IAH management is recommended in critically ill patients  even though strong evidence of its benefit remains lacking. A prospective observational study of 478 consecutive surgical patients requiring an open abdomen for the management of IAH or ACS showed a significant decrease in hospital mortality after the imple- mentation of a comprehensive management algorithm for IAH and ACS . In 23 cirrhotic patients with hepatorenal syndrome, infusion of 200 ml of 20% human albumin solution followed by large-volume abdominal paracentesis resulted in IAP reduction from a median of 22 to 9 mmHg and a significant increase in creatinine clearance during the subsequent 12 h from 23 ml/min to 33 ml/min ( p = 0.002) . Moreover, creati- nine clearance remained elevated for up to several days afterwards . Medical interventions that have been suggested to treat IAH include sedation, neuromuscular blockade, gastric or colonic decompression, hypertonic fluids or colloids, forced diuresis and hemofiltration Table 3 Stepwise multivariate logistic regression analysis for three outcomes: mortality in the ICU, hospital and need for RRT.
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APP is a parameter combining both the pathogenesis incriminated in renal dysfunction in acute critical care settings. The cause of renal dysfunction in ACS is multifactorial , available evidence suggests that the most important factor involves alterations in renal blood flow  and decreased arterial visceral perfusion , while The presence of IAH as a risk factor for acute kidney injury (AKI) has been shown in many clinical settings.
Abdominal surgery with primary fascial or tight closure, major trauma, major burns, prone positioning, colonic pseudo-obstruction, hemoperitoneum or pneumoperitoneum; other intra-abdominal injuries and damage control laparotomy are not included due to the very low number of patients with these risk factors. APACHE II, APP, abdominal perfusion pressure; Acute Physiology and Chronic Health Evaluation; CRF, categorized risk factors; IAH, intra-abdominal hypertension; IAP, intra-abdominal pressure (mmHg); ICU, intensive care unit; NS, not significant; SOFA, Sequential Organ Failure Assessment. Data are presented as mean ± standard deviation, unless otherwise indicated.
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Correlations were seen between abdominal perfusion pressure on the one hand and abdominal edema and TNF- a in intestine on the other. Edema is a hallmark of inflammation, but one may speculate that edema can also cause inflammation. Interactions between vascular permeability and inflammation were discussed in a recent review on the procoagulant and proinflammatory plasma contact system , and in high-altitude pul- monary edema, inflammation appears to be a late effect of the edema [19-21]. In a review , it is concluded that “although high altitude pulmonary edema develops in the absence of any local or systemic inflammation, inflammatory activation occurs in later stages”. To what extent it can explain the inflammation in the present study certainly requires more investigation but remains an interesting possibility. Our finding that low abdom- inal perfusion pressure was accompanied by increased inflammatory marker concentration may suggest another, parallel, mechanism of inflammation, or the lowered perfusion pressure may be a consequence of the edema. Lowered perfusion pressure can disturb cellular metabolism that triggers an inflammatory response [23-25]. It may be emphasized that the correlation between abdominal perfusion pressure and inflammatory markers was seen although MAP was kept above 65 mm Hg and thus in accordance with the guidelines in the Surviving Sepsis Campaign .
ACS: Abdominal compartment syndrome; APP: Abdominal perfusion pressure; BIPAP: Biphasic positive airway pressure; BMI: Body Mass Index; BP: Blood Pressure; BSA: Burnt Surface Area; CCU: Critical care unit; CPAP: Continuous Positive Airway Pressure; CT: Computed tomography; HB: Hemoglobin; IAH: Intra-abdominal hypertension; IAP: Intra-abdominal pressure; IP: Intra- peritoneal; IV: Intravenous; KNH: Kenyatta National Hospital; MAP: Mean arterial pressure; MmHg: Millimeters of mercury; NG: Nasogastric; PSV: Positive pressure ventilation; RAAS: Rennin angiotensin aldosterone system; SD: Standard Deviation; SIMV: Synchronized Intermittent Mandatory Ventilation; SIRS: Systemic Inflammatory Response Syndrome; SPSS: Statistical Package for Social Sciences; UON: University Of Nairobi; WSACS: World society of abdominal compartment syndrome; TAC: Temporary Abdominal Closure
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As of the guidelines by the World Society of the Ab- dominal Compartment Syndrome (WSACS) published in 2013, abdominal compartment syndrome (ACS) is de- fined as a sustained intraabdominal pressure (IAP) > 20 mmHg (with or without an abdominal perfusion pres- sure (APP) < 60 mmHg) which is associated with new onset organ failure. It can be divided into primary and secondary, where primary ACS is associated with injury or disease in the abdominopelvic region while secondary ACS refers to those that are not. The pathogenesis of ACS is multifactorial, developing from a combination of diminished abdominal wall compliance, increased intra- abdominal contents, increased intra-luminal contents, capillary leakage, fluid resuscitation as well as age, bac- teraemia, shock and sepsis. In pancreatitis, this revolves around pancreatic inflammation causing pancreatic and visceral oedema with surrounding fluid collections, as well iatrogenic processes such as aggressive fluid resusci- tation. Ascites from capillary leak, paralytic ileus and gastric distension by duodenal obstruction raises IAP . This ultimately leads to hypoperfusion and ischae- mia of abdominal viscera.
