Asnaghi, M., A. Lucchini, et al. (2002). "Monitoring of intra-abdominal pressure." Minerva Anestesiol 68(5): 485-7.

Intra-abdominal pressure monitoring is a very important parameter in the ICU setting, since pathological alterations of this value are significant and are responsible for functional alterations involving cardio-respiratory system, kidneys and central nervous system. Responsibility of the professional nurse in the ICU is to perform a tight and adequate monitoring of those patients who are at risk for a rise in intra-abdominal pressure.

Increased intra-abdominal pressure (IAP) may occur in a number of different situations encountered by intensivists, such as tense ascites, abdominal hemorrhage, use of military antishock trousers, abdominal obstruction, during laparoscopy, large abdominal tumors and peritoneal dialysis.1-3 Both clinical and experimental evidence indicate that increased IAP may adversely affect cardiac, renal, respiratory and metabolic functions.1-5 Despite this, increased IAP is rarely recognized and treated in Intensive Care Unit (ICU) settings. There appears to be two reasons for this: the physiologic consequences of increased IAP are not well know, to most physicians and, more importantly, the capability of easily measuring IAP has not been well documented. In this chapter, we will discuss: 1) the different methods proposed to evaluate IAP in ICU; 2) the physiopathological consequences of increased IAP; 3) the existing clinical data about IAP in critically ill patients. Considering overall our data, we can conclude that: 1) different techniques are available at the bedside to estimate the IAP; 2) the IAP ranges between 10 and 20 cmH2O, substantially increased compared to normal subjects. Most of the patients have IAH, while few of them (<5%) present clinical characteristics of ACS; 3) the IAP is different among different categories of patients and its increase is not limited to surgical patients only; 4) the increase in IAP appears to influence respiratory function, homodynamic, kidney, gut and brain physiology; 5) the IAP seems to be correlated with severity scores but its relation to mortality is controversial; 6) the routine measurements of IAP by means of bladder pressure are not associated with an increased rate of urinary tract infections.

BACKGROUND: The term secondary abdominal compartment syndrome (ACS) has been applied to describe trauma patients who develop ACS but do not have abdominal injuries. The purpose of this study was to describe major trauma victims who developed secondary ACS during standardized shock resuscitation. METHODS: Our prospective database for standardized shock resuscitation was reviewed to obtain before and after abdominal decompression shock related data for secondary ACS patients. Focused chart review was done to confirm time-related outcomes. RESULTS: Over the 30 months period ending May 2001, 11 (9%) of 128 standardized shock resuscitation patients developed secondary ACS. All presented in severe shock (systolic blood pressure 85 +/- 5 mm Hg, base deficit 8.6 +/- 1.6 mEq/L), with severe injuries (injury severity score 28 +/- 3) and required aggressive shock resuscitation (26 +/- 2 units of blood, 38 +/- 3 L crystalloid within 24 hours). All cases of secondary ACS were recognized and decompressed within 24 hours of hospital admission. After decompression, the bladder pressure and the systemic vascular resistance decreased, while the mean arterial pressure, cardiac index, and static lung compliance increased. The mortality rate was 54%. Those who died failed to respond to decompression with increased cardiac index and did not maintain decreased bladder pressure. CONCLUSIONS: Secondary ACS is an early but, if appropriately monitored, recognizable complication in patients with major nonabdominal trauma who require aggressive resuscitation.

Laparoscopic surgery is an emerging procedure in the treatment of many surgical pathologies. Laparoscopy in the paediatric patient reduces surgical trauma and improves cosmetic RESULTS. Physiological changes during laparoscopic surgery are mainly related to the increased intra-abdominal pressure (IAP) associated with CO2 insufflation of the abdomen, the patient's postural modifications (head-up or head-down) and CO2 absorption and its general effects. Increases in IAP affect both ventilation and circulation. Increased IAP induces a mechanical compression of the diaphragm that reduces pulmonary compliance, vital capacity, functional residual capacity (FRC) and total lung volume. Pneumoperitoneum in children has a major impact on cardiac volumes and function, mainly through the effect on ventricular load conditions. The acute increase in IAP affects both preload and afterload, while the systolic cardiac performance remains unchanged. During anaesthesia for videolaparoscopy it is important not to exceed an intrabdominal pressure of 6 mmHg in newborns and infants and 12 mmHg in older children. In our clinical experience the respiratory, cardiocirculatory and temperature parameters have been slightly influenced during laparoscopy, but have always been maintained within the normal ranges. Laparoscopic videosurgery in newborns, infants and paediatric age group patients can be performed safely and with satisfactory clinical results.

There is growing interest in measuring intra-abdominal pressure (IAP) in postsurgical and critically ill patients because increased pressure can impair various organs and functions. The aim of this study was to evaluate the effect of different IAP levels on the postoperative renal function of subjects undergoing orthotopic liver transplantation. IAP was measured every 8 hours with the urinary bladder pressure method for at least 72 hours after surgery. At the end of the study, the patients were classified on the basis of their IAP values: < or = 18 mm Hg (group A), 19 to 24 mm Hg (group B), > or = 25 mm Hg (group C). The three groups were compared in terms of the incidence of acute renal failure (defined as blood creatinine > 1.5 mg/dL or an increase in the same of > 1.1 mg/dL within 72 hours of surgery), hourly diuresis, blood creatinine, the filtration gradient, hemodynamic variations, and outcome. The incidence of renal failure was higher among the subjects in group C (P < .05 versus group A and < .01 versus group B), who also had higher creatinine levels (P < .01), a greater need for diuretics (P < .01) and a worse outcome (P < .05). Receiver Operator Characteristic curve analysis showed that an abdominal pressure of 25 mm Hg had the best sensitivity/specificity ratio for renal failure. An intra-abdominal pressure of > or = 25 mm Hg is an important risk factor for renal failure in subjects undergoing liver transplant.

