Botulinum Toxin Type A Injection Improves the Intraperitoneal High Pressure in Rats Treated with Abdominal Wall Plasty.

The aim of the study is mainly to study the subject of BoNT-A injection to improve IAH in rats undergoing abdominal angioplasty. The study problem in surgery, especially in ICU, burn, and trauma centers, intra-abdominal hypertension (IAH), and abdominal compartment syndrome (ACS) are common complications. At present, there are various treatments for IAH. The intramuscular injection of Botulinum toxin type A (BoNT-A) into the abdominal wall has received a lot of attention. Based on this, this study proposes a method for measuring abdominal pressure, applies BoNT-A to reduce abdominal pressure in the IAH state of abdominal wall angioplasty, and explores a way to increase the compliance of the abdominal wall under the premise of maintaining the sealing of the abdominal cavity, so as to realize the expansion of the abdominal cavity. A method is achieved to reduce intra-abdominal pressure and eliminate or alleviate ACS. The results of the experiment showed that when the rats in the control group were injected with the same amount of normal saline as the rats in the experimental group, the IAP was significantly higher than that in the experimental group (P < 0.05). This shows that BoNT-A increases the compliance of the abdominal wall while maintaining the closure of the abdominal cavity, thereby increasing the volume of the abdominal cavity and alleviating the state of IAH in rats.

Basic Fibroblast Growth Factor (bFGF) Protects the Blood-Brain Barrier by Binding of FGFR1 and Activating the ERK Signaling Pathway After Intra-Abdominal Hypertension and Traumatic Brain Injury.

BACKGROUND Intra-abdominal hypertension (IAH) is associated with high morbidity and mortality. IAH leads to intra-abdominal tissue damage and causes dysfunction in distal organs such as the brain. The effect of a combined injury due to IAH and traumatic brain injury (TBI) on the integrity of the blood-brain barrier (BBB) has not been investigated. MATERIAL AND METHODS Intracranial pressure (ICP) monitoring, brain water content, EB permeability detection, immunofluorescence staining, real-time PCR, and Western blot analysis were used to examine the effects of IAH and TBI on the BBB in rats, and to characterize the protective effects of basic fibroblast growth factor (bFGF) on combined injury-induced BBB damage. RESULTS Combined injury from IAH and TBI to the BBB resulted in brain edema and increased intracranial pressure. The effects of bFGF on alleviating the rat BBB injuries were determined, indicating that bFGF regulated the expression levels of the tight junction (TJ), adhesion junction (AJ), matrix metalloproteinase (MMP), and IL-1ß, as well as reduced BBB permeability, brain edema, and intracranial pressure. Moreover, the FGFR1 antagonist PD 173074 and the ERK antagonist PD 98059 decreased the protective effects of bFGF. CONCLUSIONS bFGF effectively protected the BBB from damage caused by combined injury from IAH and TBI, and binding of FGFR1 and activation of the ERK signaling pathway was involved in these effects.

Successful treatment of abdominal compartment syndrome with chemotherapy in a patient with a newly diagnosed Burkitt lymphoma.

Mortality of patients treated on the intensive care unit suffering from cancer is high, especially when admitted with an unknown malignancy. Still, anti-tumor therapy in critically ill patients requiring mechanical ventilation is a clinical challenge. Over the last years, successful chemotherapy has been reported, even in critically ill patients with infections and organ failure. In this report, we present a 42-year old male patient who later was been diagnosed for a highly-malignant lymphoma (Burkitt) developed an abdominal compartment syndrome due to ileus, ascites and progressive intestinal tumor manifestation. During the course, he required mechanical ventilation and developed several organ failures including need for renal replacement therapy. After laparotomy the abdomen was left open and managed by a vacuum dressing. The patient received systemic chemotherapy and broad anti-infective treatment in presence of markedly elevated markers of inflammation. Fortunately, he was successfully weaned from vasopressor and respiratory support. By obtaining negative fluid balances closure of the abdomen succeeded 18 days after laparotomy. The patient was transferred to the normal ward without organ dysfunction on day 27 and discharged home after a second cycle of chemotherapy. In conclusion, aggressive treatment using chemotherapy in critically ill patients with initially unkown malignancy may be successful.

