ACS in overall is a predictor of both MOF (odds ratio = 9.2; 95% confidence intervals, 3.8–22.8;p < 0.0001) and mortality (odds ratio = 8.4; 95% confidence intervals, 3.5–20.6;p < 0.0001).
Postinjury 1° ACS became evident with the widespread application of damage control laparotomy. 21–23 More recently it was recognized that ACS can also occur in cases where only extraperitoneal injuries are present (2° ACS). 4,5,12 The early case studies and reviews characterized 1° and 2° ACS by impaired renal function, high ventilator pressures, and poor cardiac function, which are reversed after surgical decompression of the abdomen. 7,24 Despite good physiologic response to decompression, the reported outcome of ACS is consistently very poor. 11 Recognizing that primary fascial closure after damage control was frequently associated with ACS, preventive “Bogota Bag” open abdomen closure has been recommended. 22 Several authors have suggested that routine UBP monitoring could lead to earlier decompression and better outcome. 1,7–9 Not surprisingly, patients whose ACS was recognized during the first 24 hours had lower mortality than those who were decompressed after 48 hours. 4,5 In contrast, we have previously reported that when early decompression (<12 hours from admission) was unvaryingly performed, there is no difference in time to decompression between patients who survived versus those who died. 12 The utilization of damage control techniques acutely saves the lives of severely injured patients with critically impaired physiology, but we now have to face the unsolved complication of ACS. Despite the liberal use of UBP measurements and early decompression, the ACS remains a difficult challenge. Believing that the inadequate epidemiologic characterization and the failure to identify the syndrome’s risk factors are the key points in the recent years’ stagnation in the ACS prevention and treatment, we focused our efforts on providing the necessary epidemiology, early prediction models, and outcome determinants of the ACS and its subgroups.
The exact incidence of ACS is difficult to determine, and it is dependent on both the definition of the ACS (numerator) and the patient population used for the actual study (denominator). Some authors used mixed (trauma, general surgery, burns) populations, which makes it difficult to compare their findings with the postinjury cohorts. The incidence of ACS in our high-risk shock/trauma ICU resuscitation cohort was 14 percent. If all patients admitted to the shock trauma ICU are used as the denominator, the incidence of ACS is 1.2 percent. In terms of the 1° ACS, our results are comparable with those of Meldrum et al. 7 Fourteen percent incidence of ACS in a group of ICU admitted patients with an ISS >15 who had undergone emergency laparotomy and ISS >1515” used twice in this sentence -- meaning not understood. Please reword for clarity.‘. Ertel et al. 25 had similar inclusion criteria (abdominal or pelvis AIS >3 and/or laparotomy) but used only clinical assessment with no UBP to diagnose ACS in the majority of patients, and they reported a 5.5 percent incidence. Study populations including only damage control laparotomy patients report higher (33–36%) incidence of ACS. 1,2 We identified nine 1° ACS patients and 45 nonACS patients among the 54 damage control patients. This 17 percent (9/54) incidence of 1° ACS among damage control patients is lower than the previous studies. This may be attributable to the fact that our damage control patients had their abdominal fascia left open (i.e., underwent Bogota bag closure). Only four patients (4/54, 7%) had towel clip closure. Our results are comparable with Offner et al.’s. 2 For all damage control patients their incidence was 33 percent, but the incidence in those patients with fascial closure was 80 percent compared with the subset of Bogota bag closure patients incidence of 17 percent. Less data are available to establish the incidence of the 2° ACS, which is more elusive and recognized only in the last 5 years. Maxwell et al. 4 reported six 2° ACS patients from 1216 ICU admissions (0.5%), while we had 15 patients from 2258 Shock Trauma ICU admissions (0.7%). To date, there is no data comparing the relative incidence of 1° ACS and 2° ACS in the same institution among patients treated in a standardized fashion. According to our results, 1° and 2° ACS had very similar incidence (6% vs. 8%) in this high-risk major-torso trauma group.
