重症急性胰腺炎合并腹腔室隔综合征诊治分析

目的总结重症急性胰腺炎合并腹腔室隔综合征的早期诊断及临床治疗经验。方法回顾分析17例重症急性胰腺炎合并腹腔室隔综合征临床治疗资料。结果腹腔置管或开腹减压引流组13例死亡4例,3例穿刺引流减压不充分,腹腔室隔综合征(abdominal compartment syndromes,ACS)持续进展,并发多器官功能衰竭综合征(multiple organ dysfunction syndrome,MODS)死亡,1例开腹减压延迟关腹术后低蛋白血症,合并腹腔感染死亡;未引流减压组4例中3例并发MODS,2周内死亡。结论重症急性胰腺炎基础治疗的同时不能忽略腹腔内压的监测,一旦腹腔室隔综合征确诊应及时行腹腔减压。     

重症急性胰腺炎并发腹腔间隔室综合征11例的诊治体会

目的 总结重症急性胰腺炎(SAP)并发腹腔间隔室综合征(ACS)的诊断和治疗经验.方法 回顾性分析11例SAP并发ACS病例,根据临床特征得出ACS诊断.一旦确诊,立即开腹减压,用3升静脉营养输液袋暂时性关腹.结果 第1例经上腹正中切口开腹减压,减压不够,再发ACS死亡,第2～11例皆作腹正中剑突至耻骨联合大切口开腹减压,减压效果较好.本组死亡4例,病死率为36.4%(4/11).结论 ACS是SAP的严重并发症,早期诊断是关键,一旦确诊,应尽早开腹减压,用3升静脉营养输液袋是理想的暂时性关腹方法.     

重症急性胰腺炎并发腹腔室隔综合征的诊断和治疗

总结重症急性胰腺炎(SAP)并发腹腔室隔综合征(ACS)的诊治经验。方法结合SAP病史,复苏液体量已足够时,在腹膨胀、腹壁紧张后出现心肺肾功能不全即可诊断ACS,膀胱测压作诊断辅助。诊断确立后及时开腹减压引流,3升静脉营养袋暂时性关腹。结果21例(23例次)。ACS患者中,行开腹减压术18例次,死亡3例(16．7％),未手术5例次,死亡4例(80％),总死亡率33．3％(7／21);7例死亡中,4例合并急性梗阻性化脓性胆管炎;诊断ACS5h内手术者无死亡;正规关腹多在开腹减压术后3～5d进行,最迟1例为术后8d;6例迟发性Acs均由腹腔腹膜后感染性坏死引起。结论SAP患者在SIRS和感染期均可发生ACS,并在病理基础上有其特殊性;及时诊断ACS和开腹充分减压,3升静脉营养袋暂时性关腹是治疗ACS的关键。     

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目的　总结重症急性胰腺炎 (SAP)并发腹腔室隔综合征 (ACS)时继发性器官功能不全的特点。方法　 1998～ 2 0 0 3年 345例SAP中 2 1例发生ACS病人 ,确诊时继发的心、肺、肾功能不全的特点 ,比较治疗前后的变化和缓解因素。结果　 2 1例 (2 3例次 )ACS病人紧随腹膨胀、腹壁紧张后出现心肺肾功能不全。表现为血压下降 ,CVP反而升高 ;PaO2 下降 ,但PaCO2 和PAP增高 ;无尿或少尿 ;液体复苏、呼吸机支持、多巴胺及速尿等保守治疗无效。 18例次行开腹减压引流术及 3L静脉营养袋暂时性关腹者中的 15例次成活者迅速逆转 ,APACHEⅡ评分由术前的 2 3 7± 13 9降至术后 6h的 13 3± 3 6 ,术后 2 4h平均尿量增至 (180 1± 6 7 8)mL/h。 5例未手术者中 4例病情进行性恶化直至死亡。结论　及时诊断ACS ,开腹充分减压和 3L袋暂时性关腹是逆转器官功能不全的关键。     

