Assessment of efficacy of postinfusion tubing flushing in reducing risk of cytotoxic contamination

2020 ◽  
Vol 77 (22) ◽  
pp. 1866-1873
Author(s):  
Pauline Claraz ◽  
Isabelle Riff ◽  
Charlotte Vert ◽  
Elina Wolff ◽  
Sophie Perriat ◽  
...  

Abstract Purpose Infusion of cytotoxic drugs carries the risk of occupational exposure of healthcare workers. Since disconnecting an infusion line is a source of contamination, flushing of tubing after infusion of cytotoxic agents is recommended, but the optimal volume of rinsing solution is unknown. The objective of this study was to assess whether postinfusion line flushing completely eliminates cytotoxics. Methods Infusions were simulated with 3 cytotoxics (gemcitabine, cytarabine, and paclitaxel) diluted in 5% dextrose injection or 0.9% sodium chloride injection in 250-mL infusion bags. Infusion lines were flushed using 5% dextrose injection or 0.9% sodium chloride solution at 2 different flow rates. The remaining concentration of cytotoxics in the infusion line was measured by a validated high-performance liquid chromatography (HPLC) method after passage of every 10 mL of flushing volume until a total of 100 mL had been flushed through. Results All cytotoxics remained detectable even after line flushing with 80 mL of flushing solution (a volume 3-fold greater than the dead space volume within the infusion set). Gemcitabine and cytarabine were still quantifiable via HPLC even after flushing with 100 mL of solution. Efficacy of flushing was influenced by the lipophilicity of drugs but not by either the flushing solvent used or the flushing flow rate. After 2-fold dead space volume flushing, the estimated amount of drug remaining in the infusion set was within 0.19% to 0.56% of the prescribed dose for all 3 cytotoxics evaluated. Conclusion Complete elimination of cytotoxics from an infusion line is an unrealistic objective. Two-fold dead space volume flushing could be considered optimal in terms of administered dose but not from an environmental contamination point of view. Even when flushed, the infusion set should still be considered a source of cytotoxic contamination.

Author(s):  
Santiago C. Arce ◽  
Fernando Chiodetti ◽  
Eduardo L. De Vito

1984 ◽  
Vol 64 (2) ◽  
pp. 505-543 ◽  
Author(s):  
J. M. Drazen ◽  
R. D. Kamm ◽  
A. S. Slutsky

Complete physiological understanding of HFV requires knowledge of four general classes of information: 1) the distribution of airflow within the lung over a wide range of frequencies and VT (sect. IVA), 2) an understanding of the basic mechanisms whereby the local airflows lead to gas transport (sect. IVB), 3) a computational or theoretical model in which transport mechanisms are cast in such a form that they can be used to predict overall gas transport rates (sect. IVC), and 4) an experimental data base (sect. VI) that can be compared to model predictions. When compared with available experimental data, it becomes clear that none of the proposed models adequately describes all the experimental findings. Although the model of Kamm et al. is the only one capable of simulating the transition from small to large VT (as compared to dead-space volume), it fails to predict the gas transport observed experimentally with VT less than equipment dead space. The Fredberg model is not capable of predicting the observed tendency for VT to be a more important determinant of gas exchange than is frequency. The remaining models predict a greater influence of VT than frequency on gas transport (consistent with experimental observations) but in their current form cannot simulate the additional gas exchange associated with VT in excess of the dead-space volume nor the decreased efficacy of HFV above certain critical frequencies observed in both animals and humans. Thus all of these models are probably inadequate in detail. One important aspect of these various models is that some are based on transport experiments done in appropriately scaled physical models, whereas others are entirely theoretical. The experimental models are probably most useful in the prediction of pulmonary gas transport rates, whereas the physical models are of greater value in identifying the specific transport mechanism(s) responsible for gas exchange. However, both classes require a knowledge of the factors governing the distribution of airflow under the circumstances of study as well as requiring detail about lung anatomy and airway physical properties. Only when such factors are fully understood and incorporated into a general description of gas exchange by HFV will it be possible to predict or explain all experimental or clinical findings.


1983 ◽  
Vol 55 (2) ◽  
pp. 472-478 ◽  
Author(s):  
V. Brusasco ◽  
T. J. Knopp ◽  
K. Rehder

During high-frequency small-volume ventilation (HFV), the transport rate of gas from the mouth to a lung region is a function of two conductances (conductance is the transfer rate of a gas divided by its partial pressure difference): regional longitudinal gas conductance along the airways (Grlongi) and gas conductance between lung regions (Ginter). Grlongi per unit regional lung (gas) volume [Grlongi/(Vr beta g)] was determined during HFV in 11 anesthetized paralyzed dogs lying supine. The distribution of Grlongi/(Vr beta g) was nearly uniform during HFV when stroke volumes were less than approximately two-thirds of the Fowler dead-space volume. By contrast, the distribution of Grlongi/(Vr beta g) was nonuniform when the stroke volume exceeded approximately two-thirds of the Fowler dead-space volume and the oscillation frequency was 5 Hz. Gas conductance along the airways per unit lung gas volume [average Glongi/(V beta g)], for the entire lung, increased with stroke volume at all frequencies, but for a given product of oscillation frequency and stroke volume, the average Glongi/(V beta g) was greater when stroke volume was large and oscillation frequency was low. The average Glongi/(V beta g) increased with frequency up to a maximal value; the frequency at which the maximum occurred depended on the kinematic viscosity of the inspired gas mixture.


