(1/300) Expiratory flow limitation during exercise in COPD: detection by manual compression of the abdominal wall.
Manual compression of the abdomen (MCA) during spontaneous expiration is a simple method for the detection of flow limitation in the chronic obstructive pulmonary disease (COPD) patients during resting breathing, based on comparison of flow/volume curves obtained during MCA with that of the preceding control breath. It was assessed whether this nonstandardized technique is also feasible during exercise. MCA was performed during resting breathing and constant-exercise work at one- and two-thirds maximal mechanical power output (W'max) in six normal subjects and 12 COPD patients. Changes in end-expiratory lung volume (EELV) were also studied. With the aid of inspection, abdominal palpation and lung auscultation, MCA could always be applied during expiration. Flow limitation was never detected in the six normal subjects, whereas four of the COPD patients were flow limited at rest, seven during exercise at one-third W'max and nine during exercise at two-thirds W'max. Expiratory flow limitation detected by MCA was always associated with an increase in EELV during exercise, indicating dynamic hyperinflation occurrence or increase. It is concluded that manual compression of the abdomen is a very simple and reliable method for the detection of flow limitation during exercise. (+info)
(2/300) How should an infected perinephric haematoma be drained in a tetraplegic patient with baclofen pump implanted in the abdominal wall? - A case report.
BACKGROUND: We present a case to illustrate controversies in percutaneous drainage of infected, perinephric haematoma in a tetraplegic patient, who had implantation of baclofen pump in anterior abdominal wall on the same side as perinephric haematoma. CASE PRESENTATION: A 56-year-old male with C-4 tetraplegia had undergone implantation of programmable pump in the anterior abdominal wall for intrathecal infusion of baclofen to control spasticity. He developed perinephric haematoma while he was taking warfarin as prophylactic for deep vein thrombosis. Perinephric haematoma became infected with a resistant strain of Pseudomonas aeruginosa, and required percutaneous drainage. Positioning this patient on his abdomen without anaesthesia, for insertion of a catheter from behind, was not a realistic option. Administration of general anaesthesia in this patient in the radiology department would have been hazardous. RESULTS AND CONCLUSION: Percutaneous drainage was carried out by anterior approach under propofol sedation. The site of entry of percutaneous catheter was close to cephalic end of baclofen pump. By carrying out drainage from anterior approach, and by keeping this catheter for ten weeks, we took a risk of causing infection of the baclofen pump site, and baclofen pump with a resistant strain of Pseudomonas aeruginosa. The alternative method would have been to anaesthetise the patient and position him prone for percutaneous drainage of perinephric collection from behind. This would have ensured that the drainage track was far away from the baclofen pump with minimal risk of infection of baclofen pump, but at the cost of incurring respiratory complications in a tetraplegic subject. (+info)
(3/300) Presence of Chlamydia pneumoniae in abdominal aortic aneurysms is not associated with increased activity of matrix metalloproteinases.
OBJECTIVE: to test the hypothesis that the presence of Chlamydia pneumoniae (C. pneumoniae) in the wall of abdominal aortic aneurysms (AAA) is associated with increased activity of matrix metalloproteinase (MMP)-2 and/or MMP-9. DESIGN: case-control study. MATERIAL AND METHODS: in a series of 40 patients with AAA > or =5cm in maximal cross-sectional diameter, C. pneumoniae-DNA was identified in the aneurysm wall by nested PCR in 14 (35%) patients. Another 14 C. pneumoniae-DNA-negative AAA patients from the same series, matched for gender and aneurysm diameter, were used as controls. In each group there were 7 asymptomatic (aAAA) and 7 ruptured (rAAA) aneurysms. MMP-2 and -9 activity was estimated in AAA wall biopsies by gelatin zymography. RESULTS: patients with a C. pneumoniae-DNA-positive aneurysm wall specimen showed an over-all lower activity of MMP-2 and MMP-9 (pro- and active enzyme) compared to the C. pneumoniae-DNA negative patients. However, there were no statistically significant differences in MMP activity between the two groups of patients with aAAA. Among patients with rAAA both pro-MMP-9 (p=0,026) and active-MMP-9 (p=0.007) were significantly lower in C. pneumoniae-DNA-positive patients compared to C. pneumoniae-DNA-negative patients, whereas there were no significant differences in pro-MMP-2 or active-MMP-2. CONCLUSION: this preliminary study does not support the hypothesis that the presence of C. pneumoniae in the AAA wall is associated with increased activity of MMP-2 and MMP-9. (+info)
(4/300) Involvement of the mural thrombus as a site of protease release and activation in human aortic aneurysms.
