Bloomfield, G. L., C. R. Blocher, et al. (1997). "Elevated intra-abdominal pressure increases plasma renin activity and aldosterone levels." J Trauma 42(6): 997-1004; discussion 1004-5.

OBJECTIVE: To study the effects of elevated intra-abdominal pressure upon renal function and the renin-angiotensin-aldosterone system. MATERIALS AND METHODS: Two groups of anesthetized, ventilated swine were studied. Intra-abdominal pressure was increased in experimental animals (n = 6) by incrementally instilling an isosmotic ethylene glycol solution into the peritoneal cavity until intra-abdominal pressure was 25 mm Hg above baseline. The intravascular volume was then expanded until cardiac index returned to baseline. Lastly, the solution was drained to decompress the abdomen. Control animals underwent surgical preparation but did not have their intra-abdominal pressure raised. Changes in systemic and pulmonary hemodynamic parameters, renal venous pressure, and urine output were recorded. Venous samples for plasma renin activity, aldosterone, and atrial natriuretic factor were drawn after each change in either intra-abdominal pressure or intravascular volume in experimental animals, and at the same time points in control animals. MEASUREMENTS AND MAIN RESULTS: Elevated intra-abdominal pressure significantly (p < 0.05, analysis of variance) increased renal venous pressure, pleural pressure, wedge pressure, and pulmonary artery pressure compared to both baseline and control animals; whereas cardiac index and urine output decreased significantly. Both plasma renin and aldosterone levels increased significantly compared with baseline and controls. Intravascular volume expansion significantly increased urine output and decreased significantly both plasma renin activity and aldosterone levels. Abdominal decompression further significantly decreased both plasma renin activity and aldosterone levels. There were no significant changes in atrial natriuretic factor at any time point. CONCLUSIONS: Elevated intra-abdominal pressure decreases urine output and significantly up-regulates the hormonal output of the renin-angiotensin-aldosterone system. Intravascular volume expansion in combination with abdominal decompression reverses the effects of acutely elevated intra-abdominal pressure upon renal function and the renin-angiotensin-aldosterone system.

OBJECTIVES: To determine the effect of acutely increased intra- abdominal pressure on pleural pressure, intracranial pressure, and cerebral perfusion pressure, and to clarify the relationship between these parameters. DESIGN: Nonrandomized, controlled study. SETTING: Laboratory at a university medical center. SUBJECTS: Yorkshire swine, weighing 15 to 20 kg. INTERVENTIONS: Anesthetized, ventilated swine had a balloon inserted into the peritoneal cavity and catheters placed for measurement of intracranial pressure, pleural pressure, central venous pressure, pulmonary artery occlusion pressure, and mean arterial pressure. Following baseline measurements, intra-abdominal pressure was increased by incrementally inflating the intraperitoneal balloon. All parameters were remeasured 30 mins after each increase in intra- abdominal pressure. Two groups were studied: a) group 1 (n = 9) animals had intra-abdominal pressure increased to 25 mm Hg above baseline, then released; b) group 2 (n = 3) animals underwent sternotomy and pleuropericardotomy to prevent an increase in pleural pressure with increasing intra-abdominal pressure. MEASUREMENTS AND MAIN RESULTS: Increase of intra-abdominal pressure to 25 mm Hg above baseline caused significant (p < .05) increases in intracranial pressure (7.3 +/- 0.6 [SEM] to 16.4 +/- 1.9 mm Hg), pleural pressure (4.3 +/- 1.3 to 11.8 +/- 1.9 mm Hg), pulmonary artery occlusion pressure (9.0 +/- 0.6 to 14.3 +/- 0.8 mm Hg), and central venous pressure (6.6 +/- 0.7 to 10.7 +/- 0.9 mm Hg). The cardiac index (3.4 +/- 0.3 to 1.6 +/- 0.1 L/min/m2) and cerebral perfusion pressure (75.6 +/- 3.6 to 62.0 +/- 6.8 mm Hg) deceased significantly (p < .05), whereas mean arterial pressure (82.8 +/- 3.2 to 78.4 +/- 6.6 mm Hg) remained essentially constant. Sternotomy and pleuro-pericardotomy negated all effects of increased intra-abdominal pressure except the decreased cardiac index (1.6 +/- 0.1 to 2.5 +/- 0.2 L/min/m2). CONCLUSIONS: Acutely increased intra- abdominal pressure causes a significant increase in intracranial pressure and a decrease in cerebral perfusion pressure. Increased intra- abdominal pressure appears to produce this effect by augmenting pleural and other intrathoracic pressures and causing a functional obstruction to cerebral venous outflow via the jugular venous system. It is possible that the same phenomenon may be why persons with chronically increased intra-abdominal pressure, such as the morbidly obese, suffer from a high frequency rate of idiopathic intracranial hypertension.

