Agusti, M., J. I. Elizalde, et al. (2000). "Dobutamine restores intestinal mucosal blood flow in a porcine model of intra-abdominal hyperpressure." Crit Care Med 28(2): 467-72.

OBJECTIVE: To assess the effects of dopamine and dobutamine administration on the systemic and mesenteric (macro- and microvascular) circulatory disturbances induced by intra-abdominal hyperpressure. DESIGN: Prospective, randomized study. SETTING: Animal research laboratory in a university hospital. SUBJECTS: Twenty-five pigs of either gender, weighing 30-35 kg. INTERVENTIONS: Animals were anesthetized, and their lungs were mechanically ventilated. Pulmonary artery flotation and carotid artery catheters were inserted for hemodynamic monitoring and blood sampling. A perivascular flow probe was placed around the superior mesenteric artery, and a laser Doppler probe was positioned in the lumen of the ileum to measure arterial and intestinal mucosal blood flows, respectively. CO2 was insufflated into the peritoneal cavity to reach an intra-abdominal pressure of 15 mm Hg, and 60 mins later, animals received dopamine (5 microg/kg/min; n = 10), dobutamine (5 microg/kg/min; n = 10), or saline (n = 5) for 30 mins. MEASUREMENTS AND MAIN RESULTS: Peritoneal CO2 insufflation induced significant increases in heart rate, arterial pressure, and systemic vascular resistance with concomitant decreases in cardiac output and superior mesenteric arterial and intestinal mucosal blood flows. Although dobutamine infusion reversed the decrease in cardiac output, it failed to restore superior mesenteric artery blood flow; however, intestinal mucosal blood flow returned to baseline levels. Dopamine also attenuated the decrease in cardiac output, but it had no beneficial effect on splanchnic hemodynamic variables. CONCLUSIONS: Low- dose infusion of dobutamine, but not dopamine, corrects the intestinal mucosal perfusion impairment induced by moderate increases in intra- abdominal pressure.

Intra-abdominal hypertension (IAH) associated with organ dysfunction defines the abdominal compartment syndrome (ACS). Elevated intra-abdominal pressure (IAP) adversely impacts pulmonary, cardiovascular, renal, splanchnic, musculoskeletal/integumentary, and central nervous system physiology. The combination of IAH and disordered physiology results in a clinical syndrome with significant morbidity and mortality. The onset of the ACS requires prompt recognition and appropriately timed and staged intervention in order to optimize outcome. The history, pathophysiology, clinical presentation, and management of this disorder is outlined.

A 13-year-old male with a history of chronic congenital megacolon presented to the emergency department with a 1-day history of increasing abdominal pain, distension, and emesis. The patient was admitted for bowel disimpaction and irrigation. The patient rapidly developed an acute abdominal compartment syndrome because of his massive colonic dilation. Surgical decompression resulted in a reperfusion phenomenon and ultimately resulted in coagulopathy and patient demise. This case presents a unique cause of the abdominal compartment syndrome and discusses the implications to the emergency physician.

OBJECTIVE: Determine if increased intra-abdominal pressure (IAP) alone can cause systemic hypertension in a chronic canine model. DESIGN: Evaluate effects of increase in IAP with progressive inflation and deflation of an intra-abdominal balloon on systemic blood pressure in experimental and control animals. SUBJECTS: Male dogs weighing 15-25 kg underwent placement of an intra-abdominal balloon which was progressively inflated on a weekly basis in the experimental animals (5) over 4 weeks to 25 mmHg above baseline and kept there for an additional 2 weeks before gradual deflation over 2 weeks. Control animals (5) had the balloon placed but not inflated. Pain was controlled with osmotic analgesic pumps. MEASUREMENTS: The animals were anesthetized, blood pressure (BP) measured and blood drawn for plasma renin activity (PRA), aldosterone, atrial naturetic peptide (ANP), catecholamines, and serum sodium (Na). A right heart catheter was inserted for measuring cardiac output (CO) and pulmonary artery occlusion pressure (PAOP) at baseline, week 5 (maximal IAP) and week 7 (after balloon deflation). The animals were weighed and urinary bladder pressures recorded weekly before and after abdominal balloon inflation. RESULTS: Systolic (122+/-3 to 155+/-5 mmHg, P<0.05) and diastolic (82+/-4 mmHg to 107+/-7 mmHg, P<0.05) BP rose at 5 weeks at 25 mmHg IAP>baseline and returned to control with balloon deflation. Both systolic and diastolic BP rose (P<0.05) above control animals BP at 15 mmHg IAP at 2 weeks and remained elevated until abdominal decompression, at week 7. There were no significant changes in net animal weight, PRA, aldosterone, ANF, catecholamines, Na, CO or PAOP. CONCLUSION: Increased IAP from progressively inflating an intra-abdominal balloon in dogs was associated with significant increases in systolic and diastolic BP that resolved with balloon deflation. Increased IAP may be a cause for systemic hypertension in central obesity and pre-eclampsia.