Acquired abdominal aortic aneurysms are usually associated with a mural thrombus through which blood continues to flow. Some early data suggest that aneurysmal evolution correlates with the biological activity of the thrombus. Our hypothesis was therefore that the thrombus could adsorb blood components and store, release, and participate in the activation of proteases involved in aneurysmal evolution. For this purpose, we have explored both the metalloproteinase and fibrinolytic systems in the thrombus and the wall of human aneurysms. We have first investigated blood clot formation and lysis in vitro. Spontaneous clotting induces a release of promatrix metalloproteinase (pro-MMP)-9 into the serum that was fourfold higher than in paired control plasma (P < 0.001). Fibrinolysis progressively released more MMP-9 in a time-dependent manner (P < 0.01). After selective isolation, we demonstrated that polymorphonuclear leukocytes are the main source of MMP-9 release during clot formation. Protease content was then analyzed in 35 mural thrombi and walls of human abdominal aortic aneurysms sampled during surgical repair. In 15 aneurysms, the liquid phase at the interface between the thrombus and the wall was sampled separately. Both thrombus and wall contained MMP-2 and MMP-9 but the ratio MMP-9/MMP-2 was higher in the thrombus than in the wall. The liquid interface also contained active MMP-9. Immunohistochemistry of the thrombus confirmed these findings, showing the presence of polymorphonuclear leukocytes at the luminal pole of the thrombus, co-localizing with MMP-9 storage. In contrast, MMP-3 and MMP-7 were only present in the aneurysmal wall. Plasminogen was present in the mural thrombus but plasmin activity was present in both thrombus and wall. In the liquid interface, plasmin-alpha(2)-anti-plasmin complexes were detected demonstrating in vivo the activation of plasminogen. In contrast, u-PA and t-PA were detectable only in the wall, suggesting that plasminogen present in the thrombus could be activated by factors secreted by the arterial wall. This was demonstrated in vitro, in which co-incubation of thrombus and wall extracts generated plasmin in the presence of a fibrin matrix and activated MMPs. In conclusion, our study strongly suggests that the mural thrombus, by trapping polymorphonuclear leukocytes and adsorbing plasma components could act as a source of proteases in aneurysms that may play a critical role in enlargement and rupture. (+info)
(5/300) The tetrapeptide AcSDKP, an inhibitor of primitive hematopoietic cell proliferation, induces angiogenesis in vitro and in vivo.
The tetrapeptide acetyl-Ser-Asp-Lys-Pro (AcSDKP), purified from bone marrow and constitutively synthesized in vivo, belongs to the family of negative regulators of hematopoiesis. It protects the stem cell compartment from the toxicity of anticancer drugs and irradiation and consequently contributes to a reduction in marrow failure. This current work provides experimental evidence for another novel biologic function of AcSDKP. We report that AcSDKP is a mediator of angiogenesis, as measured by its ability to modulate endothelial cell function in vitro and angiogenesis in vivo. AcSDKP at nanomolar concentrations stimulates in vitro endothelial cell migration and differentiation into capillary-like structures on Matrigel as well as enhances the secretion of an active form of matrix metalloproteinase-1 (MMP-1). In vivo, AcSDKP promotes a significant angiogenic response in the chicken embryo chorioallantoic membrane (CAM) and in the abdominal muscle of the rat. Moreover, it induces the formation of blood vessels in Matrigel plugs implanted subcutaneously in the rat. This is the first report demonstrating the ability of AcSDKP to interact directly with endothelial cells and to elicit an angiogenic response in vitro and in vivo. (+info)
(6/300) The ultrasonic trocar provides an easy, sharp, bloodless, and repeatable approach to the abdominal cavity.
