Effect Of Intra-abdominal Hypertension Research Articles

Effect of intraabdominal hypertension on splanchnic blood flow in children with appendicular peritonitis.

Background and Aims:Intraabdominal hypertension (IAH) is poorly diagnosed condition that cause splanchnic hypoperfusion and abdominal organs ischemia and can lead to multiple organ failure. There are no scientific data regarding effect of intraabdominal pressure (IAP) on splanchnic circulation in children.Material and Methods:Ninety-four children after surgery for appendicular peritonitis were enrolled in the study. After IAP measurement children were included in one of two groups according IAP levels: “without IAH” (n = 51) and “with IAH” (n = 43). Superior mesenteric artery (SMA) and portal vein (PV) blood flows (BFSMA, BFPV, mL/min) were measured, and SMA and PV blood flow indexes (BFISMA, BFIPV, ml/min*m2) and abdominal perfusion pressure (APP) were calculated in both groups.Results:Median BFISMA and BFIPV in group “with IAH” were lower by 54.38% (P < 0.01) and 63.11% (P < 0.01) respectively compared to group “without IAH”. There were strong significant negative correlation between IAP and BFISMA (rs = –0.66; P < 0.0001), weak significant negative correlation between IAP and BFIPV (rs = –0.36; P = 0.0001) in group “with IAH” and weak significant negative correlation between IAP and BFISMA (rs = –0.30; P = 0.0047) in group “without IAH”. There were no statistically significant correlations between IAP and BFIPV in group “without IAH”, between BFISMA and APP in both groups and between BFIPV and APP in both groups.Conclusion:Elevated IAP significantly reduces splanchnic blood flow in children with appendicular peritonitis. BFISMA and BFIPV negatively correlate with IAP in these patients. There is no correlation between BFISMA/BFIPV and APP in children with IAH due to appendicular peritonitis.

Effect of intra-abdominal hypertension on the strength of the postoperative scar of a laparotomic wound

Annotation. One of the main factors of postoperative eventration is intra-abdominal hypertension, which occurs in various surgical pathologies of the abdominal cavity. Despite the presence of a large number of scientific papers on the negative effect of intra-abdominal hypertension on the morphological state of granulation tissue in the area of the laparotomy wound, there are no publications on the impact on the strength of the postoperative scar. Therefore, the study aimed to investigate in an experiment on small laboratory animals the effect of intra-abdominal hypertension on the mechanical strength of the postoperative scar of a laparotomy wound. The experiment was performed on 120 laboratory rats, which underwent a median laparotomy and brought together the edges of the musculoaponeurotic layer of the anterior abdominal wall with simple nodal sutures. The main group consisted of 72 animals who developed intra-abdominal hypertension by inserting a container (condom) with a certain amount of Furacilin into the abdominal cavity. The comparison group consisted of 48 animals who had an empty condom inserted into the abdominal cavity after laparotomy. The mechanical strength of the postoperative scar of the laparotomy wound was determined by the method of G. V. Petrovich (2010) on the 1st, 3rd, and 5th day after the creation of intra-abdominal hypertension, by measuring the level of intra-abdominal pressure at the time of rupture of the postoperative scar of the laparotomy wound. Statistical analysis of the results was performed using Microsoft Excel spreadsheets and a package of statistical processing software PAST. Differences between study groups were determined using Mann-Whitney criteria. The results of the study indicate that the created intra-abdominal hypertension leads to a decrease in the mechanical strength of the postoperative scar of the laparotomy wound. The degree of the negative impact of intra-abdominal hypertension on the strength of the postoperative scar is inversely proportional to the level of intra-abdominal pressure.

Relavance of peritoneal drainage fluid lactate level in patients with intra-abdominal hypertension

Objective: The aim of this study was to assess the effect of intra-abdominal hypertension (IAH) on peritoneal fluid lactate, local and systemic organ dysfunctions in patients after major abdominal ...

Varying models of intra-abdominal hypertension and their effect on renal function in a porcine model

Intra-abdominal hypertension (IAH) is an independent predictor of renal impairment and mortality [1]. Organ dysfunction caused by the pressure effect of IAH is well understood, but how this is modified in the presence of bowel obstruction is unclear. The aim of this study was to determine how different IAH models cause renal dysfunction in a pig model.

