Beck, R., M. Halberthal, et al. (2001). "Abdominal compartment syndrome in children." Pediatr Crit Care Med 2(1): 51-6.

OBJECTIVE: To investigate the frequency, predisposing factors, clinical presentation, and outcome of abdominal compartment syndrome (ACS) in critically ill pediatric patients. DESIGN: A prospective study over a 5-yr period. SETTING: Pediatric intensive care unit of a tertiary care, university hospital. PATIENTS: All patients admitted to the pediatric intensive care unit were screened for the presence of ACS and were treated with a uniform protocol. ACS was defined as abdominal distention with intra-abdominal pressure (IAP) > 15 mm Hg, accompanied by at least two of the following: oliguria or anuria; respiratory decompensation; hypotension or shock; metabolic acidosis. MEASUREMENTS AND MAIN RESULTS: Of 1762 patients admitted over 5 yrs, ten patients (0.6%) had a total of 15 episodes of ACS. Of 406 trauma cases, three had ACS (0.7%). Three of the ten patients had primary abdominal conditions (mesenteric vein thrombosis, intussusception, enterocolitis), three had abdominal surgery (trauma, Kasai operation, esophageal perforation and peritonitis), three had primary central nervous system involvement, and one had meningococcemia. At laparotomy, bowel ischemia or necrosis was found in four episodes of ACS (27%). Mean IAP at diagnosis of ACS was 23.9 +/- 3.8 (range 17-31) mm Hg. Physiologic parameters were compared during 4 hrs before the development of ACS, during ACS, and after abdominal decompression. Mean arterial pressure, Pao(2), Pao(2)/Fio(2) ratio, and urinary output decreased significantly, whereas Paco(2), peak inspiratory pressures, positive end-expiratory pressures, and base deficit increased significantly after the development of ACS. After decompressive laparotomy, the condition of the patients improved promptly and these variables returned to pre-ACS values. Overall mortality rate in this group was 60%. CONCLUSIONS: Although relatively infrequent compared with adults, ACS occurs in critically ill children. Timely decompression of the abdomen results in uniform improvement, but overall mortality is still high. In contrast with adults, children with ACS have diverse primary diagnoses, with a significant number of primary extra-abdominal-mainly central nervous system-conditions. Ischemia and reperfusion injury appear to be the major mechanisms for development of ACS in children. Clinical presentation is similar to adults, but children may develop ACS at a lower IAP (as low as 16 mm Hg).

BACKGROUND: Lately renewed attention has been given to the abdominal compartment syndrome. Despite of this there still remain a lot of controversies with regard to the pathophysiological mechanisms underlying this syndrome and the therapeutic options. METHODS: Two cases of patients with this syndrome are described and the data from animal and human trials concerning the abdominal compartment syndrome are presented and discussed. RESULTS: A variety of clinical disorders may lead to the abdominal compartment syndrome. It mainly affects the cardiovascular, pulmonary and renal organ systems. Although some clinical effects are clearly described, the exact mechanisms underlying these changes in humans are incompletely understood. It is still unclear why some patients develop abdominal compartment syndrome and others do not. The intra-abdominal pressure can easily be assessed by measuring the urine bladder pressure, which correlates well with the actual intra-abdominal pressure. All authors agree that a decompression of the abdomen by means of a laparotomy is the treatment of choice for the abdominal compartment syndrome. Which parameters should determine the indication however, remains controversial, since the correlation between clinical signs and pressure is not straightforward. CONCLUSIONS: The abdominal compartment syndrome is a well-recognised disease entity related to acutely increased abdominal pressure. Urgent laparotomy can be lifesaving in some cases. However no single threshold of abdominal pressure can be applied universally. Pending further clinical trials the best therapeutic option seems to be to decompress the abdomen surgically if the intravesical pressure is 25 mmHg or higher in patients with refractory hypotension, acute renal failure or respiratory failure due to abdominal distension.

BACKGROUND: Recent reports have described resuscitation-induced, "secondary" abdominal compartment syndrome (ACS) in trauma patients without intra-abdominal injuries. We have diagnosed secondary ACS in a variety of nontrauma as well as trauma patients. The purpose of this review is to characterize patients who develop secondary ACS. METHODS: Our prospective ACS database was reviewed for cases of secondary ACS. Physiologic parameters and outcomes were recorded. Data are expressed as mean +/- SEM. RESULTS: Fourteen patients (13 male, aged 45 +/- 5 years) developed ACS 11.6 +/- 2.2 hours following resuscitation from shock. Eleven (79%) had required vasopressors; the worst base deficit was 14.1 +/- 1.9. Resuscitation included 16.7 +/- 3.0 L crystalloid and 13.3 +/- 2.9 red blood cell units. Decompressive laparotomy improved intra-abdominal, systolic, and peak airway pressures, as well as urine output; however, mortality was 38% among trauma and 100% among nontrauma patients. CONCLUSIONS: Secondary ACS may be encountered by general surgeons in a variety of clinical scenarios; resuscitation from severe shock appears to be the critical factor. Early identification and abdominal decompression are essential. Unfortunately, in our experience, this is a highly lethal event.

