IAH and pHi
Forty-two patients, who were treated more recently, had gastric tonometry and pHi monitoring. Eleven of these patients developed IAH. At the time that they had IAH, eight of the 11 patients (72.7%) had gastric mucosal acidosis with a pHi of 7.10 +/- 0.2. However, none had the classic features of the abdominal compartment syndrome at this time (cardiac index, 4.4 +/- 1.2 L/min/m2; oxygen delivery index, 1096 +/- 247.2 mL/min per m2; oxygen consumption index, 174.4 +/- 44.4 mL/min per m2; PaCO2, 38 +/- 6 mm Hg; PaO2/FiO2 ratio, 280.1 +/- 93.2). All had excellent urine output and renal function and none exhibited high peak inspiratory pressures. Of the eight patients with gastric mucosal acidosis, six had improvement in their pHi after abdominal decompression and recovered without developing ACS. The two patients who had no sustained response in pHi and IAH after abdominal decompression went on to manifest ACS and MODS and died subsequently. Both of these patients had a delayed onset of IAH (fifth and seventh day) which responded only transiently to abdominal decompression. In both of these patients, the bowel was noted to be extremely edematous, thickened, and leathery.
The three patients who had IAH but did not have gastric mucosal acidosis were not clinically different from the eight patients who had a low pHi. They did not have prior, chronic elevation of IAP (ascites, cirrhosis, etc.).
Of the 70 patients, 56 patients (80%) survived. One patient died suddenly 2 weeks after injury due to secondary hemorrhage from an iliac artery PTFE graft in the absence of overt sepsis or MODS. Three patients died within 48 hours from uncontrolled hemorrhage from coagulopathy. One of these patients had an associated macronodular cirrhosis of the liver and another patient had an associated head injury as contributing factors. Ten patients expired secondary to MODS. Survival was better in the absence of IAH (42 of 47; 89.4%) than when the complication had occurred (14 of 23; 60.9%; p = 0.003). Excluding the patient that died of head trauma, survival was also better in group I (mesh closure as prophylaxis for IAH), 40 of 44 or 90.1% compared with that in group II (fascial suture) (17 of 25; 68%; p = 0.035). ISS and mesh closure were found to be the best predictors for survival on stepwise multiple regression analysis.
Sixteen patients developed MODS. Ten of these patients died. MODS points were less in patients who did not develop IAH than in those who had this complication (0.8 +/- 1.9 vs. 4.3 +/- 3.7; p = 0.0001). MODS points were also less in patients in group I (mesh closure as prophylaxis for IAH) than in group II (fascial suture) patients (1.3 +/- 2.4 vs. 3.1 +/- 3.9; p = 0.023).
Open Abdomen Management
Forty-five patients had initial open abdomen approach by placement of a mesh at the cutaneous or fascial level. Thirteen patients had the abdomen left open at reoperation. Of the 58 patients, 12 died and 46 recovered. In 21 surviving patients (45.6%), the fascia was closed by either primary fascial closure or by a prosthetic mesh between 2 and 17 days. In 25 patients, the abdomen was closed by mobilization and suture of skin flaps, allowing a large ventral hernia for a subsequent repair. None of these patients needed skin grafting. The open abdomen in the mesh closure group provided several advantages. It facilitated a prompt bedside exploration for IAH. In three patients surgical bleeders in the abdomen were identified and controlled during the bedside exploration. One patient with a gunshot wound to the abdomen had, among other injuries, a nonbleeding kidney injury at the initial operation. Postoperative development of IAH prompted a bedside laparotomy through the mesh at which time active bleeding of the kidney at the hilum was noted. It was promptly controlled by hilar clamping, and the patient was transferred to the operating room for a nephrectomy. There were no complications of bowel fistula observed as a direct complication of the open abdomen approach, even though one patient had a colon anastomotic breakdown and required a colostomy.