BACKGROUND: We hypothesized that hemorrhagic shock followed by the abdominal compartment syndrome (ACS) resulted in bacterial translocation (BT) from the gastrointestinal (GI) tract. METHODS: Nineteen Yorkshire swine (20-30 kg) were divided into two groups. In the experimental group, group 1 (n = 10), animals were hemorrhaged to a mean arterial pressure (MAP) of 25-30 mm Hg for a period of 30 minutes and resuscitated to baseline MAP. Subsequently, intra-abdominal pressure (IAP) was increased to 30 mm Hg above baseline by instilling sterile normal saline into the peritoneal cavity. The IAP was maintained at this level for 60 minutes. Acid/base status, gastric mucosal ph (pHi), superior mesenteric artery (SMA) blood flow, and hemodynamic parameters were measured and recorded. Blood samples were analyzed by polymerase chain reaction (PCR) for the presence of bacteria. Spleen, lymph node, and portal venous blood cultures were obtained at 24 hours. Results were analyzed by ANOVA and are reported as mean +/- SEM. The second group was the control. These animals did not have the hemorrhage, resuscitation, or intra-abdominal hypertension (IAH) but were otherwise similar to the experimental group in terms of laparotomy and measured parameters. RESULTS: SMA blood flow in group 1 (baseline of 0.87 +/- 0.10 l/min) decreased in response to hemorrhage (0.53 +/- 0.10 l/min, p = 0.0001) and remained decreased with IAH (0.63 l/min +/- 0.10, p = 0.0006) as compared to control and returned towards baseline (1.01 +/- 0.5 l/min) on relief of IAH. pHi (baseline of 7.21 +/- 0.03) was significantly decreased with hemorrhage (7.04 +/- 0.03, p = 0.0003) and decreased further after IAH (6.99 +/- 0.03, p = 0.0001) in group 1 compared to control, but returned toward baseline at 24 hours (7.28 +/- 0.04). The mean arterial pH decreased significantly from 7.43 +/- 0.01 at baseline to 7.27 +/- 0.01 at its nadir within group 1 (p = 0.0001) as well as when compared to control (p = 0.0001). Base excess was also significantly decreased between groups 1 and 2 during hemorrhage (3.30 +/- 0.71 vs. 0.06 +/- 0.60, p = 0.001) and IAH (3.08 +/- 0.71 vs. -1.17 +/- 0.60, p = 0.0001). In group 1, 8 of the 10 animals had positive lymph node cultures, 2 of the 10 had positive spleen cultures, and 2 of the 10 had positive portal venous blood cultures for gram-negative enteric bacteria. Only 2 of the 10 animals had a positive PCR. In group 2, five of the nine animals had positive lymph node cultures, zero of the nine had positive spleen cultures, and one of the nine had positive portal venous blood cultures. Two of the nine animals had positive PCRs. There was no significant difference in cultures or PCR results between the two groups (Fisher's exact test, p = 0.3). CONCLUSION: In this study, hemorrhage followed by reperfusion and a subsequent insult of IAH caused significant GI mucosal acidosis, hypoperfusion, as well as systemic acidosis. These changes did not appear to be associated with a significant bacterial translocation as judged by PCR measurements, tissue, or blood cultures.

BACKGROUND/PURPOSE: Abdominal compartment syndrome (ACS) may complicate abdominal closure in patients with abdominal wall defects, abdominal trauma, intraperitoneal bleeding, and infection. Increased intraabdominal pressure (IAP) leads to respiratory compromise, organ hypoperfusion, and a high mortality rate. This study evaluates the efficacy of continuous direct monitoring of IAP and gastric tissue pH in detecting impending ACS. METHODS: Ten mongrel puppies weighing 2.8 to 6.4 kg underwent general endotracheal anesthesia, placement of an intraabdominal inflatable balloon to simulate ACS and a Swan-Ganz catheter to measure direct IAP. A gastric tonometer, nasogastric tube, foley catheter, and arterial catheter also were inserted. Half-hourly inflation's of the intraabdominal balloon were used to simulate the development of ACS. Direct intraabdominal (IAP), gastric (GP), bladder (BP), and peak airway pressures (PAP) were measured. Gastric tonometry fluid and arterial blood gas levels were obtained during inflation, and the gastric tissue pH level was calculated. Data were statistically analyzed using Pearson's correlation coefficients. RESULTS: Baseline pressures were 2 to 5 cm H(2)O in the stomach and bladder catheters, 1 to 3 mm Hg in the intraabdominal catheter, and correlated with a gastric tissue pH level of 7.4. Significantly high correlation coefficients (cc) were observed between IAP versus BP (cc, 0.77; P <.002). IAP versus GP (cc, 0.79; P <.002) and IAP versus PAP (c, 0.83; P <.0004). A high negative correlation coefficient was noted between gastric pH and IAP (cc, 0.61; P <.026). The pH level dropped to 7.0 with BP and GP of 20 cm H(2)O and IAP of 10 mm Hg, to 6.8 at 30 cm H(2)O and 20 mm Hg, and 6.5 at 40 cm H(2)O and 30 mm Hg, respectively. However, correlation coefficients between gastric tissue pH and BP, GP, or PAP were not significant. CONCLUSIONS: These data suggest that continuous direct intraabdominal pressure monitoring is a simple and effective method that correlates well with indirect bladder or gastric pressure measurement. Changes in gastric tissue pH in association with increased intraabdominal pressure may be an early indicator of impending abdominal compartment syndrome. These observations indicate that these techniques may be more sensitive than current methods of indirect measurement, which may be associated with delayed recognition of ACS.

Abdominal compartment syndrome (ACS) is caused by pathological elevation of intra-abdominal pressure (IAP) leading to multiple organ dysfunction syndrome. Since the condition is highly lethal, early diagnosis is imperative. We evaluated the pre-operative abdominal CT scans of three children with proven ACS to identify signs of elevated IAP. Findings common to these patients included narrowing of the inferior vena cava (IVC), direct renal compression or displacement, bowel wall thickening with enhancement and a rounded appearance of the abdomen. The aim of recognising the CT findings in such cases is to plan emergency surgical decompression. Although these findings are not specific for increased IAP, radiologists should be aware of this life-threatening condition and, in the proper clinical setting, should communicate the presence and significance of these findings to the referring clinician.

Many daily activities cause acute elevations of intra-abdominal pressure (IAP). In portal hypertensive cirrhotic patients, increased IAP increases absolute portal pressure and azygos blood flow, suggesting that it may have detrimental consequences at the esophageal varices. The aim of this study was to investigate the effects of increased IAP on variceal pressure, size, and wall tension. Endosonography and a noninvasive endoscopic pressure gauge were used to measure variceal pressure, radius, wall tension, and volume in baseline conditions and after increasing IAP by 10 mm Hg using an inflatable girdle in 14 patients with cirrhosis and esophageal varices. Increasing IAP markedly increased variceal pressure (from 13.3 +/- 4.2 to 17.4 +/- 4.6 mm Hg; P =.0001) and radius (from 2.9 +/- 1.0 to 3.9 +/- 1.1 mm; P =.0001). Consequently, wall tension dramatically increased (from 38.7 +/- 13.6 to 65.9 +/- 23.8 mm Hg. mm, +78%; P =.0001). Variceal volume increased significantly from 1,264 +/- 759 to 2,025 +/- 1,129 mm(3) (P =.0001). In conclusion, in portal hypertensive cirrhotic patients, increases in IAP have deleterious effects on variceal hemodynamics, markedly increasing the volume, pressure, and wall tension of the varices. Increases in IAP may contribute to the progressive dilatation that precedes the rupture of the varices in portal hypertension.