Hemodynamic, respiratory, and functional parameters Using transpulmonary thermodilution measurement (PiCCO ® , PULSION Medical Systems, Munich, Germany), the following hemodynamic parameters and ‘ filling volumes ’ were investigated: cardiac index (CI = cardiac output related to the body surface area), mean arterial pressure (MAP), global end-diastolic volume index (GEDVI), and extravascular lung water index (EVLWI). CI and MAP were continuously surveyed via pulse contour analysis, while the other above-mentioned parameters were measured hourly [24,25]. Furthermore, heart rate (HR), central venous pressure (CVP), and urine output (UO) were recorded (AS/3, Datex Ohmeda, Helsinki, Finland). Afterwards, abdominal perfusion pressure (APP = MAP - IAP) and renal filtration gradient (RFG = MAP - 2·IAP) were calculated . Every 2 h, blood gas analyses were performed.
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ALAT: alanine aminotransferase; APACHE: acute physiology and chronic health evaluation; APP: abdominal perfusion pressure; ASAT: aspartate aminotransferase; AUROC: area under the ROC curve; γ GT: gamma- glutamyltranspeptidase; IAH: intra-abdominal hypertension; IAP: intra- abdominal pressure; ICG: indocyanine green; INR: international normalized ratio; LDH: lactate dehydrogenase; MAP: mean arterial pressure; PDR: plasma disappearance rate; PDR ICG : plasma disappearance rate of indocyanine green;
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vessels selected for tumor-specific infusion; HAP: hypoxic abdominal perfusion - the perfusion of chemotherapy utilizing arterial inflow catheters, venous return catheters and an extra-corporeal circuit; MTD: maximum tolerated dose - the highest dose that induces dose limiting toxicity in no more than 1 patient among a cohort of 6 patients; DLT: dose limiting toxicity - defined as all grade 3 or greater toxicities with the exception of grade 3 constitutional symptoms that persist for less than 72 hours, grade 3 and 4 myelosuppression (neutrophils and platelets) of less than 5 days duration, and grade 3 metabolic/laboratory events that are correctable within 24 hours; ECOG: Eastern Cooperative Oncology Group; AST: aspartate aminotransferase; ALT: alanine aminotransferase; PT/INR: prothrombin time/ international normalized ratio; RECIST: Response Evaluation Criteria In Solid Tumors; EASL: European Association for the Study of the Liver
syndrome as an IAP ≥ 20 mmHg combined with the failure of more than one organ [1, 5]. Ever since then, WSACS have updated consensus definitions and clinical practice guide- lines for the patients with IAH . The prevalence of IAH on admission to the intensive care unit (ICU) ranges from 31 to 58.8 % [4, 7, 8], and the incidence increases with the length of ICU stay. Clinical conditions that increase IAH include blood and ascites in the peritoneal cavity, bowel distension and edema [4, 9], high-volume resuscitation and massive transfusion, damage control surgery in trau- matic patients, excessive tension after abdominal closure, postoperative ileus, echar in burn patients [10, 11], and hemodilution . IAH causes not only abdominal organ dysfunction by decreasing the abdominal perfusion
ALI: acute lung injury; ANOVA: analysis of variance; APACHE: acute physiology and chronic health evaluation; APP: abdominal perfusion pressure; CI: cardiac index; CLI: capillary leak index; CO: cardiac output; CRP: C-reactive protein; CRRT: continuous renal replacement therapy; EVLW(I): extravascular lung water (index); GEDV(I): global end diastolic volume (index); GEF: global ejection fraction; IAH: intra-abdominal hypertension; IAP: intra- abdominal pressure; ICU: intensive care unit; MAP: mean arterial pressure; MV: mechanical ventilation; PAL-treatment: PEEP + albumin + Lasix (furosemide); PEEP: positive end-expiratory pressure; SAPS: simplified acute physiology score; SOFA: sepsis and organ failure assessment; SVV: stroke volume variation; vs: versus.