Increased intra-abdominal pressure or IAH causes significant changes in almost all organ systems. The cardiovascular, respiratory, and renal effects [1-15,20] have been recognized for some time and are recently redocumented in trauma patients. [8,9,16] Recently, the consequences of IAH on cerebral circulation as well as splanchnic bed have attracted considerable attention. Bloomfield and associates presented evidence of increased ICP during IAP elevations and showed in animal experiments that these changes were related to an increase in pleural pressure and a functional obstruction of the jugular venous system. [21-23] Diebel and associates, in a series of swine experiments [24-26] showed that the intestinal mucosal blood flow diminished to 61% of the baseline at an IAP of 20 mm Hg and 28% of the baseline at an IAP of 40 mm Hg. Corresponding to these changes, the intestinal mucosa, as studied by the tonometer, showed severe degrees of acidosis. They also demonstrated that hepatic microvascular blood flow was 71% of the control and the portal vein blood flow was 65% of the control at an IAP of 40 mm Hg. The decreases were exaggerated with higher levels of IAP. Very recently, Bongard and colleagues  noted in ventilated swine that tissue oxygen partial pressure in the bowel fell progressively as the IAP was increased, whereas the subcutaneous tissue oxygen partial pressure remained unchanged. These changes were found to be independent of changes in cardiac output. Eleftheriadis and co-workers [27,28] noted splanchnic ischemia and oxygen free radical production during pneumoperitoneum induced elevations in IAP.
These recognized effects of IAH are particularly relevant in patients with massive abdominal injuries. These patients are at a high risk for the development of IAH from several causes: the use of bulky abdominal packs to control diffuse bleeding,  continued bleeding into the abdominal cavity from coagulopathy, edema, and thickening of the bowel wall from extensive resuscitation volumes, bowel distension, and edema from mesenteric vascular injuries or failed repairs, and closure of skin or fascia under tension. The true incidence of IAH in abdominal trauma patients has not been established, because routine bladder pressure measurements were not available in the published series of ACS. In the current series with IAP monitoring, IAH (IAP > 25 cm of H2 O) was seen in one third of the patients. It was significantly higher (52%) in patients having a primary fascial closure. Even with attempted prophylaxis by the use of an absorbable mesh at the skin or fascial level, 25% of the patients developed this complication. The incidence of IAH was also higher in patients with a greater anatomic and physiologic severity of injury. Half of the patients who had intra-abdominal packing developed IAH.
The present report also noted that the incidence and severity of MODS and death were higher in patients with IAH than in those without IAH, despite an aggressive policy of monitoring IAP and treating IAH. This finding may be related to the greater injury severity of patients who developed IAH with a contribution from a direct effect of IAH. The complications of IAH, MODS, and death, however, were less in the mesh closure group compared with the primary fascial suture group. All of these data, together with the published experience, [13-15] suggest that IAH should be predicted by the risk factors mentioned previously and that the patients should be monitored for the complication. It may also be of benefit to attempt prevention of IAH in the patient with massive abdominal injuries, coagulopathy, and abdominal packing  by rapid placement of a prosthetic mesh at the fascial (preferably) or cutaneous level. This mesh closure of the abdomen and the "open abdomen" approach offered several advantages. It provided a rapid method of abbreviating the laparotomy to reach the SICU for resuscitation. In a significant number of patients, it prevented IAH. It facilitated an expedient bedside decompression of the abdomen with the onset of IAH. When continued blood transfusion requirements and IAH suggested on-going bleeding and ineffective packing, it enabled a more efficient repacking and identification and control of surgical bleeders. Although others have suggested that approximation of skin or fascia is needed for better tamponade effect from abdominal packs,  the mesh closure approach was noted to be equally effective, as was also noted in a recent report.  As our experience with the open abdomen approach evolved, the incidence of iatrogenic bowel fistulas reduced. Careful covering of the bowel with omentum under the mesh and meticulous care in avoiding serosal tears during dressing changes are two notable precautions to avoid bowel fistulization. The loss of fascial closure by the open abdomen technique was also noted to be infrequent. Fifty percent of these patients had a successful closure of the fascia as late as 17 days after the initial laparotomy. Approximately another 25% had other reasons (presence of ostomies and the necessity for a later operation) for not attempting a fascial closure. The technique of skin flap mobilization obviated the need for skin grafting.
Our experience is very similar to the recent series from Mayberry and associates.  These authors analyzed 73 consecutive patients who had an absorbable mesh closure, 47 at the initial celiotomy (group 1) and 26 at a subsequent celiotomy (group 2). The two groups had similar injury severity but group 2 had a higher incidence of postoperative ACS (35% vs. 0%). The mesh closure, however, did not change the mortality rate in their experience. One possible explanation may be that the authors did not routinely measure bladder pressures and that abdominal decompression was used only when ACS was manifested clinically. In our experience, the most important benefit of mesh closure and IAP monitoring was prevention and an earlier diagnosis of IAH. It might have prevented the progression of IAH to the full manifestations of ACS.
