[Acute meningitis after transrectal prostate biopsy]. / Akute Meningitis nach transrektaler Prostatapunktion.

Acute meningitis caused by Escherichia coli is a rare disease in adulthood. Medical procedures, e.g. surgical interventions, have been described as a cause. Infection by blood transmission of fecal E. coli is also known. We report a case of acute meningitis after transrectal prostate biopsy. E. coli could be identified both in the cerebrospinal fluid and in the blood culture. A broad initial antibiotic therapy was administered. After cultural isolation of E. coli the therapy was switched to cefotaxime. The initially comatose patient recovered swiftly.

[Myxedema coma as a rare differential diagnosis of severe consciousness disturbance]. / Myxödemkoma als seltene Differenzialdiagnose einer schweren Bewusstseinsstörung.

Myxedema coma is a rare and life-threatening complication of untreated hypothyroidism. Therefore, it must be part of the differential diagnosis in comatose patients. We report one patient who presented with CO(2) narcosis,hypothermia, bradycardia,hyporeflexia, tetraparesis, ascitis, pleural effusions, and heart insufficiency. Examination of the CSF, cranial CT, MRI, and MR angiography were normal. In suspicion of myxedema coma,the patient was treated with high dose L-thyroxine and hydrocortisone for preventing secondary adrenal insufficiency. A fast clinical recovery, decreased T4 (7.2 ng/l) and T3 (0.93 ng/l), and increased TSH (20.19 mU/l) together with the following anamnesis of radio iodine therapy and insufficient thyroxine intake confirmed the diagnosis. In conclusion, treatment of the myxedema coma must be started as soon as the laboratory results are confirmatory, since its course depends on the time of initiation of treatment.

[Continuous monitoring of patients with extensive strokes. Importance of monitoring on the neurological intensive care unit]. / Kontinuierliches Monitoring bei Patienten mit ausgedehnten Schlaganfällen. Stellenwert der Uberwachung auf neurologischen Intensivstationen.

One of the main functions of neurologic intensive care units (NICU) is to provide continuous monitoring of critically ill patients. Space-occupying stroke is a disease with high mortality. While clinical assessment of these comatose patients is difficult, additional monitoring is of key importance. With this information, intensive care physicians may recognize pathophysiologic changes earlier, thus making the right timing of therapeutic interventions easier. Every patient admitted to the NICU receives a basic monitoring which combines noninvasive and invasive methods. Additionally, some specialized centers are exploring the new method of multimodal monitoring. This allows continuous monitoring of physiologic parameters of brain function and compliance. The following article attempts to explain methods of neurointensive care monitoring and its importance for the treatment of stroke. Furthermore, we describe new developments in patient monitoring.

Proliferation of villous trophoblast of the human placenta in normal and abnormal pregnancies.

The proliferation of villous trophoblast in the human placenta was estimated throughout normal gestation and in term placentae from preeclamptic and smoking mothers by two different methods. These were: 1) labeling of DNA producing cells by bromodeoxyuridine (BrdU) followed by immunohistochemistry using a monoclonal anti-BrdU antibody, and 2) immunohistochemical identification of all proliferating cells by the monoclonal antibody Ki67. Both methods revealed comparable results. In uncomplicated pregnancies there was a remarkable decrease in the labeling indices from early gestation to term. This was the result of a diminution of the number of Langhans' cells, although the cell division rate within the Langhans' cell layer remained nearly constant throughout gestation. A prolongation of the cell cycle in the cytotrophoblast cells at term was indicated by an increase in the Ki67/BrdU ratio. Compared with normal term placentae, there was an increase in the trophoblast proliferation rate in preeclampsia, but not in placentae from smoking mothers. Moreover, the number of Langhans' cells was diminished in placentae from smokers. The results indicate that there are different pathogenetic mechanisms of placental impairment in preeclampsia and in maternal smoking. In preeclampsia an injury to the syncytiotrophoblast seems to lead to a repair hyperplasia of the cytotrophoblast, whereas in maternal smoking, there seems to be a direct toxic effect on the cytotrophoblastic cells.