经补液升压治疗血压、心率恢复正常,1例放弃治疗死亡。结论 早期置管减压治疗MAACS是安全的,随着腹腔引流量的增加,心率、呼吸逐渐下降,血压维持平稳,在减压后24 h内仍需密切观察心率、呼吸、血压变化情况。     

筋膜间隔区综合征的诊疗体会

筋膜间隔区综合征(Compartment Syndrome,CS),系肢体创伤后发生在四肢特定的筋膜室内的进行性病变,是创伤严重合并症之一,如不能及时诊治,将导致严重后果[1-4]。我院于1991年3月至2000年3月,共收治CS患者16例,获得一定经验,现报告如下。1资料与方法1.1临床资料本组共16例CS患者     

基于生物材料创面敷料封闭负压引流在骨筋膜室综合征切开减压中的应用

背景：骨筋膜室综合征切开减压后往往出现肌肉膨出体外、大量组织液渗出导致肌肉创面不新鲜、易发生感染等不利于患者恢复,应用封闭负压引流可以保护创面,避免局部毒素入血。 目的：观察基于自主研发的生物材料创面敷料封闭负压引流在骨筋膜室综合征切开后的临床疗效。 方法：发生骨筋膜室综合征患者切开减压后采取自愿的原则,给予基于自主研发生物材料创面敷料封闭负压引流、合成材料创面敷料封闭负压引流和常规切开减压敷料包扎治疗。观察治疗后3 d患者肝肾功能指标及肉芽颗粒的新鲜度。 结果与结论：采用自主研发生物材料创面敷料、合成材料创面敷料封闭负压引流后均能明显保护患者的肝肾功能,肉芽组织颗粒的新鲜度为满意,优于常规切开减压敷料包扎组(P < 0.05)。采用合成材料创面敷料封闭负压引流组打开封闭负压时部分患者出现周围区域水泡。提示自主研发新型生物材料创面敷料能有效引流,避免患者毒素入血保护肝肾功能,同时肉芽组织颗粒的新鲜度满意,可为后期植皮提供良好的组织创面,并且具有良好的生物相容性。     

Mechanical and biochemical analyses of tibial compartment fascia in chronic compartment syndrome

Increases in compartment pressure associated with chronic compartment syndrome (CCS) may be due to changes in the mechanical properties and/or thickness of fascia (4,22). To explore this possibility, we compared the mechanical and biochemical characteristics (stiffness, thickness, time-dependent response, collagen content, and collagen crosslinking) of fascia from patients with symptomatic anterior compartment syndrome to fascia from adjacent collateral compartments. We tested 43 specimens harvested from 20 individuals during surgical fasciectomy. Properties of normal (lateral)-compartment (NC) and pathological (anterior)-compartment (PC) fascia were mechanically tested in the axial and transverse directions forming four groups. An external control group (EX) of six specimens of anterior and lateral-compartment fascia harvested from amputated legs was also included in the study. PC fascia was found to be thicker and structurally stiffer (elastic modulus times thickness) in the axial direction than was NC fascia (p≤0.05). No significant differences were found between NC and PC time-dependent response, although significant differences between percent relaxation in the pooled axial and transverse direction specimens were observed. No differences were found in the collagen content, as measured by hydroxyproline (Hyp) concentration, between NC and PC fascia. PC fascia was found to have less collagen crosslinking by hydroxylyslpyridinoline (HP) concentration. In conclusion, although this study does not elucidate etiological factors in CCS, the changes found in PC fascia suggest that fascial mechanical properties contribute to the pathology.     

A tale of two syndromes: ovarian hyperstimulation and abdominal compartment

Abdominal compartment syndrome complicated severe ovarian hyperstimulation in a 35 year old woman with multiple bowel resections due to Crohn's disease. Pain from ovarian enlargement necessitated hospital admission. Despite intravenous fluid administration and heparin prophylaxis, ilio-femoral deep vein thrombosis developed. Treatment by intravenous heparin was complicated by repeated intra-ovarian bleeding, anaemia and acute renal failure requiring haemodialysis. Intra-abdominal pressures were elevated. After placement of an inferior vena caval filter and discontinuation of heparin, there was slow spontaneous recovery without surgery.     

