Ali, S. Z., B. D. Freeman, et al. (2003). "Abdominal compartment syndrome in a patient resulting from pneumothorax." Intensive Care Med 29(9): 1614.

BACKGROUND: It is recommended that patients with impending abdominal compartment syndrome (ACS) should be volume loaded to insure the adequate preload. We evaluated our prospective resuscitation database to determine how patients who developed ACS differ from non-ACS patients in response to early volume loading. METHODS: Over 36 months, 152 consecutive high-risk patients were resuscitated by a standard intensive care unit (ICU) protocol that escalates interventions in nonresponders. Interventions, responses, and outcomes are prospectively collected and the characteristics of ACS and non-ACS patients were compared. RESULTS: Twenty-three patients (15%) developed ACS and were decompressed 8 +/- 1 hours after ICU admission. The ACS and non-ACS patients had similar demographics and injury severity. The severity of pre-ICU shock tended to be greater in the ACS patients. During the first 8 hours of ICU resuscitation, patients who developed ACS received more blood transfusions (11 +/- 2 versus 2 +/- 0.2 units; P<0.05) and crystalloids (13 +/- 2 versus 4 +/- 0.3 L; P<0.05). As a result, pulmonary capillary wedge pressure increased more in the ACS patients (20 +/- 1.5 versus 15 +/- 0.5 mm Hg; P<0.05), but comparatively the cardiac index did not (3.2 +/- 0.2 versus 4.2 +/- 0.1 L/min/m(2); P<0.05) and the ACS patients developed pathologic elevations of gastric regional CO(2) pressures (70 +/- 7 versus 48 +/- 1 mm Hg P<0.05). CONCLUSIONS: Conventional preload directed resuscitation to enhance cardiac function is not effective in patients with impending ACS, and this traditional resuscitation strategy is detrimental in this subgroup of patients.

HYPOTHESIS: Normal resuscitation (oxygen delivery index [DO2I] >/=500 mL/min per square meter), compared with supranormal trauma resuscitation (DO2I >/=600 mL/min per square meter), requires less crystalloid volume, thus decreasing the incidence of intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS). DESIGN: Retrospective analysis of a prospective database. SETTING: Twenty-bed intensive care unit (ICU) in a regional level I trauma center. PATIENTS: Patients with major trauma (injury severity score >15, initial base deficit >/=6 mEq/L, or need for >/=6 units of packed red blood cells in the first 12 hours) or age 65 years or older with any 2 of the previous criteria. INTERVENTIONS: Shock/trauma resuscitation protocol: pulmonary artery catheter, gastric tonometry, urinary bladder pressure measurements, lactated Ringer infusion, packed red blood cell transfusion, and moderate inotrope support, as needed, in that sequence, to attain and maintain a DO2I greater than or equal to 600 mL/min per m2 (16 months, ending January 1, 2001, n = 85) or a DO2I greater than or equal to 500 mL/min per square meter (16 months, starting January 1, 2001, n = 71) for the first 24 hours in the ICU.Main Outcome Measures: Lactated Ringer infusion volume (liters) at ICU admission, gastric partial carbon dioxide minus end-tidal carbon dioxide(GAPCO2), IAH (urinary bladder pressure measurements >20 mm Hg), ACS (urinary bladder pressure measurements >25 mm Hg with organ dysfunction), multiple organ failure, and mortality. RESULTS: Demographics, injury severity, and shock severity parameters were similar in both groups. The supranormal resuscitation group required more lactated Ringer infusion volume in the first 24 hours in the ICU (mean +/- SD, 13 +/- 2 vs 7 +/- 1 L; P<.05) and had higher GAPCO2 (16 +/- 2 vs 7 +/- 1 mm Hg; P<.05). In the supranormal group, IAH (42% vs 20%; P<.05) and ACS (16% vs 8%; P<.05) were more frequent. The conventional trauma outcomes, such as multiple organ failure (22% vs 9%; P<.05) and mortality (27% vs 11%; P<.05) were less favorable in the supranormal resuscitation group. CONCLUSION: Supranormal resuscitation, compared with normal resuscitation, was associated with more lactated Ringer infusion, decreased intestinal perfusion (higher GAPCO2), and an increased incidence of IAH, ACS, multiple organ failure, and death.

Abdominal compartment syndrome (ACS) has emerged to be a significant problem in patients who develop postinjury multiple organ failure (MOF). Current laboratory research suggests that ACS could be a second hit for the development of MOF. Recent studies demonstrate that ACS is an independent predictor of MOF and that the prevention of ACS decreases the incidence of MOF. The Trauma Research Centers at the University of Colorado and the University of Texas-Houston Medical School are focused on defining the role of the gut in postinjury MOF. Because ACS is a plausible modifiable risk factor, our interest has been to 1) describe the epidemiology of ACS, 2) build prediction models, 3) provide strategies for prevention and treatment of ACS, and 4) develop relevant laboratory models. This review summarizes our findings.

BACKGROUND: Primary abdominal compartment syndrome (ACS) is a known complication of damage control. Recently secondary ACS has been reported in patients without abdominal injury who require aggressive resuscitation. The purpose of this study was to compare the epidemiology of primary and secondary ACS and develop early prediction models in a high-risk cohort who were treated in a similar fashion. METHODS: Major torso trauma patients underwent standardized resuscitation and had prospective data collected including occurrence of ACS, demographics, ISS, urinary bladder pressure, gastric tonometry (GAP(CO2) = gastric regional CO(2) minus end tidal CO(2)), laboratory, respiratory, and hemodynamic data. With primary and secondary ACS as endpoints, variables were tested by uni- and multivariate logistic analysis (MLA). RESULTS: From 188 study patients during the 44-month period, 26 (14%) developed ACS-11 (6%) were primary ACS and 15 (8%) secondary ACS. Primary and secondary ACS had similar demographics, shock, and injury severity. Significant univariate differences included: time to decompression from ICU admit (600 +/- 112 vs. 360 +/- 48 min), Emergency Department (ED) crystalloid (4 +/- 1 vs. 7 +/- 1 L), preICU crystalloid (8 +/- 1 vs. 12 +/- 1L), ED blood administration (2 +/- 1 vs. 6 +/- 1 U), GAP(CO2) (24 +/- 3 vs. 36 +/- 3 mmHg), requiring pelvic embolization (9 vs. 47%), and emergency operation (82% vs. 40%). Early predictors identified by MLA of primary ACS included hemoglobin concentration, GAP(CO2), temperature, and base deficit; and for secondary ACS they included crystalloid, urinary output, and GAP(CO2). The areas under the receiver-operator characteristic curves calculated upon ICU admission are primary= 0.977 and secondary= 0.983. Primary and secondary ACS patients had similar poor outcomes compared with nonACS patients including ventilator days (primary= 13 +/- 3 vs. secondary= 14 +/- 3 vs. nonACS = 8 +/- 2), multiple organ failure (55% vs. 53% vs. 12%), and mortality (64% vs. 53% vs. 17%). CONCLUSION: Primary and secondary ACS have similar demographics, injury severity, time to decompression from hospital admit, and bad outcome. 2 degrees ACS is an earlier ICU event preceded by more crystalloid administration. With appropriate monitoring both could be accurately predicted upon ICU admission.

The abdominal compartment syndrome results from gradual increase of intra-abdominal pressure and affects many bodily systems. It is usually associated with abdominal trauma or surgery. We report the first case of this syndrome developing after a penetrating wound to the chest and heart.