ACS is a clinical syndrome characterized by increased intra-abdominal pressure, increased airway pressures, hypoxia, difficulty in ventilation, oliguria or anuria, and improvement in these parameters after abdominal decompression. [11-15] Morris et al.  defined ACS as present when the abdomen was tensely distended, peak inspiratory pressures were greater than 85 cm of H2 O on controlled mechanical ventilation or oliguria was present. Others used IAH and ACS interchangeably. [11,13]
The current experience with the routine use of IAP monitoring and gastric tonometry suggests that IAH may be an earlier phenomenon that, when persistent, may lead to the complete manifestations of ACS. In the 11 patients who had gastric tonometry and who developed IAH, the majority (72.7%) had a supranormal oxygen delivery and consumption, hyperdynamic cardiac index, normal oxygenation, normal peak inspiratory pressures, normal base deficit and lactate, and excellent urine output and renal function, despite having severe gastric mucosal acidosis (pHi < 7.3). Correction of the IAH and continued resuscitation reversed the gut mucosal acidosis and none of these responders went on to develop ACS. It is of interest that Diebel and associates  noted a similar phenomenon of IAH and gastric mucosal acidosis without the other manifestations of ACS. Other recent clinical studies [29-31] also support the concept that increased IAP may be associated with gut mucosal acidosis. Sugrue et al.  prospectively evaluated postoperative patients with IAP and pHi monitoring. Compared with patients with normal pHi, patients with a pHi < 7.32 were 11.3 times more likely to have an IAP greater than 20 mm Hg. Abnormal pHi was also associated with a poor outcome.
The present experience suggests that splanchnic hypoperfusion and gut mucosal acidosis are yet another manifestation of the adverse effects of IAH and may occur at much lower abdominal pressures than was previously recognized, long before the classic manifestations of ACS become evident. This finding may be related to the additive effects of a prior insult of hemorrhagic shock and resuscitation and the subsequent complication of IAH, as we noted in a recent swine model. In this study, in animals subjected to a hemorrhage of 20% of the circulating blood volume followed by resuscitation and then had increased IAP to 10 and 20 mm Hg, the PaO (2/FiO)2 ratios were significantly lower than in a control group of animals with elevated IAP but without prior shock and resuscitation.  It is conceivable that a similar cumulative effect may be the mechanism for the gastric mucosal acidosis that was noted in the current series. Even though the critical level of IAP in the severely injured patient with damage control treatment is unclear, a level 25 cm of H2 O should trigger careful monitoring of IAP and prompt treatment if it continues to increase. The data from Meldrum and colleagues  support this level of IAP as IAH requiring intervention. Although other well-known manifestations of ACS should trigger abdominal decompression,  IAP monitoring, measurement of pHi, and detection of gut mucosal acidosis may also provide an earlier indication for reexploration and correction of IAH.
A hypothesis, suggested by the experimental and clinical evidence from the literature and the data from the current report, is presented in Figure 1. ACS may be akin to the established compartment syndrome in the extremities. Just as muscle and nerve ischemia begins long before clinical signs such as neurovascular deficits are evident, gut mucosal ischemia may commence long before ACS is clinically recognizable. In similarity to the extremity compartment syndrome in which prompt fasciotomy may prevent a compartment syndrome, prompt relief of IAH may prevent the onset of ACS.
There are several limitations in this study, notably the absence of randomization, the potential for type I error, and the small number of patients with pHi monitoring. Larger studies, perhaps multi-institutional, incorporating the routine measurement of IAP and gut-specific monitoring, need to verify our observations.
In conclusion, IAH is frequent after major abdominal trauma, especially in patients treated by abbreviated laparotomy. A mesh fascial prosthesis (nonsuture of the fascia) at the initial celiotomy in high-risk patients may provide several advantages in addition to preventing the deleterious effects of IAH. A distinction should be made between IAH and ACS, and these conditions should be considered different stages of the pathophysiology of increased IAP. Surgical intervention should be indicated by IAH and not delayed until ACS is clinically apparent.
Dr. Jon Burch (Denver, Colorado): Dr. Ivatury and his colleagues have attempted to answer three important questions. First, what is the incidence of intra-abdominal hypertension? Second, what level of intra-abdominal hypertension requires treatment? And third, what are the implications of intra-abdominal hypertension toward the development of multiple organ failure?