Abdominal compartment syndrome is a well-described condition in which increased intra-abdominal pressure causes various physiologic derangements with adverse effects on cardiac, pulmonary, and renal function. A patient presented with radiation-induced distal colonic obstruction, abdominal distention, and severe bilateral leg edema. We performed a diverting transverse loop colostomy as treatment for her obstruction. This resulted in massive, spontaneous diuresis with complete resolution of her lower-limb edema. Abdominal compartment syndrome due to colonic obstruction can contribute to the development of lower-extremity edema. Colon decompression with reduction of intra-abdominal pressure can lead to resolution of edema in this situation.

Percutaneous endoscopic gastrostomy is a commonly performed procedure for enteral access. In the past decade surgeons have used the open abdomen technique with increased frequency for the treatment of intra-abdominal compartment syndrome. Because these patients often have associated malnutrition long-term enteral access is complicated by the massive ventral hernia. We reviewed the records of two patients with an open abdomen who needed long-term enteral access. Both patients had a large midabdominal soft tissue defect, which posed a concern about the technique for gastrostomy creation. Both patients underwent percutaneous endoscopic gastrostomy. In each case the entrance site was located on a portion of intact abdominal wall lateral to the open abdomen tissue defect. No intraoperative or postoperative complications were noted. We conclude that percutaneous endoscopic gastrostomy can be safely performed in patients with an open abdomen. Adherence to standard principles of performing percutaneous endoscopic gastrostomy allows for enteral access in these patients.

BACKGROUND: Nonoperative management has been validated as a standard of care for patients with blunt hepatic trauma. We herein study the correlation of intra-abdominal pressure (IAP) and other clinical parameters to predict the failure of nonoperative management, and attempt to use IAP to determine further therapeutic options. METHODS: During a 9-month period, 25 hemodynamically stable patients sustaining grades III to V blunt hepatic injuries were prospectively studied. They were admitted to the intensive care unit for clinical reevaluation, and hemodynamic and IAP monitoring. If the patient developed an IAP greater than 25 cm H(2)O, then an emergent laparotomy or laparoscopy was performed to achieve hemostasis and decompression of intra-abdominal hypertension (IAH). On the basis of an IAP of 25 cm H(2)O, the correlation between the IAP and an estimated amount of liver-related transfusion, the Pao(2)/Fio(2) ratio and peritoneal signs were analyzed. RESULTS: Of the 25 patients being studied, 20 (80%) had an IAP below 25 cm H(2)O, 1 of whom was found to have a pelvic abscess from an amputated segment of liver. On the other hand, five other patients with an IAP greater than 25 cm H(2)O received decompression and laparoscopic examinations, and one needed an open hepatorrhaphy. In general, though, 19 patients (76%) were successfully treated without operation. All recovered well after different therapeutic regimens; however, two developed liver abscesses, for a morbidity rate of 8% (2 of 25). This analysis revealed a strong association between the IAP value and the presence of peritoneal signs (Phi coefficient = 0.890, p < 0.001), but not in the estimated amount of liver-related transfusion and Pao(2)/Fio(2) ratio. CONCLUSION: This preliminary investigation suggests that IAH or abdominal compartment syndrome can develop while patients receive nonoperative management for grade III to V blunt hepatic injuries. There were no parameters that precisely reflected ongoing hepatic hemorrhage or predicted hemodynamic instability. Although the amount of hepatic hemorrhage was not accurately measured by the IAP, it could be reflected by an increased IAP. During nonoperative management, IAP monitoring may be a simple and objective guideline to suggest further intervention for patients with blunt hepatic trauma. Laparoscopic hepatic evaluation and abdominal decompression may be helpful in this situation.

OBJECTIVE: To evaluate the effect of a stepwise increase in intra-abdominal pressure (IAP) on intracranial pressure (ICP) and to further define the pressure transmission characteristics of different body compartments. DESIGN: A prospective, nonrandomized study. SETTING: A multidisciplinary intensive care unit at a university medical center. PATIENTS: Fifteen patients with moderate-to-severe head injury. INTERVENTIONS: All patients were studied after the initial stabilization and resolution of intracranial hypertension. Measurements were carried out before and 20 mins after IAP was increased by positioning a soft, 15-L water bag on the patient's abdomen. MEASUREMENTS AND MAIN RESULTS: Placing weights upon the abdomen generated a significant increase in IAP, which rose from 4.7 +/- 2.9 to 15.5 +/- 4.1 mm Hg (p <.001). The rise in IAP caused concomitant and rapid increases in central venous pressure (from 6.2 +/- 2.4 to 10.4 +/- 2.9 mm Hg; p <.001), internal jugular pressure (from 11.9 +/- 3.2 to 14.3 +/- 2.4 mm Hg; p <.001), and ICP (from 12.0 +/- 4.2 to 15.5 +/- 4.4 mm Hg; p <.001). Thoracic transmural pressure, calculated as the difference between central venous pressure and esophageal pressure, remained constant during the protocol. Respiratory system compliance decreased from 58.9 +/- 9.8 to 44.9 +/- 9.4 mL/cm H2O (p <.001) in all patients because of decreased chest wall compliance. The mean arterial pressure increased from 94 +/- 11 to 100 +/- 13 mm Hg (p <.01), which allowed the maintenance of a stable cerebral perfusion pressure (82.4 +/- 10.3 vs. 84.7 +/- 11.5 mm Hg; p = NS) despite the ICP increase. CONCLUSIONS: Increased IAP causes a significant rise in ICP in head trauma patients. This effect seems to be the result of an increase in intrathoracic pressure, which causes a functional obstruction to cerebral venous outflow. Routine assessment of IAP may help clinicians to identify remediable causes of increased ICP. Caution should be used when applying laparoscopic techniques in neurotrauma patients.