OBJECTIVE: To assess the clinical utility of abdominal perfusion pressure (mean arterial pressure minus intra-abdominal pressure) as both a resuscitative endpoint and predictor of survival in patients with intra-abdominal hypertension. METHODS: 144 surgical patients treated for intra-abdominal hypertension between May 1997 and June 1999 were retrospectively reviewed. Multivariate logistic regression and receiver operating characteristic curve analysis of common physiologic variables and resuscitation endpoints were performed to determine the decision thresholds for each variable that predict patient survival. RESULTS: Abdominal perfusion pressure was statistically superior to both mean arterial pressure and intravesicular pressure in predicting patient survival from intra-abdominal hypertension and abdominal compartment syndrome. Multiple regression analysis demonstrated that abdominal perfusion pressure was also superior to other common resuscitation endpoints, including arterial pH, base deficit, arterial lactate, and hourly urinary output. CONCLUSION: Abdominal perfusion pressure appears to be a clinically useful resuscitation endpoint and predictor of patient survival during treatment for intra-abdominal hypertension and abdominal compartment syndrome.

Abdominal compartment syndrome (ACS) can occur in a variety of surgical conditions, particularly those with major life-threatening hemorrhage, massive volume resuscitation, prolonged operation times, and coagulopathy. In severely traumatized patients, the incidence of ACS is reported to be as high as 14% to 15% after damage control laparotomies. Although favorable results have been achieved with nonsurgical management of adult blunt hepatic trauma, the failure rates still range from 0% to 19%. Exploratory laparotomy is considered the intervention of choice in patients with blunt hepatic trauma who fail nonsurgical treatment. Expedient abdominal decompression currently is the treatment of choice after ACS. Oliguria, tachypnea, and tachycardia developed in two blunt hepatic trauma patients with grade IV and V injuries while they were receiving nonsurgical treatment. The intra-abdominal pressures measured more than 35 and 25 cm H 2O, respectively. Two patients with grade II and III ACS received laparoscopic examination instead of laparotomy. Their ACS was decompressed effectively via laparoscopy without any adverse effects. Therefore, we suggest that laparoscopy can be used as a safe alternative for the decompression of ACS.

Abdominal compartment syndrome complicated severe ovarian hyperstimulation in a 35 year old woman with multiple bowel resections due to Crohn's disease. Pain from ovarian enlargement necessitated hospital admission. Despite intravenous fluid administration and heparin prophylaxis, ilio-femoral deep vein thrombosis developed. Treatment by intravenous heparin was complicated by repeated intra-ovarian bleeding, anaemia and acute renal failure requiring haemodialysis. Intra-abdominal pressures were elevated. After placement of an inferior vena caval filter and discontinuation of heparin, there was slow spontaneous recovery without surgery.

Abdominal assessment is one of a number of continuous assessments that critical care nurses undertake. Since 1988 in the Department of Critical Care Medicine (DCCM), the technique of abdominal decompression has become another therapy for severe critical illness. The critical care nurse requires to have an understanding of raised intra-abdominal pressure assessment, pressure measurement and the care of abdominal polypropylene mesh insertion in the critical care setting. Our experience has been that the use of polypropylene mesh insertion halved since 1993. A retrospective study (Torrie et al. 1996) of 68 occasions (64 patients) of polypropylene mesh insertion, showed that seven patients developed fistulas and 32 patients died. There was no dehiscence of the mesh from the fascia. Forty-two wounds had primary fascial closure (28 with primary skin closure, 3 with secondary skin closure, 11 left to granulate) and 3 of them later dehisced. At follow- up (27 patients, median 7.5 months), 6 had stitch sinuses, and 5 had incisional hernias. Care of patients with polypropylene mesh inserted requires vigilant nursing practice but decompression of raised intra- abdominal pressure can be life-saving and complications are manageable.

