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1.
Z Orthop Unfall ; 160(4): 422-430, 2022 08.
Artigo em Inglês, Alemão | MEDLINE | ID: mdl-33873224

RESUMO

BACKGROUND: Reconstruction of lower extremity soft tissue defects is an exceptional surgical challenge, especially in multimorbid, elderly and severely ill patients with their thin and tense local soft-tissue conditions and increased perioperative risk. The distally based peroneus brevis muscle flap (DPBM), a local flap based on the muscular branches of the fibular artery, could pose a pragmatic solution. The objective of this study was to evaluate and quantify DPBM defect reconstruction in the lower leg, especially in elderly, multimorbid and severely ill patients. MATERIAL AND METHODS: The DPBM as a surgical option in defect reconstruction in multimorbid, elderly, severely ill patients (inclusion criteria: at least 3 pre-existing comorbidities, patient age: at least 55 years, ASA status: at least III) was evaluated in a retrospective single-centre study from 01 April 2014 to 31 December 2019. The electronic SAP health records (EHR) were analysed according to 18 criteria, including patient details, extent of multimorbidity, defect characteristics, clinical outcome, and complications. OUTCOME: Ten patients with a mean age of 72.6 years, a mean number of 8.5 pre-existing comorbidities and a mean ASA status of 3.1 met the inclusion criteria. The leading causes of defects, each with exposed tendons, bones, joint capsule, or joint, were chronic ulcers (n = 5) and soft tissue defects resulting from fractures (n = 3). In case of DMPB the success rate was 100% (no partial or total loss) with a short operating time (mean: 103 min) and a brief postoperative length of stay (mean: 11 d). In 2 patients (20%), DPBM surgery had to be discontinued intraoperatively and an alternative technique of defect reconstruction had to be adopted. The reasons included impaired muscle perfusion and fatty degeneration of the peroneus brevis muscle. CONCLUSION: The DPBM flap allows straightforward, fast and safe defect reconstruction in the lower extremity, particularly in elderly, multimorbid and severely ill patients at risk. In patients with inadequate peroneal brevis muscle, however, DMPB surgery should be discontinued intraoperatively and the defect reconstructed using alternative techniques.


Assuntos
Traumatismos da Perna , Procedimentos de Cirurgia Plástica , Lesões dos Tecidos Moles , Idoso , Humanos , Perna (Membro)/cirurgia , Traumatismos da Perna/cirurgia , Extremidade Inferior/cirurgia , Multimorbidade , Músculo Esquelético/cirurgia , Procedimentos de Cirurgia Plástica/métodos , Estudos Retrospectivos , Lesões dos Tecidos Moles/cirurgia
2.
Infect Immun ; 82(6): 2585-94, 2014 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-24686054

RESUMO

Meningitis and meningoencephalitis caused by Escherichia coli are associated with high rates of mortality and neurological sequelae. A high prevalence of neurological disorders has been observed in geriatric populations at risk of hypovitaminosis D. Vitamin D has potent effects on human immunity, including induction of antimicrobial peptides (AMPs) and suppression of T-cell proliferation, but its influence on microglial cells is unknown. The purpose of the present study was to determine the effects of vitamin D deficiency on the phagocytosis rate, intracellular killing, and immune response of murine microglial cultures after stimulation with the Toll-like receptor (TLR) agonists tripalmitoyl-S-glyceryl-cysteine (TLR1/2), poly(I·C) (TLR3), lipopolysaccharide (TLR4), and CpG oligodeoxynucleotide (TLR9). Upon stimulation with high concentrations of TLR agonists, the release of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) was decreased in vitamin D-deficient compared to that in vitamin D-sufficient microglial cultures. Phagocytosis of E. coli K1 after stimulation of microglial cells with high concentrations of TLR3, -4, and -9 agonists and intracellular killing of E. coli K1 after stimulation with high concentrations of all TLR agonists were lower in vitamin D-deficient microglial cells than in the respective control cells. Our observations suggest that vitamin D deficiency may impair the resistance of the brain against bacterial infections.


Assuntos
Escherichia coli/fisiologia , Imunidade Inata/fisiologia , Meningite devida a Escherichia coli/fisiopatologia , Microglia/fisiologia , Fagocitose/fisiologia , Deficiência de Vitamina D , Vitamina D/fisiologia , Análise de Variância , Animais , Calcifediol/sangue , Sobrevivência Celular , Células Cultivadas , Quimiocinas/metabolismo , Contagem de Colônia Microbiana , Citocinas/metabolismo , Modelos Animais de Doenças , Lipopolissacarídeos/farmacologia , Meningite devida a Escherichia coli/imunologia , Camundongos , Camundongos Endogâmicos C57BL , Microglia/efeitos dos fármacos , Microglia/microbiologia , Óxido Nítrico/metabolismo , Receptores Toll-Like/agonistas , Deficiência de Vitamina D/imunologia
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