BACKGROUND: The currently prevailing paradigm calls for non-operative management of severe acute pancreatitis for as long as there is no evidence of infection. Our purpose in presenting this anecdotal experience is to propose that there is a subset of patients who may need a laparotomy in the absence of infection in order to decompress a clinically significant abdominal compartment syndrome (ACS), which is associated with the acute pancreatitis. METHODS: We present our recent experience with three patients suffering from severe acute pancreatitis. The three developed intra-abdominal hypertension (IAHT) and clinical ACS, which necessitated abdominal decompression and a laparostomy. One patient survived. CONCLUSIONS: The notion that patients with severe acute pancreatitis may develop ACS, which necessitate emergency abdominal decompression, has been ignored by current surgical literature. Only increased awareness to the syndrome of IAHT-ACS in acute pancreatitis and transvesical measurement of intra-abdominal pressure will reveal its prevalence and significance.

BACKGROUND: Multiple methods exist to manage in the intensive care unit the patient with an open abdomen. An increasingly common method is the vacuum packed technique. This method accommodates considerable expansion of intra-abdominal contents and should obviate the potential development of the abdominal compartment syndrome (ACS). Despite this, some patients with these temporary abdominal dressings will go on to develop ACS. For the purpose of this study we have defined this clinical entity as the open abdomen ACS. HYPOTHESIS: Patients with an open abdomen who develop ACS have a poor prognosis. Fluid requirements and resuscitative indices may predict which of these patients will develop open abdomen ACS. METHODS: A retrospective review was performed of patients with trauma who had an open abdomen treated with vacuum packed dressings at our urban level I trauma center. Over 1 year (July 1, 1999-June 30, 2000), 5 patients managed with an open abdomen developed ACS. These patients were compared with 15 consecutive patients with an open abdomen who did not develop clinical ACS during that same period. Fluid resuscitation, base deficit, pH, lactate level, systolic blood pressure, prothrombin time, temperature, peak inspiratory pressure, and PCO(2) were abstracted. The Fisher exact test was used for statistical analysis. RESULTS: In patients managed with an open abdomen, ACS developed between 1.5 and 12 hours (mean [SD], 7.5 [3.9] hours) after placement of the vacuum packed dressing. The base deficit, pH, peak inspiratory pressure, PCO(2,) and lactate level were more abnormal and the crystalloid requirements were significantly higher in the ACS group. The systolic blood pressure, temperature, and prothrombin time did not differ between groups. Three patients with ACS developed a second episode of ACS. Mortality in the ACS group was 3 (60%) of 5 patients vs 1 (7%) of 15 patients in the control group. CONCLUSIONS: Management of the open abdomen with the temporary abdominal closure does not prevent the development of ACS. Mortality is high when ACS occurs in this scenario. Severe physiologic derangement and high crystalloid requirements may predict which patients will develop ACS.

OBJECTIVE: Intra-abdominal pressure (IAP) can be measured in different ways but is usually measured indirectly via the urinary bladder. The aim of the study was to: 1) compare urinary bladder pressure, femoral vein pressure, and inferior caval vein pressure with IAP at different levels of IAP; and 2) try to find an optimal amount of fluid to be instilled into the urinary bladder before measurement of the bladder pressure, and to compare changes in blood flow in the femoral vein with that in the caval vein at different pressure levels. DESIGN: Experimental study. SETTING: Animal research laboratory. SUBJECTS: Eight domestic swine of both sexes, weighing 30.6+/-2.9 kg (mean+/-SD). INTERVENTIONS: Catheters connected to pressure transducers were placed into the urinary bladder, the inferior caval vein, the femoral vein, and the superior caval vein. Transit time flow probes were placed around the inferior caval vein and the femoral vein. After a stabilizing period, the abdominal pressure was increased stepwise by instillation of Ringer's solution into the abdomen and then decreased. Thereafter, we instilled fluid into the bladder at an IAP of 8 mmHg and at 20 mmHg and measured the amount of fluid needed to elevate the intra- vesical pressure by 2 mmHg. RESULTS: The pressures recorded in the urinary bladder, the inferior caval vein, and the femoral vein reflected the pressure in the abdominal cavity very well. The fluid volume needed to increase the bladder pressure by 2 mmHg was significantly lower at 20 mmHg IAP than at 8 mmHg. Blood flow in the femoral vein and the inferior caval vein showed a similar pattern and decreased when the intra-abdominal pressure increased. CONCLUSIONS: In our porcine model, and increasing the IAP by means of instillation of Ringer's solution, a reliable estimation of the IAP was obtained by measuring the pressure in the urinary bladder, the femoral vein or the inferior caval vein. The IAP estimated indirectly as the urinary bladder pressure is affected by the amount of fluid in the bladder, which should not exceed 10-15 ml. The decrease in femoral vein blood flow reflects the changes in inferior caval vein flow during increased IAP.

OBJECTIVE: To invstigte the physiologic effects and therapeutic management ofthe abdominal kompartm sendrome (ACS) Methods : A review ofthe recent Iiterature, experiences and opinions ofthe author are expressed in the papei: RESULTS AND CONCLUSIONS : Intraabdominal bleeding, peritonitis, ileus, shock-reperfusion syndrome, intestinal edema, Iaparoscopic procedures with gas, ciosure ofthe abdomen in spite ofincreased pressure and burns are some ofthefactors that take place in etiology. The critical intrabdominal pressure value that requires decompression is debatable. In patients with high abdominal pressures, the pressure should be decreased with Iaparotomy immediately and the abdomen should not be ciosed primarily. These measures will help us to Iower the rates of mortality and morbidity and improve the quality ofhealth services.

OBJECTIVE: We report the first patient to developed abdominal compartment syndrome (ACS) with intrahepatic portal venous gas (IHPVG) and pneumatosis cystoides intestinalis following emergency upper gastrointestinal endoscopy. CASE PRESENTATION: A 53-year-old man underwent an emergency upper gastrointestinal endoscopy for suspicion of upper gastrointestinal bleeding. The patient developed intra-abdominal hypertension and ACS associated with IHPVG after the endoscopy. Although the patient developed severe shock following ACS, he was managed conservatively and successfully recovered. CONCLUSIONS: An emergency upper gastrointestinal endoscopy may be associated with intra-abdominal hypertension and ACS. Our report provides an additional case of a survivor who required no surgical intervention for ACS and IHPVG following endoscopy.