Analysis on curative effect of intra-abdominal hypertension in patients with severe acute pancreatitis treated by laparoscopic surgery

Objective To explore the importance of monitoring intra-abdominal hypertension (IAH)through bladder and early application of laparoscopic techniques for the patients with severe acute pancreatitis (SAP).Methods Data of intra-abdominal pressure (IAP) from 201 SAP patients hospitalized in the past 12 years was observed and 60 cases (IAP＞25 mmHg)were included.According to the order of admission,patients were randomly divided into singular group (observation) and dual groups (control) (n=30).Group A was treated by laparoscopic irrigation,drainage and removing necrotic tissue,while the group B was given traditional comprehensive treatment including dual fast,gastrointestinal decompression,resistance to infection,somatostatin and laparotomy in case of abdominal abscess formation.Results Case fatality rate in the two groups were 16.7％ and 23.3％ respectively and concurrent arterial occlusive diseases (AODs) rate were 10.0％ and 20.0％.For the complications and prognosis,IAH duration and hospitalization time in group A were significantly shortened (P＜0.05)while abdominal cavity infection rate was decreased obviously (P＜0.05) compared with those of group B.Hemorrhagic infection incidence and mortality rate in group A were also reduced (P＜0.05).Conclusion Once SAP diagnosis established (IAP＞25mmHg),early treatment by laparoscopic irrigation,drainage and removing necrotic tissue via peritoneal outside diameter should be conducted. Key words: Severe acute pancreatitis (SAP); Laparoscope; Intra-abdominal pressure (IAP)

Effect of intra-abdominal hypertension on left ventricular relaxation: a preliminary animal study

In the intensive care unit, intra-abdominal hypertension (IAH) is a frequently encountered, life-threatening condition. The aim of this animal study was to evaluate the effect of IAH on left ventricular (LV) relaxation (i.e. the active phase of diastole). Seven male rabbits were anaesthetized before mechanical ventilation. A 20 mm Hg increase in intra-abdominal pressure (IAP) was then induced by intraperitoneal infusion of 1.5% glycine solution. Haemodynamic parameters were recorded and the relaxation time constant tau (considered to be the best index of left ventricle relaxation) was calculated. All haemodynamic measurements were recorded at baseline and then after induction of IAH. A 20 mm Hg increase in IAP was not followed by a significant change in arterial pressure, but was associated with increases in central venous pressure (from 2 [-2 to 6] to 7 [-2 to 12] mm Hg, P= 0.03), LV end-diastolic pressure (from 7 [6-8] to 15 [11-19] mm Hg, P= 0.04) and the relaxation time constant tau (from 16 [14-18] to 43 [34-52] ms, P= 0.048). In this animal study, a 20 mm Hg increase in IAP impaired LV relaxation. Further studies are necessary to identify the causes of this impairment.

Hemostatic effect of non-insufflation intra-abdominal compression on liver injury