We report on 4 cases of abdominal compartment syndrome complicated by acute renal failure that were promptly reversed by different abdominal decompression methods. Case 1: A 57-year-old obese woman in the post- operative period after giant incisional hernia correction with an intra- abdominal pressure of 24 mm Hg. She was sedated and curarized, and the intra-abdominal pressure fell to 15 mm Hg. Case 2: A 73-year-old woman with acute inflammatory abdomen was undergoing exploratory laparotomy when a hypertensive pneumoperitoneum was noticed. During the surgery, enhancement of urinary output was observed. Case 3: An 18-year-old man who underwent hepatectomy and developed coagulopathy and hepatic bleeding that required abdominal packing, developed oliguria with a transvesical intra-abdominal pressure of 22 mm Hg. During reoperation, the compresses were removed with a prompt improvement in urinary flow. Case 4: A 46-year-old man with hepatic cirrhosis was admitted after incisional hernia repair with intra-abdominal pressure of 16 mm Hg. After paracentesis, the intra-abdominal pressure fell to 11 mm Hg.

OBJECTIVE: To describe a complication of low-molecular-weight heparin (enoxaparin) in the setting of critically ill patients. DESIGN: Case report. SETTING: The medical and surgical intensive care units of a tertiary care university teaching hospital. PATIENTS: Two adult patients receiving enoxaparin developed retroperitoneal hematoma and abdominal compartment syndrome. Both patients became anuric and required high-dose intravenous fluids and vasopressors to maintain blood pressure. INTERVENTION: Discontinuation of enoxaparin, followed by exploratory laparotomy and evacuation of the hematoma. MEASUREMENTS AND RESULTS: Immediate clinical improvement following evacuation of hematoma. CONCLUSIONS: High-risk patients receiving low-molecular-weight heparin should be identified and closely monitored to prevent serious bleeding complications.

We report on 4 cases of abdominal compartment syndrome complicated by acute renal failure that were promptly reversed by different abdominal decompression methods. Case 1: A 57-year-old obese woman in the post-operative period after giant incisional hernia correction with an intra-abdominal pressure of 24 mm Hg. She was sedated and curarized, and the intra-abdominal pressure fell to 15 mm Hg. Case 2: A 73-year-old woman with acute inflammatory abdomen was undergoing exploratory laparotomy when a hypertensive pneumoperitoneum was noticed. During the surgery, enhancement of urinary output was observed. Case 3: An 18-year-old man who underwent hepatectomy and developed coagulopathy and hepatic bleeding that required abdominal packing, developed oliguria with a transvesical intra-abdominal pressure of 22 mm Hg. During reoperation, the compresses were removed with a prompt improvement in urinary flow. Case 4: A 46-year-old man with hepatic cirrhosis was admitted after incisional hernia repair with intra-abdominal pressure of 16 mm Hg. After paracentesis, the intra-abdominal pressure fell to 11 mm Hg.

Abdominal compartment syndrome (ACS) is defined by the deleterious effects of intraabdominal hypertension (IAH) on the pulmonary, cardiovascular, splanchnic, urinary and central nervous system. Abnormal and sudden increase in the volume of any component of the intraperitoneal or retroperitoneal space (occurRing postoperatively or subsequent to hemorrhagic trauma, referfusion edema, penumoperitoneum, intestinal distention, acute pancreatitis...) causes IAH. Sustained IAH leads to ACS which if left unrecognized or untreated is always fatal. Measurement of urinary bladder pressure is the best validated technique for diagnosis of IAH. It should be used routinely for minimally invasive surveillance of intra-abdominal pressure (IAP) in patients with severe thoraco-abdominal trauma or after major abdominal operations. Medical management of IAH is of limited efficacy making expedient surgical decompression the treatment of choice for ACS. Surgical decompression of the abdomen and temporary closure is generally recognized as effective in clinically patent ACS but the pressure threshold indicating the need for decompression remains controversial. No data are available from controlled randomized trials and current guidelines are based on the experience of large trauma centers. The few available prospective clinical series report survival rates in the 38 to 71% range after surgical decompression for ACS. These studies are difficult to compare due to methodological features but it would appear that centers using the lowest pressure threshold for decompensation (< 20 mmHg) have the highest survival rates. Despite the available physiological arguments, indications for prophylactic temporary abdominal coverage (TAC), e.g. in trauma patients or for early decompression in IAH patients without clinical ACS, have not been validated in clinical practice. The potential morbidity of decompression procedures, TAC, and subsequent abdominal wall reconstructions require comparative studies of these treatment options with available pharmacological and non-surgical means to lower IAP.

