Bloomfield, G., B. Saggi, et al. (1999). "Physiologic effects of externally applied continuous negative abdominal pressure for intra-abdominal hypertension." J Trauma 46(6): 1009-14; discussion 1014-6.

BACKGROUND: To determine the ability of an externally applied continuous negative abdominal pressure device (CNAP) to reverse the effects of elevated intra-abdominal pressure on the central nervous and cardiovascular systems. METHODS: Anesthetized, ventilated swine had catheters placed for measurement of intra-abdominal (IAP), intracranial (ICP), central venous, pulmonary artery, pulmonary artery occlusion, mean arterial, peak inspiratory, inferior vena cava, and femoral vein pressures. After the animals stabilized, baseline measurements were obtained. IAP was increased by incrementally instilling an isosmotic polyethylene glycol solution into the peritoneal cavity until it was 25 mm Hg above baseline. IAP was maintained at 25 mm Hg above baseline for 2 hours. CNAP was then applied for 2 hours. All parameters were remeasured 30 minutes after each increase in IAP, at 2 hours after attaining maximum IAP, and lastly at 2 hours after abdominal decompression. Cardiac index was maintained near baseline by volume expansion. RESULTS: Elevation of IAP to 25 mm Hg above baseline for 2 hours caused increases (p<0.05) in central venous pressure (10.3+/-0.9 to 15.2+/-1.7), inferior vena cava pressure (13.0+/-1.0 to 29.5+/-1.5), femoral vein pressure (13.5+/-0.5 to 33.3+/-1.3), ICP (10.6+/-1.5 to 21.0+/-1.5), and peak inspiratory pressure (18.3+/-0.3 to 34.2+/-1.0). The mean arterial pressure (106.3+/-3.5 to 125.8+/-3.4), pulmonary artery pressure (24.3+/-2.3 to 31.3+/-1.7), and pulmonary artery occlusion pressure rose (12.3+/-0.9 to 17.5+/-3.5), but not significantly. Cardiac index (3.3+/-0.5 to 3.4+/-0.4) remained essentially unchanged. CNAP significantly (p<0.05) decreased IAP (30.7+/-1.3 to 18.2+/-1.3), central venous pressure (15.2+/-1.7 to 12.4+/-2.1), inferior vena cava (29.5+/-1.5 to 19.2+/-1.3), and ICP (21.0+/-1.5 to 16.2+/-1.3). Pulmonary artery occlusion pressure (17.5+/-3.5 to 15.0+/-3.1) and peak inspiratory pressure (34.2+/-1.0 to 29.7+/-1.1) decreased, but not significantly. CONCLUSION: Acutely elevated IAP causes a significant increase in ICP and impaired cardiovascular and pulmonary function. Abdominal decompression remains the standard of care for abdominal compartment syndrome. However, in patients in whom an increased IAP does not require surgical decompression, the results of this study suggest that externally applied CNAP may be of value.

BACKGROUND: Intra-abdominal hypertension and abdominal compartment syndrome cause significant morbidity and mortality in surgical and trauma patients. Maintenance of intravascular preload and use of open abdomen techniques are essential. The accuracy of pulmonary artery occlusion pressure (PAOP) and central venous pressure (CVP) in patients with intra-abdominal hypertension has been questioned. METHODS: Twenty surgical and trauma patients with intra-abdominal hypertension requiring open abdominal decompression were monitored using volumetric thermodilution pulmonary artery catheters. Hemodynamic, oxygenation, inspiratory, and intravesicular pressure measurements were collected prospectively. PAOP, CVP, and right ventricular end-diastolic volume index (RVEDVI) were compared as estimates of preload status. RESULTS: Multiple regression analysis demonstrated that cardiac index correlated significantly better with RVEDVI (r = 0.69) than with PAOP (r = -0.27) or CVP (r = -0.28) during resuscitation after open abdominal decompression (p < 0.0001). CONCLUSION: RVEDVI is superior to PAOP and CVP as an estimate of preload status in patients with an open abdomen.