BACKGROUND: Abdominal compartment syndrome (ACS) has rarely been described as a complication of burn injury. This study describes cases of ACS in patients with burn injury and the physiologic results of abdominal release. METHODS: Charts for all patients admitted to two major burn center intensive care units from January 1998 through August 2000 were reviewed for ACS. Physiologic parameters were compared before and after abdominal release. RESULTS: Ten of 1,014 patients developed ACS. Abdominal release improved peak inspiratory pressures and Acute Physiology and Chronic Health Evaluation II scores (p < 0.03). The amount of fluid required to maintain adequate urine output also decreased substantially. Forty percent of patients with ACS survived to discharge. CONCLUSION: Abdominal release for patients with ACS and severe burn injury results in physiologic improvement and a 40% survival rate. We recommend bladder pressure monitoring for all patients with severe burn injuries and abdominal decompression in any patient who develops pressures greater than 30 mm Hg if they have signs of physiologic compromise. Aggressive expectant management can effect a 40% survival rate in this group of severely injured patients.

BACKGROUND: Intra-abdominal hypertension has been recognized as a source of morbidity and mortality in the traumatized patient following laparotomy. Multiple organ dysfunction attributable to intra-abdominal hypertension has been called the abdominal compartment syndrome. The epidemiology and characteristics of these processes remain poorly defined. METHODS: Intra-abdominal pressure was measured prospectively in all patients admitted to a trauma intensive care unit over 9 months. Data were gathered on all patients with intra-abdominal hypertension. RESULTS: Some 706 patients were evaluated. Fifteen (2 per cent) of 706 patients had intra-abdominal hypertension. Six of the 15 patients with intra-abdominal hypertension had abdominal compartment syndrome. Half of the patients with abdominal compartment syndrome died, as did two of the remaining nine patients with intra-abdominal hypertension. Patients with abdominal compartment syndrome had a mean intra-abdominal pressure of 42 mmHg compared with 26 mmHg in patients with intra-abdominal hypertension only (P < 0.05). CONCLUSION: The incidence of intra-abdominal hypertension and abdominal compartment syndrome was 2 and 1 per cent respectively. Intra-abdominal hypertension did not necessarily lead to abdominal compartment syndrome, and often resolved without clinical sequelae. Abdominal compartment syndrome did not occur in the absence of earlier laparotomy. Abdominal compartment syndrome was associated with a marked increase in intra-abdominal pressure (above 40 mmHg).

BACKGROUND: The purpose of this study was to assess the effects of abdominal compartment syndrome (ACS) on the kidneys. METHODS: Intra abdominal pressures (IAP) were indirectly measured through urinary bladder. The patients were categorised into four groups according to IAP levels. Serum urea and creatinine levels and IAP were measured once a day. Abdominal decompression was planned according to IAP as well as clinical assessment. RESULTS: The number of patients in this study was 25. Serum urea and creatinine levels were highest in the group IV (group in which abdominal pressure was above 31 cmH2O) (t > 0.05). Five of the 25 patients were died and anuria developed in these five patients before death. In three of five patients abdominal decompression operations were performed. CONCLUSION: ACS is an unusual and often lethal syndrome. The most important treatment is abdominal decompression and we conclude that it should be done in patients with IAP 30 cmH2O or above to protect renal function.

Abdominal Compartment Syndrome (ACS) has multiple causes, and decompressive laparotomy has been the most frequent modality to prevent worsening cardiovascular, respiratory, and renal function. This pilot study evaluated the utility of percutaneous drainage (PD) of peritoneal fluid compared with decompressive laparotomy in burn patients. A 26-month review was conducted. Nine of 13 (69%) study patients developed intra-abdominal hypertension (IAH) that progressed to abdominal compartment syndrome in 4 (31%). All were treated with PD using a diagnostic peritoneal lavage catheter. Peritoneal fluid analysis revealed a sterile plasma ultrafiltrate with electrolyte and other chemistries reflecting patient serum levels. Five patients underwent PD successfully, and their IAH did not progress to ACS. Four patients with greater than 80% TBSA and severe inhalation injury did not respond to PD and required decompressive laparotomy. There was no evidence of bowel edema, ischemia, or necrosis. All patients requiring decompressive laparotomies died either from sepsis or respiratory failure. Percutaneous decompression is a safe and effective method of decreasing IAH and preventing ACS in patients with less than 80% TBSA thermal injury.

BACKGROUND: Previous methods described to measure bladder pressure require additional setup, making these techniques complex and time consuming. We describe a simple U-tube technique and investigate its accuracy for measuring intra-abdominal pressure (IAP). METHODS: Warm saline was infused into the peritoneum of five pigs to increase IAP. Indirect methods of measuring IAP included bladder, inferior vena cava (IVC), and gastric pressures. Bladder pressure was measured by both the standard and U-tube technique. IVC pressure was measured via a femoral line and gastric pressure was transduced through an orogastric tube. In addition, 30 patients undergoing laparoscopy were prospectively investigated. Insufflated abdominal pressure readings were obtained and compared with bladder pressures measured by the U-tube technique (n = 20) and standard technique (n = 10). RESULTS: In the animal study, U-tube manometry had the highest degree of correlation (r(2) = 0.98) and the lowest bias (0.51 +/- 1.63 mm Hg). The bladder pressure measured by the U-tube technique was between 0.1 and 0.9 mm Hg less than the directly measured IAP (95% confidence interval). There was a high degree of correlation between IAP and the standard technique for bladder pressure (r(2) = 0.93), IVC pressure (r(2) = 0.93), and gastric pressure (r(2) = 0.90). Strong correlation also existed between the U-tube and standard techniques for measuring bladder pressure (r(2) = 0.96). In humans, a strong correlation between insufflated abdominal pressure and bladder pressure (U-tube technique, r(2) = 0.79; standard technique, r(2) = 0.53) was also encountered. CONCLUSION: The accuracy of the U-tube manometry technique for measuring intra-abdominal pressure is comparable to previously described techniques. The U-tube technique is simple, does not require additional equipment, and can be performed by any member of the medical team.

Abdominal wall closure after transverse rectus abdominis myocutaneous (TRAM) flap breast reconstruction is often performed under considerable tension and may theoretically cause a component of abdominal compartment syndrome. This prospective study examined intraabdominal pressure after TRAM reconstruction and correlated the findings with clinical course and outcome.All patients who underwent pedicled TRAM flap breast reconstruction from November of 1999 to December of 2000 (n = 77) were included and compared with nonoperative controls (n = 24). Intraabdominal pressures were measured indirectly using the urinary catheter in the postanesthesia care unit on postoperative days 1 and 2. Outcome measures included vital signs, urinary output, net 24-degree fluid balance, and complications. The preoperative variables were age, body mass index, parity, and presence of an epidural. For statistical analysis, the TRAM patients were divided into three groups on the basis of type of closure (bipedicle, unipedicle, and mesh), which were compared by analysis of variance. A multivariate logistic regression was performed to identify risk factors for patients with intraabdominal pressures > or =20 mmHg who were thought to have a component of abdominal compartment syndrome. The incidence of complications was compared by chi-square, with statistical significance determined for p < 0.05.Average intraabdominal pressures were significantly higher in the bipedicled TRAM (14.1 mmHg) and unipedicle TRAM (9.9 mmHg) groups when compared with the mesh group (5 mmHg) and controls (3.7 mmHg; p < 0.001). Increased intraabdominal pressure was transient and peaked on postoperative day 1. Elevated pressure was associated with decreased urinary output, decreased net fluid balance, and increased respiratory rate. Patients with intraabdominal pressures > or =20 mmHg (n = 10) had a higher incidence of complications (60 percent) compared with patients who had pressures <20 mmHg (18 percent; p < 0.05). Elevated intraabdominal pressures were strongly associated with donor-site and general complications. Positive predictive factors for elevated pressure included body mass index and type of closure (bipedicled or bilateral). Multiple pregnancies seemed to have a protective effect.A transient component of abdominal compartment syndrome does exist after TRAM flap breast reconstruction. Bipedicle closure, nulliparous women, and increased body mass index were risk factors for elevated intraabdominal pressures. Tension-free mesh closure seemed to have a protective effect. Symptomatic trends and certain complications were associated with, and possibly explained by, an elevated intraabdominal pressure.