[CORRECTION OF INTRAABDOMINAL PRESSURE IN RATS IN AN ACUTE PANCREATITIS, USING INFUSION OF MYORELAXANT OF A DURABLE ACTION PIPECURONIUM BROMIDE].

Impact of a durable action of myorelaxant pipecuronium bromide on intraabdominal pressure (IAP) in rats in experimentally simulated acute peritonitis was studied. In the rats in purulent pancreatitis, іnduced by L-аrginin, IAP was in 4,5 times high (p < 0.001), than in intact laboratory animals. Pipecuronium bromide have lowered IAP by 33.4%, witnessing efficacy of application of myorelaxants in treatment of intraabdominal hypertension in purulent pancreatitis.

Effect of traditional Chinese medicine on intra-abdominal hypertension and abdominal compartment syndrome: A systematic review and Meta-analysis.

OBJECTIVE: Traditional Chinese medicine (TCM) recently become a widely used treatment option for treating intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS). However, we still lack large-scale, high-quality, randomized controlled trials (RCTs). The purpose of this systematic review was to evaluate the existing clinical trials and to provide additional specific evidence. METHODS: A systematic review of randomized controlled trials (RCTs) of TCM for IAH/ACS was conducted. The following databases were searched to identify relevant studies: PubMed, Medline (Ovid SP), The Cochrane Library, China Biology Medicine Database, Wanfang Database, Chinese Periodical Database, Chinese Clinical Trial Registry, and China Knowledge Resource Integrated Database. Meta-analysis was performed using Rev. Man 5.3. RESULTS: Fifteen studies involving 735 participants were included in the analysis. Compared to conventional therapy, TCM has a significant effect on reducing intra-abdominal pressure (IAP) [15 studies, 700 patients, standard mean difference (SMD)=-0.93, 95% credibility interval (CI): -1.35- -0.52], improving the APACHE II (five studies, 199 patients, SMD=-0.75, 95% CI: -1.30- -0.21), and shortening the length of hospitalization (LOH) (six studies, 214 patients, SMD=-1.21, 95% CI: -1.50- -0.91). The influence of mortality (six studies, 241 patients) was not significant [The pooled risk ratio (RR) was -0.07 (95% CI: -0.17- 0.03)]. CONCLUSIONS: TCMs seem to be effective for patients with IAH and ACS; however, most of the reviewed trials are of poor quality. Large-scale, high-quality clinical trials are warranted.

Melatonin prevents secondary intra-abdominal hypertension in rats possibly through inhibition of the p38 MAPK pathway.

Exogenous administration of melatonin has been demonstrated to down-regulate inflammatory responses and attenuate organ damage in various models. However, the salutary effect of melatonin against secondary intra-abdominal hypertension (IAH) remains unclear. This study sought to test the influence of melatonin on secondary IAH in a pathophysiological rat model and the underlying mechanisms involved. Before resuscitation, male rats underwent a combination of induced portal hypertension, applying an abdominal restraint device, and hemorrhaging to mean arterial pressure (MAP) of 40mmHg for 2h. After blood reinfusion, the rats were treated with lactated Ringer solution (LR) (30mL/h), melatonin (50mg/kg) +LR, and SB-203580 (10µmol/kg)+LR. LR was continuously infused for 6h. MAP, the inferior vena cava pressure and urine output were monitored. Histopathological examination, immunofluorescence of tight junction proteins, and transmission electron microscopy were administered. Intestinal permeability, myeloperoxidase activity, malondialdehyde, glutathione peroxidase, and levels of TNF-a, IL-2, and IL-6, were assessed. The expression of extracellular signal-regulated kinase, p38, c-Jun NH2-terminal kinase, translocation of nuclear factor kappa B subunit, signal transducers and activators of transcription and tight junction proteins were detected by Western blot. We found that melatonin inhibited the inflammatory responses, decreased expression of p38 MAPK, attenuated intestinal injury, and prevented secondary IAH. Moreover, administration of SB203580 abolished the increase in p38 MAPK and also attenuated intestinal injury. These data indicate that melatonin exerts a protective effect in intestine in secondary IAH primarily by attenuating the inflammatory responses which are in part attributable to p38 MAPK inhibition.