腹腔开放治疗肠瘘并严重腹腔感染73例分析

目的 研究腹腔开放治疗肠外瘘并腹腔感染的时机、方法与效果。比较不同暂时关腹技术,研究消化道与腹壁重建的时机与效果。方法 回顾性分析1999年1月至2008年12月南京军区南京总医院73例接受腹腔开放疗法的肠外瘘并严重腹腹腔感染的临床资料。结果 56例（76.7%）行腹腔开放疗法后存活（存活组）,10例（13.7%）死亡,7例（9.6%）放弃治疗（死亡及放弃治疗者统称为死亡及放弃治疗组）。死亡原因主要是腹腔出血（5例）、感染和脏器功能衰竭（5例）。腹腔开放前的APACHE II评分在存活组和死亡及放弃治疗组分别为13.5±4.3和16.0±5.8,腹腔开放后第5天时分别降至9.2±4.5和12.9±5.5;腹腔开放第15天时,存活组APACHEII评分降至8.1±6.2,而死亡及放弃治疗组评分重新升高至腹腔开放前水平（16.3±11.8）。脏器功能障碍评分亦有类似变化。结论 腹腔开放可有效治疗肠外瘘并严重腹腔感染病人。在多脏器功能严重损害前及时行腹腔开放疗法可有效改善肠瘘并严重腹腔感染的疾病严重度。腹腔开放后第15天左右的疾病严重度可提示病人的转归。行腹腔开放的病人可分为暂时关腹、创面植皮和永久重建3个阶段。消化道与腹壁重建可同时进行。     

腹腔室隔综合征的诊断和治疗（附5例报告）

目的　总结腹腔室隔综合征 (ACS)的诊断和治疗经验。方法　回顾性分析 5例ACS病例 ,皆以其临床特征得出诊断 ;ACS一旦确诊 ,立即开腹减压 ,用 3升静脉营养输液袋暂时性关腹。结果　例 1经上腹正中切口开腹减压 ,减压不够 ,再发ACS死亡 ;后 4例作剑突至耻骨联合大切口开腹减压 ,其中 1例术后 12小时呕吐误吸死亡 ,3例治疗出院。死亡率 40 % (2 / 5 )。结论　密切观察腹部体征和全身变化是发现ACS的关键 ;ACS一旦确诊应及时开腹减压 ,唯有作剑突至耻骨联合正中大切口开腹才能充分减压 ,用 3升静脉营养输液袋暂时性关腹是理想选择。     

严重创伤后腹腔间隙综合征行腹腔扩容术1例报道

目的总结腹腔扩容术(IAVI)治疗创伤后腹腔间隙综合征(ACS)的效果及其关键技术。方法回顾性分析2011年5月笔者所在医院收治的1例严重创伤后ACS患者的临床资料。结果该例患者先行IAVI,手术时间为80 min,术中出血50 m L,手术顺利。术后监测膀胱压(1次/4 h),于IAVI后14 d行腹壁创面植皮以形成计划性腹疝。该例患者术后无出血、感染等并发症发生,恢复顺利,于术后20 d出院。于出院后9个月再行改良双侧腹直肌推徙术治疗巨大计划性腹疝。行改良双侧腹直肌推徙术后该患者获访24个月,随访期间腹壁疝无复发,未见其他不适。结论 IAVI能够有效防治ACS,提高严重创伤患者的生存率。     

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腹部创伤、严重腹腔感染、急性重症胰腺炎等严重腹部疾患常导致腹内高压(intraabdominal hypertention,IAH),不但限制腹式呼吸,减少机体氧供,而且对循环系统、消化系统、肾脏及中枢神经等系统带来一系列严重影响。如不及时进行开腹减压,将造成腹腔间室综合征(abdominal com-partment syndrome,ACS),导致一系列病理生理紊乱,甚至危及病人生命。因此,对腹腔高压病人,必须及时开放腹腔,降低腹内压。1ACS时腹腔开放的适应证ACS时腹腔开放的主要目的是降低腹内压,一般认为,如果腹内压>20mmHg(1mmHg=0.133kPa),必须进行开腹减压。造成腹内高…     

腹腔室隔综合征五例的诊断和治疗

目的 总结腹腔室隔综合征（ACS）的诊断和治疗经验。方法 5例ACS病例,皆以其临床特征得出诊断,行开腹减压,用3升静脉营养输液袋暂时性关腹。结果 1例经上腹正中切口开腹减压术后死亡;4例作剑突至耻骨联合大切口开腹减压,其中1例术后窒息死亡,余3例治愈出院。死亡率40％（2／5）。结论 密切腹部体征和全身变化是发现ACS的关键;ACS一旦确诊应及时开腹充分减压,可用3升静脉营养输液暂时性关腹。     

