Ertel W, Oberholzer A, Platz A, Stocker R, Trentz O
Division of Trauma Surgery, University Hospital Zurich, Switzerland.
Crit Care Med. 2000 Jun;28(6):1747-53. doi: 10.1097/00003246-200006000-00008.
To investigate the incidence, main physiologic effects, and therapeutic management of the abdominal compartment syndrome (ACS) after severe abdominal and/or pelvic trauma.
Retrospective analysis from January 1991 to December 1996; prospective study from January 1997 to August 1998.
Level I trauma center, intensive care unit.
A total of 311 patients with severe abdominal and/or pelvic trauma and "damage-control" laparotomy on day of admission.
The ACS was defined as the development of significant respiratory compromise, including elevated inspiratory pressure of >35 mbar, a decreased Horowitz quotient (<150 torr [<20 kPa]), renal dysfunction (urine output, <30 mL/hr), hemodynamic instability necessitating catecholamines, and a rigid or tense abdomen. Beginning with January 1997, urinary bladder pressure as an additional variable for the diagnosis of ACS was continuously measured in patients (n = 12) at risk. Bladder pressures of >25 mm Hg indicated ACS.
Seventeen patients (5.5%) developed ACS because of persistent intra-abdominal/retroperitoneal bleeding (n = 12; 70.6%) or visceral edema (n = 5; 29.4%). All patients with ACS underwent primary fascial closure. In eight of these patients (47%), abdominal and/or pelvic packing for hemostasis was performed. All patients with ACS required decompressive emergency laparotomies because of physiologic derangements. The time between primary laparotomy and decompressive laparotomy was 12.9 +/- 2.0 hrs. Emergency decompression of the abdomen resulted in a significant increase in the cardiac index (+146%), tidal volume (+133%), Horowitz quotient (+156%), and urine output (+1557%), whereas bladder pressure (-63%), heart rate (-19%), central venous pressure (-30%), pulmonary artery occlusion pressure (-43%), peak airway pressure (-31%), partial pressure arterial carbon dioxide (-30%), and lactate (-40%) markedly (p < .05) decreased. In two multiply injured patients with additional head trauma, ACS caused a critical increase of the intracranial pressure, which markedly dropped after the release of abdominal tension.
Risk factors for the occurrence of ACS are severe abdominal and/or pelvic trauma, which require laparotomy and packing for the control of hemorrhage. The ACS occurs within hours and causes life-threatening physiologic derangements and a critical rise in intracranial pressure in patients with combined abdominal/pelvic and head trauma. Decompressive laparotomy immediately restores impaired organ functions. In patients at risk, the continuous measurement of urinary bladder pressure as a simple, noninvasive, and less expensive diagnostic tool for early detection of elevated intra-abdominal pressure is mandatory.
探讨严重腹部和/或盆腔创伤后腹腔间隔室综合征（ACS）的发生率、主要生理影响及治疗处理。
1991年1月至1996年12月为回顾性分析；1997年1月至1998年8月为前瞻性研究。
一级创伤中心，重症监护病房。
共311例严重腹部和/或盆腔创伤患者，入院当天行“损伤控制”剖腹术。
ACS定义为出现明显的呼吸功能不全，包括吸气压力>35 mbar升高、霍洛维茨商数降低（<150 torr [<20 kPa]）、肾功能不全（尿量<30 mL/小时）、需要使用儿茶酚胺维持血流动力学稳定以及腹部僵硬或紧张。从1997年1月开始，对有风险的患者（n = 12）持续测量膀胱压力作为诊断ACS的另一个变量。膀胱压力>25 mmHg提示ACS。
17例患者（5.5%）因持续性腹腔内/腹膜后出血（n = 12；70.6%）或内脏水肿（n = 5；29.4%）发生ACS。所有ACS患者均进行了一期筋膜缝合。其中8例患者（47%）进行了腹部和/或盆腔填塞止血。所有ACS患者因生理紊乱均需行减压性急诊剖腹术。初次剖腹术至减压性剖腹术的时间为12.9±2.0小时。腹部急诊减压后，心脏指数显著增加（+146%）、潮气量（+133%）、霍洛维茨商数（+156%）和尿量（+1557%），而膀胱压力（-63%）、心率（-19%）、中心静脉压（-30%）、肺动脉闭塞压（-43%）、气道峰压（-31%）、动脉血二氧化碳分压（-30%）和乳酸（-40%）明显降低（p <.05）。在2例合并头部创伤的多发伤患者中，ACS导致颅内压急剧升高，腹部张力解除后颅内压明显下降。
ACS发生的危险因素是严重腹部和/或盆腔创伤，需要剖腹术和填塞以控制出血。ACS在数小时内发生，可导致危及生命的生理紊乱，并使腹部/盆腔合并头部创伤患者的颅内压急剧升高。减压性剖腹术可立即恢复受损的器官功能。对于有风险的患者，必须持续测量膀胱压力，作为一种简单、无创且成本较低的诊断工具，用于早期检测腹腔内压力升高。