Severe hemorrhagic shock was uniformly present in the whole cohort (Table 1), but both 1° and 2° ACS patients had a lower initial SBP and higher transfusion requirement than the nonACS group. All patients had high base deficit on hospital arrival (∼10 mEq/L), but nonACS patients responded well to the initial resuscitation, and by the time of ICU admission, their BD had improved (4 mEq/L), contrary to the 1° and 2° ACS groups (still ∼10 mEq/L) (Table 4). Hemorrhagic shock is consistently reported in the literature as a prerequisite of ACS. Although ACS can happen in patients with moderate injuries, 5 ACS patients typically have a high ISS. In the present study there was no difference among the groups in terms of injury severity. The injury pattern, however, was rather different (Table 1); the typical 1° ACS patient had severe abdominal injuries, while the classic 2° ACS patient had severe pelvic fractures or major extraperitoneal vascular injuries with multiple long bone fractures. Because of these differences in injury pattern, the 1° and 2° ACS patients’ hospital course was also different (Fig. 2). 1° ACS patients had a very short ED course because of the obvious need to go to the operating room for abdominal hemorrhage control. The OR intervention uniformly included quick damage control procedures because of the bloody “vicious cycle” physiology, 23 while they received massive transfusions. Only two 1° ACS patients did not have primary damage control laparotomy. In these two cases, 1° ACS presented as a failure of nonoperative management of blunt liver injuries. 2° ACS patients typically had more prolonged diagnostic work-up, and most frequently, they required pelvic embolization in the interventional radiology suite.
ACS patients received more crystalloid infusions and PRBC transfusions during their first 24 hours of hospital stay (Fig. 5 and 6). 2° ACS patients received more crystalloid, but not more blood compared with 1° ACS patients. The most remarkable difference between 1° and 2° ACS patients was during their interventional period (operating room and/or interventional radiology) when the 2° ACS group’s crystalloid/PBRC ratio was 1.92 ± 0.3 L/unit while the 1° ACS patients’ ratio was only 0.55 ± 0.1 L/unit (Fig. 7). The possible role of crystalloid overload in the pathogenesis of 2° ACS has been suggested, but until now crystalloid volume had not been shown to be an independent risk factor for ACS. 4,5,12,26 Our data showed that ≥3 L of crystalloid infusion in the ED predicts both 1° and 2° ACS. More than 7.5 L of crystalloid infusion before ICU admission strongly predicts 2° ACS. Both 1° and 2° ACS can be accurately predicted at the time of ICU admission (Table 7, ROC results). Some characteristics of the two syndromes are different (injury pattern, fluid resuscitation, preICU course), and they have distinct predictors. The risk factors for 1° ACS are the clinical markers of the “bloody vicious cycle,” while 2° ACS occurs in patients with low urinary output despite massive crystalloid resuscitation in those who have a high GAPCO2. Our data confirm the previous observation that gastric tonometry may be an important monitoring tool for ACS. 1,27,28
Due to the abundant monitoring inherent to our resuscitative process, ACS patients were diagnosed and treated relatively early in their ICU course (Fig. 3). While there was no difference between 1° and 2° ACS times to decompression from hospital admission, 2° ACS occurred earlier after ICU admission. This could be because 1° ACS patients’ abdomens were predominantly open, and therefore, they needed longer times to develop the critical UBP level that is known to cause ACS symptoms. The other fact is that 2° ACS patients had longer pre-ICU courses where the resuscitation was less controlled compared with the ICU.