Reusable trocars have the advantage of being more cost-effective than disposable trocars. However, the reusable trocar does lose its sharpness on insertion with repetitive insertion. Nonreusable trocars are expensive, but the sharpness of the knife facilitates insertion. Nonreusable trocars have a safety shield system designed to decrease abdominal organ injury, though the potential problem of bleeding from the abdominal wall port site has yet to be resolved. We therefore developed a novel ultrasonic vibrating trocar that does not lose its sharpness even with repetitive insertion. This trocar prevents bleeding by means of an ultrasonic cavitation effect. The ultrasonic vibrating trocar has the advantage of ease of insertion, and the force required for new reusable trocar insertion was only 34% of the force required for insertion of commercially available nonreusable trocars. The force required for multiply used conventional reusable ultrasonic vibrating trocar insertion, ie, 900 insertions, was maintained at less than 46% of the force required by the corresponding nonreusable trocars. Bleeding from the abdominal wall was prevented by an ultrasonic cavitation effect. (+info)
(7/300) The abdominal compartment syndrome following aortic surgery.
BACKGROUND: multi-organ failure is a leading cause of death following aneurysm surgery, especially in the emergency setting. Intra-abdominal hypertension is an important factor in the development of multi-organ failure. Prevention, early recognition and prompt treatment of abdominal hypertension and the abdominal compartment syndrome may reduce mortality following aneurysm surgery. METHODS: a descriptive review of the literature from a Medline search. RESULTS AND CONCLUSIONS: the abdominal compartment syndrome is the result of diverse physiological effects caused by increased intra-abdominal pressure. The syndrome has been most widely described in trauma victims, but occurs in patients following aortic surgery, particularly following ruptured aneurysm repair. Preventative therapy should be instituted to minimise its development in patients at risk, and monitoring of intra-abdominal pressure may allow prompt treatment of this condition. (+info)
(8/300) Definitive surgical treatment of infected or exposed ventral hernia mesh.
OBJECTIVE: To discuss the difficulties in dealing with infected or exposed ventral hernia mesh, and to illustrate one solution using an autogenous abdominal wall reconstruction technique. SUMMARY BACKGROUND DATA: The definitive treatment for any infected prosthetic material in the body is removal and substitution. When ventral hernia mesh becomes exposed or infected, its removal requires a solution to prevent a subsequent hernia or evisceration. METHODS: Eleven patients with ventral hernia mesh that was exposed, nonincorporated, with chronic drainage, or associated with a spontaneous enterocutaneous fistula were referred by their initial surgeons after failed local wound care for definitive management. The patients were treated with radical en bloc excision of mesh and scarred fascia followed by immediate abdominal wall reconstruction using bilateral sliding rectus abdominis myofascial advancement flaps. RESULTS: Four of the 11 patients treated for infected mesh additionally required a bowel resection. Transverse defect size ranged from 8 to 18 cm (average 13 cm). Average procedure duration was 3 hours without bowel repair and 5 hours with bowel repair. Postoperative length of stay was 5 to 7 days without bowel repair and 7 to 9 days with bowel repair. Complications included hernia recurrence in one case and stitch abscesses in two cases. Follow-up ranges from 6 to 54 months (average 24 months). CONCLUSIONS: Removal of infected mesh and autogenous flap reconstruction is a safe, reliable, and one-step surgical solution to the problem of infected abdominal wall mesh. (+info)