Chronische Transplantatdysfunktion

Chronic transplant dysfunction is a complex dynamic pathogenic process. Clinically, a decrease in glomerular filtration rate (GFR) becomes apparent leading to chronic renal insufficiency and dialysis or death from cardiovascular events. Chronic transplant dysfunction can develop into a chronic alIograft nephropathy (CAN) as a specific entity with dynamic progression. CAN includes a collection of immunologic and non-immunologic factors, rejection, ischemia time, donor and recipient characteristics and toxicity of calcineurin inhibitors. Despite improvements in immunosuppression, the long-range prognosis of renal allografts has not improved. Whether modern immunosuppressive concepts with reduction or avoidance of calcineurin inhibitors and a therapy based on antimetabolites, such as mycophenolate or mTOR-inhibitors could lead to a prolongation of transplant survival, remains to be seen.     

Multimodal—was ist das überhaupt?

In chronic pain syndromes multimodal treatment has proved its efficacy. However, multimodal treatment does not mean randomly combining different interventions in a potpourri of methods. Multimodal treatment must closely follow a well-proved conceptual framework. Those concepts may be well illustrated by therapy of back pain. The most elaborate model for understanding the transition from acute to chronic pain is fear avoidance. Based on this model chronic pain status is understood as a learned consequence, which resulted from patients’ anxious avoidance of body movements. In these cases, treatment of a physical pathology is not the main aim of therapy but rather functional restoration. Those multimodal programs meanwhile have demonstrated their effectiveness. However, good results not only depend on recognition of imperative elements in therapy but also on adhering to essential principles (avoidance of negative anticipation, adequate information with assurance techniques, no training of avoidance, recognition of elements of fear therapy).     

Meningitis

The most frequent pathogens causing bacterial meningitis in Germany are Neisseria meningitidis, Streptococcus pneumoniae, Borrelia burgdorferi, Listeria monocytogenes and staphylococci. Since immunization against Haemophilus influenzae has become a routine vaccination procedure, this pathogen no longer plays a significant role in the etiology of bacterial meningitis. A number of pilot studies have indicated that selected PCR methods most probably represent the future etiological diagnosis of bacterial meningitis. The easiest and most rapid diagnostic method is, however, still a simple gram stain preparation. In fatal cases that ran a peracute course, especially in the Waterhouse-Friderichsen syndrome, only increased congestion of the surface of the brain is detectable at autopsy. In such cases, there is hardly any histological evidence of an inflammatory reaction of the leptomeninges. In cases of purulent meningitis, in addition to the typical infiltration of the subarachnoid space with abundant granulocytes, after some days of illness there is a wide-spread histomorphological picture of pathological alterations with fibrinoid vessel wall necroses, thromboses, ventriculitis, infarctions as well as venous and arterial vasculitis. The breakdown of the integrity of the blood-brain-barrier in bacterial meningitis is obviously due to a separation of intercellular tight junctions of the endothelium of the capillaries of the leptomeninges. The cause of death in meningitis, depending on the severity and duration of a concomitant sepsis, is an increase in intracranial pressure that leads to a circulus vitiosus (via a reduced central perfusion associated with metabolic acidosis) with cerebral vasodilatation. This is followed by an additional rise of intracranial pressure and finally a reduced cerebral blood supply and central dysregulation. The medico-legal expert is occasionally confronted with this topic against the background of a possible misjudgement of the disease due to insufficient diagnostics or delayed diagnosis and in the light of a posttraumatic or nosocomial origin of the illness.     

Sonographische Messung der Fruchtwassermenge

Ohne Zusammenfassung     

Operative Versorgung von Achillessehnenverletzungen

Rupture of the Achilles tendon is typically associated with sportive activities with increasing tendency; it occurs most commonly in the third to fourth decade of life with a male-to-female ratio of 5–10:1. Ruptures are caused predominantly by a sudden, unexpected overextension of the tendon while direct trauma is less frequent. The recommended treatment of the injury remains controversial. In Germany, due to the good functional results, the open surgical repair represents the standard therapy since many years. The open suture technique offers the advantage of a lower re-rupture rate but is associated with the risk of wound-related complications including infection. By percutaneous suture techniques a significant decrease in the rate of infections and complications in wound healing could be achieved by minimal-access with reduced soft tissue trauma; on the other hand an increased rate of lesions of the sural nerve is reported. Dynamic imaging assessment of ultrasound or MRI allows a more accurate localisation of the ruptured ends of the tendons which is the prerequisite for the non-operative primary functional treatment of Achilles tendon ruptures. This conservative treatment regime is recommended when adaptation of the ends of the ruptured tendon is possible in 20° plantar flexion of the foot. Moreover, the desired level of daily activity and the patients’ degree of compliance has to be considered. Operative management should be avoided in the elderly patient or patients with risk factors like immunosuppressive therapy, diabetes mellitus, steroid use or failure to comply.