An interesting additional finding is that the UBP of the nonACS patients (Fig. 4) was relatively high (≥15 mm Hg) and, according to Burch’s classification, represents Grade II intra-abdominal hypertension. 9 The normal UBP in a mixed group of nontrauma hospitalized patients was 6.5 mm Hg (range, 0.2–16.2 mm Hg), 29 however the UBP of critically ill patients is reported to be higher. 30 Recent basic science research suggests that sequential hemorrhagic shock and abdominal compartment syndrome resulted in more severe inflammatory response than either insult alone. 31,32 Critically ill injured patients who require massive fluid resuscitation may not tolerate even lower levels of intra-abdominal pressure. The possible adverse effect on the outcome of this elevated intra-abdominal pressure without meeting the ACS criteria needs to be evaluated.
In our cohort both ACS subgroups had the same good physiologic response to decompression (Table 2). The uniform improvement in hemodynamic and respiratory parameters is well described in previous studies. 1–12 More recently it was pointed out that the good response to decompression is not necessarily associated with better outcome. 11–12 We identified only two variables that predict better outcome: cardiac index and urinary output improvement were better among survived patients than those who died. Note that an hourly urinary output of 100 mL can be an alarming sign for impaired renal function, although this is far above the generally accepted value of 0.5 mL/kg/h.
Fascial closure of open abdomens was achieved earlier and with less number of operations in the 2° ACS group compared with the 1° ACS and nonACS damage control groups (Table 3). The 2° ACS patients had no abdominal injuries and appeared to resolve their intestinal edema more quickly. While time to fascial closure was not pre-defined outcome of this study, our patients on average achieved fascial closure 7 days earlier than was reported in previous series. 33 The possible beneficial effect of the vacuum assisted closure in the prevention of fascial retraction needs further evaluation. 15
The outcome of ACS patients measured by ventilator days, the incidence of MOF and mortality was significantly worse than that of the nonACS patients’ with similar demographics, shock, and injury severity (Table 1Outcomes). In terms of outcome the ACS patients were similar regardless of the type of ACS. Several papers suggested the possible connection between ACS and poor outcome intuitively, 2,12,26,33,34 but our present study has proven statistically that ACS is a predictor for both MOF and mortality based on logistic regression analysis.
Studies in the last 15 years, including our cohort, have failed to document a convincing improvement in the outcome of ACS despite earlier decompression and the liberal use of the temporary open abdomen techniques. This suggests that efforts directed at prevention will be more fruitful than efforts directed at early recognition and decompression. The multiple logistic regression analysis showed that high-risk patients are identifiable very early during resuscitation. 1° ACS patients develop the “bloody vicious cycle” physiology at which point abbreviated surgical intervention is the only way to save their lives. Packing the abdomen is an efficient tool to achieve hemorrhage control, but the space occupied by packs, the edematous bowel, and the recurrent bleeding after optimization of the circulation are important factors in 1° ACS. Prevention requires the avoidance of tight packing, the application of large Bogota bags, the elimination of hypothermia, and re-evaluation for possible bleeders are essential. In the future, novel hemorrhage control techniques without significant space occupying nature could have an important role. 35 While the incidence of 1° ACS can be decreased by alternative damage control techniques, trauma surgeons will continue to face this complication in patients with life threatening abdominal injuries. In the nonoperative management of abdominal solid organ injuries 1° ACS, until most recently, meant the failure of the nonoperative management and mandated exploration. Novel case reports allude to decompression that can be done without laparotomy by draining the peritoneal cavity. 36