BACKGROUND/PURPOSE: Abdominal compartment syndrome (ACS) is defined as cardiopulmonary or renal dysfunction caused by an acute increase in intraabdominal pressure. Although the condition is well described in adults, particularly trauma patients, little is known about ACS in children. METHODS: Three girls, ages 4, 5, and 5 years, were treated for ACS by silo decompression. Each child presented in profound shock, required massive fluid resuscitation, and had tremendous abdominal distension. The first child sustained a thoracoabdominal crush injury, underwent immediate celiotomy for splenic avulsion and a liver laceration, and required decompression 5 hours postoperatively. The second underwent ligation of her bluntly transected inferior vena cava; because of massive edema, her abdominal wall could not be closed, and prophylactic decompression had to be performed. The third presented with shock of unknown etiology, and ACS developed acutely with a bladder pressure of 26 mm Hg. RESULTS: Respiratory, renal, and hemodynamic function improved immediately in all 3 patients after decompression. Subsequently, each child underwent abdominal wall reconstruction and recovered uneventfully. CONCLUSIONS: ACS is a potentially lethal complication of severe trauma and shock in children. To prevent the development of renal or cardiopulmonary failure in these patients, decompression should be considered for acute, tense abdominal distension.

OBJECTIVE: Acute renal failure is seen with the acute abdominal compartment syndrome (AACS). The cause of acute renal failure in AACS is thought to be multifactorial, including increased renal venous pressure, renal parenchymal pressure (RPP), and decreased cardiac output. Previous studies have established the role of renal venous pressure as an important mediator of this renal derangement. In this study, we evaluate the role of renal parenchymal compression on renal function. METHODS: Two groups of swine (20-26 kg) were studied after left nephrectomy and placement of a renal artery flow probe and ureteral cannula. Two hours were allowed for equilibration, and an inulin infusion was begun to calculate inulin clearance as a measurement of glomerular filtration. In group 1 animals (n = 6), RPP was elevated by 30 mm Hg for 2 hours with renal parenchymal compression. RPP then returned to baseline for 1 hour. In group 2 (n = 6), the RPP was not elevated. The cardiac index, preload, and mean arterial pressure remained stable. Blood samples for plasma renin activity and plasma aldosterone were taken at baseline and at hourly intervals. RESULTS: Elevation of RPP in the experimental group showed no significant decrease in renal blood flow index or glomerular filtration when compared with control animals. There were no significant elevations of plasma aldosterone or plasma renin activity in the experimental animals when compared with control. CONCLUSION: Elevated renal compression alone did not create the pathophysiologic derangements seen in AACS. However, prior data from this laboratory found that renal vein compression alone caused a decreased renal blood flow and glomerular filtration and an increased plasma renin activity, plasma aldosterone, and urinary protein leak. These changes are partially or completely reversed by decreasing renal venous pressure as occurs with abdominal decompression for AACS. These data strengthen the proposal that renal vein compression, and not renal parenchymal compression, is the primary mediator of the renal derangements seen in AACS.

OBJECTIVE: To investigate the incidence, main physiologic effects, and therapeutic management of the abdominal compartment syndrome (ACS) after severe abdominal and/or pelvic trauma. DESIGN: Retrospective analysis from January 1991 to December 1996; prospective study from January 1997 to August 1998. SETTING: Level I trauma center, intensive care unit. PATIENTS: A total of 311 patients with severe abdominal and/or pelvic trauma and "damage-control" laparotomy on day of admission. INTERVENTIONS: The ACS was defined as the development of significant respiratory compromise, including elevated inspiratory pressure of >35 mbar, a decreased Horowitz quotient (<150 torr [<20 kPa]), renal dysfunction (urine output, <30 mL/hr), hemodynamic instability necessitating catecholamines, and a rigid or tense abdomen. Beginning with January 1997, urinary bladder pressure as an additional variable for the diagnosis of ACS was continuously measured in patients (n = 12) at risk. Bladder pressures of >25 mm Hg indicated ACS. MEASUREMENTS AND MAIN RESULTS: Seventeen patients (5.5%) developed ACS because of persistent intra-abdominal/retroperitoneal bleeding (n = 12; 70.6%) or visceral edema (n = 5; 29.4%). All patients with ACS underwent primary fascial closure. In eight of these patients (47%), abdominal and/or pelvic packing for hemostasis was performed. All patients with ACS required decompressive emergency laparotomies because of physiologic derangements. The time between primary laparotomy and decompressive laparotomy was 12.9 +/- 2.0 hrs. Emergency decompression of the abdomen resulted in a significant increase in the cardiac index (+146%), tidal volume (+133%), Horowitz quotient (+156%), and urine output (+1557%), whereas bladder pressure (-63%), heart rate (-19%), central venous pressure (-30%), pulmonary artery occlusion pressure (-43%), peak airway pressure (-31%), partial pressure arterial carbon dioxide (-30%), and lactate (-40%) markedly (p < .05) decreased. In two multiply injured patients with additional head trauma, ACS caused a critical increase of the intracranial pressure, which markedly dropped after the release of abdominal tension. CONCLUSIONS: Risk factors for the occurrence of ACS are severe abdominal and/or pelvic trauma, which require laparotomy and packing for the control of hemorrhage. The ACS occurs within hours and causes life-threatening physiologic derangements and a critical rise in intracranial pressure in patients with combined abdominal/pelvic and head trauma. Decompressive laparotomy immediately restores impaired organ functions. In patients at risk, the continuous measurement of urinary bladder pressure as a simple, noninvasive, and less expensive diagnostic tool for early detection of elevated intra-abdominal pressure is mandatory.

