| ObjectiveAn intra-abdominal pressure (IAP) exceeding12mmHg is considered to bepathologically elevated and has been termed intra-abdominal hypertension (IAH). And IAPexceeding20mmHg which is associated to new organ functional impairment or failure istermed abdominal compartment syndrome (ACS). IAH/ACS is a kind of common disease inclinic, which is mainly distributed in departments of burns, trauma surgery, and intersivecare unit. Moreover, it has higher mortality, and the mortality of primary ACS is more than60%. Facors contributed to parthological increase of IAP not only include trauma,large-area burns, abdominal surgery, but also include compliance decrease of abdominalwall (mechanical ventilation, obesity, head of bed elevation,abdominal wall burns,abdominal wall scar), increase of abdominal content (intestinal obstruction,ascites),increase of capillary permeability,interintestinal fluid (acidosis, sepsis, large fluidresuscitation, large amount of blood transfusion, severe pancreatitis, coagulopathy).Although more than ten years of efforts has been taken, how to prevent, diagnose and treatIAH/ACS is still a big challenge in clinic. Truama and burns patients with hemodynamicinstability require massive fluid resuscitation, which is one of the causes of the secondaryACS. However, their effects on the body and the therapeutic effect are not very clear.IAH/ACS treatments are involved of operative and non-operative treatment, and openabdomen is the fastest method to decrease IAP. However, open abdomen is at a great risk,as disastrous consequences are likely to occur. Hence, the clinical application indicationsof open abdomen are more cautious, what is more, it is only applied when organ failureoccurs following ACS, but no significant reduction in mortality is demonstrated, despite ofrapid decrease of IAP. Therefore, the preventive effect of open abdomen is worth to exploring. The intraperitoneal management strategy following open abdomen is crucial toreduce the risk. Vacuum assisted closure (VAC) method can achieve good effect inmanaging the abdominal cavity of open abdomen, intra-abdominal volume increment(IAVI) is a modified VAC technique. This paper establishes incomplete blockage of portalvein, and IAH animal models with hemorrhagic shock resuscitation, investigates the effectof intra-abdominal volume increment (IAVI) assisted by vacuum sealing drainage (VSD) onintra-abdominal hypertension (IAH) in kidneys and livers, so as to provide reference forIAVI in treating IAH/ACS.MethodsTwelve healthy adult minipigs were established models of hemorrhagic shock (meanarterial pressure50mmHg，1h). Animals were generally anesthetized and fixed on thebench followed by skin disinfection with0.5%iodophors. After the tracheotomy surgery,animals were connected to the anesthesia machine. The right femoral artery and vein wereisolated; single lumen catheters were inserted. The catheter was connected, via a triplet, totransducer and multifunctional monitor. The catheterized artery was used for bleeding,while the catheterized vein was used for fluid transfusion and pressure detection in theinferior vena cava. After incision along the midline in the abdomen, a cystostomy wasperformed. The portal vein was isolated and ligated with a hard plastic tube with an externaldiameter of5mm by using a silk line. The hard plastic tube was then removed, creating amodel of incomplete blockage of the portal vein to simulate the process of perihepaticpacking for treatment of serious hepatic injury.5mm diameter is chosen based on thepreliminary experiment, the portal vein pressure reached35cmH2O at time of portal veinblockage. The abdomen incision was sutured layer by layer. Exsanguination from thefemoral artery caused the mean arterial pressure to reach approximately50mmHg and theblood was stored in the blood bags. One hour after the shock, all of the lost blood, alongwith Ringer’s solution (twice the amount of the blood), was transfused. Ringer’s solutionwas continuously administered to achieve over-resuscitation. The IAH model wasconsidered to be successfully established when an IAP of≥12mmHg was maintained for1h.Eight animals were resuscitated successfully to establish the IAH model with the portal veins incompletely blocked. The8minipigs were randomly divided into the IAVI treatmentgroup and the sham operation control group. Data was recorded before shock,2h after theinitiation of IAH, and22h after surgery,26h after surgery, respectively.1.Intravesical pressure(IVP): after the bladder was evacuated,50ml of physiologicalsaline was injected into the bladder, then the silicone tube was erected; the vertical heightof the water column above the pubic symphysis was taken as intravesical pressure when thecolumn declined to a steady level; Inferior vena cava pressure (IVCP): IVCP was measuredwith a multi-function monitor via inferior vena cava catheter; urine volume per hour.2.DXC800automatic biochemistry analyzer was used to analyze glutamic-oxalacetictransaminease (AST), glutamic-pyruvic transaminase (ALT), urea(Ur), creatinine (Cr).3. Enhanced abdominal CT scan was applied to observe the appearance of liver andkidney. The ratio of the anteroposterior diameter of the abdomen to the transverse diameterwas measured (measured at the level where the left renal vein crosses the aorta andexcluding the subcutaneous fat). Renal thickness, separation of the renal pelvis and renalcalyx, renal pelvis diameter were measured, based on the data obtained from the rightkidney.4.Animals were sacrificed at26h after surgery,50g of right liver tissues and upper1/8of the right kidney tissue were reserved, and divided