HYPOTHESIS: Intra-abdominal hypertension frequently threatens renal function early after orthotopic liver transplantation (OLT). DESIGN: A prospective study of consecutive patients who underwent OLT. SETTING: The intensive care unit of a National Health Service teaching hospital. PATIENTS AND MAIN OUTCOME MEASURES: The intra-abdominal pressure (IAP) of 108 consecutive patients who underwent OLT was postoperatively measured 3 times a day for 72 hours using the urinary bladder technique. Intra-abdominal hypertension was defined as an IAP of 25 mm Hg or higher. RESULTS: Thirty-four patients (31%) had a high IAP. Acute renal failure developed in 17 recipients (16%), 11 (65%) of whom had intra-abdominal hypertension (P<.01), with a mean +/- SD IAP of 27.9 +/- 9.9 mm Hg vs 18.6 +/- 5.2 mm Hg in those without acute renal failure (P<.001). The subjects with a high IAP were more frequently administered loop diuretics to maintain adequate diuresis (P<.001) and had a low mean arterial pressure on the day of surgery (P<.01), despite the fact that they were given more intravenous fluids (P<.01) and did not differ in the need for inotropic drugs. Logistic regression analysis showed that intraoperative transfusions of more than 15 U, respiratory failure, and intra-abdominal hypertension (P<.01) were independent risk factors for renal failure. The length of intensive care unit stay was similar in the patients with a normal and a high IAP, but mortality was higher among the latter (P =.02). CONCLUSIONS: Intra-abdominal hypertension is common after OLT and is significantly associated with renal failure, reduced urinary output, and intensive care unit mortality. It is, therefore, worth monitoring IAP in those undergoing OLT.

OBJECTIVE: No data are available on the incidence and clinical relevance of increased intra-abdominal pressure after orthotopic liver transplantation. This study assessed abdominal hypertension in a population of transplanted patients as this may be an important cofactor in early postoperative complications. DESIGN AND SETTING: Prospective clinical study in an intensive care unit of a national health system teaching hospital PATIENTS AND MEASUREMENTS: Abdominal pressure was measured every 6 h using the urinary bladder method and was considered elevated when it was 25 mmHg or higher. Hemodynamic status was evaluated at the same times. Renal function was assessed on the basis of hourly urinary output by calculating serum creatinine on postoperative days 2 and 4 and the filtration gradient; patient outcomes were also considered. RESULTS: Intra-abdominal hypertension was observed in 32% of cases; the subjects with high abdominal pressure had significantly lower mean artery pressure values but did not differ in terms of central venous pressure or cardiac output. High intra-abdominal pressure was more frequently associated with renal failure, a lower filtration gradient, delayed postsurgical weaning from ventilation, and a worse outcome. CONCLUSIONS: Abdominal hypertension is frequent after liver transplantation and may be associated with a complicated post-operative course.

OBJECTIVE: To observe different degrees of intra-abdominal pressure and different duration on the intestinal permeability and endotoxin/bacteria translocation in rabbit model, so as to explore the mechanism of the development of abdominal compartment syndrome (ACS) and MODS. METHODS: Rabbit model of intra-abdominal hypertension was established by injection of gaseous nitrogen into the peritoneal cavity. Thirty-nine New Zealand white rabbits were employed in the study. The change in intestinal permeability was determined by fluorescein isothiocyanate dextran (FITC-D) and two kinds of molecular probes of type II horseradish peroxidase (HRP-II). The effects of intra-abdominal hypertension on the endotoxin/bacteria translocation were also detected. RESULTS: The contents of FITC-D and HRP-II in portal veins increased evidently (P < 0.01) when intra-abdominal pressure (IAP) was higher than 20 mmHg. The endotoxin (ET) content in portal vein in rabbits with IAP of 10 mmHg for 1, 2 and 4 hours exhibited no difference compared with that in normal control, while the ET content increased obviously after 1 hour with IAP of 20 mmHg and increased thereafter along with the prolongation of IAP, and increase in pressure. The bacterial translocation rates were 33.3%, 66.7% and 100% when IAP was maintained at 20 mmHg for 1, 2 and 4 hours, respectively, and there was evidence of bacterial translocation to the liver. The rate of bacterial translocation to intestinal mesenteric lymph nodes was 100% when IAP was 30 mmHg for 1 and 2 hours. There was no bacterial translocation to the spleen in all experimental rabbits. CONCLUSION: Intestinal mucosal permeability increased significantly with increased endotoxin content in portal vein when IAP was higher than 20 mmHg. At the sane time, the bacteria could be translocate to intestinal mesenteric lymph nodes and liver, which might be constitute one of the important factors leading to the development of ACS and MODS.

OBJECTIVE. To study the effects of noninvasive positive pressure ventilation (NIPPV) on intra-abdominal pressure. DESIGN AND SETTING. Single case report from a tertiary teaching hospital. PATIENTS AND METHODS. A 65-year-old man who experienced a sudden respiratory and cardiovascular collapse during NIPPV. This was caused by gastric overdistension due to aerophagia followed by raised intra-abdominal pressure leading to intra-abdominal hypertension and abdominal compartment syndrome. RESULTS. The respiratory and cardiovascular problems resolved immediately after the introduction of a nasogastric tube. This resulted in normalization of IAP. CONCLUSIONS. This is the first case reported of an abdominal compartment syndrome related to NIPPV. Clinicians should be aware of this possible complication while using NIPPV.

Incisional hernia represents the most common wound complication after abdominal surgery. The repair of large incisional hernias requires an accurate knowledge of the interactions between the tissues of the abdominal wall, the prosthetic materials and the bowel. At the same time a careful attention must be placed on the physiopathology of abdominal hypertension. Repair of giant incisional hernias with heavy loss of substance may take to a sudden increase of intra-abdominal pressure and, sometimes, to Abdominal Compartment Syndrome (ACS). The aim of preventing recurrences very often requires the use of a prosthesis, which must be placed on a low-tension environment to avoid early failures and excessive increase of intra-abdominal pressure. It is also necessary to employ as much parietal tissues as possible to prevent visceral adhesions and lesions and to pay attention to an appropriate employment of prosthesis. Utilization of composite materials, absorbable prosthesis or of combinations of mesh and flaps looks promising in preventing endoabdominal hypertension without increasing the rate of recurrences, infections and adhesive complications.

INTRODUCTION: Abdominal compartment syndrome (ACS) is an entity that represents a latent problem in the patient subjected to laparotomy. OBJECTIVE: To evaluate the effectiveness of decompressive treatment of ACS. MATERIAL AND METHODS: We studied patients subjected to decompressive treatment for diagnosis of SCA from May 1 to November 30, 2001 prospectively. We evaluated intraabdominal pressure (IAP), peak pressure of air way (J)PVA), oxygen available index (OAi), ventilation-perfussion index and uresis, before, after, and at 48 h of decompressive surgery. The data were treated statistically with paired student t test taking as significant p < 0.05 using percentages for qualitative variables and average with standard deviation for quantitative variables. RESULTS: We included 10 patients; three died (30%). Alone it VP & it descended significantly after compression (1 > < 0.05). Uresis, PPVA, OlA and VPI were carried out 48 h of decompressive surgery. CONCLUSIONS: Decompressive treatment is effective in ACS, showing immediate decreased of IAP and improvement of the hemodynamic variables after 48 h post-surgery.