INTRODUCTION: Low gastric intramucosal pH (pHi) after shock resuscitation is associated with organ dysfunction and death in trauma patients. However, the relationship between hemodynamic performance, global oxygen transport, and pHi is unclear. Our purpose was to evaluate the relationship between intravascular volume status, splanchnic hypoperfusion, and outcome after shock resuscitation in trauma patients. DESIGN/SETTING: Cohort study of 79 consecutive critically ill patients at a Level I trauma center stratified by normal (NORM, > or = 7.32) or low (LOW, < 7.32) pHi when lactate normalized (< 2.2 mmol/L). MAIN OUTCOME MEASURES: Differences during resuscitation in mean values of right ventricular end-diastolic volume index (RVEDVI), pulmonary artery occlusion pressure, cardiac index, oxygen delivery index, and oxygen consumption index. The incidence of multiple organ failure and death in the NORM and LOW groups were analyzed via odds ratio and chi 2. RESULTS: Patients in the NORM group (n = 45) had a lower incidence of multiple organ failure (4 of 45 vs. 11 of 34, odds ratio 5.0, p < 0.01) and death (5 of 45 vs. 11 of 34, odds ratio 3.8, p < 0.05) than patients in the LOW group (n = 34). NORM patients had a higher initial RVEDVI (116 +/- 31 vs. 95 +/- 25 mL/m2, p < 0.001) and maintained a significantly higher RVEDVI (114 +/- 27 vs. 97 +/- 17 mL/m2, p = 0.003) throughout resuscitation than the LOW group did. There were no differences in the other studied variables. CONCLUSIONS: Supranormal levels of preload during shock resuscitation are associated with better outcome. Maintaining a RVEDVI higher than 100 mL/m2 during shock resuscitation may be of benefit in critically injured patients.

BACKGROUND AND METHODS: Major trauma or abdominal injury may lead to the development of increased intra-abdominal pressure (IAP) and the onset of the abdominal compartment syndrome. Although the effect of raised IAP on systemic and splanchnic hemodynamics have been described, the consequences of the resultant gut hypoperfusion in this setting are unknown. Bacterial translocation (BT) occurs after a period of splanchnic ischemia and may contribute to later organ failure. A rodent model was used to examine the effect of raised IAP on ileal mucosal blood flow (MBF) and BT. IAP was increased to 25 mm Hg for 60 minutes and mean arterial blood pressure was maintained with fluid. Animals were killed 24 hours later and examined for BT. RESULTS: Increased IAP resulted in a decrease of MBF to 63% of baseline despite maintaining normal mean arterial blood pressure. BT occurred principally to the mesenteric lymph nodes after 60 minutes of IAP at 25 mm Hg. CONCLUSIONS: Increased IAP leads to decreased MBF and to BT, which may contribute to later septic complications and organ failure.

Intra-abdominal hypertension is an unusual and often lethal syndrome. It is most often seen in critically ill surgical patients. The most important component of therapy is reduction of intra-abdominal pressure. Unfortunately, even with appropriate treatment, mortality is still high.

IAH causes multiple and profound physiologic abnormalities both within and outside the abdomen. IAP monitoring is easily performed by bladder measurements. Careful monitoring and prompt recognition and treatment of IAP are critical in patients after damage control surgery because IAH is extremely common in these patients. Use of mesh fascial prostheses at the initial celiotomy in high-risk patients may prevent the deleterious effects of IAH. IAH should be considered an earlier manifestation of ACS. Surgical intervention should be indicated by IAH and not delayed until ACS is clinically apparent.

