Alberti, A., G. Giannetto, et al. (1998). "[Abdominal compartment syndrome in video laparoscopic surgery. Etiopathogenetic aspects, physiopathology and personal experience]." Chir Ital 50(2-4): 35-42.

The abdominal compartment syndrome (ACS) is a very seven pathology, consequence oh abdominal injuries and traumatism, acute pancreatitis, aortic aneurism rupture, acute peritonitis. The etiopatogenesis is the increase of intra-abdominal pressure with systemic consequences for cardiorespiratory and renal failure. The authors after careful physiopathologic consideration, describe, a case report of ACS in the laparoscopic cholecystectomy for acute cholecystitis. To conclusion, we report very important the accurate intraoperative monitoring of vital parameters (PCO2, PO2, Pa, Fc, PVC, Ph, Diuresis) and immediate decision at laparotomic conversion for abdominal decompression.

BACKGROUND: A previous study disclosed 'unexplained' disturbances in postoperative liver function tests (LFTs) in up to 80% of 67 patients undergoing laparoscopic cholecystectomy (LC). No cause for these elevations was documented. Our objective was to assess the incidence, cause and clinical significance of 'unexplained' disturbances in liver enzymes following LC. PATIENTS AND METHODS: A retrospective chart review of 270 patients who underwent LC and 64 patients undergoing open cholecystectomy (OC) was conducted. Exclusion criteria: any preoperative abnormality in bilirubin or liver enzyme levels, history of chronic liver disease, gallbladder empyema, gangrene or perforation, any evidence or suggestion of choledocholithiasis or other ductal pathology on preoperative or intraoperative imaging or surgical exploration. Preoperatively and on postoperative day 1, alanine transaminase (ALT), alkaline phosphatase and bilirubin levels were measured. There 'unexplained' disturbances were defined as a 50% increase from preoperative values and/or above the normal range. At LC the pneumoperitoneum was maintained at a pressure not exceeding 15 mm Hg. RESULTS: In the groups undergoing OC and LC the respective early elevations in bilirubin occurred in 5 and 9% of patients (NS), and in alkaline phosphatase in 0 and 4% patients (NS). Postoperative ALT was elevated in 15% of patients following OC and in 34% after LC (p = 0. 004). 'Unexplained' LFT disturbances were not associated with any morbidity. CONCLUSIONS: 'Unexplained' disturbances in ALT following LC occur in 34% of the patients and appear to be clinically nonsignificant. It is suggested that the reason for this phenomenon is the pneumoperitoneum-related intra-abdominal hypertension; the only variable not present in the OC group.

BACKGROUND/PURPOSE: Standard treatment of large hepatoomphaloceles has been SILASTIC (Dow Corning, Midland, MI) silo placement followed by closure. This requires two operations, and complications from the silo may occur. The authors have looked for a safe and simpler alternate method of closure. Delayed external compression reduction of an omphalocele (DECRO), appears to have a low complication rate and a rapid time to closure. METHODS: The authors reviewed retrospectively the records of six patients with hepato-omphaloceles treated with DECRO from August 1993 to July 1997. All defects were evaluated by the attending surgeon and could not be closed primarily. All data are expressed as mean +/- SEM. RESULTS: The average gestational age was 36.5 +/- 0.67 weeks with mean weight of 2,780 +/- 256 g. Two patients had congenital cardiac disease. The mean size of the defects was 6.2 x 5.7 cm. All defects had the liver out of the abdomen. No patients required silo placement. The mean time to reduction and final closure was 5.6 +/- 0.49 days. The average postoperative time on the ventilator was 7.1 +/- 3.5 days. Mean time to full feeds was 18.8 +/- 3.4 days. One patient had superficial necrosis of the skin flap. Mean time to discharge was 30.5 +/- 5.5 days. All patients had DECRO completed without complications. CONCLUSIONS: This procedure decreases the number of operations needed from two to one. No complications were seen from the procedure and the time of mechanical ventilation required was low. The abdominal compartment syndrome developed in none of the patients. DECRO is a safe and very effective alternative to SILASTIC silo placement in moderate and large omphaloceles that cannot be closed primarily.