Melanocortin-4 receptor agonists alleviate intestinal dysfunction in secondary intra-abdominal hypertension rat model.

BACKGROUND: Intra-abdominal hypertension (IAH) is a potentially life-threatening disease. Melanocortin-4 (MC4) receptor activation exhibits life-saving properties. The aim of the present study was to examine whether treatment with the MC4 receptor agonist RO27-3225 ameliorates intestinal injury in IAH rats. METHODS: A total of 72 male Sprague-Dawley rats were randomized into six groups. Group 1 was the sham group. Group 2, the sham + RO group, received RO27-3225 (180 µg/kg, intraperitoneally). IAH was induced in group 3, the IAH group, by blood draw (mean arterial pressure = 30 mm Hg for 90 min) followed by shed blood and/or Ringer solution reinfusion. Intra-abdominal pressure was increased to 20 mm Hg by injecting air into the peritoneal cavity. Group 4, the RO group, was administered RO27-3225 at 5 min after blood draw. Groups 5 and 6 were the chlorisondamine (Chl) and HS024 groups, in which the rats were pretreated with the nicotinic acetylcholine receptor antagonist Chl or selective MC4 receptor antagonist (HS024), respectively, at 2 min before RO27-3225 was administered. RESULTS: RO27-3225 restored mean arterial pressure, reduced tumor necrosis factor-α, and interleukin-1ß messenger RNA expression increased by IAH, alleviated histologic damage, and improved superoxide dismutase activity in the intestine. Compared with the IAH group, the levels of intestinal fatty acid-binding protein, intestinal edema and intestinal permeability were lower in the RO group. Furthermore, the RO27-3225 treatment increased the expression of Rho-associated coiled-coil-containing protein kinase 1 and phosphorylated myosin light chain. Chl and HS024 abrogated the protective effects of RO27-3225. CONCLUSIONS: These data indicate that the MC4 receptor agonist counteracts the intestinal inflammatory response, ameliorating intestinal injury in experimental secondary IAH by MC4 receptor-triggered activation of the cholinergic anti-inflammatory pathway. It may represent a promising strategy for the treatment of IAH in the future.

Melanocortin MC4 receptor agonists alleviate brain damage in abdominal compartment syndrome in the rat.

Intra-abdominal hypertension (IAH) is accompanied by high morbidity and mortality in surgical departments and ICUs. However, its specific pathophysiology is unclear. IAH not only leads to intra-abdominal tissue damage but also causes dysfunction in distal organs, such as the brain. In this study, we explore the protective effects of melanocortin 4 receptor agonists in IAH-induced brain injury. The IAH rat models were induced by hemorrhagic shock/resuscitation (with the mean arterial pressure (MAP) maintained at 30 mm Hg for 90 min followed by the reinfusion of the withdrawn blood with lactated Ringer's solution). Then, air was injected into the peritoneal cavity of the rats to maintain an intra-abdominal pressure of 20 mm Hg for 4 h. The effects of the melanocortin 4 receptor agonist RO27-3225 in alleviating the rats' IAH brain injuries were observed, which indicated that RO27-3225 could reduce brain edema, the expressions of the IL-1ß and TNF-α inflammatory cytokines, the blood-brain barrier's permeability and the aquaporin4 (AQP4) and matrix metalloproteinase 9 (MMP9) levels. Moreover, the nicotinic acetylcholine receptor antagonist chlorisondamine and the selective melanocortin 4 receptor antagonist HS024 can negate the protective effects of the RO27-3225. The MC4R agonist can effectively reduce the intracerebral proinflammatory cytokine gene expression and alleviate the brain injury caused by blood-brain barrier damage following IAH.