腹腔间隔室综合征23例诊治分析

目的 探讨腹腔间隔室综合征（abdominal compartment syndrome,ACS）的病因、诊断和治疗.方法 回顾性分析鞍山市中心医院2006年1月至2013年6月收治的ACS 23例的临床资料.23例中,男性16例,女性7例;年龄35～67岁,平均45岁;未手术4例,手术治疗19例.结果 痊愈20例（86.9％）：未手术3例,术中切口一期缝合者6例,腹壁切口部分敞开4例,Proceed补片和三升袋缝合皮下筋膜7例.死亡3例（13.1％）：拒绝手术及腹主动脉瘤卒中死亡.结论 应及早诊断,及时采取腹腔减压措施.对于重症急性胰腺炎患者,如果膀胱内压大于25 mmHg时,也具有手术探查指征.ACS患者经开腹腹腔减压术后,可用暂时关腹的方法.术中给予腹壁切口部分敞开及各种暂时关腹的方法是提高治愈率的关键.     

Abdominal compartment syndrome

Abdominal compartment syndrome (ACS) is defined by the deleterious effects of intraabdominal hypertension (IAH) on the pulmonary, cardiovascular, splanchnic, urinary and central nervous system. Abnormal and sudden increase in the volume of any component of the intraperitoneal or retroperitoneal space (occurRing postoperatively or subsequent to hemorrhagic trauma, referfusion edema, penumoperitoneum, intestinal distention, acute pancreatitis...) causes IAH. Sustained IAH leads to ACS which if left unrecognized or untreated is always fatal. Measurement of urinary bladder pressure is the best validated technique for diagnosis of IAH. It should be used routinely for minimally invasive surveillance of intra-abdominal pressure (IAP) in patients with severe thoraco-abdominal trauma or after major abdominal operations. Medical management of IAH is of limited efficacy making expedient surgical decompression the treatment of choice for ACS. Surgical decompression of the abdomen and temporary closure is generally recognized as effective in clinically patent ACS but the pressure threshold indicating the need for decompression remains controversial. No data are available from controlled randomized trials and current guidelines are based on the experience of large trauma centers. The few available prospective clinical series report survival rates in the 38 to 71% range after surgical decompression for ACS. These studies are difficult to compare due to methodological features but it would appear that centers using the lowest pressure threshold for decompensation (< 20 mmHg) have the highest survival rates. Despite the available physiological arguments, indications for prophylactic temporary abdominal coverage (TAC), e.g. in trauma patients or for early decompression in IAH patients without clinical ACS, have not been validated in clinical practice. The potential morbidity of decompression procedures, TAC, and subsequent abdominal wall reconstructions require comparative studies of these treatment options with available pharmacological and non-surgical means to lower IAP.     

Abdominal compartment syndrome in children: experience with three cases

BACKGROUND/PURPOSE: Abdominal compartment syndrome (ACS) is defined as cardiopulmonary or renal dysfunction caused by an acute increase in intraabdominal pressure. Although the condition is well described in adults, particularly trauma patients, little is known about ACS in children. METHODS: Three girls, ages 4, 5, and 5 years, were treated for ACS by silo decompression. Each child presented in profound shock, required massive fluid resuscitation, and had tremendous abdominal distension. The first child sustained a thoracoabdominal crush injury, underwent immediate celiotomy for splenic avulsion and a liver laceration, and required decompression 5 hours postoperatively. The second underwent ligation of her bluntly transected inferior vena cava; because of massive edema, her abdominal wall could not be closed, and prophylactic decompression had to be performed. The third presented with shock of unknown etiology, and ACS developed acutely with a bladder pressure of 26 mm Hg. RESULTS: Respiratory, renal, and hemodynamic function improved immediately in all 3 patients after decompression. Subsequently, each child underwent abdominal wall reconstruction and recovered uneventfully. CONCLUSIONS: ACS is a potentially lethal complication of severe trauma and shock in children. To prevent the development of renal or cardiopulmonary failure in these patients, decompression should be considered for acute, tense abdominal distension.     