We report the case of a 55 year old woman who developed abdominal compartment syndrome [ACS] following total gastrectomy for caustic ingestion. Contributing factors for the development of ACS included peritonitis and massive fluid resuscitation for cardiovascular support of septic shock. The adverse cardiovascular and pulmonary effects of intra-abdominal hypertension [IAH] were reversed with pharmacological neuromuscular blockade [NMB]. Surgical decompression of ACS was, therefore, postponed, but the patient required re-operation for intra-abdominal sepsis several days later and subsequently died. Although medical management of ACS with NMB may lower IAH and reverse its negative cardiopulmonary effects, surgical decompression may still be required for definitive treatment.

Compartment syndrome is classically considered a complication of a musculoskeletal injury. Recent research has confirmed the abdomen as a potential compartment with the capability to cause life-threatening local and systemic manifestations. Abdominal compartment syndrome (ACS) is precipitated by an acute increase in abdominal contents volume with resulting intraabdominal hypertension. Presenting signs of ACS include a firm tense abdomen, increased peak inspiratory pressures, and oliguria, all of which improve after abdominal decompression. Patients at risk for ACS include trauma (blunt or open), retroperitoneal hemorrhage, massive fluid resuscitation, pancreatitis, pneumoperitoneum, and neoplasm. Surgical decompression is the treatment of choice. The perianesthesia nurse plays a critical role in the team managing a patient at risk for abdominal compartment syndrome through intraabdominal pressure monitoring, wound care, and end organ perfusion support.

BACKGROUND/PURPOSE: Recent studies advocate the use of the open-abdomen technique for managing the abdominal compartment syndrome and uncontrolled intraperitoneal sepsis. The authors have used vacuum packing (Vac-Pac) in pediatric patients with excellent results and have developed a method for closing widely distracted fascial edges to avoid the need for skin grafting. METHODS: Patients who had an intraabdominal catastrophe best managed by a temporary open-abdomen technique were included. After damage control laparotomy, the Vac-Pac temporary closure was used. In 2 patients a corsetlike lacing was used to bring the widely separated fascial edges together gradually. RESULTS: Five patients with intraabdominal sepsis and one with the abdominal compartment syndrome were included. The length of time the Vac-Pac was used ranged from 3 to 21 days. In 2 patients, the corset closure allowed wound approximation within 5 to 7 days. One patient died of overwhelming sepsis, the remainder of the patients survived. CONCLUSIONS: The Vac-Pac technique for abdominal closure is a simple and inexpensive means by which to manage the open abdomen in the pediatric patient effectively. Use of a corset-type closure for wounds with widely distracted edges should eliminate the need for skin grafting over an open abdomen.

HYPOTHESIS: Intraoperative and postoperative variables contribute to the development of abdominal compartment syndrome (ACS) in general surgical patients. DESIGN: Case-control cohort study of 44 patients admitted to the surgical intensive care unit from March 1, 1995, to January 1, 2001. Groups were matched with respect to age, sex, diagnosis, and procedure. Prospectively collected data included demographics, ventilatory parameters, fluid requirements, hemodynamic and oxygen-derived variables, length of stay, and mortality rates. Statistical analysis was done with the Fisher exact test and/or chi(2) analysis. Continuous variables were analyzed with multivariate and univariate analysis. Data are presented as mean +/- SD. Statistical significance is defined as P<.05. SETTING: Long Island Jewish Medical Center (New Hyde Park, NY) is a large tertiary teaching hospital. PATIENTS: Twenty-two patients admitted to the surgical intensive care unit who developed ACS, and 22 case-control patients without ACS. MAIN OUTCOME MEASURES: Identification of variables that predict the development of ACS. RESULTS: Twenty-two patients with episodes of ACS (group 1) were examined and contrasted with 22 matched patients without ACS (group 2). Using univariate analysis, the groups differed with respect to 24-hour fluid administration and balance, number of emergency procedures, peak airway pressure, central venous pressure, pulmonary artery occlusion pressure, lengths of stay in the hospital and intensive care unit, and mortality rates. With multivariate analysis, only 24-hour fluid balance and peak airway pressure (group 1 vs group 2: mean +/- SD, 15.9 +/- 10.3 L vs 7.0 +/- 3.5 L, and 57.9 +/- 11.9 mm Hg vs 32.2 +/- 7.1 mm Hg, respectively; P<.05) remained significantly different. The groups did not differ with regard to age, cardiac index, operative blood loss, duration of surgery, intraoperative fluid input, or balance. A predictive equation for ACS development was created: P = 1/(1 +e(-z)), where z= -18.6763 + 0.1671 (peak airway pressure) + 0.0009 (fluid balance). CONCLUSION: The results of this study indicate that 24-hour fluid balance and peak airway pressure are 2 independent variables predictive of the development of ACS in nontrauma surgical patients.

