Meldrum DR, Moore FA, Moore EE, et al: Prospective characterization and selective management of the abdominal compartment syndrome

Department of Surgery, Denver Health Medical Center and University of Colorado Health Sciences Center, 80204, USA.
The American Journal of Surgery (Impact Factor: 2.41). 12/1997; 174(6):667-72; discussion 672-3. DOI: 10.1016/S0002-9610(97)00201-8
Source: PubMed

ABSTRACT The abdominal compartment syndrome (ACS) is now recognized as a frequent confounder of surgical critical care following major trauma; however, few prospective data exist concerning its characterization, evolution, and response to decompression.
Acutely injured patients with an injury severity scale (ISS) score >15 requiring emergent laparotomy and intensive care unit (ICU) admission were prospectively evaluated for the development of ACS. The syndrome was defined as an intra-abdominal pressure (IAP) >20 mm Hg complicated by one of the following: peak airway pressure (PAP) >40 cm H2O, oxygen delivery index (DO2I) <600 mL O2/min/m2, or urine output (UO) <0.5 mL/kg/hr. Physiologic response to decompression was similarly documented prospectively.
Over a 14-month period ending December 1995, 21 (14%) of 145 patients (ISS >15) requiring laparotomy and admitted to our surgical ICU developed ACS; mean age was 39 +/- 9 years; injury mechanism was blunt in 60%; ISS 26 +/- 6. At initial laparotomy, 67% underwent abdominal packing (57% for major liver injuries). Mean IAP was 27 +/- 2.3 mm Hg, and time from laparotomy to decompression was 27 +/- 4 hours; 24% were planned whereas the remaining were prompted by deteriorating organ function as defined above (cardiopulmonary in 43%; renal in 19%; both renal and cardiopulmonary in 14%). Following decompression, there was an increase in cardiac index, oxygen delivery, urine output, and static compliance while there was a decrease in pulmonary capillary wedge pressure, systemic vascular resistance, and peak airway pressure.
The abdominal compartment syndrome occurs in a significant number of severely injured patients, and it develops quickly (27 +/- 4 hours). Cardiopulmonary deterioration is the most frequent reason prompting decompression. Timely decompression of the ACS results in improvements in cardiopulmonary and renal function. These data support the use of the proposed ACS grading system for selective management of the syndrome.

Download full-text


Available from: Ernest E Moore, Aug 25, 2015
  • Source
    • "The development of abdominal compartment syndrome (ACS) from intraabdominal hypertension (IAH) does not occur at a precise level. ACS is thought to develop once the abdominal pressures reach 20–25 mmHg and is characterized by an increase in airway pressures, inadequate ventilation and oxygenation, altered renal function, and hemodynamic instability [1] [2]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Abdominal compartment syndrome can result from many different causes. We present a case where this dangerous syndrome occurred in the operating room during a transurethral resection of a bladder tumor. It was initially recognized by an elevation in the peak inspiratory pressure. We report the typical physiologic changes that occur with this syndrome and its treatment options.
    08/2012; 2012:870619. DOI:10.1155/2012/870619
  • Source
    • "The peak or inspiratory airway pressure (iPaw) has also been found to be highly predictive of abdominal compartment syndrome in human trauma patients (Raeburn et al., 2001; McNelis et al., 2003). For such patients, a peak airway pressure of >40 cm H 2 0 associated with an intra-abdominal pressure of > 20 mm Hg was indicative of compartment syndrome (Meldrum et al., 1997). For pigs with a C0 2 -induced intraabdominal pressure of 30 mm Hg, the peak airway pressure rose to approximately 40 mbar (40.8 cm H 2 0; 30 mm Hg; Toens et al., 2002). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Previous experiments with diverse pig models to evaluate the ability of rFVIIa to reduce hemorrhage have provided divergent results. The current study was conducted to address concerns related to previous work by using larger sample sizes, and an extended observational period of 4 hours post-injury. The objectives were to evaluate further the hemostatic efficacy and safety of rFVIIa administration after traumatic, uncontrolled hemorrhage. Anesthetized, splenectomized pigs (36.6 +/- 0.3 kg; n = 18/group) underwent an approximately 50% isovolemic blood exchange with 33 degrees C 6% hetastarch, and body temperature was adjusted to 32.5 +/- 0.5 degrees C. Subsequently, a Grade V liver injury was inflicted. After 30 seconds, either vehicle or treatment (180 microg/kg or 720 microg/kg rFVIIa) was administered intravenously as a bolus. Concomitantly, laparotomy pads were packed around the liver. Resuscitation with 33 degrees C lactated Ringer's solution (260 mL/min) was initiated and pigs were monitored for 4 hour post-injury or until death. Tissues were collected and examined histologically to assess the presence of disseminated intravascular coagulation (DIC). Liver injuries were comparable among all groups (p = 0.89). Measures associated with in vitro coagulation (prothrombin time, activated partial thromboplastin time, thromboelastographic split-point and R times) were enhanced by rFVIIa administration (p < 0.05). However, neither percent survival (p = 0.82), survival time (p = 0.56), nor blood loss (p = 0.63) were affected by treatment. DIC was not evident in lung or kidney tissue. These data indicate an inability of rFVIIa at these doses to reduce blood loss, or to increase survival time or percent survival in this pig model. Absence of DIC provides evidence for safe use of rFVIIa under conditions specific to this study.
    The Journal of trauma 07/2005; 59(1):155-61; discussion 161. DOI:10.1097/01.TA.0000174557.89804.A2 · 2.96 Impact Factor
  • Source
    • "Mortality due to ACS is extremely high, 38 – 71 % (Cullen et al, 1989; Meldrum et al, 1997; Kron et al, 1984; Schein et al, 1995; Biffl et al, 2001). It must be taken into account in context with the main diagnosis. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The abdominal compartment syndrome has received considerable attention only recently. It may be defined as adverse physiologic consequences that occur as a result of an acute increase in the intraabdominal pressure. The most common causes of ACS are haemorrhage, visceral oedema, pancreatitis, bowel distension, venous mesenterial obstruction, abdominal packs, tense ascites, peritonitis, tumor. The mostly affected organ systems include cardiovascular, pulmonary, renal, central nervous and splanchnic. The diagnosis depends on the recognition of the clinical syndrome followed by an objective measurement of intraabdominal pressure, preferably that of the urinary bladder. The treatment consists of adequate fluid resuscitation and surgical decompression when necessary. (Tab. 1, Ref. 29.).
    Bratislavske lekarske listy 02/2003; 104(1):32-5. · 0.45 Impact Factor
Show more