BACKGROUND: Intra-abdominal hypertension (IAH) has been recognized as a source of morbidity and mortality in the injured patient. Research concerning this entity has focused predominantly on the pathophysiology. We developed a model of IAH to determine whether gene expression is altered in the presence of this condition. METHODS: Using general anesthesia, adult Sprague-Dawley rats were intubated and instrumented with a carotid and jugular catheter. Three pairs of rats (three control; three IAH 25 mm Hg) were used at each time interval. Continuous measurements of heart rate, blood pressure, cardiac output, and temperature were recorded. Arterial blood gases were measured every 30 minutes. A catheter was placed in the peritoneum and warm saline was infused up to a pressure of 25 mm Hg that was measured through this catheter continuously. At 30 and 60 minutes, the kidneys were harvested and standard protocols were used to extract nucleic acid and perform cDNA microarray analysis screening for 4,000 genes. Each experimental rat was paired with a control rat and each set underwent individual cDNA array analysis. RESULTS: Hemodynamic changes occurred that were consistent with IAH, including depression of cardiac output and acidosis. Although widespread changes in gene expression were identified, only genes that were up-regulated and down-regulated by a ratio of fivefold, a difference in magnitude of 150 molecular dynamic counts, and p < 0.05 were considered significant. When comparing IAH of 25 mm Hg at 30 and 60 minutes, there was a surprising decrease in up-regulated genes from 10 to 1. In addition, there was an increase in down-regulated genes from zero to five genes. CONCLUSION: IAH causes changes in gene up- and down-regulation in the kidney. The number and types of genes change in magnitude and type over time. Further investigation into renal gene expression may offer insight into the molecular pathophysiology of IAH.

BACKGROUND: Management of blunt liver injury is predominantly nonoperative. However, complications occur in 10% to 25% of patients, with half taking place more than 24 hours after injury. Few reports have addressed the management of the new pattern of these delayed complications, which is the objective of this study. METHODS: Adult patients admitted to our level one trauma center from 1995 to 2000 with blunt liver injury were identified. Demographic, physiologic and laboratory data, computed tomography (CT) and operative findings, and complications were reviewed. RESULTS: Blunt liver injury was identified in 192 patients. Thirty-nine patients (20%) underwent immediate celiotomy. The remaining 153 patients were initially managed nonoperatively. Liver-related complications developed in 19 (12%) patients. Fifteen patients underwent delayed celiotomy to treat secondary inflammatory processes, from bile leak (6), hemorrhage (5), and hepatic abscess (1), and to treat abdominal compartment syndrome (2), and decompress hepatic compartment syndrome (1). Although no deaths or complications were directly caused by delayed celiotomy, 2 deaths (11%), occurring early in this series, were attributed to liver-related complications. CONCLUSIONS: These complications, occurring in 12% of patients with liver injuries, may be a consequence of initial nonoperative management. Although these findings do not negate nonoperative management of blunt liver injury, this approach can be hazardous and requires diligence to recognize and treat delayed and potentially fatal complications.

INTRODUCTION: Detensive laparotomy is the first choice treatment for abdominal compartment syndrome (ACS). Tension free closure of the abdominal wall with the use of prosthesis is a broadly diffused technique; the polypropylene and the ePTFE (expanded polytetrafluoroethylene--Goretex Dual Mesh) are the most commonly used materials. MATERIALS AND METHODS: We report our experience on five patients affected by ACS submitted to detensive laparotomy and positioning of a wide Goretex Dual Mesh prosthesis. RESULTS: In our initial experience ACS has been treated with success through detensive laparotomy and there were no complications related to the use of Goretex. DISCUSSION: Even though limited, our initial clinical experience is favorable to the use of Goretex Dual Mesh as first choice material for reconstruction of the abdominal wall after detensive laparotomy for ACS.

Decompressive celiotomy for the treatment of abdominal compartment syndrome (ACS) often results in wounds that are difficult to close. These complicated wounds are frequently managed with a 3-staged surgical approach employing a planned ventral hernia. The authors describe an alternative closure with a single operation using a commercially available human acellular dermis (HACD) as a fascial substitute. Soft tissue coverage is obtained at the same operation by means of bilateral bipedicle flaps. The cohort consisted of 9 patients, ages 19 to 77 years old. On average patients were closed on the ninth postoperative day (range, 3 to 30 days) and were discharged from the trauma center on average 8 days (range, 5 to 29 days) after the abdominal closure. Complications developed in 3 (33%) patients. These complications included a flap hematoma, wound infection, and recurrent hernia. There were no postoperative fistulas. This procedure allows for early, single-staged closure of the abdomen after abdominal compartment syndrome. Once closed, patients were able to be discharged from the hospital early and without need for specialized wound care. Further investigation on the usefulness of this technique is required.

We report a rare case in which abdominal compartment syndrome resulting from venous hemorrhaging developed in a patient with stable pelvic fractures, resulting in a fatal outcome. An 84-year-old man with mild pelvic fractures developed hypovolemic shock and underwent transcatheter arterial embolization. He became hemodynamically stable after the procedure, but became hypotensive for the second time 11 h after admission. Urinary bladder pressure rose to 32 mmHg from 4-7 mmHg. Rebleeding from the pelvis with the development of abdominal compartment syndrome was suspected. Repeated transcatheter arterial embolization and laparotomy were performed; however, 1 min into the procedure, both pupils symmetrically dilated and the light reflex disappeared. This case suggests that brain death can sometimes occur due to abdominal compartment syndrome.

PURPOSE: The aim of this study was to assess the effectiveness of gravity reduction of the intestines in newborns with gastroschisis. METHODS: Throughout the calendar year 2001, all newborns with gastroschisis were prospectively treated by means of an established clinical pathway protocol. Silon insertion and all subsequent therapies were performed in the neonatal intensive care unit (NICU) No physical compression of the bowel nor stretching of the abdominal wall was done, and bowel reduction was entirely passive, accomplished by the force of gravity. Demographic data along with time to abdominal wall closure, ileus resolution, and cessation of total parenteral nutrition (TPN) all were recorded. RESULTS: Sixteen babies were treated using the established pathway without prenatal selection or postnatal rejection. There were 10 boys and 6 girls. The mean maternal age was 18.5 years. Seventy-five percent of the mothers were Hispanics. Mean time to Silon removal was 5.5 days, initiation of enteric feeding was 16 days and TPN cessation 23 days. There were no significant complications in this group nor was there any mortality. CONCLUSIONS: Gravity reduction of the intestines in babies with gastroschisis is most gentle and effective. Blood flow compromise, mechanical injuries of the exposed bowel, or abdominal compartment syndrome thus were averted. The outcome analysis favorably compares this method with reported series.

Acutely increased intra-abdominal pressure (IAP) may lead to abdominal compartment syndrome (ACS), which ischaemia/reperfusion (I/R) injury plays an important role. The main goal of the management of ACS is to lower the intra-abdominal pressure despite reperfusion injury. Octreotide (OCT), a synthetic somatostatin analogue, lowers the splanchnic perfusion. The aim of this study was to investigate whether OCT improves the reperfusion injury after decompression of acute abdominal hypertension.Under anesthesia, a catheter was inserted intraperitoneally and using an aneroid manometer connected to the catheter, IAP was kept at 20mmHg (ischemia group; I) for 1h. In the I/R group, pressure applied for an hour was decompressed and 1h reperfusion period was allowed. In another group of I/R, OCT was administered (50microg/kg i.p.) immediately before the decompression of IAP. The results demonstrate that kidney and lung tissues of malondialdehyde (MDA; an end product of lipid peroxidation) levels and myeloperoxidase (MPO; index of tissue neutrophil infiltration) activity were elevated, while glutathione (GSH; a key to antioxidant) levels were reduced in I/R group (P<0.001). Moreover, OCT treatment applied in the I/R group reduced the elevations in blood urea nitrogen (BUN) and serum creatinine levels. Our results implicate that IAP causes oxidative organ damage and OCT, by reducing splanchnic perfusion and controlling the reperfusion of abdominal organs, could improve the reperfusion-induced oxidative damage. Therefore, its therapeutic role as a "reperfusion injury-limiting" agent must be further elucidated in IAP-induced abdominal organ injury.