OBJECTIVE: Acute renal failure is seen with the acute abdominal compartment syndrome (AACS). Although the cause of acute renal failure in AACS may be multifactorial, renal vein compression alone has not been investigated. This study evaluated the effects of elevated renal vein pressure (RVP) on renal function. METHODS: Two groups of swine (18-22 kg) were studied after left nephrectomy and placement of a renal artery flow probe to measure renal artery blood flow, renal vein catheter, and ureteral cannula. Two hours were allowed for equilibration and an inulin infusion was begun to calculate inulin clearance for measurement of glomerular filtration rate. Group 1 animals (n = 4) had RVP elevated by 30 mm Hg for 2 hours with renal vein constriction. RVP was then returned to baseline for 1 hour. In group 2 (n = 4), the RVP was not elevated. The cardiac index (2.9 +/- 0.5 L/min/m2) and mean arterial pressure (101 +/- 9 mm Hg) remained stable. Plasma renin activity and serum aldosterone were measured every 60 minutes. RESULTS: Elevation of RVP (0-30 mm Hg above baseline) in the experimental group showed a significant decrease in renal artery blood flow index (2.7 to 1.5 mL/min per g) and glomerular filtration rate (26 to 8 mL/min) compared with control. In addition, there was significant elevation of plasma serum aldosterone (14 to 25 microng/dL) and plasma renin activity (2.6 to 9.5 microng/mL per h) as well as urinary protein leak in the experimental animals compared with control. These changes were partially or completely reversible as RVP returned toward baseline. CONCLUSION: Elevated RVP alone leads to decreased renal artery blood flow and glomerular filtration rate and increased plasma renin activity, serum aldosterone, and urinary protein leak. These changes are consistent with the renal pathophysiology seen in AACS, morbid obesity, and preeclampsia. The changes are partially or completely reversed by decreasing renal venous pressure as occurs with abdominal decompression for AACS.

Abdominal compartment syndrome (ACS) is a well-recognized perioperative complication that occurs in patients who undergo intra-abdominal operations and who require extensive fluid resuscitation. The classic presentation of this syndrome includes high peak airway pressures; oliguria, despite adequate filling pressures; and intra-abdominal pressures of more than 25 mm Hg. A decompressive laparotomy performed at the bedside can alleviate ACS. If left untreated, sustained intra-abdominal hypertension is often fatal. In the literature, ACS has been described in pediatric patients with burns but not in adult patients with burns. This article describes 3 adults who sustained burns of more than 70% of their body surface areas, who required more than 20 L of crystalloid resuscitation, and who developed ACS during their resuscitation after the burn injury. The mortality rate among these patients was 100%, which confirms the grave consequences of this syndrome. In our institution, intra-abdominal pressure is now routinely measured as part of the burn resuscitation process in an attempt to diagnose and treat this syndrome earlier and more efficaciously. It is recommended that the possibility of ACS be considered when diagnosing any patient with burns who develops high airway pressures, oliguria, or both.

BACKGROUND: Abdominal compartment syndrome is defined as the adverse physiologic effects of increased intra-abdominal pressure. Prolonged, unrelieved pressure may lead to respiratory compromise, renal impairment, cardiac failure, shock, and death. Abdominal compartment syndrome is diagnosed by measuring intra-cystic pressure as a reflection of intra-abdominal pressure. To examine the validity of the technique, we conducted a prospective study in surgical patients by directly measuring bladder and abdominal pressures simultaneously during laparoscopic cholecystectomy using a previously described technique. RESULTS: In the present model, the bladder had higher baseline pressures than did the abdomen. Measurements across the bladder wall were not identical, but had high positive correlation coefficient when evaluated on an individual basis. Global analysis of the data for all patients showed a weak correlation coefficient. CONCLUSION: In the present study model, intra-cystic pressure did not reflect actual intra-abdominal pressure. In spite of some limitations in the study design, we feel that further research is warranted to identify other possible variables that may play a role in the relationship between the urinary bladder and the abdominal cavity pressures, providing better means for diagnosis of abdominal compartment syndrome.

Intraabdominal hypertension and abdominal compartment syndrome are increasingly recognized as potential complications in patients who have significant intraabdominal trauma. Intraabdominal hypertension and abdominal compartment syndrome affect all body systems, most notably the cardiac, respiratory, renal, and neurologic systems. This complication also affects blood flow to various intraabdominal organs and may play a significant role in the sepsis and multiple organ failure syndrome seen in many trauma patients. Nursing knowledge of the risk factors and clinical signs of intraabdominal hypertension and abdominal compartment syndrome can reduce the morbidity and mortality associated with this syndrome.