Secondary abdominal compartment syndrome: an underappreciated manifestation of severe hemorrhagic shock

OBJECTIVE: Abdominal compartment syndrome (ACS) has multiple well-described etiologies, but almost no attention has focused on ACS in the absence of abdominal injury. This study describes a secondary ACS that occurs after severe hemorrhagic shock with no evidence of abdominal injury. METHODS: The trauma registry at a Level I trauma center was reviewed for a 13-month period beginning July 1, 1997. RESULTS: During the study period, there were 46 of 1,216 intensive care unit admissions (4%) who required laparotomy and mesh closure of the abdominal wall because of visceral edema. In that subgroup, six patients (13% of mesh closures, 0.5% intensive care unit admissions) had hemorrhagic shock (5/1, blunt/penetrating trauma) but no evidence of intra-abdominal injury. Associated extremity compartment syndrome developed in two of six (33%). Overall mortality was four of six (67%), secondary to sepsis (n = 3), and head injury (n = 1). Time from admission to decompression averaged 3 hours in survivors and 25 hours in nonsurvivors (overall average = 18+/-9 hours). Resuscitation volume before abdominal decompression averaged 19+/-5 liters of crystalloid and 29+/-10 units of packed red blood cells. Bladder pressure averaged 33+/- 3 mm Hg. Decompression significantly improved peak inspiratory pressure (p < 0.003) and base deficit (p < 0.003). CONCLUSION: ACS can occur with no abdominal injury; The incidence of secondary ACS was 0.5% in this cohort trauma intensive care unit patients, so it probably occurs more frequently than is currently appreciated. Because survivors were decompressed 20 hours before nonsurvivors, early recognition might improve outcomes. On the basis of these observations, we recommend that bladder pressures should be routinely checked and acted on appropriately when resuscitation volumes approach 10 liters of crystalloid or 10 units of packed red cells.     

The abdominal compartment syndrome

The abdominal compartment syndrome (ACS) causes dysfunctions of various organs through a progressive unphysiologic increase of the intraabdominal pressure. While the primary ACS is a result of the underlying disease/injury, secondary ACS is caused by surgical interventions. In the severely injured patient intra- and/or retroperitoneal bleeding, edema of viscera due to systemic ischemia reperfusion injury following hemorrhagic shock, abdominal/pelvic packing, and laparotomy closure under tension lead to ACS. The clinical signs of ACS are a tense abdomen with a decreased abdominal wall compliance. Early signs of ACS are a rise in inspiratory pressure and oliguria. Manifest ACS results in anuria, respiratory failure, reduced intestinal perfusion, and low cardiac output syndrome. If untreated, patients die due to left ventricular failure. Diagnosis of ACS is made using the patient's history including the injury pattern, the symptoms, the time period between injury and the occurrence of organ dysfunctions, and the physiologic response to decompression. Frequent determinations of the bladder pressure represent the "golden standard" for early recognition of ACS. Decompressive laparotomy should be performed with a bladder pressure > or = 20 mmHg and rapidly restores impaired organ functions. In the case of a multiple injured patients in shock or with associated severe head injury decompressive laparotomy may even be carried out at a lower bladder pressure. The abdomen is left open. In most patients staged laparotomy is necessary. The final closure of the abdominal wall is carried out after the edema have resolved between day 6 and 8 after primary laparotomy.     

Secondary abdominal compartment syndrome is an elusive early complication of traumatic shock resuscitation

BACKGROUND: The term secondary abdominal compartment syndrome (ACS) has been applied to describe trauma patients who develop ACS but do not have abdominal injuries. The purpose of this study was to describe major trauma victims who developed secondary ACS during standardized shock resuscitation. METHODS: Our prospective database for standardized shock resuscitation was reviewed to obtain before and after abdominal decompression shock related data for secondary ACS patients. Focused chart review was done to confirm time-related outcomes. RESULTS: Over the 30 months period ending May 2001, 11 (9%) of 128 standardized shock resuscitation patients developed secondary ACS. All presented in severe shock (systolic blood pressure 85 +/- 5 mm Hg, base deficit 8.6 +/- 1.6 mEq/L), with severe injuries (injury severity score 28 +/- 3) and required aggressive shock resuscitation (26 +/- 2 units of blood, 38 +/- 3 L crystalloid within 24 hours). All cases of secondary ACS were recognized and decompressed within 24 hours of hospital admission. After decompression, the bladder pressure and the systemic vascular resistance decreased, while the mean arterial pressure, cardiac index, and static lung compliance increased. The mortality rate was 54%. Those who died failed to respond to decompression with increased cardiac index and did not maintain decreased bladder pressure. CONCLUSIONS: Secondary ACS is an early but, if appropriately monitored, recognizable complication in patients with major nonabdominal trauma who require aggressive resuscitation.     