Abdominal compartment syndrome may occur after any elective or emergent abdominal operations that are complicated by postoperative hemorrhage or in the trauma patient who has massive fluid replacement for intra-abdominal bleeding. Once the abdomen is decompressed the type of closure varies as much as the surgeon performing the procedure. We have devised a simple, reproducible, inexpensive, and safe method to close the abdomen at the bedside. Serial abdominal closure (SAC) was performed on three patients 45, 54, and 14 years of age who had developed abdominal compartment syndrome secondary to an upper gastrointestinal bleed requiring massive transfusion, a tear of the superior mesenteric vein, and a grade 4 liver laceration respectively, all necessitating abdominal decompression. All three patients had their abdominal wounds closed at the bedside over the course of several days with our SAC technique. Subsequent postoperative course was uneventful and the abdominal wall was free of defects at one-year follow-up. SAC is an efficient, inexpensive, and easily reproducible method of managing the open abdomen. The use of SAC prevented abdominal closure-related complications such as enteric fistula and hernia formation in our three patients.

The Abdominal Compartment Syndrome (ACS) is a clinical entity, which can be defined as the adverse physiologic consequences that occur as a result of a severe increase in intra-abdominal pressure (IAP) ( ), and is characterized by cardiovascular, pulmonary, renal, splanchnic, and intra-cranial disturbances regardless of the cause. The level of IAP at which ACS occurs is not known in children, therefore we suggest that the clinical signs of tensely distended abdomen, inability to palpate the femoral pulses, cyanosis of the lower extremities, progressive oliguria and hypoxia due to increasing airway pressures are sufficient to justify abdominal decompression. We report three cases of ACS and review the management of this condition.

OBJECTIVE: Since the introduction of a preformed silo to the authors' practice in 1997, there has been a decrease in primary closure of gastroschisis. To clarify the impact of this change, the authors reviewed their results over the past 10 years. METHODS: From patient records, the authors abstracted the closure method, mechanical ventilation days, time to full feeds, mechanical and infectious complications, and length of stay. The authors compared groups using the Student t test and the Mann-Whitney test, as appropriate. RESULTS: Between 1993 and the present, 124 patients were identified. Between 1993 and 1997, 38 children presented with gastroschisis. Thirty-two (84.2%) closures were primary and six (18.8%) were staged. After 1997, the authors treated 80 children with gastroschisis. There were 27 (33.8%) primary and 53 (66.2%) staged closures. Six patients with other lethal anomalies were excluded. Length of stay and ventilator days were higher for the staged closure group, but infection and mechanical complications were less common in the staged closure group. The time to full feeds did not differ. CONCLUSIONS: A lower incidence of infection and complications related to abdominal compartment syndrome has made staged closure of gastroschisis more common in the authors' practice. While it has resulted in a longer hospital stay, staged closure decreases the risk of long-term bowel dysfunction and need for reoperation.

Since hepatorenal syndrome is a functional renal failure due to renal ischemia in cirrhotics with refractory ascites, we investigated whether increased intra-abdominal pressure (IAP) impairs the renal function and perfusion in cirrhotic portal hypertensive rats. Eight groups of 32 rats each were studied, including 4 control and 4 CCl(4) cirrhotic groups. These were subdivided into two groups each, with and without an increased IAP, and further subdivided into groups of rats with and without NO inhibition. IAP was increased to 20 mm Hg for 7 consecutive days by means of an intraperitoneally placed balloon filled with water. The animals were studied in normal conditions and after inhibition of NO synthesis. Changes in mean arterial pressure and renal microcirculation by means of femoral artery catheterization and laser-Doppler technique, respectively, were recorded. Venous samples for determination of plasma renin-aldosterone activity, biochemical parameters of liver and renal function, and plasma nitrite/nitrate levels as an index of NO synthesis were drawn. Cirrhotic rats showed decreased renal microcirculation (P = 0.05), while elevated IAP produced a further decrease (P = 0.01). Renin-aldosterone levels found increased (P = 0.001) in cirrhotics, and elevated IAP produced a further increase (P = 0.01] in both groups. Inhibition of NO synthesis resulted in a nonsignificant decrease in both renal microcirculation and renin-aldosterone levels in all experimental groups. Liver and renal function was found to be impaired in cirrhotics, but increased IAP had a nonsignificant further functional impairment in both organs. In conclusion, chronically elevated IAP in cirrhotic rats is associated with an increase in renin-aldosterone levels and significant impairment of renal perfusion.

AIM: Oliguria is seen during elevated intraperitoneal pressure, but the physiological mechanisms are not yet clarified. The purpose of the present study was to investigate the changes in renal function, cardiac output and distribution of systemic blood flow (BF) that occur in connection with an elevation of intra-abdominal pressure (IAP) in a rat model by isotope-labelled microsphere technique. METHODS: A 5 or 10 mmHg IAP was created by CO2 insufflation and maintained for 90 min in anaesthetized and mechanically ventilated rats. Rats with normal IAP served as controls. Blood flow and cardiac output measurements by injection of isotope-labelled microspheres were conducted at three time points. Acid-base balance, urine output, glomerular filtration rate (GFR) and urinary excretion products were also followed. RESULTS: Glomerular filtration rate decreased [0.7-0.1 mL min(-1) g(-1) kidney weight (KW)] with elevated IAP, as did urine output (8.5-0.6 microL min(-1) g(-1) KW). Dramatic decreases were seen in renal excretion of sodium (by 97%), potassium (by 94%) and osmotic active substances (by 93%). Cardiac output was diminished by 54% at 5 mmHg and by 65% at 10 mmHg intraperitoneal pressure and systemic vascular resistance (SVR) was elevated threefold. CONCLUSION: Cardiac output, measured by microsphere technique, decreased during elevated intraperitoneal pressure by CO2 in anaesthetized rats, while SVR was elevated and renal excretory functions were decreased to a large extent.

BACKGROUND: The effects of increased intra-abdominal pressure (IAP) and volume expansion on renal function in the rat were studied to gain more knowledge of the oliguria seen during laparoscopic procedures and to reduce the detrimental renal effects of IAP. METHODS: IAP was elevated to 5 or 10 mmHg by insufflation of CO(2) and maintained for 2 h in anaesthetized and mechanically ventilated rats. Rats with normal IAP served as controls. An angiotensin II receptor I antagonist, candesartan, was given as a bolus injection and a 5% volume expansion was achieved by i.v. saline infusion. An angiotensin-converting enzyme (ACE) inhibitor was also given. Renal parameters were the glomerular filtration rate (GFR), urine production, the urinary concentrations of sodium and potassium and the osmolality in the urine. The arterial acid-base balance and blood pressure were also monitored. RESULTS: The GFR deteriorated by 70% during pneumoperitoneum (PP) of 10 mmHg. There was a dramatic drop in sodium excretion (88-97%). With candesartan and elevated IAP, there was a drop in mean arterial pressure (from 90 to 55 mmHg) and the negative renal effects were very pronounced. Renal function was better preserved during elevated IAP in combination with volume expansion. CONCLUSIONS: Capnoperitoneum suppresses renal function, especially in combination with angiotensin II receptor 1 blockade and ACE inhibition. Volume expansion reduces the deleterious effects of PP on renal function during elevated IAP. The results suggest that patients should not be given pharmaceuticals blocking the renin-angiotensin-aldosterone system prior to procedures that may increase IAP. It may be beneficial, however, to reduce angiotensin II tension by volume expansion.