OBJECTIVE: Abdominal compartment syndrome (ACS) has multiple well-described etiologies, but almost no attention has focused on ACS in the absence of abdominal injury. This study describes a secondary ACS that occurs after severe hemorrhagic shock with no evidence of abdominal injury. METHODS: The trauma registry at a Level I trauma center was reviewed for a 13-month period beginning July 1, 1997. RESULTS: During the study period, there were 46 of 1,216 intensive care unit admissions (4%) who required laparotomy and mesh closure of the abdominal wall because of visceral edema. In that subgroup, six patients (13% of mesh closures, 0.5% intensive care unit admissions) had hemorrhagic shock (5/1, blunt/penetrating trauma) but no evidence of intra-abdominal injury. Associated extremity compartment syndrome developed in two of six (33%). Overall mortality was four of six (67%), secondary to sepsis (n = 3), and head injury (n = 1). Time from admission to decompression averaged 3 hours in survivors and 25 hours in nonsurvivors (overall average = 18+/-9 hours). Resuscitation volume before abdominal decompression averaged 19+/-5 liters of crystalloid and 29+/-10 units of packed red blood cells. Bladder pressure averaged 33+/- 3 mm Hg. Decompression significantly improved peak inspiratory pressure (p < 0.003) and base deficit (p < 0.003). CONCLUSION: ACS can occur with no abdominal injury; The incidence of secondary ACS was 0.5% in this cohort trauma intensive care unit patients, so it probably occurs more frequently than is currently appreciated. Because survivors were decompressed 20 hours before nonsurvivors, early recognition might improve outcomes. On the basis of these observations, we recommend that bladder pressures should be routinely checked and acted on appropriately when resuscitation volumes approach 10 liters of crystalloid or 10 units of packed red cells.

OBJECTIVE: To determine the current opinion of American trauma surgeons on the use of the open abdomen to prevent the abdominal compartment syndrome (ACS). METHODS: On a questionnaire survey of expert trauma surgeons regarding 12 clinical factors influencing fascial closure at trauma celiotomy, surgeons graded their willingness to close the fascia in various scenarios on a scale of 1 to 5. The impact of six signs of clinical deterioration on willingness to perform abdominal decompression in a patient with postceliotomy elevated intra-abdominal pressure (IAP) was also queried. Of 292 members of the American Association for the Surgery of Trauma active in abdominal trauma management, 248 members (85%) had experience with ACS one or more times in the previous year. RESULTS: Surgeons' responses to factors found at trauma celiotomy were divided into two distinct categories: factors decreasing willingness to close the fascia, and factors not changing or increasing willingness to close the fascia (p < 0.001). Factors disfavoring fascial closure were pulmonary or hemodynamic deterioration with closure, massive bowel edema, subjectively tight closure, planned reoperation, and packing. Factors not changing or favoring fascial closure were fecal contamination/peritonitis, massive transfusion, hypothermia, multiple abdominal injuries, acidosis, and coagulopathy. Five of the six signs of clinical deterioration increased surgeons' willingness to decompress a patient with elevated IAP (increased O2 requirement, decreased cardiac output, increased acidosis, increased airway pressures, and oliguria). Lowered gastric mucosal pH did not affect willingness. Seventy-one percent of surgeons indicated they would decompress elevated IAP in postceliotomy patient if one or two signs of clinical deterioration were present, but only 14% would decompress a patient for elevated IAP alone. CONCLUSION: A majority of expert American trauma surgeons have experience with ACS and would leave the abdomen open if ACS occurred. A majority would reopen a closed abdomen in cases of elevated IAP with signs of clinical deterioration. A minority would leave the abdomen open when there was only a risk of developing ACS.

OBJECTIVE: The abdominal compartment syndrome is a potentially fatal condition resulting from pathologic elevation of intraabdominal pressure. We evaluated preoperative abdominal CT scans of four patients with proven abdominal compartment syndrome to identify signs of increased intraabdominal pressure. CONCLUSION: CT findings common to all four patients included tense infiltration of the retroperitoneum out of proportion to peritoneal disease, extrinsic compression of the inferior vena cava by retroperitoneal hemorrhage or exudate, and massive abdominal distention with an increased ratio of anteroposterior-to-transverse abdominal diameter (positive round belly sign; ratio > .80; p < .001). Direct renal compression or displacement, bowel wall thickening with enhancement, and bilateral inguinal herniation were each present in two of the four patients. Radiologists should be aware of this life-threatening syndrome. In the appropriate clinical setting, CT findings of increased intraabdominal pressure should be swiftly communicated to other physicians involved in treating the patient because the abdominal compartment syndrome requires emergent surgical decompression.

