Prospective observational study of emergency airway management in the critical care environment of a tertiary hospital in Melbourne.

The objective of this study is to describe the population of patients receiving emergency airway management outside operating theatres at our institution, a tertiary referral centre in Melbourne. A registry of all patients receiving emergency airway management in the emergency department, ICU and on the wards as part of Medical Emergency Response teams' care, was prospectively collected. There were 128 adults and one paediatric patient requiring emergency airway management recruited to the study. Data for analysis included patient demographics, pre-oxygenation and apnoeic oxygenation, staff, drugs, details of laryngoscopic attempts, adjuncts, airway manoeuvres, complications sustained and method of confirmation of endotracheal tube placement. Over a 12-month period, there were 139 intubations of 129 patients, requiring a total of 169 attempts. Respiratory failure was the most common indication for intubation. Intubation was successful on the first episode of laryngoscopy in 116 (83.5%) patients. Complications occurred in 48 patients. In the cohort of patients without respiratory failure, nasal cannulae apnoeic oxygenation significantly reduced the incidence of hypoxaemia (0 out of 31 [0.0%] versus 10 out of 60 [16.7%], P=0.016; absolute risk reduction 16.7%; number needed to treat: 6). Waveform capnography was used to confirm endotracheal tube placement in 133 patients and there were four episodes of oesophageal intubation, all of which were recognised immediately. In the critical care environment of our institution, emergency airway management is achieved with a first-attempt success rate that is comparable to overseas data. Nasal cannulae apnoeic oxygenation appears to significantly reduce the risk of hypoxaemia in patients without respiratory failure and the use of waveform capnography eliminates episodes of unrecognised oesophageal intubation.

In vivo evolution of a novel, syncytium-inducing and cytopathic feline leukemia virus variant.

Studies of feline leukemia virus (FeLV) have illustrated the importance of the genotype of the infecting virus in determining disease outcome. In FeLV infections, as in other retroviral infections, it is less clear how virus variants that evolve from the transmitted virus affect pathogenesis. We previously reported an analysis of the genotypic changes that occur in the viral envelope gene (env) in cats infected with a prototype transmissible FeLV clone, 61E (J. Rohn, M. Linenberger, E. Hoover, and J. Overbaugh, J. Virol. 68:2458-2467, 1994). In one cat, each variant (81T) had evolved, in addition to scattered amino acid changes, a four-amino-acid insertion with respect to 61E. This insertion was located at the same site in the extracellular envelope glycoprotein where the immunodeficiency-inducing molecular clone 61C possesses a six-amino-acid insertion critical for its pathogenic phenotype, although the sequences of the insertions were distinct. To determine whether acquisition of the four-amino-acid insertion was associated with a change in the replication or cytopathic properties of the virus, we constructed chimeras encoding 81T env genes in a 61E background. One representative chimeric virus, EET(TE)-109, was highly cytopathic despite the fact that it replicated with delayed kinetics in the feline T-cell line 3201 compared to the parental 61E virus. The phenotype of this virus was also novel compared to other FeLVs, including both the parental virus 61E and the immunodeficiency-inducing variant 61C, because infection of T cells was associated with syncytium formation. Moreover, in single-cycle infection assays, the 81T-109 envelope demonstrated receptor usage properties distinct from those of both 61E and 61C envelope. Thus, these studies demonstrate the evolution of a novel T-cell cytopathic and syncytium-inducing FeLV in the host. The 81T virus will be valuable for dissecting the mechanism of T-cell killing by cytopathic variants in the FeLV model.