Abdominal compartment syndrome develops whenever the mean intraperitoneal pressure rises above the physiological pressure, leading to renal and mesenteric ischemia and respiratory decompensation due to pressure on the diaphragm. Abdominal compartment syndrome may occur after conditions such as peritonitis, intestinal obstruction, laparoscopic procedures, or abdominal tumors. Leakage from the urinary tract may cause accumulation of urine in the peritoneal cavity which commonly manifests as single or multiple urinomas, or urinary ascites. The case of a patient who had delayed identification of a ureteral perforation following the abdomino-perineal resection of a rectal carcinoma is presented. Massive urinary leakage into the peritoneal cavity led to the abdominal compartment syndrome. Peritoneal drainage and ureteral stenting improved her condition. A high index of suspicion is necessary in order to diagnose this rare condition.

OBJECTIVE: To determine whether prevention of the abdominal compartment syndrome after celiotomy for trauma justifies the use of absorbable mesh prosthesis closure in severely injured patients. DESIGN: Retrospective analysis of case series from July 1, 1989, to July 31, 1996. SETTING: University-based level I trauma center. PATIENTS: Seventy-three consecutive trauma patients requiring celiotomy who received absorbable mesh prosthesis closure and 73 control patients matched for injury severity and trauma type who received celiotomy without a mesh prosthesis closure. INTERVENTIONS: Absorbable mesh prosthesis closure was used in cases of excessive fascial tension, abdominal compartment syndrome, necrotizing fasciitis, traumatic defect, or planned reoperation. MAIN OUTCOME MEASURES: Demographics, Injury Severity Score, Abdominal Trauma Index, highest abdominal Abbreviated Injury Scale score, number of abdominal/pelvic injuries, highest head Abbreviated Injury Scale score, shock, indication for mesh closure, complications, number of operations and time required for closure, days in the intensive care unit, length of stay, and mortality were determined. The highest abdominal Abbreviated Injury Scale score was multiplied by the number of abdominal/pelvic injuries to calculate the abdominal pelvic trauma score. RESULTS: Group 1 consisted of 47 patients who received mesh at initial celiotomy, and group 2, 26 patients who received mesh at a subsequent celiotomy. These 2 groups were statistically similar in demographics, injury severity, and mortality. However, group 2 had a significantly higher incidence of postoperative abdominal compartment syndrome (35% vs 0%), necrotizing fasciitis (39% vs 0%), intra-abdominal abscess/peritonitis (35% vs 4%), and enterocutaneous fistula (23% vs 11%) compared with group 1 (P < .001). Group 1 patients with preoperative abdominal compartment syndrome had more abdominal/ pelvic injuries and higher abdominal trauma index than matched controls (P < .05). There was a trend toward higher abdominal pelvic trauma score in patients who developed abdominal compartment syndrome. The Pearson coefficient of correlation between the abdominal trauma index and the more easily calculated abdominal pelvic trauma score was 0.91 (P < .001). CONCLUSION: The use of absorbable mesh prosthesis closure in severely injured patients undergoing celiotomy was effective in treating and preventing the abdominal compartment syndrome.

