Comparing External Ventricular Drains-Related Ventriculitis Surveillance Definitions.

OBJECTIVE To evaluate the agreement between the current National Healthcare Safety Network (NHSN) definition for ventriculitis and others found in the literature among patients with an external ventricular drain (EVD) DESIGN Retrospective cohort study from January 2009 to December 2014 SETTING Neurology and neurosurgery intensive care unit of a large tertiary-care center PATIENTS Patients with an EVD were included. Patients with an infection prior to EVD placement or a permanent ventricular shunt were excluded. METHODS We reviewed the charts of patients with positive cerebrospinal fluid (CSF) cultures and/or abnormal CSF results while they had an EVD in place and applied various ventriculitis definitions. RESULTS We identified 48 patients with a total of 52 cases of ventriculitis (41 CSF culture-positive cases and 11 cases based on abnormal CSF test results) using the NHSN definition. The most common organisms causing ventriculitis were gram-positive commensals (79.2%); however, 45% showed growth of only 1 colony on 1 piece of media. Approximately 60% of the ventriculitis cases by the NHSN definition met the Honda criteria, approximately 56% met the Gozal criteria, and 23% met Citerio's definition. Cases defined using Honda versus Gozal definitions had a moderate agreement (κ=0.528; P<.05) whereas comparisons of Honda versus Citerio definitions (κ=0.338; P<.05) and Citerio versus Gozal definitions (κ=0.384; P<.05) had only fair agreements. CONCLUSIONS The agreement between published ventriculostomy-associated infection (VAI) definitions in this cohort was moderate to fair. A VAI surveillance definition that better defines contaminants is needed for more homogenous application of surveillance definitions between institutions and better comparison of rates. Infect Control Hosp Epidemiol 2017;38:574-579.

The relationship between oxygen and adenosine in astrocytic cultures.

Brain tissue oxygenation affects cerebral function and blood flow (CBF). Adenosine (Ado), a purine nucleoside, moderates neuronal activity, and arterial diameter. The cellular source of Ado in brain remains elusive; however, astrocytes are a logical site of production. Using astrocytic cultures, we tested the hypothesis that astrocytic derived Ado reflects cerebral oxygenation. We found that during alterations in pO(2), extracellular levels of Ado [Ado](e) changed rapidly. Graded reductions of oxygen tension revealed that[Ado](e) reached 10(-7) M to 10(-6) M with a pO(2) of 30-10mmHg, comparable with [Ado](e) and oxygen levels found in brain tissue during normoxemia. Higher O(2) levels were associated with a depression of [Ado](e). Under conditions of low pO(2) (pO(2)

Role of adenosine A2 receptors in regulation of cerebral blood flow during induced hypotension.

The mechanisms responsible for vascular autoregulation in the brain during changes in mean arterial blood pressure are ambiguous. Potentially, adenosine, a purine nucleoside and potent vasodilator, may be involved as earlier studies have documented an increase in brain adenosine concentrations with cerebral ischemia and hypotension. Consequently, we tested the hypothesis that adenosine is involved in vasodilatation during hypotension within the autoregulatory range (>50 mm Hg) by exposing adenosine 2a receptor (A2aR) knockout and wild type (WT) mice to short (2 to 5 mins) periods of hypotension. We found that autoregulation was significantly (P<0.05) impaired by 29% in A2a knockout mice as compared with WT animals. Furthermore, the A2R antagonist (A2a>A2b:10-85>1), ZM-241385, in a dose (1, 5, 10 mg/kg, intraperitoneally)-related manner, attenuated autoregulation in WT mice. In knockout mice treated with ZM-2413585 (5 and 10 mg/kg), autoregulation was further impaired indicating that A2b receptors also participated in cerebral vasodilatation. Treatment with dipyridamole (1.0 mg/kg) that increases extracellular concentrations of adenosine improved autoregulation in the A2aR knockout mice. We would conclude that adenosine through both A2a and A2b receptors is involved in physiologic vascular regulation during hypotension even within the autoregulatory range.

The role of adenosine in hypercarbic hyperemia: in vivo and in vitro studies in adenosine 2(A) receptor knockout and wild-type mice.

OBJECT: The authors tested the hypothesis that adenosine, acting through the A(2A) receptor, is not involved in hypercarbic hyperemia by assessing the effects of increased PaCO(2) on cerebral blood flow (CBF) in vivo in wild-type and A(2A) receptor knockout mice. In addition, they evaluated the effect of abluminal pH changes in vitro on the diameter of isolated perfused penetrating arterioles harvested from wild-type and A(2A) receptor knockout mice. METHODS: The authors evaluated in a blinded fashion the CBF response during transient (60-second) hypercapnic (7% CO(2)) hypercarbia in anesthetized, ventilated C57Bl/6 wild-type and adenosine A(2A) receptor knockout mice. They also evaluated the hypercarbic response in the absence and presence of the nonselective and selective adenosine antagonists. RESULTS: Cerebral blood flow was measured using laser Doppler flowmetry. There were no differences between the CBF responses to hypercarbia in the wild-type and the knockout mice. Moreover, the hypercarbic hyperemia response was not affected by the adenosine receptor antagonists. The authors also tested the response to alteration in abluminal pH in isolated perfused, pressurized, penetrating arterioles (average diameter 63.3 +/- 3.6 microm) harvested from wild-type (6 mice) and knockout (5 mice) animals. Arteriolar dilation in response to a decrease in abluminal pH, simulating the change in vivo during hypercarbia, was similar in wild-type (15.9 +/- 2.6%) and A(2A) receptor knockout (17.7 +/- 1.3%) mice. With abluminal application of CGS 21680 (10(-6) M), an A(2A) receptor agonist, wild-type arterioles dilated in an expected manner (9.8 +/- 0.7%), whereas A(2A) receptor knockout vessels had minimal response. CONCLUSIONS: The results of the in vivo and in vitro studies in wild-type and A(2A) receptor knockout mice support the authors' hypothesis that hypercarbic vasodilation does not involve an adenosine A(2A) receptor-related mechanism.