BACKGROUND: multi-organ failure is a leading cause of death following aneurysm surgery, especially in the emergency setting. Intra-abdominal hypertension is an important factor in the development of multi-organ failure. Prevention, early recognition and prompt treatment of abdominal hypertension and the abdominal compartment syndrome may reduce mortality following aneurysm surgery. METHODS: a descriptive review of the literature from a Medline search. RESULTS AND CONCLUSIONS: the abdominal compartment syndrome is the result of diverse physiological effects caused by increased intra-abdominal pressure. The syndrome has been most widely described in trauma victims, but occurs in patients following aortic surgery, particularly following ruptured aneurysm repair. Preventative therapy should be instituted to minimise its development in patients at risk, and monitoring of intra-abdominal pressure may allow prompt treatment of this condition.

Ileus refers to the partial or complete blockage of the small and/or large intestine either by functional (adynamic or paralytic ileus) or mechanical bowel obstruction. The diffuse gastrointestinal dysmotility during functional and mechanical ileus may result in intestinal dilatation, increased luminal pressure and gut wall ischaemia which may lead to increased intra-abdominal pressure (IAP). Any type of ileus may promote abdominal fluid sequestration with severe systemic hypovolaemia, intestinal bacterial overgrowth with the evolution of bacterial translocation and systemic invasive infections and inflammation of the intestinal wall with concomitant release of cytokines and the development of the systemic inflammatory response syndrome. The most serious complications of ileus are mediated by an increase in IAP. Intra-abdominal hypertension has been found in up to 20% of critically ill patients and may lead to a broad pattern of systemic consequences with multiple organ dysfunction, including cardiovascular, hepatic, pulmonary, renal and neurological function. The abdominal compartment syndrome is an emergency condition which is defined as elevation of IAP above 20 to 25 mmHg and the presence of systemic consequences. Therapeutic considerations include the maintenance of adequate hydration status, avoidance of drugs known to impair intestinal perfusion, stimulation of gastric and intestinal motility and various nutritional aspects. Colonic tube placement after decompressive colonoscopy may be effective in reducing intestinal dilatation. In the abdominal compartment syndrome the 'open abdominal approach' with decompressive laparotomy by opening the peritoneal cavity and temporary abdominal closure is the therapy of choice.

BACKGROUND: Severely injured patients have been observed to acutely develop ascites; however, the pathogenesis of this rare phenomenon is poorly understood. OBJECTIVES: To report the factors common among severely injured patients developing ascites and to formulate a hypothesis regarding its origin. METHODS: Retrospective review of case series. RESULTS: We identified 9 injured patients between January 1, 1993, and December 31, 1998, who acutely developed significant amounts of ascites. The mean +/- SD estimated ascites volume was 2.0 +/- 0.8 L. All 9 patients had severe shock and were mechanically ventilated before abdominal decompression for the abdominal compartment syndrome. The mean +/- SD peak inspiratory pressure was 39.0 +/- 5.8 cm H2O. The mean +/- SD volumes of crystalloid and blood product infusion before decompression were 16.1 +/- 10.2 L and 5.2 +/- 4.8 L, respectively, in a mean +/- SD of 17 +/- 15 hours. In comparison, the mean +/- SD volumes of crystalloid and blood product transfusion among 100 contemporary, randomly selected patients undergoing trauma laparotomy were 5.1 +/- 5.5 L and 1.1 +/- 2.5 L, respectively (P<.001). Eight patients had only extra-abdominal injuries, while 1 patient had a combination of extra- and intra-abdominal injuries. Two patients were found to be cirrhotic by liver biopsy, but the other 7 patients had no known preexisting hepatic disease. Eight patients had absorbable mesh temporary abdominal closure, and 1 patient had primary fascial closure. There was persistent ascitic drainage in 5 patients; however, in all but 1 patient with cirrhosis, the drainage did not persist beyond 3 days. Two patients died, 1 of sepsis and the other of a closed head injury. CONCLUSIONS: Common denominators of posttraumatic ascites include shock, massive fluid resuscitation, and elevated intrathoracic pressure. The rapid onset of ascites in the setting of elevated intrathoracic pressure suggests that the patient's ability to clear ascitic fluid is overwhelmed.

PURPOSE: As part of developing a noninvasive method to measure bladder pressure using an inflatable penile cuff, we tested the hypothesis that detrusor contraction is maintained without inhibition during the test. MATERIALS AND METHODS: Five healthy volunteers and 26 male patients with lower urinary tract symptoms underwent interruption of established urine flow by controlled inflation of a cuff placed around the penis with simultaneous invasive bladder pressure monitoring. After interruption of flow the cuff was rapidly deflated and voiding was allowed to resume. The bladder pressure was recorded before, during and after interruption of flow by cuff inflation. RESULTS: During flow interruption an isovolumetric increase in detrusor pressure was observed. When the cuff was deflated the detrusor pressure quickly returned to preinflation values and urine flow immediately resumed. Intra-abdominal pressure did not change during the cuff inflation cycle. CONCLUSIONS: Mechanical interruption of urine flow by controlled inflation of a penile cuff during voiding does not inhibit detrusor contraction. This finding further validates our noninvasive technique of bladder pressure measurement and supports ongoing studies into its clinical usefulness.

PURPOSE OF REVIEWAbdominal compartment syndrome (ACS) is the end result of sustained, uncorrected intraabdominal hypertension. In clinical and laboratory settings, ACS has been shown to adversely affect all vital organ systems. Although early descriptions emanated from the trauma literature, ACS is now encountered in all intensive care unit populations. In this review, we examine the literature and identify factors that may predict the onset of ACS.RECENT FINDINGSThe pathogenesis of ACS remains unclear, and few studies have sought to identify predictive clinical variables. Peak airway pressure and net 24-hour fluid gradient are the only variables that have been identified in the available literature as predictive of ACS development in controlled studies.SUMMARYThe earlier recognition of predictive variables and identification of patients at higher risk will hopefully lead to recognition and avoidance of the sequelae and increased mortality rate associated with ACS.

BACKGROUND/AIMS: The aim of the study was to present, on the base of own experience, clinical importance of arterio-venous fistulae involving the vascular system of the abdomen. METHODOLOGY: Clinical material consists of 18 patients in whom abnormal arterio-venous leakage in the abdomen was disclosed by means of imaging diagnostic techniques and Doppler sonographic hemodynamic investigations. Three groups of patients were determined: 1. Patients in whom arterio-venous fistula was a primary cause of portal hypertension (N = 6), 2. Patients in whom the presence of arterio-venous fistulae aggravated portal hypertension due to other pathology (N = 7). 3. Patients in whom the arterio-venous fistulae did not directly affect portal flow (N = 5). As each case presented a different clinical problem, the therapeutic approach had to be individualized. In 12 patients perarterial embolization was performed, 13 patients were operated on, one patient was listed for liver transplantation. RESULTS: Perarterial embolization was fully effective only in 4 cases. In the remaining 8 cases its effect was transient, but in 4 cases of liver tumors it allowed us to proceed with chemoembolization and the others were subsequently treated surgically. In 12 surgically treated patients the operation proved to be curative. In 1 case of multiple arterio-venous fistulae related to diffuse angiomatosis, surgical procedure was unfeasible. One patient, awaiting liver transplantation, died of liver failure. CONCLUSIONS: 1. Arterio-venous fistulae (of various etiology) are rarely found in the abdominal cavity, but their presence means usually serious consequences depending on their morphology and localization. 2. Arterio-venous fistulae involving the portal system may result in severe portal hypertension. 3. Individually chosen method of treatment, aimed at the occlusion of arterio-venous fistula often proves to be curative. 4. Overlooking or ignoring the presence of intraabdominal arterio-venous fistulae leads to unsuccessful, if not harmful treatment.