The answer to the first question requires both a numerator and a denominator. The numerator is straight forward, 23, the number of patients whose intra-abdominal pressure reached 25 mm of mercury. However, the only information we are given regarding the denominator is that all patients in the study had life-threatening intra-abdominal injuries and were admitted to the ICU.
Since both these criteria are arbitrary, the incidence of 32% lacks meaning. More clearly defined inclusion criteria, such as all patients with penetrating abdominal trauma requiring operation, would yield a more meaningful incidence.
The level of intra-abdominal hypertension which requires treatment is also troubled by the study's design, since all patients whose intra-abdominal pressure reached 25 mm of mercury were decompressed, regardless of whether complications of abdominal compartment syndrome developed. Therefore, we do not know if 25 mm of mercury of intra-abdominal pressure mandates decompression.
The authors also implied that patients with intra-abdominal hypertension are more likely to develop multiple organ failure than those without. Unfortunately, risk factors for intra-abdominal hypertension and multiple organ failure were similar, if not identical. Whether intra-abdominal hypertension was a risk factor for multiple organ failure independent of other variables was not demonstrated in the present study.
While the authors have not convinced me that their primary objectives were met, they have brought two interesting issues to light. The first is the concept of prophylactic decompression. In this series, patients so treated fared better than those who were treated after intra-abdominal hypertension developed. Although I believe that patient selection may have played a role in this outcome, I certainly agree with the concept.
The second issue regards the sheer number of patients being reported in the current literature with intra-abdominal hypertension and its complications. Some have suggested that we, meaning trauma surgeons who employ these methods, have either forgotten or never learned to control hemorrhage.
This leads to my first question, which is rhetorical: Is staged or abbreviated laparotomy, which so often leads to abdominal compartment syndrome, a major advance in trauma surgery or a boondoggle?
The second question concerns the use of Vicryl mesh for abdominal decompression. Many centers have employed the use of opened and sterilized IV bags for this purpose, which cost nothing and are universally available. What are the possible advantages of Vicryl mesh over IV bags?
The last question concerns the patient with an open abdomen whose colonic suture line failed. From experience with exteriorized colonic repairs, we have learned that suture lines created in a hostile environment often fail. Will the authors continue to perform primary colonic repairs in patients who require mesh abdominal closure?
Dr. Harvey J. Sugerman (Richmond, Virginia): It is exciting to see this report of gastric mucosal pHi in a trauma population with a high incidence of acute abdominal compartment syndrome. Of 70 severely traumatized patients who underwent bladder pressure monitoring, 42 had pHi measured, and of these, 11 had intra-abdominal hypertension, of whom eight had acidic pHi. We have found that intra-abdominal hypertension may be acute, as in these trauma patients, or chronic, as seen in the morbidly obese, possibly subacute as in toxemia pregnancy, or acute on chronic as in a morbidly obese patient with peritonitis.
In a paper which we published in 1997 in the Journal of Internal Medicine, of 84 severely obese patients undergoing gastric bypass surgery, the mean bladder pressure was 18 +/- 0.7 [micro sign]m of H2 O, with a range of 12 to 42, in contrast to a nonobese group with a mean bladder pressure of > +/- 1.6 [micro sign]m of H2 O. Thirty of the obese patients had a bladder pressure >or=to 20 [micro sign]m of H2 O, 11 >or=to 25, 4 >or=to 30, and one > 40.
Thus, were your three patients without an acidic pHi and with intra-abdominal hypertension based upon bladder pressure measurements in either severely obese or cirrhotics with ascites? One needs to consider these data before taking a patient back to the operating room for a bladder pressure greater than 25 [micro sign]m H (2) O. You need the whole gestalt to make the diagnosis of the acute abdominal compartment syndrome: decreased urine output, increased peak inspiratory pressures, decreased gas exchange, and perhaps now, a decreased pHi. Thank you.
Dr. Michael Sugrue (Liverpool, Australia): Could I ask Dr. Ivatury, conceptually, can he explain to me the role of a pack in abandoning surgery, and if you are using a pack to tamponade, how can you actually conceptually support the concept of then leaving the abdomen decompressed?
My second question is, in terms of those eight patients who had improvement, six of the eight who had the improvements in their pHi, did they have some intra-abdominal procedure performed at the time that might have contributed to their improvement in intra-gastric mucosal pH? Thank you.