The abdominal compartment syndrome (ACS) causes dysfunctions of various organs through a progressive unphysiologic increase of the intraabdominal pressure. While the primary ACS is a result of the underlying disease/injury, secondary ACS is caused by surgical interventions. In the severely injured patient intra- and/or retroperitoneal bleeding, edema of viscera due to systemic ischemia reperfusion injury following hemorrhagic shock, abdominal/pelvic packing, and laparotomy closure under tension lead to ACS. The clinical signs of ACS are a tense abdomen with a decreased abdominal wall compliance. Early signs of ACS are a rise in inspiratory pressure and oliguria. Manifest ACS results in anuria, respiratory failure, reduced intestinal perfusion, and low cardiac output syndrome. If untreated, patients die due to left ventricular failure. Diagnosis of ACS is made using the patient's history including the injury pattern, the symptoms, the time period between injury and the occurrence of organ dysfunctions, and the physiologic response to decompression. Frequent determinations of the bladder pressure represent the "golden standard" for early recognition of ACS. Decompressive laparotomy should be performed with a bladder pressure > or = 20 mmHg and rapidly restores impaired organ functions. In the case of a multiple injured patients in shock or with associated severe head injury decompressive laparotomy may even be carried out at a lower bladder pressure. The abdomen is left open. In most patients staged laparotomy is necessary. The final closure of the abdominal wall is carried out after the edema have resolved between day 6 and 8 after primary laparotomy.

BACKGROUND: Increased intra-abdominal pressure (IAP) is an adverse complication seen in critically ill, injured, and postoperative patients. IAP is estimated via the measurement of bladder pressure. Few studies have been performed to establish the actual relationship between IAP and bladder pressure. The purpose of this study was to confirm the association between intravesicular pressure and IAP and to determine the bladder volume that best approximates IAP. METHODS: Thirty-seven patients undergoing laparoscopy had intravesicular pressures measured with bladder volumes of 0, 50, 100, 150, and 200 mL at directly measured intra-abdominal pressures of 0, 5, 10, 15, 20, and 25 mm Hg. Correlation coefficients and differences were then determined. RESULTS: Across the IAP range of 0 to 25 mm Hg using all of the tested bladder volumes, the difference between IAP and intravesicular pressures (bias) was -3.8 +/- 0.29 mm Hg (95% confidence interval) and measurements were well correlated (R2 = 0.68). Assessing all IAPs tested, a bladder volume of 0 mL demonstrated the lowest bias (-0.79 +/- 0.73 mm Hg). When considering only elevated IAPs (25 mm Hg), a bladder volume of 50 mL revealed the lowest bias (-1.5 +/- 1.36 mm Hg). A bladder volume of 50 mL in patients with elevated IAP resulted in an intravesicular pressure 1 to 3 mm Hg higher than IAP (95% confidence interval). CONCLUSION: Intravesicular pressure closely approximates IAP. Instillation of 50 mL of liquid into the bladder improves the accuracy of the intravesicular pressure in measuring elevated IAPs.

Different causes, for example posttraumatic and postoperative complications, can lead to an elevated intra-abdominal pressure. Increased intraabdominal pressure effects cardiovascular, pulmonary and renal systems. The abdominal compartment syndrome can be defined as organ failure caused by an increased intra-abdominal pressure. Clinically the syndrome is characterised by a tensely distended abdomen, oliguria or anuria and/or inadequate ventilation. Early decompression by simple laparotomy and delayed closure is the treatment of choice. If untreated the abdominal compartment syndrome is lethal. Even treated it has a high morbidity and mortality as shown in our series where 2 out of 7 patients with this syndrome died despite surgical decompression.

BACKGROUND: The aim of the study was to investigate the effects of prolonged intra-abdominal pressure on systemic hemodynamics and gastrointestinal blood circulation. METHODS: The intra-abdominal pressure in anesthetized pigs was elevated to 20 mmHg (7 animals), 30 mmHg (7 animals), and 40 mmHg (4 animals), respectively. These pressures were maintained for 3 h by intra-abdominal infusion of Ringer's solution. A control group of seven animals had normal intra-abdominal pressure (IAP). Transit time flowmetry and colored microspheres were used to measure blood flow. RESULTS: An IAP of 20 mmHg did not cause significant changes in systemic hemodynamics or tissue blood flow. An IAP of 30 mmHg caused reduced blood flow in the portal vein, gastric mucosa, small bowel mucosa, pancreas, spleen, and liver. Serum lactate increased in animals with an IAP of 30 mmHg, but microscopy did not disclose mucosal damage in the stomach or small bowel. An IAP of 40 mmHg was followed by severe circulatory changes. CONCLUSIONS: Prolonged IAP at 20 mmHg did not cause changes in general hemodynamics or gastrointestinal blood flow. Prolonged IAP at 30 mmHg caused reduced portal venous blood flow and reduced tissue flow in various abdominal organs, but no mucosal injury. A prolonged IAP of 40 mmHg represented a dangerous trauma to the animals.