Three patients with the abdominal compartment syndrome are presented and discussed. In one of the patients the condition was induced in an endocrine fashion, since trauma was sustained exclusively by the middle third of the left leg. The development of the syndrome as a remote effect of local trauma has never been reported previously. In all three instances only insignificant amounts of intraperitoneal fluid was found and the increase in abdominal pressure was due to severe edema of the mesentery and retroperitoneum. Since the condition is highly lethal, early diagnosis is imperative, and this starts by carrying a high index of suspicion. Measurement of the intraperitoneal pressure easily confirms this diagnosis. It is emphasized that measurements at various sites, like bladder and stomach, in each patient is essential to confirm the diagnosis, since one of the sites may be rendered unreliable due to intraperitoneal processes impinging on the affected site and affecting its distensibility.

OBJECTIVE: Increased intra-abdominal pressure (IAP) compromises cardiopulmonary function and visceral perfusion. Our goal was to characterize acute changes in these subsystems associated with operative abdominal decompression. PATIENT POPULATION: A series of 11 consecutive injured patients monitored with a pulmonary artery catheter and nasogastric tonometer in whom operative decompression was performed. Indications for decompression included oliguria or progressive acidosis despite aggressive resuscitation in the presence of elevated IAP (>25 mm Hg). MAIN OUTCOME MEASURES: Studied hemodynamic variables included pulmonary artery occlusion pressure (PAOP), right ventricular end-diastolic volume index (RVEDVI), and cardiac index (CI). Pulmonary variables included shunt fraction (Qs/Qt) and dynamic compliance (Cdyn). Visceral perfusion was assessed using hourly urine output 4 hours before and after decompression (UOP) and gastric intramucosal pH (pHi). Mean values before and after decompression were compared using the paired t test. Linear regression and Fisher's z transformation were used to evaluate the relationships between RVEDVI, PAOP, CI, and IAP. IAP was transduced via bladder pressures. Significance was defined as p < 0.05. Data are expressed as means+/-SD. RESULTS: IAP decreased with decompression (49+/-11 to 19+/-6.8 mm Hg; p < 0.0001). RVEDVI improved independent of CI and correlated better (p < 0.01) with CI (r =0.49, p=0.04) than PAOP did (r=-0.36, p=0.09). PAOP correlated significantly with IAP (r=0.45, p=0.04). Decompression resulted in significant improvements in Qs/Qt, Cdyn, UOP, and pHi. CONCLUSION: Abdominal decompression in patients with increased IAP improves preload, pulmonary function, and visceral perfusion. Elevated IAP has important effects on PAOP, which makes the PAOP an unreliable index of preload in these patients.

OBJECTIVE: To evaluate the clinical utility of right ventricular end-diastolic volume index (RVEDVI) and pulmonary artery occlusion pressure (PAOP) as measures of preload status in patients with acute respiratory failure receiving treatment with positive end-expiratory pressure. DESIGN: Prospective, cohort study. SETTING: Surgical intensive care unit in a Level I trauma center/university hospital. PATIENTS: Sixty-four critically ill surgical patients with acute respiratory failure. INTERVENTIONS: All patients were treated for acute respiratory failure with titrated levels of positive end-expiratory pressure (PEEP) with the goal of increasing arterial oxygen saturation to > or =0.92, reducing FIO2 to <0.5, and reducing intrapulmonary shunt to < or =0.2. Serial determinations of RVEDVI, PAOP, and cardiac index (CI) were recorded. MEASUREMENTS AND MAIN RESULTS: Two hundred-fifty sets of hemodynamic variables were measured in 64 patients. The level of PEEP ranged from 5 to 50 cm H2O (mean 12+/-9 [SD] cm H2O). At all levels of PEEP, CI correlated significantly better with RVEDVI than with PAOP. At levels of PEEP > or =15 cm H2O, CI was inversely correlated with PAOP, but remained positively correlated with RVEDVI. CONCLUSIONS: CI correlates significantly better with RVEDVI than PAOP at all levels of PEEP up to 50 cm H2O. RVEDVI is a more reliable predictor of volume depletion and preload recruitable increases in CI, especially in patients receiving higher levels of PEEP where PAOP is difficult to interpret.

