Necrotizing fasciitis (NF) is an uncommon soft tissue infection, usually caused by toxin-producing virulent bacteria. It is characterized by widespread fascial necrosis primarily caused by Streptococcus hemolyticus. Shortly after the onset of the disease, patients become colonized with their own aerobic and anaerobic microflora from the gastrointestinal and/or urogenital tracts. Early diagnosis with aggressive multidisciplinary treatment is mandatory. We describe three clinical cases with NF. The first is a 69 years old man with diabetes mellitus type II, who presented with NF on the posterior chest wall, shoulder and arm. He was admitted to the intensive care unit (ICU) with a clinical picture of severe sepsis. Outpatient treatment and early surgical debridement of the affected zones (inside 3 hours after admittance) and critical care therapy were performed. The second case is of a 63 years old paraplegic man with diabetes mellitus type I. Pressure sores and perineal abscesses progressed to Fournier's gangrene of the perineum and scrotum. He had NF of the anterior abdominal wall and the right thigh. Outpatient treatment and early surgical debridement of the affected zones (inside 6 hour after admittance) and critical care therapy were performed. The third patient was a 56 year old man who had NF of the anterior abdominal wall, flank and retroperitoneal space. He had an operation of the direct inguinal hernia, which was complicated with a bowel perforation and secondary peritonitis. After establishing the diagnosis of NF of the abdominal wall and retroperitoneal space (RS), he was transferred to the ICU. There he first received intensive care therapy, after which emergency surgical debridement of the abdominal wall, left colectomy, and extensive debridement of the RS were done (72 hours after operation of inquinal hernia). On average, 4 serial debridements were performed in each patient. The median of serial debridement in all three cases was four times. Other intensive care therapy with a combination of antibiotics and adjuvant hyperbaric oxygen therapy (HBOT) was applied during the treatment. After stabilization of soft tissue wounds and the formation of fresh granulation tissue, soft tissue defect were reconstructed using simple to complex reconstructive methods.
AimTo extend the microfracture procedure, which has been proven successful on osteochondritis dissecans (OCD) lesions in the knee and ankle, to OCD lesions in the elbow.MethodsNine young patients were treated by arthroscopic debridement and microfracture by a single surgeon. The average age at operation was 15.0 years (median 15; range 12-19). The average length of the follow-up was 5.3 years (median 5; range 2-9). The follow-up included physical examination and patient interview with elbow function scoring. Success of treatment was determined according to pre-operative and follow-up Mayo Elbow Performance Index scores and the patients’ return to sports.ResultsEight patients scored excellent results on the follow-up and 1 scored a good result. Four out of 9 patients were able to increase their training intensity, 2 returned to the same level of activity, 2 changed sports (due to reasons unrelated to the health of their elbow), and 1 left professional sports and started training only recreationally. No patients stopped participating in sports altogether.ConclusionsWe advocate arthroscopic microfracturing, followed by a strict rehabilitation regime, as a highly effective treatment for OCD of the humeral capitellum.
Recently, marked therapeutic effects pertaining to the recovery of injured rat spinal cords (1 min compression injury of the sacrocaudal spinal cord (S2-Co1) resulting in tail paralysis) appeared after a single intraperitoneal administration of the stable gastric pentadecapeptide BPC 157 at 10 min post-injury. Besides the demonstrated rapid and sustained recovery (1 year), we showed the particular points of the immediate effect of the BPC 157 therapy that began rapidly after its administration, (i) soon after injury (10 min), or (ii) later (4 days), in the rats with a definitive spinal cord injury. Specifically, in counteracting spinal cord hematoma and swelling, (i) in rats that had undergone acute spinal cord injury, followed by intraperitoneal BPC 157 application at 10 min, we focused on the first 10–30 min post-injury period (assessment of gross, microscopic, and gene expression changes). Taking day 4 post-injury as the definitive injury, (ii) we focused on the immediate effects after the BPC 157 intragastric application over 20 min of the post-therapy period. Comparable long-time recovery was noted in treated rats which had definitive tail paralysis: (iii) the therapy was continuously given per orally in drinking water, beginning at day 4 after injury and lasting one month after injury. BPC 157 rats presented only discrete edema and minimal hemorrhage and increased Nos1, Nos2, and Nos3 values (30 min post-injury, (i)) or only mild hemorrhage, and only discrete vacuolation of tissue (day 4, (ii)). In the day 4–30 post-injury study (iii), BPC 157 rats rapidly presented tail function recovery, and no demyelination process (Luxol fast blue staining).
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