arbon monoxide (CO) at low concentrations is an odorless and colorless gas with a molecular weight that is similar to that of air. It develops in incomplete combustion processes of substances containing carbon (e1). In addition to fires, defect gas boilers, or wood pellet storage facilities, the risk of poisoning as a result of smoking hookah has become a focus in recent years (1, e2). Relevant alerting key words and the use of portable CO meters are intended to raise awareness in rescue personnel.In the USA, 20 000-50 000 cases of carbon monoxide poisoning occur every year (2). Treatment for accidental carbon monoxide poisoning costs the US healthcare system some $1.3 billion every year (e3). For Germany, the only available data are those from the German Federal Statistical Office, for inpatients and deaths with a diagnosis of CO intoxication (T58 in ICD-10) (e4). In the USA, the total number of deaths due to CO poisoning fell between 1999 and 2014 (from 1967 cases to 1319 cases) (e5), whereas in Germany, numbers have steadily risen in recent years. In 2015, 648 patients died as a result of CO poisoning (0.8 deaths/100 000 population) (eTable). Fatality depends on exposure times to CO and its concentrations and is crucially affected by the toxicity of further gases involved (comparative case series [3]). PathophysiologyCarbon monoxide diffuses rapidly through the alveolar membrane and binds with an affinity that is 230-300 times that of oxygen, preferably to the iron ion in heme. Conformation changes lead to a leftward shift in the position of the oxyhemoglobin dissociation curve, to reduced oxygen transport capacity, and to reduced oxygen release into the peripheral tissue (2). Within tissue, CO also binds to other heme-containing proteins, such as skeletal and myocardial myoglobin. Since elimination times in tissue and blood differ (e7), tissue injury can also develop with a delay.At the cellular level, carbon monoxide leads-among others-to an activation of neutrophils, to a proliferation of lymphocytes, to mitochondrial dysfunction, and to lipid peroxidation (2, 4). The development of oxygen radicals, oxidative stress, inflammation, and apoptosis is comparable to a reperfusion injury and constitutes a substantial damage mechanism (2, 5, 6).

The investigated administration of gelatin and medium- and high-molecular-weight HES preparations did not influence respiratory burst activity under clinical conditions. However, the neutrophil respiratory burst was impaired after the administration of low-molecular-weight HES. Neutrophil respiratory burst activity may vary according to the type of colloidal plasma substitutes administered.

In an animal model of accidental hyperinfusion, BS-G1 showed the widest margin of safety and can therefore be expected to enhance patient safety in perioperative fluid management in children; HE-G5 proved significantly less safe; and G40 was found to be outright hazardous.

The airway management of children with mucopolysaccharidosis 1 remains critical, despite advances in both treatment and airway management techniques. Problems did not seem to increase as children grew older. We assume that technical improvements such as standardised use of the laryngeal mask airway or attached tube channel videolaryngoscopes as well as a stem cell transplantation treatment of the disease helped the management of older children with mucopolysaccharidosis 1.

Antiseptic coating of intravascular catheters may be an effective means of decreasing catheter-related colonization and subsequent infection. The purpose of this study was to assess the efficacy of chlorhexidine and silver sulfadiazine (CH-SS)-impregnated central venous catheters (CVCs) to prevent catheter-related colonization and infection in patients with hematological malignancies who were subjected to intensive chemotherapy and suffered from severe and sustained neutropenia. Proven CVC-related bloodstream infection (BSI) was defined as the isolation of the same species from peripheral blood culture and CVC tip (Maki technique). This randomized, prospective clinical trial was carried out in 106 patients and compared catheter-related colonization and BSI using a CH-SS-impregnated CVC (n=51) to a control arm using a standard uncoated triple-lumen CVC (n=55). Patients were treated for acute leukemia (n=89), non-Hodgkin's lymphoma (n=10), and multiple myeloma (n=7). Study groups were balanced regarding to age, sex, underlying diseases, insertion site, and duration of neutropenia. The CVCs were in situ a mean of 14.3+/-8.2 days (mean+/-SD) in the study group versus 16.6+/-9.7 days in the control arm. Catheter-related colonization was observed less frequently in the study group (five vs nine patients; p=0.035). CVC-related BSI were significantly less frequent in the study group (one vs eight patients; p=0.02). In summary, in patients with severe neutropenia, CH-SS-impregnated CVCs yield a significant antibacterial effect resulting in a significantly lower rate of catheter-related colonization as well as CVC-related BSI.