Dr. Kazuyoshi Kato (Chiba, Japan): Dr. Ivatury, could you give me an idea about high-risk patients which is also adaptable to the blunt trauma victims people? Thank you.
Dr. Gerard J. Fulda (Newark, Delaware): Two quick questions for Dr. Ivatury. One: can you elucidate for us the indications for bladder measurement?
The second question relates to the development of organ failure. It may be that we are trading off early mortality from acute hemorrhage with damage control for later mortalities from multiple organ failure. My question revolves around the timing of decompression. If you have packed a patient for damage control purposes, you may have an expectation that there is elevated abdominal pressure. Exactly when do you time the reexploration? And have you looked at the timing of reexploration with respect to the development of organ failure?
Dr. John A. Morris, Jr. (Nashville, Tennessee): Dr. Ivatury, I rise to give you one warning from experience. We found that our fistula rate patients managed with the open abdominal technique is in excess of 10%. It is a very complex complication to deal with in these patients, and I think as you get a larger series, you will find that that becomes problematic.
Dr. Susan M. Briggs (Boston, Massachusetts): I compliment you on an excellent paper. I was interested, too, in your large number of 24 patients that required packing as well as the mesh. Did you see increased blood volume requirements in this group, presumably ongoing hemorrhage, versus those who had mesh for distended bowel alone? Thank you.
Dr. Rao Ivatury (closing): I would like to thank the discussants for their interesting comments, especially Dr. Jon Burch, who has been a pioneer in this area.
I agree with you that we have not answered all the questions, but this is one of the first reports that looked at routine bladder pressure measurements, and I think we certainly need some more data before we exactly say that the incidence is so high.
We only looked at the really severely injured trauma patients. We did not want to do a random study on all trauma patients undergoing laparotomy, which would be meaningless. All moderately to severely injured patients who reached the intensive care unit, we looked at in terms of intra-abdominal hypertension.
In terms of the selection of mesh, it does not matter what mesh you use. We happen to like the Vicryl because it is nonporous; it does not create any problems in terms of fistula, etcetera. Whatever mesh you use, that is your choice. The same principles can be applied.
Colonic repair remains a problem, and we do not recommend that you do a colonic anastomosis. If you do have a colonic repair or an anastomosis in the open abdomen, I think you should make sure that it is not just underneath the mesh, because the incidence of leak is very high in those circumstances.
Dr. Sugerman, thank you for your comments. We follow your data on morbidly obese patients with great interest. We would submit that to wait for all the manifestations of abdominal compartment syndrome and not decompress this abdomen is a little bit late, and we think that the earlier you decompress the better return of physiology you will have in these patients.
Regarding the questions about packing, these patients who had packing had a lot of vascular injuries and deteriorating quite rapidly at that time, so they did require packing. I would submit to you that the presence of a pack does not necessarily indicate that the pressures in the abdomen are high. It may be one of the causes of intra-abdominal hypertension, but we certainly had patients who were packed and who had normal abdominal pressures.
This is a good time to answer Dr. Briggs' question, because it has been said in the past that if you have packing, you must close the abdomen tight for a good tamponade effect. We found that that is just not true. Even when you close the mesh with the packing inside, it does create some tamponade effect and control your abnormal bleeding from your liver and splenic lacerations.
Definition of a high-risk patient? Any patient who is undergoing an abbreviated laparotomy, multiple transfusions, major vascular injuries who continue to be hypothermic, acidotic, and coagulopathic intraoperatively. In other words, any patient you would consider doing a damage control procedure should be a candidate for mesh closure and monitoring of intra-abdominal pressures.
Dr. Fulda raised an interesting question. We did not find any correlation with the timing of reexploration. It usually happens up to about 24 to 48 hours when the pressure has started going up. I am sorry I missed your other question.
Dr. Morris, interestingly, our experience now with the open abdomen is in excess of 200 patients, and actually just as Dr. Fabian reported last year, the incidence of fistula rate has gone down in our hands. And in these 70 patients, our incidence of fistula rate is about 1 to 2%.
I agree you should take extreme caution to prevent these fistulas by laying the omentum underneath the mesh and taking extreme care in terms of dressing changes not to cause any serosal tears. Once you have a serosal tear in this open abdomen, they will fistulize eventually.
I thank you again for the interest in the paper and thank the Associations for the privilege of this presentation. Thank you.
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