ACS is due to a rapid increase in intra-abdominal pressure. Although ACS may occur in both surgical and nonsurgical patients, patients who have abdominal or pelvic trauma and/or require massive fluid replacement are at increased risk. Critical care nurses are in a unique position to recognize early signs and symptoms of increased intra-abdominal pressure to ensure timely intervention. Aggressive hemodynamic, pulmonary, and operative management is essential for the optimal outcome of patients with ACS. Without definitive treatment, multisystem organ dysfunction and death ultimately ensue.

Abdominal compartment syndrome (ACS) is characterized by increased intraabdominal pressure and a set of secondary pathophysiological changes in the abdominal. ACS has reappeared in the literature recently in relation to the surgical concept to damage control, applied particularity in contexts of severe abdominal injury polytraumatized patients. We report two cases of ACS that appeared after scheduled abdominal surgery: one after repair of a large eventration and the other in the context of septic shock due to fecaloid peritonitis. Both patients died of multisystem organ failure in spite of surgical decompression. We wish to emphasize that ACS can appear in contexts other than surgery for damage control, and we stress the need to measure intravesical pressure as a reflection of intraabdominal pressure, particularly in certain high risk patients in the postoperative recovery ward. Finally, we review the pathophysiology of ACS and its management, which is based on early treatment to prevent multisystem organ failure with an associated high risk of death.

BACKGROUND: Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are known to occur in patients after major abdominal surgery. The incidence of IAH and ACS in the burn population is not known. METHODS: We prospectively recorded the intra-abdominal pressures of major burn patients admitted to our burn center from February 1999 to September 1999. A bladder pressure greater than 25 mm Hg was diagnosed as IAH. ACS was diagnosed when pulmonary compliance decreased in association with persistent IAH and was treated with abdominal decompression. RESULTS: Ten patients were placed on the protocol; of these, seven developed IAH. Five responded to conservative treatment. Two patients with 80% body surface area burns developed ACS and required decompression. CONCLUSIONS: IAH occurs commonly in major burn patients, and ACS is seen regularly in patients with more than 70% body surface area burns. We recommend bladder pressure measurements after infusion of more than 0.25 L/kg during the acute resuscitation phase and for peak inspiratory pressures greater than 40 cm H2O. Whereas ACS warrants surgical decompression of the abdominal cavity, IAH usually responds to conservative therapy.