BACKGROUND: A 5-year experience with the modified sandwich-vacuum pack technique, using an opened 3-litre urological irrigation bag and continuous high-pressure suction, for temporary abdominal wall closure is presented. METHODS: The records of all patients who underwent temporary abdominal wall closure using this method from January 1996 to December 2000 were examined. RESULTS: The modified sandwich-vacuum pack was used 139 times in 55 patients. Forty patients sustained penetrating trauma while 15 patients sustained blunt trauma. The mean Injury Severity Score was 19 (range 9-34). Intra-abdominal sepsis (51 per cent) was the commonest indication, followed by visceral oedema (18 per cent), abdominal compartment syndrome (16 per cent), intra-abdominal packing (11 per cent) and abdominal wall defects (4 per cent). The overall mortality rate was 45 per cent. Three patients (5 per cent) developed enterocutaneous fistula. Of the 30 survivors, 16 patients underwent primary fascial closure. CONCLUSION: The modified sandwich-vacuum pack technique of temporary abdominal wall closure is easy and rapid, cost effective and provides an effective means of containing abdominal wall contents.

BACKGROUND: Damage control surgery (DCS) and treatment of abdominal compartment syndrome have had major impacts on care of the severely injured. The objective of this study was to see whether advances in critical care, DCS, and recognition of abdominal compartment syndrome have improved survival from penetrating abdominal injury (PAI). METHODS: The care of 250 consecutive patients requiring laparotomy for PAI (1997-2000) was reviewed retrospectively. Organ injury patterns, survival, and use of DCS and its impact on outcome were compared with a similar experience reported in 1988. RESULTS: Two hundred fifty patients had a positive laparotomy for PAI. Twenty-seven (10.8%) required abdominal packing and 45 (17.9%) did not have fascial closure. Seven (2.8%) required emergency department thoracotomy and 21 (8.4%) required operating room thoracotomy. Two hundred seventeen (86.8%) survived overall. Small bowel (47.2%), colon (36.4%), and liver (34.4%) were most often injured. Mortality was associated with the number of organs injured (odds ratio, 1.98; 95% confidence interval, 1.65-2.37; p < 0.001). Vascular injury was a risk factor for mortality (p < 0.001), as was need for DCS (p < 0.001), emergency department thoracotomy (p < 0.001), and operating room thoracotomy (p < 0.001). Seventy-nine percent of deaths occurred within 24 hours from refractory hemorrhagic shock. DCS was used in 17.9% (n = 45) versus 7.0% (n = 21) in 1988, with a higher survival rate (73.3% vs. 23.8%, p < 0.001). DCS was associated with significant morbidity including sepsis (42.4%, p < 0.001), intra-abdominal abscess (18.2%, p = 0.009), and gastrointestinal fistula (18.2%, p < 0.001). CONCLUSION: Penetrating abdominal organ injury patterns and survival from PAI have remained similar over the past decade. Death from refractory hemorrhagic shock in the first 24 hours remains the most common cause of mortality. DCS and the open abdomen are being used more frequently with improved survival but result in significant morbidity.

Abdominal compartment syndrome is a well-documented entity arising from multiple and various causes. The rise of intra-abdominal pressure by the increase in volume of the peritoneal and retroperitoneal contents has been shown in the resuscitation and evaluation of surgical patients. However, the incidence of constriction of the abdomen causing intra-abdominal hypertension is unknown. Previously limited to burn eschar and externally applied devices (such as MAST trousers), external compression leading to abdominal compartment syndrome has been a limited entity. We report the first documented case of an expansive abdominal wall mass, a rectus sheath hematoma, leading to impending abdominal compartment syndrome.

OBJECTIVES: Elevated intra-abdominal pressure (IAP) may cause widespread organ dysfunction (abdominal compartment syndrome) through effects on the respiratory, cardiac, renal and gastro-intestinal systems. The aim of this study was to document IAP following aneurysm surgery, and to determine the effect of IAH on outcome. DESIGN: Prospective observational study. SETTING: University Hospital. SUBJECTS: The patient cohort comprised 75 patients undergoing infra-renal aneurysm repair (53 non-ruptured [40 conventional--1 death, 13 endovascular] and 22 conventionally repaired ruptured AAA--8 deaths). IAP was quantified by bladder manometry at the termination of the procedure and at 24 h intervals in patients who remained intubated. Physiological indices of organ function were recorded. Statistical analysis utilized the unpaired t-test, Fischer's exact test and Pearson's correlation. RESULTS: IAP was significantly higher at abdominal closure following ruptured aneurysm repair (15.4 mmHg [SE 1.6]) than conventional (10.5 [0.89]) or endovascular elective repair (6.4 [1.0]) of non-ruptured AAA. The sensitivity and specificity of IAP to predict subsequent mortality was analysed using a receiver characteristic operating curve. This analysis demonstrated that a cut off of 15 mmHg was the most useful for indicating patients at risk (sensitivity 0.66, specificity 0.79). Physiological indices of organ dysfunction (pH[P = 0.027], base excess [p = 0.005], peak inspiratory pressure [p = 0.0015], CVP and urine output [p = 0.0029]) were significantly impaired in patients with IAP > or = 15 mmHg, in comparison to patients with lower pressures. IAP correlated significantly with indices of cardiac (CVP p = 0.038), respiratory (PaO2/FiO2, p = 0.026), and renal function (urine output p = 0.046). CONCLUSIONS: These data suggest that the management of IAH may have a role following repair of ruptured AAA. High intra-abdominal pressures rarely complicate elective or endovascular aneurysm repair.

Acute respiratory distress syndrome (ARDS) can be derived from two pathogenetic pathways: a direct insult on lung cells (pulmonary ARDS (ARDSp)) or indirectly (extrapulmonary ARDS (ARDSexp)). This review reports and discusses differences in biochemical activation, histology, morphological aspects, respiratory mechanics and response to different ventilatory strategies between ARDSp and ARDSexp. In ARDSp the direct insult primarily affects the alveolar epithelium with a local alveolar inflammatory response while in ARDSexp the indirect insult affects the vascular endothelium by inflammatory mediators through the bloodstream. Radiological pattern in ARDSp is characterised by a prevalent alveolar consolidation while the ARDSexp by a prevalent ground-glass opacification. In ARDSp the lung elastance, while in ARDSexp the chest wall and intra-abdominal chest elastance are increased. The effects of positive end-expiratory pressure, recruitment manoeuvres and prone position are clearly greater in ARDSexp. Although these two types of acute respiratory distress syndrome have different pathogenic pathways, morphological aspects, respiratory mechanics, and different response to ventilatory strategies, at the present, is still not clear, if this distinction can really ameliorate the outcome.

Intestinal hypoperfusion is among the factors implicated in sepsis and multiorgan failure. Splanchnic blood flow may be sacrificed to maintain supply to vital organs, even when hemodynamic alterations are minor. The sensitivity of invasive hemodynamic monitoring for detecting intestinal hypoperfusion is low. This paper aims to review current knowledge about indirect measurement of splanchnic perfusion by way of gastrointestinal tonometry. We review the pathophysiology of ischemic intestinal lesions, the basis for gastrointestinal tonometry, and the method. Finally we discuss clinical applications (early diagnosis of ischemic colitis and ischemia of the flap after esophageal reconstruction, weaning from mechanical ventilation, abdominal compartment syndrome, liver transplant, heart surgery, prognostic factors and care of the critically ill patient). An adequate understanding of this monitoring technique and management of information it provides can give an early warning of the intestinal hypoperfusion that precedes other serious systemic complications.

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.).