BACKGROUND: The abdominal compartment syndrome (ACS) is now recognized as a frequent confounder of surgical critical care following major trauma; however, few prospective data exist concerning its characterization, evolution, and response to decompression. METHODS: Acutely injured patients with an injury severity scale (ISS) score >15 requiring emergent laparotomy and intensive care unit (ICU) admission were prospectively evaluated for the development of ACS. The syndrome was defined as an intra-abdominal pressure (IAP) >20 mm Hg complicated by one of the following: peak airway pressure (PAP) >40 cm H2O, oxygen delivery index (DO2I) <600 mL O2/min/m2, or urine output (UO) <0.5 mL/kg/hr. Physiologic response to decompression was similarly documented prospectively. RESULTS: Over a 14-month period ending December 1995, 21 (14%) of 145 patients (ISS >15) requiring laparotomy and admitted to our surgical ICU developed ACS; mean age was 39 +/- 9 years; injury mechanism was blunt in 60%; ISS 26 +/- 6. At initial laparotomy, 67% underwent abdominal packing (57% for major liver injuries). Mean IAP was 27 +/- 2.3 mm Hg, and time from laparotomy to decompression was 27 +/- 4 hours; 24% were planned whereas the remaining were prompted by deteriorating organ function as defined above (cardiopulmonary in 43%; renal in 19%; both renal and cardiopulmonary in 14%). Following decompression, there was an increase in cardiac index, oxygen delivery, urine output, and static compliance while there was a decrease in pulmonary capillary wedge pressure, systemic vascular resistance, and peak airway pressure. CONCLUSIONS: The abdominal compartment syndrome occurs in a significant number of severely injured patients, and it develops quickly (27 +/- 4 hours). Cardiopulmonary deterioration is the most frequent reason prompting decompression. Timely decompression of the ACS results in improvements in cardiopulmonary and renal function. These data support the use of the proposed ACS grading system for selective management of the syndrome.

The abdominal compartment syndrome refers to the alterations in respiratory mechanics, hemodynamic parameters and renal function that occur as a result of a sustained increase in intra-abdominal pressure. The syndrome may follow a diverse series of insults, including laparotomy for severe abdominal trauma, ruptured abdominal aortic aneurysm and intra-abdominal infection. Diagnosis depends on recognizing the clinical picture in patients at risk, followed by an objective measurement of intra-abdominal pressure. Successful management may require abdominal decompression with temporary abdominal closure. Despite urgent decompression, the death rate is high because of the severity of the patients' underlying illness.

TOPIC: Abdominal compartment syndrome (ACS) in blunt and penetrating abdominal trauma. PURPOSE: To review the clinical manifestations, pathophysiology, and nursing management of patients with ACS. SOURCES: Published literature, case study. CONCLUSIONS: Trauma nurses play a key role in early identification and management of ACS. Priorities include knowledge of signs and symptoms, methods of measurement of ACS; specifics of wound care, psychosocial interventions, and key factors in discharge planning.

BACKGROUND: Resuscitative measures associated with ruptured abdominal aortic aneurysm (rAAA) repair may result in massive edema of the bowel, retroperitoneum and abdominal wall. The resulting "abdominal compartment syndrome" may compromise abdominal closure and may be associated with respiratory, renal and cardiovascular deterioration. METHODS: The medical records of 23 patients surviving initial operative repair of a rAAA were retrospectively reviewed. Eight underwent delayed abdominal closure after early approximation with silastic sheets (n = 6) or of the skin only (n = 2). Ultimate outcome, as well as several pulmonary and cardiovascular parameters, were compared with patients undergoing standard primary fascial closure (n = 15). RESULTS: A trend toward improved survival was apparent in the group undergoing delayed abdominal wall closure. Significant improvements in oxygenation and mixed venous oxygen saturation were observed in these patients, and there were fewer late deaths due to multiple organ failure. No patient undergoing delayed abdominal closure developed a graft infection. CONCLUSIONS; As in massively resuscitated trauma victims, delayed laparotomy closure in rAAA patients may confer a physiologic and survival benefit.

PURPOSE: Two cases of abdominal compartment syndrome are described and the pathophysiology associated with it is reviewed. CLINICAL FEATURES: The first patient was a 46-yr-old man who sustained extensive blunt abdominal injuries following a fall. The second was a 54-yr-old man involved in a motor vehicle accident with blunt abdominal trauma. In both cases, the patients developed an extremely tense abdomen, increasing peak inspiratory pressures, hypercarbia and oliguria. Both demonstrated improvement in cardiac performance and ventilatory variables following an emergency decompressive celiotomy. CONCLUSION: Abdominal compartment syndrome results in impairment of organ function secondary to increased intraabdominal pressure. These patients require emergency decompressive celiotomy to relieve the symptoms. However, the incidence of intractable asystole and hypotension during this procedure is high and vigilance must be maintained during the release of the increased intraabdominal pressure.