2° ACS is predictable in patients with shock and massive crystalloid resuscitation without intra-peritoneal injuries. The standard of care crystalloid fluid based resuscitation seems to be effective in the vast majority of this high-risk cohort, but not among patients who are prone to 2° ACS. The application of alternative resuscitation fluids, such as hypertonic saline and colloids, should be considered in this subgroup. The analysis of fluid resuscitation before ICU admission. Figure 7 shows the uncontrolled nature of resuscitation in terms of PRBC/crystalloid ratio of the 2° ACS patients. To prevent this, pre-ICU needs to be better controlled. Of note, 73 percent (11/15) of the 2° ACS patients had major pelvic fracture, and 47 percent (7/15) of them required urgent angiographic embolization prompted by hemodynamic instability. The interventional radiologic embolization of the pelvic arterial bleeding is a valuable adjunct, but bleeding from the broken cancellous bony surfaces and from the retroperitoneal venous plexuses is more common. In these types of bleedings reduction of the pelvic ring and compression between the oozing cancellous bony surfaces are essential. The minimally invasive urgent pelvic stabilization techniques need to be applied in selected cases. The continuous oozing from these fractures and veins can lead to cyclic crystalloid resuscitation/re-bleeding, which may cause transient hemodilution, decreased capillary oncotic pressure, and intestinal edema. As described earlier, the increased pelvic content with the intestinal edema are key elements of the mechanism of the 2° ACS. 12
In summary, based on postoperatively collected data from a high-risk group of patients who were resuscitated in a similar manner, we conclude that ACS is a frequent early complication and is associated with massive volume loading. 1° and 2° ACS patients have different injury characteristics and undergo different preICU resuscitation, but both can be predicted as early as 6 hours after hospital admission with adequate monitoring. The outcome of ACS remains very poor and despite earlier recognition mortality did not improve. Further efforts should focus on prevention of the syndrome, most likely by: (1) standardizing and better monitoring the pre-ICU phase of the resuscitation; (2) alternative resuscitation strategies; and (3) use of novel hemorrhage control techniques in patients who are at high-risk to develop ACS.
Dr. Patrick Reilly (Philadelphia, Pennsylvania): Dr. Balogh and the group from Houston have presented data from their prospectively collected database which includes 188 major torso trauma patients undergoing a standardized resuscitation in the ICU at Memorial Herman Hospital.
From this patient population, 26 patients were identified who developed abdominal compartment syndrome.
Most of these patients were identified and treated within 14 hours of hospital presentation. Despite a heightened level of awareness and an increased urgency for prompt treatment of ACS, mortality in the group remained nearly 60 percent.
An enormous amount of information about these patients is provided, and rigorous statistical analysis ultimately leads to a predictive model for the development of abdominal compartment syndrome.
It should be noted these 26 patients compromised only 1.2 percent of all ICU admissions and a much smaller percentage of all admitted patients during this study period.
Still, they represent an important population with tremendous basic science and clinical relevance.
It is, therefore, not surprising that a recent Medline search of the key words “abdominal compartment syndrome” yielded 158 citations, most of which have been published in the last 5 years.
Unfortunately, the overwhelming majority of these citations are case reports, case series, and small clinical studies that have attempted to characterize the population in question.
So, with the addition of this manuscript, are we better off? I think the answer is clearly, yes, and clearly, no.
The epidemiology of this patient population has been eloquently described. A potentially helpful predictive model, taking into account degree or depth of shock and volume of resuscitation fluid, among other variables, is created that could be employed after resuscitation in the emergency department or ICU.
Many of these results confirm my own, and most likely most of the audience’s, clinical sense that sicker patients, especially those who receive significant crystalloid resuscitations, are at an increased risk for ACS.
It’s always nice to have your clinical suspicions confirmed by scientific review, and in that sense, I am better off.
However, I’m left with the nearly 60 percent mortality in the ACS group presented here—this from a Herman Hospital team that has written extensively about this subject and clearly is clinically “keyed in” to the phenomenon of abdominal hypertension and abdominal compartment syndrome.
I have a few questions for the authors. First, you arbitrarily divide your study patients into primary and secondary ACS groups based on whether abdominal injury is present.
However, the remaining nonACS patients are lumped together into one control group regardless of whether they have abdominal injury.
Have you examined your data comparing ACS patients with abdominal injuries to nonACS patients with abdominal injury and performed a similar analysis for those patients without abdominal injury?
Perhaps other variables could be identified that are associated with the development of ACS and that are lost in the current analysis.