2018 ◽  
Vol 51 (5) ◽  
pp. 1702251 ◽  
Author(s):  
Paolo Biselli ◽  
Kathrin Fricke ◽  
Ludger Grote ◽  
Andrew T. Braun ◽  
Jason Kirkness ◽  
...  

Nasal high flow (NHF) reduces minute ventilation and ventilatory loads during sleep but the mechanisms are not clear. We hypothesised NHF reduces ventilation in proportion to physiological but not anatomical dead space.11 subjects (five controls and six chronic obstructive pulmonary disease (COPD) patients) underwent polysomnography with transcutaneous carbon dioxide (CO2) monitoring under a metabolic hood. During stable non-rapid eye movement stage 2 sleep, subjects received NHF (20 L·min−1) intermittently for periods of 5–10 min. We measured CO2 production and calculated dead space ventilation.Controls and COPD patients responded similarly to NHF. NHF reduced minute ventilation (from 5.6±0.4 to 4.8±0.4 L·min−1; p<0.05) and tidal volume (from 0.34±0.03 to 0.3±0.03 L; p<0.05) without a change in energy expenditure, transcutaneous CO2 or alveolar ventilation. There was a significant decrease in dead space ventilation (from 2.5±0.4 to 1.6±0.4 L·min−1; p<0.05), but not in respiratory rate. The reduction in dead space ventilation correlated with baseline physiological dead space fraction (r2=0.36; p<0.05), but not with respiratory rate or anatomical dead space volume.During sleep, NHF decreases minute ventilation due to an overall reduction in dead space ventilation in proportion to the extent of baseline physiological dead space fraction.


2004 ◽  
Vol 97 (5) ◽  
pp. 1755-1762 ◽  
Author(s):  
Holger Schulz ◽  
Anne Schulz ◽  
Gunter Eder ◽  
Joachim Heyder

Carbon dioxide labeled with 18O (C18O2) was used as a tracer gas for single-breath measurements in six anesthetized, mechanically ventilated beagle dogs. C18O2 is taken up quasi-instantaneously in the gas-exchanging region of the lungs but much less so in the conducting airways. Its use allows a clear separation of phase II in an expirogram even from diseased individuals and excludes the influence of alveolar concentration differences. Phase II of a C18O2 expirogram mathematically corresponds to the cumulative distribution of bronchial pathways to be traversed completely in the course of exhalation. The derivative of this cumulative distribution with respect to respired volume was submitted to a power moment analysis to characterize volumetric mean (position), standard deviation (broadness), and skewness (asymmetry) of phase II. Position is an estimate of dead space volume, whereas broadness and skewness are measures of the range and asymmetry of functional airway pathway lengths. The effects of changing ventilatory patterns and of changes in airway size (via carbachol-induced bronchoconstriction) were studied. Increasing inspiratory or expiratory flow rates or tidal volume had only minor influence on position and shape of phase II. With the introduction of a postinspiratory breath hold, phase II was continually shifted toward the airway opening (maximum 45% at 16 s) and became steeper by up to 16%, whereas skewness showed a biphasic response with a moderate decrease at short breath holding and a significant increase at longer breath holds. Stepwise bronchoconstriction decreased position up to 45 ± 2% and broadness of phase II up to 43 ± 4%, whereas skewness was increased up to twofold at high-carbachol concentrations. Under all circumstances, position of phase II by power moment analysis and dead space volume by the Fowler technique agreed closely in our healthy dogs. Overall, power moment analysis provides a more comprehensive view on phase II of single-breath expirograms than conventional dead space volume determinations and may be useful for respiratory physiology studies as well as for the study of diseased lungs.


1997 ◽  
Vol 156 (6) ◽  
pp. 1834-1839 ◽  
Author(s):  
E. M. WILLIAMS ◽  
R. M. HAMILTON ◽  
L. SUTTON ◽  
J. P. VIALE ◽  
C. E. W. HAHN

2010 ◽  
Vol 111 (6) ◽  
pp. 1427-1431 ◽  
Author(s):  
Damien Lannoy ◽  
Bertrand Décaudin ◽  
Sophie Dewulf ◽  
Nicolas Simon ◽  
Alexandre Secq ◽  
...  

2015 ◽  
Vol 60 (9) ◽  
pp. 1247-1251 ◽  
Author(s):  
I. Amirav ◽  
A. S. Luder ◽  
A. Halamish ◽  
C. Marzuk ◽  
M. Daitzchman ◽  
...  

PLoS ONE ◽  
2015 ◽  
Vol 10 (12) ◽  
pp. e0146088
Author(s):  
Mawuena Binka ◽  
Elijah Paintsil ◽  
Amisha Patel ◽  
Brett D. Lindenbach ◽  
Robert Heimer

1984 ◽  
Vol 67 (5) ◽  
pp. 493-497 ◽  
Author(s):  
George Tatsis ◽  
Keith Horsfield ◽  
Gordon Cumming

1. The first four breaths from a multi-breath nitrogen wash-out have been analysed in 20 normal subjects by differentiation and data smoothing of phase II of the expired concentrations of nitrogen and carbon dioxide. 2. This procedure yields a distribution curve which is skewed to the right, the mode of which represents the usual value of dead space. The minimum and maximum values were found by excluding 2.5% of data points at each end of the distribution. 3. The values of minimum, mode and maximum in men were 67.6, 147 and 300 ml. For women the values were 55.4, 109 and 235 ml. 4. It is suggested that this distribution reflects the asymmetrical nature of the bronchial tree and comparison with anatomical data suggests that anatomy is the principal determinant of the distribution of dead space. 5. The contribution made by the spread of the stationary interface within individual bronchioles is evident but small.


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