In our recent clinical study of damage control laparotomy, the abdominal compartment syndrome (ACS) emerged as an independent risk factor for postinjury multiple organ failure (MOF). We and others have shown previously that the ACS promotes the systemic production of proinflammatory cytokines. Our study objective was to develop a clinically relevant two-event animal model of postinjury MOF using the ACS as a second insult during systemic neutrophil priming to provoke organ dysfunction. Male adult rats underwent hemorrhagic shock (30 mmHg x 45 min) and were resuscitated with crystalloids and shed blood. The timing of postshock systemic neutrophil (PMN) priming was determined by the surface expression of CD11b via flow cytometry. Finding maximal PMN priming at 8 h, but no priming at 2 h (early) and 18 h (late), the ACS (25 mmHg x 60 min) was introduced at these time points. At 24 h postshock, lung injury was assessed by lung elastase concentration and Evans blue dye extravasation in bronchoalveolar lavage. Liver and renal injuries were determined by serum alanine aminotransferase, serum creatinine, and blood urea nitrogen. The ACS during the time of maximal systemic PMN priming (8 h) provoked lung and liver injury, but did not if introduced at 2 or 18 h postshock when there was no evidence of systemic PMN priming. The 24-h mortality of this two-event model was 33%. These findings corroborate the potential for the ACS to promote multiple organ injury when occurring at the time of systemic PMN priming. This clinically relevant two-event animal model of PMN organ injury may be useful in elucidating therapy strategies to prevent postinjury MOF.

BACKGROUND: The purpose of the study was to examine hemodynamic parameters and intravascular volume in a porcine model in the presence of intra-abdominal hypertension (IAH) lasting for 24 hours. METHODS: Twelve pigs (52.5 +/- 4.9 kg) were studied over a period of 24 hours. In six animals, the intra-abdominal pressure was increased to 30 mm Hg via carbon dioxide-pneumoperitoneum. The others served as controls. Using the double-indicator dilution technique, intrathoracic blood volume (ITBV), total circulating blood volume, and cardiac output (CO) were measured. Standard parameters (e.g., central venous pressure [CVP]), were also recorded. RESULTS: In the presence of IAH, ITBV and total circulating blood volume were significantly reduced to 55% and 67% of control values. CO decreased to 27% and CVP increased fourfold. CONCLUSION: IAH leads to significant intravascular volume depletion that is not reflected by the CVP. Assessment of CO and ITBV in the presence of a critically increased intra-abdominal pressure is therefore recommended.

Acutely increased intra-abdominal pressure (IAP) can lead to multiple organ failure. As blood flow to intra-abdominal organs is reduced by high venous resistance, ischemia-reperfusion (I/R) injury plays an important role in the pathogenesis of abdominal compartment syndrome (ACS) following IAP. Melatonin, a secretory product of the pineal gland, is known to have free radical scavenging and antioxidative properties in several oxidative processes. The objective of this study was to examine the potential protective properties of melatonin on the oxidative organ damage in a rat model of ACS. Under ketamine anesthesia, an arterial catheter was inserted intraperioneally (i.p.) and using an aneroid manometer connected to the catheter, IAP was kept at 20 mmHg (ischemia group; I) for 1 hr. In the ischemia/reperfusion (I/R) group, pressure applied for an hour was decompressed and a 1-hr reperfusion period was allowed. In another IR group, melatonin was administered (10 mg/kg, i.p.) immediately before the decompression of IAP. The results demonstrate that tissue levels of malondialdehyde (MDA) and myeloperoxidase activity (MPO; index of tissue neutrophil infiltration) were elevated, while glutathione (GSH; a key to antioxidant) levels were reduced in both I and I/R groups (P < 0.05-0.001). Melatonin treatment in I/R rats reversed these changes (P < 0.01-0.001). Moreover, melatonin given to the I/R group reduced the elevations in serum aspartate aminotransferase, alanine aminotransferase and blood urea nitrogen levels and abolished the increase in serum creatinine levels. Our results indicate that melatonin, because of antioxidant and free radical scavenging properties, ameliorates reperfusion-induced oxidative organ damage. In conclusion, the results of the present study suggest that the therapeutic value of melatonin as a 'reperfusion injury-limiting' agent must be considered in ACS.

The inability for abdominal closure in critically ill surgical patients provides a complex problem. Often, these patients are left with a large ventral hernia, which requires readmission for abdominal wall repair. We are reporting on the use of a vacuum-assisted device (VAD) to facilitate abdominal wall closure. Fifteen patients were enrolled for placement of a VAD. Selection was based on the diagnosis of abdominal compartment syndrome, the inability for abdominal closure at the initial operation, or the inability to close the abdomen upon re-exploration. Ten (67%) patients were successfully closed within 11 days using the VAD. Predictors of successful closure were the duration of VAD placement (< 12 days, P < 0.001), the total amount of VAD output (< 3 L, P < 0.04), the patient's cumulative fluid balance within the first 2 weeks (< 2 L, P < 0.002), or the presence of a systemic infection at the time of attempted closure (P < 0.001). After 6 months, there have been no complications in patients successfully closed with this device. There have been a few recent reports describing VAD abdominal closures. While not successful for every case, the majority of our patients were able to have their abdominal wall closed primarily. We plan to use this technique to help shorten hospital stay and prevent readmission for hernia repair.

Presented in this paper is our experience in the diagnosis and management of abdominal compartment syndrome during severe acute pancreatitis. On the basis of the history of severe acute pancreatitis, after effective fluid resuscitation, if patients developed renal, pulmonary and cardiac insufficiency after abdominal expansion and abdominal wall tension, ACS should be considered. Cystometry could be performed to confirm the diagnosis. Emergency decompressive celiotomy and temporary abdominal closure with a 3 liter sterile plastic bag must be performed. It is also critical to prevent reperfusion syndrome. In 23 cases of ACS, 18 cases received emergency decompressive celiotomy and 5 cases did not. In the former, 3 patients died (16.7%) while in the later, 4 (80%) died. Total mortality rate was 33.3% (7/21). In 7 death cases, 4 patients developed acute obstructive suppurative cholangitis (AOSC). All the patients who received emergency decompressive celiotomy 5 h after confirmation of ACS survived. The definitive abdominal closure took place mostly 3 to 5 days after emergency decompressive celiotomy, with longest time being 8 days. 6 cases of ACS at infection stage were all attributed to infected necrosis in abdominal cavity and retroperitoneum. ACS could occur in SIRS stage and infection stage during SAP, and has different pathophysiological basis. Early diagnosis, emergency decompressive celiotomy and temporary abdominal closure with a 3L sterile plastic bag are the keys to the management of the condition.

Damage control laparotomy for life-threatening abdominal conditions has gained wide acceptance in the management of exsanguinating trauma patients as well as septic patients with acute abdomen. Survivors considered too ill to undergo definitive abdominal wall closure are temporized, often with skin grafting on granulated viscera. These maneuvers compromise the integrity of the anterior abdominal wall and result in a subset of patients with loss of abdominal domain and massive, debilitating ventral hernias. A retrospective review was conducted of 21 such patients (16 men, five women) who underwent elective abdominal wall reconstruction at the Hospital of the University of Pennsylvania between November of 1998 and October of 2000. The purpose of this study was to report the authors' experience with these complex abdominal wall reconstructions. A double-layer, subfascial Vicryl mesh buttress was used in all repairs to aid in reestablishing abdominal wall integrity. The mean hernia size was 813 cm2 (range, 75 to 1836 cm2), and the average interval to definitive repair was 24.4 months (range, 3 weeks to 11 years). Mean follow-up was 13.5 months (range, 1 month to 40 months). Twenty patients (95 percent) had successful ventral hernia repair. Four patients with massive hernias (924 to 1836 cm2) required submuscular Marlex mesh implantation. Two patients (10 percent) developed abdominal compartment syndrome that required surgical decompression. One patient (5 percent) developed an incisional hernia at a prior colostomy site. Four patients (19 percent) had superficial skin dehiscence that healed secondarily with daily wound care. There were no mesh infections. In most cases, successful single-stage repair of large ventral hernias following damage control laparotomy can be achieved using a subfascial Vicryl mesh buttress in combination with other established reconstructive techniques. Massive defects exceeding 900 cm2 typically require permanent mesh implantation to achieve fascial closure and to minimize the risk of postoperative abdominal compartment syndrome and recurrent herniation. This technique represents an improved solution to a complicated problem and optimizes the aesthetic and functional outcome for these debilitated patients.