In humans, intra-abdominal pressure (IAP) is elevated during many everyday activities. This experiment aimed to investigate the extent to which increased IAP--without concurrent activity of the abdominal or back extensor muscles--produces an extensor torque. With subjects positioned in side lying on a swivel table with its axis at L3, moments about this vertebral level were measured when IAP was transiently increased by electrical stimulation of the diaphragm via the phrenic nerve. There was no electromyographic activity in abdominal and back extensor muscles. When IAP was increased artificially to approximately 15% of the maximum IAP amplitude that could be generated voluntarily with the trunk positioned in flexion, a trunk extensor moment (approximately 6 Nm) was recorded. The size of the effect was proportional to the increase in pressure. The extensor moment was consistent with that predicted from a model based on measurements of abdominal cross-sectional area and IAP moment arm. When IAP was momentarily increased while the trunk was flexed passively at a constant velocity, the external torque required to maintain the velocity was increased. These results provide the first in vivo data of the amplitude of extensor moment that is produced by increased IAP. Although the net effect of this extensor torque in functional tasks would be dependent on the muscles used to increase the IAP and their associated flexion torque, the data do provide evidence that IAP contributes, at least in part, to spinal stability.

INTRODUCTION: Intra-abdominal hypertension is becoming increasingly recognised in intensive care patients. The objective of this paper was to review the modern published literature to establish a representative consensus view of the incidence, causes, pathophysiology, management and outcome of intra-abdominal hypertension. METHODS: A computerised MEDLINE search from 1966 to November 2000 was conducted using the Medical Subject Heading and textwords "abdominal", "compartment syndromes", "intra-abdominal" and "hypertension" and "pressure". The references of recent articles were checked for additional relevant citations. Papers were independently assessed for relevance by authors SJR and GMJ using a data collection format. Data were assessed qualitatively and papers detailing physiologic variables, effects of decompression and outcome were abstracted in table form. CONCLUSIONS: Intra-abdominal hypertension exists when intra-abdominal pressure exceeds 10 to 12 mmHg as physiological aberrations are manifest above this pressure. Incidence is 5% to 40% in high-risk surgical patients. Pathophysiological changes caused by intra-abdominal hypertension include effects on the gastrointestinal, cardiovascular, renal, respiratory and central nervous systems. An association between intra-abdominal hypertension and subsequent multiple organ failure has been repeatedly shown, although causation remains unproven. Monitoring intra-abdominal pressure (IAP) by measuring urinary bladder pressure is easy and accurate. However, it is unclear what level of intra-abdominal pressure requires intervention (decompression), or what length of time intra-abdominal hypertension can be tolerated before significant end organ damage occurs. In the absence of good outcome data, expert consensus is that an acute increase of IAP to above 20 to 25 mmHg and/or evidence of abdominal compartment syndrome warrants urgent decompression. While some progress has been made in describing and managing this clinical entity, further studies are needed to fully understand the clinical implications and confirm appropriate management of this condition.

Abdominal compartment syndrome may be defined as the deleterious pathophysiologic consequences of a significant increase in intra-abdominal pressure. These alterations can affect respiratory mechanics, cardiovascular system, regional blood flow, renal function, urine output, and intracranial pressure. Although the syndrome may be associated with many clinical situations, the most common are severe abdominal trauma and ruptured abdominal aortic aneurysm. Diagnosis depends upon recognition of the clinical syndrome followed by an objective measurement of intra-abdominal pressure, the most common being the measurement of bladder pressure. Treatment consists of adequate fluid resuscitation and surgical decompression when necessary.

The abdominal compartment syndrome is an increasingly recognized complication of both medical and surgical patients in the ICU setting. This syndrome has been described in a wide variety of clinical scenarios and results from a persistent elevation in intra-abdominal pressure characterized by graded organ system dysfunction. Manifestations of abdominal compartment syndrome include cardiovascular, pulmonary, renal, splanchnic, and neurologic impairment. The diagnosis of abdominal compartment syndrome requires a high level of clinical suspicion combined with an increased intra-abdominal pressure, usually obtained via urinary bladder pressure measurement. Patients at risk for abdominal compartment syndrome warrant close monitoring and we recommend prompt abdominal decompression following documentation of increased intra-abdominal pressure in the setting of physiologic compromise. Abdominal compartment syndrome can significantly contribute to the morbidity and mortality of both medical and surgical patients alike in the ICU. The signs and symptoms of abdominal compartment syndrome should become familiar to all critical care practitioners.

BACKGROUND: Increased intra-abdominal pressure (IAP) postoperatively can adversely affect cardiovascular, pulmonary, and renal function. In this prospective, randomized trial, we compared the IAP in morbidly obese patients after laparoscopic and open gastric bypass (GBP) surgery. METHODS: 64 patients with a body mass index of 40 to 60 kg/m2 were randomized to undergo laparoscopic or open GBP. IAPs were obtained at baseline (after induction of anesthesia), immediately after the operation, and on post-operative day (POD) 1, 2, and 3. Intraoperative and postoperative fluid requirements, urine output, and creatinine clearance were recorded. RESULTS: Demographics of the two groups were similar. IAP increased from baseline immediately after laparoscopic and open GBP (p < 0.05). IAP returned to baseline by POD 2 after laparoscopic GBP but remained elevated through POD 3 after open GBP. In fact, IAP was lower after laparoscopic GBP than after open GBP on POD 1, 2 and 3 (p < 0.05). The amount of intraoperative IV fluid was similar between groups, but laparoscopic GBP required less IV fluid and facilitated higher urine output postoperatively than open GBP. There was no significant difference in creatinine clearance between groups. CONCLUSIONS: Laparoscopic GBP resulted in significantly lower IAP, less postoperative fluid required, and greater postoperative urine output than open GBP.