OBJECTIVES: To determine the rate of elevated intra-abdominal pressure (IAP) and to evaluate the accuracy of clinical abdominal examination in the assessment of IAP in the critically injured trauma patient. DESIGN: A prospective blinded study. SETTING: The medical-surgical critical care unit of a university-affiliated regional adult trauma centre. PATIENTS: Forty-two adult blunt trauma victims, who had a mean injury severity score of 36. INTERVENTIONS: Urinary bladder pressure was measured daily and classified as normal (10 mm Hg or less), elevated (more than 10 mm Hg) or significantly elevated (more than 15 mm Hg). A blinded clinical assessment of abdominal pressure was concurrently performed and recorded as elevated or normal. MAIN OUTCOME MEASURES: The sensitivity, specificity and accuracy and the positive and negative predictive values of the 2 interventions in identifying elevated IAP. RESULTS: Twenty-one patients (50%) had an elevated IAP at some point during the study. Of the 147 bladder pressure measurements done in these 42 patients, 47 (32%) were more than 10 mm Hg and 16 (11%) were more than 15 mm Hg. The sensitivity, specificity, positive predictive value, negative predictive value and accuracy of clinical abdominal examination for identifying elevated IAP were 40%, 94%, 76%, 77% and 77%, respectively. Clinical abdominal examination had a sensitivity, specificity, positive predictive value, negative predictive value and accuracy of 56%, 87%, 35%, 94% and 84% respectively, for significantly elevated IAP. CONCLUSIONS: Urinary bladder pressure was commonly elevated among our population of critically injured adults. Compared with bladder pressure measurements, clinical abdominal assessment showed poor sensitivity and accuracy for elevated IAP. These findings suggest that more routine measurements of bladder pressure in patients at risk for intra-abdominal hypertension should be performed.

Experimental studies and clinical experience suggest that the combination of positive end-expiratory pressure (PEEP) ventilation and intra-abdominal hypertension might alter splanchnic hemodynamics to a significantly greater degree than the effect of either of them alone. Therefore, we assessed the intestinal and hepatic hemodynamics in two steps of PEEP ventilation, adding tense pneumoperitoneum in a pig model. The hepatic artery, portal vein, and superior mesenteric artery blood flow, as well as the hepatic and intestinal mucosal microcirculation, and the hepatic pO2 and intestinal mucosal pH, were assessed before, then with 5 cmH2O and 10 cmH2O PEEP alone, and in combination with a 12-mmHg pneumoperitoneum, in ten domestic pigs. Statistical analysis of the hepatic and intestinal measurements revealed a significant decrease (P = 0.001) in all parameters in relation to the baseline, during the 5-cmH2O and 10-mmH2O PEEP ventilation period. The addition of 12 mmHg intra-abdominal pressure led to an extreme deterioration in all parameters (P = 0.001), in relation to both the baseline and the 10-cmH2O PEEP measurement. These findings demonstrate that PEEP and intra-abdominal hypertension act cumulatively on the abdominal viscera, producing conditions of extremely low hypoperfusion and ischemia.

BACKGROUND/PURPOSE: Abdominal compartment syndrome (ACS) is the cardiac, pulmonary, and renal dysfunction that occurs as a result of elevated intraabdominal pressure. The authors present their experience with patch abdominoplasty (PA) in pediatric patients as a means to treat and prevent ACS. METHODS: The charts of patients who underwent PA were reviewed retrospectively. ACS was defined as the increased oxygen requirements and elevation of peak inspiratory pressures (PIP) associated with abdominal distension and worsening renal and or cardiac function. RESULTS: A total of 23 patients (13 boys) were treated (average age, 23 months). Diagnoses included necrotizing enterocolitis (NEC, n = 13), trauma (n = 3), Hirschsprung's enterocolitis (n = 2), perforated bowel (n = 4), and bilateral Wilms' tumor with bowel obstruction (n = 1). Oxygen requirements decreased after patch abdominoplasty (mean preoperative FIO2, 0.87 +/- 24, mean postoperative, 0.67 +/- 24 [P = .01]). The PIP decreased significantly in the 13 patients who survived (mean preoperative PIP, 33 +/- 8, mean postoperative PIP, 27 +/- 7 [P = .01]). These PIPs failed to respond in the 8 nonsurvivors (mean preoperative PIP, 35 +/- 10, mean postoperative PIP, 33 +/- 14 [P value not significant]). Six of the 8 nonsurvivors had NEC. Complications of intraabdominal abscess and enterocutaneous fistula were seen in 5 patients, all of who had NEC. CONCLUSIONS: Patch abdominoplasty effectively decreases airway pressures and oxygen requirements associated with ACS. Complications with PA occur primarily in patients with NEC. Failure to respond with a decrease in PIP and FIO2 requirements is an ominous sign.