Objective To assess the effectiveness and safety of non-insufflation intra-abdominal compression as a prehospital hemostatic technique in treatment of liver injury.Methods Twenty-nine male Wistar rats were enrolled and randomly assigned into four experimental groups:IAP0 group ( n =8 ),IAP5 group (n =8),IAP10 group (n =8) and IAP15 group (n =5).Then,the anticoagulated rat models of severe liver injury were established with different intra-abdominal pressures ( 0,5,10 and 15 mm Hg) by using a non-expansible insufflated gas bag.Once the mean artery pressure (MAP) was less than 95 mm Hg,Lactated Ringer' s solution was infused through the right jugular vein at speed of 3.3 ml · min-1 · kg-1 until MAP reached 100 mm Hg.Thirty minutes later,the animals were killed by intravenous injection of 0.2 ml saturated potassium chloride solution to measure the intraperitoneal total blood loss,liver weight,volume of infused solution and MAP.Results No death was observed in IAP0,lAP5 and IAP10 groups and four rats (4/5) died at 10-15 minutes following exposure to the 15 mm Hg intra-abdominal pressure in IAP15 group.Total blood loss was reduced to ( 54.20 ±11.30)ml/kg in IAP0 group,(43.98 ±9.2) ml/kg in IAP5 group,(32.49 ±7.40) ml/kg in IAP10group and (25.77 ± 14.16) ml/kg in IAP15group ( P ＜0.01 ).The infused volume of resuscitation solution was (31.06 ± 3.14) ml in IAP10 group,which was higher than (24.94 ±6.67) ml in IAP0 group,(23.06 ± 7.98) ml in IAP5 group and (16.50 ±7.27) ml in IAP15 group (P ＜0.05).Liver weight was ( 11.18 ± 1.45) g in IAP5 group,( 12.13 ± 0.96) g in IAP10 group and ( 11.41 ± 1.20) g in IAP15 group,which was significantly higher than (10.03 ±0.58) g in IAP0 group (P＜0.05).The MAP was (64.81 ± 19.65) mm Hg in IAP5 group and (65.80 ± 15.36) mm Hg in IAP10 group ( insignificant difference between groups,P ＞ 0.05 ),which was higher than (41.22 ± 10.00) mm Hg in IAP0 group and (44.50 ±28.60) mm Hg in IAP15 group (P ＜0.05).Conclusions Non-pneumatic intra-abdominal compression can effectively control bleeding in rat models of severe liver injury,while the adverse effect of intra-abdominal hypertension should be avoided. Key words: Liver; Wounds and injuries; Hemorrhage; Hemostatsis; Prehospital

Mission to Eliminate Postinjury Abdominal Compartment Syndrome

To determine the current incidence of postinjury abdominal compartment syndrome (ACS), the effect of intra-abdominal hypertension (IAH) on trauma outcomes, and the independent predictors of postinjury IAH. Prospective cohort study. University-affiliated level 1 trauma center. Eighty-one consecutive shock/trauma patients admitted to the intensive care unit (mean [SD] values: age, 41[2] years; 70% male; injury severity score, 29[1]; base deficit, 6[0.5] mmol/L; lactate level, 29.73[4.5] mg/dL; transfusions of packed red blood cells, 5[0.5] U in first 24 hours; mortality rate, 2.5%; and multiple organ failure [MOF], 6%) had second hourly intra-abdominal pressure (IAP) monitoring. Intensive care unit length of stay, ACS, IAH, MOF, mortality. The mean (SD) IAP was 14(1) mm Hg. No patients developed ACS. Sixty-one patients (75%) had sustained IAH. Both patients with IAH and those without had similar demographics and injury severity. Patients with IAH had worse metabolic acidosis (P=.02), received more crystalloids (P=.03), and underwent laparotomy more frequently (P=.005). One patient with IAH and one without died. MOF occurred in 1 patient without IAH (5%) vs 4 with IAH (7%). The mean (SD) intensive care unit length of stay was 11(3) days in patients without IAH vs 8(1) days in those with IAH. Intra-abdominal hypertension was poorly predictive of MOF (odds ratio, 1.17; 95% confidence interval, 0.96-1.43; P=.13). Of the 30 variables in multiple logistic regression analysis, only base deficit, laparotomy, and emergency department crystalloids were identified as weak predictors of IAP greater than 12 mm Hg. No predictors were found for the clinically more relevant IAP greater than 15 mm Hg and IAP greater than 18 mm Hg. Most of the severe shock/trauma patients developed sustained IAH. Based on univariate and multivariate analyses, there was no difference in outcomes between the trauma patients with IAH and those without. Multiple logistic regression analysis failed to show IAH as a predictor of MOF. The attenuation of the deadly ACS to a less deleterious IAH could be considered a success of the last decade in trauma and critical care.