HYPOTHESIS: Abdominal compartment syndrome (ACS) is a morbid complication of damage-control laparotomy. Moreover, the technique of abdominal closure influences the frequency of ACS. DESIGN: Retrospective cohort study. SETTING: Urban level I trauma center. PATIENTS: We studied 52 patients with trauma who required damage-control laparotomy during the 5 years ending December 31, 1999, and who survived longer than 48 hours. MAIN OUTCOME MEASURES: Abdominal compartment syndrome, acute respiratory distress syndrome (ARDS), and multiple organ failure (MOF). RESULTS: Mean (+/- SD) age was 33 +/- 2 years; 38 (73%) were male. Mechanism of injury was blunt in 29 patients (56%), and mean (+/- SD) Injury Severity Score was 28 +/- 2. Development of ARDS and/or MOF was seen in 23 patients (44%); ARDS and MOF increased mortality from 12% (3/26) to 42% (11/26). Abdominal compartment syndrome was a common complication (17/52), and was associated with an increase in ARDS and/or MOF (12 patients [71%] vs 11 patients [31%] without ACS; P =.02, chi(2) test) and death (6 [35%] vs 8 patients [23%] without ACS). Primary fascial closure (n = 10) at the initial laparotomy was associated with ACS in 8 (80%) (P =.001, chi(2) test) and ARDS and/or MOF in 9 (90%) (P =.01, chi(2) test); skin closure (n = 25), with ACS in 6 (24%) and ARDS/MOF in 9 (36%); and Bogota bag closure (n = 17), with ACS in 3 (18%) and ARDS/MOF in 8 (47%). CONCLUSIONS: Damage-control laparotomy is associated with frequent complications. In particular, ACS is a serious complication that increases ARDS and/or MOF and mortality. Avoiding primary fascial closure at the initial laparotomy can minimize the risk for ACS.

The importance of splenic preservation in the setting of penetrating and blunt trauma has led to the development of more sophisticated and noninvasive methods for controlling splenic hemorrhage. Although controversy exists, transcatheter embolotherapy has challenged the use of splenectomy in patients suffering from persistent bleeding after splenic trauma. We describe a case of a 41-year-old man with hepatitis C, ethanol-induced liver disease, and portal hypertension who presented with splenic rupture secondary to blunt trauma. Continued intra-abdominal hemorrhage was successfully controlled by superselective embolotherapy using microcoils and gelatin sponge pledgets.

French physicians dealing with abdominal emergencies are not very familiar with the abdominal compartment syndrome (ACS). Increased abdominal pressure has deleterious consequences on local (intestine, liver, kidney) circulation, leading to death in the absence of correct treatment. Abdominal trauma and ruptured aortic aneurism are the main causes of ACS. Clinical presentation may be misleading: respiratory failure, oliguria or circulatory symptoms are often predominant. Abdominal palpation is inefficient for evaluating intra-abdominal pressure (IAP); only measurement of cystic pressure allows precise evaluation of IAP. Abdominal decompression is the treatment of choice. It must be performed as soon as IAP exceeds 25 mmHg. The procedure may be risky with a high incidence of severe complications when ischaemic territories are reperfused. Recent data underline the importance of compensation of hypovolemia before decompression. Abdominal closure may necessitate various techniques (aponevrotomy, Bogota bags, etc.). At any rate, IAP must remain low at the end of the procedure. In case of suspicion of ACS, early measurement of IAP is mandatory. If pressure is over 25 mmHg, a decompressive procedure must be initiated.

BACKGROUND: The abdominal compartment syndrome (ACS) is a recognized complication of damage control surgery (DCS). The purposes of this study were to (1) determine the effect of ACS on outcome after DCS, (2) identify patients at high risk for the development of ACS, and (3) determine whether ACS can be prevented by preemptive intravenous bag closure during DCS. METHODS: Patients requiring postinjury DCS at our institution from January 1996 to June 2000 were divided into groups depending on whether or not they developed ACS. ACS was defined as an intra-abdominal pressure (IAP) greater than 20 mm Hg in association with increased airway pressure or impaired renal function. RESULTS: ACS developed in 36% of the 77 patients who underwent DCS with a mean IAP prior to decompression of 26 +/- 1 mm Hg. The ACS versus non-ACS groups were not significantly different in patient demographics, Injury Severity Score, emergency department vital signs, or intensive care unit admission indices (blood pressure, temperature, base deficit, cardiac index, lactate, international normalized ratio, partial thromboplastin time, and 24-hour fluid). The initial peak airway pressure after DCS was higher in those patients who went on to develop ACS. The development of ACS after DCS was associated with increased ICU stays, days of ventilation, complications, multiorgan failure, and mortality. CONCLUSIONS: ACS after postinjury DCS worsens outcome. With the exception of early elevation in peak airway pressure, we could not identify patients at higher risk for ACS; moreover, preemptive abdominal bag closure during initial DCS did not prevent this highly morbid complication.