The incidence of the abdominal compartment syndrome (ACS) after severe abdominal and/or pelvic trauma is 3%. ACS occurs within hours and causes severe organ dysfunction. Decompressive emergency laparotomy restores this impaired organ function.

Prolonged pneumoperitoneum during laparoscopic surgery has been associated with oliguria in clinical experimental studies. Although the pathophysiology of this oliguria is thought to be renal parenchymal and venous compression, the role of the potent vasoconstrictor endothelin (ET) has not been studied. The purpose of this study was to investigate the effect of pneumoperitoneum on endothelin release and renal function in a canine model. Two groups of dogs were studied during pneumoperitoneum (Group 1, N = 7) or isolated left renal vein compression (Group 2, N = 6). Urine and plasma samples were collected for urine output, glomerular filtration rate (GFR), urine sodium, and plasma endothelin measurements. In Group 1, GFR fell significantly (p < 0.05) by 49% from a control of 0.88 +/- 0.12 mL/min per gram of kidney weight. Urine volume fell by 79% (p < 0.05) from a control value of 0.014 +/- 0.003 mL/min/gkw. Sodium excretion was decreased by 88%. Sodium reabsorption was significantly enhanced during pneumoperitoneum (99.56 +/- 0.15% v 98.44 +/- 0.25%). Arterial plasma ET concentrations were elevated by 8% during the first 20 minutes of pneumoperitoneum (30.8 +/- 3.6 v 33.3 +/- 3.4 pg/mL; p < 0.05). In Group 2, left renal vein compression resulted in a 31% decrease (p < 0.05) in GFR in the left kidney and a 25% decrease in the right kidney. Urine volume fell by 67% in the left kidney and 40% in the right. Renal venous ET concentrations also increased after renal vein compression. Although the mechanism by which oliguria occurs during pneumoperitoneum is not fully understood, the ET concentration was elevated. Because ET can decrease RBF, GFR, and sodium excretion, it may contribute to the oliguria observed during long periods of pneumoperitoneum.

AIMS/BACKGROUND: Increased intra-abdominal pressure during laparoscopic cholecystectomy changes pressure values in the thoracic cavity, in blood vessels, and in biochemical blood values. METHODOLOGY: In this prospective study, we investigate whether CO2 pneumoperitoneum causes blood absorption and whether there is an increased risk of thromboembolism because of its mechanical influence on reographic and biochemical blood attributes. We analyzed pH, BE and arterial blood pCO2 pre-operatively, three times during surgery and post-operatively; and blood coagulation values pre-, during and 30 minutes after the operation. Blood samples were taken from 75 patients, divided into two groups. The first group consisted of 50 patients on whom laparoscopic cholecystectomies were performed, while the second (control) group consisted of 25 patients who were operated on by open laparotomy. All patients had a pre-operative physical status of ASA I and ASA II. RESULTS: There was no statistically significant difference in pCO2 in any measurement, but in the group of patients treated with a laparoscopy there were statistically significant increases in pCO2 in three measurements during the operation. CONCLUSIONS: The data show that during the laparoscopy the pneumoperitoneum had no physical or biochemical influence on coagulation values and so reduced the risk of thromboembolism.