Second, patients in the study were standardized by the uniform resuscitation guidelines that were followed in the ICU; however, in your manuscript, you mentioned the relatively “uncontrolled” resuscitation that occurred in some patients before their arrival in the ICU.
Crystalloid volumes were quite significant and crystalloid packed red blood cell ratios high. A number of studies have identified an association between significant crystalloid resuscitations and ACS.
We also have found a relationship in damage control patients between these same crystalloid resuscitations and an increased incidence of complications associated with hollow viscus injury repairs as well as a decreased ability to obtain delay primary fascial closure during the initial hospitalization.
How do you plan to change the resuscitation philosophy at Memorial Herman Hospital in this patient population at risk?
Do you think taking your resuscitation guideline out of the ICU and to the patient will impact the incidence of abdominal compartment syndrome?
Is there a role for a colloid resuscitation in these select patients? How useful do you really think your predictive model will ultimately be?
The ED model is less sensitive, although rapidly available. The ICU model is more sensitive but relies on some numbers such as crystalloid resuscitation greater than 7.5 liters that might only be obtained after the horse is already out of the barn.
The majority of your damage control patients already are left open rather than having fascial or even skin closure.
How will your predictive model really change your clinical practice? Have you preemptively opened an abdomen with a bladder pressure less than 25 or other clinical signs of abdominal compartment syndrome based solely on your model?
I greatly enjoyed this presentation, and the manuscript that accompanied it is well written. I commend the Houston group on their past efforts and look forward to their future projects, both at the basic science bench and the bedside.
Hopefully, in the not too distant future we can all build on this current project and come up with a resuscitative and/or operative strategy to prevent the development of this highly lethal complication.
I would like to thank the Association and the Program Committee for the opportunity to discuss this paper.
Dr. Zsolt Balogh (Houston, Texas): Thank you very much for your questions and comments, Dr. Reilly. I’ll try to answer all of them.
First of all, your first question was about the study design. We attempted to design and perform the most comprehensive clinical ACS study on post-injury ACS, and we spent months on thinking how to allocate our patients in study groups.
Originally, we had four groups. The first group was a primary ACS, and the control was the other resuscitation patients with abdominal injuries.
The third group was secondary ACS, and their controls were those resuscitation patients who had no abdominal injuries.
This resulted in four groups and less patients in each group, higher standard errors, and less statistical power.
This analysis didn’t help us to find more predictors than what we included in the manuscript. The other thing that this manuscript, together with epidemiology, prediction, outcome, and all the decompression responses, otherwise quite lengthy, and further groups would cause further expansion and even confusion.
The second question was about the less-controlled preICU resuscitation. It’s a very good observation from our manuscript.
Early on, our resuscitation protocol was criticized that probably the ICU protocol causes and the resuscitation protocol causes the abdominal compartment syndromes.
Our very first observation was that ACS occurs very early during the ICU course, so there is virtually no time to over resuscitate these patients on the ICU.
However, the pre-ICU resuscitation is less controlled and, as was clear from the presentation, is driven by the vital signs such as blood pressure and heart rate.
We already started to implement or modify the resuscitation protocol to the pre-ICU setting and possibly prevent abdominal compartment syndrome during the early hospital course.
The question about the use of alternative fluid resuscitation is another good one. I think crystalloid and blood resuscitation is presently the standard of care in the United States trauma centers.
At first, we wanted to know what we had. As Dr. Reilly alluded, most of the studies are case reports, retrospective reviews, and reviews of the reviews, and that’s why we wanted to perform an epidemiologic study and find out how the crystalloid volume affects the outcome and the development of ACS.
Based on these results, those patients who are at high risk of ACS, alternative resuscitation either with colloids or hypertonic saline may be warranted.
We can tell you that on that 85 percent of the shock resuscitation patients, the crystalloid and blood resuscitation seems to work.
If you can predict the 15 persons who are at high risk at ACS, you can actually prevent them. The third question was about the use of our prediction model in the future.