BACKGROUND: Elevated intra-abdominal pressure (IAP) increases intracranial pressure (ICP) and reduces cerebral perfusion pressure (CPP). We evaluated a nonsurgical means of reducing IAP to reverse this process. METHODS: Swine with a baseline ICP of 25 mm Hg produced by an intracranial balloon catheter were studied. In group 1 (n = 5), IAP was increased by 25 mm Hg. Continuous negative abdominal pressure (CNAP) was then applied. Group 2 (n = 4) had neither IAP elevation nor CNAP. Group 3 (n = 4) had CNAP without IAP elevation. RESULTS: Elevation of IAP by 25 mm Hg above baseline led to deleterious changes in ICP (25.8+/-0.8 to 39.0+/-2.8; p < 0.05) and CPP (85.2+/-2.0 to 64.8+/-2.6; p < 0.05). CNAP led to a reduction in IAP (30.2+/-1.2 to 20.4+/-1.3; p < 0.05) and improvements in cerebral perfusion (ICP, 33+/-2.7; CPP, 74.4+/-1.2; both p < 0.05). Group 2 had stable ICP (25.8+/-0.25 to 28.7+/-1.7; p > 0.05) and CPP (80.8+/-1.4 to 80.5+/-1.8; p > 0.05). In group 3, CNAP decreased cardiac index (2.9+/-0.2 to 1.1+/-0.4; p < 0.05), mean arterial pressure (105.2+/-4.0 to 38.2+/-12.0; p < 0.05), and CPP (74.2+/-4.7 to 14.5+/-12.2; p < 0.05). CONCLUSION: Elevations in IAP led to increased ICP and decreased CPP. CNAP ameliorated these intracranial disturbances. With normal IAP, CNAP impaired cerebral perfusion.

Acutely increased intraabdominal pressure can lead to multisystem organ dysfunction. Organ dysfunction consists of acute pulmonary failure secondary to compressive atelectasis and associated with high peak inspiratory pressures and impaired gas exchange, acute renal failure with marked oliguria without hypernaturia, intestinal and hepatic ischemia possibly leading to bacterial translocation or necrosis with peritonitis, increased intracranial pressures which may cause brain dysfunction or aggravate head injury edema, venous thrombosis and thromboembolism, and abdominal wall ischemia or necrosis. The diagnosis is made clinically in a patient with high peak inspiratory pressures, oliguria and an apparently tight abdomen, although urinary bladder pressure > or = 20 cm H2O pressure is suggestive. However, chronically increased intraabdominal pressure as is seen in the morbidly obese, pregnancy and cirrhosis may be misleading. As to treatment, once the diagnosis is made, the patient's abdomen should be opened and the tension relieved. The intestinal contents need to be protected and evaporative water loss minimized by either closing the skin and not the fascia or, if this is not possible, using an impermeable protective dressing. If the abdomen is difficult to close at the primary operation, it is best to prevent the development of an acute abdominal compartment syndrome by closing only the skin or leaving it open and using an impermeable dressing. In conclusion, the acute abdominal compartment syndrome has become increasingly recognized as a cause for multisystem organ failure. Recognition of the problem or prevention is mandatory for optimal patient survival.

HYPOTHESIS: Intra-abdominal hypertension exerts an effect on renal function independent of other confounding variables. DESIGN: A prospective study of all patients admitted to an intensive care unit following abdominal surgery was undertaken between September 1, 1994, and July 31, 1997, in a single university hospital. MAIN OUTCOME MEASURES: Intra-abdominal pressure (IAP) was measured every 8 hours (normal IAP, 0-17 mm Hg); 18 mm Hg or higher was considered increased. Forward stepwise logistic regression determined whether intra-abdominal hypertension is an independent cause of renal impairment. RESULTS: A total of 263 patients (174 after emergency surgery), whose mean +/- SD age was 61.0 +/- 18.7 years and Acute Physiology and Chronic Health Evaluation II score was 14.6 +/- 7.7, were studied. Intra-abdominal pressure was increased in 107 (40.7%) of the 263 patients. Renal impairment occurred in 35 (32.7%) of the 107 patients with intra-abdominal hypertension and in 22 (14.1%) of the 156 with a normal IAP (odds ratio, 1.62-5.42). Using the Wald maximizing model, renal impairment was independently associated with 4 antecedent factors: hypotension (P= .09), sepsis (P = .006), age older than 60 years (P = .03), and increased IAP (P = .004). CONCLUSIONS: To our knowledge, for the first time in a large clinical study, IAP has been shown to be an independent cause of renal impairment, and it ranks in importance after hypotension, sepsis, and age older than 60 years. Surgeons need to be aware of the importance of intra-abdominal hypertension in patients postoperatively.

BACKGROUND: Abdominal compartment syndrome is a rare condition in which increased intra-abdominal pressure adversely affects perfusion and viability of the viscera, and the cardiovascular, respiratory, and renal systems. The syndrome follows acute abdominal events such as abdominal trauma, intraperitoneal hemorrhage, or intra-abdominal infection. CASES: Two women who had abdominal hysterectomies postoperatively developed clinical features of multisystem failure with markedly elevated intra-abdominal pressures. The women, one with intra-abdominal infection and diffuse intestinal edema and one with intra-abdominal hemorrhage, were diagnosed by clinical exam and intravesical pressure measurements. Both had follow-up exploration and temporary placement of the small bowel and colon into an intestinal bag until adequate resuscitation was achieved. CONCLUSION: Abdominal compartment syndrome is a rare complication in gynecology that can be diagnosed early and decompressed promptly.