We report an episode of acute abdominal compartment syndrome, with pulseless electrical activity, in a patient undergoing colonoscopic examination of a recently constructed mucus fistula.Associated clinical features of this acute abdominal compartment syndrome (tension pneumoperitoneum) were abdominal distention, which was very impressive, cardiopulmonary arrest, severe cyanosis, and progressive bradycardia.In general, increased intraabdominal pressure can have numerous adverse physiologic effects, which may include decreased cardiac output, altered ventilation-perfusion relationships, and decreased venous return. The magnitude of each effect likely depends on the magnitude of the increased intraabdominal pressure.Success with initial resuscitation efforts should not diminish further vigilance with these patients, as other problems may be discovered.

OBJECTIVE: To compare tissue pH in the stomach, bowel, and abdominal wall muscle during hemorrhagic shock and recovery using tissue electrodes; also, to compare tissue electrode pH measurements to gastric intramucosal pH (pHi), gastric luminal PCO2, and PCO2 gap (gastric luminal CO2--arterial CO2) measured with an air-equilibrated tonometer. DESIGN: Prospective animal study. SETTING: University animal research laboratory. SUBJECTS: Eight anesthetized, mechanically ventilated Yorkshire swine. INTERVENTIONS: Hemorrhagic shock was initiated by withdrawing blood over a 15-min period to lower systolic blood pressure to 45 mm Hg. Shock was maintained for 45 mins and was followed by a 5-min resuscitation to normal blood pressure with a blood/lactated Ringer's (1:2) mixture. Recovery was monitored for 60 mins. MEASUREMENTS AND MAIN RESULTS: pH was measured with electrodes in the submucosa of the stomach, the submucosa of the small bowel, and the abdominal wall muscle. Gastric luminal PCO2 was measured with an air- equilibrated tonometer and pHi and PCO2 gap were calculated. Each organ showed a different sensitivity to shock and resuscitation. The bowel pH responded most rapidly to the onset of hemorrhagic shock and had the largest change in tissue pH. The bowel also showed the most rapid recovery during resuscitation. The submucosal pH of the stomach responded more slowly than the bowel, but faster than the abdominal wall muscle pH, gastric PCO2 gap, or pHi. The smallest changes in organ pH as a result of hemorrhagic shock were seen in the abdominal wall muscle and the stomach as assessed by gastric tonometry. CONCLUSIONS: Direct measurement of tissue pH indicates that intra-abdominal organ pH varies during hemorrhagic shock. The small bowel pH changes the most in magnitude and rapidity compared with stomach pH or abdominal wall muscle pH. Tonometrically derived parameters were not as sensitive in the detection of tissue acidosis during shock and resuscitation as pH measured directly in the submucosa of the stomach or small bowel.

Laparoscopic techniques for surgery are gradually becoming established in paediatric surgery. Technical aspects, such as the maximum safe gas insufflation pressure, are still open to discussion. We used transoesophageal echocardiography to study the haemodynamic changes in eight small children undergoing laparoscopic herniorrhaphy, with two different levels of intra-abdominal pressure (IAP), 6 and 12 mm Hg. End- tidal carbon dioxide tension was maintained constant at 4.3-4.7 kPa. After baseline measurements, an IAP of 12 mm Hg was applied for 10 min. Next, IAP was decreased to 6 mm Hg, followed by a second period of 12 mm Hg. Haemodynamic measurements were obtained at each stage. A further measurement was obtained 10 min after abdominal deflation at the end of surgery while anaesthesia was unchanged. Cardiac index (CI) decreased significantly only after the first 12 mm Hg level of IAP. The subsequent decrease in IAP to 6 mm Hg caused return of CI to baseline levels. The second increase in IAP did not cause any reduction in CI. The initial reduction in CI, although statistically significant, did not appear to be clinically important. We conclude that an IAP of up to 12 mm Hg appeared to be safe in healthy small children undergoing laparoscopic herniorrhaphy.

The abdominal compartment is limited by the abdominal wall, Mm. Psoas, vertebral column, diaphragm and the pelvis. Thus the retroperitoneum is included. Elevated intraabdominal pressure may profoundly impair the function of the entire gastrointestinal tract, the cardiovascular, respiratory, and renal system. Reduction of increased intraabdominal pressure may reverse all these adverse effects. The most common causes of elevated intraabdominal pressure are abdominal operations, abdominal trauma, diffuse peritonitis, ascites and peritoneal edema following resuscitation. Excessively increased intraabdominal pressure may result in a total loss of function and may lead to death. Such a condition is called an abdominal compartment syndrome. It usually requires operative decompression. According to animal experiments and clinical experiences suggestions for treatment are given. Diagnostic suspicion of elevated intraabdominal pressure may be confirmed with objective measurements. Since bedside manometry using a Foley catheter provides a valuable estimate of intraabdominal pressure and is easy to perform, intraabdominal pressure values may contribute to medical decision making. At this time there is a great need of controlled clinical trials to point out the importance of increased intraabdominal pressure and the abdominal compartment syndrome.

