Model Of Abdominal Compartment Syndrome Research Articles

A New Model for the Study of the Abdominal Compartment Syndrome in Rats

The purpose of the present study was to develop of a rodent model of abdominal compartment syndrome (ACS), which allows detailed analysis of intra-abdominal hypertension (IAH)- and decompression-associated reperfusion injury. In 20 anesthetized and ventilated Sprague-Dawley rats an IAH of 20 mmHg was induced for 3 h by intraperitoneal infusion of gelatin polysuccinate. After decompression, an additional 3-h period of reperfusion was studied. Sham-operated animals, undergoing identical procedures without IAH induction, served as controls. Controlled hyperventilation and intravenous fluid substitution were adapted to keep PCO(2) <60 mmHg and mean arterial pressure (MAP) >100 mmHg. IAH of 20 mmHg could successfully be maintained for the entire 3-h period. MAP was not affected during IAH, however, decreased upon decompression despite forced fluid resuscitation. CVP was markedly elevated during IAH, but returned to baseline after decompression. Of interest, the IAH-induced reduction of PaO(2) did not recover to baseline after decompression, indicating a persistent deterioration of gas exchange. In contrast, IAH-associated elevation of PaCO(2) normalized during reperfusion. IAH was further accompanied by metabolic acidosis, which persisted after decompression, indicating reperfusion injury. IAH was further associated with a significant increase of serum potassium, lactate, AST, LDH, bilirubin, urea, and creatinine as well as creatine kinase (CK) and CK-MB. Histomorphological analysis revealed parenchymal injury in liver, lung, intestine, and myocardium. We established an easily reproducible ACS model in the rat, demonstrating hemodynamic deteriorations and organ dysfunctions similar as known from patients with IAH. Decompression did not restore functional deteriorations, indicating persistent post-ACS reperfusion injury. The model may be suitable to study mechanisms and novel treatment strategies in ACS.

Subcutaneous Endoscopic Fasciotomy in a Porcine Model of Abdominal Compartment Syndrome: A Feasibility Study

Treatment of abdominal compartment syndrome (ACS) involves abdominal decompression via a laparotomy, which can result in significant wound-related morbidity. Our aim was to determine if subcutaneous endoscopic abdominal fasciotomy in a porcine model of ACS is feasible and what effect it may have on intra-abdominal pressure (IAP) and superior mesenteric artery (SMA) blood flow. A total of 6 female pigs weighing 50 kg each were used for the study. Each animal underwent placement of an arterial line, pulmonary artery catheter, SMA blood flow probe, IAP catheter, and intra-abdominal saline infusion line. After endoscopic dissection of a subcutaneous pocket overlying the rectus muscles, saline was infused into the abdomen to a pressure of 40 mm Hg. Physiologic parameters were measured before and after bilateral endoscopic anterior rectus fasciotomies were performed, and analyzed with a paired t-test. Mean subcutaneous dissection time was 42.5 +/- 11.3 minutes, and mean fasciotomy time was 5.5 +/- 2.3 minutes. There were no significant changes in heart rate, cardiac output, pO(2), or pH during the experiment. IAP increased exponentially as fluid was instilled into the abdomen. SMA blood flow decreased reliably and linearly with increasing IAP. Mean baseline IAP was 4.0 +/- 1.7 mm Hg. IAP decreased from 37 mm Hg to 25 mm Hg after fasciotomy (P < 0.001). Mean baseline SMA blood flow was 629 +/-164 mL/min. SMA blood flow improved from 265 mL/min to 389 mL/min after fasciotomy (P< 0.01). Subcutaneous endoscopic abdominal fasciotomy is feasible and appears to lower IAP and raise SMA blood flow in a porcine model of ACS.

Subcutaneous Endoscopic Fasciotomy in a Porcine Model of Abdominal Compartment Syndrome: A Feasibility Study

Purpose: Treatment of abdominal compartment syndrome (ACS) involves abdominal decompression via a laparotomy, which can result in significant wound-related morbidity. Our aim was to determine if subcutaneous endoscopic abdominal fasciotomy in a porcine model of ACS is feasible and what effect it may have on intra-abdominal pressure (IAP) and superior mesenteric artery (SMA) blood flow. Materials and Methods: A total of 6 female pigs weighing 50 kg each were used for the study. Each animal underwent placement of an arterial line, pulmonary artery catheter, SMA blood flow probe, IAP catheter, and intra-abdominal saline infusion line. After endoscopic dissection of a subcutaneous pocket overlying the rectus muscles, saline was infused into the abdomen to a pressure of 40 mm Hg. Physiologic parameters were measured before and after bilateral endoscopic anterior rectus fasciotomies were performed, and analyzed with a paired t-test. Results: Mean subcutaneous dissection time was 42.5 ± 11.3 minutes, and mean fasciotomy time was 5.5 ± 2.3 minutes. There were no significant changes in heart rate, cardiac output, pO2, or pH during the experiment. IAP increased exponentially as fluid was instilled into the abdomen. SMA blood flow decreased reliably and linearly with increasing IAP. Mean baseline IAP was 4.0 ± 1.7 mm Hg. IAP decreased from 37 mm Hg to 25 mm Hg after fasciotomy (P < 0.001). Mean baseline SMA blood flow was 629 ±164 mL/min. SMA blood flow improved from 265 mL/min to 389 mL/min after fasciotomy (P< 0.01). Conclusion: Subcutaneous endoscopic abdominal fasciotomy is feasible and appears to lower IAP and raise SMA blood flow in a porcine model of ACS.