BACKGROUND: Elevated intraabdominal pressure (IAP) is observed in various clinical situations, the most common of which are severe abdominal trauma and laparoscopic surgery. Extreme pressures may lead to Abdominal Compartment Syndrome (ACS), but even with lower pressures adverse effects are apparent. The cardiovascular system, the respiratory system, the kidneys and the visceral circulation are all affected, but the exact physiological mechanism is not well defined. AIMS: To discuss possible mechanisms which explain the observed hemodynamic effects of increased IAP. METHODS: Large animal model observations and review of current literature regarding the correlation between IAP and intracranial pressure (ICP). RESULTS: It was shown that the elevation of abdominal pressure leads to elevation of ICP. Transfer of pressure through the central venous system or by the cerebrospinal fluid (CSF) has been proposed as an explanation. In response to elevated ICP, various stress hormones are secreted by the central nervous system, including vasoconstricting agents such as vasopressin and catecholamines. It is hypothesized that the central nervous system is the link between the increased abdominal pressure and its adverse hemodynamic effects. This may be a protective mechanism of the brain, aimed to increase the mean arterial pressure when the ICP is elevated, in order to preserve the cerebral perfusion pressure. CONCLUSION: ICP is elevated in response to IAP elevation, and may be responsible for its adverse hemodynamic effects. Antagonists to vasopressin may have a role in the treatment of this condition.

The causes and effects of increased intra-abdominal pressure and abdominal compartment syndrome have been well documented. However, there have been no large series to determine normal intra-abdominal pressure in hospitalized patients. The purpose of this study was to determine normal intra-abdominal pressure in randomly selected hospitalized patients and to identify factors that predict variation in normal intra-abdominal pressure. A total of 77 patients were prospectively enrolled between September 1998 and July 1999. Data obtained included patient demographics (i.e., age, gender, height, weight, and body mass index), reason for hospitalization and bladder catheterization, previous and current surgical status, comorbidities, and intra-abdominal pressures. Intra-abdominal pressure readings were obtained through an indwelling transurethral bladder (Foley) catheter. Data were analyzed by analysis of variance and multiple regression analysis. There were 36 females and 41 males with a mean age of 67.7 years. Average weight, height, and body mass index were 79.6 kg, 1.70 m, and 27.6 kg/m2, respectively. Mean intraabdominal pressure was 6.5 mm Hg (range 0.2-16.2 mm Hg). Body mass index was positively related to intra-abdominal pressure (P < 0.0004). Gender, age, and medical and surgical histories did not significantly affect intra-abdominal pressure. However, using multiple regression analysis, a relationship between intra-abdominal pressure, body mass index, and abdominal surgery was discovered. Intra-abdominal pressure is related to a patient's body mass index and influenced by recent abdominal surgery. Thus, the normal intra-abdominal pressure can be estimated in hospitalized patients by using the derived equation. Knowledge of the expected intra-abdominal pressure can then by used in recognizing when an abnormally high intra-abdominal pressure or abdominal compartment syndrome exists.

BACKGROUND: The effects of increased intra-abdominal pressure in various organ systems have been noted over the past century. The concept of abdominal compartment syndrome has gained more attention in both trauma and general surgery in the last decade. This article reviews the current understanding and management of intra-abdominal hypertension and abdominal compartment syndrome. METHODS: Relevant information was gathered from a Medline search of the English literature, previous review and original articles, references cited in papers, and by checking the latest issues of appropriate journals. RESULTS AND CONCLUSION: Akin to compartment syndrome in extremities, the pathophysiological effects of increased intra-abdominal pressure developed well before any clinical evidence of compartment syndrome. These effects include cardiovascular, pulmonary, renal and intracranial derangement, reduction of intestinal and hepatic blood flow, and reduction of abdominal wall compliance. Although abdominal compartment syndrome is more commonly noted in patients with abdominal trauma, it is now evident that non-trauma surgical patients could also develop the condition. Early initiation of treatment for intra-abdominal hypertension is currently advocated in view of the possibility of subclinical progress to the full-blown abdominal compartment syndrome.

OBJECTIVE: We studied the validity and reproducibility of a new abdominal ultrasound protocol for the assessment of intra-abdominal adipose tissue. MEASUREMENTS: Intra-abdominal adipose tissue was assessed by CT, MRI, anthropometry and ultrasonography on a single day. By ultrasonography the distance between peritoneum and lumbar spine was measured using a strict protocol, including the location of the measurements, pressure on the transducer and respiration. All measurements were repeated after 3 months. RESULTS: The study population consisted of 19 overweight patients with a body mass index (BMI) of 32.9 kg/m(2) (s.d. 3.7), intra-abdominal adipose tissue on CT 140.1 cm(2) (s.d. 55.9), and a mean ultrasound distance of 9.8 cm (s.d. 2.5). There was a strong association between the CT and ultrasonographic measures: Pearson correlation coefficient was 0.81 (P<0.001). The correlation between ultrasound and waist circumference was 0.74 (P<0.001), the correlation between CT and waist circumference was 0.57 (P=0.01). Ultrasound appeared a good method to diagnose intra- abdominal obesity: the area under the ROC curve was 0.98. During the follow-up period of 3 months, the patients lost on average almost 3 kg of body weight. The correlation coefficient between changes in intra- abdominal adipose tissue assessed by CT and ultrasound was 0.74 (P<0.001). The correlation coefficient of the mean ultrasound distance assessed by two different sonographers at baseline was 0.94 (P<0.001), the mean difference 0.4 cm (s.d. 0.9), and the coefficient of variation 5.4%, indicating good reproducibility of the ultrasound measurements. CONCLUSIONS: The results of this validation study show that abdominal ultrasound, using a strict protocol, is a reliable and reproducible method to assess the amount of intra-abdominal adipose tissue and to diagnose intra-abdominal obesity.