OBJECTIVE: To standardise a direct method for measuring intra-abdominal pressure (IAP), to correlate the results with intrarectal pressure, and to compare the results in various conditions. DESIGN: Prospective open study. SETTING: Teaching hospital, Egypt. SUBJECTS: 34 Subjects in 4 groups: control (n = 11), hernia (n = 8; 6 umbilical and 2 incisional), mass (n = 7; 6 enlarged spleen and 1 carcinoma of sigmoid), and obese (n = 8; a mean of 40% above expected weight). INTERVENTIONS: Measurement of IAP with a Verres needle connected to a pressure transducer with the patient at rest, straining, supine, erect, and before and after anaesthesia. Intrarectal pressure was measured simultaneously. MAIN OUTCOME MEASURES: Reproducibility and correlation between the two measurements. RESULTS: The hernia group had significantly lower IAP than controls both at rest and on straining (mean (SD) 2.7 (1.5) cm H2O compared with 7.0 (5.09) and 6.1 (2.7) compared with 20.5 (7.9), p < 0.01 in each case). Neither the mass nor the obese group differed from the controls at rest, but the pressure was higher on straining (31.2 (1.4) and 33.5 (2.07) cm H2O, respectively, compared with 21.9 (7.3), p < 0.05 in each case). There was a significant drop in IAP after anaesthesia in all groups, and no significant difference between intrarectal pressure and IAP in any group. CONCLUSION: The method of measuring IAP is reproducible. Intrarectal pressure is similar to IAP and can therefore be used instead of it.

BACKGROUND: Intra-abdominal hypertension has been associated with pulmonary and cardiac dysfunctions. We have noted in the clinical scenario of hemorrhagic shock and resuscitation that avoidance of even moderate levels of increased intra-abdominal pressure, using prophylactic decompression, improves outcomes when compared with patients who were decompressed when intra-abdominal pressures went over 20 cm H2O. We hypothesized that prior hemorrhage and resuscitation exacerbates the cardiopulmonary dysfunction associated with intra-abdominal hypertension. METHODS: Ten anesthetized pigs underwent placement of arterial and pulmonary artery catheters and a Silastic intra-abdominal catheter for measuring and manipulating intra-abdominal pressure. Group 1 animals (n = 5) were subjected to increasing intra-abdominal pressures at 10 mm Hg increments up to a level of 40 mm Hg. Group 2 animals (n = 5) were exposed to a severe hemorrhage and resuscitation before the increasing intra-abdominal pressure protocol. RESULTS: Compared with baseline, hemorrhage and resuscitation caused a significant deterioration in cardiac output at intra-abdominal pressures of 10 mm Hg and above. Oxygenation was reduced at 30 and 40 mm Hg. These changes were not seen in group 1 animals. A significant difference was found between groups 1 and 2 in VT, PaCO2, and PaCO2/FIO2 ratio at an intra-abdominal pressure of 20 mm Hg. This difference was not seen at lower or higher pressures. CONCLUSIONS: Prior hemorrhage and resuscitation caused an earlier decline in cardiopulmonary function in the setting of increased intra-abdominal pressure. These data suggest that, when interpreting intra-abdominal pressures, the clinical scenario must be considered. Prior hemorrhage and resuscitation produce the adverse consequences of intra-abdominal hypertension at lower pressures than when intra-abdominal hypertension is the only insult.

OBJECTIVES: To determine relationship of intra-abdominal pressure to central obesity and the comorbidity of obesity. DESIGN: Non-randomized, prospective. SETTING: University hospital, operating room. SUBJECTS: Eighty-four anaesthetized consecutive patients prior to gastric bypass for morbid obesity and five non-obese patients before colectomy for ulcerative colitis. MAIN OUTCOME MEASURES: Weight, body mass index (BMI), co-morbid history, sagittal abdominal diameter, waist:hip (W:H) ratio and urinary bladder pressure, as an estimate of intra-abdominal pressure. RESULTS: Urinary bladder pressure was greater in the obese than the non-obese (18 +/- 0.7 vs. 7 +/- 1.6 cm H2O, P < 0.001), correlated with sagittal abdominal diameter (r = +0.67, P < 0.001) and was greater (P < 0.05) in patients with, than those without, morbidity probably (hypoventilation, gastroesophageal reflux, venous stasis, stress incontinence, incisional hernia) or possibly (hypertension, diabetes) due to increased abdominal pressure. W:H ratio correlated with urinary bladder pressure in men (r = +0.6, P < 0.05) but not women (r = -0.3). CONCLUSIONS: Increased sagittal abdominal diameter was associated with increased intraabdominal pressure which contributed to obesity-related comorbidity. W:H ratio was not a reliable indicator of intra-abdominal pressure for women who often have both peripheral and central obesity. Further studies are needed to evaluate the relationship between intra-abdominal pressure and Type II diabetes and hypertension.