Yes, that’s true. A prediction model is absolutely worthless if it’s not implemented into the clinical practice.
So, we already started to use this model in the clinical practice. As you see, there are distinct predictors for primary and secondary ACS.
The primary ACS predictors are indicators of the bloody vicious cycle that can help us to leave these abdomens open and have a higher level of suspicion to decompress these patients earlier.
For the secondary ACS patients, there are two important things. One is the crystalloid limits that we implement into the resuscitation protocol as an alarming sign.
If the patient starts to reach this amount of crystalloid, an alternative resuscitation may start. The other thing is the 150 milliliters per hour urine output may be adequate in other patients, but in these aggressively resuscitated patients, that output may be low—an alarming sign of renal failure.
Yes, we do decompress patients with bladder pressure lower than 25, as we already started, because bladder pressure is not a very sophisticated method, and it cannot be treated as an absolute number.
If the physiology worsens and the predictors show that these patients are on the tract to develop ACS, they should be decompressed or treated as an ACS.
Dr. Steven R. Shackford (Burlington, Vermont): This is a very nicely presented paper, and I congratulate you on the delivery.
I would like to focus, just for a second, on that secondary abdominal compartment group with the large crystalloid resuscitation.
Now, did I understand you to say that most of the resuscitation of those patients was carried out before they got to the ICU—is that right?
Dr. Zsolt Balogh (Houston, Texas): Yes, when they reached the ICU, they were decompressed between 3 to 4 hours.
So most of the resuscitation occurred in the pre-ICU setting in the diagnostic evaluation.
Dr. Steven R. Shackford (Burlington, Vermont): So, what were the end points of resuscitation? I saw your ICU resuscitation protocol began with the first step of being driven by a relatively arbitrary or target DO2 or oxygen delivery, but down in the ER, or your resuscitation space, you couldn’t do that because you probably didn’t have a pulmonary artery catheter in and couldn’t obtain a cardiac output to calculate the DO2, correct?
Dr. Zsolt Balogh (Houston, Texas): Yes.
Dr. Steven R. Shackford (Burlington, Vermont): So, what were the end points of resuscitation in that group? What were you using to titrate: the amount of crystalloid you were giving those patients?
Dr. Zsolt Balogh (Houston, Texas): Our resuscitation protocol, which will extend to the pre-ICU setting, will be a modified one, and it will be driven by the CVP and the SvO2.
According to the primary reports, SvO2 can be a very good predictor for these adverse outcomes.
Dr. Steven R. Shackford (Burlington, Vermont): That’s a central –
Dr. Zsolt Balogh (Houston, Texas): Yes, it’s a central venous line.
Dr. Dennis Wang (Washington, D.C.): I just want to caution you not to rise to the bait of Dr. Reilly in actually implementing releasing abdominal compartment syndrome based on your predictive model, because some of the issues have not been addressed specifically—things such as why the patient died.
Is this from multi-organ failure due to resuscitation, or was resuscitation failure not specifically addressed?
Also, you may have to look at this compounding factor: is your resuscitation pre-ICU, or is it the actual resuscitation protocol that lead to your morbidity and mortality?
These are things that have to be addressed before you go ahead and actually start opening abdomens, before you reach the compartment pressure greater than 25.
Dr. Zsolt Balogh (closing): Thank you very much. The patients are not decompressed according to the prediction model, but they are decompressed at this time according to the measured organ dysfunction parameters such as cardiac index, respiratory, and renal failure. I think we answered the question in the presentation that the less controlled pre-ICU resuscitation and the physiology which leads to damage control surgery are important predictors of postinjury primary and secondary ACS. Once these patients reach the ICU, the syndrome is already there, and there is virtually no time to over-resuscitate them by the ICU resuscitation protocol.
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Keywords:© 2003 Lippincott Williams & Wilkins, Inc.
Intraabdominal hypertension; Abdominal compartment syndrome; Multiple organ failure; Gastric tonometry