Experimental study of prognosis of chronic compartment syndrome

There is little in the literature concerning the pathobiology and repair processes of impaired skeletal muscle after decompressive operation for chronic compartment syndrome (CCS), which would be valuable for prognosis. Repeated tourniquet compression through cuff inflation on rabbits' claves was performed daily for 2 hr, then stopped for 30 min, and applied for another 2 hr. The contralateral hindlimb, which was not compressed, served as a control. Rabbits were allocated to four groups: groups I and II were pressured with 80 and 120 mmHg for 3 days, and groups III and IV were pressured with 80 and 120 mmHg for 14 days. Skeletal muscle specimens from each group were obtained for histological and ultrastructural observation at day 1, 7, 14, and 28 post-compression. In groups I and II, a few necrotic fibers were observed and basal lamina was intact at 1 day after compression. Seven days after compression, there was an observable increase in the proliferation of satellite cells and development of myotube structures. Fourteen days after compression, regeneration of muscles was complete, and there was no significant difference compared with the control group. In groups III and IV, 1 day post-compression examination revealed a large area of necrotic fibers, fibrotic interstitium, and disintegratin basal lamina. Seven days later, proliferation of satellite cells was observed around the surviving basal lamina, and 28 days after compression we could see a large area of fibrosis. The degree of recovery of impaired muscle in rabbit's CCS-induced tissues is related to pressure and duration of compression. Complete recovery of the impaired muscle is determined by survival of basal lamina.     

胃肠减压在腹部手术中的最佳应用时机探讨

目的探讨腹部手术患者胃管留置的最佳方法及时机,为临床高效性护理提供借鉴。方法临床收集210例行腹部手术的患者,随机分成3组,每组70例,其中A组在手术前30 min未麻醉时置入胃管,B组在麻醉后置入胃管,前两组均为徒手置入,而C组在麻醉后喉镜直视下置入胃管。之后比较3组患者的相关反应情况、一次性成功率及置管时间等。结果 A组患者置管时与置管后2 min的收缩压、舒展张压、心率及心脏耗氧率同置管前相比均具有统计学差异(P<0.05);在置管时及置管后2min的收缩压、舒张压、心率及心脏耗氧率方面,B组和C组分别同A组相比较,也均具有统计学差异(P<0.05)。在恶心及呕吐发生率、一次性成功率与置管所需时间方面,B组和C组分别与A组相比均具有统计学差异(P<0.05),B组与C组相比也均具有统计学差异(P<0.05)。结论胃管置入的最佳时机为全麻后,在喉镜直视下置入的效果最佳,不仅可以减轻了患者痛苦,还可提高护理的工作效率。     

Arthroscopic decompression for subacromial impingement syndrome.

Arthroscopic decompression and cuff debridement was performed on 47 cases in 45 consecutive patients with either stage II or stage III impingement syndrome: 19 with no actual tear of the cuff (stage II); 13 with a partial thickness tear (stage IIIa); 10 with complete tear less than 3 cm long (stage IIIb); and 5 with complete tear longer than 3 cm (stage IIIc). Patients were classified into impingement syndrome without tear (Group I), impingement syndrome with partial thickness tear (Group II), and impingement syndrome with full thickness tear (Group III). Group I had 19 cases, group II had 13 cases, and group III had 15 cases. Patients were followed up for an average of 39.3 months (24 approximately 62 months). In group I, postoperative UCLA ratings improved in 18 cases (95%) to satisfactory result rate. In group II, 11 patients (85%) had improvement to satisfactory result rate. In group III, 12 cases (80%) had improvement to satisfactory result rate. The arthroscopic subacromial decompression and rotator cuff debridement was effective in the treatment of subacromial impingement syndrome.     

Anatomical dissection of the deep posterior compartment and its correlation with clinical reports of chronic compartment syndrome involving the deep posterior compartment

Patients with clinical presentation of deep posterior chronic compartment syndrome (CCS) frequently have symptoms limited to either proximal or distal components of the deep posterior compartment. In this study the posterior aspect of 15 cadaver legs was dissected to document anatomical separations and delineate boundaries, if any, of the deep posterior compartment and to correlate the findings to these patients. Origins of flexor hallucis longus (FHL), flexor digitorum longus (FDL), and tibialis posterior (TP), as well as whether TP existed in its own osseofascial compartment, were noted. Ten specimens had an identifiable distinct layer of tissue separating the deep posterior compartment into two potentially clinically relevant components. Much of this layer was derived from origins of FDL and its anatomical position in relation to the TP muscle. In seven of these cases, FDL had a significant fibular origin in addition to the well-established tibial origin. This essentially compartmentalized the distal third of the tibialis posterior as it descends anterior and medial to FDL in the lower one-third of the leg in five specimens. No cadaver possessed a significant fascial septum encasing TP and separating it from other deep posterior muscles. This study confirms the existence of a proximal and distal sub-compartment of the deep posterior compartment as a variant and supports the most frequent clinical presentation of deep posterior CCS as involving either the distal or proximal deep compartment, rather than the entire deep posterior compartment. The anatomic arrangement of muscles in the deep posterior compartment creates sub-compartments, which may explain the successful outcomes following a deep compartment release limited to symptomatic portion(s) of the deep compartment. Clin. Anat. 10:104–111, 1997 © 1997 Wiley-Liss, Inc.     