into2parts: one part of specimenwere weighed and then placed in a60°C drying oven for3days. The other part of specimenwere fixed in10%formalin, embedded in paraffin, sliced, performed hematoxylin-eosin(HE) staining, and then observed under the light microscope.Results1.The IAH model was successfully established in8of12minipigs(66.7%),3minipigsdied due to arhythmia when anesthetized,1due to portal vein rupture,2due to hemorrhagicshock. The average body weight was22.9±1.7Kg，with baseline MAP of118±14.3mmHg. Exsanguination was performed until achieving a MAP of50mmHg, withexsanguination volume of648±98ml. The required time for achieving successful animalmodel was3.20±0.60h. Two animals (maximum IVP of17.6mmHg and19.2mmHg,respectively) showed rectal prolapse and stress urinary incontinence. The ratio of anteroposterior diameter to the transverse diameter showed remarkable increase whencompared with at2h after IAH and pre-shock time point(1.22±1.41vs0.96±0.08，P＜0.01).2..Effects of decompression with IAVITwo hours after IAH, IVP and IVCP were remarkably higher than those of pre-shocklevel (21.16±4.63mmHg vs.6.65±0.5mmHg,21.15±4.59mmHg vs.6.59±0.52mmHg,P<0.01). When compared with the IAVI treatment group and sham-operation control groupat22h after surgery, urinary volume increased (120.00±23.00ml/h vs10.00±1.00ml/h，P＜0.01)；IVP(10.90±0.60mmHg, vs29.50±0.70mmHg) and IVCP(10.80±0.50mmHgvs31.60±2.00mmHg) showed significant decrease (P＜0.01)3.Effects of IAVI on liver in minipigs with IAH following hemorrhagic shockAt2h after IAH, blood AST and ALT were higher than those before shock (589.96±14.94U/L vs36.43±2.1U/L,77.03±12.59U/L vs37.86±3.48U/L, P＜0.01); but itdecreased after IAVI treatment(215.25±73.4U/L vs589.96±14.94U/L，60.45±3.88U/Lvs77.03±12.59U/L，P＜0.01); in the sham-operation control group, the two indices weresignificantly higher than those in other groups (661.3±14μU/L vs118.25±3.3U/L，P＜0.01) Liver CT value at2h IAH were significantly lower than those before shock(42.73±4.92HU vs60±6.85HU, P＜0.05); at22h after operation, the CT value in the IAVItreatment group was recovered while compared with the sham-operation control group(46.08±2.69HU vs31.45±4.21HU, P＜0.05). At22h after operation, the liver wet/dryratio was significantly higher in sham-operation control group than that in IAVI treatmentgroup (5.14±0.71vs2.32±0.25，P＜0.01). At22h after operation, sham-operated controlgroup indicated that obvious blood stasis was observed in the liver tissue accompanied byinfiltration of inflammatory cells. While in the IAVI group, only mild blood stasis or noblood stasis and slight infiltration of inflammatory cells were observed.4.Effects of IAVI on kidney in minipigs with IAH following hemorrhagic shockAt2h after IAH, blood Cr, Ur values increased, but the difference was not statisticallysignificant (66.5±8.5μmol/L vs72.3±6.1μmol/L,3.87±1.05mmol/L vs4.12±0.85mmol/L，P＞0.1); following IAVI treatment, both values still increased slowly, but Ur value showed no differences (4.73±0.71mmol/L vs4.12±0.85mmol/L, P>0.1), Crcontinued to increase (89.50±9u mol/L vs72.30±6.10u mol/L. P <0.05); the twovalues in the sham-operated control group were significantly higher than those in othergroups (200.01±1.43mol/L,9.62±0.14mmol/L, P <0.01). There was no significantdifference in the right renal thickness (mm) between2h after IAH and22h after operation(14.80±2.90vs15.70±1.81, P>0.1), but the renal thickness became higher at22h afteroperation in the sham-operation control group while compared with the IAVI treatmentgroup (19±1.39vs15.70±1.81, P <0.05); at22h after operation, renal cortical thickness inthe right kidney was measured by B ultrasound, showing no significant difference betweenat22h after operation and2h after IAH in the IAVI treatment group(6.53±1.19vs6.78±0.51, P>0.1), but significant difference with the sham-operated control group(6.53±1.19vs9.25±0.29, P <0.01);Right renal pelvis diameter measured by CT indicated no obvious change at2h afterIAH (41.30±7.23vs41.38±9.40>0.1). There was no hydronephrosis or separation of therenal pelvis and renal calyx as determined by B ultrasound and CT at any phase point in allanimals. At22h after operation, the renal wet-to-dry ratio in the sham-operated controlgroup was significantly higher than that in IAVI treatment group (5.80±0.70vs3.70±0.60,P <0.01). In the sham-operated control group, obvious blood stasis was observed in thekidney accompanied by infiltration of inflammatory cells at22h after operation. While inthe IAVI treatment group, only mild blood stasis or no blood stasis and slight infiltration ofinflammatory cells were observed.conclusions1. Our model can well be established by uncomplete occlusion of the portal vein,whichcan minic twist of the portal vein because of abdominal packing following hemorrhagicshock. The model can achieve IAP of greater than12mmHg after resuscitation. It is moresuitable to clinical practice that haemorrhage or systemic inflammation together withresuscitation lead to abdominal fluid accumulation and increased intra-abdominal pressure.than that is created by inserting gas or liquid into abdominal cavity.2. The IAVI treatment can significantly reduce IVP and IVCP and mortality of IAH/ACS. Moreover, various indices in the IAVI treatment group are better than those inthe sham-operated control group. Therefore, IAVI is helpful to prevent and treat liver andkidney function disorder following IAH,. Prophylactic use of IAVI for treating IAH canavoid the MODS following ACS. The model for the clinical application of IAVI controlACS provides experimental basis... |
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