Modified extraperitoneal endoscopic separation of parts for abdominal compartment syndrome

Standard therapy for abdominal compartment syndrome (ACS) is laparotomy and temporary abdominal wall closure with significant morbidity. The component separation technique allows for difficult abdominal closure. We studied a modified extraperitoneal endoscopic separation of parts technique on an animal model of ACS. Twelve anesthetized pigs were instrumented for measurement of central venous pressure, arterial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, cardiac output, and intraabdominal pressure (IAP). ACS to 25 mmHg was created by infusing saline into an intraabdominally placed bag. Animals were divided in two equal groups. Pigs in group A underwent minimally invasive resection of the nerves supplying the rectus muscles bilaterally. Pigs in group B underwent minimally invasive modified component separation technique bilaterally. Change in IAP and other physiological parameters were recorded. (Group A) IAP increased significantly from 7.3 mmHg +/- 3.8 to 25.2 mmHg +/- 1.5 with infusion of saline. Following nerve transection on the right side there was a nonsignificant decrease in IAP from 25.2 mmHg +/- 1.5 to 22.3 mmHg +/- 1.4 and following nerve transection on the left side there was a further decrease in IAP to 20.3 mmHg +/- 1.9. (Group B) IAP increased significantly from 3.8 mmHg +/- 0.4 to 24.7 mmHg +/- 0.5 with infusion of saline. Following separation of parts on the right side there was a significant decrease in IAP from 24.7 mmHg +/- 0.5 to 15.0 mmHg +/- 1.7 and there was a further decrease in IAP to 11.3 mmHg +/- 1.4 following separation of parts on the left side. The only significant change in the physiological parameters measured was observed in CVP in both groups. We present a porcine model of extraperitoneal endoscopic release of abdominal wall components as a treatment option for ACS.

Melatonin ameliorates oxidative organ damage induced by acute intra-abdominal compartment syndrome in rats.

Acutely increased intra-abdominal pressure (IAP) can lead to multiple organ failure. As blood flow to intra-abdominal organs is reduced by high venous resistance, ischemia-reperfusion (I/R) injury plays an important role in the pathogenesis of abdominal compartment syndrome (ACS) following IAP. Melatonin, a secretory product of the pineal gland, is known to have free radical scavenging and antioxidative properties in several oxidative processes. The objective of this study was to examine the potential protective properties of melatonin on the oxidative organ damage in a rat model of ACS. Under ketamine anesthesia, an arterial catheter was inserted intraperioneally (i.p.) and using an aneroid manometer connected to the catheter, IAP was kept at 20 mmHg (ischemia group; I) for 1 hr. In the ischemia/reperfusion (I/R) group, pressure applied for an hour was decompressed and a 1-hr reperfusion period was allowed. In another IR group, melatonin was administered (10 mg/kg, i.p.) immediately before the decompression of IAP. The results demonstrate that tissue levels of malondialdehyde (MDA) and myeloperoxidase activity (MPO; index of tissue neutrophil infiltration) were elevated, while glutathione (GSH; a key to antioxidant) levels were reduced in both I and I/R groups (P < 0.05-0.001). Melatonin treatment in I/R rats reversed these changes (P < 0.01-0.001). Moreover, melatonin given to the I/R group reduced the elevations in serum aspartate aminotransferase, alanine aminotransferase and blood urea nitrogen levels and abolished the increase in serum creatinine levels. Our results indicate that melatonin, because of antioxidant and free radical scavenging properties, ameliorates reperfusion-induced oxidative organ damage. In conclusion, the results of the present study suggest that the therapeutic value of melatonin as a 'reperfusion injury-limiting' agent must be considered in ACS.

Endoscopic components separation for abdominal compartment syndrome

Background Sustained intraabdominal pressures of 14 to 20 mm Hg have significant pathophysiological consequences, but there is currently no satisfactory low-morbidity procedure appropriate for intervention early in the disease process of abdominal compartment syndrome (ACS). The anatomical principles of abdominal wall components separation were used to develop a percutaneous procedure that increased abdominal capacity and decreased abdominal pressure. Methods Using a porcine model, we determined abdominal capacity changes by helium insufflation. Corn oil was then used to create an episode of sustained intraabdominal hypertension and changes in intraabdominal pressure and intestinal mucosal oxygenation were determined. Results Endoscopic abdominal wall components separation (EACS) increased abdominal capacity by 1 L (from 0.89 ± 0.39 L to 1.95 ± 0.48 L; P <0.001). During intraabdominal hypertension, EACS decreased abdominal pressure by 31.6% (from 15.9 ± 2.1 to 11.0 ± 1.5 mm Hg; P <0.001). Intestinal P o 2 was increased by 61% (18.8 ± 11.4 to 30.3 ± 11.7; P = 0.012) Conclusions A minimally invasive procedure (EACS) is feasible and has demonstrated effectiveness in a porcine model of ACS.