The preventive effect of dopamine infusion in rats with abdominal compartment syndrome.

BACKGROUND: The most significant perfusion disorder of the intra-abdominal viscera occurs in the abdominal compartment syndrome (ACS). Free oxygen radicals diffuse into the body during the reperfusion phase of ACS. Our aim was to determine the effects of dopamine infusion (3 µg/kg/min) on renal perfusion, cytokine levels, free oxygen radicals, and renal histopathological changes in the presence of ACS in a prospective randomized manner. METHODS: Twenty-four male Sprague-Dawley rats were randomly divided into four groups (n = 6). Group 1 was used as control. In group 2, air was inflated until the intra-abdominal pressure (IAP) reached 20 mmHg. In group 3, dopamine was infused for 60 min meanwhile IAP was kept at 20 mmHg. In group 4, dopamine was infused for 60 min before IAP rise. After this phase, renal artery (RA) perfusion was measured continuously. Myeloperoxidase activity (MPO), glutathione (GSH), and lipid peroxidation (MDA) levels were measured in tissue samples and histopathological scoring was performed. RESULTS: Dopamine treatment before and during ACS significantly decreased MPO and MDA levels and also increased renal blood flow and GSH levels. However, histopathological damage was improved simultaneously. CONCLUSION: Dopamine infusion before and during ACS, increases renal perfusion and decreases free oxygen radicals. According to our findings, dopamine infusion may be proposed for the treatment of ACS and perfusion disorders in critically ill patients.

Minocycline ameliorates lung and liver dysfunction in a rodent model of hemorrhagic shock/resuscitation plus abdominal compartment syndrome.

BACKGROUND: We sought to elucidate whether minocycline, a broad-spectrum tetracycline antibiotic with potent anti-inflammation capacity, could mitigate inflammatory response and organ dysfunction in the lungs and liver induced by hemorrhagic shock/resuscitation (HS) plus abdominal compartment syndrome (ACS). MATERIALS AND METHODS: Adult male rats were randomized to receive HS plus ACS or HS plus ACS plus minocycline (denoted as the HS/A and HS/A-M group, respectively; n = 12). Sham-instrumentation groups were employed to serve as the controls. Hemorrhagic shock/resuscitation was induced by blood drawing (mean arterial pressure: 40-45 mm Hg for 60 min) followed by shed blood/saline mixture reinfusion. Subsequently, intra-abdominal pressure (IAP) was increased to 25 mm Hg by injecting air into the preplaced intraperitoneal latex balloon to induce ACS. Minocycline (20 mg/kg) was intravenously administered immediately after resuscitation. IAP was maintained at 25 mm Hg for 6 h. Then, all rats were euthanized. RESULTS: The levels of polymorphonuclear leukocyte infiltration, the wet/dry weight ratio, and the concentrations of inflammatory molecules (e.g., chemokine, cytokine, and prostaglandin E2) in lung and liver tissues of the HS/A group were significantly higher than those of the HS/A-M groups (all P < 0.05). Moreover, the levels of lung dysfunction (assayed by arterial blood gas) and liver dysfunction (assayed by plasma concentrations of bilirubin, aspartate aminotransferase, and alaninine aminotransferase) of the HS/A group were significantly higher than those of the HS/A-M group (all P < 0.05). CONCLUSIONS: Minocycline ameliorates inflammatory response and organ dysfunction in the lungs and liver induced by hemorrhagic shock/resuscitation plus abdominal compartment syndrome.

Modified Da-Cheng-Qi Decoction reduces intra-abdominal hypertension in severe acute pancreatitis: a pilot study.