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The following data were acquired from the patients: general characteristics, AGI grade, IAP (highest value obtained on bladder manometry in the first 3 days, with each measurement being performed at a set time of the day; measurements were performed at least 4 times a day, if the IAP exceeded 12 mm Hg, and mean values were used ), abdominal perfusion pressure (APP; difference between mean blood pres- sure and IAP, determined at the time of IAP meas- urement), Acute Physiology and Chronic Health Evaluation (APACHE) II score (in the first 24 h after ICU admission), Sepsis-related Organ Failure Assess- ment (SOFA) score (in the first 24 h after ICU ad- mission), and 28-day mortality.
Early initiation of conservative measures has been rec- ommended to optimize abdominal perfusion pressure, and potentially prevent surgical indication and associ- ated morbidity and mortality. Medical management in- volves evacuation of abdominal contents (for example, insertion of nasogastric and rectal tubes, use of proki- netic agents, paracentesis, percutaneous drainage of space-occupying lesions); improvement of abdominal compliance (for example, sedation, analgesia, neuromus- cular blockade, head of bed elevation <30 degrees); optimization of systemic perfusion (for example, judi- cious use of intravenous fluid and vasoactive medica- tions); and IAP monitoring at least every 4 hours [4, 23]. Refractory cases evolving with IAP >20 mmHg with pro- gressive organ failure should be promptly considered for surgical decompression, since delayed surgical indication has been associated with increased mortality [24, 25].
or repeated pathological elevation in IAP ≥12 mmHg. ACS was diagnosed when sustained increase of the IAP >20 mmHg and one new organ dysfunction were detected . Abdominal perfusion pressure (APP) was calculated in all patients with IAH and defined as the mean arterial pressure (MAP) minus the IAP. The decision to discon- tinue negative-pressure therapy and to perform permanent closure of the abdominal cavity was based on preoperative evidence of stable regression of the inflammatory response, regression of organ dysfunction and sepsis. Intraoperative evidence of a visually clean abdomen (absence of abscesses or purulent exudate, disappearance of fibrin) and well-perfused bowels with recovered transit determined the decision to close the abdomen. Bacteriolo- gical samples from the abdominal cavity were taken during all operations; however, we did not wait until all intrao- perative cultures would become negative. Blood cultures from the abdominal effluent were collected until regres- sion of sepsis and stable decrease of the C-reactive protein (CRP) in the blood were achieved. Positive blood culture was defined as septicaemia. The complication rate, hospi- tal and ICU stay and main outcomes were analysed for all patients. Application of NPT was approved by the institu- tional ethics committee. Informed consent was obtained according to institutional practice. Statistical data analysis was done using SPSS version 17.0. All data have been changed to median values and range.
Finally, end-stage liver disease is associated with pro- gressive loss of functional liver capacity. Conventional laboratory assessment of liver function is mainly based on liver enzymes, bilirubin and the coagulation param- eter international normalized ratio (INR) . Dynamic tests of liver function at bedside might be more precise and objective relating to actual, short-term functional status . Promising experiences were achieved with noninvasive measurement of plasma disappearance rate of indo-cyanine green (ICG-PDR). ICG is injected intra- venously, distributed via blood circulation and excreted hepatobiliary . ICG-PDR reflects both hepatos- planchnic blood flow and hepatocellular and excretory function [20, 21]. Some previous data described an inter- action of ICG-PDR with intraabdominal pressure level [22–24]. Recently, one of these studies affirmed that ICG- PDR correlates inversely with IAP, suggesting that IAH restrains hepatosplanchnic and sinusoidal perfusion . The abdominal perfusion pressure (APP), defined as dif- ference between mean arterial pressure (MAP) and IAP, was positively correlated with ICG-PDR.