OBJECTIVE: Using a standardized massive splenic injury model of uncontrolled hemorrhagic shock, we studied the effect of vigorous fluid resuscitation on the hemodynamic response and survival time in rats. DESIGN: Randomized, controlled study. Duration of follow-up was 4 hrs. SETTING: University research laboratory. SUBJECTS: Adult male Sprague- Dawley rats, weighing 240-430 g. INTERVENTIONS: Standardized massive splenic injury was induced by two transverse incisions in the rat's spleen. The animals were randomized into four groups: group 1 (n = 8) underwent sham operation; in group 2 (n = 15), massive splenic injury was untreated; in group 3 (n = 15), massive splenic injury was treated with 41.5 mL/kg 0.9% sodium chloride (large-volume normal saline); and in group 4 (n = 15), massive splenic injury was treated with 5 mL/kg 7.5% sodium chloride (hypertonic saline). MEASUREMENTS AND MAIN RESULTS: The hemodynamic and metabolic variables in the sham-operated group 1 were stable throughout the experiment. Mean arterial pressure in group 2 decreased from 86.5 +/- 4.0 to 50.3 +/- 6.3 mm Hg (p < .001) in the first 15 mins after massive splenic injury. Mean survival time in group 2 was 127.5 +/- 17.0 mins; total blood loss was 33.8% +/-2.6% of blood volume; and the mortality rate at 1 hr was 13.3%. Bolus infusion of large-volume normal saline after 15 mins resulted in an early increase in mean arterial pressure from 48.6 +/-7.4 to 83.3 +/- 7.2 mm Hg (p < .01); it then rapidly decreased to 24.6 +/- 8.6 mm Hg (p < .001) after 60 mins. The mean survival time (95.3 +/- 16.4 mins) was significantly lower than in group 2 (p < .01); total blood loss (48.0% +/- 4.3%) was significantly higher than in group 2 (p < .01); and mortality rate in the first hour was 33.3% (p < .05). Bolus infusion of hypertonic saline also decreased survival time to 93.3 +/- 20.3 mins (p < .01), but total blood loss was 35.2% +/- 3.0%, which was not significantly different from the blood loss in group 2. The mortality rate in the first hour (60.0%) was significantly higher than in group 2 (p < .005). CONCLUSIONS: Vigorous infusion of normal saline after massive splenic injury resulted in a significant increase in intra- abdominal bleeding and decreased survival time. The hemodynamic response to crystalloid infusion in blunt abdominal trauma is primarily dependent on the severity of injury and the rate of blood loss.

Abdominal compartment syndrome is defined by increased intraabdominal pressure above 20 mmHg with increased pulmonary peak pressure and oliguria. In primary abdominal compartment syndrome the increased intraabdominal pressure is caused directly by peritonitis, ileus or abdominal and pelvic trauma. Secondary compartment syndrome is a result of forced closure of the abdominal wall after abdominal surgery. The effects are decreased cardiac output, pulmonary atelectasis, oliguria to anuria and hepatic as well as intestinal reduction of perfusion. Effective monitoring is done by standardised measuring of urinary bladder pressure. Normal values are between 0 and 7 cm H2O, after elective laparotomies 5-12 cm H(2)0. Above 25 cm H(2)0 they are definitely pathological. For the prevention and therapy of manifested abdominal compartment syndrome the application of a laparostomy using a resorbable mesh is recommended. Between 1988 and 1999 we applied a laparostomy to lower the intraabdominal pressure in 377 patients. In 16% of the cases it was indicated by primary abdominal compartment syndrome with a bladder pressure of 31 +/- 4 cm H(2)0 preoperatively, which could be lowered to 17 +/- 4 cm H(2)0 by laparostomy. An early reconstruction of the abdominal wall could be performed in 18% of the cases. CONCLUSIONS: The abdominal compartment syndrome is an often underestimated problem in abdominal surgery involving multiple organ systems. The temporary laparostomy lowering intraabdominal pressure rather than a forced closure of the abdominal wall should be used in all circumstances.