BACKGROUND: Intra-abdominal hypertension (IAH) is a recognized prognostic marker for severity of severe acute pancreatitis (SAP) and has a strong impact on the clinical course of SAP. Previous studies indicate that a Da-Cheng-Qi Decoction (DCQD) is beneficial in the treatment of SAP. The purpose of this study was to evaluate the effect of modified DCQD on IAH in patients with SAP. METHODS: Between January 2008 and December 2008, 42 patients from the West China Hospital were randomized into either the DCQD or control group (n = 21 in each group). Mortality, intra-abdominal pressure (IAP), Acute Physiology and Chronic Health Evaluation II (APACHE II) score, C-reactive protein (CRP), oxygenation index, Balthazar CT score, rate of renal failure, decompression rate, intensive care unit (ICU) transfer rate, and length of hospital stay (LOS) were compared between the two groups. RESULTS: Compared to the control group, the modified DCQD treatment significantly decreased IAP (P < 0.05) and APACHE II (P < 0.05) scores on days 4 - 8, CRP on day 8 (P < 0.01), renal failure rate (P < 0.05), and LOS (P < 0.05). The oxygenation index was significantly improved in the DCQD group compared with the control group (P < 0.05). No significant differences in the Balthazar CT score, shock rate, ICU transfer rate, or mortality occurred between the two groups. CONCLUSIONS: The modified DCQD can effectively relieve IAH and decrease LOS for patients with SAP. Larger clinical trials are needed to confirm these findings.

Tissue plasminogen activator-assisted hematoma evacuation to relieve abdominal compartment syndrome after endovascular repair of ruptured abdominal aortic aneurysm.

PURPOSE: To describe our experience with a novel technique to decompress abdominal compartment syndrome after endovascular aneurysm repair (EVAR) of ruptured abdominal aortic aneurysm (rAAA). METHODS: From January 2003 to April 2010, 13 patients (12 men; mean age 75 years) treated for rAAA with EVAR underwent tissue plasminogen activator (tPA)-assisted decompression for intra-abdominal hypertension. All of the patients but one had intra-abdominal pressure >20 mmHg, with signs of multiple organ failure or abdominal perfusion pressure <60 mmHg. With computed tomography guidance, a drain was inserted into the retroperitoneal hematoma, and tPA solution was injected to facilitate evacuation of the coagulated hematoma and decrease the abdominal pressure. RESULTS: In the 13 patients, the mean intra-abdominal pressure decreased from 23.5 mmHg (range 12-35) to 16 mmHg (range 10-28.5). A mean 1520 mL (range 170-2900) of blood was evacuated. Urine production (mean 130 mL/h, range 50-270) increased in 7 patients at 24 hours after tPA-assisted decompression; among the 5 patients in which urine output did not increase, 3 underwent hemodialysis by the 30-day follow-up. One patient did not respond with clinical improvement and required laparotomy. The 30-day, 90-day, and 1-year mortality was 38% (5/13 patients); none of the deaths was related to the decompression technique. CONCLUSION: tPA-assisted decompression of abdominal compartment syndrome after EVAR can decrease the intra-abdominal pressure and could be useful in preventing multiple organ failure. It is a minimally invasive technique that can be used in selected cases but does not replace laparotomy or retroperitoneal surgical procedures as the gold standard treatments.

[Effects of somatostatin in a rabbit model of abdominal compartment syndrome induced by prolonged intra-abdominal hypertension].