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It is critically important to identify patients whose perfusion pressure is below the autoregulation thresh- old because from the point downward, organ blood flow is usually inadequate and organ perfusion will solely depend on perfusion pressure. This is the rationale for using vasopressors to restore organ perfusion pressure during acute resuscitation in fluid resuscitated patients with septic shock. Regrettably, there is not one threshold MAP because each organ system has a different inflow and outflow pressures and internal control systems linked to their individual physiologic roles . For example, the kidney increases filtration as renal perfusion pres- sure increases because its role is to filter solute from the blood, whereas the liver maintains a relatively constant flow from the combined hepatic artery and portal vein so as to maintain hepatic clearance and metabolic functions.
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Objectives: To investigate the influence of cold renal perfusion on renal func- tion and clinical outcomes in cases where the renal ischemia time exceeded 30 min during pararenal and juxtarenal abdominal aortic aneurysm (P/JAAA) surgery. Methods and Results: Fifty-four patients who underwent open re- pair for P/JAAAs were retrospectively analyzed. Thirty-nine patients received renal perfusion with cold Ringer’s solution (perfusion group) and 15 pa- tients did not receive renal perfusion (non-perfusion group). There were no significant differences in preoperative serum creatinine level (Cr) (1.08 ± 0.42 vs. 1.35 ± 0.71 mg/dL, p = 0.09), percentage of patients with Cr > 2 mg/dL [2/38 (5%) vs. 2/15 (13%), p = 0.8], and renal ischemia time during proximal aortic clamping (49 ± 21 vs. 47 ± 11 min; p = 0.8) between the groups. Postoperative Cr was significantly lower in the perfusion group than in the non-perfusion group (1.48 ± 0.76 vs. 2.23 ± 1.21 mg/dL, p < 0.01). The percentage of patients with postoperative Cr > 2 mg/dL was also significantly lower in the perfusion group than in the non-perfusion group [5 (13%) vs. 7 (47%), p < 0.01)]. At discharge, Cr returned to preoperative levels in both groups. All patients were discharged from the hospital without incidents. Conclusion: Renal artery perfusion with cold Ringer’s solution clearly re- duced the deterioration of postoperative renal function compared to non-renal perfusion.
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The effect of IAH on CO is controversial with some studies showing a decrease in CO, while other studies do not show a change or even an increase in CO in the pre- sence of IAH [7,10-12,31]. This controversy can be explained by IAH having a biphasic and potentially opposing effect on CO which itself may be explained by the dependence of venous return on the level of IAP [7,10,31]. Low levels of IAP have been shown to increase venous return as a result of a redistribution of abdominal blood to the thoracic compartment, thus increasing stroke volume and CO [10,31]. However, further increase in IAP overcomes the compensatory effect of blood redis- tribution from the abdominal compartment to the thor- acic compartment decreasing venous return and therefore stroke volume and CO [10,31]. In our study,
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Induction of IAP in this animal study was clearly mechanical, without developing conditions either of capillary leakage which could interfere in interpretation of cytokines and lactate measurements or intravascular depletion (e.g. hemorrhage) interfering with hemody- namic measurements. A net effect of mechanically increased IAP on CNS pressures, cytokines and lactate was attempted. We didn’t use a gradual increase of IAP, but rather a first level of 20 mmHg, commonly seen in clinical settings, and then an abrupt increase to 45 mmHg, in order to augment the impact of IAH on CNS and draw safer conclusions for this relationship. Finally, the increase of IAP in phase T3 is considered as ACS, according to definitions of the World Society of the Abdominal Compartment Syndrome (WSACS).
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domly picked rats for fibrosis model confirmation and 15 rats for further experiments: A) the control group without ADMSCs: 2 × 10 6 irrelevant cells (BRL-3A, a rat liver cell line) was injected in portal vein. B) The portal vein group: rats were anesthetized and exposed with an upper midline incision inferiorly from the xiphoid, and the abdominal cavity was exposed with a retractor. Portal vein was gently isolated and directly injected with 2 × 10 6 ADMSCs using a 25-gauge needle connected to a 2 ml syringe [15,16]. The abdominal wall was closed after bleeding stopped by pressure. C) The tail vein group: 2 × 10 6 ADMSCs were injected in the tail vein.