The abdominal compartment syndrome (ACS) is a clinical entity that develops after sustained and uncontrolled intra-abdominal hypertension. ACS has been demonstrated to affect multiple organ systems including the cardiovascular, respiratory, gastrointestinal, genitourinary, and neurologic systems. To date most descriptions of ACS are found in the trauma literature, but the development of ACS in the general surgical population is being increasingly observed. In this study the development of ACS in a nontrauma surgical population is described and examined. The records of 18 surgical intensive care unit patients with documented ACS were reviewed retrospectively. Data acquired included demographics, urine output in mL/hour, cardiac index in L/m2/min: systemic vascular resistance index in mm Hg/L/m2/min: and pulmonary artery occlusion pressure, peak inspiratory pressure, partial pressure of oxygen in arterial blood, pH, partial pressure of carbon dioxide, and intra-abdominal pressure (all in mm Hg). When they were available values were obtained before and after decompression. Data are presented as mean +/- standard deviation and are analyzed by Student's t-test; significance was accepted to correspond to a P value <0.05. Nineteen episodes of ACS were identified in 18 patients. The average age was 69.2 years, and the observed mortality of the group was 61.1 per cent (11 of 18). Diagnoses included abdominal aortic aneurysm (eight), postoperative laparotomy (six), pancreatitis (three), and cerebral aneurysm (one). Of the parameters examined urine output, peak inspiratory pressure, and cardiac index demonstrated a significant change before and after decompression. The average intra-abdominal pressure was 43.4 mm Hg. Five of 18 patients (two with abdominal aortic aneurysm, two with postoperative laparotomy, and one with pancreatitis) were found to have necrotic bowel on decompressive laparotomy. The development of ACS is described in a surgical intensive care unit. ACS is the end result of uncontrolled intra-abdominal hypertension and results in systemic derangements. Surgical decompression of ACS significantly reduces peak inspiratory pressure while increasing urine output and cardiac index. The observed association between ACS and ischemic bowel may result from decreased mucosal perfusion as a direct result of abdominal hypertension. In our patient population ACS resulted in a 61.1 per cent mortality.

The acute intra-abdominal hypertension causes profound physiologic abnormalities, both within and outside the abdomen. Just as in compartment syndrome in the extremities, gut mucosal ischemia begins long before clinical signs are evident, explaining the name of "abdominal compartment syndrome" given to the acute, markedly increased intra-abdominal pressure. The abdominal compartment syndrome was initially described in patients with severe abdominal injuries and massive transfusions and crystalloid infusions, caused by the closure of fascia or skin under tension, the use of bulky abdominal packs to control diffuse bleeding, the massive bowel distension and edema, and the continued bleeding into the abdominal cavity. Intra-abdominal pressure can be monitored by measuring the urinary bladder pressure with a manometer, connected to the transurethral Foley catheter, with the symphysis pubis as the zero point. A persistent elevation of the intra-abdominal pressure beyond 20-25 cmH2O, with significant respiratory, hemodynamic and renal dysfunction is an indication for abdominal decompression, before the manifestations of abdominal compartment syndrome became clinically evident. The mortality in patients with abdominal compartment syndrome is over 40%, even when adequately treated.

"Bogota bags" are often used for temporary abdominal closure after damage control or staged laparotomy for trauma or release of abdominal compartment syndrome. After placement of the Bogota bag serial operative closures are required to return abdominal contents to their original location before definitive closure. Unnecessary operative procedures may be avoided when binder clips are used to facilitate the gradual approximation of the wound edges before abdominal closure.

We present a case report of a child with intussusception who underwent air reduction which was complicated by bowel perforation. Life threatening tension pneumoperitoneum developed rapidly and immediate needle decompression was life saving in this case. The pathophysiology of hyperacute abdominal compartment syndrome is discussed.

The aim of the study was to assess whether increased intra-abdominal pressure affects the clinical course and reflects on the effectiveness of the conservative treatment in patients with severe acute pancreatitis. Data on 37 consecutive patients with severe acute pancreatitis that were collected prospectively included APACHE II score, daily measurement of the intra-abdominal pressure, and clinical routine. Group A consisted of 26 patients with intra-abdominal pressure < 25 cm/H2O during their treatment period, and group B consisted of 11 patients with intraabdominal pressure > or = 25 cm/H2O. SIRS, MODS, complication rate and mortality were analysed. The age, APACHE II scores and hospital stay were similar in both groups. ICU stay was 9.1 +/- 9.6 vs. 20.7 +/- 16.8 days in groups A and B, p < 0.05. SIRS and MODS developed less frequently in group A. More pulmonary complications developed in group B, reaching 64% compared to 19% in group A, p < 0.05. Intra-abdominal pressure had negative interrelation with enterally provided volume (r = -0.45, p < 0.001) and positive interrelation with parenterally provided volume (r = +0.27, p < 0.01) in all. Mortality was zero in group A vs. 36% in group B, p < 0.01. Increase of the intra-abdominal pressure is common during the clinical course of severe acute pancreatitis and can be associated with aggressive fluid replacement therapy. Routine measurement of the intra- abdominal pressure is rational in the clinical setting of the ICU and gives additional criteria for the evaluation of the clinical course and the effectiveness of the treatment. Marked increase of the intra- abdominal pressure should be considered a serious prognostic sign in patients with severe acute pancreatitis.

OBJECTIVE: The objectives of this study were the comparison of patients who needed mesh closure of the abdomen with patients who underwent standard abdominal closure after ruptured abdominal aortic aneurysm repair and the determination of the impact of timing of mesh closure on multiple organ failure (MOF) and mortality. METHODS: We performed a case-control study of patients who needed mesh-based abdominal closure (n = 45) as compared with patients who underwent primary closure (n = 90) after ruptured abdominal aortic aneurysm repair. RESULTS: Before surgery, the patients who needed mesh abdominal closure had more blood loss (8 g versus 12 g of hemoglobin; P <.05), had prolonged hypotension (18 minutes versus 3 minutes; P <.01), and more frequently needed cardiopulmonary resuscitation (31% versus 2%; P <.01) than did the patients who underwent primary closure. During surgery, the patients who needed mesh closure also had more severe acidosis (base deficit, 14 versus 7; P <.01), had profound hypothermia (32 degrees C versus 35 degrees C; P <.01), and needed more fluid resuscitation (4.0 L/h versus 2.7 L/h; P <.01). With this adverse clinical profile, the patients who needed mesh closure had a higher mortality rate than did the patients who underwent primary closure (56% versus 9%; P <.01). However, the patients who underwent mesh closure at the initial operation (n = 35) had lower MOF scores (P <.05), a lower mortality rate (51% versus 70%), and were less likely to die from MOF (11% versus 70%; P <.05) than the patients who underwent mesh closure after a second operation in the postoperative period for abdominal compartment syndrome (n = 10). CONCLUSION: This study reports the largest experience of mesh-based abdominal closure after ruptured abdominal aortic aneurysm repair and defines clinical predictors for patients who need to undergo this technique. Recognition of these predictors and initial use of mesh closure minimize abdominal compartment syndrome and reduce the rate of mortality as the result of MOF.

