[Management of seasonal influenza in 2017/2018 at a German tertiary-care hospital]. / Management der saisonalen Influenza 2017/2018: Erfahrungen an einem deutschen Universitätsklinikum.

BACKGROUND: There are only few structured reports on inpatient management of a seasonal influenza epidemic. OBJECTIVES: A systematic description of a seasonal influenza patient population at a German university hospital to improve risk stratification and clinical care. METHODS: In this monocentric, retrospective observational study of the 2017/2018 influenza season at the University Medical Center Hamburg-Eppendorf, patients with confirmed influenza infection were included. RESULTS: Of all influenza swabs performed in the emergency department, 24% (n = 162/676) were positive. A total of 255 patients (median age 66 years) had an influenza infection (influenza A n = 79, influenza B n = 176); 27 (15.3%) were nosocomial infections. Of the 179 (70.2%) patients that were hospitalized, 51 (20%) received intensive medical care. Patients with subsequent need for intensive care had an elevated CRP level (69.5 mg/dl [SD 62.8] vs. 141.7 [SD 127.2] mg/dl) at the time of influenza diagnosis and more frequent infiltrates in X­ray/CT of the thorax (n = 43 [33.6%] vs. n = 43 [84.3%]). Antiviral therapy with oseltamivir was administered for 74 (29.0%) patients and 11 (6.1%) patients were treated with extracorporeal membrane oxygenation (ECMO). Of the 23 (9.0%) patients who died, only four of them had been vaccinated (trivalent). Those four had an influenza B infection. CONCLUSION: The structured use of diagnostic tests (influenza PCR, X­ray/CT chest and CRP) and antiviral therapy (oseltamivir) as well as targeted management of admission, intensive care capacities, and an increase in vaccination rates are important for improving patient care and optimizing the use of resources during seasonal influenza epidemics.

A randomized, double-blind, phase 2 study of erythropoietin in optic neuritis.

OBJECTIVE: Based on findings in animal models of autoimmune optic nerve inflammation, we have assessed the safety and efficacy of erythropoietin in patients presenting with a first episode of optic neuritis. METHODS: Patients with optic neuritis who attended the University Hospitals of Homburg/Saar, Göttingen, or Hamburg (Germany) were included in this double-blind, placebo-controlled, phase 2 study (ClinicalTrials.gov, NCT00355095). They were randomly assigned to groups receiving either 33,000IU recombinant human erythropoietin intravenously daily for 3 days or placebo as an add-on therapy to methylprednisolone. The primary outcome parameter was change in retinal nerve fiber layer (RNFL) thickness after 16 weeks. Secondary outcome parameters included optic nerve atrophy as assessed by magnetic resonance imaging, and changes in visual acuity, visual field, and visual evoked potentials (VEPs). RESULTS: Forty patients were assigned to the treatment groups (21/19 erythropoietin/placebo). Safety monitoring revealed no relevant issues. Thirty-seven patients (20/17 erythropoietin/placebo) were analyzed for the primary endpoint according to the intention-to-treat protocol. RNFL thinning was less apparent after erythropoietin treatment. Thickness of the RNFL decreased by a median of 7.5µm by week 16 (mean ± standard deviation, 10.55 ± 17.54µm) compared to a median of 16.0µm (22.65 ± 29.18µm) in the placebo group (p = 0.0357). Decrease in retrobulbar diameter of the optic nerve was smaller in the erythropoietin group (p = 0.0112). VEP latencies at week 16 were shorter in erythropoietin-treated patients than in the placebo group (p = 0.0011). Testing of visual functions revealed trends toward an improved outcome after erythropoietin treatment. INTERPRETATION: These results give the first indications that erythropoietin might be neuroprotective in optic neuritis.

Motor strokes: the lesion location determines motor excitability changes.

BACKGROUND AND PURPOSE: The purpose of this research was to investigate the impact of lesion location on motor excitability and motor performance. METHODS: We studied patients with pure motor strokes in 4 different brain areas: motor cortex lesions (n=7), striatocapsular lesions (n=13), lacunar lesions of the internal capsule (n=13), and paramedian pontine lesions (n=10). Motor performance tests included the 9-hole-peg test and grip strength recordings. Motor excitability was determined by transcranial magnetic stimulation. Motor thresholds, stimulus-response curves, silent periods, motor cortical inhibition, and facilitation were investigated. RESULTS: The 4 groups were clinically similar but showed major differences in motor excitability. Only motor cortex lesions had a loss of intracortical inhibition in the affected hemisphere. In the internal capsule lesion group and the pontine lesion group, stimulus-response curves were depressed on the affected side. All of the subcortical lesions showed a prolongation of the silent period in the paretic side. Motor thresholds were predominantly elevated in the lesioned hemisphere of patients with internal capsule or pontine lesions. Motor performance was correlated with silent period duration in internal capsule lesions and with motor thresholds in internal capsule and pontine lesions. CONCLUSIONS: Motor cortex lesions exhibited deficient inhibitory properties. In contrast, subcortical lesions displayed an enhancement of inhibition. Internal capsule and pontine lesions affecting the corticospinal tract on different levels particularly impaired neuronal recruitment. Our results suggest that the lesion location determines a specific pattern of motor excitability changes.