[Septic arthritis]. / Die septische Arthritis.

Septic arthritis Abstract. A painful, red, and swollen joint may have different causes. Septic arthritis is one of the most serious conditions and should be diagnosed and treated right away. In the native joint, an infection can damage the cartilage within the first 24 hours with impacts on joint function including lingering joint problems leading to possible future joint destruction. An interdisciplinary approach is essential for achieving optimal results. Most infections are caused by bacteria from the patient's own microbiome. In general, the incidence of native joint infections is growing, whether it is due to more appropriate diagnostics, or an actual increase cannot be determined at this point. In case of an acute infection, the patients usually describe a relatively short and acute period of pain, redness, and swelling of the affected joint. For diagnostic purposes the common blood serum laboratory work-up serves as a basis, complemented by puncture of the affected joint. Cell count and cell differentiation in the synovial liquid, microbiological and histopathological workup serve as gold standard in detecting septic arthritis. Septic arthritis lacks a distinctive presentation and other inflammatory conditions, like CPPD and gout must be considered. Prior to antibiotic therapy, joint lavage is the most important method to reduce bacterial load, leading to an improved outcome. Prognosis is determined by a swift diagnosis and initiation of therapy. The patient's comorbidities are significant, especially immunocompromising factors such as rheumatoid arthritis, diabetes or immunomodulating therapy. In case of a second focus of infection, chronic kidney disease or older age, patients are at greater risk for an inferior outcome.

Disproportionate Vertebral Bodies and Their Impact on Lumbar Disc Herniation.

BACKGROUND: The aim of this study was to determine whether the presence of disproportionate vertebral bodies is a risk factor for disc herniation (DH). METHODS: Sixty-seven consecutive patients (m: 31 f: 36) who underwent lumbar discectomy for symptomatic DH at one level between L3 and S1 were retrospectively included. The last three motion segments (3 × 67 = 201) were assessed on sagittal MRI scans. A disproportionate motion segment was defined as the difference of more than 10% of the antero-posterior diameter of two adjacent endplates. RESULTS: DH was present in 6/67 (9%), 26/67 (38.8%), and 35/67 (52.2%) patients at L3/4, L4/5, and L5/S1, respectively. A total of 14 of 67 patients demonstrated a disproportionate motion segment at the discectomy level (20.9%). A total of 23 of the 201 (11.4%) investigated motion segments met our criteria for a disproportionate motion segment. In our study population, when one of the 201 segments was disproportionate, the positive predictive value (PPV) for DH increased toward the lower segments: the PPV at the L5/S1 level was 83.0%. The odds ratio of disproportion for DH was the highest at the L5/S1 level, with 6.0 ± 0.82 (p = 0.017). CONCLUSIONS: The presence of a disproportionate motion segment in the lower spine may lead to a significant higher risk for DH in patients undergoing discectomy.

Effects of the α2-adrenergic agonist clonidine on the pharmacodynamics and pharmacokinetics of 3,4-methylenedioxymethamphetamine in healthy volunteers.

The mechanism of action of 3,4-methylenedioxymethamphetamine (MDMA; ecstasy) involves the carrier-mediated and potentially vesicular release of monoamines. We assessed the effects of the sympatholytic α2-adrenergic receptor agonist clonidine (150 µg p.o.), which inhibits the neuronal vesicular release of norepinephrine, on the cardiovascular and psychotropic response to MDMA (125 mg p.o.) in 16 healthy subjects. The study used a randomized, double-blind, placebo-controlled crossover design with four experimental sessions. The administration of clonidine 1 h before MDMA reduced the MDMA-induced increases in plasma norepinephrine concentrations and blood pressure but only to the extent that clonidine lowered norepinephrine levels and blood pressure compared with placebo. Thus, no interaction was found between the cardiovascular effects of the two drugs. Clonidine did not affect the psychotropic effects or pharmacokinetics of MDMA. The lack of an interaction of the effects of clonidine and MDMA indicates that vesicular release of norepinephrine, which is inhibited by clonidine, does not critically contribute to the effects of MDMA in humans. Although clonidine may be used in the treatment of stimulant-induced hypertensive reactions, the present findings do not support a role for α2-adrenergic receptor agonists in the prevention of psychostimulant dependence.