This article gives an overview, citing animal and clinical studies, of the effects of increased intra-abdominal pressure (IAP) in severe obesity. Animal studies demonstrate that increased IAP increases pleural pressure, cardiac filling pressures, femoral venous pressure, renal venous pressure, systemic blood pressure, and vascular resistance, renin and aldosterone levels, and intracranial pressure. Thus, the comorbidities presumed secondary to increased IAP in obese patients include congestive heart failure, hypoventilation, venous stasis ulcers, gastroesophageal reflux, urinary stress incontinence, incisional hernia, pseudotumor cerebri, proteinuria, and systemic hypertension.

OBJECTIVE: To study the effects of an externally applied negative abdominal pressure device designed to lower the effects of intra-abdominal pressure (IAP) on headaches and pulsatile tinnitus in severely obese women with pseudotumor cerebri (PTC). DESIGN: Short-term clinical intervention trial in the Clinical Research Center. Days 1 and 3 were 'control' days; on days 2 and 4-6 patients were in the device from 8:00 am to noon and from 1:00 to 5:00 pm, and on nights 7-11 they were in the device from 10:00 pm to 8:00 am. The last four patients were treated in a device with a counter-traction mechanism. SUBJECTS: Seven centrally obese women with PTC. MEASUREMENTS: Headache and pulsatile tinnitus severity were graded by the patient using visual analog scale (1-10) and averaged for the time that the device was in use or not in use. IAP was estimated from urinary bladder pressure (UBP) before and during device use. The internal jugular vein (IJV) elliptical cross-sectional area was measured with B-mode ultrasonography; the timed average velocity was measured by Doppler. RESULTS: There was a decrease in both headache (6.8+/-0.8 to 4.2+/-0.8, P<0.05) and pulsatile tinnitus (4.2+/-0.5 to 1.8+/-0.5, P<0.02) within 5 min, and in headache (to 2.2+/-0.8, P<0.01) and tinnitus (to 1.7+/-0.5, P<0.01) within 1 h of device activation. UBP decreased (P<0.001) from 19.1+/-3 to 12.5+/-2.8 cmH2O. Headache remained improved throughout time that the device was used. During the second week, five of seven patients slept in the device without difficulty and four awoke without headache. There was a progressive decrease (P<0.01) in headache during the day after sleeping in the device at night as compared with days 1 and 3 when it was not used (6.5+/-0.5, day 1; 4.1+/-0.7, day 3; 3.1+/-0.8, day 8; 2.3+/-0.8, day 10). Headaches returned late in the afternoon in two patients; the device was reactivated and headache again improved. Five patients underwent IJV sonography; the IJV area decreased (129+/-53 to 100+/-44 mm2, P=0.06) without a change in IJV flow (1004+/-802 to 1000+/-589 ml/min) with the device. When activated, the device was pulled into the patient, creating discomfort that was alleviated with the counter-traction mechanism in the last four patients. One patient developed a 5 cm area of blisters that resolved when the device was worn over a hospital gown. CONCLUSIONS: Decreasing IAP relieved headaches and pulsatile tinnitus in PTC. When patients slept in the device, they awoke without headache or tinnitus, which remained markedly improved throughout most of the following day. This study supports the hypothesis that PTC in obese women is secondary to an increased IAP.

Abdominal compartment syndrome (ACS) results from increased pressure within the abdominal cavity leading to multisystem organ dysfunction. The most common cause of ACS is increased intraperitoneal volume from any source, but extrinsic compression can also cause increased intra-abdominal pressure. Although ACS has been well described in patients with trauma, little has been reported on ACS in postoperative patients without traumatic injuries. We report on a patient who had acute ACS 2 days after surgical revascularization for chronic mesenteric ischemia. With appropriate treatment, the patient made a rapid and complete recovery. We present this case of acute ACS in the postoperative patient without trauma to increase awareness and help minimize death caused by this devastating syndrome.

In the last few years, physiological changes, symptoms, diagnostic tools, and treatment of abdominal compartment syndrome interest surgeons, trauma surgeons and anaesthetists. Sudden, dangerous basic vital function deterioration in patients managed in the intensive care unit, may be results of abdominal compartment syndrome. Abdominal compartment syndrome is secondary to massive intraabdominal haemorrhages, hepatic or retroperitoneal space "packing", fluid collection in tissues, including abdominal organs. Circulatory, respiratory and kidney dysfunction occur, when intraabdominal pressure measured in urinary bladder is 25 H2O or higher. In this condition, rapid surgical decompression is necessary. During decompression abdominal organs reperfusion may produce arterial hypotension and asystole. Abdominal closure must prevent abdominal hypertension. Temporary plastic patch, simple and cheap is the most popular technique.