Acute renal failure due to abdominal compartment syndrome

To observe the effect of intra-abdominal hypertension on renal function. 30 intra-abdominal hypertension patients, 26 mals and 4 femals, age 42 +/- 17, were observed. Intra-abdominal pressure, mean arterial pressure, central venous pressure and serum creatinine were recorded and tested at the same time every day. When the intra-abdominal pressure increased, the urine output decreased (from 78 ml/h +/- 26 ml/h to 31 ml/h +/- 11 ml/h, P < 0.01), serum creatinine increased (from 110 mmol/L +/- 98 mmol/L to 224 mmol/L +/- 147 mmol/L, P < 0.01) with high central venous pressure (6.0 mm Hg +/- 2.1 mm Hg to 8.8 mm Hg +/- 2.5 mm Hg, 1 mm Hg = 0.133 kPa, P < 0.01) and high mean arterial pressure (from 79 mm Hg +/- 8 mm Hg to 86 mm Hg +/- 10 mm Hg, P < 0.01). There is a significant negative correlation between the intra-abdominal hypertension and urine output (r = -0.747, P < 0.01), and a significant positive correlation between the intra-abdominal hypertension and serum creatinine (r = 0.816, P < 0.01). During the ICU stay, 12 patients died, amoung which 8 died from multiple organ dysfunction due to septicemia and 4 died from abdominal hemorrhage. Intra-abdominal hypertension is correlated with lower urine output and increased blood creatinine significantly, and these results can be inversed when the intra-abdominal pressure decreases.

Increased susceptibility to oxidant injury in hepatocytes from rats with intra-abdominal hypertension.

Intra-abdominal hypertension leads to visceral organ hypoperfusion, and subsequent decompression may cause ischemia-reperfusion, releasing toxic metabolites. This study focuses on the effect of intra-abdominal hypertension on hepatic antioxidant store and the susceptibility of hepatocytes to oxidant injury. Sprague-Dawley rats (150-180 g) were acclimatized to an environment for 3 days and then divided into two groups according to challenge based on intra-abdominal pressure (0 and 30 cm H2O for control and experimental groups, respectively). After a 90-minute challenge, the rats underwent immediate laparotomy for decompression; after a further 30 minutes, one fragment of liver from the lingual lobe (>0.1 g) was excised to measure glutathione (GSH) in vivo before portal vein perfusion. After hepatocyte isolation (viability rate > 85%), the cell density was set at 1 x 10/mL for each well. The samples were cultured in an incubator for 12 hours, after which varying concentrations of t-butyl hydroperoxide (TBHP) (0.0, 0.5, 1.0, and 2.0 mmol/L) were added into the wells. After another 5-hour incubation, the total store of intracellular GSH in vitro (GSHVT) and the hepatocyte survival rates were measured for different groups of TBHP challenge using GSH assay and MTT kits. The control and experimental groups consisted of 10 and 8 rats, respectively, that successfully completed the entire experimental procedure. Compared with the control group, the in vivo GSH store was significantly reduced after the intra-abdominal pressure challenge (mean +/- SE, 968.1 +/- 63.5 vs. 1,581.0 +/- 115.3 nmol/g of protein; p = 0.001). After the hepatocyte isolation, the GSHVT stores at various TBHP concentrations in the experimental rats were also similarly and significantly decreased relative to the control animals (894.4 +/- 56.4, 804.2 +/- 118.4, 586.9 +/- 86.6, and 410.2 +/- 87.4 nmol/g of protein vs. 1,282.2 +/- 112.0, 1,156.6 +/- 91.0, 995.2 +/- 92.7, and 866.8 +/- 62.4 nmol/g of protein for TBHPs of 0.0, 0.5, 1.0, and 2.0 mmol/L, respectively; all p < 0.05). Moreover, from photocytometry, the hepatocyte survival rates were significantly reduced for the experimental rats compared with the control animals after challenge with various TBHP concentrations (survival was 100%, 91.1%, 81.3%, and 72.8% vs. 100%, 99.2%, 95.0%, and 88.2%, respectively, for TBHPs of 0.0, 0.5, 1.0, and 2.0 mmol/L; p < 0.05 for the last two). This animal study demonstrated that intra-abdominal hypertension and subsequent decompression deplete the total in vivo GSH store in rat livers, probably via the mechanism of ischemia-reperfusion injury, and the GSHVT after hepatocyte isolation, which makes the isolated hepatocytes of rats more susceptible to oxidant challenge.