OBJECTIVES: To determine whether intra-abdominal pressure (as estimated from urinary bladder pressure) is elevated in patients with central obesity (as measured by sagittal abdominal diameter) and pseudotumor cerebri and whether this increased intra-abdominal pressure is associated with increased pleural pressure and cardiac filling pressure, implying a resistance to venous return from the brain. DESIGN: Nonrandomized, prospective. SETTING: University hospital, operating room. MAIN OUTCOME MEASUREMENTS: Intracranial pressure, urinary bladder pressure, sagittal abdominal diameter, transesophageal pleural pressure, central venous pressure, pulmonary artery pressure, and pulmonary artery occlusion pressure. SUBJECTS: Six women with pseudotumor cerebri (one with CSF leak, one with lumboperitoneal shunt). RESULTS: Urinary bladder pressure (22 +/- 3 cm H2O) and sagittal abdominal diameter (29 +/- 3 cm) were significantly elevated in these patients with elevated intracranial pressure (293 +/- 80 mm H2O) compared with a previously reported group of nonobese control patients. The transesophageal pleural pressure (15 +/- 10 mm Hg), central venous pressure (20 +/- 6 mm Hg), mean pulmonary artery pressure (31 +/- 6 mm Hg), and pulmonary artery occlusion pressure (21 +/- 7 mm Hg) were all markedly elevated compared with published normal values and with previous data from obese patients without pseudotumor cerebri. CONCLUSIONS: These data support the hypothesis that central obesity raises intra-abdominal pressure, which increases pleural pressure and cardiac filling pressure, which impede venous return from the brain, leading to increased intracranial venous pressure and increased intracranial pressure associated with pseudotumor cerebri.

Five cases are reviewed in which intra-abdominal pressures were used to decide whether critically ill patients would undergo exploratory laparotomy. This is a retrospective case series of a convenience sample of five critically ill, postoperative patients with a variety of underlying illnesses admitted to a surgical intensive care unit in a university hospital. Intra-abdominal compartment pressures were measured using the indirect method of urinary bladder pressure. In patients with signs of abdominal compartment syndrome, intra-abdominal pressures were measured. The pressures were measured every 6 hours until the signs had resolved or the patient was taken for exploratory laparotomy. All patients had Foley catheters. The drainage tubing to the catheters was clamped after the infusion of 200 cc of sterile water. An 18-gauge needle was inserted into the sampling port of the drainage tubing proximal to the clamp, and the needle was connected to a pressure transducer. An elevated abdominal compartment pressure was considered at greater than 25 mm Hg. The case series were reviewed to determine in critically ill patients whether intra-abdominal pressures could assist in deciding which patients required emergent exploratory laparotomy. The patients underwent frequent venous and arterial blood gas and hemodynamic measurements. If the clinical course of the patients worsened as indicated by requiring additional pressors, ventilator support and/or oliguria intra-abdominal pressures were measured every 6 hours. The five patients whose intra-abdominal pressures were elevated were taken for exploratory laparotomy. Four patients were found to have urgent surgical conditions. Intra-abdominal pressures can be used to help decide which patients can be aggressively supported and observed and which patients need re-exploration. At exploration the patient may be found to have necrotic large or small intestines instead of the classical abdominal compartment syndrome findings of ascites, hematoma, and bowel wall edema. In symptomatic patients with abdominal compartment pressures greater than 30 mm Hg, the patient should be taken for exploration. It is not necessary to perform any further diagnostic tests before exploring the patient.