A hydrodynamic model is proposed to describe one of the most critical problems in intensive medical care units: the formation of biofilms inside central venous catheters. The incorporation of approximate solutions for the flow-limited diffusion equation leads to the conclusion that biofilms grow on the internal catheter wall due to the counter-stream diffusion of blood through a very thin layer close to the wall. This biological deposition is the first necessary step for the subsequent bacteria colonization.
Deep Dive into Hydrodynamics of catheter biofilm formation.
A hydrodynamic model is proposed to describe one of the most critical problems in intensive medical care units: the formation of biofilms inside central venous catheters. The incorporation of approximate solutions for the flow-limited diffusion equation leads to the conclusion that biofilms grow on the internal catheter wall due to the counter-stream diffusion of blood through a very thin layer close to the wall. This biological deposition is the first necessary step for the subsequent bacteria colonization.
Hydrodynamics of catheter biofilm formation
Oscar Sotolongo-Costa1,2, Manuel Arias-Zugasti3, Daniel Rodríguez-Pérez3, Sergio Martínez Escobar1,4,
Antonio Fernández-Barbero1
1Complex Fluids Physics Group, Department of Applied Physics, University of Almeria, 04120-Almeria, Spain.
2Cátedra de Sistemas Complejos “Henri Poincaré”. Universidad de La Habana, 10400, Cuba.
3Departamento de Física-Matemática y Fluidos, UNED, Madrid, Spain.
4 Intensive Care Unit. University Hospital Torrecardenas. Public Andalucian Health Service, 04009-Almeria, Spain.
Abstract
A hydrodynamic model is proposed to describe one of the most critical problems in intensive medical care
units: the formation of biofilms inside central venous catheters. The incorporation of approximate solutions for
the flow-limited-diffusion equation leads to the conclusion that biofilms grow on the internal catheter wall due
to the counter-stream diffusion of blood through a very thin layer close to the wall. This biological deposition
is the first necessary step for the subsequent bacteria colonization.
Introduction
Growing of microorganism in association with a surface is frequently named biofilm formation. It needs a
material substrate as demonstrated by the presence of non-infectious fibrin layers onto the catheters lumen. (1-
3) As the sole possibility of substrate formation comes from the accumulation of bood proteins, it is of special
importance the study of the mechanisms of catheter blood penetration (CBP).
From a clinical point of view, central venous catheterization use to cause undesired and critical
complications, being one of the most frequent the bloodstream infection.(4, 5) This process is strongly related
to the biological interactions between the catheter polymer surface and the bloodstream. These interactions
have been largely studied during the last decades, including those between polymers, polymers at interfaces
and scrambles polymer-cells-bacteria.(3, 6-10)
1
To our knowledge, despite the great deal of basic and applied information in literature about biological
colonization, there is not any realistic analysis about the first necessary process of protein migration, previous
to bacteria colonization.
In this paper we analyze several possible mechanisms for CBP formation, rejecting those impossible or out
of range. We also propose a physical model describing how blood penetrates into the catheter, which captures
the basic physical phenomenology under clinical practice conditions.
The main ideas
Two fluids have to be considered: a perfusion flow injected into the venous system trough a catheter,
composed by water and medical drugs and the blood at certain pressure trying to rise against the main
perfusion stream.
In a first approximation, the perfusion fluid dominates the general hydrodynamics at the catheter tip since
blood pressure into veins is not enough to overcome the perfusion pressure. However, there are several
mechanisms that could cause at least, partial bood rising against the perfusion flow. Capillarity due to surface
tension could force blood to ascend the catheter. This is only possible if the blood surface tension coefficient
largely overcomes that of the perfusion fluid. It never happens in our case since both coefficients are of the
same order of magnitude and the difference is not enough to surpass drag forces over the blood.
It is well known that a fluid flowing through a region bounded by walls exhibits a parabolic velocity
profile. The fluid velocity just on the walls is zero (or very low) while it reaches a maximum value at the
center. This velocity distribution is only true under laminar flow for which, dissipative forces dominate over
kinematic ones. The Reynolds number = vR/ ν accounts for this feature, where ν, v and R are the kinematic
viscosity, velocity and the tube radius, respectively. The flow becomes turbulent for Reynolds number > 1000
and the velocity distribution turns disordered. In the present case, a small lumen section, a low injection rate
and the value for kinematic viscosity of the perfusion fluid (water), warrant a laminar flow over all working
real conditions. The Reynolds number for the catheter and clinical conditions employed in this study is about
few tenths. Thus a laminar Poiseuille flow is warranted and phenomena as fluid entrainment, produced by a
boundary layer separation and/or turbulent diffusion are not expected.
Due to the parabolic profile of the flow, the velocities in the region near the wall are very low and,
consequently, blood can diffuse there without too much difficulty, whereas near the center of the cross section
2
the relative high velocities makes more difficult the upstream diffusion process. The extent to which this
happens will be examined in the next sections.
In fact, this phenomenon of diffusion under the influence of a field of velocities has been under study for a
long time since the pionee
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