Bogota-VAC – A Newly Modified Temporary Abdominal Closure Technique

Background  We present Bogota-VAC, a newly modified temporary abdominal closure (TAC) technique for open abdomen condition after abdominal compartment syndrome (ACS). Methods  A thin isolation bag (Bogota bag) and a vacuum assisted closure (VAC) system were combined. A matching bag was tension-free fixed on the abdominal fascia by fascia suture. A ring shaped black polyurethane foam of the VAC system was placed into the gap between Bogota bag, abdominal fascia and the wound edge. A constant negative topic pressure of 50–75 mmHg was used in the VAC system. Results  Intra-abdominal pressure (IAP: 22 ± 2 mmHg) of four patients with ACS after severe traumatic brain injury and one patient with isolated ACS after blunt abdominal trauma decreased significantly (p = 0.01) after decompressive laparotomy and treatment with Bogota-VAC (IAP: 10 ± 2 mmHg) and remained low, measured via urinary bladder pressure. Intracranial pressure (ICP) in the four traumatic brain injury patients decreased from 42 ± 13 mmHg to 15 ± 3 mmHg after abdominal decompression. Cerebral perfusion pressure (57 ± 14 mmHg) increased to 74 ± 2 mmHg. Conclusion  The advantage of the presented Bogota-VAC is leak tightness, wound conditioning (soft tissue/fascia), skin protection and facilitation of nursing in combination with highest volume reserve capacity (VRC), thus preventing recurrent increased intra-abdominal and intracranial pressure in the initial phase after decompression of ACS compared to other TAC techniques.     

Postinjury abdominal compartment syndrome does not preclude early enteral feeding after definitive closure

BACKGROUND: Critically injured patients are susceptible to the abdominal compartment syndrome (ACS), which requires decompressive laparotomy with delayed abdominal closure. Previous work by the University of Texas Houston group showed impaired gut function after resuscitation-associated gut edema. The purpose of this study was to determine if enteral nutrition was precluded by the intra-abdominal hypertension and bowel edema of the ACS. METHODS: Patients developing postinjury ACS from January 1996 to August 2003 at our level-I trauma center were reviewed. Patient demographics, time to definitive abdominal closure, and institution and tolerance of enteral nutrition were evaluated. RESULTS: Thirty-seven patients developed postinjury ACS during the study period; 26 men and 11 women with a mean age of 36 +/- 4 and injury severity score of 33 +/- 4. Mean intra-abdominal pressure before decompression was 32 +/- 3 mm Hg, and concurrent mean peak airway pressure was 50 +/- 4 cm oxygen. Enteral feeding was never started in 12 patients; 4 died within 48 hours of admission, 7 required vasoactive agents until their death, and 1 developed an enterocutaneous fistula requiring parenteral nutrition. Enteral feeding was initiated in the remaining 25 patients: 13 had feeds started within 24 hours of abdominal closure; 5 were fed with open abdomens; and 7 had a delay because of vasopressors (n = 2), multiple trips to the operating room (n = 2), paralytics (n = 2), and increased intra-abdominal pressures (n = 1). Once advanced, enteral feeding was tolerated in 23 (92%) of the 25 patients with attainment of goal feeds in a mean of 3.1 +/- 1 days. CONCLUSIONS: Despite the bowel edema and intra-abdominal hypertension related to the ACS, early enteral feeding is feasible after definitive abdominal closure.     

Abdominal compartment syndrome among surgical patients

Abdominal compartment syndrome(ACS) develops when organ failure arises secondary to an increase in intraabdominal pressure. The abdominal pressure is determined by multiple factors such as blood pressure, abdominal compliance, and other factors that exert a constant pressure within the abdominal cavity. Several conditions in the critically ill may increase abdominal pressure compromising organ perfusion that may lead to renal and respiratory dysfunction. Among surgical and trauma patients, aggressive fluid resuscitation is the most commonly reported risk factor to develop ACS. Other conditions that have also been identified as risk factors are ascites, hemoperitoneum, bowel distention, and large tumors. All patients with abdominal trauma possess a higher risk of developing intra-abdominal hypertension(IAH). Certain surgical interventions are reported to have a higher risk to develop IAH such as damage control surgery, abdominal aortic aneurysm repair, and liver transplantation among others. Close monitoring of organ function and intra-abdominal pressure(IAP) allows clinicians to diagnose ACS rapidly and intervene with target-specific management to reduce IAP. Surgical decompression followed by temporary abdominal closure should be considered in all patients with signs of organ dysfunction. There is still a great need for more studies to determine the adequate timing for interventions to improve patient outcomes.