OBJECTIVE: To define the incidence, prophylaxis, and treatment of intra-abdominal hypertension (IAH) and its relevance to gut mucosal pH (pHi), multiorgan dysfunction syndrome, and the abdominal compartment syndrome (ACS). METHODS: Seventy patients in the SICU at a Level I trauma center (1992-1996) with life threatening penetrating abdominal trauma had intra-abdominal pressure estimated by bladder pressure. pHi was measured by gastric tonometry every 4 to 6 hours. IAH (intra-abdominal pressure> 25 cm of H2O) was treated by bedside or operating room laparotomy. RESULTS: Injury severity was comparable between patients who had mesh closure as prophylaxis for IAH (n = 45) and those who had fascial suture (n = 25). IAH was seen in 10 (22.2%) in the mesh group versus 13 (52%) in the fascial suture group (p = 0.012) for an overall incidence of 32.9%. Forty-two patients had pHi monitoring, and 11 of them had IAH. Of the 11 patients, eight patients (72.7%) had acidotic pHi (7.10 +/- 0.2) with IAH without exhibiting the classic signs of ACS. The pHi improved after abdominal decompression in six and none developed ACS. Only two patients with IAH and low pHi went on to develop ACS, despite abdominal decompression. Multiorgan dysfunction syndrome points and death were less in patients without IAH than those with IAH and in patients who had mesh closure. CONCLUSIONS: IAH is frequent after major abdominal trauma. It may cause gut mucosal acidosis at lower bladder pressures, long before the onset of clinical ACS. Uncorrected, it may lead to splanchnic hypoperfusion, ACS, distant organ failure, and death. Prophylactic mesh closure of the abdomen may facilitate the prevention and bedside treatment of IAH and reduce these complications.

The results of the study indicate that elevated pressure during gas incubation in vitro leads to suppression of tumor growth probably due to direct damage of the cells. In vivo, laparoscopy with carbon dioxide and slightly elevated intraperitoneal pressure (5 and 10 mmHg) leads to promotion of intraperitoneal tumor growth while higher pressure (15 mmHg) causes again suppression of intraperitoneal tumor growth. Subcutaneous tumor growth is stimulated by carbon dioxide insufflation in all groups with elevated intraperitoneal pressures. The hypothesis that elevated intraperitoneal pressure might influence the immune system of the tumor host and increase immune suppression after laparoscopy remains theoretically and has to be investigated in further studies.

BACKGROUND: Intra-abdominal hypertension is known to decrease hepatic blood flow, but its effect on hepatic energy level has not described. METHODS: Fifty-three rabbits were mechanically ventilated and divided into five groups. Intra-abdominal hypertension was induced by saline infusion and maintained for 30 minutes. Hepatic sinusoidal functional blood flow was evaluated by means of indocyanine green disappearance rate (ICG-K), hepatic mitochondrial redox status was evaluated by arterial ketone body ratio, and tissue energy level was evaluated by energy charge (EC). RESULTS: At an intra-abdominal pressure of 20 mm Hg, ICG-K was significantly decreased, with no decrease in EC. At 30 mm Hg, hypoxemia developed and the ICG-K decreased further, with significant decreases observed in arterial ketone body ratio and EC. The latter were not increased by administration of oxygen. CONCLUSION: At an intra-abdominal pressure of 20 mm Hg, a slight decrease in sinusoidal flow did not affect hepatic energy level. At 30 mm Hg, a reduced hepatic mitochondrial redox status and a decreased energy level were attributed to a decrease in sinusoidal flow in this animal model.

Abdominal compartment syndrome refers to a complex of negative effects of intra-abdominal hypertension. Its most common cause is complicated abdominal trauma. The syndrome includes mainly hemodynamic and respiratory manifestations but may involve other systems as well. It may present as a life-threatening emergency in the multi-trauma patient. Awareness of the syndrome may enable the surgeon to take preventive measures or to diagnose it earlier and to treat it effectively. We describe a 21-year old man who developed this syndrome after multiple gunshot wounds, with severe liver injury. After 2 operations the typical manifestations of the syndrome were diagnosed. He was re-operated to release intra-abdominal hypertension and then slowly recovered.

A 61-year-old man received an aorto-iliac reconstruction after he was admitted because of a ruptured abdominal aortic aneurysm. Postoperatively, he developed cardiopulmonary insufficiency with anuria. After the intra-abdominal pressure had risen to 40 cmH2O (measured by a urinary bladder catheter), it was decided to perform a relaparotomy. Immediately after abdominal decompression--without correction of any other intra-abdominal pathology--the diuresis increased and several other cardiopulmonary parameters improved significantly. When a critically ill patient shows a rapid increase of the intra-abdominal pressure above a critical level an acute abdominal compartment syndrome may develop. This syndrome consists mainly of potentially fatal cardiopulmonary and renal insufficiency, for which (re)laparotomy with abdominal decompression is the only correct treatment.