BACKGROUND: The abdominal compartment syndrome (ACS) has been implicated in the pathogenesis of postinjury multiple organ failure. The ACS is defined as intra-abdominal hypertension causing adverse physiologic response. This study was designed to determine the effects of IAH on the production of interleukin-1b (IL-1beta), interleukin-6 (IL-6), tumor necrosis factor (TNF-alpha), and the effects on remote organ injury. METHODS: IAH was induced in Sprague-Dawley rats which were divided into 5 groups, 10 animals each. Intra-abdominal pressure (IAP) was increased to 20 mm Hg for 60 and 90 minutes in two different groups. In a third group following IAP of 20 mm Hg the abdomen was decompressed for 30 minutes before samples were collected. The other animals were used as controls. Hemodynamic response was monitored throughout the procedure. Cytokine levels were assessed in the plasma. Remote organ injury was assessed by histopathology and myeloperoxidase activity. RESULTS: IAH caused a significant decrease in MAP. After abdominal decompression MAP returned to baseline levels. A significant decrease in arterial pH was also noted. Increase in the levels of TNF-alpha and IL-6 was noted 30 minutes after abdominal decompression. Plasma concentration of IL-1b was elevated after 60 minutes of IAH. Abdominal decompression, however, did not cause a significant increase in the levels of this cytokine. Lung neutrophil accumulation was significantly elevated only after abdominal decompression. Histopathological findings showed intense pulmonary inflammatory infiltration including atelectasis and alveolar edema. CONCLUSIONS: IAH provokes the release of pro-inflammatory cytokines which may serve as a second insult for the induction of MOF.

We here report the case of a patient with systemic capillary leak syndrome (SCLS). This syndrome is a rare condition characterized by recurrent episodes of hypotension with hemoconcentration and hypoproteinemia. It is due to unexplained episodic capillary hyperpermeabilty that results in fluid and protein shift from the intravascular to the interstitial space: generalized edema, shock and renal failure follow. A 59 yo man was admitted to our intensive care unit because of unexplained shock with hemoconcentration, renal failure, and metabolic acidosis. Previous attemps to reverse shock in a medical ward with crystalloids and dopamine failed. An abdominal CT scan, a TEE, and chest X ray study were inconclusive. No sign or history of major infections or anaphylaxis were present. The patient was resuscitated with massive fluid infusions and norepinephrine on the guide of a Swan Ganz catheter. The diagnosis was made on the basis of a previous episode of severe shock complicated with renal failure and a compartment syndrome, the hemoconcentration, and the negative cardiopulmonary findings. A small amount of monoclonal immunoglobulin G, kappa chain, found in the serum confirmed the diagnosis. The SCLS should be considered in the differential diagnosis of idiopathic and anaphylactic shock. Patients may benefit from a prophylactic treatment with theophilline and terbutaline.

BACKGROUND: Laparostomy is frequently performed in the surgical therapy of mechanical obstruction, peritonitis, or trauma to prevent abdominal compartment syndrome (ACS). Extended incisional hernia is inevitable when fascial closure is missed (up to 90% of cases). Intra-abdominal pressure (IAP) has not yet been evaluated as a criterion for the feasibility of fascial closure. PATIENTS AND METHODS: Over 12 months laparostomy was carried out in 40 patients. Definitive closure of the abdomen was performed after 4.4+/-3.7 days in 23 of these. Intravesical pressure was used to assess IAP before and after fascial closure. The resulting IAP was compared to the values of 90 patients undergoing elective abdominal surgery. Parameters of cardiocirculatory, renal, pulmonary, and liver function were also recorded. RESULTS: After closure of the laparostomy IAP increased significantly from 6.5+/-3.3 to 12.0+/-4.1 mmHg. Urine output decreased by 27% on the first postoperative day but regained normal levels thereafter. The central venous pressure increased by 31%. Other parameters of cardiocirculatory, renal, pulmonary, and liver function were unchanged. No case of ACS occurred. In the patients undergoing elective abdominal surgery IAP ranged from 6.5+/-2.1 to 10.0+/-4.0 mmHg. CONCLUSIONS: Fascial closure increased the IAP, which was accompanied by short-termed decrease in urine output. At these levels of IAP fascial closure appears to be harmless, but further prospective studies are needed to determine the critical level of IAP for allowing a safe repair of large fascial defects.

BACKGROUND: An intra-abdominal pressure (IAP) of 15 mm Hg reduces intestinal organ perfusion in humans and animals, but it is unknown whether this results in organ damage. The purpose of this study was to evaluate if an IAP of 15 mm Hg lasting for 24 h in a porcine model will lead to morphologic impairment of intestinal and adjacent organs. METHODS: We examined 12 intubated and anesthetized domestic pigs (51.8 +/- 4.4 kg). Using CO2 pneumoperitoneum, the IAP was raised to 15 mm Hg (study group, n = 6) for an investigation period of 24 h. In the control group, the IAP remained unchanged. Investigated parameters were cardiac output (CO), peak inspiratory pressure (PIP), and urine output (UO), as well as serum creatinine, alanine aminotransferase (ALT), lactate, lipase, and alkaline phosphatase (AP). Additionally, histopathological examinations were performed.Results. In comparison to the control, CO did not change, while UO decreased significantly by 59% and PIP increased significantly to more than 30 mbar. Serum ALT and AP increased significantly while there was no change in creatinine, lactate, and lipase. Histopathologically, low-grade liver necrosis (12% of liver lobuli), low-grade proximal tubular epithelial necrosis, and low bowel mucosal damage were observed.Conclusion. In this porcine model, an IAP of 15 mm Hg lasting for 24 h was found to result in functional and morphologic impairment of lungs, liver, kidneys, and bowel. These results imply that a prolonged IAP of 15 mm Hg predisposes to multiorgan dysfunction and that a safe duration of increased IAP still has to be determined.

An 11-year-old boy sustained a grade IV liver injury and complete disruption of the left hepatic duct (LHD) secondary to a sledding accident. Although he became hemodynamically stable after initial resuscitation in the emergency department and the intensive care unit (ICU), serial paracentesis procedures were necessary to manage abdominal compartment syndrome (ACS). The fluid initially was serosanguinous but subsequently became bile stained. A bile leak was confirmed by a technetium 99m dimethyliminodiacetic acid (HIDA) scan and an endoscopic retrograde cholangiogram (ERCP). The LHD transection was treated with percutaneous drainage of the subhepatic space and a transampullary biliary stent. The leak sealed within 8 days, and follow-up ERCP as an outpatient showed no extravasation but could not visualize the LHD. Repeat computed tomography (CT) scan 3(1/2) months after injury showed the liver laceration to be healed with atrophy of the left lobe and no ductal dilatation. The patient has had a complete recovery, resumed all activities, and currently is 20 months after his injury with no sequelae.

This study was designed to establish if clinical examination can accurately predict intraabdominal pressure (IAP). Between August 1998 and March 2000 a prospective blinded observational study of postoperative intensive care unit patients was undertaken at a major trauma center. IAP was measured using an intravesicular technique and compared with clinical evaluation. An IAP of at least 18 mmHg was considered elevated. The sensitivity, specificity, positive predicative value (ppv), negative predictive value (npv), kappa score, and reliability analysis were calculated. A total of 110 patients provided 150 estimates of IAP, which was elevated in 21%. The kappa score was 0.37; sensitivity, 60.9%; specificity, 80.5%; ppv, 45.2%; npv, 88.6%. The mean difference in IAP values between intravesicular readings and clinical estimates was -1.0 +/- 4.1. Prediction of IAP using clinical examination is not accurate enough to replace intravesicular IAP measurements.

