A Painless Method of Ultrasonically Assisted Debridement of Chronic Leg Ulcers: A Pilot Study

ObjectivesDevitalized tissue in a recalcitrant leg ulcer is common and may impede healing. The aim of this study was to evaluate the use of a non-invasive low frequency ultrasound device to debride chronic leg ulcers as an adjunct to compression bandages therapy.Methods19 patients with leg ulceration of at least 6 months were recruited. Low frequency ultrasound at 25kHz was delivered by a portable Sonaca® – 180 via a handheld probe, using normal saline as the irrigation/coupling medium. The ultrasound was applied for 10–20 seconds per probe head area onto the ulcer. Each leg underwent treatment at an interval of 2–3 weeks with compression bandages reapplied at the end of the treatment. Serial colour photographs were taken to evaluate the response at each visit.ResultsEach patient received on average 5.7 treatments each ranged from 5–20 minutes depending on the ulcer size. Symptomatic relief (pain and odour reduction) was achieved in 6 patients. 7 patients achieved complete ulcer healing (mean ulcer size=4.72±SD 1.872cm2) but no response was observed in 8 patients. There were no major complications of the treatment which was relatively painless.ConclusionsThe application of low frequency ultrasound debridement may heal some recalcitrant ulcers when standard compression regimens have failed. It is cheap and does not require admission. The role of simple wound cleansing requires further investigation

Cysteine protease activity in the wall of abdominal aortic aneurysms

BackgroundCysteine proteases are potent elastolytic enzymes and together with their inhibitor, cystatin C, have been linked with the growth of abdominal aortic aneurysms (AAAs). These enzymes and their inhibitors have previously been studied in AAAs, but comparisons have always been made with wall from normal aorta. Atherosclerosis is a feature of aneurysmal disease and may therefore confound comparisons with normal wall. This study compared the expression and activity of cysteine proteases and their inhibitors in aneurysm wall with their expression in the aortic wall of patients with aortic occlusive disease (AOD).MethodsAortic wall was obtained from 82 patients with AAA and 13 with AOD. Protein expression and activity of cathepsin B, H, K, L and S, and cystatins A, B, and C were measured by enzyme-linked immunosorbent assay and specific fluorogenic substrate assays. Matrix metalloproteinase 9 (MMP-9) activity was measured by quantitative bioimmunoassay in the same extracts.ResultsAAA wall had 330% more cathepsin H protein (P = .007) and >30% less cystatin C (P = .03) than the aortic wall from patients with AOD. The activity of cathepsins B, H, L, and S was significantly greater in AAA than AOD (376%, [P < .0001], 191%, [P = 0.019], 223%, P = 0.002, and approximately 20% [P = 0.045] respectively). MMP-9 activity was also increased in AAA compared with AOD (P<0.0001) and levels in the wall of AAA correlated positively with cathepsin L activity (r = 0.42, P<.0001) and negatively with cystatin C (r = -0.75, P<.0001).ConclusionsThe activity of four cathepsins B, H, L, and S was higher in the aneurysm wall than in aortic wall of patients with occlusive disease. This was associated with a reduced level of cystatin C in the aneurysmal wall. Cathepsin H was the only protein in which there was a correlation between protein level and activity, which suggests that post-translational modifications were responsible for activation of the other cathepsins. Increased cathepsin activity may influence the activity of MMP-9, which is thought to have an important role in aneurysm development.Clinical RelevanceThe incidence of abdominal aortic aneurysms has been steadily increasing for the last 3 decades. The condition is associated with a progressive loss of structural proteins such as elastin and collagen from the wall of the aorta through increased protease activity. Metalloproteinases have been the most predominantly studied enzymes, but there is increasing evidence that other protease systems such as the cysteine proteases may also be involved. Controlling the activity of proteases may form the basis for the development of novel medical treatments that inhibit aneurysm expansion and thereby reduce the need for surgery

Neuroprotective Strategies Can Prevent Permanent Paraplegia in the Majority of Patients Who Develop Spinal Cord Ischaemia After Endovascular Repair of Thoracoabdominal Aortic Aneurysms

ObjectivesSpinal cord ischaemia (SCI) following endovascular thoracoabdominal aortic aneurysm (TAAA) repair is a devastating and unpredictable complication. This study describes a single unit's experience of SCI in patients who have had endovascular TAAA repair.MethodsA prospectively maintained database of patients having endovascular TAAA repair using branched and fenestrated stent grafts between 2008 and 2014 at a single high volume centre was reviewed. Patients who developed neurological symptoms and signs related to SCI were identified and factors associated with onset and recovery of neurology were analysed.ResultsSixty-nine patients (median age 73 years, 52 male; Crawford classification type I [n = 4], type II [n = 11], type III [n = 33], type IV [n = 14], type V [n = 7]) underwent endovascular TAAA repair. Twelve patients developed neurological symptoms/signs related to SCI but this was successfully reversed in eight patients, leaving four (5.8%) with permanent paraplegia. The median length of aorta covered was not significantly different in the 12 patients who developed SCI compared with the cohort that did not. Eleven of the patients who developed SCI had an intraoperative mean arterial pressure (MAP) below 80 mmHg. Cutaneous atheroemboli were noted in half of the patients in the SCI group compared with 11% of the non-SCI group (p < .05). Strategies used to reverse SCI included raising MAP, cerebrospinal fluid drainage, angioplasty of stenosed internal iliac arteries, and restoring perfusion to the aneurysm sac.ConclusionsThis series highlights some of the risk factors associated with the development of SCI after endovascular repair of TAAAs. It also illustrates the importance of a dedicated institutional protocol aimed at ensuring the early diagnosis of SCI and prompt intervention to reverse permanent paraplegia in the majority of cases