The ACS is a clinical entity that develops from progressive, acute increases in IAP and affects multiple organ systems in a graded fashion because of differential susceptibilities. The gut is the organ most sensitive to IAH, and it develops evidence of end-organ damage before the development of the classic renal, pulmonary, and cardiovascular signs. Intracranial derangements with ACS are now well described. Treatment involves expedient decompression of the abdomen, without which the syndrome of end-organ damage and reduced oxygen delivery may lead to the development of multiple organ failure and, ultimately, death. Multiple trauma, massive hemorrhage, or protracted operation with massive volume resuscitation are the situations in which the ACS is most frequently encountered. Knowledge of the ACS, however, is also essential for the management of critically ill pediatric patients (especially those with AWD) and in understanding the limitations of laparoscopy. The role of IAH in the pathogenesis of NEC, central obesity co-morbidities, and pre-eclampsia/eclampsia remains to be fully studied.

This study prospectively analyzed outcomes in 49 consecutive patients undergoing temporary abdominal closure (TAC) between 1993 and 1996 at a single university hospital. There were 37 males and 12 females, mean age was 57 years (range, 25-79 years), mean Acute Physiology and Chronic Health Evaluation score was 27 (+7.8 SD), and mean Simplified Acute Physiology II score was 53.0 (+/-15.4). The reason for TAC was decompression in 22 patients, inability to close the abdomen in 10 patients, to facilitate reexploration for sepsis in 8 patients, and multifactorial in 9 patients. After TAC, there was a significant reduction in intra-abdominal pressure from 24.2+/-9.3 to 14.1+/-5.5 mm Hg and improvement in lung dynamic compliance from 24.1+/-7.9 to 27.6+/-9.4 mL/cm H2O (p < 0.05). Although 10 patients experienced brisk diuresis, there was no significant improvement in renal function; in fact, serum creatinine increased. The median length of stay was 35 days (range, 1-232 days). The mean number of abdominal operations after mesh insertion was 2.6+/-2.4. There were 21 deaths, for a standardized mortality rate of 0.80. Although it achieved significant reductions in abdominal pressures and improved lung dynamic compliance, TAC did not result in improved renal function or patient oxygenation.

BACKGROUND: The abdominal compartment syndrome (ACS) is a newly appreciated and potentially fatal consequence of increased intra-abdominal pressure. It can be due to either trauma or surgery, as well as numerous medical conditions. Prolonged, unrelieved elevation of intra-abdominal pressure can produce pulmonary compromise, renal impairment, cardiac failure, shock, and death. A high index of suspicion is imperative. Measurement of the intravesical pressure provides a urometric window for detecting and monitoring this condition. CONCLUSIONS: Reopening the abdominal incision (decompressive celiotomy) has proven a life-saving intervention. Use of delayed wound closure (staged celiotomy) may prevent development of this condition in high-risk surgical patients. It is urgent that all physicians, and surgeons in particular, be alerted to this potentially lethal complication.

BACKGROUND AND STUDY AIMS: The accuracy of transurethral bladder catheter pressure in reflecting intra-abdominal pressure is well defined in experimental studies and case reports but not in controlled clinical trials. PATIENTS AND METHODS: We compared bladder pressure with insufflator pressure during laparoscopic cholecystectomy in 40 patients. Measurements were made at four pressure levels of the insufflator: 0, 5, 10 and 15 mmHg. RESULTS: When the insufflator displayed 0, 5, 10, and 15 mmHg (0, 6.8, 13.6 and 20.4 cmH2O), and the mean bladder pressures measured 2.5 +/- 1.4, 7.3 +/- 1.5, 12.9 +/- 1.6 and 19.7 +/- 1.5 cmH2O, respectively. The two measurements correlated well with each other (r = 0.973, P < 0.0001). CONCLUSION: We concluded that bladder pressure measured by transurethral catheter was equal to insufflator pressure during laparoscopy, and that this was a valid indicator of intra-abdominal pressure.