OBJECTIVE: To establish a rabbit model of abdominal compartment syndrome (ACS) induced by prolonged intra-abdominal hypertension (IAH) and evaluate the therapeutic effect of somatostatin on ACS. METHODS: Twelve New Zealand rabbits were randomized equally into normal saline (NS) group and somatostatin group. ACS model was established by intra-abdominal bleeding (IAB) and intra-abdominal infusion with nitrogen gas to achieve an intra-abdominal pressure of 15 mmHg. The hemodynamics (SP, HR, CVP), hepatic function (ALT), renal function (BUN), antioxidation level (SOD, MDA) and blood electrolyte level (pH, [Na(+)], [Cl(-)], [CaNa(2+)], [KNa(+)]) of the rabbits were recorded 1-6 h after establishment of IAH. RESULTS: Prolonged IAH caused decreased hemodynamic functions and antioxidation level as well as hyperkalemia and hypocalcemia (P<0.05), but these changes showed no significant differences between NS group and somatostatin group. CONCLUSION: Prolonged IAH causes cardiovascular function damages in rabbits possibly related to acidosis, electrolyte disturbances, and oxidative damage due to tissue ischemia and hypoxia. Somatostatin produces no obvious protective effects against the occurrence and progression of ACS.

Cytomegalovirus enterocolitis presenting as abdominal compartment syndrome in a premature neonate.

BACKGROUND: Cytomegalovirus (CMV) enterocolitis is an uncommon intestinal disorder of newborns that is often initially misdiagnosed as necrotizing enterocolitis. METHODS: We treated a premature twin boy with CMV enterocolitis who presented with abdominal compartment syndrome requiring urgent decompression. All patients with neonatal CMV enterocolitis reported were reviewed. RESULTS: Nine previously reported patients with neonatal CMV enterocolitis presented with abdominal distention and signs of sepsis. At the time of surgery, either perforation or stricture was identified. The current report is the first to present with clinical signs of abdominal compartment syndrome. CONCLUSION: CMV is a rare cause of neonatal enterocolitis. Surgical intervention is required for bowel perforation, stricture, or abdominal compartment syndrome.

[The influnence of dachengqi tang on acute lung injury and intra abdominal hypertension in rats with acute pancreatitis].

OBJECTIVE: To test the hypothesis "lung and large intestine are interior exteriorly related" through investgating into the effect of Dacheng qi tang (DCQT) on intra abdominal hypertension (IAH) and acute lung injury (ALI) in rats with acute pancreatitis. METHODS: Male SD rats were randomly divided into three groups with ten rats for each group: rats with sham-operations (SO); rats with acute necrosis pancreatitis (ANP); rats with ANP plus DCQT treatment. ANP was induced by retrograde infusion of 5% taurocholic acid into pancreatic duct. Two hours after operations, 10 mL/kg of normal saline was orally adminstered to the rats in both SO and ANP groups, whereas 10 mL/kg DCQT was adminstered to the rats in the treatment group. Aterial blood, pancreas and lung tissues were collected for biomarkers and histopathology 24 hours after operations. Intra-abdominal pressure and intestinal propulsion rate were also measured. RESULTS; DCQT treatment reduced intra-abdominal pressure and improved intestinal propulsion rate compared with those treated with saline (P < 0.05). The ANP rats treated with DCQT had lower wet to dry weight ratio, and milder myeloperoxidase activity and histopathology changes in pancreas and lung than those treated with saline (P < 0.05). Higher pressure of oxygen (PO2) was found in the rats treated with DCQT, while no difference in PCO2 was found between the DCQT and ANP groups (P > 0.05). Only two rats in the ANP group died. CONCLUSION: DCQT can effectively relieve IAH and cure ALI at the same time in rats with acute pancreatitis. The result provides evidence to support the hypothesis "lung and large intestine are interior exteriorly related".

Nonoperative management of intra-abdominal hypertension and abdominal compartment syndrome: evolving concepts.

Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are associated with significant morbidity and mortality. Nonoperative medical management strategies play an important role in the current treatment of IAH and ACS. There are five medical treatment options to be considered to reduce elevated intra-abdominal pressure (IAP): 1) improvement of abdominal wall compliance; 2) evacuation of intraluminal contents; 3) evacuation of abdominal fluid collections; 4) optimization of systemic and regional perfusion; and 5) correction of positive fluid balance. Nonsurgical management is an important treatment option in critically ill patients with raised IAP.