Efficacy of enalapril in the treatment of steroid resistant idiopathic nephrotic syndrome

Fifteen patients of idiopathic nephrotic syndrome who failed to respond to 8 weeks of corticosteroid therapy formed the material for this study. There were 10 males and 5 females, age ranging from 4 to 56 years. Three patients had hypertension. Histological lesions were focal and segmental glomerulosclerosis (FSGS) in 8; membranous glomerulonephritis in 3; mesangial proliferative glomerulonephritis in 2 and membranoproliferative glomerulonephritis in 2 patients. Proteinuria ranged from 3.64 to 8.66 g/1.73 m2/day. Serum albumin ranged between 2.2 to 3.3 g/dl. Serum creatinine was elevated > 1.5 mg/dl in 3 cases. After discontinuing steroids, enalapril was started in a dose of 2.5 mg/day and increased by 2.5 mg/day every 3-4 days till the maximum tolerated dose but not exceeding 20 mg/day. Proteinuria, serum albumin and serum creatinine estimations were done every 4 weeks for six months and every three months thereafter. Patients were followed up for 6 to 30 months. Proteinuria decreased to < 1.5 g/1.73 m2/day in 12 patients (80%) and to < 0.5 g/1.73 m2/day in 10 patients (66.7%) by 8 weeks. There was no significant decrease in proteinuria in 3 (20%) patients; two of these were cases of FSGS and one of membranoproliferative glomerulonephritis. Oedema, hypoalbuminaemia and hypercholesterolaemia returned to normal in all patients who had a decrease in the proteinuria. There was no correlation between the histological lesion and response to enalapril. There was no rise in the serum creatinine level above the baseline in any of the patients. Except for cough in one patient, no other significant side effects were observed. We conclude that enalapril is effective in reducing proteinuria and thereby the morbidity in steroid resistant nephrotic syndrome irrespective of the underlying pathology.     

利妥昔单抗在难治性微小病变型肾病综合征中的疗效及分析

目的 回顾性分析利妥昔单抗(rituximab,RTX)治疗难治性微小病变型肾病综合征(minimal-change nephrotic syndrome,MCNS)的疗效和安全性,探讨影响其疗效的可能因素.方法 纳入2018年12月至2020年6月于我院肾内科接受RTX治疗的MCNS患者23例,根据发病年龄分为儿童组...     

A rabbit model of peripheral compartment syndrome with associated rhabdomyolysis and a regenerative medicine approach for treatment

Peripheral compartment syndrome (PCS) has a complex etiology, with limited treatment options and high patient morbidity. Animal models of PCS have been hampered by differences in cross-species anatomy, physiology, and the relative rarity of the naturally occurring syndrome in animals. In the present study, the combination of saline infusion with intermittent crushing of skeletal muscle consistently caused increased intracompartmental pressure, hypocalemia, and hypercreatinine-phophokinasemia, signs diagnostic of PCS. This method was used to evaluate both the standard PCS treatment, specifically a fasciotomy, and a regenerative medicine approach for treatment-consisting of a fasciotomy with local administration of a biologic scaffold material composed of porcine small intestinal submucosa extracellular matrix (SIS-ECM). The use of this SIS-ECM scaffold in conjunction with a fasciotomy was associated with myogenesis and constructive tissue remodeling in the SIS-ECM-treated animals. At 1 and 3 months after treatment innervated muscle tissue was present at the site of injury. No myogenesis was present in the fasciotomy only treated animals. RAM11+ macrophages, which are associated with constructive tissue remodeling, were present within the injury site in the SIS-ECM-treated animals at 1 month. The present study provides a reproducible animal model with which to study PCS, and shows the potential of a regenerative medicine approach to PCS treatment.     

Acute compartment syndrome of the muscle in intensive care patients

Acute compartment syndrome of the muscle occurs when elevation of tissue pressure in closed fascial compartments results in muscle and nerve ischemia. Prompt diagnosis and decompression is essential to avoid the devastating local complications with permanent disabilities and systemic even lethal complications. Despite its drawbacks, clinical assessment is still the diagnostic cornerstone of acute compartment syndrome. In critically multisystem injured patients, it often presents silently and clinical examination alone may be insufficient. Intracompartmental pressure measurement is a useful adjunct and can confirm the diagnosis when clinical assessment is difficult. In this article, the etiology, clinical signs, diagnosis and therapy is discussed and underscores the importance of routine surveillance for acute compartment syndrome of muscle.