Through clinical observation of 11 patients with abdominal compartment syndrome (ACS), the author explored the effects of acutely elevated abdominal pressure on systemic circulation, respiration and renal function. Based on the experience in diagnosis and treatment of ACS, the author suggests that early identification and timely surgical depressurization are essential to reduce mortality and improve the prognosis.

BACKGROUND: Acute compartment syndrome is both a limb- and life-threatening emergency that requires prompt treatment. To avoid a delay in diagnosis requires vigilance and, if necessary, intracompartmental pressure measurement. This review encompasses both limb and abdominal compartment syndrome, including aetiology, diagnosis, treatment and outcome. METHODS: A Pubmed and Cochrane database search was performed. Other articles were cross-referenced. RESULTS AND CONCLUSION: Diagnosis of limb compartment syndrome is based on clinical vigilance and repeated examination. Many techniques exist for tissue pressure measurement but they are indicated only in doubtful cases, the unconscious or obtunded patient, and children. However, monitoring of pressure has no harmful effect and may allow early fasciotomy, although the intracompartmental pressure threshold for such an undertaking is still unclear. Abdominal compartment syndrome requires measurement of intra-abdominal pressure because clinical diagnosis is difficult. Treatment is by abdominal decompression and secondary closure. Both types of compartment syndrome require prompt treatment to avoid significant sequelae.

The purpose of this study was to investigate whether an intra-abdominal pressure (IAP) of 30 mmHg lasting 24 h in a porcine model will lead to a condition comparable with the abdominal compartment syndrome (ACS) in humans. We examined 12 intubated and anesthetized domestic pigs with a mean body weight of 52.5 +/- 4.9 kg. Using a CO2 pneumoperitoneum, the IAP was increased to 30 mmHg (study group, n = 6) for an investigation period of 24 h. In the control group, the IAP remained unchanged. Investigated parameters were cardiac output (CO), peak inspiratory pressure (PIP), urine output (UO), as well as serum alanine aminotransferase (ALT), lactate, lipase, and alkaline phosphatase (AP). Additionally, histopathological examinations were performed. In the study group, CO was significantly reduced compared with the control group. All animals of this group became anuric and their PIP exceeded 40 cm H2O. Furthermore, ALT, AP, lipase, and lactate were significantly increased. Histopathologically, high-grade atelectasis in the lower lobes of the lung together with medium grade liver necrosis, medium grade proximal tubular epithelial necrosis, and medium grade mucosal bowel damage were observed. In this porcine model, an intra-abdominal pressure of 30 mmHg led to a condition comparable with the ACS. Because function or integrity of additional organ systems was impaired, an IAP of 30 mmHg has to be considered a predisposition for the multi-organ dysfunction syndrome in this porcine model.

BACKGROUND. To decide "how and when to treat intra-abdominal infection" is one of the most important challenges for surgeons interested in abdominal sepsis. The minimally invasive approach to intra-abdominal infection, both diagnostic and therapeutic, has gained great popularity in recent years: the cause of infection is assessed as soon as possible by means of sophisticated radiography and minimally invasive surgery, patients with intra-abdominal infection are treated with the least surgical injury in order not to aggravate the systemic response ("second hit"), and clinicians rely on clinical scoring combined with new imaging techniques to decide for reintervention. In some patients with severe intra-abdominal infection damage control followed by a few planned relaparotomies seems necessary to provide a solid basis for the patient to start recovering. Paying close attention in these patients to maximal support vital systems and preventing local complications seems crucial for their eventual prognosis. DISCUSSION. In this context we discuss important surgical topics such as primary resection and anastomosis in perforated diverticulitis, planned relaparotomy vs. relaparotomy "on demand," intra-abdominal hypertension, and primary and delayed abdominal wall closure techniques after operation for severe intra-abdominal infection.

The rat is increasingly being used to study the physiological response to elevated intra-abdominal pressure (IAP) during laparoscopic surgery. Although decreased portal venous flow associated with the elevated IAP has been reported in large animals, little information is available in rats. Furthermore, the relative blood flow changes in the hepatic artery and portal vein have not been reported. Therefore, this study was performed to elucidate the change in systemic and splanchnic circulation, including hepatic arterial and portal venular flow, during pneumoperitoneum in rats. Sprague-Dawley rats were assigned into either a ventilated or nonventilated group and then subjected to various levels of IAP (0, 5, 10, and 20 mm Hg) using carbon dioxide gas. At each pressure, both cardiac output and splanchnic organ flow were determined using fluorescent microspheres. There was no obvious hemodynamic difference between the ventilated and nonventilated groups. Mean arterial pressure and cardiac index were significantly lower with 20 mm Hg of IAP compared to 0 mm Hg in both groups. Flow to the spleen, stomach, duodenum, total intestine, and portal vein was all decreased by increasing IAP (P < 0.05 at 20 mm Hg compared to 0 mm Hg) and was significantly correlated to the decrease in cardiac index. However, the hepatic arterial flow was relatively preserved throughout all levels of IAP, suggesting activation of the hepatic arterial buffer response. We conclude that the decreased splanchnic flow during pneumoperitoneum largely depends on the decreased cardiac index. Hepatic artery flow, however, is selectively preserved and may provide protection for liver function during sustained elevations in IAP.

In Stone's milestone article on damage-control surgery (DCS) (Ann Surg 1983; 197:532-535), detailed clinical observations of abdominal compartment syndrome (ACS) were presented although the concept of ACS had not yet been established at that time. Since then the concept of ACS has been developed concomitantly with the widespread application of DCS for severe trauma victims. Intraabdominal pressure (IAP) is the most important factor for determining the severity of pathophysiological consequences in patients with ACS. Increased IAP pushes the diaphragm upward, which may cause deterioration of pulmonary function. Increased IAP decreases the glomerular filtration rate and urinary secretion. Patients with severe torso injury may have intraabdominal and/or retroperitoneal hematomaor edema formation in the mesentery, and all those can be factors that elevate IAP. About one-third of patients who undergo DCS develop ACS. Decompression of IAP clearly ameliorates physiological parameters in those patients, although the, mortality rate may not be improve despite adequate control of IAP. This suggest that in addition to elevated IAP other factors such as increased cytokine production might be important in ACS. Inserting a plastic infusion bag between intraabdominal organs and the abdominal wall rather than suturing a plastic bag to the edge of the opened abdominal wall may be preferable for further reconstruction of the wall.