Intraabdominal hypertension (IAH) can occur in critically ill patients who have undergone surgery, who have required fluid resuscitation after intraabdominal operations, or whose abdominal surgical wound closure was under tension. If IAH remains unrelieved, it can lead to development of the abdominal compartment syndrome (ACS). The latter presents with severe cardiorespiratory and urinary symptoms such as hypotension, hypoventilation, and oliguria, and it can become fatal if it is not diagnosed early and treated properly. Moreover, IAH has been documented in the context of major burns, complicating the initial resuscitation of these patients. This study was set up to investigate the role of full-thickness burns of the thoracic and abdominal areas in IAH during the early resuscitation period, to determine whether escharotomy could influence its levels. During the past 2 years 10 burn patients were enrolled in this study, as they fulfilled the necessary criteria: >35% total body surface area (TBSA) full-thickness burn affecting the anterior, lateral, and most of the posterior surface of the thorax and abdomen (torso), no respiratory mechanical support at admission, and initial evaluation at another facility and transfer to our burn center 2-6 h postburn. Upon admission, the following parameters (indicative of intraabdominal hypertension, IAH) were measured: bladder pressure and gastric pressure. Also, we monitored inferior vena cava pressure, and as a routine, central venous pressure, systolic blood pressure, and arterial blood gases. Elevated intraabdominal pressure to hazardous levels was documented in all patients included in our study. The same escharotomy pattern was performed in every case, and 5-10 min after the procedure all measurements were repeated. Immediate improvement of all the parameters measured was recorded, and the alterations were found statistically significant. These results were indicative of significant relief of the elevated intraabdominal pressure in all patients after escharotomy, as well as the efficacy of the procedure. It is thus demonstrated that full-thickness burns of the thoracic and abdominal areas can cause a significant early increase in intraabdominal pressure that, if left untreated, can lead to the development of ACS. However, the application of simple decompression techniques can offer remarkable, immediate, and often lifesaving results and is absolutely indicated for this reason, as well as for its well-known beneficial effects on respiratory function.

OBJECTIVE: To investigate the possibility of artificially decreasing intra-abdominal pressure (IAP) by applying continuous negative pressure around the abdomen. MATERIAL AND METHODS: We investigated the effects of negative extra-abdominal pressure (NEXAP) on IAP and central venous pressure (CVP) in 30 patients admitted to our intensive care unit (age 57+/-17 years, BMI 26.1+/-4.0 kg/m2, SAPS II 41.8+/-17.0). Patients with severe hemodynamic instability and/or those admitted following a laparotomy were not studied. Measurements included bladder pressure as an estimate of IAP, CVP, invasive mean arterial pressure (MAP) and heart rate (HR). In five patients extensive hemodynamic measurements were also taken using a Swan-Ganz catheter. Following measurements at baseline (Basal), NEXAP (Life Care - Nev 100, Respironics) was applied on the abdomen, in random order, at a pressure equal to IAP (NEXAP0), 5 cmH(2)O (NEXAP-5) or 10 cmH(2)O (NEXAP-10) more negative than NEXAP0. RESULTS: Basal IAP ranged from 4 to 22 mmHg. NEXAP decreased IAP from 8.7+/-4.3 mmHg to 6+/-4.2 (Basal vs NEXAP0 p<0.001). There was a further decrease of IAP when more negative pressure was applied: 4.3+/-3.2 mmHg, 3.8+/-3.7 mmHg (NEXAP-5 and NEXAP-10 vs NEXAP0, respectively, p<0.001). Similarly, CVP decreased from 9.3+/-3.4 mmHg to 7.5+/-3.8 (Basal vs NEXAP-10, p<0.001). The lower the IAP when NEXAP was applied, the lower the CVP (r2=0.778, p<0.001, multiple linear regression). When measured, cardiac output did not significantly change with NEXAP. CONCLUSIONS: Negative extra-abdominal pressure may be applied in critically ill patients to decrease intra-abdominal pressure non-invasively.

PURPOSE: To report an unusual case of abdominal compartment syndrome (ACS) following endovascular repair of a ruptured abdominal aortic aneurysm (rAAA) that had been treated with a stent-graft 3 years prior. CASE REPORT: A 68-year-old man with a 3-year-old Vanguard bifurcated aortic stent-graft experienced sudden back pain and collapse. Aneurysm rupture documented by computed tomography was due to dislocation of the left graft limb. A Talent aortomonoiliac graft was deployed, followed by a femorofemoral bypass. No endoleak was evident. A few hours later, the patient became oliguric and hemodynamically unstable. Increased intra-abdominal pressure (IAP) was recorded. Abdominal decompression was performed, removing 1500 mL of blood from the retroperitoneum through an 18-cm lumbotomy; the peritoneum was opened, and another 500 mL of blood was aspirated. The IAP fell immediately, followed by diuresis a few hours later. The patient recovered and was discharged after 27 days. CONCLUSIONS: Some of the perioperative complications seen after conventional rAAA repair are also encountered after endovascular treatment. ACS requires urgent decompression, and less invasive approaches, such as translumbar extraperitoneal decompression, may be a good alternative to a midline laparotomy.

BACKGROUND: Sustained intraabdominal pressures of 14 to 20 mm Hg have significant pathophysiological consequences, but there is currently no satisfactory low-morbidity procedure appropriate for intervention early in the disease process of abdominal compartment syndrome (ACS). The anatomical principles of abdominal wall components separation were used to develop a percutaneous procedure that increased abdominal capacity and decreased abdominal pressure. METHODS: Using a porcine model, we determined abdominal capacity changes by helium insufflation. Corn oil was then used to create an episode of sustained intraabdominal hypertension and changes in intraabdominal pressure and intestinal mucosal oxygenation were determined. RESULTS: Endoscopic abdominal wall components separation (EACS) increased abdominal capacity by 1 L (from 0.89 +/- 0.39 L to 1.95 +/- 0.48 L; P <0.001). During intraabdominal hypertension, EACS decreased abdominal pressure by 31.6% (from 15.9 +/- 2.1 to 11.0 +/- 1.5 mm Hg; P <0.001). Intestinal PO(2) was increased by 61% (18.8 +/- 11.4 to 30.3 +/- 11.7; P = 0.012) CONCLUSIONS: A minimally invasive procedure (EACS) is feasible and has demonstrated effectiveness in a porcine model of ACS.

Abdominal compartment syndrome is a potentially lethal condition caused by any event that produces intra-abdominal hypertension; the most common cause is blunt abdominal trauma. Increasing intra-abdominal pressure causes progressive hypoperfusion and ischemia of the intestines and other peritoneal and retroperitoneal structures. Pathophysiological effects include release of cytokines, formation of oxygen free radicals, and decreased cellular production of adenosine triphosphate. These processes may lead to translocation of bacteria from the gut and intestinal edema, predisposing patients to multiorgan dysfunction syndrome. The consequences of abdominal compartment syndrome are profound and affect many vital body systems. Hemodynamic, respiratory, renal, and neurological abnormalities are hallmarks of abdominal compartment syndrome. Medical management consists of urgent decompressive laparotomy. Nursing care involves vigilant monitoring for early detection, including serial measurements of intra-abdominal pressure.